Neurosurgical Operative Atlas 21

NEUROSURGICAL OPERATIVE ATLAS
Volume 2
Part 1
AANS Publications Committee
Editors SETTI S. RENGACHARY ROBERT H. WILKINS
The American Association of Neurological Surgeons
Contents
Volume I
Optic Gliomas. Edgar M. Housepian / 1-13 Fibrous Dysplasia Involving the Craniofacial Skeleton. James T. Goodrich, Craig D. Hall / 14-22 Depressed Skull Fracture in Adults. Fred H. Geisler / 23-33 Cervical Hemilaminectomy for Excision of a Herniated Disc. Robert H. Wilkins, Sarah J. Gaskill / 34-38 Lateral Sphenoid Wing Meningioma. Joseph Ransohoff / 39-45 Selective Microsurgical Vestibular Nerve Section for Intractable Mnires Syndrome. Edward Tarlov / 46-53 Chiari Malformations and Syringohydromyelia in Children. W. Jerry Oakes / 54-60 Carotid Body Tumors. Fredric B. Meyer, Thoralf M. Sundt, Jr. / 61-69 Olfactory Groove Meningiomas. Joshua B. Bederson, Charles B. Wilson / 70-78 Cerebral Aneurysms at the Bifurcation of the Internal Carotid Artery. Eugene S. Flamm / 79-88 Treatment of Unilateral or Bilateral Coronal Synostosis. John A. Persing, John A. Jane / 89-98 Convexity Meningioma. Sarah J. Gaskill, Robert H. Wilkins / 99-105 Occipital Lobectomy. Milam E. Leavens / 106-112 Spinal Meningiomas. Michael N. Bucci, Julian T. Hoff / 113-116 Percutaneous Trigeminal Glycerol Rhizotomy. Ronald F. Young / 117-123 Lumbar Hemilaminectomy for Excision of a Herniated Disc. Patrick W. Hitchon, Vincent C. Traynelis / 124-129 Transoral Surgery for Craniovertebral Junction Anomalies. Arnold H. Menezes / 130-135 Anterolateral Cervical Approach to the Craniovertebral Junction. Dennis E. McDonnell / 136-153 Correction of Malposition of the Orbits. John A. Persing / 154-163 Removal of Cervical Ossified Posterior Longitudinal Ligament at Single and Multiple Levels. Ralph B. Cloward / 164-170 Technique of Ventriculostomy. Joseph H. Piatt, Jr., Kim J. Burchiel / 171-175 Cerebellar Medulloblastoma. Arthur E. Marlin, Sarah J. Gaskill / 176-183 Shunting of a Posttraumatic Syrinx. David J. Gower / 184-190 Direct Surgical Treatment of Vein of Galen Malformations. Harold J. Hoffman / 191-200 Spinal Nerve Schwannoma. Phyo Kim, Burton M. Onofrio / 201-206 Combined Craniofacial Resection for Anterior Skull Base Tumors. Ehud Arbit, Jatin Shah / 207-217 Diagnostic Open Brain and Meningeal Biopsy. Richard P. Anderson, Howard H. Kaufman, Sydney S. Schochet / 218-222 Ventriculoperitoneal Shunting. David C. McCullough / 223-230 Ventriculoatrial Shunting. Paul J. Camarata, Stephen J. Haines / 231-239 Excision of Acoustic Neuromas by the Middle Fossa Approach. Derald E. Brackmann / 240-248 Upper Thoracic Sympathectomy by a Posterior Midline Approach. Prem K. Pillay, Issam A. Awad, Donald F. Dohn / 249-255 Carotid Endarterectomy. Daniel L. Barrow, Christopher E. Clare / 256-266 Transsphenoidal Excision of Macroadenomas of the Pituitary Gland.
NEUROSURGICAL OPERATIVE ATLAS: TABLE OF CONTENTS
George T. Tindall, Eric J. Woodard, Daniel L. Barrow / 267-278 Computer-Directed Stereotactic Resection of Brain Tumors. Patrick J. Kelly / 279-293 Sagittal Synostosis. A. Leland Albright / 294-300 Glossopharyngeal Rhizotomy. Burton M. Onofrio / 301-304 Occipitocervical and High Cervical Stabilization. Volker K.H. Sonntag, Curtis A. Dickman / 305-315 Petroclival Meningiomas. Ossama Al-Mefty, Michael P. Schenk, Robert R. Smith / 316-326 Facial Reanimation without the Facial Nerve. Mark May, Steven M. Sobol / 327-336 Omental and Musculocutaneous Free Flaps for Coverage of Complicated Neurosurgical Wounds. Daniel L. Barrow, Foad Nahai / 337-348 Repair of Growing Skull Fracture. Tadanori Tomita / 349-354 Occipital Encephaloceles. William O. Bell / 355-362 Foramen Magnum Meningiomas and Schwannomas: Posterior Approach. Chad D. Abernathey, Burton M. Onofrio / 363-371 Penetrating Wounds of the Spine. Edward C. Benzel / 372-378 Percutaneous Radiofrequency Rhizolysis for Trigeminal Neuralgia. James Fick, John M. Tew, Jr. / 379-390 Extended Costotransversectomy. Eddy Garrido / 391-396 Surgical Resection of Posterior Fossa Epidermoid and Dermoid Cysts. Lee Kesterson / 397-406 Luque Rod Segmental Spinal Instrumentation. Edward C. Benzel, / 407-412 En Bloc Anterior Temporal Lobectomy for Temporolimbic Epilepsy. Michel F. Levesque / 413-422 Cingulotomy for Intractable Pain Using Stereotaxis Guided by Magnetic Resonance Imaging. Samuel J. Hassenbusch, Prem K. Pillay / 423-432 Cerebellar Astrocytomas. A. Leland Albright / 433-439 Extreme Lateral Lumbar Disc Herniation. Robert S. Hood / 440-444 Tentorial Meningiomas. Laligam N. Sekhar, Atul Goel / 445-455
Volume II
Surgical Repair of Trigonocephaly. Ken R. Winston, Michael J. Burke / 1-8 Dorsal Root Entry Zone (DREZ) Lesioning. Blaine S. Nashold, Jr., Amr O. Ei-Naggar / 9-24 Ophthalmic Segment Aneurysms. Arthur L. Day / 25-41 Chronic Subdural Hematoma. James E. Wilberger, Jr. / 42-48 Tailored Temporal Lobectomy Using Subdural Electrode Grids. Issam A. Awad, Joseph F. Hahn / 49-55 Gunshot Wounds of the Brain. Suzie C. Tindall, Ali Krisht / 56-59 Transtorcular Occlusion of Vein of Galen Malformations. J. Parker Mickle, Ronald G. Quisling, Keith Peters / 60-66 Detection of an Epileptic Focus and Cortical Mapping Using a Subdural Grid. Sumio Uematsu / 67-78 Anteromesial Temporal Lobectomy for Epilepsy. Issam A. Awad, Prem K. Pillay / 79-87 Anastomosis of the Facial Nerve After Resection of an Acoustic Neuroma. Charles M. Luetje / 88-90 An Extended Subfrontal Approach to the Skull Base. Chandranath Sen, Laligam N. Sekhar / 91-100
Pansynostosis: Surgical Management of Multiple Premature Suture Closure. James T. Goodrich, Craig D. Hall / 101-112 Distal Anterior Cerebral Artery Aneurysms. H. Hunt Batjer, Duke Samson / 113-126 Tethered Spinal Cord, Intramedullary Spinal Lipoma, and Lipomyelomeningocele. W. Jerry Oakes / 127-135 Interstitial Brachytherapy. Jeffrey D. McDonald, Philip H. Gutin / 136-144 Lateral Extracavitary Approach to the Thoracic and Lumbar Spine. Dennis J. Maiman, Sanford J. Larson / 145-153 An Extreme Lateral Transcondylar Approach to the Foramen Magnum and Cervical Spine. Chandranath Sen, Laligam N. Sekhar / 154-162 Retrolabyrinthine Presigmoid Approach for Sectioning of the Vestibular Nerve for Mnires Disease. Charles M. Luetje / 163-166 Stereotactic Surgical Ablation for Pain Relief. Ronald F. Young / 167-177 Anterior Screw Fixation of Odontoid Fractures. Ronald I. Apfelbaum / 178-188 Carpal Tunnel Syndrome. Setti S. Rengachary / 189-199 Transantral Ethmoidal Orbital Decompression For Graves Ophthalmopathy. Lawrence W. DeSanto / 200-206 Middle Fossa Approaches for Invasive Tumors Involving the Skull Base. Laligam N. Sekhar, Atul Goel, Chandranath Sen / 207-218 Transthoracic Excision of a Spinal Metastasis with Vertebral Body Reconstruction. Gregory J. Bennett / 219-228 Anterior Cervical Discectomy and Fusion-the Cloward Technique. Ralph B. Cloward / 229-240 Cubital Tunnel Syndrome. Setti S. Rengachary / 241-245 Caspar Plating of the Cervical Spine. H. Louis Harkey, Wolfhard Caspar, Yaghoub Tarassoli / 246-256 Surgical Management of Anterior Communicating Artery Aneurysms. Timothy C. Ryken, Chistopher M. Loftus / 257-265 Basilar Bifurcation Aneurysm: Pterional (Transsylvian) Approach. H. Hunt Batjer, Duke S. Samson / 266-281 Thalamotomy for Tremor. Roy A. E. Bakay, Jerrold L. Vitek, Mahlon R. Delong / 282-295 Endovascular Treatment of Carotid Cavernous Fistulas. Arvind Ahuja, Lee R. Guterman, Kimberly Livingston, Leo N. Hopkins / 296-304 Combined Transsylvian and Middle Fossa Approach to Interpeduncular Fossa Lesions. Chandranath Sen, Laligam N. Sekhar / 305-311 Aneurysms of the Ophthalmic Segment of the Internal Carotid Artery. Daniel L. Barrow / 312-322 Lumbar-Peritoneal Shunting. Setti S. Rengachary / 323-333 Surgery of the Cavernous Sinus. Harry van Loveren, Magdy El-Kalliny, Jeffrey Keller, John M. Tew, Jr. / 334-344 Encephaloceles of the Anterior Cranial Base. Alan R. Cohen / 345-353 Cotrel-Dubousset Instrumentation: Internal Fixation for Thoracolumbar Fractures and Tumors. Bruce E. van Dam / 354-358 Posterior-Lateral Lumbar Spinal Fusion. Edward S. Connolly / 359-366 Correction of Exorbitism. Constance M. Barone, Ravelo V. Argamaso, David F. Jimenez, James T. Goodrich / 367-372 Meralgia Paresthetica. Setti S. Rengachary / 373-379 Depressed Skull Fracture in Infants. Lyn C. Wright, Marion L. Walker / 380-383 Combined Presigmoid-Transtransversarium Intradural Approach to the Entire Clivus and
Anterior Craniospinal Region. Mario Ammirati, Melvin Cheatham / 384-395 Partial Median Corpectomy with Fibular Grafting for Cervical Spondylotic Myelopathy. Setti S. Rengachary / 396-409 Correction of Orbital Hypertelorism and Orbital Dystopia. Constance M. Barone, David F. Jimenez, Ravelo V. Argamaso, James T. Goodrich / 410-416 Percutaneous Radiofrequency Rhizotomy for the Treatment of Paraplegic Spasms. Sumio Uematsu / 417-427 Endocrine-Inactive Pituitary Adenomas. Charles B. Wilson / 428-437 Posterior Decompression and Fusion for Cervical Spondylotic Myelopathy. Paul Kurt Maurer, Charles Nussbaum / 438-447 Surgical Correction of Swan Neck Deformity. Peter M. Klara, Kevin T. Foley / 448-461
Volume III
Tuberculum Sellae Meningiomas. Ossama Al-Mefty / 1-11 Craniofacial Techniques Used in Resection of Anterior Skull Base Tumors. James T. Goodrich, Ravelo V. Argamaso / 12-20 Occipital Transtentorial Approach to Pineal Region Neoplasms. James I. Ausman, Balaji Sadasivan / 21-26 Meningioma of the Lateral Ventricle. Edward Tarlov / 27-30 Preauricular-Infratemporal Fossa Approach to Tumors that Involve the Lateral Cranial Base. Robert L. Grubb, Peter G. Smith / 31-37 Repair of the Myelomeningocele. David G. McLone / 38-44 Anterior Clinoidal Meningiomas. Franco DeMonte, Ossama Al-Mefty / 45-57 Dandy-Walker Malformation. Arthur E. Marlin, Sarah J. Gaskill / 58-65 Acoustic Neuromas: Surgical Anatomy of the Suboccipital Approach. Martin B. Camins, Jeffrey S. Oppenheim / 66-75 Exposure of the Skull Base via the Midface. James T. Goodrich, Sidney Eisig, George J. Cisneros, Allen B. Kantrowitz / 76-83 Exposure of the Skull Base by Transoral, Translabial, and Transmandibular Routes. James T. Goodrich, Sidney Eisig, Joseph G. Feghali, Allen B. Kantrowitz / 84-93 Surgical Management of Chiari I Malformations and Syringomyelia. Richard B. Morawetz / 94-102 Open-Door Maxillotomy Approach for Lesions of the Clivus. H. Louis Harkey, Vinod K. Anand, H. Alan Crockard, Michael P. Schenk / 103-112 Peripheral Nerve Repair. Allan J. Belzberg, James N. Campbell / 113-128 Surgical Management of Split Cord Malformations. Dachling Pang / 129-143 Tethered Cord Syndrome Secondary to Previous Repair of a Myelomeningocele. Timothy A. Strait / 144-150 Craniofacial Techniques for Managing Orbital Trauma. James T. Goodrich, Simeon A. Lauer, Ravelo V.Argamaso / 151-158 Transoral-Transclival Approach to Basilar Artery Aneurysms. R. A. de los Reyes, Paul W. Detwiler / 159-166 Frontal Lobectomy. Setti S. Rengachary / 167-175 Thoracic Outlet Syndrome: Supraclavicular First Rib Resection and Brachial Plexus Decompression. Susan E. Mackinnon, G. A. Patterson / 176-182 Transfacial Approaches to the Clivus and Upper Cervical Spine. Ivo P. Janecka / 183-192 Surgical Management of Prolactinomas. Andrew D. Parent / 193-202
Sectioning of the Filum Terminale. Frederick A. Boop, William M. Chadduck / 203-209 Repair of Diastematomyelia. Frederick A. Boop, William M. Chadduck / 210-214 Repair of a Lipomyelomeningocele. Frederick A. Boop, William M. Chadduck / 215-219 Untethering of the Spinal Cord After a Previous Myelomeningocele Repair. Frederick A. Boop, William M. Chadduck / 220-224 Secondary Carpal Tunnel Syndrome. Susan E. Mackinnon / 225-234 Spheno-Orbital Craniotomy for Meningioma. Joseph C. Maroon, John S. Kennerdell, Danko V. Vidovich / 235-243 Surgical Treatment of Anterior Sacral Meningocele. K. Stuart Lee / 244-251 Acrylic Cranioplasty. Setti S. Rengachary / 252-259 Preauricular Transzygomatic Infratemporal Craniotomy for Skull Base Tumors. Stephen L. Ondra, Michael G. Donovan / 260-269 Medial Sphenoid Ridge Meningiomas. Vallo Benjamin, Jules M. Nazzaro / 270-282 Surgical Treatment of Arteriovenous Malformations of the Cerebral Convexity. Wink S. Fisher III / 283-291 Lumbar Microdiscectomy. Peter M. Klara, Kevin T. Foley / 292-301 Microvascular Decompression of the Facial Nerve. Robert H. Wilkins / 302-311 Craniofacial Resection of Neoplasms of the Anterior Skull Base. Vincent C. Traynelis, Timothy M. McCulloch, Henry T. Hoffman / 312-323 Postlaminectomy Instability: Posterior Procedures. Seth M. Zeidman, Thomas B. Ducker / 324-336 Vertebral Artery and Posterior Inferior Cerebellar Artery Aneurysms: Surgical Management. Fernando G. Diaz, Richard D. Fessler / 337-343 Anterior Cervical Discectomy and Fusion: Smith-Robinson Technique. Philip R. Weinstein / 344-358 Management of Basilar and Posterior Cerebral Artery Aneurysms by Subtemporal Approaches. Robert M. Crowell, Christopher S. Ogilvy / 359-374 Subcutaneous Transposition of the Ulnar Nerve for Tardy Ulnar Palsy. Melvin L. Cheatham, Fredric L. Edelman, Martin Holland / 375-381 Image-Guided Neurosurgery: Frame-Based and Frameless Approaches. Lucia Zamorano, Lutz Nolte, Charlie Jiang, Majeed Kadi / 482-401 Anterior Stabilization of the Cervical Spine Using a Locking Plate System. Setti S. Rengachary / 402-413 Endoscopic Neurosurgery. Alan R. Cohen / 414-426 Surgical Management of Brain Abscess. Timothy C. Ryken, Christopher M. Loftus / 427-435 Submuscular Transposition of the Ulnar Nerve at the Elbow: Musculofascial Lengthening Technique. A. Lee Dellon / 436-443 Superficial Temporal Artery to Middle Cerebral Artery Bypass Grafting. Issam A. Awad / 444-456
Volume IV
Spinal Vascular Malformations. Edward H. Oldfield / 1-18 Posterior C1-2 Screw Fixation for Atlantoaxial Instability. Ronald I. Apfelbaum / 19-28 Supracerebellar Infratentorial Approaches to the Pineal Region. Michael L. Levy, Michael L. J. Apuzzo / 29-36 Third-Ventricle Exposure by the Interhemispheric Corridor. Peter Gruen, Michael L. J. Apuzzo / 37-42
Arteriovenous Malformations of the Basal Ganglia, Thalamus, and Adjacent Ventricles. Ghaus M. Malik, Fady T. Charbel / 43-58 Selective Denervation for Spasmodic Torticollis. Antonio A. F. DeSalles / 59-66 Unilateral Coronal Synostosis. James T. Goodrich, Ravelo Argamaso / 67-74 Neurosurgical Approaches to the Orbit. Part 1: Orbital Anatomy and Lateral Orbitotomy. Johnny B. Delashaw, Jr. / 75-84 Neurosurgical Aproaches to the Orbit. Part 2: Craniotomy for Surgical Exposure of the Orbit. Johnny B. Delashaw, Jr. / 85-94 Fourth Ventricular Ependymoma. J. Gordon McComb, John H. Schneider / 95-106 Sectioning of the Corpus Callosum for Epilepsy. Issam A. Awad / 107-116 Surgical Treatment of Intracranial Glomus Tumors. Vinod K. Anand, Michael P. Schenk, John P. Leonetti, Ossama Al-Mefty / 117-130 Technique of Temporal Lobectomy. Allen R. Wyler / 131-138 Treatment of Moyamoya Syndrome in Children with Pial Synangiosis. Richard G. Ellenbogen, R. Michael Scott / 139-146 Isthmic Spondylolysis and Spondylolisthesis: Treatment by Reduction, Interbody Fusion, and Lateral Stabilization. Timothy C. Wirt / 147-158 Translabyrinthine Removal of Acoustic Neuromas. John T. McElveen, Jr. / 159-164 Transsphenoidal Surgical Treatment of Cushings Disease. William F. Chandler / 165-172 Upper Thoracic Spinal Exposure Through a Lateral Parascapular Extrapleural Approach. Richard G. Fessler, Donald Dietze, David Peace / 173-182 Selective Dorsal Rhizotomy for the Spasticity of Cerebral Palsy. T. S. Park / 183-190 Surgical Treatment of the Subclavian Steal Syndrome. George E. Pierce / 191-198 Surgery for Tumors Affecting the Cavernous Sinus. Franco DeMonte, Vinod K. Anand, Ossama Al-Mefty / 199-208 Lambdoidal Synostosis. David F. Jimenez, Constance M. Barone, Ravelo V. Argamaso, James T. Goodrich / 209-214 Gamma Knife Radiosurgery of Intracranial Lesions. Robert J. Coffey / 215-224 Submuscular Transposition of the Ulnar Nerve at the Elbow. Susan E. Mackinnon / 225-234 Ulnar Nerve Entrapment at the Wrist. V. Leroy Young, Jill M. Young / 235-249
Volume V
Endoscopic Pituitary Surgery. Hae-Dong Jho, Ricardo L. Carrau, Yong Ko / 1-12 Torcular and Peritorcular Meningiomas. Griffith R. Harsh IV / 13-22 Surgical Resection of Lower Clivus-Anterior Foramen Magnum Meningioma. Vallo Benjamin, Ramesh P. Babu / 23-32 Basilar Bifurcation Aneurysms: Transsylvian Transclinoidal Transcavernous Approach. Murali Guthikonda, Fernando G. Diaz / 33-42 Surgical Management of Posterior Plagiocephaly. Richard G. Ellenbogen, Michael H. Mayer / 43-56 Acute Subdural Hematoma. Fred H. Geisler / 57-64 Intracranial Pressure Monitoring. Andrew D. Firlik, Donald W. Marion / 65-74 Temporal Lobectomy Under General Anesthesia. Diana L. Abson Kraemer, Dennis D. Spencer / 75-84 Far-Lateral Disc Herniation Treated by Microscopic Fragment Excision. Bruce V. Darden II, J. Robinson Hicks / 85-90 Stabilization of the Cervical Spine (C3-7) with Articular Mass (Lateral Mass) Plate and
Screws. T. Glenn Pait, Luis A. B. Borba / 91-100 Stabilization of the Cervical Spine with the Orion Anterior Cervical Plate System. Gary L. Lowery / 101-108 Texas Scottish Rite Hospital System for Internal Stabilization of Thoracolumbar Fractures. Bradford M. Mullin, Gary L. Rea / 109-120 Application of Frameless Stereotaxy in the Management of Intracranial Lesions. Dennis A. Turner, Paul B. Johnson / 121-128 A Modified Transfacial Approach to the Clivus. Brooke Swearingen, Michael P. Joseph, Matthew Cheney, Robert G. Ojemann / 129-134 Management of the Vertebral Artery During Excision of Extradural Tumors of the Cervical Spine. Chandranath Sen, Mark Eisenberg / 135-142 Posteroventral Pallidotomy for Patients with Parkinsons Disease. Robert P. Iacono, Shokei Yamada / 143-154 Functional Hemispherectomy. Joseph R. Smith, Mark R. Lee / 155-164 Microsurgical Decompresson of the Root Entry Zone for Trigeminal Neuralgia. Chandranath Sen / 165-170 The Anterior Cervical Approach to the Cervicothoracic Junction. Julian K. Wu / 171-176 Management of Extradural Non-Neoplastic Lesions of the Craniovertebral Junction via the Transcondylar Approach. Luis A. B. Borba, Ossama Al-Mefty, T. Glenn Pait, Ronald Tribell / 177-184 Far Lateral Lumbar Disc Herniation. Nancy E. Epstein, Joseph A. Epstein / 185-198 Repair and Reconstruction of Scalp and Calvarial Defects. Warren Schubert, Jeffrey Aldridge / 199-218 Sagittal Synostosis. Larry A. Sargent, Timothy A. Strait / 219-226 Microsurgical Lumbar Decompression Using Progressive Local Anesthesia. Stephen D. Kuslich / 227-232 Banked Fibula, the Locking Anterior Cervical Plate, and Allogeneic Bone Matrix in Anterior Cervical Fusions Following Cervical Discectomy. Scott Shapiro / 233-240 Endoscopic Third Ventriculostomy for Obstructive Hydrocephalus. Jonathan J. Baskin, Kim H. Manwaring / 241-246
Volume VI
Treatment of Carotid-Cavernous Sinus Fistulas Using a Superior Ophthalmic Vein Approach. Neil R. Miller, Lee H. Monsein, Rafael J. Tamargo / 1-4 The Separation of Craniopagus Twins. Harold J. Hoffman, James T. Rutka / 5-12 Posteroventral Pallidotomy for Parkinsons Disease Patients. Kim J. Burchiel, Jamal M. Taha, Jacques Favre / 13-26 Microelectrode-Guided Pallidotomy. Andres M. Lozano, William D. Hutchison / 27-34 Anterolateral Transforaminal Approach for a Large Dumbbell-Shaped Cervical Neurinoma. Isao Yamamoto / 35-42 Bridge Bypass Coaptation for Cervical Nerve Root Avulsion. Shokei Yamada, Russell R. Lonser, Robert P. Iacono / 43-50 Sinus Skeletonization Technique: A Treatment for Dural Arteriovenous Malformations at the Tentorial Apex. Evandro De Oliveira, Helder Tedeschi / 51-56 Microsurgical Carotid Endarterectomy. Julian E. Bailes, Patrick P. Flannagan / 57-64 Endoscopic Approaches to the Ventricular System. David F. Jimenez / 65-74 Surgical Management of Cranial Dural Arteriovenous Fistulas. Lokesh S. Tantuwaya, Julian E. Bailes / 75-84
Intraventricular Endoscopy: Diagnostic Ventriculoscopy, Tissue Biopsy, Cyst Fenestration, and Shunting. Jonathan J. Baskin, Kim H. Manwaring / 85-98 Endoscopic Carpal Tunnel Release Through a Monoportal Approach. Jay Menon / 99-108 Endoscopic Excision of Colloid Cysts. Jonathan J. Baskin, Kim H. Manwaring / 109-114 Surgical Anatomy of the Temporal Lobe. Steven N. Roper / 115-124 Multiple Subpial Transection. Walter W. Whisler / 125-130 Stereotactic Depth Electrode Implantation in the Evaluation of Candidates for Ablative Epilepsy Surgery. Joseph R. Smith, Mark R. Lee / 131-146 Trans-Sulcal Approach to Mesiotemporal Lesions. Isabelle M. Germano / 147-156 Anterior Cervical Spine Stabilization with the Codman Locking Plate System. R. John Hurlbert, Volker K. H. Sonntag / 157-166 Posterior Cervical Fusion with Tension Band Wiring. Thomas J. Lovely / 167-172 Primary Anterior Treatment of Thoracolumbar Burst Fractures. David W. Polly, Jr., Richard G. Ellenbogen / 173-182 Technique for Reduction of Spondylolisthesis Using Custom Texas Scottish Rite Hospital Forceps. Gary L. Lowery, David A. Fernandez, Atul L. Bhat, A. Eugene Pennisi / 183-192 Surgical Management of Infected Ventriculoperitoneal Shunt. Timothy M. George, Sohaib A. Kureshi / 193-200 Combined Fronto-Orbital and Occipital Advancement for Total Calvarial Reconstruction. Ian F. Pollack, H. Wolfgang Losken / 201-212 Repair of Meningoceles. Timothy M. George, Eric M. Gabriel / 213-220 Installation of a Dorsal Column Stimulator for Pain Relief. John P. Gorecki / 221-236 Implantation of Drug Infusion Pumps. John P. Gorecki / 237-250 Stereotactic Microsurgical Craniotomy for the Treatment of Third Ventricular Colloid Cysts. Kyle L. Cabbell, Donald A. Ross / 251-256 Hemispherectomy. Benjamin S. Carson, Aaron L. Zuckerberg / 257-264
Volume VII
Posterior Lumbar Interbody Fusion Augmented With the Ray Threaded Fusion Cage. Peter Klara, Berkley Rish, Charles D. Ray / 1-10 Total Sacrectomy. Ziya L. Gokaslan, Marvin M. Romsdahl, Stephen S. Kroll, Theresa A. Gillis, David W. Wildrick, Milam E. Leavens / 11-20 Treatment of Fractures at the Thoracolumbar Junction with Kaneda Anterior Spinal Instrumentation System. Seth M. Zeidman, Randy F. Davis / 21-28 Cannulated Screws for Odontoid and Atlantoaxial Transarticular Screw Fixation. Curtis A. Dickman, R. John Hurlbert / 29-42 Anterior Microforaminotomy for Cervical Radiculopathy: Disc Preservation Technique. Hae-Dong Jho / 43-52 Pedical Subtraction and Lumbar Extension Osteotomy for Iatrogenic Flatback. Gary L. Lowery, Atul L. Bhat, A. Eugene Pennisi / 53-58 The Surgical Treatment of Dolichoectactic and Fusiform Aneurysms. Michael T. Lawton, John A. Anson, Robert F. Spetzler / 59-68 Petrosal Approach for Resection of Petroclival Meningiomas. William T. Couldwell / 69-82 Surgical Resection of Esthesioneuroblastoma. Scott L. Henson, John A. Jane, Sr. / 83-92 Stereotactic Radiosurgery of the Trigeminal Nerve Root for Treatment of Trigeminal Neuralgia. Ronald F. Young / 93-98 Techniques of Peripheral Neurectomy for Control of Trigeminal Neuralgia. Raj Murali / 99-106
Percutaneous Balloon Compression for the Treatment of Trigeminal Neuralgia. Jeffrey A. Brown, Jan J. Gouda / 107-116 Microvascular Decompression for Hemifacial Spasm. Thomas J. Lovely / 117-124 Thalamic Deep Brain Stimulation for the Control of Tremor. Andres Lozano / 125-134 Magnetic Resonance Image-Guided Stereotactic Cingulotomy for Intractable Psychiatric Disease. Osama S. Abdelaziz, G. Rees Cosgrove / 135-140 Magnetic Resonance Image-Guided Pallidotomy. Antonio A.F. De Salles, Marwan Hariz / 141-148 Endoscopic Carpal Tunnel Release via a Biportal Approach. David F. Jimenez / 149-156 Thoracic Sympathectomy. J. Patrick Johnson, Samuel S. Ahn / 157-162 Blood Flow-Monitored Transthoracic Endoscopic Sympathectomy. Ricardo Segal, Peter M. Ferson, Edwin Nemoto, Sidney K. Wolfson Jr. / 163-172 Surgical Management of Craniopharyngiomas. Harold J. Hoffman / 173-182 Surgical Resection of Craniopharyngiomas. Ali F. Krisht, Ugur Tre / 183-190 Optic Nerve Sheath Fenestration in the Management of Pseudotumor Cerebri. Eric L. Berman, Jonathan D. Wirschafter / 191-200 Surgical Correction of Unilateral and Bilateral Coronal Synostosis. Ann Marie Flannery, Jack C. Yu / 201-210 Tethered Cord Syndrome: Management of Myelomeningocele, Diastematomyelia, and Hypertrophied Filum Terminale. Robert F. Keating, James Tait Goodrich / 211-218 Tethered Cord Syndrome: Management of Lipomyelomeningoceles. James Tait Goodrich / 219-226 Excision of Colloid Cyst via the Transcallosal Approach. Deepak Awasthi, John J. Kruse / 227-234 Laparoscopy Assisted Lumboperitoneal Shunt Placement in the Management of Pseudotumor Cerebri. Florence C. Barnett, Dennis E. McConnell / 235-240 The Transparaspinal Approach to Dumbbell-Shaped Spinal Tumors. Stephen T. Onesti, Ely Ashkenazi, W. Jost Michelsen / 241-248 Posterior Occipito-axial Fusion for Atlantoaxial Dislocation Associated with Occipitalized Atlas. Vijendra K. Jain, Sanjay Behari / 249-256 Evaluation and Management of Severe Facial Nerve Injury Resulting From Temporal Bone Trauma. Aijaz Alvi / 257-260
Volume VIII
Surgical Management of Paraclinoid Carotid Aneurysms. Murali Guthikonda, Fernando G. Diaz / 1-12 Surgical Management of Middle Cerebral Artery Aneurysms. Philip E. Stieg, Robert M. Friedlander / 13-22 Surgical Removal of Tentorial and Posterior Fossa Dural Arteriovenous Malformations. Adam I. Lewis, John M. Tew Jr. / 23-34 Surgical Resection of the Arteriovenous Malformations of the Posterior Fossa. Thomas Kopitnik, Duke Samson, Michael Horowitz / 35-46 Surgical Treatment of Arteriovenous Malformations of the Ventricular Trigone. Daniel L. Barrow, Roger H. Frankel / 47-56 Dural Arteriovenous Malformations of the Transverse and Sigmoid Sinuses. Todd A. Kuether, Gary M. Nesbit, Stanley L. Barnwell / 57-68
Operative Management of Anterior Fossa, Superior Sagittal Sinus, and Convexity Dural Arteriovenous Malformations. Aman B. Patel, Wesley A. King, Neil A. Martin / 69-78 Use of the Operating Arm System in Skull Base Surgery. Jeffrey J. Larson, Ronald E. Warwick, John M. Tew Jr. / 79-86 The Orbitocranial Zygomatic Approach to Aneurysms of the Upper Basilar Trunk. T. C. Origitano / 87-94 Extradural Approaches for Resection of Trigeminal Neurinomas. J. Diaz Day / 95-106 Surgical Management of Trigeminal Schwannomas. Madjid Samii, Ramesh Pitti Babu, Marcos Tatagiba / 107-120 Surgical Management of Cholesterol Granulomas of the Petrous Apex. Mark B. Eisenberg, Ossama Al-Mefty / 121-126 Surgical Management of Angiographically Occult Vascular Malformations of the Brainstem, Thalamus, and Basal Ganglia. Gary K. Steinberg, Steven D. Chang / 127-134 Management of Jugular Foramen Tumors. Jeffrey Bruce, Ian Storper / 135-142 Surgical Management of Esthesioblastomas. Ramesh Pitti Babu, Mark S. Persky / 143-152 Surgical Treatment of Brainstem Gliomas. Mark R. Lee, Michael Cowan / 153-160 Brainstem Gliomas. Harold J. Hoffman / 161-170 The Contralateral Transcallosal Approach to Lesions In or Adjacent to the Lateral Ventricle. Michael T. Lawton, Robert F. Spetzler / 171-178 Posterior Fossa Decompression Without Dural Opening for the Treatment of Chiari I Malformation. Jonathan Sherman, Jeffrey J. Larson, Kerry R. Crone / 179-184 Computed Tomography-Assisted Preformed Prosthesis for Repair of Cranial Defects. Manuel Dujovny, Celso Agner, Fady T. Charbel, Lewis L. Sadler, Raymond Evenhouse, Dierdre McConathy / 185-194 Chronic Subthalamic Nucleus Stimulation for Parkinsons Disease. Ali R. Rezai, William Hutchison, Andres M. Lozano / 195-208 Arthroscopic Microlumbar Discectomy. Kenneth F. Casey, Parviz Kambin, Marc Chang / 209-216 Excision of Herniated Thoracic Disc Via the Transthoracic Approach. Mary Louise Hlavin, Russell W. Hardy / 217-224 Surgical Management of Advanced Degenerative Disease of the Lumbar Spine with Multiplanar Deformity. Michael F. OBrien, Gary L. Lowery, A. Eugene Pennisi / 225-234 The Retropleural Approach to the Thoracic and Thoracolumbar Spine. Theodore H. Schwartz, Paul C. McCormick / 235-242 Surgical Treatment of Lateral Lumbar Herniated Discs. Giuseppe Lanzino, Christopher I. Shaffrey, John A. Jane, Sr. / 243-252 Trap Door Exposure of the Cervicothoracic Junction. Ziya L. Gokaslan, Garrett L. Walsh / 253-260 Peripheral Nerve Suture Techniques. Rajiv Midha, Margot Mackay / 261-269
A
Ablative epilepsy surgery, 6:131-146 Acoustic neuromas, 4:159-164 Acrylic cranioplasty, 5:214-215 Acute subdural hematoma, 5:57-63 Allogeneic bone matrix, 5:233-239 Aneurysms basilar bifurcation, 5:33-42 broad-based siphon, 8:3-4; 8:10-11 carotid cave, 8:3-4 carotid ophthalmic, 8:2-3; 8:10-11 carotid-superior hypophyseal, 8:3-4 dolichoectatic, 7:59-67 fusiform, 7:59-67 middle cerebral artery, 8:13-22 paraclinoid carotid artery, 8:1-12 superior hypophyseal, 8:1-2; 8:10-11 upper basilar trunk, 8:87-94 ventral paraclinoid, 8:3-4; 8:10-11 Angiographically occult vascular malformations, 8:127-133 Angioma, cavernous, 4:13-18 Anterior cervical spine discectomy, 5:233-239 implant systems, 5:101-108 stabilization, 6:157-166 Anterior foramen magnum meningioma, 5:23-32 Anterior fossa dural AVMs, 8:69-78 Anterior microforaminotomy, 7:43-52 Apert syndrome, 7:201 Arteriovenous fistulas (AVFs) cranial dural, 6:75-84 dural, 4:3-7; 6:51-56 intradural, 4:11-16 perimedullary, 4:11-13 Arteriovenous malformations (AVMs) anterior fossa, 8:69-78 basal ganglia, 4:43-58 cerebellar hemisphere, 8:36; 8:40-42 cerebellar tonsil, 8:36; 8:43-44 cerebellar vermis, 8:35-36, 8:38-40 deep parenchymal, 8:36 dural, 8:23-34; 8:69-79 glomus, 4:9-10 juvenile, 4:8-10 posterior fossa, 8:23-46 spinal cord, 4:7-10
superior sagittal sinus dural, 8:69-78 tentorial dural, 8:23-34 thalamic, 4:43-58 upper basilar trunk, 8:87 ventral paraclinoid, 8:3-4; 8:10-11 ventricular trigone, 8:47-56 Astrocytomas brainstem, 8:162; 8:164; 8:165-169 craniocervical, 8:169-170 Atlantoaxial dislocation with occipitalized atlas, 7:249-256 Atlantoaxial instability, C1-2 screw fixation, 4:19-28 Atlantoaxial transarticular screw fixation, 7:29-41
A B C D E F G H I J K L M N O P Q R S T U V W X Y Z
B
Banked fibula, 5:233-239 Basal ganglia AVMs, 4:43-58 Basilar bifurcation aneurysms, 5:33-42 Bilateral coronal synostosis, 7:201-210 Birth defects, 5:219-225 Bone graft harvesting fractures, 7:24-25 atlantoaxial dislocation, 7:251-254 calvarial defects, 5:199-217; 6:201-211 posterior lumbar interbody fusion, 7:6-10 Bone-wiring procedures, 5:91-100 Brainstem AVMs, 8:36; 8:43; 8:45-46 craniocervical astrocytomas, 8:169-170 dorsally exophytic gliomas, 8:161-163 diffuse intrinsic astrocytomas, 8:162; 8:164 focal intrinsic astrocytomas, 8:165-169 gliomas, 8:153-159 Bridge bypass coaptation, 6: 43-50 Broad-based siphon aneurysms, 8:3-4; 8:10-11 Burst fractures, 5:110; 6:173-182
C
Callostomy, 7:227-233 Calvarial defects, 5:199-217 Calvarial reconstruction, 6:201-211 Cannulated screws, 7:29-41
Carotid cave aneurysms, 8:3-4 Carotid endarterectomy, 6:57-64 Carotid-cavernous sinus fistulas, 6:1-4 Carotid ophthalmic aneurysms, 8:2-3; 8:10-11 Carotid-superior hypophyseal aneurysms, 8:3-4 Carpal tunnel syndrome, 6:99-108; 7:149-156 Cavernous angiomas, 4:13-18 Cavernous sinus tumors, 4:199-207 Cerebellar hemisphere AVMs, 8:36; 8:40-42 Cerebellar tonsil AVMs, 8:36; 8:43-44 Cerebellar vermis AVMs, 8:35-36; 8:38-40 Cerebral palsy, 4:183-190 Cervical fusion, 5:233-239; 6:167-171 Cervical nerve root avulsion, 6:43-50 Cervical neurinoma, 6:35-41 Cervical radiculopathy, 7:43-52 Cervical spine C1-2 screw fixation, 4:19-28 degenerative disc disease, 7:43-52 discectomy, 5:233-239 extradural tumors, 5:135-141 implant systems, 5:101-108 stabilization, 6:157-166 stabilization (articular mass), 5:91-100 stabilization (Orion system), 5:101-108 Chiari I malformation, 8:179-183 Children cerebral palsy, 4:183-190 moyamoya syndrome, 4:139-146 Cholesterol granulomas of petrous apex, 8:121-125 Chondrosarcoma, 5:129 Cingulotomy for psychiatric disease, 7:135-140 Clivus, 5:129-133 Codman locking plate system, 6:157-166 Colloid cyst, 6:109-114; 6:251-256; 7:227-233 Complex spinal schwannomas, 7:241-242 Convexity dural AVMs, 8:69-78 Coronal synostosis, 4:67-73; 6:201-211; 7:201-210 Corpus callosum sectioning, 4:38-39; 4:107-116 Cranial defects, 8:185-194 Cranial dural arteriovenous fistulas,
6:75-84 Craniocervical brainstem astrocytomas, 8:169-170 Craniopagus twins, 6:5-11 Craniopharyngiomas, 7:173-181; 7:183-190 Craniovertebral junction lesions, 5:177-184 Crouzons syndrome, 7:201 Cubital tunnel syndrome, 4:235-249 Cushings disease, 4:165-172 Cyst colloid, 6:109-114; 6:251-256; 7:227-233 fenestration, 6:85-98
D
Decompressive corpectomy, 5:101 Deep brain stimulation control of tremor, 7:125-134 subthalamic nucleus, 8:169-197; 8:200-201; 8:205-206 Deep parenchymal AVMs, 8:36 Degenerative disc disease, 7:43-52; 8:225-233 Denervation for spasmodic torticollis, 4:59-65 Diastematomyelia, 7:219-226 Direct end-to-end repair of peripheral nerves, 8:263-269 Disc herniation far lateral, 5:85-89 far lateral lumbar, 5:185-197 lateral, 8:243-251 thoracic, 8:217-224 Disc preservation, 7:43-52 Discectomy, cervical, 5:233-239 Dolichoectatic aneurysms, 7:59-67 Dorsal column stimulation, 6:221-235 Dorsal lipomyelomeningocele, 7:221-225 Dorsal rhizotomy, 4:183-190 Drug infusion pumps, 6:237-250 Dumbbell-shaped cervical neurinoma, 6:35-41 Dumbbell-shaped spinal tumor, 7:241-248 Dural AVFs, 4:3-7; 6:51-56; 6:75-84 Dural AVMs anterior fossa, 8:69-78 convexity, 8:69-78 inferior petrosal sinus, 8:29-32
petrous apex, 8:24-27 posterior fossa, 8:23-46 superior sagittal sinus, 8:69-78 tentorial, 8:23-34
E
Elbow, ulnar nerve transposition, 4:225-233 Electrode implantation, 6:131-146 Endarterectomy, carotid, 6:57-64 Endoscopy approaches to the ventricular system, 6:65-74 carpal tunnel release, 6:99-107; 7:149-156 colloid cysts, 6:109-114 fenestration of the third ventriculostomy, 5:241-246 intraventricular, 6:85-98 pituitary surgery, 5:1-12 thoracoscopic sympathectomy, 7:157-162; 7:163-171 Ependymoma, fourth ventricular, 4:95-106 Epilepsy ablative surgery, 6:131-146 corpus callosum sectioning, 4:107-116 medial temporal onset, 5:75-83 Esthesioblastomas, 7:83-91; 8:143-151 Exophytic gliomas, 8:161-163 Extradural non-neoplastic lesions, 5:177-184 Extradural cervical spine tumors, 5:135-141
Focal intrinsic brainstem astrocytomas, 8:165-169 Foramen magnum, 5:23-32 Fourth ventricular ependymoma, 4:95-106 Frameless stereotaxy, intracranial lesions, 5:121-128 Full facetectomy, 5:190-191 Full thickness calvarial bone graft, 5:215-217 Functional hemispherectomy, 5:155-164 Fusiform aneurysms, 7:59-67 Fusion tension band wiring, 6:167-171
G
Galen, vein of, 8:32-34 Gamma Knife radiosurgery, intracranial lesions, 4:215-224 Gliomas, brainstem, 8:153-159 Glomus AVM, 4:9-10 Glomus tumors, intracranial, 4:117-130 Grafts, 5:233-239; 8:267-269 bone, 5:199-217; 7:6-10; 7:24-25; 7:251-254 Granulomas, petrous apex cholesterol, 8:121-125
H
Hematoma, acute subdural, 5:57-63 Hemicorticectomy, 5:155 Hemifacial spasm, 7:117-124 Hemispherectomy, 5:155-164; 6:257-264 Herniation far lateral disc, 5:85-89 far lateral lumbar disc, 5:185-197 thoracic disc, 8:217-224 Horners syndrome and anterior microforaminotomy, 7:51 complication of thoracoscopic sympthectomy, 7:162 Hydrocephalus, 5:241-246; 6:65; 6:76; 6:98; 6:261-264 Hyperhidrosis, 7:158 Hypertrophied filum terminale, 7:219-226
F
Facial nerve injury, 7:257-260 Facial pain, 5:227-232 Far lateral disc herniation, 5:85-89; 5:185-197 Fascicular peripheral nerves repair, 8:267 Fields of Forel, 8:200 Fistulas carotid-cavernous sinus, 6:1-4 dural arteriovenous, 4:3-7; 6:51-56; 6:7584 intradural, 4:11-16 Flat-back syndrome, 7:53-58
I
Idiopathic intracranial hypertension,
7:191-200 Implantation of drug infusion pumps, 6:237-250 Infection of ventriculoperitoneal shunt, 6:193-200 Inferior dental neurectomy, 7:103-104 Inferior petrosal sinus dural AVMs, 8:29-32 Infraorbital neurectomy, 7:101-103 Interbody fusion, 4:147-157 Intercostal neuralgia, 7:162 Interhemispheric corridor and thirdventricle exposure, 4:37-42 Internal stabilization, 5:109-119; 5:233-239 Intervertebral disc damage, 7:51-52 Intracranial glomus tumors, 4:117-130 Intracranial hypertension, 7:191-200 Intracranial lesions, 4:75-83; 4:85-93; 4:215-224; 5:121-128 Intracranial pressure monitoring, 5:65-74 Intradural arteriovenous fistulas, 4:11-16 Intraventricular endoscopy, 6:85-98 Intraventricular shunt, 6:85-98 Isthmic spondylolysis/spondylolisthesis, 4:147-157
Locking plate system, 6:157-166 Low back pain, 5:227-232 Lower clivus-anterior foramen magnum meningioma, 5:23-32 Lumbar decompression, 5:227-232 Lumbar disc herniation, far-lateral, 5:185197 Lumbar extension osteotomy for flat-back syndrome, 7:53-58 Lumbar spine arthroscopic microlumbar, 8:209-216 degenerative disease, 8:225-233 far lateral disc herniation, 5:85-89 far lateral lumbar disc herniation, 5:185-197 foraminal stenosis, 8:227 thoracolumbar fractures, 5:109-119 Lumboperitoneal shunt placement for pseudotumor cerebri, 7:235-240
M
Meningioma anterior foramen magnum, 5:23-32 lower clivus, 5:23-32 petroclival, 7:69-81 torcular/peritorcular, 5:13-21 Meningoceles, 6:213-219 Mental neurectomy, 7:103-106 Mesiotemporal lesions, 6:147-156 Microelectrode-guided pallidotomy, 6:27-33 Microforaminotomy, anterior, 7:43-52 Microsurgery carotid endarterectomy, 6:57-64 craniotomy for colloid cysts, 6:251-256 lumbar decompression, 5:227-232 root entry zone decompression, 5:165-170 Microvascular decompression for hemifacial spasm, 7:117-124 Middle cerebral artery aneurysms, 8:13-22 Moyamoya syndrome, 4:139-146 MRI-guided pallidotomy, 7:141-148 MRI-guided stereotactic cingulotomy, 7:135-140 Multiple subpial transection, 6:125-129 Myelomeningocele, 7:219-226
J
Jugular foramen tumors, 8:135-142 Juvenile AVMs, 4:8-10
K
Kambin instrumentation for microlumbar discectomy, 8:211 Kaneda anterior spinal instrumentation system, 7:21-27
L
Labb, vein of, 8:58-60 Lambdoidal synostosis, 4:44-45; 4:209-214 Lateral disc herniation, 8:243-251 Lateral mass plate and screws, 5:91-100 Lateral orbitotomy, 4:81-83 Lateral ventricles, 5:67-69 Lipomyelomeningoceles, 7:219-226 Lobectomy, temporal, 4:131-137; 5:75-83 Locking anterior cervical plate, 5:233-239
N
Nerve root avulsion, 6: 43-50 Nerve root injury, 7:51 Neurectomy for trigeminal neuralgia, 7:99-106 Neurinoma, 6:35-41; 8:95-105 Neuroblastomas, olfactory, 7:83-91; 8: 143-151 Neuroma, acoustic, 4:159-164 Non-neoplastic lesions of the craniovertebral junction, 5:177-184
O
Obstructive hydrocephalus, 5:241-246 Occipitalized atlas, 7:249-254 Occipitoaxial fusion, 7:249-254 Odontoid transarticular screw fixation, 7:29-41 Olfactory neuroblastomas, 7:83-91; 8:143-151 Operating Arm System, 8:79-85; 8:133 Optic nerve injury, 8:12 Optic nerve sheath fenestration, 7:191-200 Orbit anatomy, 4:75-81 craniotomy, 4:85-93 lateral orbitotomy, 4:81-83 Orbitotomy, 4:81-83 Orion anterior cervical plate system, 5:101-108
P
Pain facial, 5:227-232 low back, 5:227-232 relief, 6:221-235 trigeminal neuralgia, 5:165-170 Pallidotomy microelectrode-guided, 6:27-33 MRI-guided, 7:141-148 posteroventral, 5:143-153; 6:13-26 subthalamic nucleus, 8:196-197; 8:200-201; 8:205-206 Paraclinoid carotid artery aneurysms, 8:1-12
Parkinsons disease deep brain stimulation for control of tremor, 7:125-134 MRI-guided pallidotomy, 7:141-148 posteroventral pallidotomy, 5:143-153; 6:13-26 subthalamic nucleus, 8:196-197; 8:200-201; 8:205-206 Pedical screw, 5:112-113; 5:116-117 Pedicle subtraction for flat-back syndrome, 7:53-58 Percutaneous balloon compression for trigeminal neuralgia, 7:107-116 Perimedullary AVFs, 4:11-13 Peripheral nerve suture techniques, 8:261-269 Peripheral neurectomy for trigeminal neuralgia, 7:99-106 Peritorcular meningiomas, 5:13-21 Petroclival meningiomas, 7:69-81 Petrous apex cholesterol granulomas, 8:121-125 dural AVMs, 8:24-27 Pfeiffers syndrome, 7:201 Pial synangiosis, 4: 139-146 Pineal region masses, 4:29-36 Pituitary Cushings disease, 4:165-172 surgery, 5:1-12 Plagiocephaly, posterior, 5: 43-55 Pneumothorax, postoperative, 7:162 Posterior C1-2 screw fixation, 4:19-28 Posterior cervical fusion with tension band wiring, 6:167-171 Posterior fossa dural AVMs, 8:23-46 Posterior lumbar interbody fusion, 7:1-10 Posterior occipitoaxial fusion for atlantoaxial dislocation, 7:249-254 Posterior plagiocephaly, 5: 43-55 Posterior stabilization, 5:91-100 Posterolateral tentorium dural AVMs, 8:25-29 Posteroventral pallidotomy, 5:143-153; 6:13-26 Pseudotumor cerebri lumboperitoneal shunt placement, 7:235-240
optic nerve sheath fenestration, 7:191-200 Psychiatric disease, surgery for, 7:135 Pulse generator for subthalamic nucleus stimulation, 8:205-206
R
Radiosurgery of intracranial lesions, 4:215-224 Radiosurgical dose planning, 7:94-96 Radiosurgical localization, 7:94-96 Ray Threaded Fusion Cage, 7:1-10 Raynauds syndrome, 7:158 Revascularization and dolichoectatic/fusiform aneurysms, 7:61-65 Rhizotomy dorsal, 4:183-190 spasmodic torticollis, 4:59-65 Rod placement and thoracolumbar junction fractures, 7:24-27 Root entry zone decompression, 5:165-170
S
Sacrectomy, 7:11-20 Sacrum tumors, 7:11-20 Sagittal synostosis, 5:219-225 Sathre-Chotzen syndrome, 7:201 Scalp reconstruction, 5:199-217 Schwannomas complex spinal, 7:241-242 trigeminal, 8:107-120 Screw fixation atlantoaxial instability, 4:19-28 atlantoaxial transarticular, 7:29-41 odontoid transarticular, 7:29-41 Seizures ablative epilepsy surgery, 6:131-146 corpus callosum sectioning, 4:38-39; 4:107-116 temporal lobectomy, 4:131-137 Shunt intraventricular, 6:85-98 ventriculoperitoneal, 6:193-200 Sinus fistulas, carotid-cavernous, 6:1-4 Sinus skeletonization technique, 6:51-56
Sinus, sagittal, 8:74-77 Sinus, transverse-sigmoid, 8:57-68 Spasmodic torticollis, 4:59-65 Spasticity, 4:183-190 Spina bifida, 7:219-226 Spinal cord AVMs, 4:7-10 Spinal exposure, upper thoracic, 4:173-182 Spinal instrumentation, 7:21-27 Spinal plate/screw placement, 7:23-25 Spinal stabilization cervical spine, 6:157-166 cervical spine with articular plates and screws, 5:91-100 cervical spine with the Orion system, 5:101-108 posterior, 5:91-100 thoracolumbar fractures, 5:109-119 Spinal tumor, dumbell-shaped, 7:241-248 Spinal vascular malformations, 4:1-18 Spondylolisthesis, 4:147-157; 6:183-191 Spondylolysis, 4:147-157 Stabilization cervical, 6:157-166 lateral, 4:147-157 posterior, 5:91-100 thoracolumbar fractures, 5:109-119 Stereolithography for cranial repair, 8:188 Stereotactic cingulotomy for psychiatric disease, 7:135-140 Stereotactic depth electrode implantation, 6:131-146 Stereotactic imaging and deep brain stimulation for control of tremor, 7:127-128; 7:141 Stereotactic microsurgical craniotomy, 6: 251-256 Stereotactic radiosurgery of trigeminal nerve root, 7:93-97 Stereotaxy, frameless, 5:121-128 Subclavian steal syndrome, 4:191-198 Subdural hematoma, 5:57-63 Substantia nigra pars reticulata/pars compacta, 8:201 Subthalamic nucleus, 8:196-197; 8:200-201; 8:205-206 Superior hypophyseal aneurysm, 8:1-2; 8:10-11 Superior sagittal sinus dural AVMs, 8:69-78 Supraorbital, supratrochlear neurectomy,
7:99-101 Sympathectomy, 7:157-162 Synostosis coronal, 4:67-73; 6:201-211; 7:201-210 lambdoidal, 4:44-45; 4:209-214 sagittal, 4:219-225
T
Temporal bone trauma, 7:257-260 Temporal lobe, 4:131-137; 5:75-83; 6:115-124 Tension band wiring, 6:167-171 Tentorial apex, 6:51-56 Tentorial dural AVMs, 8:23-34 Tethered cord syndrome, 7:219-226 Texas Scottish Rite Hospital forceps, 6:183-191 system, 5:109-119 Thalamic AVMs, 4:43-58 Thalamic mapping for control of tremor, 7:125-134 Third ventricular colloid cysts, 6:251-256 Third ventriculostomy for obstructive hydrocephalus, 5:241-246 Third-ventricle exposure, 4:37-42 Thoracic disc herniation, 8:217-224 Thoracic spine exposure, 4:173-182 Thoracolumbar spine burst fractures, 6:173-182 fractures, 5:109-119 junction fractures, 7:21-27 Thoracoscopic sympathectomy, 7:157-162 Thrombectomy, 7:61-62 Torcular/peritorcular meningiomas, 5:13-21 Transthoracic endoscopic sympathectomy, 7:163-171 Transverse-sigmoid sinus, 8:57-68 Tremor, 7:125-134 Trigeminal neuralgia percutaneous balloon compression, 7:107-116 peripheral neurectomy, 7:99-106 microvascular decompression of root entry zone, 5:165-170 stereotactic radiosurgery of the trigeminal nerve root, 7:93-97 Trigeminal schwannomas, 8:107-120
Tumors cavernous sinus, 4:199-207 dumbell-shaped spinal, 7:241-248 ependymomas, 4:95-106 extradural cervical spine, 5:135-141 intracranial glomus, 4:117-130 jugular foramen, 8:135-142 orbital region, 4:87-90 pineal region, 4:36 sacrum, 7:11-20 Twins, craniopagus, 6:5-11
U
Ulnar nerve entrapment, 4:235-249 submuscular transposition, 4:225-233 Unilateral coronal synostosis, 4:67-73; 7:201-210 Upper basilar trunk aneurysms, 8:87-94 AVMS, 8:87 Upper clivus dural AVMs, 8:24-27
V
Vascular malformations angiographically occult, 8:127-133 spinal, 4:1-18 Vein of Galen, 8:32-34 Vein of Labb, 8:58-60 Ventral intermediate thalamotomy, 7:125; 7:134 Ventral paraclinoid aneurysms, 8:3-4, 8:10-11 AVMs, 8:3-4; 8:10-11 Ventricular AVMs, 8:52-58 Ventricular system, 6:65-74 Ventricular trigone AVMs, 8:47-56 Ventriculoperitoneal shunt, 6:193-200 Vertebral artery, 5:135-141
W
Wrist, ulnar nerve entrapment, 4:235-249
Z
Zona incerta, 8:200
SURGICAL REPAIR OF TRIGONOCEPHALY

KEN R. WINSTON, M.D. MICHAEL J. BURKE, D.V.M., M.D.
INTRODUCTION The metopic suture is functional for approximately the first two years of life. Premature fusion of this suture is typically associated with a specific cranial dysmorphia, termed trigonocephaly. While associated brain deformities have been reported (i.e., holoprosencephaly and arhinencephaly), trigonocephaly is most commonly an isolated type of cranial dysmorphia in a neurologically normal child. DESCRIPTION OF THE DEFECT The dysmorphia is apparent at birth. When the head is viewed from the vertex, the frontal area has a wedge or triangular shape. A keel of bone extends vertically across the forehead and may appear to continue below the frontonasal suture. The keel does not necessarily extend posteriorly to the bregma. Very characteristic of trigonocephaly is the severely retropositioned lateral parts of the supraorbital ridges. The bifrontal cranial dimension is abnormally narrow, with a widening of the biparietal diameter which accommodates normal brain volume but accentuates the cosmetic defect. Although the eyes often appear hyperteloric, measurement of the orbits may show hypotelorism. The lateral canthal angles and therefore the lateral eyebrows may appear elevated, but extraocular muscle functions are normal. The term startled coon has been applied to the facies of these children. The diagnosis is made by inspection of the head. If the characteristic abnormality cannot be identified, then either there is no trigonocephaly or it is clinically insignificant. Skull films will show the suture to be absent anteriorly (lower portion). Computed tomography scanning should be done on patients with other congenital malformations (i.e., palatal defects). These patients with trigonocephaly are at higher risk for forebrain abnormalities.
INDICATIONS FOR SURGERY Surgery for trigonocephaly is cosmetic. Most parents of children with trigonocephaly find the dysmorphia to be very noticeable and extremely undesirable. The defect does not improve with time; there is no reason to delay the corrective procedure. We strongly prefer surgical repair by four to six weeks of age but there is no upper age limit. RISKS Risks associated with this procedure include blood loss and the need for transfusion. Dural lacerations, if not recognized and repaired, can lead to enlarging skull defects with cerebral herniation and brain injury. The osteotomies may fuse too early or, conversely, reossification may be incomplete. Additional surgical procedures may be required to achieve a desired satisfactory cosmetic result. Injury to an eye or to periocular structures is possible, with resulting damage to the visual system. Although rare, it is possible for the brain to be injured. Parents should also be informed that, while most children have an excellent cosmetic result, a perfectly shaped skull is not likely to be achieved. A good result is one in which the childs resulting craniofacial morphology will not adversely affect normal psychosocial development. After surgery, the region of the forehead and orbits is usually normal in appearance to all but the most detailed examination. PREPARATION FOR SURGERY Preoperative laboratory evaluation generally consists of routine complete blood counts, electrolyte determinations, and urinalysis. A prothrombin time, partial thromboplastin time, and platelet count are also usually obtained. A shampoo with a chlorhexidine solution is done 8-24 hours before surgery. Prophylactic antibiotics are started in the operating room and continued for 24 hours. SELECTION OF SURGICAL REPAIR Children under six months of age, and perhaps up to
1992 The American Association of Neurological Surgeons
NEUROSURGICAL OPERATIVE ATLAS, VOL. 2
age nine months, are repaired by the floating forehead procedure. This method corrects the almond shape of the orbits and midline ridge and takes advantage of the progressively expanding brain to correct any remaining abnormality. Children who are one year of age or older and some children under this age are best repaired by the tongue-in-groove procedure. In older children, the brain is expanding more slowly and it is necessary to make a more rigidly structured repair. Also, it is not safe to leave large bony defects because they occasionally do not reossify satisfactorily. DESCRIPTION OF FLOATING FOREHEAD OPERATION Position, Preparation of Scalp, and Draping The patient is placed in the supine position with the shoulders elevated by a transverse roll and the neck slightly extended. An arterial line (usually a radial artery), a single peripheral venous line, and a Foley catheter are placed. We do not shave or clip the hair, although this is commonly done by most neurosurgeons. Using a sterile comb or hemostat, the hair is parted along the proposed incision line. The scalp, including the ears and cheeks, are scrubbed with a chlorhexidine solution and the head is draped for a transcoronal incision. Chemical Hemostasis The skin is infiltrated with 0.5% lidocaine with epinephrine (1/400,000) along the planned incision line. Initial Soft Tissue Dissection A coronal incision is made, beginning about 5 mm above the insertion of each pinna and crossing the midline near the anterior fontanelle (Fig. 1). Skin edges are retracted and clips (preferably childrens or Cone clips) are applied to the scalp edge for hemostasis. Periosteal elevators are used to free the pericranium anteriorly to the level of the supraorbital rims. The periorbita are then dissected from the superior half of each orbit. Medially this dissection is continued well below the frontonasal suture and laterally below the frontozygomatic sutures. The supraorbital nerves can be preserved by using a thin osteotome to open the supraorbital foramen and reflecting the nerve anteriorly with the skin. Osteotomies The frontal convexity and supraorbital rims are removed separately. A high-speed craniotome (e.g., Midas Rex) is used for all osteotomies in the frontal convexity. No burr holes are made. Blunt dissection in the anterior fontanelle is used to separate the dura from the frontal bone
and is the starting point for the osteotomies. If the anterior fontanelle is closed, a small oval hole just anterior to the coronal suture can be made with the craniotome. The frontal convexity bone is removed first. An osteotomy is made just anterior to each coronal suture. The osteotomy is continued anteriorly across the forehead approximately 1.5 cm superior to the supraorbital rims (Fig. 1). The resulting triangular piece of bone is separated from the underlying dura. and removed from the field. The only firm dural attachment to the frontal bone is at the midline along the area of the superior sagittal sinus. A wide periosteal elevator will usually disrupt this attachment with safety. Bleeding from the dura. is controlled with bipolar coagulation and microfibrillar collagen (Avitene). Bleeding from bone is controlled with microfibrillar collagen. Bone wax is used only if the above measures fail to control a point of active bleeding. Both supraorbital ridges are removed with a frontal bar en bloc, using osteotomes (Fig. 2). The frontal dura is retracted superiorly and posteriorly. This necessitates separation of the dura. from the midline of the frontal fossa anterior to the crista galli. An osteotomy is made across the floor of the frontal fossa (i.e., across each orbital roof) and extended laterally across the sphenoid wings (Fig. 2). This osteotomy is approximately 1-1.5 cm posterior to the supraorbital rims. The zygomaticofrontal suture is divided vertically with an osteotome. A vertical osteotomy is made in the sphenoid bones down to the level of the frontozygomatic suture. When necessary, a horizontal osteotomy is made to connect the above two osteotomies. An inverted V-shaped osteotomy is made through the region of the frontonasal suture to free the supraorbital rim. If an abnormal nasal ridge exists, it is removed with a high-speed burr. Remodeling of the Supraorbital Rims, Frontal Bar, and Forehead The supraorbital bar is straightened. This almost always requires division in the midline. Posterior reinforcement with a strip of bone taken from the frontal convexity may be required. Straightening of the bar causes the lateral orbital margins to swing medially. A large Leksell rongeur is used to resect this protrusion and also to remodel the superior orbit (Fig. 3). Remodeling of the forehead first involves division of the frontal bone in its midline (Fig. 1). Switching right for left and rotating the two fragments 90 often achieves an acceptable appearance but sometimes other incisions in the frontal fragments are performed as needed to mold them into an acceptable cosmetic appearance. Prior to replacing the above remodeled bones, the narrow anterior biparietal diameter is addressed.
WINSTON AND BURKE : SURGICAL REPAIR OF TRIGONOCEPHALY
Figure 1. Removal and remodeling of the forehead bone. A, a coronal incision is made. The dura is bluntly separated from bone at the anterior fontanelle and is the starting point for osteotomies. Osteotomies are made just anterior to the coronal sutures and 1.5 cm superior to the supraorbital
rim (inset). B, the forehead bone is removed and divided in its midline. C and D, switching right for left and rotating the fragments 90 will often give a satisfactory shape. E, other osteotomies and smoothing of the frontal bone are performed as needed to improve the shape of the forehead.
Figure 2. Removal of the supraorbital bar. The supraorbital ridges and a 1.5-cm frontal bar are removed en bloc. This necessitates separation of the dura from the frontal fossa anterior to the crista galli. Osteotomies across the frontal fossa (orbital roofs) are indicated. The zygomaticofrontal suture
is divided. An inverted V-shaped osteotomy through the frontonasal suture is made. If the tongue-in-groove technique is required, osteotomies are made posteriorly to form a 2-4 1.5-cm tongue of bone which is continuous with the frontal bar.
Figure 3. Remodeling of the supraorbital bar. A and B, the supraorbital bar is straightened by division in the midline. B, straightening of the bar causes the lateral orbital margins to protrude antermedially and may increase the distance between the orbits. C, on each side, the lateral orbital protrusion is resected and the interorbital distance is narrowed by vertical
osteotomies from glabella to nasion; using a large Leksell rongeur, the superior orbital margin is rounded. D and E, osteotomies are made in the bone of the frontal fossa, facilitating a more natural curve to each supraorbital margin. F, the supraorbital bar is reinforced posteriorly with a strip of bone (generally obtained from the remodeled forehead bone).
Using the high-speed craniotome, the anterior 1-2 cm of the parietal bone is morcellated and the resulting two to four fragments are left attached to the dura (Figs. 5 and 6). Replacement of Remodeled Forehead The frontal bones are sutured together at the midline
with 2-0 Vicryl (Figs. 1 and 4). The forehead is then attached to the supraorbital bar with 2-0 Vicryl sutures (Fig. 4). Only rarely do we use a few wires and then only in children over one year of age. The entire rigid complex is then replaced and anchored with a single 30 Vicryl suture in the frontonasal region (Fig. 4). The result is a floating forehead (Fig. 5).
Figure 4. Replacement of remodeled bone. The forehead bone is attached to the supraorbital bar using 2-0 absorbable sutures. The entire rigid complex is replaced and anchored with a 3-0 absorb6
able suture in the frontonasal region. Wire is occasionally used to attach the forehead to the supraorbital bar in children over one year of age.
Closure and Dressing If the upper face has been prepared and draped appropriately, the scalp should be returned to its normal position, temporarily at first, so that the appearance of the upper face and orbits can be assessed. It may be necessary to make some corrective adjustments in the forehead and orbits at that time. After the surgeon is satisfied with the appearance, the galea and underlying pericranium are sutured (single layer) with 3-0 Vicryl sutures (interrupted or continuous technique). Skin edges are approximated with staples. Drains are occasionally required. Postoperatively the head is wrapped snugly but never tightly. DESCRIPTION OF TONGUE-IN-GROOVE OPERATION This procedure is identical to that described above for the first three steps. The removal of the convexity of the frontal bone and the osteotomy in the orbital roofs (floor of frontal fossa) are the same as in Step 4 above. The lateral osteotomies are, however, totally different. The hightorque craniotome is used to outline a posteriorly directed tongue of bone which remains in continuity with the
frontal bar (Fig. 6). This tongue should be at least 1.5 cm wide and about 2-4 cm in length. This tongue always extends posteriorly into the squamous portion of the temporal bone beyond the coronal suture. The osteotomies along the lateral orbits are the same as described above. The remodeling of the supraorbital rim and frontal bar should include all the steps described above. As a result, the tongue of bone will rotate outward on each side when the midline angle in the frontal bar is corrected. Therefore, the sphenoid ridges will need to be notched on their inner (medial) surfaces and the lateral bony fragments bent (green stick fracture) inward. It is very important that the fragment to which the tongue is attached remain firmly continuous with the whole frontal bar. The remodeled forehead is returned to the operative field and sewed in the middle with one or two 3-0 Vicryl sutures. The posteriorly directed tongues of bone are returned to their respective grooves and secured 11.5 cm anterior to their original location to give the desired correction. The tongues are sewed in place with wire and/or 2-0 Vicryl (Fig. 6). The closure and application of the dressing are accomplished as described above.
Figure 5. The floating forehead operation. This technique is used in children under nine months of age. The remodeled forehead is replaced and anchored with an absorbable suture at the frontonasal region. The entire 7
complex then floats over the growing brain. Morcellation of the anterior parietal bones, leaving the fragments attached to the dura, corrects the narrow anterior biparietal diameter.
Figure 6. The tongue-in-groove operation. This technique is used in older children where a more rigid reconstruction is required. A posteriorly directed tongue of bone which is continuous with the frontal bar is created while the lateral osteotomies are performed. The tongue is 1.5 cm wide and 2-4 cm long. Upon straightening the supraorbital bar the tongue protrudes laterally. Notching of the sphenoid wing facilitates moving the tongue of
bone medially. The tongue must remain attached to the supraorbital bar. The forehead bone is replaced and secured in the frontonasal region. The tongues of bone are secured 1-1.5 cm anterior to their previous location, thereby rigidly fixing the supraorbital bone in an advanced position. Biparietal morcellation is performed to correct the narrow anterior biparietal diameter.
POSTOPERATIVE MANAGEMENT The head of the patients bed is elevated. A hematocrit is checked in the immediate postoperative period and twice daily for the first 48 hours. We transfuse packed red cells when the hematocrit drops to 22 or below. The dressing should be monitored at approximately 4-hour intervals for the first 24 hours to ensure that it is not too tight. Facial swelling reaches its maximum at around 48 hours. The worst of the periorbital and facial edema resolves over the next 24 hours and the child is generally discharged at about the time both eyes are clearly open (usually the third to fifth postoperative day). A helmet is not used unless the child is a toddler.
FOLLOW-UP AND EXPECTED OUTCOME The child is usually seen five to seven days postoperatively for staple removal. Examinations are at about the six-week, six-month, and one-year anniversaries. Follow-up radiographs are not necessary unless the cosmetic result is questionable or clearly unsatisfactory. An enlarging skull defect should alert the surgeon to the presence of a dural tear and is an indication for immediate surgical attention. No clinically significant defects in bone should be palpable at a one-year postoperative follow-up.
DORSAL ROOT ENTRY ZONE (DREZ) LESIONING

BLAINE S. NASHOLD, JR., M.D. AMR O. EL-NAGGAR, M.D.
INTRODUCTION The dorsal root entry zone (DREZ) operation was originally reported in 1976 as a focal destruction of the substantia gelatinosa of Rolando. It was done on a patient with intractable arm pain following a brachial plexus avulsion injury. Since then it has been performed at the Duke University Medical Center in over 500 patients with intractable pain of various etiologies. Pain due to deafferentation responds best to the DREZ operation, which involves the creation of lesions in the dorsal root entry zone areas, destroying Rexed layers I through V using a radiofrequency current delivered through a specially designed thermocouple electrode. These lesions are mainly targeted toward the cells of origin of the second-order neurons in Rexed layers II and V which give rise to the spinothalamic and spinoreticular tracts. The dorsal root entry zone extends from the upper cervical cord to the conus medullaris deep to the intermediolateral sulcus. It intermingles cephalad with the trigeminal nucleus caudalis which is the caudal portion of the trigeminal nucleus. The nucleus caudalis receives the major pain afferents from the trigeminal system. Radiofrequency (RF) lesions in the nucleus caudalis have the same functional effect as the dorsal root entry zone lesions, and are performed to treat intractable pain of head and facial origin, especially pain caused by deafferentation. PATIENT SELECTION Careful patient selection is the key to the success of any operative procedure. Patients with deafferentation pain syndromes, especially brachial and sacral plexus avulsion pains, benefit the most from this operation. The DREZ operation is also very successful in paraplegic patients with intractable pain, including central pain and radicular pain, in postamputation phantom pain, and in postherpetic neuralgia. Trigeminal nucleus caudalis le-
sions are successful in the treatment of intractable facial pain secondary to postherpetic neuralgia or anesthesia dolorosa, as well as in patients with trigeminal dysesthesia for whom all other surgical treatments have failed. Combined nucleus caudalis-nucleus solitarius lesions in the floor of the fourth ventricle are performed for the treatment of intractable visceral pain of pharyngeal origin. The nucleus solitarius contains the second-order neurons encoding pain from cranial nerves IX and X from the tongue, pharynx, larynx, and esophagus. PREOPERATIVE EVALUATION A thorough evaluation of the patients pain is thus essential, especially for patients who have undergone previous multiple surgical procedures. Plain roentgenograms are obtained routinely to study the details of the bone anatomy, which is especially helpful in patients who have had previous operative interventions. Other preoperative radiological studies are essential in most cases to confirm the diagnosis (as in cases of brachial plexus or sacral plexus avulsion injuries where myelography and magnetic resonance imaging (MRI) usually show evidence of pseudomeningoceles along the avulsed roots (Fig. 1)) as well as to visualize the spinal cord at the proposed operative site for evidence of scar tissue or traumatic syringomyelia (Fig. 2). All patients are given 10 mg of dexamethasone by mouth the evening prior to surgery. We do not use perioperative antibiotics. OPERATIVE PROCEDURE All DREZ operations are performed under general anesthesia with appropriate physiologic monitoring as determined by the patients general condition; however, a Foley catheter and an arterial line are essential. The patient is then placed in the prone position. Patients undergoing nucleus caudalis lesions as well as patients undergoing cervical DREZ lesions or lesions involving the upper four thoracic segments require immobilization of their head in a Mayf ield head holder
Figure 1. A, a cervical myelogram showing traumatic pseudomeningoceles along several cervical nerve roots in a case of brachial plexus avulsion injury. B, a lumbar myelogram showing traumatic
pseudomeningoceles along the L5 and S1 nerve roots in a case of sacral plexus avulsion injury.
Figure 2. A cervical MRI showing a traumatic syrinx in a patient with cervical spinal cord injury.
to ensure anatomical alignment. Full flexion and elevation of the head is also essential in nucleus caudalis cases as well as in cases involving the uppermost cervical levels. A reverse Trendelenburg position is then used to position the operative site horizontally (Fig. 3). Patients undergoing lesions below T4 are placed in the prone position with the head turned to one side. Adequate cushioning by placing soft rolls under the chest, hips, arms, and legs will prevent pressure injuries (Fig. 4). Particular care should be taken to avoid injury to the ulnar and peroneal nerves. Intraoperative steroids are given in the form of intravenous 1-2 mg/kg/hr Solu-Medrol throughout the procedure along with 50 mg of ranitidine intravenously every eight hours. Muscle relaxants are used in cases where intraoperative evoked potential monitoring is used. The level and extent of the surgical exposure relates directly to the level and number of dermatomes affected. Patients undergoing cervical DREZ lesions require laminectomies extending one level rostral to the highest dermatome affected, whereas those undergoing thoracic DREZ lesions require laminectomies two levels higher. The number of laminectomies per-
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NASHOLD AND EL-NAGGAR : DORSAL ROOT ENTRY ZONE LESIONING
Figure 3. Positioning of a patient undergoing nucleus caudalis DREZ lesions or cervical DREZ lesions.
Figure 4. Positioning of a patient undergoing thoracic or conus medullaris DREZ lesions.
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formed is based directly, in a one-to-one ratio, upon the number of painful dermatomes. For patients undergoing a conus medullaris DREZ lesioning for intractable lower extremity pain, as in patients with phantom pain, T10 through L1 laminectomies are performed. For trigeminal nucleus caudalis lesions a small suboccipital craniectomy and C1-C2 laminectomies are performed (Fig. 11, upper left). Determination of the level is based on palpation of the spinous processes and is confirmed by obtaining an intraoperative radiograph as necessary. The anatomy of the spinal roots varies according to the level of their origin from the spinal cord. The cervicodorsal roots are made up of five to eight individual rootlets that form the main sensory branch and exit via the intervertebral foramen at the level of origin from the spinal cord. In contrast, the thoracic dorsal roots are made up of two to four rootlets which are much smaller in diameter that form the main dorsal root and they exit at least two to three vertebral levels below their origin from the spinal cord. Whereas the cervical sensory rootlets originate close together, the thoracic roots often are separated by several millimeters with a distance of 5 mm between successive thoracic dorsal roots. This so-called blank space between the thoracic roots should also be included in the DREZ lesioning. At the level of the conus medullaris, the lower lumbar and sacral roots are close to each other and may overlap the conus and hide the lower sacral sensory roots. The
avulsed area on the spinal cord at the level of the conus is often hidden by these superficial sensory rootlets from higher levels and the surgeon must carefully retract these roots to expose the avulsed area. Anatomical identification of the sacral sensory roots is often difficult. The S1 dorsal root is the largest, and the best way to identify it visually is for the surgeon to find the last sacral root, which is extremely small, and count up from that point to the largest dorsal root which should be the level of S1. The most accurate method of dorsal root localization is the use of somatosensory evoked potentials. Electrical stimulation over the femoral triangle, stimulating the femoral nerve, will give a good L1 localization. With the recording electrodes placed on the spinal cord while stimulating over the popliteal fossa (posterior tibial or sciatic nerve) and recording on the conus will give good S1 localization. Where there is an area of unilateral avulsion on the conus or loss of a leg from trauma, the intact leg can be used for somatosensory localization (Fig. 5). The thoracic dorsal roots are the most difficult to identify precisely at their origin on the spinal cord. We use the rule of two: the origin of the dorsal root from the spinal cord is approximately two vertebral levels above its exit at the intervertebral foramen. In patients with postherpetic pain involving the thoracic or abdominal areas, the surgeon may note after opening the dura that certain of the dorsal roots appear abnormal. This is a good indication that the proper roots for
Figure 5. Localization by somatosensory evoked potential monitoring. The site for DREZ lesioning is determined by the
most positive wave recorded when stimulating the affected dermatome.
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the DREZ lesion have been localized. These involved herpetic dorsal roots usually appear thin, dull, and grayish-red in color. A biopsy of the dorsal root reveals loss of the large myelinated fibers. The advantage of the DREZ lesion is that the clinical effect can be localized to specific dermatomes or dermatomal levels. As we have indicated above, precise anatomical localization is important to restrict the lesion just to the painful areas of the body. Following a thorough skin preparation and draping, a midline incision is made down to the subcutaneous tissue, and using electrocautery the midline cervical or lumbodorsal fascia is incised. In most instances a standard multilevel bilateral laminectomy is done following a subperiosteal dissection of the paraspinous muscles from the spinous processes and laminae. After adequate confirmation of the desired levels, bilateral laminectomies are performed in almost all patients. Hemilaminectomies are performed in patients with thoracic postherpetic neuralgia and in patients with unilateral intractable radicular pain secondary to spinal cord injury. Postoperative recovery is faster and incisional pain is less in patients undergoing hemilaminectomy. We prefer to use the Midas Rex drill to perform the laminectomies to save operative time and for its safety when used by an experienced surgeon. We use the S-1 drill bits for lumbar and thoracic laminectomies and hemilaminectomies, and the B-1 drill bits for the cervical region. We first use the AM-8 drill bit to drill the lower portion of the most caudal lamina to expose the ligamentum flavum bilaterally. The S-1 or B-1 bit is then used to cut through the laminae one after the other, rostrally (Fig. 6A). This is performed on both sides. The supraspinous and interspinous ligaments above and below are cut with Mayo scissors and the laminae and spinous processes are removed en toto. The AM-8 bit is then used to widen the laminectomy as necessary. The use of the Midas Rex drill is not essential and the laminectomies can be performed the conventional way using rongeurs. A hemilaminectomy is used to expose the dorsal roots in the thoracic region in patients with postherpetic pain. The dorsal roots are well visualized using the microscope. Lesser postoperative pain and early mobility are advantages in this group of patients who are often elderly. We do not use the Midas Rex drill in cases where epidural scarring is suspected from previous surgery, trauma, or infection. Bone bleeding is controlled by applying bone wax to the edges of the laminae. Epidural venous bleeding is controlled with bipolar cautery and small pieces of Surgicel. Cottonoid strips are placed over the sides of the wound and the dura is then opened. In patients undergoing nucleus caudalis lesions, the suboccipital craniectomy is performed using a perforator
and rongeurs or using the Midas Rex M-3 bit as a perforator followed by a suboccipital craniotomy and removal of the bone in one piece. Care should be taken during dissection of the paraspinal muscles at the C1-2 area due to the presence of large veins in that location. Careful dissection of the periosteum above and underneath the posterior arch of C1 should be performed prior to the use of rongeurs or the drill. The craniectomy needs to extend about one-third to one-half the distance from the foramen magnum to the inion and extend bilaterally just short of the mastoid processes. The rim of the foramen magnum is carefully dissected and preferably removed piecemeal. The atlanto-occipital membrane is then dissected and cut using Dandy scissors. Bone wax and Surgicel are used to control bleeding as mentioned above and the dura is then opened. The dural opening is accomplished with or without the aid of the operative microscope. Either way a 2-mm opening in the midline is made with a small-blade scalpel, sparing the arachnoid. The dura is then opened sharply in the midline along the entire extent of the bony exposure (Fig. 6B). Using 4-0 silk sutures placed approximately 1 cm apart, the dural edges are retracted laterally, thus maximizing the exposure. In patients with trauma or prior operative procedures, the dura and arachnoid may be adherent and scarred down to the spinal cord. Gentle and blunt dissection using the microscope is required to separate them. In nucleus caudalis DREZ operations, care should be taken when opening the dura across the area of the foramen magnum due to the frequent presence of a circular sinus. Control of bleeding, from the sinus is achieved using hemostatic clips until the dura is opened followed by replacing the clips with a running 4-0 silk suture. Once the dura is opened beyond this point the incision is then curved laterally toward the side of the pain. If the microscope was not used for the dural opening it is then brought into the field to open the arachnoid. The arachnoid is opened directly over the dorsal root entry zone in patients undergoing unilateral DREZ lesions. The arachnoid is first opened in the middle of the exposure by the use of a sharp hook and scissors and then its edges are secured to the dural edges using small hemostatic clips (Fig. 6C). It is then opened caudally and rostrally using a microbayonet forceps and sharp microscissors. It is important to keep the arachnoid edge secured to the dural edge with hemostatic clips so that when the dura is closed the subarachnoid space is maintained and adhesion of the dura to the spinal cord is prevented. In patients undergoing nucleus caudalis lesions, the posterior inferior cerebellar artery is almost always encountered and care should be taken to avoid injury to this impor-
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Figure 6. A, a laminectomy performed using the Midas Rex AM-8 and S-1 drills. B, opening of the dura. C, opening of the arachnoid.
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tant vessel. This is especially important in patients who have undergone a previous retromastoid craniectomy for microvascular decompression of the fifth cranial nerve for tic douloureux, in whom scarring and thickening of the arachnoid can obscure the vessel. Once the arachnoid is satisfactorily opened, any adherent structures over the dorsal root entry zone should be dissected and retracted. Commonly, multiple serpentine vessels located along the intermediolateral sulcus must be mobilized to allow for the introduction of the DREZ electrode. If bleeding is encountered, a small piece of Surgicel placed on the vessel is almost always sufficient for hemostasis; if the bleeding is significant, bipolar coagulation at a low setting is used. The description of the DREZ electrodes as well as the specifics of the operation for various indications are mentioned later. In general, the DREZ electrode is placed first into the most caudal aspect of the region to be lesioned, and is then moved stepwise in cephalad direction. This allows the neurosurgeon to visualize the upper dorsal rootlets as a guide. The electrode is placed into the entry zone at the same angle as the dorsal root, i.e., approximately 45. The electrode is placed into the spinal cord to a depth of 2 mm, at which point the insulating collar prevents further ingress. Lesions are made at 75C for 15 seconds using the radiofrequency generator. The lesions are made at 1-mm intervals along the entire affected dorsal root entry zone. The spinal region to be lesioned can be measured, and if the distance is 10 mm then 10 lesions should be made. A comparison of the improvement in pain after DREZ procedures between the earlier patients operated on in the late 1970s and the more recent cases reveal improved results with a greater number of DREZ lesions. Blood vessels which are encountered are gently retracted and the electrode slipped into the entry zone avoiding the coagulation of all except the smallest vessels adherent to the DREZ area. The laser has been used by some neurosurgeons to create DREZ lesions, and the early clinical reports regarding relief of pain and complications appear to be satisfactory. We believe the laser lesion may be more difficult to control because of the lack of detailed laboratory studies, but this may be corrected in the future. After all lesions are made, total hemostasis is obtained within the thecal sac and all residual blood is gently irrigated away. The dura and arachnoid are reapproximated in a single layer of continuous 4-0 Vicryl suture, removing the silver clips gradually as the suture approaches the site of the clip to avoid any gaps in the arachnoid closure. Dural tack-up sutures are placed to avoid compression in the event of the development of a postoperative epidural hematoma. A tack-up suture is
placed at each end of the dural exposure between the suture line and the adjoining supraspinous or interspinous ligament. Central tack-up stitches are also used: two in four-level laminectomies and three in five-level laminectomies. These are placed between the dural suture line and the connective tissue overlying the adjoining joint capsule in the lumbar and thoracic regions, or to the cervical fascia and nuchal ligament in the cervical region. We prefer to place tack-up stitches in all cases, whether bilateral laminectomies or hemilaminectomies are performed. Copious amounts of bacitracin irrigation are used after each layer of the wound is closed. The paraspinal muscles are sutured with 2-0 Vicryl sutures, followed by closure of the subcutaneous tissue in two or three layers of 2-0 Vicryl sutures depending on its thickness. The skin is then sutured using 4-0 continuous nylon sutures. We ordinarily do not use epidural drains. If drains are used they are preferably removed on the first postoperative day to avoid infection and the development of a cerebrospinal fluid (CSF) fistula. ELECTRODES AND LESION PARAMETERS The three types of DREZ electrodes in use at Duke are manufactured by Radionics who also make the RF lesion generator used in the DREZ operation (Fig. 7). The standard DREZ electrode has a lesion tip of 2 mm and is 0.25 mm in diameter (Fig. 7A). The caudalis nucleus electrode has a tip length of 3 mm, a diameter of 0. 25 mm, a 1-mm proximal insulation, and a 2-mm lesion tip (Fig. 7B). The proximal 1-mm insulation at the base is designed to prevent lesioning the ascending spinocerebellar tract which lies superficial to the trigeminal nucleus caudalis. A new type of caudalis electrode is made with a 90 angle at the tip to facilitate its use at the higher levels of the cervicomedullary junction (Fig. 7C). The electrodes are made of a hollow stainless steel tube tapered and pointed at the end with an internal thermister at the tip to measure the temperature of the lesion. The RF lesions are made at 75C for 15 seconds and this results in a lesion (2 4-5 mm) which will destroy the upper 5 or 6 Rexed layers in the dorsal horn. Two postmortem studies have confirmed the focal nature of the lesions of the Rexed layers. The heat produced at the tip of the electrode is produced by the radiofrequency current generator. Spinal cordotomy-type electrodes are not satisfactory to make DREZ lesions. BRACHIAL PLEXUS AVULSION INJURY A laminectomy usually extending from C5 to T1 is performed, although it is imperative that at least a portion of the healthy roots above and below the avulsion be visualized to avoid any residual postoperative pain. The intermediolateral sulcus marking the entry
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Figure 7. The various DREZ electrodes: A, standard DREZ electrode. B, nucleus caudalis DREZ electrode. C, El-NaggarNashold right-angled nucleus caudalis DREZ electrode.
zone of the avulsed rootlets is readily identified in most cases and is easily seen along an imaginary line connecting the entry zone of the first attached root above and the first attached root below the avulsed area. Also, identification of the DREZ area on the normal contralateral side helps in identifying the overall anatomy of the area. DREZ lesions are then placed 1 mm apart extending between the healthy rootlets above and below as described above (Fig. 8). CONUS MEDULLARIS ROOT AVULSIONS Avulsion injuries of the conus medullaris differ from those in the cervical region in that usually only one or two lumbosacral roots are avulsed (L5 or S1). When the conus is exposed at operation, the lumbosacral dorsal roots on either side can be seen along with the avulsed area on the conus. The dorsal roots on the side of the avulsion must be carefully retracted laterally until the avulsed root level is visualized (Fig. 9). PARAPLEGIA WITH INTRACTABLE PAIN Meticulous dissection of the arachnoidal scarring and adhesions commonly found in these cases is necessary to identify the DREZ area. Intraoperative ultrasound is also used whenever there is a suspicion of the presence of a traumatic syrinx either on clinical, radiological, or surgical grounds. If present, the syrinx should be drained by placement of a syringo-subarachnoid or syringo-peritoneal shunt in addition to the DREZ lesions (Fig. 10). POSTHERPETIC NEURALGIA Evoked potentials are very helpful in localizing the re16
sponsible dorsal rootlets as shown below; we find this to be crucial to avoid incomplete pain relief. Both somatosensory evoked potential (SEP) and motor evoked potential (MEP) studies are carried out intraoperatively. Anatomic localization is most difficult with the thoracolumbar dorsal roots and those dorsal roots originating from the conus medullaris. Careful SEP studies from the painful areas of the body give a precise dorsal root localization, allowing the neurosurgeon to confine the DREZ lesions to the involved painful area of the body. We now routinely monitor somatosensory evoked potentials intraoperatively. The potential recorded is produced by simultaneous firing of dorsal horn neurons, the maximal discharge being in the spinal cord segment(s) of entry of the nerve stimulated (Fig. 5). This allows for precise localization of the level for lesion production. Stimulating electrodes are placed bilaterally near affected nerves as determined from the preoperative sensory exam, and also on the contralateral side near the comparable intact nerves. This allows for a comparison of normal with abnormal signals. For stimulating the body or the extremities, we use subcutaneous bipolar needle electrodes; bipolar gold discs are used when stimulating the face. The evoked potentials are recorded from the surface of the spinal cord or the cervicomedullary junction using platinum-irridium multicontact disc electrodes and also from the depth using the lesion-generating electrode. The largest amplitude negativity is determined after stimulation of the intact side. The negativity is usually comparatively much reduced or otherwise ab-
Figure 8. DREZ lesions in brachial plexus avulsion injuries.
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Figure 9. DREZ lesions in conus medullaris sacral avulsion injuries.
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first and wired or plated into position (labeled C in Fig. 6). The nasal bone and cribriform plate are usually the most solid structures to work with. The medial canthal ligament also has to be reattached, which can be done easily through a small drill hole. Next, a piece of bone is fashioned to form the orbital roof. This is an important structure which must be solidly placed (Fig.
Figure 10. DREZ lesions and drainage of a traumatic spinal cyst in cases with intractable pain due to spinal cord injury.
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normal on the affected side. We have found that in many instances after DREZ lesions are produced, the negative wave is replaced by a positive one. This positive potential generally signals the volume-conducted approach toward the electrode of neural activity, but without neuronal discharge at the electrode site. This positivity, then, provides for an immediate feedback on the technical success of the operation. NUCLEUS CAUDALIS DREZ LESIONING The DREZ lesions are made using the special caudalis electrodes described above. The special design of these electrodes takes into account that the caudalis nucleus lies beneath the surface of the cervicomedullary junction. Therefore, the electrode tip is 3 mm in length and 0.25 mm in diameter, with a proximal 1 mm insulated area and a distal 2-mm lesion tip. The RF lesions are made along the same line as the cervical dorsal root entry zones over a distance of 15-20 mm from the level of the C2 dorsal rootlets to the tuberculum cinereum of the medulla at a level slightly above the obex. Due to the larger cross-sectional diameter of the nucleus caudalis, two rows of RF lesions are made 1 mm apart using the same parameters of 75C for 15 seconds. The first row of lesions begins at the level of the dorsal rootlets of C2 and is extended cephalad to 5 mm above the obex. The second row begins at C2 but just dorsal to the exit of the rootlets of the spinal accessory nerve (Fig. 11, middle and lower left). Currently, we perform a unilateral limited exposure of the nucleus caudalis. This is associated with less postoperative pain and earlier ambulation. It involves a paramedian skin incision (Fig. 12A). The incision is carried down to the subcutaneous tissue, cervical fascia, and trapezium muscle using electrocautery. The semispinalis capitis muscle is then split at the point of emergence of the greater occipital nerve (Fig. 12B). The rectus capitis posterior minor muscles are divided at their insertion on the posterior tubercle of C1 and reflected upward. The rectus capitis posterior major is retracted downward and laterally using a Leyla retractor (Fig. 12C). A unilateral suboccipital craniectomy with removal of the ipsilateral half of the arch and whole tubercle of C1 is then performed. The ligamentum flavum between C1 and C2 is also removed (Fig. 12D). The C2 lamina and the muscles attached to C2 are left intact. The dura and arachnoid are then opened as discussed previously. The lesions are made using the right-angled nucleus caudalis DREZ electrode (Fig. 13A), which provides a better angle to target the lesion on the nucleus caudalis (Fig. 13B). The lesions are made starting above the C2 rootlets in line with the DREZ area of the spinal cord in the intermediolateral sulcus proceeding upward until the C1 rootlets are encountered. The lesions are then made into the
trigeminal tubercle between the border of the cuneate tubercle and the emerging cranial roots of the accessory nerve (Fig. 13C). Only one row of lesions is made. Familiarity with the bilateral exposure of the nucleus caudalis is advised prior to performing the unilateral exposure. COMBINED NUCLEUS CAUDALIS-NUCLEUS SOLITARIUS DREZ LESIONING The exposure is the same as for nucleus caudalis DREZ lesioning. After arachnoid dissection, standard nucleus caudalis DREZ lesions are made; then two lesions are made to destroy the nucleus solitarius in the floor of the fourth ventricle 1 mm above the obex and 1 mm lateral to the midline on the side of the pain (Fig. 11, middle). The RF lesions are made using the straight nucleus caudalis electrode, thereby avoiding injury to the overlying cranial nerve nuclei. Transient bradycardia and a slight drop of the blood pressure may occur during lesioning. The use of 0.5-1 mg of atropine intravenously will prevent the vascular changes which are due to the proximity of the afferent input from the carotid body into the ventral portion of the nucleus solitarius. The combined nucleus caudalis and solitarius lesions give good pain relief in patients with head and neck cancer, especially those with posterior pharyngeal and esophageal pain. POSTOPERATIVE CARE Postoperative care is the same as for laminectomy patients. We prefer, however, progressive ambulation of the patients depending upon the clinical condition. Patients who undergo conus medullaris DREZ lesioning or lower thoracic procedures are nursed in the flat position for three to four days followed by progressive ambulation. Patients with upper thoracic, cervical, and caudalis DREZ surgery are kept with the head of the bed up 30 for three days followed by progressive ambulation. Steroids are continued in the postoperative period for three days followed by rapid tapering over three to four days to avoid the deleterious effect of steroids on wound healing. Analgesics are limited to those necessary to control postoperative pain. Parenteral narcotics for 24-48 hours are used followed by oral codeine or oxycodone for a few days. We prefer not to give narcotics in high doses for extended periods of time to be able to assess the results of surgery. COMPLICATIONS Postoperative complications are in the order of 3-5%, including CSF leakage and postoperative epidural hematoma formation, in addition to ipsilateral lower extremity weakness or incoordination, especially following DREZ lesions in the thoracic cord. Nucleus caudalis DREZ lesioning can be especially compli-
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Figure 11. Nucleus caudalis DREZ lesions using a bilateral exposure. Nucleus solitarius lesions are also shown.
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Figure 12. Unilateral exposure of the nucleus caudalis.
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Figure 13. Precise location of lesions of the nucleus caudalis.
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cated by upper and/or lower extremity ataxia, usually resolving in a few days. Cerebrospinal fluid leakage can be prevented by having a tight dural closure and nursing the patient in the appropriate position postoperatively. In nucleus caudalis DREZ operations we almost invariably place a dural graft at the time of closure to avoid undue tension on the dura, which in turn allows for a better, tighter closure. Epidural hematomas can be prevented by having a dry field prior to closure in addition to the use of tackup stitches as mentioned above. Rou-
tine antibiotics are not used; however, if signs of infection develop, we obtain blood cultures as well as wound cultures followed by the administration of broad spectrum antibiotics until the final results of the cultures are obtained. Neurologic deficits in the form of ipsilateral or bilateral upper and lower extremity weakness can be avoided by careful monitoring of evoked potentials as well as downstream electromyographic recording in addition to thorough adherence to the above mentioned principles of lesion making.
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OPHTHALMIC SEGMENT ANEURYSMS

ARTHUR L. DAY, M.D.
PERTINENT ANATOMY The ophthalmic segment (OphSeg) is the longest subarachnoid portion of the internal carotid artery (ICA). It begins below the level of the anterior clinoid process at the point where the ICA penetrates the dura to enter the subarachnoid space and ends at the origin of the posterior communicating artery (PComArt) (Fig. 1). Removal of the anterior clinoid process (AC) to expose the proximal portion of the OphSeg reveals an ICA segment that lies beneath the subarachnoid space and outside the cavernous sinus. This portion, known as the clinoidal segment (ClinSeg), is limited superiorly by the dural reflections from the medial roof of the anterior clinoid process toward the optic nerve and canal that mark ICA entry into the subarachnoid space, a point known as the dural ring (DR). Inferiorly, the clinoid segment is bordered by a thin layer of periosteum, bridging from the ICA to the oculomotor nerve (carotid-oculomotor membrane (COM) or membranous ring), that separates this segment from the venous wall of the cavernous sinus. Two named branches arise from the OphSeg, both of which typically originate just above the dural ring. The ophthalmic artery (OphArt) usually arises from the dorsal or dorsomedial ICA surface. Several perforating vessels also arise from this segment, the largest of which has been named the superior hypophyseal artery (SupHypArt). These perforators typically arise from the medial or ventromedial ICA surface. Their ventromedial origin, together with the gentle downward slope of the dural ring posteriorly, often places the SupHypArt origins on a horizontal plane below the level of both the anterior clinoid process and OphArt. Ophthalmic segment aneurysms are divided herein into two large categories, depending on association of the aneurysm neck with the named arterial branches within the segment. Aneurysms arising in clear relation to the ophthalmic artery are termed OphArt aneurysms (Fig. 2). These lesions arise from the ICA just distal to the origin of the ophthalmic artery, and initially project dorsally or dorsomedially from the carotid surface toward the lateral half of the optic nerve.
Other aneurysms originating within this segment invariably incorporate the perforating branches to the hypophysis and are herein called SupHypArt aneurysms (Fig. 3). Small SupHypArt aneurysms usually arise from the inferior or inferomedial surface of the ICA just opposite and slightly distal to the origin of the OphArt. These lesions may remain lateral to the sella, burrowing beneath and medial to the ICA under the anterior clinoid process. Because the space beneath the carotid is limited, however, most larger lesions will eventually expand medially or superomedially above the diaphragma sellae into the suprasellar space. PATIENT SELECTION The typical patient harboring an OphSeg aneurysm is a female in her mid-fifties who presents with a subarachnoid hemorrhage (SAH) or visual changes, or whose aneurysm is discovered incidentally. If bleeding has occurred, surgery is performed on the earliest day possible following the hemorrhage, as long as the patient is not a poor medical risk or has not sustained significant and irreversible brain injury. Approximately one-half of symptomatic OphSeg aneurysms are giant lesions presenting with visual loss. The high frequency of OphSeg lesions reaching large or giant proportions without bleeding is probably explained by their reinforcement by adjacent structures, such as the optic nerve or dura of the lateral sellar wall and cavernous sinus. Lesions presenting with mass-related symptoms are often much larger on computed tomography than the angiographically apparent lumen size would suggest, indicating a significant incidence of partial luminal thrombosis. Because 40-50% of patients with one OphSeg lesion also have at least one other intracranial aneurysm, the surgeon often must decide which lesion bled. Small SupHypArt lesions that remain purely paraclinoid have a very low rate of hemorrhage compared with those at other locations, and asymptomatic lesions are often best treated conservatively unless intervention is planned for other reasons. Larger aneurysms, or those with medial suprasellar extension, appear to bleed with higher frequency. If intervention is planned, the ideal treatment of
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DAY : OPHTHALMIC SEGMENT ANEURYSMS
Figure 1. Paraclinoid anatomy. A, lateral view (schematic) with the clinoid intact. The three paraclnoid segments of the ICA can be identified, including the intracavernous segment (CavSeg), the clinoidal segment (ClinSeg), covered by the anterior clinoid process (AC), and the ophthalmic segment (OphSeg). The OphSeg begins just proximal to the OphArt origin and ends at PComArt. Note the posterior bend of the ICA just beyond the ophthalmic artery (OphArt) origin, which is usually obscured by the AC. ON = optic nerve; SupHypArt = superior hypophyseal artery; PComArt = posterior communicating artery; AChorArt = anterior choroidal artery; CavSin = cavernous sinus. B, lateral view (schematic) with the clinoid removed. The dura overlying
and reflecting from the medial surface of the AC delineates the paraclinoid segments. DR = dural ring; COM = carotid-oculomotor membrane (also called membranous ring); OSt = optic strut. In most instances, the OphArt and SupHypArt arise from the OphSeg, above the dural ring. C, dorsal view (schematic) with the anterior clinoid intact. Note the medial-to-lateral curve of the ICA that actually begins just beyond the anterior bend of the CavSeg. The SupHypArt perforators usually arise from the inferomedial surface of the OphSeg as the ICA curves laterally. The right ON has been retracted superiorly to expose the OphArt origin. Occasionally, both or either branch may arise from the ClinSeg, beneath the dural ring. Pit = pituitary gland.
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Figure 2. Typical anatomy of ophthalmic artery aneurysms. A, a large ophthalmic artery aneurysm (schematic, lateral view, clinoid intact). Note the position of the optic nerve (ON) and the sharp angulation of its superior surface (arrow) against the edge of the falciform ligament. Note also that the anterior clinoid process (AC) limits the view of the proximal aneurysm neck and the origin of the ophthalmic artery (OphArt). DR = dural ring; OphSeg = ophthalmic segment; AN = aneurysm. B, a large OphArt aneurysm (schematic, dorsal view, clinoid intact). Note the medial dis-
placement of the lateral aspect of the optic nerve. The ON often creates a groove in the superomedial surface of the aneurysm, and its position restricts medial extension of the AN across the midline until late in the clinical course. FalcLig = falciform ligament. C, a lateral arteriogram of a typical large OphArt aneurysm. Note that the lesion originates just beyond the OphArt takeoff and projects largely dorsally, above the bend of the carotid artery. As the lesion expands, the superior restriction imposed by the overlying optic nerve tends to close the carotid siphon.
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Figure 3. Typical anatomy of superior hypophyseal artery aneurysms. A, a small superior hypophyseal artery aneurysm. 1, lateral view (schematic). The aneurysm (AN) arises ventromedially above the dural ring (DR), opposite the ophthalmic artery (OphArt) origin, and appears to project into the cavernous sinus. The AN lies partly below the level of the anterior clinoid process (AC) but is still within the subarachnoid space. ON = optic nerve. 2, anteroposterior (AP) view (schematic). The AN projects ventromedially above the DR toward the lateral sellar wall. SupHypArt = superior hypophyseal artery; Pit = pituitary gland. B, a larger superior hypophyseal artery aneurysm. The lesion size now exceeds its ventral confines and expands into the suprasellar space below the optic nerves and chiasm. 1, lateral view (schematic). Note that the AN projects both dorsal and ventral to the OphSeg of the ICA, and its lumen is widely splayed. The SupHypArt drape over the aneurysms superior surface, while the posterior communicating artery (PComArt) is displaced posteriorly and laterally. The AC limits the view of the ventral and medial aspects of
the aneurysm neck. Note also that the AN does not sharply angulate the optic nerve at the falciform ligament. 2, AP view (schematic). Note the two bulges at the aneurysm, one ventrally at the site of aneurysm origin. and the second into the suprasellar space. To totally obliterate this lesion, the ventral bulge (arrow) lateral to the sella must be incorporated in the clip down to the dural ring. C, a giant superior hypophyseal aneurysm, dorsal view (schematic). Note the suprasellar extension beneath the chiasm, with the pituitary stalk (PitSt) displaced and allowing extension across the midline. D, a lateral arteriogram of a typical large SupHypArt aneurysm. In this projection, the AN balloons both above and below the projected course of the ICA, which appears to run through the aneurysm lumen. The part of the aneurysm below the ICA represents the initial ventral origin, whereas the suprasellar extension lies superior. The carotid siphon appears to open as the lesion enlarges, due to the bulge beneath and medial to the ICA. Note that the region of the typical OphArt origin is independent of the aneurysm.
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OphSeg aneurysms is clipping, with preservation of the internal carotid artery and its branches. Major risks of surgery include blindness, stroke, or inability to completely secure the aneurysm neck. With proper exposure and a firm understanding of parasellar and vascular anatomy, however, most of these lesions are clippable, with low risks to the brain or visual apparatus. Carotid ligation should be considered a secondary alternative, as the risks of stroke are higher from parent vessel sacrifice, the visual system is not as effectively decompressed, and complete thrombosis of the aneurysm is not ensured. PREOPERATIVE PREPARATION Bleeding from OphSeg aneurysms is managed in the same fashion as SAE from aneurysms in other locations, using such measures as bedrest, calcium channel blockers, hydration, ventricular drainage (when indicated), steroids, and anticonvulsants. Prophylactic antibiotics are given to all patients when they enter the operating suite and are continued for 24 hours. Preoperative bedside testing of visual fields is often overlooked in the SAH patient, but should be dutifully performed in those harboring large or giant OphSeg aneurysms. The early visual sign of an OphArt aneurysm (an inferior nasal field cut) is often not noted by the patient. Establishment of this visual field loss pattern not only documents the deterioration preoperatively, but also
provides key knowledge to the surgeon about the anatomy likely to be encountered in the operating room. SURGICAL TECHNIQUE Anesthesia and Monitoring The ispilateral cervical carotid region should be unencumbered by any anesthetic equipment. If temporary clipping of the ICA is anticipated, intravenous barbiturates are administered until burst suppression is achieved on electroencephalography (EEG) and are continued until patency in the carotid system is restored. Blood pressure, monitored with an indwelling radial artery catheter, is generally maintained at normal levels. Continuous evoked potential and EEG monitoring is also utilized, and the blood pressure is elevated during ICA clipping if focal changes are noted. Spinal drainage is not utilized routinely. Operative Positioning and Draping The patient is placed in the supine position, with the head elevated above the heart to promote good venous drainage (Fig. 4). The patients head is turned 45 toward the opposite side, with the vertex lowered, to allow gravitational distraction of the frontal and temporal lobes from the skull base. A shoulder roll is used to minimize distortion of the cervical carotid bifurcation.
Figure 4. Operative position and craniotomy exposure (schematic). The arrow points to the keyhole, marking the external surface of the sphe-
noid ridge. The carotid incision is draped into the operative field but is not opened in most instances.
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The head is draped to permit visualization of the frontal and temporal regions from the midline to below the zygoma. For giant lesions, especially those with calcifications or luminal thrombosis, the cervical region is also draped to allow sterile access to the carotid bifurcation for proximal control or bypass source as desired. Operative Procedure The skin incision for craniotomy extends from the midline to the zygoma, one fingers breadth behind the hairline (Fig. 4). An incision is also marked over the cervical carotid bifurcation, paralleling the anterior margin of the sternocleidomastoid muscle, but is not opened in most instances. The temporalis fascia is sectioned 1 cm below its skull attachment superiorly, and just posterior to the fat pad containing the frontal branch of the facial nerve. The temporalis muscle with its remaining fascial covering is reflected inferiorly and posteriorly to expose the pterion. A frontotemporal free bone flap is elevated, opening low enough anteriorly so that 2-3 cm of the posterior frontal fossa floor is exposed. The sphenoid ridge is removed extensively, and a temporal craniectomy is enlarged to allow an unobstructed view of the anterior aspect of the middle cranial fossa. Proximal visualization of the carotid and ophthalmic arteries is mandatory for both aneurysm types (OphArt and SupHypArt), and, at this point, a decision is made whether to remove the anterior clinoid process extradurally. While not always necessary for smaller lesions, clinoidal removal is frequently required for safe and accurate clipping of large or giant lesions. With unruptured aneurysms, extradural clinoid removal can usually be done quite safely, without exposing the subarachnoid space to bone debris. Generally, and especially following SAH, the clinoidal tip is removed intradurally while the surgeon simultaneously visualizes the aneurysm, thereby avoiding inadvertent rupture during extradural manipulation. If done extradurally, the posterior roof of the orbit and the lesser wing of the sphenoid bone covering the superior and medial surface of the superior orbital fissure are removed with a rongeur (Fig. 5). As the base of the clinoid process and optic nerve are approached, a highspeed diamond drill is utilized to thin the bone, which is then fractured away with microcurettes. After the dura has been stripped away from the remaining clinoid tip, the process is grasped with a hemostat, gently rocked free of any remaining attachments, and removed. Bleeding is quite easily controlled with bone wax, Gelfoam, and Surgicel. This extensive bone removal exposes the extradural optic nerve and the clinoidal space, a pocket of vari-
able size (usually <5 mm) that houses an ICA segment (clinoidal segment) below the dural ring but outside the main venous channels of the cavernous sinus. Although covered by thin reflections of periosteum and small venous channels, the ClinSeg can be freed up from its loose attachments, thus providing proximal exposure for temporary clipping if required. The dura is then opened and reflected to expose the proximal portions of the sylvian fissure. The fissure is split widely to allow an unobstructed view of the optic nerve, ICA, and aneurysm with minimal retraction. If indicated and not already performed, the clinoid process is now removed intradurally (Fig. 6). After cauterization, a cruciate incision is made into the dura covering the anterior clinoid process and the optic canal roof. The clinoid process is then carefully thinned and removed with small rongeurs and a highspeed drill. The removal should extend laterally to include the medial roof of the superior orbital fissure, inferomedially to trim the optic strut, and superomedially to unroof the optic canal. Optic nerve displacement, if not already done by the aneurysm, is often necessary to visualize the proximal neck. The falciform ligament should be sectioned before any aneurysm dissection is undertaken. This structure forms a knife-like edge against the superior aspect of the optic nerve, and mobilization of the nerve against it may further increase visual morbidity. The neck of the aneurysm is now ready to be defined. Before beginning the dissection, the ClinSeg should be prepared to receive a temporary clip if the need is anticipated. Extradural clinoidal removal requires that the clinoidal dura now be opened from within, thereby delineating clearly the dural ring and the clinoidal ICA segment. The dural ring is thicker laterally but thins on its medial surface. Its circumferential section allows mobilization of the ICA and accurate identification of the OphArt and aneurysm neck. Cervical carotid exposure is a reasonable alternative to proximal control within the clinoidal space, but neither is a substitute for extensive clinoidal and optic strut removal. The proximal neck of OphArt aneurysms originates just distal to the OphArt and can be separated with gentle retraction of the aneurysm base and spreading dissection with micro-bayonetted forceps (Fig. 7). The distal neck is usually unencumbered by major branch attachments, but any perforators to the optic nerves, chiasm, or hypophysis should be dissected free. Straight or side-angled clips, closed down parallel to the course of the ICA and sparing the OphArt, satisfactorily secure most OphArt lesions. Clips placed perpendicular to the ICA are often ineffective in collapsing larger lesions and risk avulsion of the proximal aneurysm neck.
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Figure 5. Extradural clinoid removal (schematic). A, the extent of the osseous removal is outlined in the crosshatched area. OC = optic canal; AC = anterior clinoid process; SOF = superior orbital fissure; OSt = optic strut. B, the operative view. 1, the right frontal and temporal lobes are retracted extradurally to expose and permit removal of the posterior portions of the orbital roof back to the sphenoid ridge. The SOF is unroofed, advancing toward the AC and the extradural portion of the optic nerve (ON). 2, the AC is removed with a high-speed irrigating drill until only a
thin shell remains, which is then fractured off the optic strut and detached from the dura. The superior, lateral, and inferior walls of the extradural portion of the ON are removed carefully. 3, the completed exposure reveals the clinoidal segment (ClinSeg) of the carotid artery, and the optic strut (OSt). The cavernous sinus lies posterior, inferior, and lateral to the ClinSeg and is covered by the inferior projection of dura from the AC known as the carotid-oculomotor membrane (COM). DR = dural ring, the point where the ICA penetrates the dura to enter the subarachnoid space.
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Figure 6. Intradural clinoid removal, operative view (schematic). A, the dural incision (right pterional frontotemporal craniotomy). The sylvian fissure has been opened widely, and the frontal and temporal lobes retracted. The dotted lines mark a cruciate dural incision overlying the anterior clinoid process (AC), with an additional limb sectioning the falciform ligament (FalcLig) to untether the optic nerve (ON). OphArt = ophthalmic artery; SupHypArt = superior hypophyseal artery; ICA = internal carotid artery; ACA = anterior cerebral artery; PComArt = posterior communicating artery. B, the AC, roof, and lateral wall of the optic canal, and adjacent orbital
roof have been removed. The clinoidal segment (ClinSeg) has been exposed, covered by the thin dura medial to the AC. The dural ring (DR) surrounds the ICA and marks its entrance into the subarachnoid space. The carotid-oculornotor membrane (COM) covers the cavernous sinus (CavSin). The oculomotor nerve (III) can be seen through the COM, in the wall of the CavSin. Bleeding is usually due to small venous tributaries that traverse the area and is easily controlled with pledgets of Gelfoam and gentle suction. Extensive removal of the optic strut (OSt) provides enough exposure of the ClinSeg to permit temporary ICA clipping if necessary.
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SupHypArt aneurysms project medially and inferiorly, just distal to the dural ring (Fig. 8). Small SupHypArt aneurysms may be initially hidden from the surgeon by the overlying ICA and anterior clinoid process. In large and giant varieties, the ICA is displaced slightly laterally and superiorly toward the surgeon, and the neck of the lesion often appears so wide and long that the entire carotid wall appears incorporated into the aneurysm. As SupHypArt aneurysms enlarge, their walls become adherent to the dura of the sella, diaphragma, and lateral cavernous sinus wall. Although the arteriogram may suggest otherwise, these lesions rarely if ever project into the cavernous sinus, and the walls of the two structures can be separated. By carefully adhering to the dural ring surface, the part of the aneurysm wall that bulges beneath the clinoid process is separated from the clinoidal dura, thus freeing up the proximal neck. The hypophyseal stalk may be adherent to the posterior and medial surface of larger SupHypArt lesions. The posterior communicating artery or its thallamoperforating branches are often draped over the distal end of the aneurysm, and these vessels must be carefully identified, separated, and preserved. SupHypArt lesions are usually best obliterated with a fenestrated clip whose blades pass over and then run parallel to the ICA, spanning the distance between the PComArt and the dural ring. Although the OphSeg perforators (superior hypophyseal arteries) do not generally supply brain parenchyma, some reach the optic chiasm, and every attempt should be made to spare them from the surgical clip. Visual loss, either unimproved or somewhat worsened following surgery, can perhaps be caused by interruption of these vessels. The pituitary stalk receives blood supply from both sides, however, and endocrine deficits secondary to unilateral interruption of these branches are rarely noted. When large, both types of lesions (OphArt and SupHypArt) tend to be associated with arteriosclerosis in the carotid artery and/or adjacent aneurysm neck. Broad necks are commonplace and are best secured by placing the clip parallel to the parent (ICA) vessel. The bulk of these aneurysms and the thickness of their necks often cause the initial clip to slip downward and partially obstruct the parent artery lumen. A second clip, applied more
distally on the neck and in the same direction as the first, is often helpful in keeping the neck and aneurysm collapsed. If placement of the first two clips results in a compromised ICA lumen, a third clip is applied distal to the second, and the original clip is removed. This process is repeated until wide carotid patency is ensured. The aneurysm is then opened and its contents evacuated without bleeding. The entire aneurysm wall does not need to be removed, but the visual apparatus must be thoroughly decompressed. Some OphSeg lesions may be judged unclippable because of marked calcification within their walls. Using barbiturate anesthesia and temporary ICA clipping, the laminated calcific walls are removed through an incision into the aneurysm interior. The resultant neck is much more pliable and accepting of the clip, with less risk of parent vessel compromise by fractured or displaced calcification or atheroma. A hemostat may occasionally be used to facilitate creation of a surgical neck, but this instrument must be applied distal enough so as not to injure the parent vessel. Debris should be irrigated thoroughly from the parent vessel before final clip placement. Because of their superior or medial projection, small OphSeg aneurysms can often be clipped from a contralateral approach between or behind the optic nerves. OphArt aneurysms are much easier to clip from a contralateral approach than are SupHypArt lesions. This capability may be quite important when deciding which side to treat first in a patient harboring bilateral lesions, one of which is an OphSeg type. In general, the craniotomy should be done on the side of the symptomatic aneurysm. The surgeon may then choose to explore the opposite carotid artery, with plans to obliterate the contralateral lesion if feasible. Attempted clipping of large or giant OphSeg lesions from a contralateral approach should be avoided except in emergent situations. Once the aneurysm is clipped and aspirated, the dura is closed, including the opening over the anterior clinoid process. The clinoid often incorporates an extension of the sphenoid sinus, and the residual bone edges must be inspected and carefully sealed with muscle, bone wax, or acrylic to prevent cerebrospinal fluid leakage. A drain is left in the epidural space, and brought out posterior to the skin incision through a
Figure 7. Ophthalmic artery aneurysm clipping (right side, schematic). A, exposure (see also Fig. 6B). The falciform ligament (FalcLig) is sectioned before any aneurysm manipulation is undertaken. AN = aneurysm; ON = optic nerve; OphArt = ophthalmic artery; SupHypArt = superior hypophyseal artery; PComArt = posterior communicating artery; ClinSeg = clinoidal segment; OphSeg = 37
ophthalmic segment; DR = dural ring; OSt = optic strut. B, defining the proximal neck with microforceps dissection and suction-retraction. C, defining the distal neck. D, clip application. A side-angled clip has been placed parallel to the long axis of the ICA. The AN is then aspirated and carotid artery patency inspected.
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Figure 8. Superior hypophyseal artery aneurysm clipping (right side, schematic). A, exposure (see also Fig. 6B). AN = aneurysm; ON = optic nerve; OphArt = ophthalmic artery; SupHypArt = superior hypophyseal artery; PComArt = posterior communicating artery; ClinSeg = clinoidal segment; OphSeg = ophthalmic segment; DR = dural ring; OSt = optic strut. B, defining the proximal neck with microforceps and suction-retraction. Separation of the ventral AN bulge from the dura adjacent to the DR is often aided by circumferential section of
the dura alongside the ring. C, defining the distal neck. D, clip application. A right-angled fenestrated clip is passed over the broadened carotid wall and carefully placed parallel to the ICA, with the fenestration reconstructing the parent vessel lumen. The butt of the clip must spare the PComArt, while the tips are advanced to the ventral border (arrow) of the DR. The AN is then aspirated, and carotid patency confirmed. If possible, the SupHypArt should also be spared, as they may provide critical blood supply to the ON or chiasm.
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Figure 9. Clinoidal segment aneurysm (schematic). A, AP view. The aneurysm (AN) arises below the dural ring (DR) and erodes through this membrane to enter the subarachnoid space medial and usually anterior to the ICA. AC = anterior clinoid process; ON = optic nerve; COM = carotid-oculomotor membrane. B, operative view, right side. Removal of the optic strut (OSt) is essential to gain access to the aneurysm neck, which usually originates just above the COM anteromedially. Note that the clinoidal segment (ClinSeg) is not avail-
able for proximal arterial control, and cervical exposure may be very useful. Circumferential section of the DR is required to allow passage of a fenestrated clip around the ICA. The clip tips are then advanced as far proximally as to obliterate the neck, using great care to avoid injury to the cranial nerves within the cavernous sinus. Bleeding can be easily controlled with gentle Gelfoam or Surgicel packing and suction. III = oculomotor nerve within cavernous sinus wall; OSt = optic strut.
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separate stab wound. When the frontal sinus is violated by the craniotomy, the mucosa should be removed, and the space packed with Gelfoam soaked with an antibiotic. The sinus is then obliterated with acrylic and in questionable cases is oversewn with periosteum. The bone flap is then anchored in position, and the temporalis muscle and skin are closed in traditional fashion. POSTOPERATIVE CARE Patients are thereafter managed according to their presenting symptoms. Patients with an unruptured aneurysm are mobilized the following day, with rapid normalization of medications and fluid intake. SAH patients with high vasospasm potential are hydrated aggressively for the duration of their risks. COMPLICATIONS AND THEIR MANAGEMENT Transient or fixed postoperative hemibody deficits may be an indication of carotid compromise and occur with higher frequency in patients with a calcified or partially thrombosed aneurysm with atherosclerosis within the ICA wall. Digital subtraction arteriography can be useful in the operating room or immediately postoperatively when parent vessel patency or embolization is questioned. Visual deterioration after surgery may occur if the optic nerve, already distorted medially and superiorly by the underlying aneurysm, is further manipulated against the falciform ligament. Perforator sacrifice may harm the
blood supply of the optic nerve and chiasm. Postoperative diplopia may be due to either an abducens or oculomotor nerve paresis. When the dural ring is opened, these nerves lie in a relatively superficial position within the wall of the clinoidal space. They may be disturbed within the cavernous sinus either by clinoid removal or by the clip blades as they are advanced proximally beyond the aneurysm neck. Aneurysms may arise from the clinoidal segment and may be quite difficult to differentiate from OphSeg lesions (Fig. 9). These aneurysms probably account for some lesions formerly termed ophthalmic aneurysms which at surgery were unclippable or ruptured catastrophically. ClinSeg aneurysms probably represent cases in which the OphArt or SupHypArt arises from the clinoidal rather than the ophthalmic segment of the carotid artery. As the space beneath the dural ring is limited, these lesions may eventually erupt through the dura into the subarachnoid space, where they appear alongside the ICA and resemble OphSeg aneurysms. Proximal exposure is much more difficult to obtain in these lesions, as the dural ring does not define its proximal extent. Clinoidal segment aneurysms are often adherent to the undersurface of the anterior clinoid process and optic strut, and extradural clinoidal removal may cause premature aneurysm rupture before proximal or distal vascular control has been established. If this type of aneurysm is anticipated, proximal ICA exposure in the cervical region is essential.
41
CHRONIC SUBDURAL HEMATOMA

JAMES E. WILBERGER, JR., M.D.
INTRODUCTION Since first described by Virchow in 1875 as pachymeningitis haemorrhagica interna, the pathophysiology and treatment of chronic subdural hematoma (SDH) has been a controversial neurosurgical topic. Through the years, concepts on the pathophysiology of chronic SDH have been reviewed and revised. Similarly, a variety of treatments have been advocatedobservation for spontaneous resolution, steroid and osmotic therapy, manipulation of intracranial pressure, radical calvariectomy to collapse the subdural space, shunting procedures, and exteriorization of the subdural space. Currently, the favored surgical treatments for chronic SDH are twist drill or burr hole craniostomy with or without closed system external drainage of the subdural space. More extensive procedures are now usually reserved for the 10-25% of patients who do not respond clinically to these treatments. This chapter will focus on the techniques of twist drill and burr hole craniostomy for chronic SDH. DIAGNOSIS The incidence of chronic SDH has been estimated to be 1-2 per 100,000 population per year with an increasing occurrence as age advances. Over 50% of patients may have no history of trauma and, even in those that do, the inciting incident is often mild and poorly remembered. Predisposing factors have been shown to include advanced age, chronic alcoholism, epilepsy, coagulopathy, and intracranial shunting procedures. Chronic SDH may present in a variety of ways, making the clinical diagnosis difficult. A frequent misdiagnosis is dementia because the patient is often elderly, a history of trauma is missing, and symptoms such as memory loss and personality change may be prominent and slowly progressive. Chronic SDH can present with acute or slowly progressing focal neurologic signs, mimicking a stroke or tumor. Other infrequent but well described presentations include meningismus, seizures, and ataxia. Chronic SDH is not commonly associated with
impaired consciousness, but headache may be a very prominent complaint. In the era before computed tomography (CT), the diagnosis of chronic SDH was not made until postmortem examination in over one-third of patients. Presently, CT is rarely incorrect in confirming or establishing the diagnosis. The typical finding is a focal hypodense lentiform lesion over the surface of the hemisphere. Occasionally, the CT may be unreliable if the SDH is isodense with the brain. In such situations, use of intravenous contrast may result in visualization of the vascularized subdural membranes, giving indirect evidence of the hematomas existence. Magnetic resonance imaging (MRI) can also assist in diagnosis when the CT is normal or equivocal. An acute subdural hematoma is slightly hypointense on T1 weighted images and markedly hypointense on T2 images. The hypointense signal is due to the presence of deoxyhemoglobin, a strong paramagnetic substance. As the deoxyhemoglobin is converted to methemoglobin, the T2 image becomes very intense. When the subdural hematoma becomes chronic, and the conversion to methemoglobin is complete, the hematoma will appear intense on both T1 and T2 images (Fig. 1). When considering radiographic imaging for chronic SDH, it should be borne in mind that there is no clear correlation between hematoma size and clinical symptoms and signs. Thus, selection of patients for surgical treatment should rely more on clinical than on radiographic criteria. In addition, a significant finding in many chronic SDH treatment series has been that remission of the clinical syndrome may significantly precede radiographic resolution of the SDHan important consideration in evaluating treatment results and the need for further intervention. PATHOPHYSIOLOGY The initial stages in the formation of a chronic SDH involve a proliferative response to blood in the subdural space. Fibroblasts from the dura invade the area to form both an outer and an inner membrane to encapsulate the SDH within approximately three weeks of its initial presence.
42
WILBERGER : CHRONIC SUBDURAL HEMATOMA
SURGICAL TREATMENT The surgical treatment for chronic SDH has evolved from craniotomy for radical membranectomy to burr hole and twist drill drainage of the fluid collection. Given the fact that chronic SDH may resolve spontaneously with complete and lasting recovery, it is not unreasonable to treat alert patients who have few signs of cerebral dysfunction with repeated clinical and CT follow-up. In those patients whose clinical symptoms and signs from the subdural fluid collection warrant intervention, burr hole or twist drill craniostomy with or without closed system external drainage has become the preferred initial treatment option. Twist Drill Craniostomy with External Closed System Drainage This treatment approach should be considered when CT and/or MRI demonstrates subdural fluid of homogenous liquid character without septations and with sufficient thickness (>1 cm) to ensure safety of blind dural perforation. This procedure maybe performed at the bedside under aseptic conditions using local anesthesia supplemented by intravenous sedation if necessary (Fig. 2). The site for drainage is selected based on CT findingsplacement of the twist drill hole is over the maximal thickness of the SDH. The scalp in this area is shaved to cover an area 3-4 cm in diameter from the selected twist drill hole site. After skin preparation with Betadine or other antiseptic solutions, sterile drapes are placed about the site. Xylocaine (0.5% with 1:100,000 epinephrine) infiltration of the surrounding skin is accomplished, a No. 15 scalpel blade is used to nick the skin, a 5/8-inch twist drill bit attached to a hand-powered drill is placed perpendicular to the skulls outer table, and drilling is begun (Fig. 2A). Drilling may be continued in a perpendicular direction or may then be slanted obliquely. Perforation of the outer table is appreciated by a lessening of tension on the drill bit; engagement of the inner table results in a binding of the drill bit and should lead to caution as only one to two more turns on the drill are usually needed to break through into the epidural space. The dura and outer SDH membrane are then blindly perforated with a sharp trocar or a 14- or 16-gauge needle to enter the subdural space. Only rarely does a significant amount of subdural fluid escape spontaneously at this point. A standard ventriculostomy catheter may be used as the subdural drain. This catheter is modified by cutting off the blunt end and adding several side holes along the shaft to facilitate fluid and particulate drainage. The stylet is left in the catheter as it is passed through the twist drill hole and is removed as soon as the catheter is in the subdural space to prevent intracerebral penetration. The catheter is then directed
Figure 1. MRI appearance of a chronic subdural hematoma.
Theories about the subsequent enlargement of the hematoma have been numerous. For years, it was held that an osmotic gradient developed across the membranes and that fluid was drawn into the subdural hematoma. Others have held that fragile neocapillaries within the membranes rupture repeatedly and fill the subdural cavity with recurrent hemorrhage. Recent research has focused on disordered hemostatic mechanisms with increased fibrinolytic activity within the membranes. Following the initial hemorrhage, abundant tissue thromboplastin is released into the subdural space, activating local clotting mechanisms. Thrombin is generated and crossed-linked fibrin is formed from fibrinogen. Clotting activation leads to mobilization of the intrinsic fibrinolytic system. Fibrin is split into fibrin degradation products which affect further clot formation. Defective clot formation causes recurrent hemorrhage. As this process is repeated, the dura reacts to fibrin nonspecifically to gradually form the vascularized outer membrane. As this membrane proliferates, the extrinsic fibrinolytic system is activated and a self-perpetuating vicious cycle is repeated. It has been postulated that the primary effect of surgical drainage procedures is to remove such self-perpetuating factors from the subdural space and to allow restoration of normal hemostatic mechanisms.
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Figure 2. Twist drill craniostomy with external closed system drainage. A, placement of the twist drill hole after the injection of a local anesthetic and the creation of a small stab wound in the scalp. B,
introduction of the subdural drainage catheter. C, tunneling of the drainage catheter. D, connection of the catheter to an external drainage system.
44
anteriorly or posteriorly for approximately 10 cm depending on the location of the hole in relation to the SDH cavity (Fig. 2B). The catheter is then checked for patency by allowing spontaneous gravity drainage of fluid or by aspirating 15-20 ml of the hematoma. Subcutaneous tunnelling of the catheter is accomplished after first anesthetizing the skin for 2-3 cm lateral to the twist drill site (Fig. 2C). A trocar is used to guide the catheter to an exit site 2-3 cm away from the twist drill site. The catheter is rechecked for patency before connecting to a sterile closed drainage system (Fig. 2D). All wounds are sutured closed with 3-0 nylon sutures. Postoperatively, prophylactic antibioticsnafcillin and cefotaximeare given during the time the subdural drain is left in place. Anticonvulsants are not given routinely unless there is a seizure history. The collection bag of the drainage system is positioned 10-15 cm below head level to promote gravity drainage of the subdural fluid. The patient is kept in bed with the head elevated no more than 30. Hydration, intravenous and oral, is encouraged to promote brain reexpansion. Within 24 hours, a follow-up CT scan is obtained (Fig. 3). If the patients initial symptoms and signs have resolved, the CT scan shows substantial reduction (>50%) in the size of the fluid collection, and/or output from the subdural catheter is minimal or clear, the catheter is removed. If these criteria are not met, the catheter may be left in place for several more days, and CT scans obtained daily. Subdural fluid samples are sent daily and on removal of the catheter for Gram stains, cultures, and sensitivity determinations. If the clinical symptoms and signs are not satisfactorily resolved after two to three days and the CT scan shows persistence of a significant SDH, alternative treatment approaches should be considered. Burr Hole Craniostomy Burr hole craniostomy holds several advantages over the twist drill technique: burr holes permit wider visualization of the subdural space and of the outer and inner subdural membranes; hemostatic control of the vascularized outer membrane can be accomplished; the larger opening permits freer drainage of thicker blood collections and particulate matter; the subdural space may be cross-irrigated between burr holes for more complete emptying of the hematoma; brain reexpansion may be directly visualized; and, if necessary, the burr holes can be converted to a full craniotomy for further treatment as indicated. Burr hole craniostomy can be accomplished with local anesthesia supplemented by intravenous sedation. Siting of the burr holes should be done with two factors in mind: they should relate to the location of the maximal subdural fluid collection, but skin incisions and hole place-
ments should be able to be converted to a full craniotomy without compromise of the vascular supply of the scalp (Fig. 4A). Once the site is selected, the scalp is shaved for 34 cm around the area; antiseptic skin preparation is accomplished and local anesthesia is induced with Xylocaine (0.5% with 1:100,000 epinephrine). A 2.53.0-cm skin incision is made to accommodate an airpowered cranial perforator and the periosteum is stripped away from the area. A small mastoid retractor can be used to retract the skin edges. After the burr hole is made, the inner table is removed with a small curette or a Penfield No. 1 dissector. Bipolar coagulation of the dura is accomplished and a No. 11 scalpel blade is used to incise the dura in a cruciate fashion. The outer subdural membrane is also coagulated and opened sharply. The subdural fluid often runs out or gushes out spontaneously at this point. A small red rubber catheter (7 or 9 French) can then be directed into the subdural space. Warm saline irrigation is carefully flushed through the subdural space until the effluent is clear and the inner membrane brain surface is visualized (Fig. 4B). A subdural catheter and closed external drainage system can then be left in place as described previously. Careful hemostatic closure of the skin incision with galeal and subcutaneous sutures should be performed to avoid any bleeding that may gain access to the subdural space and cause an acute reaccumulation of the hematoma. If the subdural fluid is too thick to evacuate through the burr hole, or septations are encountered which prevent effective drainage of the subdural space, conversion to a full craniotomy is possible for stripping of the inner and outer membranes and complete evacuation of the hematoma (Fig. 4C). The postoperative management of patients with burr hole craniostomy is not significantly different from that described for twist drill craniostomy. COMPLICATIONS AND TREATMENT RESULTS The outcome of surgical treatment of patients with chronic SDH is quite variable. A compilation of treatment results over the past 30 years yields a cure rate ranging from 39 to 100%, a recurrence rate of 1-37%, a rate of neurologic sequelae of 7-32%, and a mortality rate of 0-28%. Such variation could not be explained adequately by a difference in surgical techniques alone, but more likely it reflects varying trends in patient selection and the means and mechanisms of follow-up. Comparison of burr hole versus twist drill techniques yields somewhat more consistent results, yet 1025% of patients usually require some form of addi-
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Figure 3. A, CT scans of a chronic SDH immediately after twist drill drainage. B, 24 hours later with the subdural drain still in place.
C, 4 weeks later showing substantial resolution of the SDH.
46
Figure 4. Burr hole craniostomy. A, siting of the burr holes. B, cross-irrigation of the subdural space between holes. C, conversion of burr holes to a full craniotomy.
47
tional treatment. When evaluating results of treatment in any given patient, however, as noted previously, it must be borne in mind that remission of the clinical syndrome of chronic SDH does not necessarily require radiographic resolution of the fluid collection. Camel et al. found in their series of twist drill craniostomy treatment that 41 of 45 patients (91%) having residual SDH on follow-up CT scan had complete or nearly complete resolution of symptoms. Similarly, CT scans did not normalize following burr hole treatment until after three weeks in 92% of cases reported by Richter and after 40 days in 84% of cases described by Markwalder. Thus recurrence of the SDH after twist drill or burr hole treatment must be considered in light of such findings. Excluding the need for reoperation, the compli-
cation rate from burr hole or twist drill drainage is quite low. Infection rates range from 1.5% to 4.2%; subdural empyema has been reported in approximately 2% of treated patients. Richter reported two epidural hematomas in a series of 120 patients after burr hole SDH evacuation. Several authors have reported tension pneumocephalus after drainage of the subdural space. Burr hole or twist drill craniostomy thus appears to be a safe and reliable method of dealing with a clinically symptomatic chronic SDH. Other more invasive and extensive procedures, however, may be necessary in the few patients who are not appropriate candidates for these procedures or who have recurrent or residual clinical problems in spite of this mode of treatment.
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TAILORED TEMPORAL LOBECTOMY USING SUBDURAL ELECTRODE GRIDS

ISSAM A. AWAD, M.D., M.S. JOSEPH F. HAHN, M.D.
PATIENT SELECTION Patients with intractable epilepsy where noninvasive techniques do not clearly define the zone of epileptogenicity to the mesial temporal lobe structures need further delineation of the epileptic zone prior to resective surgery. In these cases, noninvasive electroencephalographic (EEG) recording or the presence of a structural lesion may suggest basal frontal or lateral temporal epileptogenicity. Especially on the dominant side, these regions cannot be resected safely without tailored mapping. In the following illustrated text, we describe the technique of insertion of subdural electrodes in the circumstance where surface recording alone suggests left frontotemporal epileptogenicity (interictal epileptiform activity and seizure-onset EEG data) but does not define it further to the mesial temporal structures. The strategy for electrode implantation is designed to allow coverage of basal frontal areas, lateral frontotemporal structures, and basal temporal structures. The electrodes are subsequently used to map interictal and ictal-onset epileptiform activity. Subsequent extraoperative stimulation using these electrodes defines areas of cortex involved in speech function (zones of Broca and Wernicke). A tailored temporal resection is then designed to accomplish maximal resection of epileptogenic tissue, while sparing eloquent regions of brain involved in speech function. The general techniques of subdural electrode insertion and brain mapping may also be used in extratemporal regions of the brain, or in cases where a structural lesion (i.e., neoplasm, vascular malformation, etc.) is located adjacent to eloquent brain. PREOPERATIVE PREPARATION Anticonvulsant therapy is titrated to levels near the toxic range prior to the insertion of subdural electrodes. Intravenous antibiotics aimed to cover the skin flora (i.e.,
oxacillin, vancomycin, etc.) are administered at the time of skin incision for electrode implantation and are continued prophylactically until electrode removal and resection of the epileptogenic tissue. The patient would have donated autologous blood two to three weeks prior to surgery and/or would have been typed and screened for possible blood transfusion. Partial thromboplastin time, prothrombin time, and bleeding time are checked preoperatively to rule out coagulopathy which may be related to chronic anticonvulsant use.
SURGICAL TECHNIQUE Operative Positioning The patient is placed in the supine position on the operating table; the head is extended 45 and rotated 60 away from the operative side (Fig. 1). It is helpful to place the head at the foot of the operating table to provide more knee room for the sitting surgeon and to allow the anesthetist or nurse to raise or lower the operating table at the request of the operating team. The head is fixed in the desired position using a Mayfield head clamp or other skull fixation device. The whole head is shaved because meticulous scalp hygiene will be required in view of the exiting electrode cables. The presence of hair near the electrode exit sites will invariably interfere with proper care and hygiene at these sites. Draping and Skin Incision A skin incision is marked to allow wide exposure of potential areas of brain resection. Because the precise extent of the zone of resection is not known at this time, a large frontotemporal incision is generally performed. Draping should allow exposure of not only the skin incision but also sites of potential cable exit. Because of this, the scalp is prepared in a wide area beyond the proposed incision. Otherwise, draping is performed as for a routine craniotomy.
49
Figure 1. Patient positioning for frontotemporal insertion of subdural electrodes.
Implantation of Subdural Electrodes The skin is incised through the galea aponeurotica, and Raney clips are applied to both edges of the scalp. The scalp is reflected in the subgaleal plane, preserving attachment of the underlying temporalis muscle to the cranial bone for subsequent osteoplastic craniotomy. Osteoplastic bone removal (with a muscle nutrient pedicle attached) is thought to minimize the risk of flap infection in the setting of chronically implanted subdural electrodes. If a free bone flap is elevated, consideration must be given to maintaining this bone in a sterile fashion in a freezer until removal of the subdural electrodes and final replacement of the bone. The scalp is reflected in the subgaleal plane and is held anteriorly and inferiorly using fishhooks (Fig. 2). The temporalis muscle is then incised in the line of the proposed osteoplastic flap, making sure to preserve a viable vascularized muscle pedicle inferiorly. Three burr holes are placed, one at the pterion, one in the posterior temporal area, and one in the posterior frontal area. These are connected using a power craniotome, except inferiorly where the bone is rongeured under the preserved muscle pedicle (Fig. 2). This facilitates elevation of the osteoplastic flap and its reflection inferiorly along the temporalis muscle pedicle. The dura mater is tacked to the edges of the surrounding craniotomy using 4-0 Nurolon sutures. The dura mater is opened in a C-shaped fashion and flapped anteriorly (Fig. 3). Prior to dural opening, if the brain appears tense,
intravenous mannitol is administered in the dose of 1 g/ kg, in addition to ensuring hyperventilation to a pCO2 of 25-30 mm Hg. The dural opening should allow exposure of the inferior frontal regions and the lateral temporal lobe. The selection of subdural grids, including size and number of electrodes, is dictated by the areas of the brain to be covered. Subdural electrode grids consist of stainless steel (or platinum for magnetic resonance imaging compatibility) discs embedded in a sheet of Silastic, typically 1 cm apart. These are available through several commercial manufacturers. In the particular instance being described, a 4 4 grid is used to cover the basal frontal region (orbitofrontal cortex). A large 8 8 grid is used to cover the lateral frontotemporal neocortex, and this is folded inferiorly to cover the inferior temporal and fusiform gyri. Another two 1 4 strips of electrodes are inserted transversely under the temporal lobe to cover the anterior and posterior basal temporal areas (Fig. 3). Wound Closure Additional mannitol may be infused intravenously to ensure continued brain relaxation prior to dural closure. The dura mater is closed in a watertight fashion around the electrode cables using 4-0 Nurolon sutures (Fig. 4). The suture is passed in purse-string fashion around the electrode cables for maximal watertight effect. A piece of Gelfoam is placed around the site of cable exit from the dura mater. The osteoplastic flap is replaced and kept free-floating or fixed loosely using
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AWAD AND HAHN : TAILORED TEMPORAL LOBECTOMY USING SUBDURAL ELECTRODE GRIDS
Figure 2. Elevation of an osteoplastic bone flap.
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Figure 3. Insertion of subdural electrodes. The choice of size and number of electrode grids depends on the areas of the brain to be covered. In this particular instance, a 4 4 electrode grid is used to cover the basal
frontal regions (orbital frontal cortex), an 8 8 grid is used over the lateral frontotemporal convexity, and two 1 4 strips are placed transversely to cover the basal temporal area.
Figure 4. Wound closure including watertight dural closure around the cable exit sites. The cables are tunneled subcutaneously and are brought out via a separate scalp incision. 52
temporalis muscle sutures. The cables are brought out via the posterior burr hole and are tunneled subcutaneously to a separate stab scalp incision from which they exit. At the site of skin cable exit, 3-0 Nurolon sutures are used once again in a purse-string fashion to ensure a watertight closure. The scalp is then closed in two layers using inverted interrupted 2-0 Vicryl sutures for the galea aponeurotica and interrupted 3-0 Nurolon sutures for the skin (Fig. 4). BRAIN MAPPING Following electrode implantation, the patient is nursed in a critical care unit for 24-48 hours. Throughout this period, close attention is paid to the serum electrolyte values, ensuring a sodium level greater than 140 mEq/dl. Frequent infusions of mannitol or other diuretics and strict fluid restriction are adopted. Inappropriate antidiuretic hormone secretion and other factors may induce significant brain edema during this critical period, necessitating removal of the subdural electrodes. We have not encountered the need to remove electrodes because of brain edema in any patient maintained on strict fluid restriction and where the serum sodium concentrations were maintained in an elevated range. Intravenous dexamethasone is also administered at a dose of 4 mg every six hours. Two to three days following electrode implantation, fluid restriction may be eased as tolerated, and the steroids are tapered. The patient is transferred to a special epilepsy monitoring unit where the anticonvulsant medications are gradually tapered for the first phase of brain mapping. This first phase of brain mapping will consist of interictal and ictal-onset monitoring of epileptiform activity. The special monitoring unit is equipped with videoEEG capabilities for real-time correlation of seizure symptomatology with EEG phenomena. Monitoring of epileptiform activities is continued until sufficient interictal abnormalities are recorded and mapped and until several of the patients typical seizures have been recorded. This phase of the monitoring typically lasts 5-10 days. Following this, the serum anticonvulsant levels are gradually titrated once again to near-toxic ranges, in preparation for cortical stimulation. The second phase of brain mapping will consist of stimulation of each of the subdural electrodes in a systematic fashion, to map eloquent brain regions. This is performed in the epilepsy monitoring unit in an unhurried fashion, with retesting performed as needed to ensure accurate localization of frontal and temporal speech areas. The location of the electrodes is correlated closely with surface landmarks as noted intraoperatively and as documented by intraoperative drawings and photographs. Each electrode is stimulated during wakefulness starting initially with a current intensity of 1 mA. As long as there are no clinical symptoms or EEG afterdischarge, subsequent trials are used with gradu-
ally increasing amperage. If there are no symptoms or signs with stimulation at a maximum of 15 mA or at amperage just below the afterdischarge threshold, then testing is repeated for reading or speech interference. Information gathered from recording and electrical stimulation will consist of delineation of zones of maximal interictal epileptiform activity, seizure-onset epileptiform activity, and eloquent cortical regions (Fig. 5). A plan of resection is then designed to excise a maximal extent of epileptogenic brain, while staying at least 1 cm away from eloquent brain regions. In the particular case illustrated here, epileptiform regions are noted in lateral and basal temporal areas. These can be resected just close to but not including the temporal speech area (Wernickes area). Electrical stimulation may induce speech interference near the temporal tip and in the fusiform gyrus (basal temporal speech area). Resection of these areas (non-Broca, non-Wernicke) has not been associated with any untoward sequelae. In addition to cortical stimulation, evoked potential studies of the lateral cortical plate may be performed to define the rolandic fissure (as per standard neurophysiologic techniques). Other specialized studies of
Figure 5. Results of cortical mapping in a hypothetical case. Frontal and temporal speech areas have been delineated by cortical stimulation. Prolonged monitoring has revealed a zone of interictal epileptiform activity, and another zone of seizure-onset epileptiform activity. The planned resection (dashed line) will include maximal excision of these epileptogenic areas while sparing mapped eloquent brain regions.
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Figure 6. Tailored temporal lobectomy. At the second operation, the wound is reopened and the subdural plate is used to guide the planned
resection line. This will extend posteriorly to (but not include) the mapped temporal lobe speech area (Wernickes area).
Figure 7. Temporal lobectomy is performed along the planned resection line using bipolar electrocautery and suction. The Cavitron ultrasonic aspirator used at low settings is very helpful for such brain inci54
sions. The diagram illustrates the extent of temporal lobectomy as guided by extraoperative brain mapping.
speech and memory and of movement-induced potentials can be performed as per institutional protocols. The whole period of brain mapping (recording of epileptiform activity and electrode stimulation) usually does not exceed three weeks (mean, 10 days). Throughout this time, prophylactic antibiotic coverage is continued and meticulous scalp hygiene is maintained. Leakage at the cable exit sites is not infrequent during this time. If it becomes excessive, additional purse-string sutures at the cable exit sites may be placed at the bedside. REMOVAL OF SUBDURAL ELECTRODES AND TAILORED TEMPORAL LOBECTOMY The patient is returned to the operating room following the period of brain mapping and is placed once again under endotracheal anesthesia. The head is fixed in the same position and the areas of previous scalp incision and cable exit sites are prepared and draped according to routine neurosurgical procedures (Fig. 6). The wound is reopened with cultures taken from every layer prior to copious antibiotic irrigation. At this time, the cable is cut and removed (by pulling out) prior to dural opening. The dura mater is opened and the cortical surface is once again examined through the subdural grids, and correlations are made with previous photographs and diagrams. The proposed line of resection is then marked on the cortical surface prior to removal of the subdural electrodes (Fig. 6). Basal electrodes are left in place until completion of the basal resection, for they can be quite helpful in delineating the extent of such resection. Cortical resection is performed along the proposed line using bipolar electrocautery and suction (Fig. 7). The Cavitron ultrasonic aspirator used at low setting is particularly helpful in this regard. Following excision of the desired portion of the temporal lobe, a decision must be made whether to also excise mesial temporal structures. Meticulous hemostasis is ensured. The wound is closed in layers, including watertight dural closure. A piece of the osteoplastic bone flap is sent for culture along with
the multiple cultures obtained during wound opening. The subdural plates themselves are sent for cultures. The cable exit site is debrided and closed in a single layer. Sterile dressings are applied. POSTOPERATIVE CARE Postoperatively, anticonvulsants are continued at or near toxic levels, and intravenous antibiotics are maintained until final intraoperative culture results. Frequently (onethird of cases), these cultures reveal bacterial colonization of at least one layer of the wound or the subdural plates. In this case, intravenous antibiotics are continued for 14 days following surgery and are followed by one month of oral antibiotics, all aimed against the cultured organism. This is done even in the absence of any clinical evidence of wound infection. In the circumstance of a positive bone culture, intravenous antibiotics are continued for four weeks even in the absence of clinical evidence of wound infection. The above aggressive regimen of antibiotic treatment of bacterial colonization of the wound has eliminated frank wound infections (purulence or meningitis) in the last 80 consecutive cases of subdural electrode insertion. Prior to this, wound purulence in the setting of implantation of subdural electrodes was not infrequent at our institution. OUTCOME AND COMPLICATIONS Using the above precautions, infection should not be more frequent with this procedure than with any other neurosurgical operation. Other complications are related to the area of cortical resection. As long as the zone of resection is at least 1 cm away from mapped eloquent areas, we have not encountered any instances of permanent neurologic deficit related to focal cortical function. Favorable seizure outcome is accomplished in nearly two-thirds of patients undergoing this operation. This is highly dependent on patient selection and other factors related to the etiology and severity of the epilepsy.
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GUNSHOT WOUNDS OF THE BRAIN

SUZIE C. TINDALL, M.D. ALI KRISHT, M.D.
PATIENT SELECTION Most patients with gunshot wounds to the head require surgery. Any depressed fracture due to a penetrating missile is an open fracture and requires exploration, debridement, and elevation in order to prevent complications such as infection or cerebrospinal fluid (CSF) leakage. As patients reach the more serious end of the injury spectrum, decisions regarding surgical intervention become more difficult, as surgery may have little to offer. We list some criteria for and against surgical intervention, realizing that each situation will need individual assessment.
Criteria in favor of surgical intervention: Glasgow coma scale (GCS) 8 or above; GCS 5-8 with good response to cerebral resuscitation; Limited nondominant hemisphere injury; Tangential wounds; Young age. Criteria against surgical intervention: GCS 3-5; GCS 5-8 with no response to cerebral resuscitation; Extensive dominant hemisphere injury; Brain stem injury; Injuries crossing the midline; Old age; Associated major multisystem injuries.
head completes the preoperative radiological evaluation. SURGICAL PROCEDURE The goals of surgery in patients with gunshot wounds to the head are to remove all devitalized tissue, debris, and hematoma, to control hemorrhage, and to provide dural closure and scalp coverage. General endotracheal anesthesia is induced and the pCO2 is maintained between 28 and 32 torr. Mannitol and furosemide are used if increased intracranial pressure is believed to be a potential problem. The head is widely shaved. Hair and debris are removed from the irregular edges of the scalp defect. The head is positioned to facilitate extension of the scalp incision if necessary. For uncomplicated superficial wounds, the head may rest softly on a foam headrest, but for more complicated deep wounds in which brain retractors will be needed a three-point head fixation device is used. The scalp is prepared with a gentle scrub of Betadine soap followed by painting with Betadine solution. Sterile towels are secured circumferentially with a surgical stapler and cranial drapes are positioned. Three major objectives are kept in mind when planning the scalp incision:
1. 2. 3. To preserve blood supply to the scalp edges; To incorporate the entry and/or exit wounds into the incision; To establish adequate exposure of the limits of fractured bone and any adjacent structures that might need repair.
PREOPERATIVE PREPARATION Patients with cerebral gunshot wounds are evaluated upon arrival into the emergency facility. In addition to routine trauma evaluation and care, coma grade and neurological function are assessed, and measures for cerebral resuscitation (intubation, hyperventilation, and mannitol) are instituted if indicated. Entrance and exit wounds are evaluated and temporary dressings applied. All patients receive tetanus prophylaxis and broad spectrum antibiotics. Anticonvulsants are administered if there has been obvious cortical damage. Plain anteroposterior and lateral skull radiography followed by noncontrasted CT scanning of the
We find the simple linear or modified linear incisions (Fig. 1A) to be adequate in most injuries involving the hair-bearing scalp. For injuries of the forehead, a bicoronal scalp incision is used (Fig. 1B). The anterior branch of the superficial temporal artery should be preserved. Such a scalp incision facilitates adequate exposure of the frontal cranial base and avoids cosmetically unacceptable scars about the face. Raney clips are used on healthy scalp edges, but clips are avoided on scalp edges macerated or injured at the entrance or exit sites. After completing the scalp incision, the bony defect
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TINDALL AND KRISHT : GUNSHOT WOUNDS OF THE BRAIN
Figure 1. A, for wounds within the hair-bearing scalp, the best scalp incision is usually a linear or curvilinear incision centered over the entry or exit wound. B, for injuries of the face or forehead in which wide exposure of the frontal or anterior temporal fossa may be required, a
bicoronal scalp incision is used. The incision is located behind the hairline and positioned so as to preserve the anterior branch of the superficial temporal artery if there is potential disruption of the supraorbital blood supply from the injury.
is widened to expose all edges of the torn dura (Fig. 2A). This can be achieved by craniectomy or craniotomy. Large pieces of bone are kept and soaked in Betadine solution. The dura is opened back to healthy brain all around. Control of active bleeding is accomplished using bipolar cautery or clips for very large vessels. Torn venous sinuses are oversewn or patched with pericranium and Gelfoam. The missile track is then explored and debrided. One helpful technique is illustrated in Figure 2B. The tip of an Asepto syringe is introduced into the depth of the track, and the wound is irrigated with saline under moderate pressure while the syringe is gently withdrawn. This maneuver will deliver debris and small indriven pieces of bone. Pieces of bone or bullet fragments still embedded in the wound may be localized using intraoperative ultrasound (Fig. 2C). In removing these fragments, the gelatinous pedicle should be coagulated, cut, and allowed to slip back in the wound as it frequently contains a small blood vessel that has been previously tamponaded by the bone fragment (Fig. 2D). If the track is very deep, it is a good idea to set up a self-retaining retractor system to aid in maintaining exposure. This helps to keep the track well defined and aids in obtaining hemostasis deep in the wound. Bacterial contamination of metallic bullet fragments is much lower than that of bone fragments. For this rea-
son and because bullet fragments usually travel to much greater depth, we often leave bullet fragments behind. Necrotic brain, readily identified by its purple color and soft fragile texture is removed with suction. Hemostasis is achieved with bipolar coagulation and gentle tamponade with Gelfoam. We try not to leave foreign hemostatic agents in the wound, as we think that they might serve to increase the incidence of cerebritis and brain abscess. Once all bleeding has been controlled, hemostasis is checked by asking the anesthesiologist to increase the patients intrathoracic pressure as in Valsalvas maneuver. At this stage, the wound is ready to be closed. A pericranial patch is used to close the dura (Fig. 2E). Watertight dural closure helps to prevent CSF leakage or fungus cerebri. Sometimes taking a pericranial graft may prove difficult because of a lack of exposure; in certain circumstances, attempts at harvesting a graft may further threaten an already tenuous blood supply to the injured scalp edges. Under such circumstances, graft material may be taken from fascia lata or other body fascia through a separate incision. Whether or not to replace the bone remains a controversial issue. If the wound is extremely dirty and contaminated, the bone is left out and the patient brought back for cranioplasty in six months; if the wound is relatively clean, large (cleansed) fragments of bone or a craniotomy bone flap is replaced and an-
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Figure 2. A, adequate exposure of the injured area is essential. Bone removal by craniectomy or craniotomy back to normal dural edges is desirable. B, an excellent technique for removing indriven bone fragments and other debris is with gentle warm saline irrigation with an Asepto syringe. C, intraoperative ultrasound is occasionally useful for
localizing residual bone or bullet fragments. D, the gelatinous strand adherent to an extracted bone fragment is best coagulated before it is divided as it often contains a small vascular pedicle. E, watertight dural closure helps to prevent CSF leakage and fungus cerebri.
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TINDALL AND KRISHT : GUNSHOT WOUNDS OF THE BRAIN
chored with nonabsorbable, monofilament, synthetic sutures. Scalp closure or scalp coverage is critical in preventing later complications. Routinely, the scalp is closed in a single layer with interrupted vertical mattress sutures using 3-0 nylon. This prevents placing foreign suture material in the galeal layer and brings galea and epidermis into anatomical alignment. The closure should not be under excessive tension. If simple closure of this type is not possible, arrangements should be made to adequately cover the injured area by use of rotational scalp flaps or a free vascularized flap. SPECIAL SURGICAL SITUATIONS Injuries of the major dural venous sinuses may be difficult to repair. In most cases, a sinus laceration may be simply oversewn. Generous exposure of the injured sinus is mandatory for more severe sinus injuries, where sacrifice of the sinus would prove potentially detrimental to the patient. In such cases, the sinus can be patched with pericranium or temporalis muscle. Bleeding can be controlled temporarily by digital pressure or occlusion with a No. 7 Fogarty catheter. Gunshot wounds of the frontal area frequently prove to be very challenging. The face, orbits, and frontal and temporal fossae may be involved. A generous frontal, and sometimes bifrontal, exposure is required for adequate debridement and repair. The involved sinuses should be exenterated. Intradural graft repair using pericranium or fascia is very important for preventing eventual CSF leak-
age. Foreign and avascular materials should be avoided in attempts to reconstruct the bony floor. Wounds involving the temporal bone area are associated with a high incidence of vascular injury. Hemorrhage may be controlled with packing of the external ear canal or indirect balloon occlusion of the involved vessel or sinus. COMPLICATIONS Disseminated intravascular coagulation may develop at the time of operation. It is usually first recognized by noting diffuse oozing of blood at the operative site which is difficult to control with the usual methods. Laboratory evaluation will document elevated coagulation times and fibrin split products in conjunction with reduced platelet counts and fibrinogen levels. The condition is treated with infusions of fresh blood products, including frozen plasma and platelets. CSF leakage may occur in the form of a cutaneous fistula, otorrhea, or rhinorrhea. Hydrocephalus must be ruled out, and the leak may stop with temporary placement of a spinal or ventricular drain. If the leak persists, the wound should be reexplored with adequate dural closure. Meningitis, abscess, and empyema are possible infectious complications. All are treated with appropriate antibiotics, and surgical drainage is frequently necessary with abscess or empyema. Subarachnoid hemorrhage from a traumatic aneurysm may occur occasionally. Under these circumstances, a cerebral angiogram should demonstrate the lesion.
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TRANSTORCULAR OCCLUSION OF VEIN OF GALEN MALFORMATIONS

J. PARKER MICKLE, M.D. RONALD G. QUISLING, M.D. KEITH PETERS, M.D.
INTRODUCTION The transvenous therapy for vascular malformations involving high- and low-flow shunts is nothing new. Sean Mullan and others have been advocates for the incorporation of this route of therapy for various lesions for many years. The concept that the arterial side of high-flow fistulas needed to be attended to first in the obliteration of these lesions virtually eliminated the discussion and use of the transvenous approach to these lesions for decades. The great risk of venous outlet obstruction and therefore marked increased pressure in the thinly walled veins just distal to the shunts could very easily result in massive hemorrhage, producing major neurologic deficit or death. This threat and potential outcome has been demonstrated graphically to occur with transarterial endovascular therapy for certain malformations when the embolic material, principally glue, escaped into the venous outlets, solidifying the egress and resulting in major venous outlet occlusion with hemorrhage. However, Mullans excellent results with the transvenous approach to carotid cavernous fistulas continued to stimulate interest in a transvenous approach to various vascular malformations, especially those lesions such as vein of Galen malformations which carry high mortality and morbidity statistics with the standard surgical and transarterial approaches. As the burgeoning subspecialty of interventional neuroradiology continued to grow, various technologies including new thrombolytic agents and particles have made possible the approach to lesions heretofore unreachable. The combined interventional and neurosurgical approach to vein of Galen malformations as reported by Berenstein and Epstein demonstrated the utility of this combined approach in improving morbidity and mortality statistics. We reported in 1986 the use of the transtorcular approach for the endovascular treatment of vein of Galen malformations. Our enthusiasm, because of the initial successes, became tempered after a review of 24 patients treated in a similar fashion revealed many of the problems with this new therapy. However, the overall statistics, especially in the neonate, have prompted continued interest in this technique as an adjunct of therapy for the elimination of central high-flow fistulas. Of the nine neonates we have treated with the transtorcular approach, five are alive and three are virtually normal except for mild spasticity in the lower extremities. The 15 infants and older children treated with the transtorcular approach have fared very well, with a 50% cure rate angiographically and one death. This death was secondary to an acute shunt malfunction three months after transtorcular embolization of the vein of Galen malformation. TREATMENT CONCEPTS The general concepts which are important to the understanding of the utility of the transvenous treatment of vein of Galen malformations remain fairly simple. First, in all patients the goal is to gradually occlude and thereby eliminate the fistula or fistulae such that acute thrombosis with acute venous outlet obstruction does not occur. Various guidelines and experiences obtained from our series will be discussed below as to how this goal can be attained. Second, the goal for transvenous therapy in the neonate is to produce a cardiac survivor while maintaining neurologic integrity. This goal has often resulted in converting the neonate into a surviving infant with a persistent fistula. There seems to be a delicate balance for the neonate: the therapist should produce a cardiac survivor but not eliminate the fistula completely because of the major risk of venous outlet obstruction, hemorrhage, and death. Again, how this is attained will be discussed below. The third concept of major importance in the use of this therapy revolves around the potential for continued, slow, progressive thrombosis after one or more therapies with the transtorcular route. We have been
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MICKLE ET AL. : TRANSTORCULAR OCCLUSION OF VEIN OF GALEN MALFORMATIONS
tempted in our 15 infants and older patients to consider other therapies to rid the patient of the fistula completely (stereotactic radiosurgery or direct surgery). In two instances, we have admitted patients to the hospital for prestereotactic radiosurgery angiograms and have found in one of these the total obliteration of the fistula since the childs previous angiogram three months prior to that admission and a substantial reduction in the flow in the other patient which allowed us to wait to see if continued thrombosis would occur. We have therefore treated no patients with adjunctive therapy including surgery or stereotactic radiosurgery and have had no patients hemorrhage or develop other progressive symptomologies necessitating further therapy. The bottom line, however, is that, as pointed out by Hoffman and others, the prognosis of untreated or persistent vein of Galen malformations tends to be poor. Therefore, once therapy for these malformations is undertaken by whatever route, continued perseverance and careful follow-up are essential for optimum outcome. TECHNICAL ASPECTS The key steps in the transtorcular approach to vein of Galen malformations will be discussed. This simple operation is rapid and utilizes common materials and instruments found in all operating rooms and radiology suites. Various embolic materials such as coils can be delivered to the vein of Galen malformation complex not only through the torcular approach but through a direct jugular puncture or through the femoral route if access can be obtained. The neurosurgeon, usually the primary care physician in this disorder, has control over which route is chosen for the treatment of these malformations. Today, transarterial endovascular therapy combined with transvenous occlusive therapy would seem to be the treat-
ment of choice for this very difficult group of malformations. The transarterial approach requires the cooperation of an interventionlist trained in microcatheter manipulation both on the transarterial and transvenous sides. In the neonate, access is often difficult from the transarterial side, whereas the transvenous route, especially the transtorcular route, is quick and easy. Of course, it is essential to obtain high-quality pretherapy angiograms to assess the extent of the lesion and the flow characteristics necessitating the therapy. Also, computed tomography (CT) scans and magnetic resonance imaging (MRI) of the brain and ventricular spaces are essential before therapy. Many of these individuals, especially in the neonatal group, have pretherapy lesions which can be extensive at times and can preclude therapy. Massive encephalomalacia is a relative contraindication to any form of therapy in this disease. Many of these patients have pretreatment hydrocephalus and this often necessitates shunting procedures as a major form of therapy in the vein of Galen malformations. Once the transtorcular route for therapy has been decided upon, the steps as outlined below and in the accompanying figures can be carried out rapidly and in repeated sessions to obtain optimum outcomes in the neonate, infant, and older child. Equipment and Technique The initial surgical therapy is carried out in the operating room, and therefore a standard craniotomy set is necessary. A C-arm. imaging system is necessary during the procedure for placement of wires and also during the venography (Fig. 1). Newer real-time subtraction units are available and make following the course of therapy much easier and more accurate. A large burr hole is placed over the area of the torcular herophili as identified on the angiogram. The ul-
Figure 1. An efficient arrangement of personnel and equipment during a transtorcular embolization for a vein of Galen malformation is shown. The surgeon and assistant (A and C) are seated, with the nurse (B) and equipment directly behind the patients head. The patient is positioned such that the occiput is close to the edge of the table so that manipulations with various catheters entering the torcular are unimpeded. The gantry for the C-arm fluoroscopic unit (D) can be moved easily in and out to obtain high-quality real-time fluoroscopic images during manipulation and deposition of coils during the procedure. It is very important to have the visual monitor (E) directly across from the surgeon so that all fluoroscopic manipulations can be seen easily during the procedure.
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Figure 2. These drawings depict the patient positioning (A), location of the incision (), and the appearance of the torcular through the burr hole (B). The small roll under the right shoulder allows the midline occiput to be parallel with the floor. This makes the approach through the torcular with the various catheters quite simple. If the torcular is not identified clearly after the burr hole is completed, then the craniectomy can be enlarged with rongeurs to better expose the structure for emboliza-
tion. The ultrasonic scanner can be used to identify the torcular, straight sinus, and aneurysm through this burr hole. Bleeding during the placement of the incision and burr hole is minimal, and the dura forming the outer surface of the torcular is thick and resistant to injury. It is not necessary to place a purse-string suture through the outer layer of dura and this will result in bleeding.
trasound probe is very useful in defining the torcular herophili, straight sinus, and aneurysm (Fig. 2). The area of the torcular herophili is tapped with a 25-gauge needle to ensure free return of arterialized blood (Fig. 3A). A 16-gauge Angiocath is passed through this puncture and the soft end of the Angiocath is left in place through which a short, soft guidewire is advanced under fluoroscopic control into the area of the aneurysm
(Fig. 3, B-D). Under fluoroscopy, an angiography catheter or sheath with an attached Tuohy-Borst adapter is advanced over the wire into the area of the aneurysm (Fig. 3F). The guidewire is removed and a venogram performed through the indwelling angiography catheter to assess location and flow characteristics. Various methods of measuring pressures and flows can be utilized at this point in the procedure to
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Figure 3. These drawings (A through K) represent the essential steps in the deposition of thrombogenic wires through the torcular via the straight sinus into a vein of Galen aneurysm. The area of the torcular is tapped with a 25-gauge needle (A), and brisk bleeding results. Contrast agents can be injected through this 25-gauge needle if there is any question about the location of the penetrating needle. This needle is removed and a standard 16-gauge Angiocath (B) is placed through the same hole into the straight sinus. The sharp inner needle of the Angiocath is removed, and then the soft outer sheath can be advanced further into the straight sinus (C). Bleeding can be vigorous at this point but is controlled nicely
with an occluding finger placed over the hub of the sheath. A standard soft guidewire is then placed through the sheath and advanced into the aneurysm under fluoroscopic control (D). The Angiocath sheath is then removed while maintaining the position of the guidewire with the aid of fluoroscopy. The assistant holds the guidewire in place after the sheath has been removed (E) and then the surgeon advances a short angiographic catheter or sheath with an attached Tuohy-Borst adapter over the indwelling guidewire into the aneurysm (F). It is extremely important to maintain the position of the guidewire safely within the confines of the aneurysm during the placement of this catheter.
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Figure 3. (Continued) The floppy guidewire is then removed and a venogram can now be performed through the indwelling angiographic catheter (G). A 90-145-cm floppy guidewire (the mandrel was removed prior to surgery) is now advanced through the Tuohy-Borst angiographic catheter into the aneurysm (H and I). The venogram is performed after deposition of this basket (I) and, if needed, Gianturco coils of various
sizes can be deposited on this basket lattice (J) to further reduce the flow and to encourage thrombosis (J and K). An occluding finger is used to control bleeding over the torcular once the angiographic catheter has been removed. A piece of Gelfoam is placed over this area and the skin is closed in a standard fashion (K).
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help outline the therapeutic goal (Fig. 3G). A long floppy guidewire is passed into the aneurysm very carefully in order to create a basket onto which various sizes of thrombolytic Gianturco coils are deposited (Fig. 3, H-K); all this is done under fluoroscopic control. Without the indwelling basket the potential for embolization of the coils into the general venous circulation is a real threat. At the termination of the procedure, the catheter is removed and a piece of Gelfoam is placed over the bleeding hole in the torcular herophili and held for 5 minutes. The skin is closed in layers and the patient is returned to the intensive care unit for observation. Individual Steps The positioning of the patient on the operating table is shown in Figure 1. The head is placed in a position with the sagittal suture parallel to the floor. The right shoulder is usually elevated slightly with a roll. The area of the torcular herophili should be very close to the edge of the table so that the table itself is not obstructing the surgeons hands in their approach. The C-arm gantry and the visual monitor are brought in from above and in front, respectively. The surgeon and assistant are operating as if an occipital approach is being utilized in the placement of a ventriculoperitoneal shunt. Angiographic localization of the torcular herophili on the skull is estimated and a 3-4cm midline vertical incision is marked. Preparation and draping are standard for a burr hole. A small adjacent table is draped in a sterile fashion with all the necessary equipment ready so that when embolization is begun this table can be rolled to the juncture of the operating table just below the position of the childs head. This instrument table is very useful in stabilizing the indwelling catheter during evaluation and therapy. The incision is made down to the skull and the periosteum is elevated. Bleeding is minimal. A burr hole is placed over the torcular and enlarged to 2-3 cm in diameter (Fig. 2). Again, bleeding is minimal. The red dilated torcular is easily identified from directly over the structure. If ultrasound equipment is available, ultrasonic identification of the torcular, straight sinus, and aneurysm is very useful in helping the surgeon to decide on the angle of approach to the aneurysm through the torcular. If identification of the torcular is not certain, then a 25-gauge needle can be passed easily into the area suspected of being the torcular. If bright red blood returns then one can be confident that this is the area of entry. If no blood is obtained then a further craniectomy should be carried out in an effort to identify the torcular. It is important to realize that a true torcular may not exist and an accessory straight sinus may have to be utilized in approaching these lesions. In many of the patients, venous outlet obstruction is already a part of the disease process and therefore al-
ternate routes of approach may have to be chosen. This poses no great problem, and these routes of entry can be easily identified on the preoperative angiogram. Once the torcular is identified, a 16-gauge Angiocath is passed into the hole previously made by the 25-gauge needle (Fig. 3B). Brisk bleeding will be obtained through the Angiocath and the sharp needle from it can be removed easily with advancement of the soft outer portion. Bleeding is brisk but easily controlled with an occluding finger over the hub of the catheter. Under fluoroscopic control, a soft guidewire is advanced through the catheter into the aneurysm (Fig. 3D). This distance ranges from 6 to 9 cm from the surface of the dura to the anterior surface of the aneurysm. Care must be taken not to advance even the soft guidewire forcefully into the area of the most anterior part of the aneurysm and malformation. Once the wire is in place, the 16-gauge Angiocath sheath is removed. The assistant holds the wire in place at the level of the dura and bleeding can be brisk at this point while the angiographic sheath or catheter is placed over the wire and advanced through the dura and into the area of the aneurysm (Fig. 3F). The tip of the wire is carefully observed and maintained in its original position during the passage of this catheter so that forceful impingement does not occur on the anterior face of the malformation. Once the catheter is in the aneurysm, the guidewire is removed and the angiographic catheter system is flushed with heparinized saline through a side port. A Tuohy-Borst adapter is placed on the end of the catheter so that various therapeutic embolic agents can be placed through the catheter without significant bleeding. At this point, the assistant and surgeon can rest because the catheter is in place and there is no further bleeding. This is a good point in the procedure to perform pressure measurements through the side port of the angiographic catheter and to look at the venous flow patterns produced in the malformation with venography. Our initial procedure consisted of placing Gianturco coils directly into the aneurysm to produce thrombosis. This worked in certain individuals, but in others the flow characteristics were so great that the coils themselves embolized peripherally into the sigmoid sinus and, in one instance, into the lung. Therefore, we have modified our procedure by placing within the aneurysm a nonthrombogenic stainless steel basket constructed from a long stainless steel guidewire with the indwelling mandrel removed (Fig. 3I). This is accomplished easily by cutting off the weld on the end and removing the stout thin wire with a clamp. This results in the production of a very floppy wire capable of forming a basket when placed within the aneurysm. Through the Tuohy-Borst adapter we advance this guidewire, which may
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range from 90 to 145 cm in length, carefully into the aneurysm. This often results in a major change in the venous flow pattern within the aneurysm, and in several instances we stopped the procedure at this point and elected to return later to deposit thrombogenic wires onto this basket. If a major change in the metabolic needs of the patient occurs with this deposition, such as a reduction or elimination of blood pressure support, then we suggest that the procedure be terminated and further therapy considered later. The philosophy is to do as little as is needed to get a therapeutic response, knowing that returning later for more therapy is always possible. If we elect to deposit thrombogenic material within the aneurysm we use Gianturco coils of various sizes and have found that these are easily
deposited within the basket both to produce a change in the flow pattern and to induce thrombosis in a graded fashion (Fig. 3J). At the termination of the procedure, the angiographic catheter is removed and an occluding finger is placed over the egress site in the torcular. A small pledget of Gelfoam is placed here and pressure applied for 5 minutes. No sutures are required to obtain hemostasis and the skin is closed over the Gelfoam pledget in a standard fashion (Fig. 3K). The child is returned to the intensive care unit for careful observation. Repeat embolizations can be performed in the neuroradiology suite transcutaneously if needed. In this setting the procedure takes only a few minutes after anesthesia is administered.
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DETECTION OF AN EPILEPTIC FOCUS AND CORTICAL MAPPING USING A SUBDURAL GRID

SUMIO UEMATSU, M.D.
INTRODUCTION The goal of epilepsy surgery is to remove the epileptogenic parts of the brain while sparing critical functions. To achieve this goal, two criteria are essential: precise localization of the epileptogenic focus and identification of areas with critical functions. To meet these criteria, electroencephalography (EEG) performed directly on the surgically exposed brain (electrocorticography (ECOG)) has been used intraoperatively. However, the ECOG technique has obvious limitations: it must be performed in a limited time and it does not allow EEG recording during epileptic attacks (ictal recording). Accumulated evidence indicates that the most reliable information for localization of an epileptogenic focus is obtained from the ictal recording. Epileptiform discharges not associated with the patients habitual seizures (interictal discharges) alone are not sufficient. To catch and record these habitual seizures, at least several days of continuous EEG and video monitoring are needed. Furthermore, the physician has to determine that the recorded attack is typical of the patients habitual seizures. This is best achieved by analyzing video-recorded attacks in combination with the simultaneously recorded EEG (Fig. 1). Once the epileptogenic area has been localized, the next task is to identify the functions of the areamost importantly, speech and sensorimotor functionsince resection of critical areas may result in significant functional impairment postoperatively. Critical functions, particularly speech and language, can be tested for only on fully awake patients. Intraoperative stimulation has been used for this purpose also, but it is restricted by the limited time available and by patient discomfort, particularly in children. To overcome the limitations of intraoperative studies, a technique for subdural implantation of electrodes was developed. The approach allows, if needed, coverage of broad
areas of the cortical convexity as well as the basal hemispheric regions and the interhemispheric fissure. In addition to widespread coverage of the cortical surfaces, the subdural electrodes allow direct, systematic cortical stimulation to be performed over a period of days. However, as the number of electrode contacts required in the subdural grid increases for widespread coverage, the cable may become so bulky that skin incision and undermining of the subcutaneous tissue become necessary, which raises concerns about potential cerebrospinal fluid (CSF) leakage and infection of the subdural space. Therefore, a variation of the subdural grid technique that uses a finer, multiple cable (multi-minicable) was developed. The minicable has a 2-mm diameter and can be brought out through the skin using guiding needle punctures. CSF leakage and grid infection have been minimized by sealing the burr holes with glue and placing purse-string sutures at the site where the cable exits from the scalp. Technical details include planning the craniotomy, placing the grid, closing the dura, and closing the craniotomy wound. The techniques described here for implantation and use of the multi-minicable subdural grid allow localization of epileptogenic areas and mapping of cortical function. PATIENT SELECTION The indications for grid implantation include: 1. 2. 3. 4. 5. Incapacitating epileptic attacks; Failure of medical management of the attacks; Attacks originating from one cerebral hemisphere; EEG abnormalities adjacent to or within functionally critical cortex; Discrepancy of location of EEG abnormality and abnormality seen on magnetic resonance imaging. Contraindications to implantation are:
1.
Presence of active local or systemic infection;
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Figure 1. Diagram of the epilepsy monitoring system: the video camera and the computerized EEG simultaneously record the patients behav-
ior and brain activity. Electrical stimulation for cortical mapping is carried out through the implanted grid.
2. 3.
Uncorrectable bleeding tendency; Uncooperative or violent behavior of the patient.
Age alone is not a contraindication to grid implantation. The potential risks of the procedure are common to any craniotomy, such as CSF leakage, infection, or hematoma formation. Every preventive precaution should be taken during selection of candidates for implantation. OPERATIVE METHODS To illustrate the subdural grid technique, the operative details of grid implantation for a study of the languagedominant left hemisphere are described. Preoperative Preparation Bleeding Time and Premedication Bleeding time must be checked for all patients and should be within normal limits. Prophylactic broad-spectrum antibiotics are given intravenously just prior to the skin incision and are administered daily until the removal of the grid. The serum level of anticonvulsant(s) should be checked 24 hours prior to surgery and should be kept at the therapeutic level to avoid major tonic-clonic convulsions in the immediate postoperative period. Double doses of the usual daily anticonvulsant may be given the night before surgery to make up for anticipated loss of drugs during intraoperative depletion of body fluid. Dexamethasone and other antiinflammatory drugs are avoided.
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Anesthesia and Positioning Endotracheal general anesthesia is used. The vertex of the patients head extends out 3 cm from the headboard of the operating table. The vertex is tilted down slightly to facilitate drainage of blood out of the surgical field and to aid in opening of the base of the temporal subdural space. The head, neck, and chest are elevated by tilting up the upper half of the operating table about 15, so that the vertex of the head is above heart level (Fig. 2). Grid and Operative Plan The patients entire head is shaved. The rolandic line is drawn on the scalp (details are shown in Fig. 3A). The simplified midpoint to meatal (M-M) line, extending from the external auditory meatus to the midpoint between the nasion and inion, may also be used (Fig. 3A). After determination of the amount of grid needed to encompass the entire suspected epileptogenic area, including critical sensorimotor cortex and language areas, the appropriate number (i.e., one or more) of multi-minicable electrode grids (Ad-Tech Medical Instrument Corp., Racine, WI) are autoclaved at 270F (132C) for 10 minutes just prior to implantation. For study over the language-dominant hemisphere, a 6 8 contact grid is placed over the lateral convexity of the temporal lobe and cortex superior to the sylvian fissure (Fig. 3C). The 6 8 contact grid is 9 cm long from anterior to posterior and 7 cm wide. Accordingly, the scalp incision and craniotomy opening should be
UEMATSU : DETECTION OF EPILEPTIC FOCUS AND CORTICAL MAPPING
Figure 2. A, artists view of positioning of a patient for subdural grid implantation over the left hemisphere. The vertex of the patients head extends out 3 cm from the headboard of the operating table. The upper part of the operating table is elevated so that the patients vertex is higher than heart level. B, the vertex of the head must extend out from the head-
board of the operating table to provide access for subcutaneous tunnelling using the Angiocath. C, the vertex is tilted down to allow gravitational pull to aid in opening the subdural space at the temporal base. The tilted-down position of the vertex also facilitates drainage of blood from the surgical field.
10 8 cm. The extra length (1 cm) allowance around the grid plate prevents buckling of the Silastic plate. Surgical Procedures Skin Incision After the M-M line has been drawn on the head, four points are determined: the pterion; the base of the mastoid, 10 cm posterior to the pterion; the parietal point, 8 cm superior to the mastoid base; and, finally, the frontal point, 8 cm superior to the pterion (Fig. 3B). A line connecting the four points is drawn, beginning at the pterion and extending to the frontal point, the parietal point, and toward the base of the mastoid, and ending by curving above and in front the ear. The connecting line forms the so-called Falconers question-mark incision for temporal lobectomy. During the incision, the superficial temporal artery is carefully preserved to maintain the blood supply to the skin flap. Local anesthetic with 1/200,000 epinephrine is infiltrated along the outer margin of the incisional outline and around the superficial temporal artery at the neck of the skin flap.
Burr Holes and Craniotomy Burr holes are made at each of the four corner points, and two additional burr holes are also made; one at the midpoint between the frontal and parietal points and the other halfway between the parietal and mastoid points (Fig. 3B). The multiple burr holes are connected by cuts made with the Gigli saw. The temporalis muscle should not be detached from the bone flap. The flap is turned outward using the muscle as a hinge (Fig. 4E). The dura is opened at the base of the craniotomy over the temporal lobe. The incision is extended anteriorly and posteriorly and is swung superiorly toward the vertex; finally, the dura is reflected toward the midline. The arachnoid, vessels, and cortex are inspected. The sylvian vein and the vein of Labb are identified. The sylvian vein, which drains into the sphenopalatine sinus around the tip of the temporal lobe, and the vein of Labb, which drains into the transverse sinus at the posterior part of the lobe, are examined by gentle retraction of the lobe. The location of the vein of Labb is measured from the tip of the temporal lobe.
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Placement of Grid First the 2 8 strip-grid is inserted into the temporal base (see the inset, Fig. 3C). While the anterior quarter of the strip is held with a bayonet forceps, the wet grid is slipped into the subdural space as the mid-temporal base is slightly lifted with a brain spatula. The grid is advanced with gentle force mesially and toward the tip of the temporal lobe. The first (anterior) two electrode contacts reach the temporal tip, and the remaining majority of electrodes cover the fusiform and parahippocampal gyri. The tail end of the strip emerges from the middle fossa posterior to the tympanic prominence, crossing the fusiform and inferior temporal gyri. The strip is anchored to the dural sleeve at the cross-point with a single fine suture. The 6 8 grid is placed over the lateral convexity of the temporal and frontoparietal lobes. A slit 2 cm long made between the third and fourth rows of the grid allows the upper half of the grid-leaf to be angled toward the inferior orbital gyrus and the lower half toward superior temporal gyrus. The grid leaflets straddle the sylvian vein and sphenoid wing. The multi-minicables are directed toward the posterior margin of the craniotomy (Fig. 3C). A few loosely placed stitches are used to anchor the grid to the dura. Before closure, detailed drawings are made and color photographs are taken, with attention paid to the relation of the electrodes to the major cortical sulci and vessels. The sequential relation of the color-coded cables and electrode array is confirmed and recorded. Dural Closure Dural closure begins with suturing at the posterior temporal base. The running suture goes around the individual cables and secures the cable with the dural closure. The anterior and inferior or superior dural gap created by the posterior dural approximation is closed with a dehydrated human dural patch (Fig. 4). The closure again starts from the temporal base and proceeds toward the lower vertex. This facilitates drainage of subdural blood through the dural opening, which is lower with the head tilted downward. The subdural space is irrigated a final time with
normal saline before placement of the last sutures to complete dural closure. Bone Flap and Cable Placement After retaining sutures are placed to anchor the dura to the periosteum, the bone flap is secured with sutures tied to the skull through the drill holes. The cables emerge through the craniotomy gap or multiple burr holes (Fig. 5). An epidural Hemovac drain is placed in the anteriormost frontal burr hole, sufficiently remote from the cable. Gelfoam is packed in each burr hole. Medical adhesive is used to fill in the bone gaps created by the craniotomy and burr holes, with care taken to ensure that the adhesive does not contact the dura or brain or the epidural drain tube, since the adhesive binds with the tubing and would make its subsequent withdrawal difficult. In cases with a space-occupying brain lesion, where brain may be herniated by the mass or edema, we have used a Raimondi peritoneal catheter or Raney scalp clip placed around the craniotomy flap (Fig. 6A) to elevate the bone flap off the cortical surface and avoid compression of the edematous brain (Fig. 6B). Percutaneous Cabling Before the skin flap is replaced, each cable is passed subcutaneously using an Angiocath 10GA (3.4 mm), 3 inches (7.6 cm). The Angiocath needle puncture is made as far away as possible from the craniotomy margintypically 2-3 cm is sufficient (Fig. 5). Purse-string Suture and Skin Closures After completion of the scalp closure, a purse-string suture is placed around the exit point of each cable (Fig. 7). Postoperative Measures Surgical Dressing The cable exits are painted with antibiotic ointment. A bundle of a few cables is passed through the opening of a thick, soft pad (ABD-pad) that is used to cover the
Figure 3. A, estimation of the rolandic and sylvian lines on the scalp, based on cranial landmarks, is shown. First, the halfway point (50%) between the nasion and inion along the sagittal midline of the skull is determined; the point 19 mm posterior to the halfway point is the upper rolandic point. A line is drawn from the upper rolandic point to the lower rolandic point on the sylvian fissure. The lower rolandic point is found by constructing a line from the perpendicular point to Reeds line (a line formed by connecting the lower ridge of the orbit to the preauricular point (Preaur. pt.). The rolandic line is then formed by connecting the upper and lower rolandic points. The simplified M-M
line can also be used. The line is derived by simply connecting the midpoint to meatus, as depicted in the diagram. B, a question-mark incision extends from the pterion to the zygoma just in front of the ear. The superficial temporal artery is preserved to maintain the blood supply to the skin flap. Extra burr holes are needed for multi-minicable exits. C, the upper three rows of the electrode contact (3 8) ventral to the sylvian fissure cover Brocas speech area and the motor-sensory cortex; the lower three rows cover the lateral convexity of the temporal lobe. The second grid (2 8) covers the fusiform and parahippocampal gyri.
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Figure 4. The dura is closed with a continuous running suture, similar to the technique used for closure of an arteriotomy (E). Note the dural patch, which allows the subdural space to expand, thereby minimizing compression of the arachnoid vessels and fluid space over the cortex.
Eight to ten minicables are individually passed through the dura, burr holes, and subcutaneous tunnels that traverse the midline of the vertex. An Angiocath is used for the passage of each cable through its subcutaneous tunnel (A-D).
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Figure 5. Sealing the craniotomy opening and burr holes using Silastic medical adhesive. Note the temporalis muscle on the bone flap.
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Figure 6. A and B, application of a Raimondi catheter or Raney scalp clips around the bone flap is shown. In patients with a space-occupying lesion or edema, the grid may compress the brain. The catheter or
clip elevates the bone flap off the cortical surface and prevents compression of the swollen brain underneath the grid.
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Without cushioning, the bone flap collapses, putting presure on the cerebral cortex.
Raimondi catheter technique for cushioning the bone flap.
Scalp clip technique for cushioning the bone flap.
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Figure 7. This diagram depicts the path of the cable from the grid over the cortex and through the dura, skull (burr hole), galea, and scalp. The
burr hole is sealed with Gelfoam and Silastic adhesive. The Gelfoam prevents direct contact between the adhesive and the dura.
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surgical wound. Another pad with a slit is used to cover around the ear, including the area in front of the ear. As the cable is held up out of the dressing by an assistant, an adhesive elastic bandage is applied over the skin flap and cable exit area. The tails of the cables are then covered with 3 3-inch dressing sponges. Sitting Position and Restraint Certain precautions are unique to this procedure. As soon as the patient recovers from the general anesthesia and vital signs and neurologic condition are stabilized, the patient is placed in a sitting position, tilted at 45. Both hands are restrained by the use of mittens until the patient is transferred to the epilepsy monitoring unit. Routine skull x-rays are taken in the recovery room. The epidural drain is withdrawn on the first postoperative day, and EEG recording begins immediately. Stimulation studies are typically begun on the third postoperative day. Postoperative Medications The same anticonvulsants that the patient took prior to surgery are administered postoperatively. No steroid or anti-inflammatory medications are given. Moderate analgesics are given. The patient is given nothing by mouth, with fluid intake restricted for 24 hours. Prophylactic antibiotics are continued until the grid is removed. COMPLICATIONS AND THEIR PREVENTION The success of the approach described here is heavily dependent on pre- and postoperative management as well as intraoperative technique. The discussion is divided according to these two concerns. Preoperative and Postoperative Management The use of prophylactic antibiotics has been a subject of controversy. However, we administer a prophylactic antibiotic (Ancef) until the subdural grid is removed. CSF leakage along a subcutaneously placed cable could be a major cause of grid infection. Every possible measure is taken to prevent this. In particular, the postoperative sitting position discourages CSF leakage along the subcutaneous cables. The cable should be thin and should travel an extended distance in a deep subcutaneous tunnel. Use of the finer, multicable system instead of a single, bulky cable system also reduces the chance of CSF leakage. Because even a millimeter-thin hematoma membrane between the electrode and the cortex could interfere with effective cortical stimulation and EEG recording, every effort is made to prevent a hematoma membrane: bleeding time is checked preoperatively, the head is tilted down during the grid implant, and the dural opening at the lower
part of surgical field is left open until the end of the dural closure. These measures allow blood-tinged CSF to drain out through the dural opening. Placement of an active epidural drain equipped with a suctioning reservoir (Hemovac) also helps to clear the fluid around the grid. The pressure dressing using the elastic adhesive bandage minimizes subcutaneous bleeding. Shielding the craniotomy opening and burr holes with Gelfoam and Silastic medical adhesive minimizes the escape of subgaleal blood into the cranial space. Watertight closure of the dural opening prevents the blood from running into the subdural space and thus prevents formation of a subdural hematoma membrane. These wound-closure measures for the scalp, skull, and dura minimize CSF leakage and prevent grid infection. The dressing is changed and the drainage tube is removed 24 hours after surgery. Thereafter, the dressing must be changed once a week for routine wound inspection and suture line care. Intraoperative Technique The proper positioning unique to this procedure is important. The vertex of the head must extend out from the headboard of the operating table to provide access for subcutaneous tunnelling using the Angiocath. I prefer not to use a head fixation device, because the metal arms and pins around the skull make the tunnelling procedure more difficult. Our work has shown that motor and sensory areas have considerable individual variation and cover a much broader area than is conventionally believed. Using the rolandic line (R line) for outlining the craniotomy for grid implantation (Fig. 3A) helps to ensure that the grid covers the broadest possible cortical area for functional mapping and localization of the epileptogenic area. We call the modified R-line that we use the midpoint to meatal line (M-M line). The midpoint is the halfway point between the nasion and inion, and the line is drawn from the midpoint to the external auditory meatus. Autoclaving the grid is probably safer than gas sterilization because of the potential for residual chemicals (ethylene oxide) accidentally remaining after sterilization to cause cortical irritation. Every effort should be made to reduce surgical blood loss, because the grid procedure involves two stages, one for grid implantation and another for grid removal, within a short period of time. Infiltration of the epinephrine/local anesthetic combination around the skin incision is an effective hemostatic measure. Use of every available hemostatic measure means that blood transfusion can be avoided. The superficial temporal artery should not be ligated or coagulated and the temporal muscle should
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not be detached from the bone flap, in order to keep these tissues vital, which helps to minimize surgical wound infection. Furthermore, in the event of an infection, maximum antibiotic irrigation of the wound can be achieved by the rich blood flow throughout the tissues. Although the grid currently available is only a millimeter thick, it can buckle, and buckling will compress the cortical veins and the cortex. To prevent buckling, the craniotomy opening should be 1 cm wider than the grid plate. Use of the dural patch also provides an ample subdural space and prevents compression. Craniotomy using the Gigli saw instead of a highspeed craniotome is preferable. The Gigli saw allows a beveled-edge craniotomy, which prevents the bone flap from sinking and compressing the cerebral structures beneath. The two extra burr holes, one halfway between the frontal and parietal burr holes and another at the halfway
point between the parietal and mastoid, are necessary exits for the multi-minicable. CONCLUSION A nonsurgical setting, as opposed to the intraoperative environment, provides comfort and support for the patient and allows EEG recording during the patients habitual attacks. Complex speech and language testing can be carried out with maximal cooperation of the patient. The potential for infection is a serious concern with any implanted device that has external leads. The surgical technique described here is intended to minimize CSF leakage, thereby reducing the risk of infection. However, it should be emphasized that careful, complete, routine pre- and postoperative antiseptic measures, not just intraoperative technique, are needed for ultimate reduction of the risk of infection and for surgical success.
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ANTEROMESIAL TEMPORAL LOBECTOMY FOR EPILEPSY

ISAAM A. AWAD, M.D., MS PREM K. PILLAY, M.D.
PATIENT SELECTION Temporal lobectomy is an accepted surgical treatment of intractable complex partial seizures for patients in whom the temporal lobe has been implicated as the site of electroencephalographic (EEG) seizure onset. In these patients, mesial temporal structures are the commonest site of abnormal epileptiform EEG activity. Postoperative pathologic specimens from epileptic patients commonly reveal histological abnormalities in the amygdalohippocampal region. The extent of mesiobasal resection in temporal lobectomy has been correlated directly with seizure outcome, with higher rates of seizure control achieved with more extensive resections of mesiobasal temporal lobe structures. In this chapter, we describe a modified technique of temporal lobectomy with limited lateral temporal resection and extensive microsurgical resection of mesial temporal structures. This operation may be performed on the left or right temporal lobe without mapping of speech areas, since the procedure is designed to spare all but the most anterior portion of lateral temporal lobe cortex. Candidates for this operation suffer from complex partial seizures despite optimal medical therapy. The seizures are thought to be intractable, thereby interfering with psychosocial function and having a significant impact on the patients life. Preoperative diagnostic studies should include magnetic resonance imaging (MRI) of the brain, including coronal views, to delineate any structural abnormalities in the temporal lobe. Other diagnostic information should include prolonged EEG monitoring of interictal epileptiform abnormalities and seizure onset. Detailed neuropsychological studies should be performed to define baseline preoperative cognitive and memory function. Any modality-specific impairment should be noted (such as impaired verbal memory in patients with suspected left temporal epileptogenicity or impaired vi-
sual memory in patients with suspected right temporal epileptogenicity). Intracarotid injection of amobarbital (Wada test) is performed to confirm laterality of speech and memory and to demonstrate that the contralateral temporal lobe is able to support memory function. Patients with unilateral or predominantly unilateral EEG epileptiform abnormalities arising from the anterior or anteromedial temporal lobe are selected for the operation of anterior temporal lobectomy and microsurgical resection of mesial structures. This operation is contraindicated in patients with significant contralateral temporal pathology and in patients with epileptiform activity arising primarily from lateral temporal lobe structures. Patients with mesiotemporal epileptogenicity and an adjacent temporal lobe lesion should undergo this described operation in addition to resection of the structural lesion (i.e., neoplasm, vascular malformation, etc.). PREOPERATIVE PREPARATION Anticonvulsant therapy is continued through the perioperative period at or near toxic concentrations. Preoperative prothrombin time, partial thromboplastin time, and bleeding time measurements are performed in all patients in view of possible coagulopathy from prolonged anticonvulsant therapy. The patient would have donated two units of autogenous blood two to three weeks prior to surgery, and/or would have been typed and screened for possible blood transfusion. SURGICAL TECHNIQUE Operative Positioning The patient is placed in the supine position on the operating table with the head toward the foot of a typical table to provide greater room for the knees of a sitting surgeon and to allow the anesthetist or nurse to raise and lower the operating table without disturbing the operating team. The frontotemporal area is shaved and the hair is combed away from the field. The pa-
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tients head is extended 45 and turned 60 away from the side of surgery (Fig. 1), and it is fixed in that position using a Mayfield head clamp or other skull fixation system. The incision is marked as a question mark starting just in front of the tragus, extending posteriorly above the tip of the ear and anteriorly just above the superior temporal line. The incision is extended inferiorly and anteriorly (along the forehead) enough to clearly expose the pterion when flapped forward (Fig. 2). In most patients, the incision will not extend anterior to the hairline more than 2 or 3 cm. The proposed incision is marked and the operative area is prepared and draped according to routine craniotomy techniques. Operative Procedure Myocutaneous Flap The scalp is incised through the galea aponeurotica, and Raney clips are applied on both sides of the incision. The temporalis muscle is opened along the line of the incision. The scalp and underlying temporalis muscle are turned forward as a unit in the subperiosteal plane (Fig. 3). The myocutaneous flap is dissected anteriorly to expose the orbital zygomatic ridge and inferiorly to expose the zygomatic root. The myocutaneous flap is held in this position using multiple fine fishhooks tethered tensely with rubber bands to a Yasargil Leyla bar attached to the operating table. Such tense holding forward of the flap is essential for subsequent bony exposure and intradural visualization. Bony Opening A burr hole should be placed on the pterion and an-
other burr hole should be located at the most posterior aspect of the incision. These are connected via a power craniotome to elevate a frontotemporal bone flap (Fig. 4). This free bone flap should not expose more than one or two finger breadths of the frontal lobe but should allow as much of a temporal exposure as possible. The key to further steps of this operation will consist of subsequent removal of the pterional ridge to allow a very anterior exposure of the middle (temporal) fossa. Rongeurs are used to remove the remaining portion of the inferior squamous temporal bone down to the zygomatic root. This should allow exposure nearly flush with the floor of the middle fossa. Mastoid air cells are frequently entered and should be thoroughly waxed. Anteriorly, rongeurs are used to remove the thin temporal bone covering the anterior temporal lobe dura. The pterional ridge is thoroughly rongeured and subsequently drilled medially as far as the superior orbital fissure. At this point, the tip of the temporal lobe should be seen extradurally. Further intradural portions of the operation cannot be carried out without this extensive bony removal of the pterional ridge (Fig. 5). Lateral Temporal Resection Following the administration of intravenous mannitol (1 g/kg body weight) and insuring that the arterial pCO2 tension is in the range of 25 to 30 mm Hg, the dura mater is tacked to the edges of the surrounding craniotomy and is opened in a C-shaped fashion based anteriorly (Fig. 6). The dural flap is elevated anteriorly and tensed using 4-0 silk sutures allowing a full exposure of the temporal lobe tip and the sylvian veins. Any
Figure 1. Patient positioning. The head is extended 45 and rotated 60 away from the operative side. The head is fixed in this position using a Mayfield head clamp or other skull fixation device.
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AWAD AND PILLAY : ANTEROMESIAL TEMPORAL LOBECTOMY FOR EPILEPSY
Figure 2. Scalp incision. The pterion is marked (two finger breadths above the zygoma (B) and one thumb breadth behind the lateral orbital rim (A)). A question-mark skin incision is marked extending just anterior to the tragus at the level of the zygoma, swinging posteriorly above
the tip of the ear and anteriorly just above the superior temporal line. The anterior extent of the incision (on the forehead) should allow adequate exposure of the pterion upon anterior flapping of the scalp and muscle.
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Figure 3. (Top) Myocutaneous flap. The scalp and temporalis muscle are flapped anteriorly and inferiorly as a single layer in the subperiosteal plane. The myocutaneous flap is extended anteriorly to expose the orbital zygomatic ridge and inferiorly to expose the root of the zygoma. Figure 4. (Upper middle) Free bone flap. The myocutaneous flap is held anteriorly using multiple fishhooks which are tethered tensely with rubber bands to a Leyla bar. One burr hole is placed at the pterion and a second one at the posterior aspect of the incision. These are connected using a power craniotome to elevate a frontotemporal bone flap.
Figure 5. (Lower middle) Resection of the pterional ridge. The lesser wing of the sphenoid is resected using rongeurs and then a power drill medially to the superior orbital fissure. This is essential for subsequent intradural portions of the operation. Figure 6. (Bottom) Dural opening. The previous pterional resection should allow extradural visualization of the temporal tip. The dural opening is performed in a C-shaped fashion and is flapped anteriorly.
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temporal lobe tip draining veins should be visualized at this time, coagulated, and divided. The lateral temporal lobe resection is accomplished by connecting three separate corticectomies (Fig. 7). The first or posterior cut extends obliquely across the lateral temporal surface traversing the middle temporal gyrus 3.5 cm posterior to the temporal tip. The incision slants slightly anteriorly across the superior temporal gyrus and posteriorly across the inferior temporal gyrus, and continues transversely on the basal surface of the temporal lobe to the collateral sulcus (which separates the fusiform gyrus from the parahippocampal gyrus). This posterior cut spans across four gyri: the superior, middle, and inferior temporal gyri and the fusiform gyrus. The second or superior cut extends anteromedially below the sylvian veins just inferior and parallel to the free edge of the lesser wing of the sphenoid. It extends medially to the anterior clinoid process which should be easily visualized (given the adequate bony exposure). These two cortical incisions are then joined by a third or inferior cut across the basal surface of the temporal lobe. This should totally disconnect the temporal pole which is removed in one piece. This portion of the operation is performed with a headlight. It does not involve any violation of important sylvian structures (superiorly) or incisural structures (medially).
in the subpial plane from the choroidal fissure to the tentorial incisura under direct microsurgical visualization. This cut traverses the hippocampal sulcus which separates the parahippocampal gyrus from the dentate gyrus. The arterial feeders of the hippocampus (Ammons horn arteries) traverse the hippocampal sulcus after arising from the P2 segment of the posterior cerebral artery; these arterial feeders are coagulated and divided. The leptomeninges covering the perimesencephalic cisterns are not violated. The medial and lateral cuts are extended posteriorly to the point where the tentorial edge curves medially. A third or posterior cut joins the lateral and medial cuts posteriorly to disconnect the hippocampal formation and allow its removal in one piece. At this point, the tentorial edge should be seen curving medially behind the collicular plate on the posterior aspect of the mesencephalon. During this microsurgical resection of mesiobasal structures, care should be taken not to use bipolar electrocautery at or near the tentorial incisura (where the 4th cranial nerve may be injured) or near the petrous apex (where the intratemporal portion of the facial nerve may be injured). Wound Closure After securing meticulous hemostasis, thorough irrigation of the resection cavity is performed. No pieces of Surgicel or Gelfoam are left intradurally. The operating microscope is removed and intraoperative electrocorticography may be performed if this is a part of institutional epilepsy protocols. The value of intraoperative electrocorticography and further tailoring of the resection has not been proven. The dura mater is closed in a watertight fashion using running 4-0 Nurolon sutures. The bone flap is fixed in place using 2-0 Nurolon sutures. The wound is irrigated thoroughly and the temporalis muscle is approximated using interrupted 2-0 Vicryl sutures. The galea aponeurotica is closed using inverted interrupted 2-0 Vicryl sutures. The skin is closed using interrupted 3-0 Nurolon sutures behind the hairline and 4-0 nylon sutures in a plastic fashion for any portion of the incision extending anterior to the hairline. Antibiotic ointment is used to cover the incision and a sterile head dressing is applied. The anesthetic is reversed. The patient is allowed to awaken and is examined in the operating room. OUTCOME AND COMPLICATIONS Perioperative antibiotics are administered at the time of the skin incision and are continued for 24 hours postoperatively. These are geared at our institution against the narrow spectrum of staphylococci (vancomycin or oxacillin). The patient is observed for 24 hours in a critical care unit. Fluid restriction, dex-
Resection of Mesial Structures The operating microscope is brought in at this point. A Greenberg or other self-retaining retractor system is set up, and a narrow long blade is chosen. Under the operating microscope, the stump of the temporal lobe is gently explored to locate the tip of the temporal horn of the lateral ventricle. This is opened gently using bipolar coagulation, and a long cottonoid patty is slipped into the temporal horn of the lateral ventricle. The long narrow blade of the selfretaining retractor is then inserted over the cottonoid patty within the temporal horn. This retractor blade is used to elevate the choroid plexus, thus opening the temporal horn like a fishs mouth. This allows identification of the choroidal fissure medially and the hippocampal formation in the floor of the temporal horn. Upon orientation in relation to the pes hippocampus, the remaining portion of the amygdala is removed by suction, making sure not to extend this resection superiorly above the plane of the sylvian fissure (into the caudate nucleus). Mesial basal resection is completed through three subsequent incisions into the mesiobasal temporal structures (Fig. 8). The first or lateral cut extends from the lateral edge of the floor of the temporal horn (terminal sulcus) to the collateral sulcus. The second or medial cut extends
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Figure 7. Resection of the temporal pole. This is carried out through three cortical incisions labeled 1, 2, and 3.
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Figure 8. Resection of mesial structures. A narrow self-retaining retractor blade is used to open the temporal horn of the lateral ventricle, allowing adequate exposure of mesial temporal structures at the floor of the temporal horn. The roof of the temporal horn is care-
fully protected using a cottonoid patty inserted under the retractor blade (in the temporal horn itself). Mesial structures at the floor of the temporal horn are then resected using three incisions labeled 1, 2, and 3.
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amethasone, and intermittent mannitol are used as prophylaxis against brain edema. Not uncommonly, following left temporal resections, the patient may awaken with normal speech function but may develop transient dysphasia several hours after surgery, which may last for one or two days. Permanent dysphasia is rare following this operation. Visual field abnormalities are encountered in less than one-fourth of the patients, and these consist of incomplete homonomous quadrantic field defects; they have been shown to be less frequent and less dense than following more extensive temporal lobectomies. Other focal neurologic deficits are rare. It is extremely important to protect structures at the roof of the temporal horn to avoid homonomous hemianopia (optic tract) or hemiparesis (internal capsule). It is also important to avoid injury to any structures within the perimesencephalic cistern to avoid cranial nerve or major vascular injuries. Anticonvulsants are maintained at near toxic levels
and are monitored closely in the perioperative period. Early postoperative seizures not associated with electrolyte abnormalities or low anticonvulsant levels are a marker for future recurrent seizures. Otherwise, complete control of seizures (on anticonvulsants) is expected in 7080% of the patients. This rate may be affected by preoperative selection protocols and other patient-related factors. Patients who are seizure-free for one year following surgery are likely to remain seizure-free thereafter; subsequent seizure recurrence may be related to tapering or lack of compliance with anticonvulsant therapy, and is rarely intractable. Postoperative radiographic verification of the extent of resection (Fig. 9) is performed routinely at our institution. Patients with retained temporal mesial structures are more likely to have seizure recurrence and may be helped by reoperation aimed at resection of these residual mesial structures.
Figure 9. Postoperative T1-weighted MRI performed in the axial plane of the temporal lobe (axial cuts angled along the plane of the sylvian
fissure). This reveals the extent of resection of the temporal pole and of mesial structures to the collicular level.
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ANASTOMOSIS OF THE FACIAL NERVE AFTER RESECTION OF AN ACOUSTIC NEUROMA

CHARLES M. LUETJE, M.D.
INTRODUCTION The potential for interruption of the VIIth cranial nerve during acoustic tumor removal is present for any sized tumor. It is incumbent upon the surgeon(s) to be prepared for this event and to be ready to implement an immediate plan of action should it occur. The immediate plan should be that of direct VII-VII neuroanastomosis or autogenous cable graft interposition VII-VII neuroanastomosis. The plan should not be one of delay, or inaction, waiting for a time to perform a substitution cranial nerve anastomosis. OVERVIEW OF SURGICAL PROCEDURE The authors experience has been primarily with the operation of posterolateral craniectomy with translabyrinthine exposure of the cerebellopontine angle (CPA). The details of the operative procedure will be highlighted for a clearer understanding of the VII-VII neuroanastomosis. It must be clearly understood that this procedure allows for the removal of an acoustic tumor of any size. The patient is supine on the operating table with the head lying flat on a sheepskin and turned away from the surgeon. The anesthesiologist is on the same side of the operating table as the surgeon, with a 5-foot anesthesia tubing running along the other side of the patient, crossing over to the machine at the pelvis. Appropriate monitoring equipment is used for the assessment of VIIth nerve function and the maintenance of anesthesia. A large postauricular incision is made just in the hairline, the ear is rotated forward, and if bone removal is to involve removal of the cochlea, the external ear canal is transected and sewn shut. Bone removal is accomplished with the air-driven Ototome drill. The mastoid is opened and saucerized widely posteriorly behind the sigmoid sinus to the dura. The facial recess (bounded anteriorly by
the chorda tympani nerve and posteriorly by the VIIth nerve) is opened, the incus is removed, and the eustachian tube and middle ear are filled with periosteum, fascia, and muscle to prevent postoperative cerebrospinal fluid (CSF) leakage. The sigmoid sinus is skeletonized and retracted posteriorly with the Silverstein retractor. The vestibular bony otic capsule is removed and the internal auditory canal skeletonized in an arc of 180. The area of Bills bar separating the VIIth nerve from the superior vestibular nerve is identified and the superior vestibular nerve is avulsed from its canal; positive identification of the VIIth nerve is made at this point in the operation. Once this is accomplished, certain key anatomic points have been established. These include: 1) bone removal from the superior petrosal sinus and middle fossa dural plate superiorly to the jugular bulb inferiorly; 2) posterior retraction of the sigmoid sinus; 3) opening of the cochlear aqueduct to allow egress of CSF and reduction of intracranial pressure; 4) skeletonization of the VIIth nerve from the posterior aspect through its mastoid portion, lateral to the vestibule, toward the geniculate ganglion, and at its entrance into the lateral end of the internal auditory canal (IAC); and 5) complete exposure of the posterior fossa dura as outlined above. If the cochlea is removed as in the case of tumors with extension forward and into the tentorial notch, this step is accomplished first and simultaneously with skeletonization of the VIIth nerve. In essence, the ear canal skin and ossicles are removed, the bony posterior ear canal wall is removed, and the cochlea is drilled away to expose the carotid artery below the floor of the eustachian tube. The VIIth nerve can be skeletonized in an arc of 360 and the dural exposure extended medial to the VIIth nerve, above the jugular bulb, to the carotid artery, anteromedially, inferior to the IAC. This exposure takes from a little less than two hours to three hours, depending upon the extent of
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Figure 1. Lifting the divided VIIth nerve out of its bony canal.
Figure 2. Suture anastomosis of the VIIth nerve. Left inset, abdominal fat is used to support the suture anastomosis of the VIIth nerve. Lower inset, an autogenous cable graft is interposed between the proximal and distal VIIth nerve stumps.
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aeration of the temporal bone. From the induction of anesthesia to the operation starting time is approximately 30 minutes. The dura is opened in an apron-shaped fashion and an extradural retraction with cottonoids only over the cerebellum is accomplished. The pCO2 is maintained at 23 mm Hg and the patient is not paralyzed. Tumor removal is posterior first in larger tumors using the House-Urban rotary dissector to gut the interior of the tumor, allowing for the development of arachnoid planes and for the capsule of the tumor to be moved away from cranial nerves, vessels, cerebellum, and brain stem. Once the tumor is gutted, removed partially, and reduced to smaller size, attention is turned to the lateral end of the IAC. Here, previous identification of the VIIth nerve has been made. The tumor is then carefully dissected away from the VIIth nerve using continuous suction and irrigation via the Brackmann multifenestrated suction-irrigator, the neurotologic scissors, and the insulated Crabtree dissector, both designed for us, the latter of which is attached to the Xomed Nerve Integrity Monitor. The problem of VIIth nerve preservation occurs during the dissection of the VIIth nerve at its anterior angulation out of the IAC. Many tumors spread the VIIth nerve so thinly over the anterior tumor surface that the plane of dissection can be lost in spite of lateral VIIth nerve identification in the IAC and identification of its zone of exit from the brain stem. In fact, a histological plane between tumor and VIIth nerve may not exist. It is at this site where the VIIth nerve is most commonly interrupted both anatomically and electrically, intentionally or unintentionally, during total tumor removal. VII-VII NEUROANASTOMOSIS Upon recognition of interruption of the VIIth nerve or the likelihood of little if any chance of regeneration through thin strands of tissue that resemble arachnoid, one must be ready to perform a VII-VII neuroanastomosis. Previous skeletonization of the VIIth nerve during earlier bone removal stages of the operation now becomes an advantage of the posterolateral craniectomy and translabyrinthine operation. The proximal end of the VIIth nerve is marked with a cottonoid at its root exit zone. The CPA is sealed off with cottonoids to prevent scattering of bone dust throughout. Bone removal is completed along the thin bone covering the VIIth nerve from the stylomastoid foramen to the geniculate ganglion using a diamond drill. The sharp angulation of the VIIth nerve from the geniculate ganglion into the IAC does not allow for 180 of bone removal. However, careful diamond drilling techniques can satisfactorily skeletonize the VIIth nerve, and bone re-
moval can be accomplished without damage to this labyrinthine segment, allowing removal of the VIIth nerve out of its bony canal (Fig. 1). Brisk bleeding occurs from the vessels in the canal of the greater superficial petrosal nerve. The angled neurotologic scissors can be helpful in separating the nerve from the ganglion, and Avitene can be used for immediate hemostasis. Once the nerve is mobilized, a 7-0 silk suture is first passed through the proximal stump of the VIIth nerve at the brain stem. The suture is then passed through the distal end of the nerve which is gently brought into approximation with the proximal stump (Fig. 2). The first knot should be a double (surgeons) knot so the second will hold fast. A piece of abdominal fat (taken for wound closure) and Avitene are used to support the neuroanastomosis (Fig. 2, left inset). The neuroanastomosis can be somewhat tenuous, and because the root exit area of the VIIth nerve may be pushed into the brain stem, this support is helpful and is easy to place. Rarely is it necessary to obtain an autologous cutaneous nerve for cable grafting because the length gained from the technique just described is ordinarily sufficient. If it is necessary, a segment of sural nerve from the area just behind the lateral malleolus of the ankle is obtained. While grossly this nerve may look small, under the microscope it is always much larger than the root exit segment of the VIIth nerve. In this instance, the proximal neuroanastomosis is accomplished first with the technique just described, followed by the distal neuroanastomosis (Fig. 2, lower inset). RESULTS Our patients have exhibited better facial animation results with direct VII-VII neuroanastomosis than with a delayed XII-VII neuroanastomosis. The results produce spontaneous simultaneous facial movement, do not require a second operation, and shorten the time of recovery compared with a second substitute cranial nerve neuroanastomosis. The results with an interposition autogenous cable graft are not as good as those with direct end-to-end VII-VII neuroanastomosis but are preferable when compared with paralysis or XII-VII substitution. If a patient has undergone a retrosigmoid, standard suboccipital craniectomy, the VIIth nerve can still be mobilized and a VII-VII neuroanastomosis performed. The length of nerve gained from the rerouting described is not changed because of the surgical exposure. I believe that any surgeon who performs acoustic tumor surgery should be prepared for the unfortunate situation of VIIth nerve interruption, intentional or unintentional, and should either perform the VII-VII neuroanastomosis or call in someone who can.
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Neurosurgical Operative Atlas 21

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NEUROSURGICAL OPERATIVE ATLAS

The American Association of Neurological Surgeons

NEUROSURGICAL OPERATIVE ATLAS: TABLE OF CONTENTS

NEUROSURGICAL OPERATIVE ATLAS: TABLE OF CONTENTS

NEUROSURGICAL OPERATIVE ATLAS: TABLE OF CONTENTS

NEUROSURGICAL OPERATIVE ATLAS: TABLE OF CONTENTS

NEUROSURGICAL OPERATIVE ATLAS: TABLE OF CONTENTS

NEUROSURGICAL OPERATIVE ATLAS: TABLE OF CONTENTS

NEUROSURGICAL OPERATIVE ATLAS: TABLE OF CONTENTS

NEUROSURGICAL OPERATIVE ATLAS: TABLE OF CONTENTS

NEUROSURGICAL OPERATIVE ATLAS: TABLE OF CONTENTS

SURGICAL REPAIR OF TRIGONOCEPHALY

1992 The American Association of Neurological Surgeons

NEUROSURGICAL OPERATIVE ATLAS, VOL. 2

WINSTON AND BURKE : SURGICAL REPAIR OF TRIGONOCEPHALY

1992 The American Association of Neurological Surgeons

NEUROSURGICAL OPERATIVE ATLAS, VOL. 2

1992 The American Association of Neurological Surgeons

WINSTON AND BURKE : SURGICAL REPAIR OF TRIGONOCEPHALY

1992 The American Association of Neurological Surgeons

NEUROSURGICAL OPERATIVE ATLAS, VOL. 2

1992 The American Association of Neurological Surgeons

WINSTON AND BURKE : SURGICAL REPAIR OF TRIGONOCEPHALY

1992 The American Association of Neurological Surgeons

NEUROSURGICAL OPERATIVE ATLAS, VOL. 2

1992 The American Association of Neurological Surgeons

DORSAL ROOT ENTRY ZONE (DREZ) LESIONING

1992 The American Association of Neurological Surgeons

NEUROSURGICAL OPERATIVE ATLAS, VOL. 2

1992 The American Association of Neurological Surgeons

1992 The American Association of Neurological Surgeons

NASHOLD AND EL-NAGGAR : DORSAL ROOT ENTRY ZONE LESIONING

1992 The American Association of Neurological Surgeons

1992 The American Association of Neurological Surgeons

Figure 4. Positioning of a patient undergoing thoracic or conus medullaris DREZ lesions.

NEUROSURGICAL OPERATIVE ATLAS, VOL. 2

1992 The American Association of Neurological Surgeons

most positive wave recorded when stimulating the affected dermatome.

NASHOLD AND EL-NAGGAR : DORSAL ROOT ENTRY ZONE LESIONING

NEUROSURGICAL OPERATIVE ATLAS, VOL. 2

1992 The American Association of Neurological Surgeons

NASHOLD AND EL-NAGGAR : DORSAL ROOT ENTRY ZONE LESIONING

NEUROSURGICAL OPERATIVE ATLAS, VOL. 2

1992 The American Association of Neurological Surgeons

NASHOLD AND EL-NAGGAR : DORSAL ROOT ENTRY ZONE LESIONING

1992 The American Association of Neurological Surgeons

Figure 8. DREZ lesions in brachial plexus avulsion injuries.

NEUROSURGICAL OPERATIVE ATLAS, VOL. 2

1992 The American Association of Neurological Surgeons

Figure 9. DREZ lesions in conus medullaris sacral avulsion injuries.

NASHOLD AND EL-NAGGAR : DORSAL ROOT ENTRY ZONE LESIONING

1992 The American Association of Neurological Surgeons

NEUROSURGICAL OPERATIVE ATLAS, VOL. 2

NASHOLD AND EL-NAGGAR : DORSAL ROOT ENTRY ZONE LESIONING

1992 The American Association of Neurological Surgeons

NEUROSURGICAL OPERATIVE ATLAS, VOL. 2

1992 The American Association of Neurological Surgeons

Figure 12. Unilateral exposure of the nucleus caudalis.

NASHOLD AND EL-NAGGAR : DORSAL ROOT ENTRY ZONE LESIONING

1992 The American Association of Neurological Surgeons

Figure 13. Precise location of lesions of the nucleus caudalis.

NEUROSURGICAL OPERATIVE ATLAS, VOL. 2

OPHTHALMIC SEGMENT ANEURYSMS

NEUROSURGICAL OPERATIVE ATLAS, VOL. 2