Você está na página 1de 41

M5 unit

Dr.G.Rengaraj - post-graduate

A 70 year female was brought with c/o rt. Upper eyelid drooping 1 day, associated with vomiting & giddiness associated with headache- on & off no h/o loss of vision h/o diminished sensation of the upper part of face on right side no h/o any other FND No h/o fever/trauma/altered sensorium

Past history: hypertensive on irregular treatment no other positive history no h/o prev. episodes

P 80/min , BP 190/130 mm Hg CBG -157 mg Concious, oriented No P/Ict/Cy/Cl/Nodes/PE CVS - S1S2 + RS NVBS + P/a - soft

CNS - rt. Pupil dilated 4 mm, sluggish reaction to light +, left 2mm reacting vision R - 6/60 improv. With Pinhole to 6/36 L - 6/24 doesnt improv. With PH complete ophthalmoplegia on the right sensory loss in the right V1 and V2 trigeminal nerve distribution.

Cavernous sinus syndrome - ? Thrombosis


CBC & RFT normal ECG & CXR - normal

Hyperdense area in the right parasellar region- right parasellar meningioma , suggested MRI

3 x2.9x2.5 cm sized flow void seen in right parasellar region. In T1 images it is hyperintense. Gradient images show surrounding blooming of the wall. Post-contrast MRA shows no enhancement within the lesion CEMRA shows another 1.5x1x1.2 cm saccular aneurysm in left ICA

Basilar artery ectasia present multiple saccular aneurysm of 3 mm size seen in right ICA-PCoA and right MCA bifurcation Non-specific periventricular hyperintensities noted

Giant right internal carotid artery saccular ANEURYSM[thrombosed] probably arising from the cavernous part of right ICA. Multiple intracranial saccular aneurysms. Small vessel ischemic changes

Pt. was transferred to neurosurgery ward Planned for clipping of the aneurysm and removal of the thrombus.

Patient Refused surgery sent home with anti-hypertensives & antiplatelets

cavernous sinus syndrome is presents as -orbital or facial pain; orbital swelling and chemosis due to occlusion of the ophthalmic veins; - oculomotor neuropathy affecting the third, fourth, and sixth cranial nerves; and trigeminal neuropathy affecting the ophthalmic (V1) and occasionally the maxillary (V2) divisions of the trigeminal nerve. Cavernous sinus thrombosis is the most frequent cause secondary to 1]infection from orbital cellulitis (frequently Staphylococcus aureus) or 2]sinusitis (especially with mucormycosis in diabetic patients)

other etiologies include aneurysm of the carotid artery a carotid-cavernous fistula (orbital bruit may be present) Meningioma nasopharyngeal carcinoma, other tumors an idiopathic granulomatous disorder (Tolosa-Hunt syndrome)

Sphenoid wing meningioma[MRI] Orbital apex syndrome[no V2 involvement]

The physical findings in patients with unruptured aneurysms are determined in part by the size and location of the aneurysm

Surgical Classification of Intracranial Arterial Aneurysms MORPHOLOGY Saccular Fusiform Dissecting This morphological classification is helpful in defining the different natural histories of these lesions

Saccular (berry or congenital) aneurysms are the most common aneurysms and are most often responsible for aneurysmal SAH. Saccular aneurysms may arise from defects in the muscular layer of cerebral arteries that occur at vessel bifurcations or from degenerative changes that damage the internal elastic membrane, resulting in weakness of the vessel wall. They usually occur on the first- or secondorder arterial branches of the vessel emanating from the circle of Willis.

Evidence suggests that both genetic and environmental factors contribute to the development of saccular aneurysms. Genetic connective tissue disordersmarfans , EDS, NF 1 , ADPKD Environment- smoking Hypertension

Saccular aneurysms may also be caused by infection, trauma, or neoplasm Fusiform (dolichoectatic) aneurysms are classified separately from saccular aneurysms, although in some patients these types may overlap. The basilar artery is most commonly affected

Dissecting aneurysms result from cystic medial necrosis or a traumatic tear in the endothelium and subjacent layers of the artery, allowing the formation of a false lumen Such aneurysms can occur in any portion of the extracranial or intracranial arterial circulation. Trauma is a common cause in the neck and anterior circulation

Conventional CT large aneurysm with calcification & central enhancement on contrast HRCT small aneurysm CT angio understanding the morphology MRA detects, no need for contrast.

CLIPPING OF ANEURYSM

ENDOVASCULAR COILING

ISUIA & ISAT Size[3,7 & 25 mm] Risk group Location

High risk group suffered SAH from another aneurysm, anxious, family h/o SAH from IA , ADPKD High risk location Posterior comm. Artery or vertebro-basilar system

Intracranial aneurysms are found on postmortem examination in between 1% and 6% of adults in large autopsy series . The frequency of intracranial aneurysm seen during angiography for patients not suspected of harboring an aneurysm is between 0.5% and 1.0%.

Familial occurrence of intracranial aneurysms is defined by the presence of aneurysms in two or more first- to thirddegree relatives without any known hereditary disease. The reported prevalence of cerebral aneurysms in these targeted families varies from 2.4% to 29.4

Screening studies with MRA, CT angiography, or conventional angiography for the presence of aneurysms in this group of patients appears warranted Screening with noninvasive angiography has been recommended for individuals with two first-degree relatives with intracranial aneurysms and for all patients with autosomal dominant polycystic kidney disease

anterior communicating artery visual field defects, endocrine dysfunction, and localized frontal headache. Aneurysms of the internal carotid artery oculomotor paresis, visual field deficits, impaired visual acuity, endocrine dysfunction, and localized facial pain.

Aneurysms of the internal carotid artery in the cavernous sinus can, if of sufficient size, produce a cavernous sinus syndrome. Those of the middle cerebral artery can produce aphasia, focal arm weakness, and paresthesias. Posterior circulation aneurysms can be associated with signs of cranial nerve dysfunction

A third nerve palsy secondary to an aneurysm usually is associated with a dilated pupil and ptosis, which contrasts with the paresis caused by an ischemic lesion of the nerve, in which pupillary function is usually preserved. However, this distinction is not uniformly reliable, and aneurysms should be suspected in all cases of new-onset painful third nerve dysfunction

Você também pode gostar