Radiologic Anatomy of The Brain - Finals

RADIOLOGIC
ANATOMY OF THE BRAIN

INTRODUCTION • Awarded Nobel Prize 1979
• Radiology has undergone enormous technologic
advancements and ever broadening clinical WHEN IS CT SCAN INDICATED?
applications since Roentgen discovered the x-‐ray • CT scan is a fast diagnostic procedure and is often
in 1895. indispensable, for example after VA involving
• The progressive refinement of conventional x-‐ray head injuries, stroke to detect any internal
and the development of more sophisticated injuries or bleeding.
imaging modalities such as ultrasound, CT and • Better than all other procedures at recognizing
MRI have allowed radiology to emerge as one of recent bleeding.
the most exciting and challenging fields in
medicine. ADVANTAGES OF CT VERSUS MRI
• Rapid scan acquisition
RADIOGRAPHY (X-‐RAY) • Superior bone detail
• is an electromagnetic radiation that is capable of • Demonstration of calcification
causing ionization in matter due to its high
energy content. MRI
• Wilhelm Conrad Roentgen – German physicist • Strong magnetic field is used to create images
• November 8, 1895 – x-‐ray was discovered by from the human body
accident • Tesla = unit of measurement of a magnetic field
• December 28, 1895 – thoroughly investigated the • Signal intensity
properties of x-‐ray • T1 and T2 refer to the physical properties of the
• 1901 – first Nobel Prize for Physics was awarded tissues
due to his outstanding contribution to science • MRA
• DWI
DEVELOPMENT OF MODERN RADIOLOGY
2 TYPES OF X-‐RAY PROCEDURE ADVANTAGES OF MRI OVER CT SCAN
1. Radiographic examination with fixed employs x-‐ • No ionizing radiation
ray film and x-‐ray tube • Multiplanar imaging capability (axial, coronal,
2. Fluoroscopic examinations – provides radiologist sagittal, oblique)
with moving/dynamic images portrayed on a • Better anatomic detail
fluoroscopic screen or television monitor • More sensitive in detecting subtle pathologic
tissue alterations
CT SCAN
• Ability to characterize specific types of tissue
• Is a technology that uses an x-‐ray to generate based on signal intensity
cross-‐sectional (axial) images.
• Any portion of the human body can be imaged by DISADVANTAGE OF MRI VERSUS CT
CT
• Inability to demonstrate dense bone detail or
• Current CT scanners can obtain an image of a calcification
transverse section of the body in 1-‐second or less.
• Long imaging time
• Allows radiologist to look at the inside of the • Limited spatial resolution
body
• Inavailability and expense
• Doctors can look right at the area of interest
• Contraindicated in patients with electrically,
• Takes pictures of mm-‐thin layers tissue. magnetically or mechanically active implants
• Allows doctors to see diseases in the past are only
found in autopsy and surgery
• Non-‐invasive, safe and well-‐tolerated
• Provides detailed look at many different parts of
the body

HISTORY OF CT SCAN
• 1974 – CT scan was first installed
• Sir Godfrey Hounsfield
• Dr. Alan Cormack
kirstie

RADIOLOGIC ANATOMY OF THE BRAIN

x-‐ray CT scan MRI Scout view. Magnified view of the 2"d box, 1,1 row of
Images Appears as Cross Cross fig.9-‐2. The Scout view of a CT scan looks like a plain
if looking sectional sectional radiograph of the patient in profile. 6 lines are drawn on
through the images images the diagram to indicate the levels at which the 6 essential
body CT images are taken (PICTURE BELOW)
Method Radiation Radiation (x-‐ Magnetic field
(x-‐ray) ray) and radio
waves
Cost Inexpensive Expensive Most
expensive
Duration Few few seconds 10-‐30 minutes
of minutes
procedur
e
Indication Accurate in Better Much better
diagnosing evaluate soft detailed
pneumonia tissue (brain, tissue
, arthritis liver, differentiatio
and abdominal n
fracture organs) The X. 1st basic slice taken near the base of the skull.
Evaluates A. Diagram of normal anatomy.
abnormalitie
s that are not
apparaent on
x-‐ray

LATERAL VIEW OF THE BRAIN

B. CT image of normal anatomy.

CT of the head: Usual location of the patient's I.D. Scout
view, and the 6 essential CT images. The other boxes
represent images taken between the essential images.
(PICTURE BELOW) C. MRI of the author's head (Hopefully normal).

kirstie


The Star 2nd basic slice.
A. Diagram of normal anatomy. B. CT image of normal anatomy.

C. MRI of the author's head.

C. MRI of the author's head. Mr. Sad 4th basic slice.
A. Diagram of normal anatomy.

Mr. Happy 3rd basic slice.


kirstie


C. MRI of the author's head. The Coffee Bean 6th basic slice.

The Worms 5th basic slice.

C. MRI image of the author's head.


BLOOD SUPPLY -‐ CIRCLE OF WILLIS

C. MRI image of the author's head.

kirstie


Vascular territories b. vasospasm due to nontraumatic subarachnoid
A. The anterior, middle and posterior cerebral arteries hemorrhage (4%)
grossly supply the anterior, middle and posterior part of c. veno-‐occlusive disease (1%) – sinus thrombosis
the brain from the X to the Mr. Sad levels.
• Stroke may be preceded by transient ischemic
attack (TIA)
• 10-‐14% of all strokes are preceded by TIA
• 60% of all stroke ascribed to carotid disease are
preceded by TIA

 INFARCTION
• brain cell death leading to coagulation necrosis
• Imaging modality is CT and MRI (DWI – most
sensitive)
• Causes
-‐ large vessel occlusionof ICA/MCA/PCA (50%)
due to emboli from atherosclerotic stenosis
-‐ small-‐vessel lacunes (25%)
B. From the Worms to the Coffee Bean level, the anterior -‐ blood disorder (5%)
cerebral arteries supply most of the midline. -‐ non-‐atherosclerotic (5%)
• Differential diagnosis
-‐ ICH, subdural hematoma, cerebritis, AV
malformation, hemiplegic/hemisensory migraine,
tumor,
• Location: cerebrum : cerebellum = 19:1
a. supratentorial
-‐ cerebral mantle (70%), in territory of MCA
(50%), PCA (10%), watershed between MCA +
ACA (70%), ACA (4%)
-‐ basal ganglia + internal capsule (20%)
b. infratentorial (10%)
-‐ upper cerebellum (5%), lower cerebellum (3%)
pons + medulla (2%)
• Detection rate by CT:
-‐ 80% for cortex + mantle
-‐ 55% for basal ganglia
INTRACRANIAL INSULT/INJURY -‐ 54% for posterior fossa
NON-‐TRAUMA RELATED TYPE
• CT sensitivity
 STROKE
on the day of ictus – 48%
• Generic term designating a heterogeneous group 1-‐2 days later – 59%
of cerebrovascular disorder 7-‐10 days later 66%
• Etiology: 10-‐11 days later 74%
A. Nonvascular (5%)
• Stages :
B. Vascular (95%) 1. hyperacute ischemic infarction
1. Brain infarction – ischemic stroke (80%) -‐ <12 hours
a. occlusive atheromatous disease of extracranial -‐ CT is relatively insensitive and non specific
(35%) /intracranial (10%) -‐ insular ribbon sign
b. small vessel disease penetrating arteries -‐ hyperdense middle cerebral artery sign
c. cardiogenic emboli
d. nonatheromatous disease 2. acute ischemic infarction
e. overactive coagulation a. early acute ischemic infarction
-‐ 12-‐24 hours
2. Hemorrhagic stroke (20%) -‐ insular ribbon sign
a. primary intacerebral hemorrhage (15%)
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b. late acute ischemic infarction • pure motor/pure sensory stroke
-‐ 1-‐3-‐7 days • ataxia hemiparesis
-‐“bland infarct” may be transformed into • vascular dementia
hemorrhagic infarct after 2-‐4 days • small discrete foci of hypodensity between 3-‐15
mm in size (most < 1 cm diameter)
3. subacute ischemic infarction • may enhance in late acute/early subacute stage
-‐ 7-‐30 days • unilateral pontine infarcts are sharply marginated
-‐ paradoxical phase with resolution of at
midline
edema + onset of coagulation necrosis • higher in signal intensity than CSF (due to
-‐ “fogging phenomenon” marginal gliosis)
• Causes:
4. chronic ischemic infarction -‐occlusion of small penetrating end arteries at
-‐ months to years (>30 days) base of brain due to fibrinoid degeneration
-‐ cerebral atrophy + encephalomalcia + gliosis
• Pathophysiology:
-‐lacunae = small hole of encephalomalacia
Hemorrhagic Infarction traversed by cobweb fibrous strands
• Etiology: • Location:
-‐ lysis of thrombus / opening of -‐ upper 2/3 of putamen > caudate > thalamus >
collaterals/restoration of normal blood pressure pons > internal capsule
following hypotension / hypertension /
anticoagulation causes extravasation in  HEMATOMA/HEMORRHAGE
reperfused ischemic brain
• Bleed secondary to a ruptured vessel.
• Incidence:
• Imaging modality is CT (most sensitive) and MRI
-‐ 6% of clinically diagnosed brain infarcts
(GRE)
-‐ 20% of autopsied brain infarct

• Pathophysiology: INTRACEREBRAL
-‐ petechial hemorrhages in various degrees of 1. hematoma
coalescence -‐ blood separating relatively normal neurons/
• Location: frequently no LOC
-‐ corticomedullary junction -‐ well defined homogeneously increased density
a. shear –strain injury (most common)
Basal Ganglia Infarct b. blunt /penetrating trauma
• occlusion of small penetrating arteries at base of
brain (lenticulostriate /thalamoperforating 2. cortical contusion
arteries) – blood mixed with edematous brain
• dense homogeneous enhancement outlining -‐ poorly defined area of mixed high and low
caudate nucleus, putamen, globus pallidus, densities
thalamus
• dense round nodular enhancement/peripheral 3. intraventricular hemorrhage
ring enhancement – potential complication of intracranial
• Causes: hemorrhage
-‐ embolism
-‐ hypoperfusion Hematoma of the Brain
-‐ carbon monoxide poisoning • intracerebral hematoma
-‐ drowning • Etiology:
-‐vasculopathy (hypertension, microvasculopathy,
aging) a. very common
1. chronic hypertension (50%) – external capsule
Lacunar Infarction and basal ganglia (putamen 65%)/thalamus
• small deep infarcts in the distal distribution of (25%), pons (5%), + brainstem (10%), cerebellum
penetrating vessels (5%), cerebral hemisphere (5%)
(lentiulostriate,thalamoperforating, pontine 2. trauma
perforating arteries, recurrent artery of Heubner) 3. aneurysm

kirstie


4. vascular malformation – AVM, cavernous • Risk factors:
hemangioma, venous angioma, capillary 1. hypertension
telangiectasia 2. cardiac disorders
3. diabetes mellitus
b. common 4. cigarette smoking
1. hemorrhagic infarction – hemorrhage
transformation TYPES:
2. amyloid angiopathy (20%) – elderly 1. Carotid Transitory Ischemic Attack
3. coagulopathy (5%) -‐ carotid attacks < 6 hours in 90%
4. drug abuse(5%) -‐ transient weakness/sensory dysfunction
5. bleeding into tumor classically in:
a. primary – GBM, ependymoma, a. hand/face with embolic event
pituitary adenoma, oligodendroglioma b. proximal arm + lower extremity with
b. metastatic – melanoma, hemodynamic event (watershed area)
choriocarcinoma, renal cell CA, throid
CA, adenoCA 2. Vertebrobasilar Transient Ischemic Attack
c. uncommon – venous infarction, eclampsia, -‐ vertebrobasilar events <2 hours in 90%
Table septic emboli, vasculitis (fungal), encephalitis -‐ drop attack – sudden fall to the ground without
LOC
Stages of Cerebral Hematoma
Appearance Accelerating/Cresendo TIA
• repeated periodic events of neurologic
T1-Weighted T2-Weighted dysfunction with complete recovery to
Phase Time Hemoglobin, Location MRI MRI normal in interphase

Hyperacute <24 h Oxyhemoglobin, Isointense or Hyperintense  SUBARACHNOID HEMORRHAGE
intracellular hypointense • Bleeding into the subarachnoid space, between
the pia mater and the arachnoid
Acute 1-3 d Deoxyhemoglobin, Hypointense Hypointense • Most commonly occurs between ages of 25 to 65,
intracellular increasing in frequency with age
• Most common causes are rupture of an
Early >3 d Methemoglobin, Hyperintense Hypointense intracranial aneurysm or head trauma
subacute intracellular • Causes of SAH
o Head trauma
Late subacute >7 d Methemoglobin, Hyperintense Hyperintense o Intracranial aneurysms
extracellular -‐ Cause of approximately 80% of
nontraumatic subarachnoid hemorrhage
Chronic >14 d Ferritin and hemosiderin, Hypointense Hypointense -‐ Most occur around the circle of Willis

extracellular (berry aneurysm)
• Middle cerebral artery
bifurcation
 ISCHEMIC ATTACK • Anterior communicating artery

• Posterior communicating artery
Transient Ischemic Attack
• Ophthalmic arteries
• brief episode of transient focal neurologic
• Vertebral and basilar arteries
deficit owing to ischemia of < 24 hours
• Benign perimesencephalic hemorrhage
duration with return to pre attack status.
-‐ Blood limited to midbrain
• Cause:
• Less Frequent Causes of SAH
1. embolic – from ulcerative plaque at carotid
o Arteriovenous malformation (AVM)
bifurcation
o Extension from intracerebral
2. hemodynamic – fall in perfusion pressure
hemorrhage
distal to high grade stenosis/occlusion
o Arteriovenous fistulae

kirstie


o Meningitis  High-‐attenuation blood in the Sylvian
o Neoplasm fissures (blue arrows) and the
• Risk Factors: interhemispheric fissure (red arrow)
o Vasculitis  Normal, physiologic calcifications (white
o Fibromuscular dysplasia (FMD) and black arrows).
o Hypertension
o History of polycystic kidney disease
o Smoking

 Clinical findings
 Headache is most common symptom
 Frequently reported as severe (“worst
headache of life"), of abrupt onset,
reaches maximum intensity within
seconds (“thunderclap headache”)
 Nausea and Vomiting  Treatment
 Change in mental status -‐-‐ confusion  Relief of associated vasospasm (occurs in
 Decreased level of consciousness -‐ coma as many as 50% of patients with SAH) -‐
 Spinal fluid may be bloody calcium channel blockers
 Urgent surgical removal of blood
 Imaging findings  Early surgical clipping to prevent
 Unenhanced CT of the brain is the study rebleeding
of choice for establishing presence of  Endovascular management
SAH  Coiling
 Acute hemorrhage is most evident 2-‐3  Prognosis
days after the acute bleed  About 10 to 30% die before reaching
 CT angiography have replaced medical help with first bleed
conventional angiography in most  Nontraumatic subarachnoid hemorrhage
institutions for the identification and in patients who reach the hospital still
location of the aneurysm itself has a mortality rate of 30 to 60%
 Aneurysm size and shape can  SAH from an arteriovenous
help determine which aneurysm malformation has a better prognosis
has bled than SAH from a ruptured aneurysm
 Still considered the “gold”
standard for diagnosis of Trauma-‐related TYPE
intracranial aneurysm
 Acute hemorrhage high-‐attenuation Layers of The Meninges
(white) material that fills the normally  Dura Mater
black subarachnoid spaces, which  Arachnoid Membrane
include  Pia Mater
 The basilar cisterns
-‐ Especially the suprasellar I. Dura Mater
cistern  Outer (Periosteal) Layer
 The sulci  Consists of ELONGATED FIBROBLASTS
-‐ Especially the Sylvian fissures  Contains large extracellulars spaces,
 Over the convexities of the brain, SAH meningeal blood vessels
produces white, branching densities  Tightly applied to the inner calvarial
representing the normally black sulci vault; similar to periosteum
filled with blood  Terminates at the FORAMEN MAGNUM
 In MRI, FLAIR sequence best
demonstrates SAH.



kirstie


 Inner (Meningeal) Layer Virchow-‐Robin Spaces
 Composed of EPITHELIAL CELLS  Invaginations of pia and CSF along cortical
 Continuous with the SPINAL DURA arteries that penetrate the brain parenchyma
 Epidural Space
 Potential space between the
outer (periosteal) dura and
inner table of the skull
 OUTER
 Aka:Periosteal
 Comp: Fibroblasts
 Terminates at Foramen magnum

 INNER
 Aka: Menigeal
 Comp: Epithelial Cells
 Continuous with Spinal dura

II. Arachnoid
 Closely applied to the inner dura Acute Neurologic Conditions
 Subdural space  Extracerebral Hemorrhage
 Epidural Hematoma
 Potential space between inner dura and  Subdural Hematoma
arachnoid  Subarachnoid Hemorrhage
 Traversed by scattered trabeculae  Intraaxial Lesions
 Where cortical veins cross as they course  Diffuse Axonal Injury
from brain surface toward a dural sinus
EPIDURAL HEMATOMA
III. Pia Mater  collection of blood which forms between the
 Innermost cranial meningeal layer inner surface of the skull and outer layer of dura
 Closely applied to the cortex  torn meningeal artery, usually middle meningeal
 Invaginates into the underlying sulci artery.
 Composition  Associated skull fracture is present in 80% of
 External: Collagen Fibers cases
 Internal: Vermicular and Elastic Fibers  5 -‐ 10% of patients the EDH is posterior fossa
 Occasionally an EDH can form due to venous
LEPTOMENINGES = Arachnoid + Pia blood, typically a torn sinus with associated
fracture
Subarachnoid space  Essentially a subperiosteal hematoma (between
 Space between arachnoid and pia mater bone and outer layer of the dura)
 Occupied by delicate connective tissue  Limited by the sutures
trabeculae and intercommunicating channels  Can cross and elevate venous sinuses as long as
containing CSF. there is no suture
 Small in the normal brain  Prognosis and Treatment: good for immediate
 Over the gyri, the arachnoid membrane evacuation of clot
and pia mater are in close contact.  Smaller hematomas treated consevatively 
 In the sulci, triangular spaces develop dural calcifications
because the pia mater is closely applied  COMPLICATIONS
to the cerebral cortex and the arachnoid • Pseudoaneurysm
membrane bridges the gap between • Arteriovenous fistula
adjacent gyri without descending into
each sulci

kirstie


EPIDURAL HEMATOMA -‐ BICONVEX OR LENTIFORM SUBARACHNOID HEMATOMA (TRAUMA)
• concomitant to cerebral contusion
1. Injury to leptomeningeal vessels at the vertex
2. rupture of major intracerebral vessels (less
common)
• location:
a. focal, overlying site of contussion/subdural
hematoma
b. interhemispheric fissure, paralleling falx cerebri
c. spread diffusely throughout subarachnoid
space (rare in trauma): convexity sulci>basal
cisterns

DIFFUSE AXONAL INJURY
SUBDURAL HEMORRHAGE  Result of deceleration injuries, especially in high-‐
 Collection of blood between the dura and speed motor vehicle collisions
arachnoid mater of the meninges around the  Also a major cause of morbidity in
brain “Shaken Baby Syndrome”
 Seen in 10 to 20% of all head trauma cases and  Most frequent cause of persistent vegetative
occur in up to 30% of fatal injuries state following trauma
 Common in elderly people and they tend to occur  Result of rotational shear injuries that most often
following trivial head trauma occur at the gray-‐white matter junction
 Stretching and tearing of bridging cortical veins  Extent of injury is usually worse than
as they cross the subdural space to drain into an that depicted by imaging
adjacent dural sinus  Shearing leads to edema, axoplasmic leakage,
 Sudden change of velocity of the head shearing retraction ball formation and wallerian
forces  RUPTURE OF CORTICAL VEINS degeneration
 Arachnoid may also be torn  mixture of blood  Brainstem function is typically unaffected
and CSF in the subdural space  Damage occurs at time of injury and then when
 10 to 30% of chronic SDHs show evidence of secondary swelling occurs
repeated hemorrhage.  Immediate loss of consciousness
 SDHs are interposed between the dura and  Most, but not all, have no period of
arachnoid. lucidity
 Typically crescent-‐shaped
 Usually more extensive than EDHs  Imaging Findings
 Not limited by sutures but are limited by dural  Diffuse
reflections ( e.g. falx cerebri, tentorium, falx  Bilateral
cerebelli)  Majority of lesions (80%) are multiple
 Common sites:  Occur at the gray-‐white matter junction
 Fronto-‐parietal convexities  Lesions are most frequently ovoid, larger
 Middle cranial fossa centrally than peripherally
 -‐ 85% are unilateral
 Frequently involved sites:
SUBDURAL HEMATOMA -‐ CRESCENT-‐SHAPED  Frontal and temporal lobes
homogeneously hyperdense extraaxial collection  Posterior body and splenium of the
corpus callosum
 Caudate nuclei
 Thalamus
 Tegmentum
 Internal capsule

kirstie


 On CT  Hemorrhagic lesions appear
 50-‐89% normal CT scan on presentation hyperintense on T1-‐weighted images
 Small petechial hemorrhages located at  Non-‐hemorrhagic lesions appear
gray-‐white matter junction and corpus hyperintense on T2-‐weighted sequences
callosum are characteristic but occur in
only about 20%  Differential Diagnosis
 There may also be small. Focal areas of  Multiple sclerosis
decreased attenuation secondary to  Embolic or hemorrhagic stroke
edema  Prognosis
 Over 90% remain in persistent
DIFFUSE AXONAL INJURY -‐ Petechial hemorrhages at vegetative state
the gary-‐white matter junction, the caudate nucleus and  Chances of this occurring are greater
the corpus callosum with lesions that are supratentorial,
involve the corpus callosum or corona
radiata
 Prognosis worsens with multiplicity of
lesions

VASCULAR MALFORMATION OF THE BRAIN
 Cerebrovascular malformation (CVM) of the
brain are a heterogeneous group of disorders that
represent morphogenetic errors affecting
arteries, capillaries, veins or various combinations
of vessels
 FOUR Basic Types:
1. Arteriovenous malformations – most common
 On MRI type (brain prenchyma[pial], dural and mixed
 Gradient-‐echo sequences are very useful pial-‐dural)
in demonstrating paramagnetic effects 2. Capillary telangiectasias
of petechial hemorrhages 3. Cavernous angiomas
 Most common MRI finding 4. Venous malformations
 Presence of multiple focal areas
of abnormally bright signal on ANGIOGRAPHY (CT/MRI)
T2-‐weighted images in the
white matter of the temporal or
parietal corticomedullary
junction or in splenium of
corpus callosum.

ANGIOGRAPHY (A-‐V MALFORMATION)

kirstie

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