CEREBROVASCULAR DISEASE
OLINOR V. MAMBUAY, MD
RADIOLOGY RESIDENT
Stroke
• brain infarction (75%) or hemorrhage (25%)
• Infarction is a permanent injury that occurs when
tissue perfusion is decreased long enough to cause
necrosis, typically due to occlusion of the feeding
artery
• Transient ischemic attacks (TIAs)- transient neurologic
symptoms or signs lasting less than 24 hours, which
may serve as a “warning sign” of an infarction
occurring in the next few weeks or months
• clinical term applied to any abrupt nontraumatic
• brain insult
• The diagnosis of stroke is usually made clinically. Patients
• with suspected stroke are imaged to determine if there is
• another cause of the neurologic impairment besides
• a stroke (e.g., a brain tumor) and to identify the presence
• of blood so as to distinguish ischemic from hemorrhagic
• stroke. Whether or not hemorrhage is present
• may determine whether or not thrombolytic therapy
• will be instituted, and it may identify the infarct and
• characterize it.
• Hemorrhage is seen when blood ruptures
through the arterial wall, spilling into the
surrounding parenchyma, subarachnoid
space, or ventricles
ISCHEMIC STROKE
• Among those with an established mechanism,
about two thirds of infarcts are caused by
thrombi and one-third by emboli
Pathophysiologic Basis for Imaging
Changes
• Ischemia causes a cascade of cellular level events
leading to the gross pathologic changes detected in
clinical imaging
• Failure of membrane pumps permits efflux of K and
simultaneous influx of Ca 2, Na , and water
• Cellular (“cytotoxic”) edema
• Changes in brain water are key to understanding signs
of infarction by CT and MR
Hyperdense Artery Sign and Early
Edema on CT and ASPECTS
• Hyperdense Artery Sign and Early Edema on CT. Three
hours post occlusion, high density indicative of thrombus
is seen in the
• proximal right middle cerebral artery (MCA) ( arrows ).
Extensive right hemisphere edema is already present. The
10 regions scored by ASPECTS
• are shown in the normal left hemisphere. The ASPECTS
score is only 3, with points off for low attenuation in the
right insula, posterior lentiform
• nucleus, M1, M2, M3, M4, and M5 cortical regions. Edema
involves more than one-third MCA territory and ASPECTS is
much lower than 7,
• both predicting a poor candidate for acute thrombolysis.
Insular Ribbon Sign
• Insular Ribbon Sign. A. A noncontrast CT done 4 hours
after right middle cerebral artery (MCA) occlusion
• shows decreased attenuation and loss of gray–white
borders in the right insular region ( arrows ). B. Diagram of
the
• insula in transverse and coronal planes. The insular cortex,
claustrum, and extreme capsule are infarcted due to
occlusion
• of the MCA ( arrow ) beyond the lateral lenticulostriate
vessels. (From Truwit CL, Barkovich AJ, Gean-Marton A, et
al. Loss
• of the insular ribbon: another early CT sign of acute middle
cerebral artery infarction.
Diffusion–Perfusion Mismatch in
Acute Ischemia
Diffusion–Perfusion Mismatch in Acute Ischemia. This 86-year-old
woman with a history of atrial fi brillation developed
• sudden right hemiplegia and aphasia. The noncontrast CT shows
subtle low attenuation in the left putamen, insula, and sylvian
• cortex ( arrows ). On T2WI, the cortical gray matter shows mild
edema, confi rmed to represent cytotoxic edema on DWI and
• apparent diffusion coeffi cient (ADC). Fluid-attenuated inversion
recovery (FLAIR) image shows cortical edema and stasis in the left
• middle cerebral artery. Perfusion-weighted images (mean transit
time, MTT, and cerebral blood volume, CBV) show a larger area
• at risk extending into the parietal lobe (MTT defect in white dashes;
DWI lesion superimposed in black dashes ). The hypoperfused
• tissue not yet infarcted is considered tissue at risk, or the ischemic
penumbra. Diffusion lesions tend to “grow into” severe surrounding
• perfusion lesions if untreated. Follow-up CT shows extension of
infarction into the penumbral tissue identifi ed by MTT.
Use of Contrast in Ischemic Stroke
• A noncontrast CT remains the radiologic exam of
choice for emergency assessment of suspected
acute stroke
• The unenhanced study is necessary to help triage
the patient.
• It serves to rule out hemorrhage, may define
patterns and
• extent of ischemic injury, shows areas of
abnormal vascular
• calcifi cation (e.g., giant aneurysms), and excludes
mass lesions.
Pattern Recognition in Ischemic Stroke
• Classically strokes and
TIAs are divided into
anterior (carotid
• territory) or posterior
(vertebrobasilar
territory) events
• The relation of vascular anatomy to functional
neuroanatomy
• is at the heart of clinicoradiologic correlation in stroke.
• Homunculus. A coronal section through the precentral
• (motor) cortex depicts the topographic representation of
the
• opposite side of the body. The face and hand areas are
served by the
• middle cerebral artery territory, the leg by the anterior
cerebral artery.
Anterior Cerebral Artery (ACA)
Occlusion
• Anterior Cerebral Artery (ACA) Occlusion. An
ACA
• occlusion causes infarction of the paramedian
frontal cortex responsible
• for motor and sensory function of the
opposite leg ( stippled area ).
• If bilateral, incontinence and akinetic mutism
may also be seen.
Middle Cerebral Artery (MCA)
Occlusion
• Middle Cerebral Artery (MCA)
• Occlusion. An MCA occlusion distal to the lateral
lenticulostriates
• causes infarction of the motor and sensory
• cortex of the arm and face ( stippled area ). More
• proximal occlusion will also affect the internal
capsule,
• potentially adding leg deficits. (From Patten J.
• Neurological Differential
Posterior Cerebral
Artery (PCA) Occlusion
• Posterior Cerebral
• Artery (PCA) Occlusion. A PCA
• occlusion results in syndromes of
• memory impairment, opposite visual
• field loss, and sometimes hemisensory
• deficits. (From Patten J. Neurological
• Differential Diagnosis.
Posterior Cerebral Artery Infarction
• Posterior Cerebral Artery Infarction. Adjacent
• T2-weighted images show involvement of the
left occipital lobe and
• medial temporal lobe. The patient presented
with a dense right homonymous
• visual field defect.
HEMORRHAGE
• A noncontrast CT remains
the test of choice for
emergency evaluation of
suspected hemorrhage
• CT Versus MR in
Parenchymal Hemorrhage
Due to
• Amyloid Angiopathy. CT
shows an acute right
thalamic hematoma
• with extension into the
occipital horn of the right
lateral ventricle
• ( arrow ).
Subarachnoid Hemorrhage
• CSF-lined compartment,
which surrounds the
blood vessels and
communicates with the
ventricular system
• Sudden, severe
headache is the most
common symptom of
aneurysm rupture
• Ruptured Anterior Communicating Artery Aneurysm. This
21-year-old man collapsed immediately after
• snorting a line of cocaine. A. Noncontrast CT shows blood in
the interhemispheric fi ssure and in the dependent portions
of the lateral ventricles. Blood in the ventricles, cisterns, or
layered in the sulci is subarachnoid by defi nition. B. Lateral
view from a
• digital subtraction angiogram demonstrates a large anterior
communicating artery aneurysm ( arrow ). Over half of drug
abusers
• with intracranial hemorrhage will be found to have an
underlying aneurysm or arteriovenous malformation. CTA in a
similar
• case showing a ruptured aneurysm ( white arrows ) in sagittal
( C ) and coronal ( D ) thick two-dimensional reconstructions.
Subtle Subarachnoid Hemorrhage
by CT
• Subtle Subarachnoid Hemorrhage by CT. The
most sensitive areas for detecting subarachnoid
hemorrhage
• are the dependent parts of the occipital horns (
A, arrow ) and the interpeduncular fossa ( B,
arrow ). The choroid plexus at
• the atrium of the lateral ventricle ( A, CP )
normally appears dense due to calcifi cation or
enhancement. The nondependent
• location of the choroid differentiates it from
hemorrhage.
Parenchymal Hemorrhage
• Hypertensive hemorrhages are seen in the
putamen (35% to 50%), the subcortical white
matter (30%), the cerebellum (15%), thalamus
(10% to 15%), and pons (5% to 10%)
Vascular malformations
• Arteriovenous malformations (AVMs)
– are the most common type of brain
vascular malformation.
– Abnormal tangle of arteries directly
connected to veins without an intervening
capillary network.
– About 80% to 90% are supratentorial
• Cavernous malformations are thin-walled
sinusoidal vessels
– (neither arteries nor veins) which may present
with seizures or small parenchymal hemorrhages
• Venous malformations are congenitally
anomalous veins that drain normal brain.
Parenchymal Hemorrhage
• Hypertensive Putaminal Hemorrhage With Enhancement
at 10 Days. The precontrast study (A) shows a large
• hematoma centered in the left putamen. Dense calcifi
cation of the choroid plexus ( CP ), pineal ( P ), and
habenula ( H ) should
• not be mistaken for intraventricular extension. Moderate
mass effect and a small amount of surrounding edema are
evident. A
• ring of enhancement surrounds this benign hematoma ( B
), likely due to a vascular capsule. Resolving infarcts and
hemorrhages
• normally show enhancement at the subacute phase.
Right Frontal Arteriovenous
Malformation.
• Right Frontal Arteriovenous Malformation. An MR
was performed because of headaches. A. Transverse
• T2WI shows a large right frontal lesion ( arrow ) with a
complex mixture of hyperintensity and hypointensity
due to turbulent
• fl ow. A tortuous fl ow void headed toward the midline
indicates a large draining vein ( arrowhead ). B. Digital
subtraction
• angiography in the lateral projection (internal carotid
artery injection) depicts the large frontal nidus ( arrow
) and faintly the
• tortuous draining vein ( arrowheads ).