Brant Helm

Chapter 4- Cerebrovascular

DiseaseBrant and Helms Lecture Series

Michael Bergen PGY-2

Stroke is a clinical term referring to a non-traumatic brain insult resulting in a sudden loss of neurologic function

Infarction represents about 75% and Hemorrhage about 25% of strokes

Radiologist plays a critical role in evaluation and triage of EVERY stroke patient

Ischemic StrokesThromboembolic events are the

principle causes of ischemic events

i.e. Large artery atherosclerosis

has a higher mortality than

lacunes and are amendable to

Carotid Endarectomy

Acute Ischemia FindingsIschemia = Increased Cellular water

content = Cytotoxic edema

Brain water content is the principle to understating CT and Brain MRI in stroke

More Subtle CT findings

r/o Hemorrhage is the most critical step in HEAD CT evaluation

Early signs of infarction can be evident: Insular Ribbon Sign, Sulcal effacement, Mass effect, edema

MRI SequencingDWI: Uses a strong gradient pair that sensitizes images to microscopic BROWNIAN WATER MOTION

Brain water diffusion rapidly falls during acute ischemia.

Early infarct = BRIGHT SIGNAL ON DWI

ADC: reflects pure diffusion behavior free of any shine through and appears = DARK SIGNAL

** DDX: pyogenic abscess and tumors

MR

Pattern Recognition in Ischemic

Stroke

Vascular anatomy to functional neuroanatomy is critical

Anterior Circulation

Internal Carotid Artery- atherosclerotic disease near the carotid bifurcation is responsible for majority ICA territory events

MRA of Circle Willis

ACARepresent 5% of infarcts

3 subgroups of Branches:

1. Medial Lenticulostriates

2. Hemispheric

3. pericallosal

MCA

Represents 2/3 of Infarcts

Branches:

1. Lateral Hemispheric

2. Lateral lenticulostirates

Posterior (Vertebrobasilar) Circulation

Acute Brainstem Infarction

Posterior Cerebral ArteryRepresent 10-15% of Infarcts

Major Branches : 1. thalamic perforators 2.Posterior Choroidal 3.Cortical (med. temporal and occ. lobes)

** Normal Variant of the Circle Willis is a fetal origin of the PCA ~20% population

Contralateral homonymous Hemiaponsia

Cerebellar StrokeOften Neurosurgical emergencies and require posterior fossa decompression

85% ischemic and 15% hemorrhagic

Presents with headache, vertigo, N/V, ipsilateral ataxia

Superior Cerebellar Artery

Anterior Inferior Cerebellar Artery

Posterior Inferior Cerebellar Artery

Small Vessel IschemiaLacunes ‘little lakes’ account for 15-20% of all strokes

Secondary to long-standing HTN

Affects subcortical regions i.e Lenticular nucleus (37%), pons (16%), thalamus (14%), caudate (10%), IC (10%)

1. multiple foci of deep white matter/basal ganglia lacunar infarcts (black arrow), typical in small vessel ischemic disease

Venous InfarctionUncommon, but affects younger, OCPS, dehydration, infections

Blockage of outflow leads to stasis--neuronal death

Lesions tend to spare cortex, don’t follow normal vascular territories

CT- Empty Delta Sign; Spin Echo and MRV best imaging modality

Venous Infarction

Hemorrhagic Transformation of infarction

Reperfusion injury and develops in 15-45% of infarcts

Confined to infarcted vessel territory and intraventricular extension is UNCOMMON

Peaks 1-2 weeks post infarction

Manifest as serpiginous line of petechial blood following gyral contours of the infarcted cortex

Catastrophic hemorrhagic transformation can follow TPA

Subacute Infarction

Acute vs Subacute vs Chronic

Subacute InfarctionSubacute infarction approximately 2-14 days following initial ischemic event

Best diagnostic clue: Gyral edema and enhancement within basal ganglia and cortex

Typically wedge-shaped abnormality involving gray and white matter within vascular distribution

HT of initially ischemic infarction occurs in 15-20% of MCA occlusions, usually by 48-72 hours

"2-2-2" rule = enhancement begins at 2 days, peaks at 2 weeks, disappears by 2 months

• ↑ lactate, ↓ NAA within infarcted tissue

wedge-shaped abnormality involving gray and white matter within vascular distribution

Gyriform Enhancement

Chronic Infarction• Volume loss with gliosis along affected margins

• Classic: Wedge-shaped area of encephalomalacia

• Wallerian degeneration may be present

Chronic Infarction

HemorrhagesDivided: Subarachnoid vs Intraparenchymal

CT presents as high attenuation and MR is based on iron oxidation state

MR is best for subacute and chronic blood

FLAIR very sensitive for SAH

Gradient T2 echo is sensitive for parenchymal bleed

Biochemical evolution of hemorrhage

MR pattern signal

Subarachnoid Hemorrhage

Parenchymal HemorrhageHemorrhage has a higher mortality than infarction but less deficits on recovery

Trauma excluded DDX considerations: hypertensive, drugs, AVM, amyloid, tumors

Cases

Case 1

Case 2

Case 3

Case 4

Case 5

1

2

3