Chapter 4Cerebrovascular Disease

Brant and Helms Lecture Series

Michael Bergen PGY-2

Stroke is a clinical term referring to a nontraumatic 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 Strokes
Thromboembolic 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 Findings

Ischemia = 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 Sequencing
DWI: 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 Arteryatherosclerotic disease near the carotid bifurcation is responsible for majority ICA territory events

MRA of Circle Willis

ACA
Represent 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 Artery

Represent 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 Stroke
Often 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 Ischemia

Lacunes 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 Infarction
Uncommon, but affects younger, OCPS, dehydration, infections Blockage of outflow leads to stasis--neuronal death Lesions tend to spare cortex, dont 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 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 1520% 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

Subacute Infarction

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

Hemorrhages
Divided: 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 Hemorrhage
Hemorrhage 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