Computed Axial Tomography Scan of Cerebrovascular

Disease

By Jaymart S. CostillasRadiology Senior Clerk

Northern Mindanao Medical CenterJune 25, 2014

Non-contrast CT (Brain Plain) Remains the initial imaging of CHOICE for

emergency assessment of suspected acute stroke (within 24hrs onset)

Helps triage the patient To rule out hemorrhage Define patterns/extent of ischemic injury Shows areas of abnormal calcification Excludes mass lesion FIRST-LINE information needed for management

Objectives:

To determine if there is another cause of neurologic impairment

To distinguish between ischemic & hemorrhagic stroke

To identify infarct and characterize it

Definition: Stroke A clinical term denotes an acute loss of

neurologic function Abrupt non-traumatic brain insult Infarction (75%) or Hemorrhagic (25%) TIAs - transient neurologic symptoms or

signs lasting less than 24 hours, may serve as a “warning sign” of an infarction occurring in the next few weeks or months.

Arterial Territories

Supratentorial Territories

ISCHEMIC STROKE

Etiology Thrombi – 2/3 Emboli – 1/3

ISCHEMIC STROKE

Pathophysiologic Basis for Imaging Changes

Brain metabolism Disruption of blood flow for a few minutes

can lead to neuronal death Selective vulnerability

Gray matter is 3-4x more metabolically active than white matter

ISCHEMIC STROKE

Pathophysiologic Basis for Imaging Changes

Selective vulnerability Some subset of neurons are more

vulnerable Cells residing at “Water-Shed” zone are

more prone to infarction

ISCHEMIC STROKECT of Acute Ischemia Occlusion of feeding artery ischemia

failure of energy production ionic deregulation cellular “cytotoxic” edema (increased water content) loss of gray-white differentiation observed as decreased attenuation at CT

Key: Changes in brain water

ISCHEMIC STROKECT of Acute Ischemia Edema peaks 3-7 days post-infarction,

maximal in gray matter “Hyperacute” signs relate to

morphologic changes in the vessels rather than density changes in the parenchyma

Hyperdense artery sign

ISCHEMIC STROKECT of Acute Ischemia CT scan done within 6hrs exhibit

“Insular ribbon sign” Early edema can be most conspicuous

in putamen “Lentiform nucleus edema sign”

Loss of insular ribbon sign

Obscuration of the lentiform nucleus

Hyperdense vessel sign

Hyperdense vessel sign & loss of gray/whitejunction...

Left insular ribbon sign & effacement of sulci

ISCHEMIC STROKECT of Subacute & Chronic Ischemia Edema mass effect Peaks 3-7 days Pitfall: Fogging effect occurs 2-6 weeks after

onset, hypodensed infarcted area disappear, becoming isodense “disappeared infarct” will reappear in later phase in a form of tissue cavitation (encephalomalacia)

Ischemic stroke at 24h after onset

Fogging effect

36 hrs 18 days

Encephalomalacia

ISCHEMIC STROKEHemorrhagic transformation Peaks at 1-2weeks post infarction Caused by reperfusion (50% of cases) Mostly microscopic leakage

(diapedesis) of RBC Rarely, frank hematoma Pt rarely have new symptoms Confined to territory of infarcted vessel Intraventricular extension is uncommon

Hemorrhagic transformation

ISCHEMIC STROKE Summary of CT imaging time course

Time CTMinutes No changes

2-6 hrs Hyperdense artery sign

Insular ribbon sign

6-12hrs Sulcal effacement

Decreased attenuation

12-24hrs Decreased attenuation

3-7 days Maximal swelling

3-21 days Gyral enhancement (peak 7-14 days)

30-90 days Encephalomalacia

Loss of enhancement

Resolution of petechial blood

ISCHEMIC STROKEWatershed Infarction Transient global hypoperfusion

bilateral infarctions of watershed regions When flow of BOTH parent vessels falls

below critical level watershed region suffers first

Unilateral watershed damage occur in carotid occlusion/stenosis unmasked by hypotension

Watershed infarct

ISCHEMIC STROKESmall-vessel ischemia Lacunes - small subcortical infarcts that

may occur in any territory 15% to 20% of all strokes Are the cavities (2 to 5 mm3) left in the

brain due to occlusion of a penetrating artery, causing infarction and ensuing encephalomalacia

Long-standing HPN Lipohyalinosis Thrombosis

ISCHEMIC STROKESmall-vessel ischemia Characteristic locations:

lenticular nucleus (37%) pons (16%) thalamus (14%) caudate (10%) internal capsule/corona radiata (10%)

HEMORRHAGIC STROKE Occurs 15% of strokes Higher mortality & morbidity Occur on brain parenchyma or

subarachnoid Majority are assoc w/ chronic HPN 60% of hypertensive hemorrhage occur

in basal ganglia

Hemorrhagic Stroke

Primary Intracerebral bleed Hypertensive Amyloid angiopathy Arteriovenous malformations Neoplasms Trauma

Subarachnoid hemorrhage Aneurysm AVM’s Trauma

HEMORRHAGIC STROKE

CT imaging of Hemorrhage Non-contrast CT test of choice for

emergency evaluation Detected as increased attenuation Formation of a clot enhances diagnostic

yield

HEMORRHAGIC STROKE

Subarachnoid Hemorrhage (SAH) Aneurysm – most common AVM’s Thrombocytopenia Severe coagulopathies Drugs, trauma, dissection

HEMORRHAGIC STROKE

HEMORRHAGIC STROKESubarachnoid Hemorrhage (SAH) CT>90% sensitive for the detection of

acute SAH d/t increased density of clotted blood

Difficult to detect in pt w/: Low Hct (<30%, non-clotted isodense) Small hemorrhage Delay in scanning

Subarachnoid Hemorrhage (SAH) The most sensitive places to look for:

interpeduncular fossa far posterior aspects of the occipital horns

Prompt scanning is important, because dissolution of subarachnoid blood reduces CT sensitivity to 66% by day 3

HEMORRHAGIC STROKE

HEMORRHAGIC STROKE 15% to 20% of patients with subarachnoid

bleeding will have multiple aneurysms Because of this multiplicity, a CTA or “four-

vessel” angiogram is needed on the initial �evaluation

When multiple aneurysms are present, the largest or most irregular, has focal mass effect, is intra-aneurysmal, or shows a change on serial exams is likely to be the culprit

HEMORRHAGIC STROKESubarachnoid Hemorrhage (SAH) Follow-up studies

initial or subsequent CT may show communicating hydrocephalus requiring a ventriculostomy or shunt

Episodes of possible rebleeding are evaluated with noncontrast CT

HEMORRHAGIC STROKE Subarachnoid Hemorrhage (SAH)

Infarcts may also be seen in patients with elevated ICP or vasospasm and are the main pathologic finding in patients whose condition continues to deteriorate after the initial SAH

Post treatment angiography is used to assess adequacy of clip placement and to rule out vasospasm

HEMORRHAGIC STROKEIntraparenchymal Hemorrhage Occurs as a result of bleeding directly

into the brain substance Generally have a higher initial mortality

than infarcts But on recovery they show fewer

deficits than a similar-sized infarct hemorrhage tends to tear through and

displace brain tissue but can be resorbed

HEMORRHAGIC STROKEIntraparenchymal Hemorrhage Differential considerations:

hypertensive hemorrhage vascular malformations drug effects amyloid angiopathy bloody tumors

HEMORRHAGIC STROKE

Intraparenchymal Hemorrhage Hypertensive hemorrhage

Putamen – 35 – 50% Subcortical white matter – 30% Cerebellum – 15% Thalamus – 10 – 15% Pons – 5 – 10%

HEMORRHAGIC STROKE

Intraparenchymal Hemorrhage Hypertensive hemorrhage

Due to: lipohyalinosis Small hypertensive hemorrhages may

resolve with few deficits

HypertensiveHemorrhage

Classically involvesthe deep nucleii

THE END