CT scan of Cerebrovascular Diseases
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Computed Axial Tomography Scan of Cerebrovascular
Disease
By Jaymart S. CostillasRadiology Senior Clerk
Northern Mindanao Medical CenterJune 25, 2014
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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
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Objectives:
To determine if there is another cause of neurologic impairment
To distinguish between ischemic & hemorrhagic stroke
To identify infarct and characterize it
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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.
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Arterial Territories
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Supratentorial Territories
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ISCHEMIC STROKE
Etiology Thrombi – 2/3 Emboli – 1/3
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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
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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
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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
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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
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Hyperdense artery sign
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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”
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Loss of insular ribbon sign
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Obscuration of the lentiform nucleus
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Hyperdense vessel sign
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Hyperdense vessel sign & loss of gray/whitejunction...
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Left insular ribbon sign & effacement of sulci
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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)
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Ischemic stroke at 24h after onset
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Fogging effect
36 hrs 18 days
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Encephalomalacia
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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
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Hemorrhagic transformation
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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
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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
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Watershed infarct
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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
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ISCHEMIC STROKESmall-vessel ischemia Characteristic locations:
lenticular nucleus (37%) pons (16%) thalamus (14%) caudate (10%) internal capsule/corona radiata (10%)
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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
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Hemorrhagic Stroke
Primary Intracerebral bleed Hypertensive Amyloid angiopathy Arteriovenous malformations Neoplasms Trauma
Subarachnoid hemorrhage Aneurysm AVM’s Trauma
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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
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HEMORRHAGIC STROKE
Subarachnoid Hemorrhage (SAH) Aneurysm – most common AVM’s Thrombocytopenia Severe coagulopathies Drugs, trauma, dissection
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HEMORRHAGIC STROKE
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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
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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
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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
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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
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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
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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
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HEMORRHAGIC STROKEIntraparenchymal Hemorrhage Differential considerations:
hypertensive hemorrhage vascular malformations drug effects amyloid angiopathy bloody tumors
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HEMORRHAGIC STROKE
Intraparenchymal Hemorrhage Hypertensive hemorrhage
Putamen – 35 – 50% Subcortical white matter – 30% Cerebellum – 15% Thalamus – 10 – 15% Pons – 5 – 10%
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HEMORRHAGIC STROKE
Intraparenchymal Hemorrhage Hypertensive hemorrhage
Due to: lipohyalinosis Small hypertensive hemorrhages may
resolve with few deficits
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HypertensiveHemorrhage
Classically involvesthe deep nucleii
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THE END