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Primary intraparenchymal hemorrhage (pICH)
Acute nontraumatic intracranial hemorrhage (ICH)
Acute round or oval intracerebral hematoma
Subcentimeter “microbleeds” to massive ICH
Hematoma location for common causes of pICH
HTN: Basal ganglia > thalamus > pons > cerebellum
Amyloid angiopathy: Lobar
Arteriovenous malformation: Any location
Cavernous malformation: Any location
Venous sinus thrombosis: Subcortical white matter
Neoplasm: Any location
Recommended imaging: Begin with NECT
If HTN with striatocapsular hematoma → stop
If atypical hematoma → CTA or MR/MRA
Atypical hematoma or unclear history: MR (T2*, DWI, C+)
If standard study suggests vascular etiology → CTA/MRA
If concern for venous infarct → CTV/MRV
Pediatric patients, < 18 years old: Vascular malformation (~ 50%) > hematologic disorders, vasculopathy, venous infarct, neoplasm
Young adults, < 45 years old: Vascular malformation, drug abuse, venous thrombosis, PRES, vasculitis, neoplasm
Adults > 45 years old: HTN, amyloid > neoplasm (primary or metastatic), venous infarct, coagulopathy
ICH causes ~ 15% of acute strokes
Treatment: Control of intracranial pressure, hydrocephalus
Surgical evacuation when clinically indicated
If positive spot sign indicates active bleeding, predicts hematoma expansion and poor outcome
1-year mortality approaches 60%
Primary intraparenchymal hemorrhage (pICH), hemorrhagic stroke
Acute nontraumatic intracranial hemorrhage (ICH)
Etiology often initially unknown
Best diagnostic clue
Acute nontraumatic intracerebral hematoma
Location
Varies with etiology
Hypertension (HTN): Deep gray matter (basal ganglia, thalamus), pons, cerebellar hemisphere
Amyloid angiopathy: Lobar
Arteriovenous malformation (AVM): Any location
Cavernous malformation: Any location, common in brainstem
Venous sinus thrombosis: Subcortical white matter (WM) adjacent to occluded sinus
Neoplasm: Any location, posterior fossa common
Size
Subcentimeter “microbleeds” to massive hemorrhage
Morphology
Typically round or oval; often irregular when large
Patterns with HTN and amyloid angiopathy
Acute parenchymal hematoma
Multiple subacute/chronic “microbleeds” in deep gray matter (HTN > amyloid) &/or subcortical white matter (amyloid > HTN)
Microbleeds often seen only on GRE or SWI MR
NECT
Acute hyperdense round/elliptical mass
May be mixed iso-/hyperdense
May have fluid-fluid level
Coagulopathy
Brisk bleeding
Bleed into cystic mass
Peripheral low density (edema)
Deep (ganglionic) ICH may rupture into ventricles
CTA
Often nonrevealing
± underlying vascular malformation (AVM, aneurysm)
Look for dural sinus venous thrombosis
T1WI
Hyperacute (< 24 hours)
Isointense center (oxygenated Hgb)
Isointense periphery (deoxygenated Hgb, clot-tissue interface)
Hypointense rim (vasogenic edema)
T2WI
Hyperacute (< 24 hours)
Hyperintense, heterogeneous center
May have subtle hypointense periphery
Hyperintense rim of edema
T2* GRE
Hypointense
Multifocal hypointense lesions (“black dots”)
Basal ganglia (BG) and thalami suggests HTN
Subcortical WM suggests amyloid angiopathy
DWI
T2 shine through common; may see “DWI restriction” in core
T1WI C+
Often none in acute hematoma
May enhance if underlying neoplasm, vascular malformation
MRA
Often normal, look for vascular lesion
MRV
Look for dural sinus thrombosis
DSA, often negative
Look for dural sinus occlusion, “stagnating vessels” (thrombosed AVM)
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