Neuro5 Intracranial Hemorrhage Flashcards
Epidural hematoma
Rupture of middle meningeal artery (branch
of maxillary artery), often secondary to fracture
of temporal bone. Lucid interval. Rapid
expansion under systemic arterial pressure:
transtentorial herniation, CN III palsy.
CT shows “biconvex disk” not crossing suture
lines. Can cross falx, tentorium
Subdural hematoma
Rupture of bridging veins. Slow venous bleeding
(less pressure = hematoma develops over time).
Seen i n elderly individuals, alcoholics, blunt
trauma, shaken baby (predisposing factorsbrain
atrophy, shaking, whiplash). Crescent-shaped hemorrhage that crosses suture lines. Midline shift. Gyri are preserved, since pressure is distributed equally. Cannot cross falx, tentorium
Subarachnoid hemorrhage
Rupture of an aneurysm (usually berry aneurysm in Marfan’s, Ehlers-Danlos, ADPKD) or an AVM. Rapid time course. Patients complain of “worst headache of my life.” Bloody or yellow (xanthochromic) spinal tap. 2-3 days afterward, risk of vasospasm due to blood breakdown (not visible on C1
lntraparenchymal (hypertensive) hemorrhage
Most commonly caused by systemic hypertension, but also amyloid angiopathy, vasculitis, and neoplasm. Typically occurs in basal ganglia and internal capsule, but can be lobar.
Ischemic brain disease
Irreversible damage after 5 minutes. Most vulnerable-hippocampus, neocortex, cerebellum, watershed areas. Irreversible neuronal injury-red neurons ( 12-48 hours) , necrosis + neutrophils (24-72 hours), macrophages (3-5 clays) , reactive gliosis + vascular proliferation (1-2 weeks), glial scar (> 2 weeks) .
Atherosclerosis
thrombi lead to ischemic stroke with subsequent necrosis. Form cystic cavity with reactive gliosis
Hemorrhagic stroke
Intracerebral bleeding, often clue to hypertension, anticoagulation, and cancer (abnormal vessels can bleed). May be 2° to ischemic stroke followed by reperfusion (increases vessel fragility).
Ischemic stroke
Emboli block large vessels; etiologies include atrial fibrillation, carotid dissection, patent foramen ovale, endocarditis. Lacunar strokes block small vessels, may be 2° to hypertension. Treatment: tPA within 4.5 hours (so long as patient presents within 3 hours of onset) .
Transient ischemic attack (TIA)
brief, reversible episode of neurologic dysfunction lasting fewer than 24 hours; deficits clue to focal ischemia.
Stroke imaging
bright on diffusion-weighted MRI in 3-30 minutes and remains bright for 10 days, dark on noncontrast CT in ~ 24 hours. Bright areas on noncontrast CT indicate hemorrhage (tPA contraindicated) .