ABPN Vascular Neurology cheat sheet

Circle of Willis: anterior circulation from internal carotid arteries (ACA, MCA) and posterior circulation from the vertebrobasilar system (PCA), linked by anterior and posterior communicating arteries.

Normal cerebral blood flow is about 50 mL/100 g/min; flow below roughly 20 mL/100 g/min produces electrical failure, and below 10 mL/100 g/min causes membrane failure and infarction.

Cerebral perfusion pressure (CPP) = mean arterial pressure (MAP) − intracranial pressure (ICP); autoregulation normally maintains flow across a MAP range of about 60–150 mmHg.

ACA infarction: contralateral leg-predominant weakness and sensory loss, abulia, urinary incontinence; MCA infarction: face/arm weakness, aphasia (dominant), neglect (nondominant); PCA infarction: contralateral homonymous hemianopia.

Lacunar syndromes include pure motor, pure sensory, sensorimotor, ataxic hemiparesis, and dysarthria–clumsy hand; they arise from disease of small penetrating arteries and produce deep infarcts.

Watershed infarcts occur at ACA–MCA and MCA–PCA border zones after global hypoperfusion; they often cause proximal limb weakness or visual field deficits without a single-vessel territory.

Deep cerebral venous drainage: internal cerebral veins → vein of Galen → straight sinus; superficial cortical veins drain to the superior sagittal sinus and then to the transverse/sigmoid sinuses.

Ischemic cascade: ATP depletion → Na+/K+ pump failure → depolarization → glutamate release → calcium influx → protease, lipase, and free-radical injury → apoptosis and necrosis; the penumbra remains salvageable.

Blood–brain barrier tight junctions are disrupted by ischemia, increasing edema and hemorrhagic transformation risk, particularly after reperfusion.

Last known well determines eligibility; IV thrombolysis with alteplase or tenecteplase is approved for selected patients within 4.5 hours of symptom onset.

Absolute contraindications to IV thrombolysis include intracranial hemorrhage, severe head trauma or surgery within 3 months, active internal bleeding, and platelet count <100,000/µL.

Before IV thrombolysis, blood pressure must be <185/110 mmHg; after treatment, maintain <180/105 mmHg for at least 24 hours.

Noncontrast CT excludes hemorrhage; CT angiography identifies large-vessel occlusion; CT perfusion or MRI mismatch selects patients for thrombectomy in 6–24-hour windows.

Mechanical thrombectomy is standard for anterior circulation large-vessel occlusion within 6 hours; selected patients with salvageable tissue benefit up to 24 hours.

Aspirin is typically started 24 hours after IV thrombolysis once follow-up imaging excludes hemorrhage; dual antiplatelet therapy is used for 21 days in minor stroke or high-risk TIA.

Maintain normoglycemia, normothermia, and adequate oxygenation; treat hypoglycemia immediately because it is a common stroke mimic.

Malignant MCA infarction with progressive edema and midline shift may require decompressive hemicraniectomy, especially in patients younger than 60 years within 48 hours.

A dysphagia screen precedes oral intake; early mobilization and venous thromboembolism prophylaxis reduce complications after ischemic stroke.

Spontaneous ICH: hypertensive deep locations (basal ganglia, thalamus, pons, cerebellum) versus lobar locations, which suggest cerebral amyloid angiopathy in older adults.

For ICH, rapid systolic blood pressure lowering to about 140 mmHg (range 130–150) is reasonable within 6 hours; avoid sustained systolic pressure below 130 mmHg.

Warfarin-associated ICH: intravenous vitamin K plus four-factor prothrombin complex concentrate; dabigatran: idarucizumab; heparin: protamine sulfate.

ICH score components: GCS, hematoma volume, intraventricular hemorrhage, infratentorial origin, and age ≥80 years; higher scores predict higher mortality.

Cerebellar hemorrhage >3 cm, brainstem compression, or hydrocephalus warrants urgent surgical evacuation.

Aneurysmal SAH: secure the aneurysm early (clip or coil); oral nimodipine 60 mg every 4 hours for 21 days reduces delayed cerebral ischemia.

Vasospasm risk peaks days 3–14 after SAH; monitor with TCD (MCA mean velocity >120 cm/s) and CTA, and treat with induced hypertension and endovascular therapy when indicated.

Acute hydrocephalus after SAH may require external ventricular drainage; routine prophylactic anticonvulsants are not recommended beyond the early period.

Symptomatic carotid stenosis 70–99%: carotid endarterectomy reduces stroke risk when performed within 2 weeks of the index event in selected patients; 50–69% offers modest benefit.

Asymptomatic carotid stenosis 60–99%: consider endarterectomy in low-surgical-risk patients with life expectancy >5 years after shared decision-making.

Atrial fibrillation: DOACs are preferred over warfarin except with mechanical valves or moderate-to-severe mitral stenosis; use CHA2DS2-VASc to guide anticoagulation.

High-intensity statin therapy is standard after atherosclerotic ischemic stroke; an LDL-C goal <70 mg/dL is commonly used, with <55 mg/dL for very high-risk disease.

Blood pressure target after ischemic stroke is generally <130/80 mmHg when tolerated; smoking cessation, diabetes control (A1C ~<7%), and physical activity reduce recurrent risk.

Minor ischemic stroke or high-risk TIA: aspirin plus clopidogrel for 21 days, then single antiplatelet therapy; avoid long-term dual therapy unless a specific indication exists.

Symptomatic intracranial atherosclerosis: aggressive medical therapy (statin, blood pressure control, antiplatelet) is preferred over routine stenting.

Patent foramen ovale closure is considered for cryptogenic stroke in selected younger patients with high-risk PFO features after multidisciplinary evaluation.

RCVS: recurrent thunderclap headaches with segmental cerebral vasoconstriction, often postpartum or after vasoactive drugs; angiography normalizes over weeks.

PACNS: progressive headache, encephalopathy, and multifocal deficits with abnormal CSF; brain biopsy is the definitive test when diagnosis is uncertain.

Moyamoya disease: progressive distal ICA stenosis with lenticulostriate collaterals ('puff of smoke'); revascularization (direct or indirect bypass) is used for ischemic or hemorrhagic presentations.

CADASIL: autosomal dominant NOTCH3 mutation; anterior temporal pole and external capsule white-matter changes, migraine, lacunar strokes, and cognitive decline.

Cervical artery dissection: young adult stroke with neck pain, Horner syndrome, or posterior circulation symptoms; antithrombotic therapy for 3–6 months, with stenting for recurrent ischemia.

CVST: headache, papilledema, seizures, and venous infarcts; anticoagulation is given even with hemorrhagic infarction, and elevated opening pressure may require acetazolamide or shunt.

Spinal dural AV fistula: progressive myelopathy with T2 cord hyperintensity and flow voids; catheter angiography confirms and enables embolization or surgery.

Fibromuscular dysplasia: 'string of beads' narrowing of carotid or renal arteries; antiplatelet therapy and blood pressure control, with intervention for symptomatic high-grade stenosis.

Noncontrast CT is first-line to exclude hemorrhage; early ischemic signs include loss of insular ribbon, basal ganglia obscuration, sulcal effacement, and hyperdense MCA sign.

ASPECTS grades early ischemic change on noncontrast CT (10 normal to 0 extensive); lower scores indicate larger core and worse prognosis.

CTA identifies large-vessel occlusion; CTP core–penumbra mismatch or MRI DWI–clinical mismatch supports reperfusion in extended windows.

MRI DWI is most sensitive for acute infarction within minutes; FLAIR hyperintensity may appear after several hours and helps estimate lesion age.

TCD vasospasm: MCA mean flow velocity >120 cm/s is suggestive; Lindegaard ratio (MCA velocity / extracranial ICA velocity) >3 supports vasospasm rather than hyperemia.

Elevated ICP: CPP = MAP − ICP; head elevation 30°, normocapnia, hypertonic saline or mannitol, and short-term hyperventilation for impending herniation.

Brain death evaluation requires absent brainstem reflexes, coma, apnea test, and exclusion of confounders; ancillary tests include cerebral blood flow imaging and EEG.

Basilar artery occlusion: fluctuating consciousness, cranial nerve palsies, quadriparesis, and coma; urgent CTA and thrombectomy are indicated for eligible patients.