Cerebrovascular Disease: Causes, Symptoms, Diagnosis and Treatment — Overview, Diagnosis & Treatment Options | MyMedicPlus

Cerebrovascular disease encompasses a spectrum of conditions caused by impaired blood flow to or within the brain: ischemic stroke (85% of cases, due to arterial occlusion), hemorrhagic stroke (intracerebral hemorrhage and subarachnoid hemorrhage, 15% combined), transient ischemic attack (TIA, symptoms resolving within 24 hours without infarction on MRI), and cerebral small vessel disease progressing to vascular dementia. Stroke is the second leading cause of death globally and the leading cause of adult disability, with 12.2 million new stroke cases annually worldwide per the GBD 2019 study. Approximately 800,000 strokes occur per year in the US. The advent of intravenous thrombolysis (tPA) and mechanical thrombectomy for large vessel occlusion has transformed outcomes for ischemic stroke — mechanical thrombectomy doubles rates of functional independence and is among the most effective acute treatments in all of medicine.

Ischemic stroke etiologies (TOAST classification): cardioembolic (most commonly atrial fibrillation, accounting for 25-30% of ischemic strokes); large artery atherosclerosis (stenosis of internal carotid, vertebral, basilar arteries); small vessel lacunar disease (hypertensive lipohyalinosis of deep perforating arteries); cryptogenic (no identified cause, approximately 30%); and other determined causes (arterial dissection, hypercoagulable states). Intracerebral hemorrhage: hypertension-related rupture of deep perforating arteries (putamen, thalamus, pons, cerebellum) and cerebral amyloid angiopathy (lobar hemorrhage, elderly). Subarachnoid hemorrhage: rupture of saccular (berry) aneurysm in 85% of cases. Major modifiable risk factors (AHA/ASA guidelines): hypertension (highest population-attributable risk), diabetes mellitus, dyslipidemia, smoking, atrial fibrillation, obesity, physical inactivity, and excessive alcohol consumption.

FAST acronym captures the cardinal ischemic stroke warning signs: Face drooping (unilateral facial palsy), Arm weakness (unilateral arm or leg weakness), Speech difficulty (dysarthria or aphasia), Time to call emergency services. Additional symptoms: sudden visual loss or diplopia, severe sudden-onset vertigo or ataxia (posterior circulation), and sudden severe headache (worst headache of life) indicating subarachnoid hemorrhage (SAH) — the sentinel headache of SAH must not be missed. TIA produces identical focal neurological symptoms that fully resolve within 24 hours (by definition), but carries a 10-day stroke risk of 5-10% without treatment and is a neurological emergency. Intracerebral hemorrhage may cause progressive neurological deterioration with declining consciousness. Vascular dementia causes stepwise (not gradual) cognitive decline following recurrent infarcts.

Non-contrast CT brain is performed immediately on all patients to exclude intracerebral hemorrhage before thrombolysis. MRI DWI (diffusion-weighted imaging) detects acute ischemic infarction within minutes of onset with high sensitivity and specificity. CT angiography (CTA) from aortic arch to cerebral vessels identifies large vessel occlusion (LVO), carotid stenosis, intracranial stenosis, aneurysms, and vascular malformations. CT perfusion or MRI perfusion-diffusion mismatch identifies salvageable ischemic penumbra, guiding thrombectomy candidacy. Cardiac evaluation: 12-lead ECG, continuous cardiac monitoring for 72 hours (detects paroxysmal AF in up to 20%), echocardiography (TTE/TEE), and long-term cardiac monitoring (30-day event monitor, implantable loop recorder for cryptogenic stroke). Carotid ultrasound assesses stenosis. Full vasculopathy and thrombophilia workup for young stroke patients.

Ischemic stroke — acute phase: IV alteplase (tPA, 0.9 mg/kg, maximum 90 mg) within 4.5 hours of symptom onset for eligible patients (NINDS and ECASS-3 trials); tenecteplase 0.25 mg/kg is now preferred over alteplase in many centers. Mechanical thrombectomy (stent retriever or aspiration) for large vessel occlusion (LVO): anterior circulation up to 24 hours (DAWN, DEFUSE-3 trials). Intensive stroke unit care — dedicated acute stroke unit admission reduces mortality and disability by approximately 25% compared to general ward care. Hemorrhagic stroke: aggressive blood pressure control (target SBP <140 mmHg within 1 hour for ICH), reversal of anticoagulation (idarucizumab for dabigatran, andexanet alfa for apXa inhibitors), neurosurgical evacuation for selected cerebellar hemorrhage. Secondary prevention: DOAC (apixaban, rivaroxaban, dabigatran) for AF-related stroke; antiplatelet therapy (clopidogrel, or aspirin plus clopidogrel for 90 days for minor stroke/TIA) for non-cardioembolic events; carotid endarterectomy or stenting for symptomatic carotid stenosis >50%.

Prognosis after stroke depends on infarct volume, stroke subtype, severity on presentation, and access to acute stroke care. Overall 30-day mortality after ischemic stroke is approximately 10-15%; one-year mortality is 20-30%. Approximately 80% of stroke survivors experience some degree of disability; 40% have moderate-to-severe disability at 1 month. Functional recovery is most rapid in the first 3-6 months but can continue for up to 2 years with structured rehabilitation. With mechanical thrombectomy for large vessel occlusion, rates of functional independence at 90 days improve from approximately 26% to 46% (DAWN and DEFUSE-3 trials). Without treatment in the pre-thrombolysis era, stroke carried far higher mortality and disability. Hemorrhagic stroke (intracerebral hemorrhage) carries worse short-term prognosis: 30-day mortality approximately 30-40%, with half of deaths in the first 24-48 hours. Subarachnoid hemorrhage from aneurysm rupture: 30-day mortality approximately 30-40% including pre-hospital deaths; rebleeding and vasospasm are major complications of survivors. TIA carries a 10-day stroke risk of 5-10% without treatment but very low risk with prompt antiplatelet therapy and risk factor control. Key prognostic factors include NIHSS score on presentation, infarct volume and location, age, pre-stroke functional status, comorbidities (atrial fibrillation, hypertension, diabetes), time to treatment, and stroke mechanism. Recurrent stroke risk without secondary prevention is approximately 10-15% per year; with optimal secondary prevention it falls to 4-6% per year. Long-term monitoring after ischemic stroke requires ongoing secondary prevention, management of vascular risk factors, annual neurological and functional assessment, and cardiac monitoring (30-day Holter or implantable loop recorder) to detect paroxysmal atrial fibrillation in cryptogenic stroke.

Primary prevention: control hypertension (the most important modifiable risk factor) with antihypertensive agents targeting SBP below 130 mmHg; anticoagulate atrial fibrillation with DOACs (apixaban, rivaroxaban, or dabigatran) rather than aspirin for stroke prevention; treat dyslipidemia with high-intensity statins; achieve glycemic control in diabetes; smoking cessation (reduces stroke risk to baseline within 5 years); limit alcohol to fewer than 2 units per day; maintain healthy weight (BMI below 25); and undertake regular aerobic exercise. Secondary prevention following TIA or ischemic stroke (AHA/ASA 2021 Guidelines): antiplatelet therapy or anticoagulation based on stroke mechanism; intensive statin therapy (atorvastatin 80 mg or rosuvastatin 40 mg); carotid revascularization for symptomatic stenosis >50%; and structured risk factor management programs reducing recurrent stroke by up to 80%.

Stroke is a medical emergency — call emergency services immediately if you observe: sudden facial drooping (one side), arm or leg weakness (one side), speech difficulty or confusion, sudden vision loss in one or both eyes, sudden severe headache with no known cause, or sudden loss of balance or coordination. Time is brain — 1.9 million neurons die every minute of untreated stroke. Do not drive yourself to hospital; call emergency services. TIA — even if symptoms resolve completely within minutes — must be evaluated urgently in a hospital emergency department the same day, as stroke risk is highest in the hours to days immediately after TIA. Individuals with known atrial fibrillation, carotid stenosis, prior TIA, or multiple vascular risk factors should ensure their antiplatelet or anticoagulant therapy is optimized and discuss risk factor management with their physician.