Stroke - Comprehensive Overview

Definition

Classification

1. Ischemic Stroke

Subtypes & Causes

• Thrombotic (~33%): Clot forming at an atherosclerotic plaque, typically at vessel bifurcations (ICA, MCA). Turbulent flow at >90% stenosis triggers platelet adhesion and occlusion.
• Lacunar (~25%): Small-vessel occlusions in deep structures (basal ganglia, thalamus, pons, internal capsule). Strongly associated with hypertension and diabetes. The underlying process is lipohyalinosis of small penetrating arteries.
• Cardioembolic (~25%): Mural thrombus embolizing from the heart. Atrial fibrillation is the most common cause - AF confers a ~5x increased stroke risk.
• Cryptogenic (>33%): No identified cause despite full workup.
• Artery-to-artery embolism: e.g., amaurosis fugax from carotid plaque embolizing to the ophthalmic artery.

Causes in Young Patients (15-45 years)

2. Vascular Territory Syndromes

Anterior Circulation

• MCA territory: Contralateral hemiplegia and hemisensory loss (face and arm > leg), aphasia (dominant hemisphere), hemineglect (non-dominant), contralateral homonymous hemianopia.
• ACA territory: Contralateral leg > arm weakness, abulia, urinary incontinence.

Posterior Circulation

• Vertebrobasilar: Ipsilateral cranial nerve deficits + contralateral hemiparesis ("crossed signs").
• PCA territory: Ipsilateral CN III palsy + contralateral homonymous hemianopia.
• Wallenberg syndrome (lateral medullary syndrome): Vertigo, Horner syndrome, ipsilateral facial numbness with loss of corneal reflex, and contralateral loss of pain and temperature - a classic crossed sensory deficit.

3. Pathophysiology

• Impaired cerebral metabolic rate of O2 (CMRO2) and glucose metabolism
• Blood-brain barrier disruption
• Loss of GABA receptors
• Microglial activation and inflammatory response
• Diaschisis: remote functional impairment in connected non-infarcted areas due to disruption of neural circuits

4. Diagnosis & Investigations

Immediate Evaluation

1. Non-contrast CT head (first-line): Rapidly differentiates ischemic from hemorrhagic stroke, identifies >1 cm parenchymal hemorrhages, and detects >67% of early ischemic changes within 3 hours. Limited for posterior fossa.
2. ECG: Identifies AF and life-threatening arrhythmias.
3. Blood glucose: Hypoglycemia is the most important stroke mimic to exclude.

Early Ischemic CT Signs

• Hyperdense MCA/artery sign (visible thrombus)
• Sulcal effacement
• Loss of gray-white interface (insular ribbon sign)
• Loss of deep gray matter contours
• Acute hypodensity (develops 6-12 hours post-onset)

Advanced Imaging

• MRI DWI (diffusion-weighted imaging): Most sensitive method for acute ischemia; detects signal change within minutes of onset. ADC mapping essential.
• CT/MR angiography: Identifies large vessel occlusion (LVO), dissection, or stenosis. CTA obtained concurrently with CT head. Guides thrombectomy candidacy.
• CT perfusion (CTP): Identifies salvageable tissue in extended time windows (6-24 hours). Not typically needed in the first 6 hours.

Other Tests

• CBC, coagulation studies, renal/liver function
• Echocardiogram (if cardioembolic cause suspected)
• Carotid ultrasound / MRA neck

5. Hemorrhagic Stroke

Intracerebral Hemorrhage (ICH)

• Hypertensive vasculopathy (most common)
• Cerebral amyloid angiopathy (CAA) in elderly patients - lobar hemorrhages

6. Management

Stroke Time Targets (NINDS Protocol)

Ischemic Stroke - Acute Treatment

• Dose: 0.9 mg/kg (max 90 mg) - 10% as IV bolus, remaining 90% over 1 hour
• Window: Within 4.5 hours of symptom onset (or last known well)
• Not recommended for mild non-disabling symptoms; recommended for mild but disabling symptoms within 4.5 hours
• Risk of symptomatic ICH post-thrombolysis: 2-7%; asymptomatic ICH (microbleeds): 30-45%
• Goal: door-to-needle time of 60 minutes or less

• For large vessel occlusions (LVO)
• Window up to 24 hours from last known well (with appropriate imaging selection)
• CTA used to identify LVO and guide candidacy
• t-PA should not be delayed awaiting thrombectomy planning

• Avoid aggressive BP lowering in acute ischemic stroke (reduces perfusion pressure to penumbra)
• If thrombolytics are being given, strict BP control required to reduce hemorrhagic transformation risk
• Prognosis worsens with: fever, hypotension, hypoxia, hypo/hyperglycemia - correct these rapidly

• Oxygen only if SpO2 < 95% (avoid in normoxic patients)
• Avoid dextrose-containing fluids (hyperglycemia worsens ischemic deficit)
• Treat fever aggressively (even mild hyperthermia worsens outcomes)
• ECG monitoring throughout
• Aspirin (antiplatelet) initiated after ruling out hemorrhage

Hemorrhagic Stroke - Acute Treatment

• Reverse coagulopathy: Vitamin K + prothrombin complex concentrate (PCC) preferred over FFP (faster INR correction, lower infection risk, smaller volume). FFP if PCC unavailable.
• Blood pressure: For SBP 150-220 mmHg, acutely lower to 140 mmHg (safe and beneficial).
• Blood glucose: Maintain normoglycemia.
• Seizure control: Antiepileptic medications if seizures occur.
• ICP management (if elevated): Intubation/sedation, head-of-bed elevation to 30°, hypertonic saline/mannitol, and hemicraniectomy if necessary.
• No thrombolytics or anticoagulants in the acute phase.

7. Stroke Mimics (Differential Diagnosis)

8. Prognosis & Rehabilitation

• Post-stroke depression and immobilization significantly worsen outcomes and are important to manage.
• Falls risk is more than doubled in stroke patients vs. age-matched controls; hip fracture risk is particularly elevated within 3 months in women.
• Motor recovery occurs via recruitment of midline premotor areas and contralateral motor cortex; recovery is associated with return to a more normal restricted activation pattern.
• Transcranial magnetic stimulation (TMS) targeting contralateral hemisphere inhibition is an emerging rehabilitation strategy.
• Early mobilization and stroke unit admission improve outcomes.