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Stroke: Types, Etiology, Pathogenesis, Clinical Features, Signs, Investigations, and Complications

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1. Definition

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2. Types of Stroke

• ICH accounts for 10-15% of all strokes
• SAH accounts for ~5% of all strokes

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3. Etiology

Ischemic Stroke

• Large-vessel occlusion: Atherosclerotic plaque at vessel bifurcations (especially internal carotid artery, MCA origin). Plaque ulceration + platelet adhesion leads to clot that occludes or embolizes distally.
• Small-vessel/Lacunar (~20%): Lipohyalinosis of small penetrating arteries due to hypertension or diabetes. Infarcts 2-20mm in basal ganglia, thalamus, pons, internal capsule.

• Atrial fibrillation (most common): 5x increased stroke risk
• Mural thrombus (post-MI), valvular disease (rheumatic, prosthetic), cardiomyopathy, paradoxical embolism through PFO
• Artery-to-artery embolism (from carotid plaque)

• Carotid/vertebral artery dissection (leading cause of stroke in young; follows trauma, sneezing, chiropractic manipulation)
• Hypercoagulable states: antiphospholipid antibodies, protein C/S deficiency, factor V Leiden
• Sickle cell disease (vasculopathy)
• Pregnancy/OCP use
• Cocaine, amphetamines (vasospasm + hypertension)
• Fibromuscular dysplasia
• Migraine-associated (prolonged vasospasm)
• Vasculitis (varicella, fungal meningitis, giant cell arteritis)
• Cerebral venous sinus thrombosis (CVST)

Hemorrhagic Stroke

• Hypertensive vasculopathy (most common): Lipohyalinosis of small deep penetrating arteries → deep hemorrhages (putamen 44%, thalamus 13%, cerebellum 9%, pons 9%)
• Cerebral amyloid angiopathy (CAA): Amyloid deposits in cerebral vessel walls → lobar hemorrhages in elderly
• Arteriovenous malformations (AVMs)
• Saccular (berry) aneurysm rupture
• Drug intoxication (cocaine, sympathomimetics)
• Blood dyscrasias, anticoagulation
• Venous sinus thrombosis
• Hemorrhagic transformation of ischemic stroke
• Tumors (primary or metastatic)

• Ruptured saccular (berry) aneurysm (most common, ~85%)
• Arteriovenous malformation
• Trauma
• Cocaine use

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4. Pathogenesis

Ischemic Stroke - Cerebral Blood Flow (CBF) Thresholds

• Loss of ATP → Na⁺/K⁺-ATPase failure → membrane depolarization
• Glutamate excitotoxicity → massive Ca²⁺ influx
• Free radical production, lipid peroxidation
• Inflammatory response: microglial activation, cytokines, BBB disruption, edema
• Impaired CMRO₂ (cerebral metabolic rate of oxygen) and glucose metabolism

Hemorrhagic Stroke Pathogenesis

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5. Clinical Features by Stroke Territory

Anterior Circulation (ICA / MCA / ACA)

• Contralateral hemiplegia (face and arm > leg)
• Contralateral hemisensory loss
• Contralateral homonymous hemianopia
• Gaze preference toward lesion side (eyes "look toward the lesion")
• Aphasia (dominant hemisphere - Broca's/Wernicke's/global)
• Anosognosia, neglect, constructional apraxia (non-dominant hemisphere)

• Contralateral weakness/sensory loss (leg > arm, face spared)
• Abulia, personality change, urinary incontinence

• Combination of MCA + ACA territory
• Amaurosis fugax (transient monocular blindness from ophthalmic artery embolus) - pathognomonic for carotid disease

Posterior Circulation (Vertebrobasilar)

• Contralateral homonymous hemianopia (macular sparing)
• Memory deficits, visual agnosias, cortical blindness (bilateral)
• Thalamic syndrome (central post-stroke pain)

• "Crossed" signs: ipsilateral cranial nerve palsy + contralateral hemiplegia
• Vertigo, diplopia, dysarthria, dysphagia
• Locked-in syndrome (bilateral ventral pontine infarction): quadriplegia, mutism, preserved vertical eye movements and consciousness
• Wallenberg syndrome (PICA infarct): ipsilateral facial numbness, contralateral body pain/temp loss, dysphagia, hoarseness, Horner's syndrome, ataxia

• Ipsilateral limb ataxia, dysmetria, intention tremor
• Nystagmus, vertigo, nausea/vomiting
• Truncal ataxia

Lacunar Syndromes (Small vessel)

Hemorrhagic Stroke - Location-Specific Features

• Contralateral motor/sensory deficits
• Eyes deviate toward lesion

• Contralateral hemisensory loss
• Skew deviation (lower eye on side of lesion)
• Wrong-way eye deviation (away from lesion)
• "Peering at tip of nose" - almost pathognomonic
• Loss of vertical gaze

• Pinpoint pupils (bilateral)
• Quadriplegia
• Hyperthermia, coma
• Horizontal gaze palsy; eye movements become random ("bobbing")

• Sudden onset occipital headache, vomiting
• Inability to walk (ataxia)
• No hemiplegia (important distinguishing feature)
• Rapidly progresses to coma if untreated - surgical emergency

• Severe headache
• Focal deficits depending on lobe
• Seizures (common)
• ~50% decreased consciousness; ~20% in coma at admission

• "Thunderclap headache" - worst headache of life, sudden onset
• Meningismus (nuchal rigidity, Kernig's, Brudzinski's signs)
• Nausea, vomiting, photophobia
• Focal deficits (may be absent initially)
• Loss of consciousness (at onset)
• Subhyaloid (preretinal) hemorrhages on fundoscopy

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6. Physical Signs

• Facial droop
• Arm drift
• Speech disturbance
• Time to call emergency services

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7. Investigations

Immediate / Emergency

Neuroimaging

DWI with ADC mapping is the most sensitive method for imaging acute ischemia, detecting changes within minutes of onset. - Bradley and Daroff's Neurology in Clinical Practice

Cardiac Workup (Embolic source)

Hematologic / Other

Scoring Tools

• NIH Stroke Scale (NIHSS): Severity 0-42; used to guide thrombolysis
• ICH Score: Predicts 30-day mortality based on GCS, age, ICH volume, intraventricular extension, location
• Glasgow Coma Scale (GCS): Level of consciousness

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8. Complications

Neurological Complications

Systemic Complications

SAH-Specific Complications

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Summary Table: Ischemic vs. Hemorrhagic Stroke

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• Rosen's Emergency Medicine: Concepts and Clinical Practice - Ischemic and Hemorrhagic Stroke chapter
• Bradley and Daroff's Neurology in Clinical Practice - Stroke imaging, ischemic stroke
• Plum and Posner's Diagnosis and Treatment of Stupor and Coma - Intracerebral hemorrhage
• Frameworks for Internal Medicine - Hemorrhagic stroke classification and key facts