• Clinical science

Overview of stroke

Summary

A stroke is an acute neurologic condition resulting from a disruption in cerebral perfusion, either due to ischemia (ischemic strokes) or hemorrhage (hemorrhagic strokes). Hemorrhagic strokes are further classified as intracerebral or subarachnoid. Systemic hypertension and other cardiovascular diseases are common risk factors for both ischemic and hemorrhagic strokes. Clinically, strokes are characterized by the acute onset of focal neurologic deficits, including hemiparesis, paresthesias, and hemianopsia. The pattern of clinical features is dictated by the affected vessel. Distinguishing between ischemic and hemorrhagic strokes based on physical examination is difficult and requires initial evaluation with a noncontrast head CT. Further neurovascular imaging may be required before deciding on treatment options. In ischemic strokes, immediate revascularization of the affected vessel is vital to preserve brain tissue and prevent further damage. Hemorrhagic strokes are treated with supportive measures and neurosurgical evacuation of blood. Long-term management of all types of stroke focuses on the management of modifiable risk factors (i.e., hypertension and atherosclerosis).

For more information, see ischemic stroke, intracerebral hemorrhage, and subarachnoid hemorrhage.

Definition

References:[2][3][4]

Overview

Ischemic stroke Intracerebral hemorrhage Subarachnoid hemorrhage
Epidemiology
Etiology
  • Embolism
  • Thrombus
  • Small vessel occlusion (lipohyalinosis)
  • Systemic hypoperfusion
Risk factors
Clinical features
  • Sudden onset of focal neurologic deficits
  • Headache, confusion, nausea
  • Sudden onset of focal neurologic deficits
Diagnosis
  • Noncontrast head CT to rule out hemorrhage
  • MRI
  • CTA/MRA
  • Noncontrast head CT
  • MRI
  • CTA/MRA
Treatment
Pathology

For both ischemic and hemorrhagic strokes, age is the most important nonmodifiable risk factor and arterial hypertension is the most important modifiable risk factor!

Epidemiology

Epidemiological data refers to the US, unless otherwise specified.

Etiology

References:[6][7]

Stroke symptoms by affected vessel

Affected vessel Clinical features [8][9][10]

Middle cerebral artery (MCA) (most commonly affected vessel)

  • Contralateral weakness and sensory loss more marked in the upper limbs and lower half of the face than in lower limbs
  • Gaze deviates toward the side of infarction
  • Contralateral homonymous hemianopia without macular sparing or superior/inferior quadrantanopia [11][10]
  • Aphasia if in dominant hemisphere (usually left MCA territory)
  • Hemineglect if in nondominant hemisphere (usually right MCA territory)
    • Unawareness of and unresponsiveness to unilateral stimuli due to a brain unilateral injury, most commonly strokes (not due to a primary motor or sensory lesion)
    • Typically associated with right hemisphere damage resulting in neglect (esp. visual) of the left side [12]
    • The lesion is usually contralateral to the stimuli
      • Motor neglect
      • Sensory or perceptual neglect
Anterior cerebral artery (ACA)
Posterior cerebral artery (PCA)
Posterior inferior cerebellar artery
Anterior inferior cerebellar artery
Lenticulostriate arteries (penetrating arteries
Basilar artery
Extracranial arteries Internal carotid artery
Common carotid artery
Vertebral artery
Anterior spinal artery

References:[18][9][15][19]

Stroke symptoms by affected region

Lacunar syndromes [20][10]

Lacunar stroke type Location Clinical features
Pure motor stroke
Pure sensory stroke
  • Contralateral numbness and paresthesia of the face, arm, and leg
Sensorimotor stroke
Ataxic hemiparesis
  • Ipsilateral weakness with impaired coordination (e.g., ataxia, gait instability) [21][22]
Dysarthria-clumsy hand syndrome
  • Contralateral facial and hand weakness with dysarthria
Hemiballismus
  • Contralateral, involuntary, large flinging movements of the arm or leg

Infarction of the posterior limb of the internal capsule is the most common type of lacunar stroke and may manifest clinically with pure motor stroke, pure sensory stroke (rare), sensorimotor stroke, dysarthria-clumsy hand syndrome, and/or ataxic hemiparesis.

Brainstem syndromes [23][10]

General considerations

  • Brainstem syndromes involve the cranial nerves and/or their nuclei (procude symptoms ipsilaterally to the lesion) and major brainstem tracts (procude symptoms contralaterally to the lesion unless they are uncrossed or double-crossed).
  • Disruption of reticular activating system, if present, results in decreased level of consciousness or coma.

Midbrain syndromes [24][25][26]

Syndrome Affected vessel Affected structures Resulting symptom
Ventral midbrain syndrome (Weber syndrome)

Claude syndrome

Paramedian midbrain syndrome (Benedikt syndrome)
Dorsal midbrain syndrome (Parinaud syndrome)
Nothnagel syndrome
  • Ipsilateral or bilateral oculomotor palsy

Pontine syndromes

Syndrome Affected vessel Affected structures Resulting symptom

Ventral pontine syndrome (Millard-Gubler syndrome)

  • Ipsilateral facial muscle weakness
Lateral pontine syndrome (Marie-Foix syndrome)
  • Contralateral loss of pain and temperature sensation
  • Ipsilateral loss of facial sensation to pain and temperature
  • Ipsilateral facial muscle weakness
  • Ipsilateral decreased lacrimation and salivation
  • Ipsilateral loss of taste sensation from anteriorof the tongue
Inferior medial pontine syndrome (Foville syndrome)
  • Ipsilateral facial muscle weakness
Locked-in syndrome

Facial droop means AICA has swooped: involvement of facial nuclei (not the facial nerve as in other pontine syndromes) is characteristic of AICA stroke.

Medullary syndromes

Syndrome Affected vessel Affected structures Resulting symptom
Medial medullary syndrome (Dejerine syndrome) Paramedian branches of the anterior spinal artery and/or vertebral arteries Nucleus and fibers of the hypoglossal nerve Ipsilateral tongue palsy (deviation of the tip to the ipsilateral side)
Corticospinal tract Contralateral hemiparesis
Medial lemniscus Contralateral decrease in proprioception
Lateral medullary syndrome (Wallenberg syndrome) Posterior inferior cerebellar artery Nucleus ambiguus (CN IX, X, XI)

Ipsilateral bulbar palsy (dysphagia, dysphonia, hiccups, decreased gag reflex)

Vestibular nuclei Ipsilateral nystagmus and vertigo
Lateral spinothalamic tract Contralateral decrease in pain and temperature sensations in the trunk and limbs
Spinal trigeminal nucleus Ipsilateral decrease in pain and temperature sensations in the face
Inferior cerebellar peduncle Ipsilateral limb ataxia and dysmetria
Sympathetic fibers Ipsilateral Horner syndrome

To remember the cause and the symptoms of the lateral medullary syndrome: Try not to pick a (PICA) horse (hoarseness) that can't eat (dysphagia).

Clinical features of strokes affecting other regions

Location of lesion Clinical features [17][9][10]
Putamen
Cerebellum
Thalamus
Cortex
Watershed border-zone

References:[9][28][29][30][31]

Diagnostics

Initial evaluation

Imaging [32][33]

  • Approach:
    1. Noncontrast head CT to evaluate for acute hemorrhage
    2. Diffusion-weighted MRI to detect acute ischemia
    3. Consider further neurovascular imaging depending on the type of stroke
  • Noncontrast head CT (first-line imaging)
  • Diffusion-weighted MRI
    • Allows identification of ischemia earlier than a CT (within 3–30 minutes after onset)
    • Allows detection of hyperacute hemorrhage
    • Evaluates reversibility of ischemic injury
  • See ischemic stroke, subarachnoid hemorrhage, and intracerebral hemorrhage for specific imaging findings and other modalities.

Laboratory evaluation

  • Initial: serum glucose
  • Additional evaluation
    • Complete blood count, electrolytes
    • Coagulation parameters (e.g., INR, PTT)
    • Urine drug screen for recreational substances (e.g., cocaine), blood alcohol level
    • Serum troponin

Laboratory studies should not delay imaging for patients with acute stroke. [33]


References:[34][35][36][37][38][32]

Differential diagnoses

References:[36][39]

The differential diagnoses listed here are not exhaustive.

Treatment

If symptoms of a suspected ischemic stroke began less than 4.5 hours prior to presentation and there are no signs of intracranial bleeding, begin reperfusion therapy immediately!

Stabilization and monitoring [33]

Blood pressure management [33][40]

Nitrates should be avoided because they can increase intracranial pressure.

See ischemic stroke, subarachnoid hemorrhage, and intracerebral hemorrhage for specific management.

References:[41][40][36][38][42][43][44][45]

Complications

Medical complications [46]

Neurologic complications [47]

References:[47][46]

We list the most important complications. The selection is not exhaustive.

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