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For further information, see CMDT Part 24-08: Stroke

Key Features

Essentials of Diagnosis

  • Sudden onset of neurologic deficit of cerebrovascular origin

  • History of hypertension, diabetes mellitus, tobacco use, atrial fibrillation, or atherosclerosis

  • Distinctive neurologic signs reflect the region of the brain involved

General Considerations

  • Stroke due to cerebral infarction is caused by thrombotic or embolic occlusion of a major vessel

  • Causes are identical to the disorders predisposing to transient ischemic attacks

  • The resulting deficit depends on the particular vessel involved and the extent of any collateral circulation

Clinical Findings

Symptoms and Signs

  • Obstruction of carotid circulation

    • Ophthalmic artery or central retinal artery occlusion

      • Probably symptomless in most cases

      • Transient embolic obstruction can lead to transient monocular blindness (amaurosis fugax)

    • Anterior cerebral artery occlusion distal to its junction with the anterior communicating artery

      • Causes weakness and cortical sensory loss in the contralateral leg and sometimes mild weakness of the arm, especially proximally

      • A contralateral grasp reflex, paratonic rigidity, and abulia (lack of initiative) or frank confusion may be present

      • Urinary incontinence is not uncommon

      • Bilateral anterior cerebral infarction may cause marked behavioral changes and memory disturbances

      • Unilateral anterior cerebral artery occlusion proximal to the junction with the anterior communicating artery is generally well tolerated because of the collateral supply from the other side

    • Middle cerebral artery occlusion

      • Leads to contralateral hemiplegia, hemisensory loss, and homonymous hemianopia, with the eyes deviated to the side of the lesion

      • If the dominant hemisphere is involved, global aphasia is also present

      • In extreme cases, there may be considerable swelling of the hemisphere, leading to drowsiness, stupor, and coma

      • Anterior branch occlusion leads to an expressive dysphasia and to contralateral paralysis and loss of sensations in the arm, the face and, to a lesser extent, the leg

      • Posterior branch occlusion produces a receptive (Wernicke) aphasia and a homonymous visual field defect

      • With involvement of the nondominant hemisphere, speech and comprehension are preserved, but there may be a left hemispatial neglect syndrome or constructional and visuo-spatial deficits

  • Obstruction of vertebrobasilar circulation

    • Posterior cerebral artery occlusion

      • May lead to a thalamic syndrome in which contralateral hemisensory disturbance occurs, followed by the development of spontaneous pain and hyperpathia

      • Often a macular-sparing homonymous hemianopia and sometimes a mild, usually temporary, hemiparesis occurs

    • Vertebral artery occlusion

      • May be clinically silent when occlusion is below the origin of the anterior spinal and posterior inferior cerebellar arteries because the circulation is maintained by the other vertebral artery

      • If the remaining vertebral artery is congenitally small or severely atherosclerotic, a deficit similar to that of basilar artery occlusion is seen unless there is good collateral circulation from the anterior circulation through the circle of Willis

      • With occlusion of the small paramedian arteries arising from the vertebral artery, contralateral hemiplegia and sensory deficit occur in association with an ...

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