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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 ipsilateral cranial nerve palsy at the level of the lesion

    • Posterior inferior cerebellar artery (PICA) or ...

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