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mitral valve disease, infective endocarditis, atrial myxoma, and mural thrombi complicating myocardial infarction Atrial septal defects and patent foramen ovale may permit emboli from the veins to reach the brain ( paradoxical emboli ) An ulcerated plaque on a major artery to the brain may serve as a source of emboli In the anterior circulation, atherosclerotic changes occur most commonly in the region of the carotid bifurcation extracranially, and these changes may cause a bruit In some patients with transient ischemic attacks or strokes, an acute or recent hemorrhage is found to have occurred into this atherosclerotic plaque, and this finding may have pathologic significance Patients with AIDS have an increased risk of developing transient ischemic deficits or strokes Less common abnormalities of blood vessels that may cause transient ischemic attacks include fibromuscular dysplasia, which affects particularly the cervical internal carotid artery; atherosclerosis of the aortic arch; inflammatory arterial disorders such as giant cell arteritis, systemic lupus erythematosus, polyarteritis, and granulomatous angiitis; and meningovascular syphilis Hypotension may cause a reduction of cerebral blood flow if a major extracranial artery to the brain is markedly stenosed, but this is a rare cause of transient ischemic attack Hematologic causes of ischemic attacks include polycythemia, sickle cell disease, and hyperviscosity syndromes Severe anemia may also lead to transient focal neurologic deficits in patients with preexisting cerebral arterial disease The subclavian steal syndrome may lead to transient vertebrobasilar ischemia Symptoms develop when there is localized stenosis or occlusion of one subclavian artery proximal to the source of the vertebral artery, so that blood is stolen from this artery A bruit in the supraclavicular fossa, unequal radial pulses, and a difference of 20 mm Hg or more between the systolic blood pressures in the arms should suggest the diagnosis in patients with vertebrobasilar transient ischemic attacks.

disorders of neuromuscular transmission; or from primary disorders of muscle The clinical findings help localize the lesion and thus reduce the number of diagnostic possibilities Weakness due to upper motor neuron lesions is characterized by selective involvement of certain muscle groups and is associated with spasticity, increased tendon reflexes, and extensor plantar responses The site of upper motor neuron (pyramidal) involvement may be indicated by the presence of other clinical signs or by the distribution of the motor deficit Lower motor neuron lesions lead to muscle wasting as well as weakness, with flaccidity and loss of tendon reflexes, but no change in the plantar responses unless the neurons subserving them are directly involved Fasciculations may be evident over affected muscles In distinguishing between a root, plexus, or peripheral nerve lesion, the distribution of the motor deficit and of any sensory changes is of particular importance In patients with disturbances of neuromuscular transmission, weakness is patchy in distribution, often fluctuates over short periods of time, and is not associated with sensory changes In myopathic disorders, weakness is usually most marked proximally in the limbs, is not associated with sensory loss or sphincter disturbance, and is not accompanied by muscle wasting or loss of tendon reflexes at least not until an advanced stage

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Focal neurologic deficit of acute onset Clinical deficit resolves completely within 24 hours Risk factors for vascular disease often present

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Transient ischemic attacks are characterized by focal ischemic cerebral neurologic deficits that last for less than 24 hours (usually less than 1 2 hours) About 30% of patients with stroke have a history of transient ischemic attacks, and proper treatment of the attacks is an important means of prevention The incidence of stroke does not relate to either the number or the duration of individual attacks but is increased in patients with hypertension or diabetes The risk of stroke is highest in the month after a transient ischemic attack (particularly in the first 48 hours) and progressively declines thereafter

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