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Transient Ischemic Attack

Transient ischemic attack is defined as a focal neurologic deficit due to a cerebrovascular event from which the patient recovers completely in less than 24 hours. Most TIAs last only 2 to 30 minutes, and little if any permanent brain damage results. When clinical manifestations persist beyond 24 hours, the event is considered a stroke.

TIAs are "ministrokes" that should prompt urgent evaluation, and hospitalization in an effort to prevent devastating consequences.

The most frequent mechanism of TIA is embolization by a thrombus from an atherosclerotic plaque in a large vessel (stenotic carotid artery). TIAs may also occur as manifestations of intracranial atherosclerotic disease (lacunar TIAs) or large-vessel occlusion. In addition, they can be associated with atrial fibrillation or mitral valve prolapse, carotid or vertebral dissection, and hypercoagulable states (antiphospholipid antibody syndrome).

Evaluation. The primary objective when evaluating a patient with a transient ischemic attach (TIA) is to determine whether the ischemic insult has occurred in the anterior or posterior circulation and whether the patient falls into a high-risk category. The first point to stress is that most TIAs are, in fact, very transient. Almost 25% of patients will have resolution of their symptoms within five minutes, and 50% of patients will have resolution within 30 minutes of noticing symptoms. If the patient's deficit still persists after one hour, there is only a 15% chance that the neurological symptoms will abate over the next 24 hours. Since the patient may be neurologically normal by the time they arrive in the ED, a careful history is essential in establishing the diagnosis. Not infrequently, the emergency physician will have to seek information from EMS personnel, family members, or observers who may have observed the deficit.

Distinguishing between TIAs that involve the anterior circulation from those involving the posterior circulation has important diagnostic and treatment implications. Symptoms associated with anterior circulation ischemia usually include motor or sensory deficits of the extremities or face, amaurosis fugax, aphasia, and/or homonymous hemianopia. In contrast, patients with symptoms involving the posterior circulation ischemia may complain of motor or sensory dysfunction, but commonly such symptoms will occur in association with diplopia, dysphasia, dysarthria, ataxia, and/or vertigo.

The patient should be questioned about co-existing vascular or cardiac disease. For example, a careful inquiry may reveal that the patient may have experienced neurological symptoms but did not seek medical attention. The patient may have symptoms suggesting vasculopathies, connective tissue disorders, or intracranial mass lesions. Patients under 40 years of age should be questioned about family history of early stroke, drug use, or symptoms suggestive of a hypercoagulable state.

Patients should be considered to be at high-risk for subsequent stroke if they have had multiple TIAs within the two weeks prior to arrival in the ED, if the deficit associated with the TIA was very severe, or if the patient had crescendo symptoms. In addition, patients should be considered to be transient ischemic attack.