Transient ischemic attack (transient cerebral ischemia, TIA) is a temporary focal neurologic deficit caused by the brief interruption of local cerebral blood flow. The preva- lence of TIAs 1.6-4.1 percent. Stroke occurs in one-third of patients who have a TIA. The duration of a focal neurologic deficit that leads to cerebral infarction has arbitrarily been determined to be 24 hours or greater.
I. Pathophysiology. 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 pro- lapse, carotid or vertebral dissection, and hypercoagulable states (antiphospholipid antibody syndrome).
II. Evaluation of TIA symptoms
A. The primary objective when evaluating a patient
with a transient ischemic attack (TIA) is to deter- mine whether the ischemic insult has occurred in the anterior or posterior circulation.
B. Anterior circulation ischemia causes motor or
sensory deficits of the extremities or face, amaurosis fugax, aphasia, and/or homonymous hemianopia.
C. Posterior circulation ischemia causes motor or
sensory dysfunction in association with diplopia, dysphasia, dysarthria, ataxia, and/or vertigo.
D. Assessment should determine the activity in which
the patient was engaged and the patient's physical position at the onset of the attack. A description of the specific symptoms of the attack should be obtained, including the speed with which they developed, whether they were bilateral or unilat- eral, and their duration.
E. History of hypertension, diabetes, cardiac disease,
previous TIA or stroke, cigarette smoking, or use of street drugs should be sought.
F. Differentiating TIAs from other entities 1. Seizures almost always involve a change in the
level of consciousness or awareness, excessive motor activity and confusion, none of which characterizes a TIA.
2. Syncope. Changes in cardiac output produce
generalized, rather than focal, cerebral ischemia, characterized by loss of conscious- ness and a rapid heartbeat (often due to an arrhythmia).
3. Benign positional vertigo. Recurrent waves of
dizziness, which last 2-10 seconds and are related to movement (standing up or sitting down), are characteristic.
G. Physical examination
1. Heart rate and rhythm and the blood pressure
in both arms, peripheral pulses, skin lesions (petechiae of embolic origin), and skin manifestations of connective tissue disease
should be assessed.
2. Carotid bruits may suggest carotid stenosis.
Ophthalmoscopic examination can detect arterial or venous occlusion and emboli.
3. Neurologic examination
a. The neurologic examination should be nor-
mal in TIA patients unless the patient has had a previous stroke or is currently experi- encing a TIA or stroke.
b. Evaluation should include the level of con-
sciousness, orientation, ability to speak and understand language; cranial nerve function, especially eye movements and pupil reflexes and facial paresis. Neglect, gaze preference, arm and leg strength, sensation, and walking ability should be assessed.
III. Differential diagnosis and symptoms Common Clinical Findings Associated with Ischemia in Various Arterial Distributions Anterior cerebral artery
Weakness in contralateral leg Sensory loss in contralateral leg, with or without weakness or numbness in proximal contralateral arm
Middle cerebral artery
Contralateral hemiparesis Deviation of head and eyes toward side of lesion Contralateral hemianesthesia Contralateral hemianopia Aphasia (if dominant hemisphere is affected) Unawareness of stroke (if nondominant hemisphere is affected)
Lenticulostriate arteries
Pure motor hemiparesis (lacunar syndrome)
Posterior cerebral artery
Visual field disturbance Contralateral sensory loss Amnesia
Vertebrobasilar arteries
Vertigo
Nausea and vomiting Ataxia
Nystagmus
IV. Laboratory studies
Initial Evaluation of a Patient with Transient Ischemic Attack
Complete blood cell count with platelet count
Chemistry profile (including cholesterol and glucose levels) Prothrombin time and activated partial thromboplastin time Erythrocyte sedimentation rate
Syphilis serology Electrocardiography
Cranial computed tomography (particularly with hemi- spheric transient ischemic attack)
Noninvasive arterial imaging (ultrasonography, magnetic resonance angiography)
A. Complete blood count with differential rules out
profound anemia, polycythemia, leukocytosis, thrombocytopenia and thrombocytosis. The chem- istry profile may demonstrate hypoglycemia that can present with focal neurologic deficits or hyperglycemia that can worsen the outcome after stroke.
B. Prothrombin time and an activated partial thromboplastin time are needed to rule out
coagulopathies. The erythrocyte sedimentation rate serves as a screening test for autoimmune disorders. Syphilis serology screens for neurosyphilis.
C. Electrocardiogram (ECG) is used to detect
arrhythmias (eg, atrial fibrillation) as the cause of ischemia. Computed tomographic (CT) scanning of the head is necessary to rule out intracranial bleeding or tumors. CT may reveal the vascular distribution of previous ischemic events.
D. Carotid duplex studies are recommended in all
patients with TIA symptoms. These tests (eg, Doppler plus B-mode imaging) detect extracranial carotid disease.
E. Echocardiography may be helpful in identifying
atrial thrombus in patients with atrial fibrillation. Transcranial Doppler ultrasonography can reveal intracranial stenosis of the middle cerebral or posterior cerebral arteries.
F. Magnetic resonance angiography is used to
detect stenosis in extracranial or intracranial cerebral arteries. Arteriography is reserved for suspected intracranial vasculitis or arterial dissec- tion.
G. Special testing for hypercoagulable states
(antiphospholipid antibodies) protein C and S, antithrombin III should be reserved for use in patients less than 50 years of age, patients with a history of thrombotic disease and patients in whom no other cause of TIA is found. Holter monitoring is recommended for use in patients who had palpitations.
H. Lumbar puncture may be warranted if central
presenting symptoms suggest subarachnoid hemorrhage but the CT scan is negative.
V. Treatment
A. Reduction of risk factors
1. Aggressive treatment of chronic hypertension
should maintain the systolic blood pressure below 140 mm Hg and the diastolic blood pressure below 90 mm Hg.
2. Cigarette smoking and consumption of three or
more alcohol drinks per day should be discour- aged.
3. Atrial fibrillation is one of the strongest inde-
pendent risk factors for stroke. Warfarin (Coumadin) or aspirin is effective for stroke prevention in patients with atrial fibrillation.
B. Carotid endarterectomy guidelines
1. Surgery is recommended in symptomatic pa-
tients with 70 percent carotid stenosis.
2. Surgery may be considered in symptomatic
patients with carotid stenosis of 50 to 69 per- cent. The risks and benefits of surgery should be carefully considered in these patients.
3. Surgery should not be considered in patients
with carotid stenosis of less than 50 percent.
C. Stroke prevention, antithrombotic therapy 1. Aspirin. Because aspirin inactivates
cyclooxygenase activity for the life of platelets, thromboxane A2 cannot be produced. Aspirin in
a dosage of 75 to 325 mg per day is recom- mended for all TIA patients for stroke preven- tion. Clopidogrel or ticlopidine are alternatives for patients who cannot tolerate aspirin.
2. Clopidogrel (Plavix), 75 mg qd, is recom-
mended for patients who can not tolerate aspirin. Clopidogrel has fewer side effects than ticlopidine.
3. Ticlopidine (Ticlid) inhibits platelet aggrega-
tion and is recommended for patients who can not tolerate aspirin. The dosage is 250 mg PO bid. Adverse events include neutropenia, thrombocytopenia, diarrhea, rash, abnormal liver function tests and elevated cholesterol levels. Close monitoring of complete blood count is required for the first three months.
4. Aggrenox Cap ER (Aspirin 25 mg,
Dipyridamole 200 mg) is an alternative for patients who have an event while on aspirin alone. 1 cap bid. Side effects include GI bleed- ing, headache, diarrhea.
References, see page 282.