Transient Ischemic Attack and Stroke

Carotid Artery Transient Ischemic Attack

Platelets commonly aggregate on plaques at the common carotid artery bifurcation ( Fig. 11.1 ), and if they embolize and travel up the internal carotid artery, they can lead to cerebral hemisphere TIAs. Occasionally, auscultation over the carotid artery bifurcation reveals a harsh systolic sound ( bruit ) that suggests carotid artery stenosis. In the event of a complete carotid artery occlusion—where blood flow ceases—no bruit will be audible.

Contralateral hemiparesis and/or hemisensory loss is typical of carotid artery TIAs. A TIA also may induce neuropsychologic symptoms. Their nature will depend upon whether the involved carotid artery irrigates the dominant or nondominant hemisphere. For example, dominant hemisphere TIAs may cause transient aphasia or apraxia, while nondominant hemisphere TIAs may cause short-lived neglect or hemi-inattention with or without hemiparesis. Occasionally, TIAs cause neuropsychological symptoms but no hemiparesis or other physical deficits.

Sometimes, a TIA causes only brief visual loss in one eye (i.e., monocular blindness. Neurologists call this distinctive symptom amaurosis fugax [Greek, fleeting darkness]). The underlying mechanism consists of emboli from the internal carotid artery traveling into the ophthalmic artery—the carotid artery’s first branch—to induce several minutes of ischemia in the retina and optic nerve of the ipsilateral eye ( Box 11.1 ). Amaurosis fugax is usually painless. Funduscopy may demonstrate retinal emboli of atheromatous material (Hollenhorst plaques) that have broken off the carotid artery plaque and traveled up to the ophthalmic artery.

Basilar Artery Transient Ischemic Attack

The vertebrobasilar system —sometimes referred to simply as the posterior circulation —supplies the brainstem, cerebellum, occipital lobes, and medial-inferior portion of the temporal lobes ( Fig. 11.2 ). Emboli-generating plaques tend to develop at the origin of the vertebral arteries (from the subclavian arteries) and at their junction at the base of the brain.

Symptoms and signs of basilar artery TIAs, which usually reflect patchy brainstem ischemia, differ greatly from those of carotid artery TIAs ( Box 11.2 ). Typical basilar artery TIA symptoms include tingling around the mouth (circumoral paresthesias), dysarthria, diplopia, ataxia, and vertigo. On rare occasions, when all blood flow through the basilar artery momentarily stops, almost the entire brainstem suffers from ischemia. The brainstem ischemia interrupts consciousness and body tone, which causes patients to collapse suddenly and unexpectedly. (Such events, sometimes termed “drop attacks,” mimic cataplexy [see Chapter 17 ]).

Although vertigo represents one of the most characteristic symptoms of basilar artery TIAs, disruption of the peripheral vestibular system in the inner ear more often causes it. The term vertigo properly denotes a sensation of the patient or the surroundings revolving or otherwise moving. The thoughtful physician should label no other descriptions as vertigo. In particular, the common complaint of “dizziness” has no clinical value because patients may use the term to may mean imbalance, lightheadedness, anxiety, confusion, altered vision, or almost any other symptom.

Transient global amnesia ( TGA ), a condition characterized primarily by the acute onset of anterograde amnesia for several hours, previously was thought to represent TIA-induced ischemia of the temporal lobes (see Chapter 7 ). Various lines of evidence now point to other causes of TGA that bear some resemblance to Dissociative Amnesia .

The evaluation of basilar artery symptoms is like assessment of carotid artery symptoms and includes MRI, MRA, and evaluation for cardiac and systemic illness. In addition, a transcranial Doppler examination harmlessly uses ultrasound to measure blood flow in the vertebrobasilar system. For treatment, neurologists prescribe the same medications useful for carotid artery TIAs. Because the usual sites of vertebrobasilar stenosis are encased in the chest, vertebrae, and skull, endarterectomy is not feasible.

Risk Factors

Although some stroke risk factors are not modifiable, neurologists educate their stroke patients about those that are modifiable in the hope of preventing future strokes ( Box 11.3 ). Stroke risk factors tend to occur in combination. For example, obesity, elevated low-density lipoprotein (LDL) cholesterol, hypertension, and lack of physical activity frequently occur together in the metabolic syndrome . Some factors by themselves have a weak correlation with stroke but pose a synergistic risk when paired with others. For example, cigarette smoking correlates with stroke; however, with concomitant use of oral contraceptives or in sufferers of migraine with aura, cigarette smoking becomes a powerful risk factor. More striking, smokers who are hypertensive have a 20-fold greater risk.