A transient ischemic attack (TIA) is caused by ischemia (loss of blood flow.Ischemia in the dominant hemisphere may cause dysphagia, with impairment in the context of speech and, at times, a transient lack of understanding.
The symptoms of ischemic attack vary depending upon which area of the brain is ischemic, but there are two main types: those associated with ischemia of parts or the whole of a cerebral hemisphere and those associated with ischemia of the brainstem. The symptoms most often include transient contralateral weakness of the lower face, fingers, hand arm, or leg, but such patients may also experience fleeting sensory symptoms such as tingling, “pins and needles,” or numbness in parts of the body contralateral to the ischemia.
Patients with ischemia in the portion of the brain supplied by the posterior cerebral artery may suffer blurred vision, or may notice transient hemianopic or altitudinal visual field defects or impairment of visual acuity.
Ischemia or insufficiency due to internal carotid artery stenosis often produces transient retinal ischemia, resulting in monocular blindness or reduced acuity on the side of the stenosis, combined with contralateral weakness of the face, arm, or leg.
Ischemic attacks which result from involvement of the brain supplied by the vertebral and basilar arteries have an extremely wide range of symptoms. Common symptoms include vertigo, tinnitus, diplopia, dysarthria, dysphagia, and dysphonia. Patients may complain of unilateral or bilateral face, arm, and leg weakness and unilateral or bilateral sensations of numbness and tingling in the face, arms, or leg.
You Must Know The Causes And Symptoms of Transient Ischemic Attack
There may be tinnitus, hearing loss, and ataxia. In addition, patients with brainstem ischemia may experience “drop attacks,” in which they suddenly lose postural tone and fall to the ground without losing consciousness, then immediately regain postural control and rise quickly. The most common complaint with transient ischemic attacks from vertebrobasilar insufficiency is dizziness. However, dizziness is commonly associated with other physiologic disturbances and is rarely the only symptom of brainstem ischemia.
Symptoms of vertebrobasilar artery ischemia, although variable, tend to occur in combinations that aid in their diagnosis. Vertigo, ataxia, dysarthria, paresthesia, diplopia, tinnitus, dysphagia, and focal weakness in the face, jaw, or pharynx tend to coexist, although not always in the same sequence or combination.
Another grouping of symptoms is that of unilateral or bilateral weakness of the extremities with drop attacks, and diplopia. The reason for these differences in symptom combinations can be found by referring to the diagrams of the blood supply to the brainstem. Ischemia of the dorsal and lateral portions of the brainstem supplied by the circumferential arteries produces the first group of symptoms. Ischemia of the more ventral portions supplied by the medial perforating arteries causes the second group.
Symptomatic vertebrobasilar artery ischemia may occur with stenosis of the subclavian artery proximal to the origin of the vertebral artery. The arm on the side of the stenosis may be supplied by retrograde flow in the ipsilateral vertebral and, during exercise, enough blood can be diverted from the vertebral system to the arm to cause symptoms of brainstem ischemia. This mechanism of producing brainstem ischemia has been called the subclavian steal syndrome. However, most instances of reversed vertebral artery flow with subclavian artery stenosis or occlusion are asymptomatic.
Ischemic attacks may occur many times a day or at weekly or monthly intervals. They may be intermittently present over several months or several years. Some patients with internal carotid artery occlusion have transient ischemic attacks for as long as two years before cerebral infarction occurs. Others have clusters of attacks lasting only a few hours or days before carotid occlusion becomes complete and causes infarction. The major importance of transient ischemic attacks is that they signal the existence of significant cerebrovascular disease and clearly indicate the potential danger of cerebral infarction.
It cannot always be predicted which patients with cerebral ischemia will develop cerebral infarction or even when it will occur. Some varieties of cerebral ischemic attacks carry a better prognosis than others. Thus, symptoms suggesting involvement of the dorsal and lateral portion to the brainstem, the lateral medullary area, imply the best prognosis. Attacks suggesting ventral brainstem involvement, such as bilateral paresis or unilateral transient paresis or drop attacks, connote a considerably poorer prognosis.
Carotid ischemic attacks that occur close together in clusters carry a poor prognosis, for in a large percentage of such patients cerebral infarction rapidly follows.In the interval between transient ischemic attacks, the neurologic examination is usually entirely normal. During a transient ischemic attack, patients commonly have neurologic deficits corresponding to their symptoms.
Thus, with ischemia of a cerebral hemisphere, there may. be a hemiparesis with reflex asymmetry and an extensor plantar response, or a mild hemisensory or visual field deficit.
If the dominant hemisphere is affected, dysphasia may be noted: the patient has difficulty in naming and recognizing objects. Patients examined during a brainstem ischemic attack often exhibit nystagmus, complete facial weakness, palate and tongue weakness, and deviation, dysconjugate eye movements, sensory defects, and •weakness on one side Or on both sides of the body.
Consciousness is usually unimpaired during transient ischemic attacks, although thinking is sometimes slowed. This lack of alteration of consciousness coupled with the absence of either aura or convulsive movements helps to distinguish these attacks from convulsive seizures. Other conditions that must be considered in the differential diagnosis are Meniere’s syndrome (which is rare in the elderly), migraine headache, cerebral emboli, or the progressive neurologic deficits caused by cerebral neoplasm.
