Transient Ischemic Attacks TIAs

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A TIA is a transient episode of focal neurological or retinal dysfunction secondary to impaired blood supply in a vascular territory. Clinical signs typical of TIAs in the carotid and vertebrobasilar territories are outlined in T,aMe.2.2-;2. . It should be noted that transient vertigo, diplopia, dysarthria, or dysphagia in isolation is insufficient to establish a diagnosis of vertebrobasilar TIAs. In addition, isolated drop attacks in which the patient falls to the ground, maintains consciousness, and then arises without a deficit are seldom due to vertebrobasilar ischemia. The annual risk of stroke after a TIA is 3 to 4 percent per year. However, the risk of a subsequent stroke is at least three times greater for individuals who have had a TIA than in those individuals who have not had a TIA. y

Amaurosis fugax may be described as a sudden onset of a "fog," "haze," "scum," "curtain," "shade," "blur," "cloud" or "mist." A curtain or shade pattern with the loss of vision moving superiorly to inferiorly is described only by 15 to 20 percent of patients. y , y Less commonly, there can be a concentric visual loss presumed to be due to marginal perfusion causing diminished blood flow to the retina. The visual loss is sudden in onset, often brief in duration, and painless in nature. The length of visual loss is usually 1 to 5 minutes and rarely lasts more than 30 minutes. Positive phenomena such as scintillation, fortification spectra, or flashing lights are rarely indicative of amaurosis fugax. After an episode of amaurosis fugax, the vision is usually fully restored, although some patients may have permanent visual loss due to a retinal infarction (see Tabie,22-2 ).[28]

In amaurosis fugax, it is key to evaluate for internal carotid artery stenosis with a carotid duplex ultrasound and to exclude temporal arteritis or a cardiac abnormality as a cause.


Occlusion of the ICA can produce symptoms and signs of infarction in either the ACA or MCA territories (or both) as described below. The sole feature that distinguishes the MCA syndrome from a carotid artery syndrome is the presence of amaurosis fugax. y , y Infarctions are often large, involving multiple lobes. Cerebral edema may be a life-threatening concern. The carotid pulse may be absent ipsilaterally. Horner's syndrome may be present due to oculosympathetic involvement along the carotid artery.


An MCA infarction is one of the most common manifestations of cerebrovascular disease ( Fig 22-8 ). The clinical picture with an MCA infarction is varied and depends upon whether the site of the occlusion is in the stem, the superior division, the inferior division, or the lenticulostriate branches and whether there is good collateral blood flow.

When the stem of the MCA is occluded, there is usually a resultant large infarction with contralateral hemiplegia, conjugate eye deviation toward the side of the infarct, hemianesthesia, and homonymous hemianopia. There is associated global aphasia if the dominant hemisphere is involved and hemineglect with nondominant hemispheral lesions. The difference between an upper division MCA infarction and a MCA stem lesion is that the hemiparesis usually affects the face and arm more than the leg with upper division infarction. A Broca aphasia is more common in upper division infarcts due to preferential involvement of the anterior branches of the upper division in occlusions. With lower division MCA syndromes, a Wernicke type aphasia is seen with dominant hemisphere infarction and behavioral disturbances are seen with nondominant infarction. A homonymous hemianopia may be present. A lenticulostriate branch occlusion may cause a lacunar infarction with involvement of the internal capsule producing a syndrome of pure motor hemiparesis. These described syndromes are variable and are dependent on the presence of collaterals and whether edema is present.y , y , y

Figure 22-8 CT of a large acute right middle cerebral artery territory infarctic(Courfesy of Karen S. Caldemeyer, M.D.)

Alexia with agraphia may occur with left angular gyrus involvement. Gerstmann's syndrome, which consists of finger agnosia, acalculia, right-left disorientation, and agraphia, may be seen with dominant hemisphere parietal lesions. The perisylvian aphasias seen with dominant hemispheral infarctions may be of the Broca, Wernicke, conduction, or global type, depending on the site and extent of involvement. Anosognosia most commonly is associated with right hemispheric strokes. Nondominant infarction may cause inattention, neglect, denial, apraxia, impaired prosody, and rarely acute confusion and agitated delirium. y A contralateral homonymous hemianopia or contralateral inferior quadrantanopia can occur with infarctions in either hemisphere.


ACA territory infarctions are uncommon. They can be seen in patients with vasospasm after subarachnoid hemorrhage due to ACA or ACoA aneurysms. Excluding these causes, the percentage of acute cerebral infarcts that are in the ACA territory is less than 3 percent. y , y , y The characteristics of ACA infarction vary according to the site of involvement and the extent of collateral blood flow. y Contralateral weakness involving primarily the lower extremity and, to a lesser extent, the arm is characteristic of infarction in the territory of the hemispheric branches of the ACA (see Table.22.-2 ). Other characteristics include abulia, akinetic mutism (with bilateral mesiofrontal damage), impaired memory or emotional disturbances, transcortical motor aphasia (with dominant hemispheric lesions), deviation of the head and eyes toward the lesion, paratonia (gegenhalten), discriminative and proprioceptive sensory loss (primarily in the lower extremity), and sphincter incontinence (see Table. .22-2 ).

An anterior disconnection syndrome with left arm apraxia due to involvement of the anterior corpus callosum can be seen. Pericallosal branch involvement can cause apraxia, agraphia, and tactile anomia of the left hand. Infarction of the basal branches of the ACA can cause memory disorders, anxiety, and agitation.

Infarction in the territory of the medial lenticulostriate artery (artery of Huebner) causes more pronounced weakness of the face and arm without sensory loss due to this artery's supply of portions of the anterior limb of the internal capsule.


The AChA syndrome is often characterized by hemiparesis as a result of involvement of the posterior limb of the internal capsule, hemisensory loss due to involvement of the posterolateral nucleus of the thalamus or thalamocortical fibers, and hemianopia secondary to involvement of the lateral geniculate body or the geniculocalcarine tracty , y (see TabJe..2.2-2 ). The visual field defect that is seen with AChA infarcts is characterized by a homonymous defect in the superior and inferior visual fields that spares the horizontal meridian. y In a small number of patients, there may be left spacial hemineglect with right hemispheric

infarctions and a mild language disorder with left hemispheric infarctions. y , y With bilateral infarctions in the AChA territory, there can be pseudobulbar mutism and a variety of other features including facial diplegia, hemiparesis, hemisensory loss, lethargy, neglect, and affect changes. y

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