Transient ischemic attacks (TIAs) are focal episodes of neurologic dysfunction caused by ischemia. They are typically rapid in onset, lasting 10 seconds to 15 minutes but occasionally as long as 24 hours. According to the new International Classification of Diseases Eleventh Revision (ICD-11) (https://icd.who.int/dev11/l-m/en), TIA is defined as “a transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction in the clinically relevant area of the brain. Symptoms should resolve completely within 24 hours.” Cases formerly defined as TIAs with evidence of ischemic brain lesions are now considered as ischemic stroke. The longer the episode, the greater the likelihood of finding a cerebral infarction on computed tomography (CT) or magnetic resonance imaging (MRI), including diffusion weighting and perfusion sequences. Overall, cerebral infarction in a distribution that is appropriate for the clinical symptoms is detected by radiologic imaging in approximately 30% to 50% of patients with TIA. TIAs can usually be localized to a portion of the brain that is supplied by a single vascular system. The symptoms usually reach maximum intensity within 2 minutes, often within a few seconds. Fleeting episodes that last only 1 or 2 seconds and symptoms such as unconsciousness without other symptoms of vertebrobasilar ischemia and a prolonged “marching” of symptoms are not likely to be TIAs. Positive symptoms such as tingling, repetitive rhythmic shaking of a limb, and scintillating scotomata are also uncommonly ischemic in nature. The frequency of episodes varies: Some patients experience a single attack, but others experience multiple attacks at different intervals or at increasing frequency (crescendo TIAs).

Amaurosis fugax (transient monocular blindness) is included as part of the definition of carotid system TIA, but certain isolated symptoms, such as vertigo, light-headedness, syncope, dysarthria, dysphagia, diplopia, dizziness (or wooziness), bowel or bladder incontinence, loss of vision associated with alteration of level of consciousness, focal symptoms associated with migraine, amnesia, and confusion, are not, by definition, considered TIA.

The duration, stereotyped nature, and frequency of repetitive spells may suggest a pathophysiologic mechanism. For example, repetitive (as many as 5-10 per day), short-lived (<15 minutes), stereotyped spells suggest a hemodynamic mechanism with proximal arterial narrowing or occlusion associated with reduced cerebral perfusion (low flow) and inadequate collateral circulation or thrombosis at the low-flow arterial narrowing. Stereotyped focal spells may also result from seizures, migraine, positional vertigo, or other causes. The other end of the spectrum is the patient who presents with symptoms suggesting TIAs in multiple distributions occurring over a short period of time. This suggests a proximal source of embolus, a hypercoagulable state, or some disorder that can affect multiple arteries simultaneously, such as an inflammatory disorder.

TIAs should be differentiated from other conditions that result in transient focal neurologic deficit. Migraine is often characterized by visual auras (particularly scintillating scotoma) that march or expand across the vision of both eyes for 10 to 30 minutes. Other focal neurologic symptoms associated with migraine include marching paresthesias that characteristically start in one hand, motor disturbances (hemiplegic migraine), unilateral visual disturbances (retinal migraine), ocular movement abnormalities (ophthalmoplegic migraine), and aphasia. These symptoms sometimes occur without associated headache (migraine equivalent or migraine cine cephalgia), but they are usually followed by a unilateral throbbing headache that lasts hours to 1 or 2 days and are often associated with nausea or vomiting. Various combinations of posterior circulation symptoms that evolve over minutes, such as dysarthria, vertigo, alteration in level of consciousness, bilateral visual obscuration, and motor weakness (often occurring in young women and typically followed by a severe, often throbbing occipital headache), are referred to as basilar migraine.

Focal seizures commonly produce episodes of repetitive jerking, tingling, visual phenomena, or speech arrest, any of which may be followed by a generalized seizure. Typical electroencephalographic findings provide additional evidence of seizure. Postseizure states may also mimic or follow TIA or stroke (a focal ischemic neurologic deficit may trigger a seizure and postictal state that lasts as long as 24 hours), with the focal postictal transient deficit called a Todd’s paralysis.

Multiple sclerosis occurs mainly in young patients and usually is characterized by recurrent fluctuating subacute onset (during hours or days) of symptoms with neurologic deficits that last 1 day or longer. Less commonly, the condition may be associated with gradually progressive neurologic deficit; rarely, symptoms may involve sudden-onset, short-lived spells of neurologic dysfunction called paroxysmal symptoms of multiple sclerosis, including isolated recurrent dysarthria, ataxia with hemiparesis, hemisensory symptoms, and episodic tonic spasm of the limbs. The condition typically progresses to involve various parts of the white matter of the brain and spinal cord. The diagnosis is clinical in nature, but it may be aided by ancillary studies such as MRI.

Attacks that are clinically indistinguishable from TIA can result from small cerebral infarction or intracerebral hemorrhage. These attacks usually last hours rather than seconds or minutes. The diagnosis is established by CT or MRI. Arteriovenous malformations, brain tumors (e.g., meningiomas, gliomas, and metastases), or subdural hematomas may also be associated with TIA-like spells. Characteristic historical data and papilledema may or may not be present. The diagnosis is usually made with CT or MRI. Enlargement of a saccular aneurysm may present with transient symptoms and persistent, localized headache.
Sometimes a clot that forms within the aneurysmal sac can embolize distally and cause TIAs; the diagnosis is based on arteriographic and CT or MRI findings.

Hypoglycemia with typical prodromal autonomic symptoms may mimic TIA. Prompt improvement after intravenous administration of 50% glucose helps to establish the diagnosis. Familial paroxysmal ataxia may also be associated with transient focal neurologic deficit and is difficult to diagnose without the characteristic family history. Many patients with episodic vertigo alone have benign positional vertigo unrelated to cerebral or brainstem ischemia. These patients tend to hold their head still or avoid certain head positions that exacerbate the vertigo, and the vertigo usually decreases with repeated actions that would typically precipitate the symptom (see Chapters 2 and 4). Transient global amnesia (TGA) is associated with the relatively sudden onset of anterograde amnesia often with some degree of retrograde amnesia (see Chapter 2). Whereas some of these episodes may be caused by a posterior circulation TIA, most are likely due to a benign, possibly migrainous cause. A key issue in differentiating this syndrome from a more definite TIA is that the patient with TGA should have no other neurologic deficit. Episodic isolated diplopia seldom relates to cerebrovascular disease. A common ocular cause is divergence insufficiency, which tends to develop with increasing age (see Chapters 2 and 4).