Transient Ischemic Attack

A transient ischemic attack is a transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischemia, without acute infarction. That last clause is the modern, tissue-based definition and it replaced the old 24-hour time-based one, because diffusion-weighted MRI showed that a substantial proportion of episodes lasting under 24 hours leave permanent infarction — they are strokes, not TIAs.

The practical significance of a TIA is entirely about what comes next. It is an unstable warning: the risk of completed stroke is highest in the first 48 hours, and a meaningful proportion of strokes are preceded by one. A TIA is to the brain what unstable angina is to the heart, and it warrants the same urgency.

The mechanisms are those of ischemic stroke:

• Large artery atherosclerosis — most often artery-to-artery embolism from a carotid bifurcation plaque, less often haemodynamic failure across a tight stenosis. Identifying this matters because carotid endarterectomy substantially reduces recurrence when performed early.
• Cardioembolism — atrial fibrillation is the dominant cause, alongside recent myocardial infarction with mural thrombus, prosthetic valves, endocarditis, and patent foramen ovale in younger patients.
• Small vessel (lacunar) disease — lipohyalinosis of penetrating arterioles, driven by hypertension and diabetes.
• Less common — arterial dissection, especially in younger patients after neck trauma or manipulation; vasculitis; hypercoagulable states; and sickle cell disease.

Risk factors are the modifiable cardiovascular set — hypertension, which is the single most important, smoking, diabetes, dyslipidemia, atrial fibrillation, obesity and physical inactivity — together with age, male sex and family history.

Onset is abrupt and deficits are focal and negative — loss of function rather than positive phenomena. Most episodes resolve within an hour.

The territory determines the picture. Carotid (anterior) circulation: unilateral weakness or numbness of the face, arm or leg; dysphasia; and amaurosis fugax, a painless transient monocular visual loss classically described as a curtain descending. Vertebrobasilar (posterior) circulation: vertigo, diplopia, dysarthria, dysphagia, ataxia, bilateral or crossed sensory and motor signs, and homonymous hemianopia.

Some presentations are characteristically missed. Isolated amaurosis fugax is frequently attributed to migraine or an eye problem. Sudden severe dysphasia without weakness may be taken for confusion. Posterior circulation events are the most commonly missed of all, because vertigo and unsteadiness are so often assumed to be labyrinthine.

Symptoms that are not typical of TIA, and should prompt another diagnosis: isolated loss of consciousness, generalized weakness, confusion alone, incontinence, and marching or spreading positive symptoms such as tingling that travels over minutes, which suggests migraine or seizure.

A TIA is a medical emergency even though the symptoms have resolved, and the assessment is about preventing the stroke that may follow within days.

Specialist assessment should occur within 24 hours. Antiplatelet therapy is generally started immediately once haemorrhage is excluded, and short-term dual antiplatelet therapy reduces early recurrence in high-risk patients. The ABCD² score was widely used for risk stratification but is no longer relied on to defer urgent assessment — everyone with a suspected TIA needs prompt evaluation.

Investigation covers three questions: was it ischemic, where did the clot come from, and what are the modifiable risks.

• Imaging — MRI with diffusion-weighted sequences is preferred, and identifies infarction in a substantial minority, reclassifying the event as a stroke. CT is used mainly to exclude haemorrhage and mimics.
• Vascular imaging — carotid Doppler, CT or MR angiography, urgently, since symptomatic carotid stenosis of 50–99% warrants endarterectomy and the benefit is greatest within two weeks.
• Cardiac — ECG for atrial fibrillation, with prolonged ambulatory monitoring where none is found, since paroxysmal AF is easily missed and completely changes treatment. Echocardiography where a cardiac source is suspected.
• Bloods — full blood count, glucose and HbA1c, lipids, renal function, ESR where giant cell arteritis is possible, and a thrombophilia screen in the young.

Blood glucose must be checked immediately in every case, since hypoglycemia is the most important reversible mimic.

The conditions underlying a TIA are the ones that determine outcome: hypertension, atrial fibrillation, diabetes, dyslipidemia and carotid disease all require active management, and secondary prevention reduces subsequent stroke risk substantially. Coronary and peripheral arterial disease frequently coexist, since the pathology is the same. Vascular cognitive impairment and post-stroke depression are common downstream, and even a resolved TIA has implications for driving that must be raised at the time rather than left to be discovered.