Transient ischemic attack

Transient ischaemic attack (TIA), in the most recent definition, corresponds to a transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction.

Terminology 

In the past, TIA was arbitrarily distinguished from stroke by the duration of neurological symptoms of less than 24 hours ¹. However, this definition allowed for risk of permanent infarction to be classified as a TIA, and thus the aforementioned tissue-based definition was favoured ¹. It is well established nowadays that in most TIAs symptoms resolve in less than one hour but occasionally prolonged episodes may occur ^1,2. 

Clinical features

The clinical features are variable and dependent on the mechanism (see below):

• Lowlow-flow TIA: classic transient focal neurological symptoms, either anterior or posterior circulation symptoms, last only minutes, and are often recurrent ³
• Embolicembolic TIA: similar presentation to a thromboembolic ischaemic stroke, localised to a specific arterial territory rather than a general circulation, tend to last hours, and do not tend to be recurrent ³
• Lacunarlacunar or small penetrating vessel TIA: also known as the capsular warning syndrome, these are similar to low-flow TIAs but the transient and recurrent neurological symptoms are those of lacunar stroke syndromes⁴

Pathology

There are three pathophysiological mechanisms:

• Lowlow-flow TIA: caused by large artery stenosis (e.g. internal carotid artery stenosis) ^1,3
• Embolicembolic TIA: caused by the same aetiologies of thromboembolic ischaemic stroke ^1,3
  • There is controversy as to whether these should actually be classified as strokes as per the tissue-based definition
• Lacunarlacunar or small penetrating vessel TIA: caused by either stenosis of intracranial arteries (e.g. middle cerebral artery stenosis) or lipohyalinosis of penetrating arteries ^1,4

Radiographic features

There is uncertainty regarding the radiographical features of TIAs given that there is currently no perfect radiographic corollary to the pathology, especially when even minute regions of infarction could differentiate a stroke from a TIA ¹. While CT brain is often unremarkable, there is controversy regarding the significance of regions demonstrating high signal on DWI, a finding present in approximately half of all TIAs ⁵.

It has been proposed that if a region demonstrates high signal on DWI, and especially if there is no early DWI reversal, then that is a region of infarction and hence should be a stroke and not a TIA ⁵. However, the confusion lies if a lesion demonstrates early DWI reversal, because it has been found that these such lesions may still have some degree of infarction, and thus the patient may, in fact, have a stroke instead of a TIA ^6,7. Thus, determining which, or determining if all, "DWI-positive" TIAs should, in fact, be classified as strokes remains unclear and a subject of ongoing research ⁵. 

Treatment and prognosis

Management is complex, but in short, it revolves around determining the aetiology of the TIA, risk stratification, and then medical and surgical therapy where appropriate ⁸.