Transient ischaemic attack

Transient ischaemic attacks (TIAs) describe a transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction.

Terminology 

In the past, transient ischaemic attack 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 transient ischaemic attack, and thus the aforementioned tissue-based definition was favoured ¹. It is well established nowadays that in most transient ischaemic attacks, symptoms resolve in less than one hour but occasionally prolonged episodes may occur ^1,2. 

Epidemiology

The incidence increases with age, with approximately 0.1 million new cases per year reported world wide. A male gender predominance noted in an American population ¹⁰.

Risk factors

Risk factors are essentially typical vascular risk factors, such as hypertension, cigarette smoking, and diabetes mellitus ¹⁰.

Clinical presentation

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

• low-flow transient ischaemic attack: classic transient focal neurological symptoms, either anterior or posterior circulation symptoms, last only minutes, and are often recurrent ³

• embolic transient ischaemic attack: 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

• lacunar or small penetrating vessel transient ischaemic attack: also known as the capsular warning syndrome, these are similar to low-flow transient ischaemic attacks but the transient and recurrent neurological symptoms are those of lacunar stroke syndromes ⁴

Pathology

There are three pathophysiological mechanisms:

• low-flow transient ischaemic attack: caused by large artery stenosis (e.g. internal carotid artery stenosis) ^1,3

• embolic transient ischaemic attack: 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

• lacunar or small penetrating vessel transient ischaemic attack: 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 radiographic features of transient ischaemic attacks 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 transient ischaemic attack 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 transient ischaemic attacks 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 transient ischaemic attack 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 had a stroke instead of a transient ischaemic attack ^6,7. Thus, determining which, or determining if all, "DWI-positive" transient ischaemic attacks 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, revolves around determining the aetiology of the transient ischaemic attack, risk stratification, and then medical (e.g. aspirin, statin) and/or surgical therapy (e.g. carotid endarterectomy) where appropriate ⁸.

History and etymology

The term transient ischaemic attack was coined by Charles Miller Fisher (1913-2012), a renowned Canadian neurologist, in 1951 ⁹. The term capsular warning syndrome was coined by Geoffrey Donnan, Australian neurologist, and colleagues in 1993 ⁴.