Aetiology

Causes of TIA include:[14]

  • In situ thrombosis of an intracranial artery or artery-to-artery embolism of thrombus as a result of stenosis or unstable atherosclerotic plaque (16%).

  • Cardioembolic events (29%). Intracardiac thrombus may form in response to some secondary risk factor such as stasis from impaired ejection fraction or atrial fibrillation. The precipitating factor may be a thrombogenic nidus within the heart such as an infectious vegetation or artificial valve. Rarely, thrombus can pass from the venous system across a cardiac shunt to create paradoxical emboli.

  • Small-vessel occlusion (16%). Microatheromas, fibrinoid necrosis, and lipohyalinosis of small penetrating vessels are seen. Hypertension and diabetes predispose to small ischaemic lesions. Because these may occur in the brainstem and internal capsule, a small lesion can result in significant symptoms.

  • Occlusion due to hypercoagulability, dissection, vasculitis, vasospasm, or sickle cell occlusive disease (3%). These are less common aetiologies.

  • Uncertain mechanism (36%).

Pathophysiology

The severity of clinical neurological impairment after arterial occlusion depends on the complex interplay between the degree of obstruction, area and function of tissue supplied by the vessel, the length of time thrombus obstructs the vessel, and the ability of collateral circulation to provide supplemental perfusion to the area at risk.

Under normal circumstances, cerebral blood flow (CBF) is tightly autoregulated to maintain a blood flow of >50 mL/100 g/minute across a wide range of cerebral perfusion pressures by alteration in cerebrovascular resistance.[15] If the CBF falls to between 20 and 50 mL/100 g/minute, the brain can compensate by increasing oxygen extraction, but below this threshold, neuronal quiescence occurs with neurological deficits. Below 15 mL/100 g/minute of CBF, neuronal death occurs. Thus, if there is complete loss of cerebral blood flow, then neuronal death will occur rapidly. With partial blood flow, neuronal function is impaired, but cell death will be delayed by minutes to hours. Restoration of flow, presumably via autolysis of the occluding thrombus, can arrest the progression to infarction.

Early in the process of ischaemic neuronal injury, cytotoxic oedema causes influx of water to the intracellular space, which is observable as hyperintensity on MRI diffusion images.[16] Experimental data from animal models suggests that middle cerebral artery occlusion lasting 15 minutes or less creates little evidence of injury, whereas by 2 hours the downstream infarct is essentially complete.[17] As predicted by this model, in humans, the likelihood of spontaneous recovery from a neurological deficit falls as the symptom duration lengthens. If symptoms are present at 3 hours, the likelihood of being completely asymptomatic at 24 hours is only 2%.[18] This is part of the rationale for not withholding thrombolysis for acute neurological symptoms in the hopes of spontaneous resolution.

Classification

Oxford Community Stroke Project classification system (also known as the Bamford or Oxford classification)[4]

Based on the initial presenting symptoms and clinical signs. Depending on the extent of the symptoms, the stroke/transient ischaemic attack episode is classified as:

  • Total anterior circulation (carotid territory)

  • Partial anterior circulation

  • Posterior circulation (vertebrobasilar territory)

  • Lacunar.

Trial of Org 10172 in Acute Stroke Treatment (TOAST) criteria[5]

Based on initial presenting symptoms and signs and further investigations, the stroke/transient ischaemic attack is classified as being due to:

  • Large-artery atherosclerosis (artery-to-artery embolic or in situ thrombotic)

  • Cardioembolism (from high-risk or medium-risk source)

  • Small-vessel occlusion (lacune)

  • Other determined aetiology (such as non-atherosclerotic vasculopathies, hypercoagulability, or haematological disorders)

  • Undetermined aetiology.

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