Disease modifying treatment available:
Time critical diagnosis and management:
Lateralising:
Transient ischaemic attacks have been clinically defined as symptoms resulting from focal neurological dysfunction as a result of cerebral ischaemia lasting less than 24 hours. Signs of cerebral ischaemia may persist beyond this time - the emphasis is on symptoms having resolved. Skeptics will quite rightly be immediately suspicious of the neat 24 hour cut off.
Several potential mechanisms for transient ischaemic attacks have been proposed:
1) The vasospasm theory
2) The haemodynamic theory
3) The thromboembolic theory
The potential for arteries to contract and limit flow has been demonstrated experimentally. This contraction is referred to as vasospasm and has been suggested as a possible mechanism for reducing cerebral blood flow and causing ischaemia. Previous treatments for cerebral ischaemic events have included the use of vasodilators and cervical sympathetic blocks to alleviate potential spasm. No such treatments are currently recommended for the treatment of TIA or ischaemic stroke in the UK though vasodilators are used to reduce the risk of vasospasm in aneurysmal subarachnoid haemorrhage. Retinal vasospasm causing monocular visual deficits has been caught on fundal photography (%cite11) but there is experimental evidence suggesting the cerebral blood vessels are generally un-reactive.
The haemodynamic theory attributes transient ischaemic attacks to reduced flow within the vessel in the absence of obstruction. Hypotension can undoubtably cause ischaemic damage to organs. Among the most profound examples of this include the brain injury that follows cardiac arrest. While hypotension can cause global cerebral dysfunction in the form of syncope, the evidence that hypotension can cause focal neurological dysfunction as seen in TIA is less convincing. The fact that syncope is seldom preceded by a TIA makes the haemodynamic theory less viable. In a study which induced hypotension in individuals with TIA/ischaemic stroke focal cerebral deficits were seldom observed despite a reduction in systemic blood pressure (%cite12).
None
Transient ischaemic attack may cause the following:
The symptoms of TIA are by definition self limiting - the problem is the risk of future stroke! Not all TIAs carry an equal risk of future stroke and high risk features have been established. TIA duration is a major risk factor - the longer symptoms persist the greater the chance of future stroke. Evidence of ischaemia on MRI significantly increases the risk of further episodes. In a study of 3,206 patients with DWI imaging after stroke the risk of stroke at 7 days was 7.1% in tissue-positive events vs. 0.4% in tissue-negative events while at 90 days 7.7% of tissue-positive individuals had a stroke vs. 1% of tissue-negative stroke (%cite13).
Aspirin 300mg should be given as soon as possible. If there is concern about possible intracerebral haemorrhage a CT brain is usually obtained first.
In selected individuals with a TIA secondary to carotid atherosclerosis, carotid endarterectomy may reduce the risk of future stroke. Two different sets of criteria are used. Carotid endarterectomy should be considered if:
- >= 50% stenosis on North American Symptomatic Carotid Endarterectomy Trial (NASCET) criteria
- >= 70% stenosis on the European Carotid Surgery Trial (ECST) criteria
1) Is there any difference in the risk of recurrence of TIA or subsequent stroke in those left with signs of residual neurological dysfunction?