Transient Ischaemic Attack is a condition of focal neurological deficit lasting less than 24 hours (usually less than 1-2 hours) due to cerebrovascular insufficiency.
Most (90%) of the cause of Transient Ischaemic Attack are due to micro-thrombo-embolism, derived from atheromatous cerebral vessels (anterior or posterior circulation) or from the heart (mitral disease with or without fibrillation, infarction, atrial myxoma, Atrial Septal Defect / patient foramen ovale with paradoxical embolisation).
There is a history of Transient Ischaemic Attack in about 30% cases of stroke. In presence of AIDS there is an increased risk of TIA. Less common causes of TIA include fibromuscular hyperplasia of the internal carotid artery (cervical part), inflammatory disorder of arteries, e.g., SLE, Polyarteritis nodosa, Giant cell arteritis, Granulomatous angitis, Meningovascular syphilis etc. Blood dyscrasias, e.g, Polycythaemia, Sickle cell anemia, Severe anemia, Hyper viscosity syndrome, Sub-clavian steal syndrome are also rare causes.
Onset is sudden Consciousness is usually preserved. When the carotid system (anterior circulation) is affected there may be:
During attack, examination reveals flaccid hemiparesis of pyramidal distribution, sensory changes, brisk jerks, planter extensor on the affected side and aphasia. Subsequently neurologic deficit exists. Carotid murmur, pulse abnormality, cardiac fundings may give a clue.
When the posterior circulation (vertebrobasilar system) is affected there may be:
The natural history is variable. In some cases several attacks of TIA occur without development of stroke. Again in some others stroke develops only after few attacks. In general carotid system or anterior circulation TIA are more liable to develop stroke than vertebrobasilar or posterior circulation TIA.
Whenever the attack starts, it attains its peak within seconds and usually lasts for minutes or hours and always passes away within 24 hours. There may be evidences of carotid stenosis by thrill and murmur over it. When subclavian stenosis is present pulse volume will differ on both sides with asymmetric BP (difference of 20 mm of Hg or more between systolic pressure in two sides). Evidence of atherosclerosis may be obvious. Heart may show evidences of infective endocarditis, mitral stenosis, atrial fibrillation or infarction. Associated features like high BP, postural hypotension, diabetes, bradycardia etc. may be present. Headache is usually absent.
1. Ancillary investigations as described under cerebral thrombosis/embolism are to be done.
2. Imaging: CT scan is helpful to exclude cerebral haemorrhage or tumour. Ultrasonography or carotid duplex ultrasonography, MR angiography are done, but for better
evaluation carotid angiography is still superior.
Here convulsive seizure is present and march of events will be gradual. EEG and CT scan will settle the diagnosis.
Headache is a dominant feature here which will be absent inTIA. Visual changes are completely different.
Here the neurological deficit persists even beyond 24 hours.
TIA heralds the onset of stroke (17%). Death occurs in 25% of cases in the first attack of stroke. When TIA occurs in anterior circulation the prognosis is bad.
Same as in Cerebral infarction.
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