By: DR. WALID REDA ASHOUR
Definition: Acute, focal neurological deficit with
clinical resolution over a period of minutes or
up to an hour and which is thought to be due to
inadequate cerebral or ocular blood supply as
a result of arterial thrombosis , low flow or
brief episode of neurological dysfunction caused
by focal disturbance of brain or retinal ischemia,
with clinical symptoms typically lasting less than
1 hour and without evidence of infarction.
** Symptoms resolve following rapid
fragmentation and dissolution of the
microemboli / thrombus.
* Onset sudden & rapid, with complete resolution.
* Most TIAs last approximately 2 to 20 minutes.
* Initially should involve all affected areas relatively
* Should involve focal loss of neurologic function,
with symptoms reflecting dysfunction of cerebrum,
brainstem, or cerebellum.
Probably NOT TIA
* Ill-defined onset, waxes & wanes, or slowly worsens.
* Leaves persistent neurologic deficits, however mild.
* Neurologic dysfunction of few seconds duration
* Episode lasting for more than 1 hour.
* Marching of symptoms from one body part to another.
* Positive phenomena: involuntary movements, jerking,
* Global brain symptoms: giddiness, LOC.
The symptoms start more or less abruptly, and they
are ‘focal’, indicating a disturbance in a particular
area of brain, or in one eye.
Motor symptoms (the most common):
* Clumsiness or
in the upper limb or lower limb or face alone, or in
various combinations, usually on just one side of the
* Numbness or
Transient monocular blindness (amaurosis
Affects the upper or lower half of vision, or all the
vision of one eye, and is often described like a blind
or shutter coming down from above, or up from
Indeed, if a patient still has symptoms more than an
hour after the onset, the chances are that they will
persist for more than 24 hours and so the patient will
actually have had a stroke
Vertigo, diplopia, dysphagia, unsteadiness,
tinnitus, amnesia, drop attacks, and possibly
dysarthria are so often due to global cerebral
ischaemia, or non-vascular causes, that if one
occurs as an single symptom the diagnosis of TIA
is very uncertain
** In the clinical analysis of TIAs, it is important to
separate a single transient episode from repeated
ones that are all of uniform type. The latter are
more a warning of impending vascular occlusion,
particularly of the internal carotid artery, whereas
the former, especially when prolonged, are again
often caused by an embolus that leaves no lasting
TIAs can reflect the involvement of virtually any
cerebral artery: common or internal carotid; middle,
posterior, or anterior cerebral; ophthalmic; vertebral,
basilar, or cerebellar; or a penetrating branch. The
carotid (80 %) or vertebrobasilar vascular territories
TIAs may precede, accompany, or infrequently
follow the development of a stroke, or they can
occur by themselves without leading to a stroke.
About two thirds of all patients with TIAs are men
with hypertension, reflecting the higher incidence of
atherosclerosis in this group. Occasionally, in
younger adults, TIAs may occur as relatively benign
phenomena, without recognizable features of
atherosclerosis or risk factors for it.
come on slowly, spread and intensify over several
minutes, and fade in 20–30 min. The symptoms
tend to begin in one domain (particularly vision),
fade and move on to another. Also symptoms tend
to be positive (e.g. flashing lights, tingling) rather
than the typically negative symptoms of a TIA (e.g.
weakness, visual loss, numbness).
Partial epileptic seizures
The symptoms ‘march’ across a hand or foot, and up the limb
in a minute or so and may, eventually, be accompanied by
focal motor seizures or secondary generalization. Sudden
speech arrest seems to be more often epileptic than due to
ischaemia, which is more likely to cause dysphasic