TRANSIENT ISCHEMIC ATTACK Joshua S.

1610211083
DEFINITION
•A transient episode of neurologic dysfunction caused by focal brain, spinal
cord or retinal ischemia without acute infarction (AHA, 2009)

•Mini stroke, with classical definition : symptoms lasting as long as 24 hours

•Advances in neuroimaging proved that many of such cases represent minor

strokes with resolved symptoms rather than true TIAs, hence the latest definition
included tissue-based definition
EPIDEMIOLOGY
•Internationally, the probability of a first TIA is around 0.42 per 1000
population in developed countries

•The incidence of TIAs increases with age, from 1-3 cases per 100,000 in those
younger than 35 years to as many as 1500 cases per 100,000 in those older
than 85 years

•The incidence of TIAs in men (101 cases per 100,000 population) is

significantly higher than that in women (70 per 100,000)
 RISK FACTORS FOR TIA

Hypertension Current smoking

Hypercholesterolaemia High waist-to-hip ratio

High dietary risk score Lack of regular exercise

Diabetes mellitus Excess alcohol consumption

Psychological stress Cardiac causes (AF or previous MI)

 ETIOLOGY
•Atherosclerosis of extracranial carotid and
vertebral or intracranial arteries

•Embolic sources - Valvular disease, ventricular

thrombus, or thrombus formation from atrial
fibrillation, aortic arch disease, paradoxical
embolism via a patent foramen ovale (PFO) or
atrial-septal defect (ASD)

•Arterial dissection
ETIOLOGY
•Arteritis - Inflammation of the arteries occurring
primarily in elderly persons, especially women;
noninfectious necrotizing vasculitis (primary cause);
drugs; irradiation; local trauma; connective tissue
diseases

•Sympathomimetic drugs (eg, cocaine)

•Mass lesions (eg, tumors or subdural hematomas) –

These less frequently cause transient symptoms and
more often result in progressive persistent symptoms

•Hypercoagulable states (eg, genetic or associated with

cancer or infection)
Large-artery events:
•Caused by stenotic lesions in the internal carotid artery, anterior or middle cerebral
arteries or in the posterior circulation in the vertebral or basilar territories. Any
obstruction at these sites can cause TIA symptoms, especially if collateral circulation is
inadequate.
Embolic events:
•Usually arise from a process starting from an extracranial large artery or from the
heart, and occasionally from smaller vessels within the brain. Cardiac causes are most
commonly secondary to AF or left ventricular disease.
Lacunar or small-vessel events:
•Due to stenosis of one of the intracranial vessels, anterior from the middle cerebral
artery or its branches and posteriorly from the vertebro-basilar system. The process
involved here is usually atherosclerosis driven by risk factors such as hypertension and
hypercholesterolemia.
PATHOPHISIOLOGY
•The clinical symptoms of TIA typically
last less than 1 hour and often last for
less than 30 minutes, but prolonged
episodes can occur
SIGN AND SYMPTOMS
DIAGNOSIS •Comorbidities related to metabolic disorders,
especially diabetes
•Known coagulopathy or family history of early
Significant medical history clotting or thrombotic events

•Recent surgery (eg, carotid or cardiac) •History of arteritis

•Previous strokes or TIAs •Noninfectious necrotizing vasculitis, irradiation,

and local trauma
•Seizures
•Thromboembolic risk factors (eg, carotid artery
•Systemic or central nervous system (CNS) stenosis, venous or arterial thromboembolism,
infections patent foramen ovale or atrial septal defect,
atrial fibrillation, prior myocardial infarction, and
•Use of illicit drugs
left ventricular dysfunction)
•Complete medication regimen, including
•Other known cardiovascular disease
all over-the-counter medications
•History of migraine
NEUROLOGICAL EXAMINATION
•Subsets of the neurologic examination include the following:
•Cranial nerve testing
•Determination of somatic motor strength
•Somatic sensory testing
•Speech and language testing
•Assessment of the cerebellar system (be sure to watch the patient walk)
•For somatic motor testing: test muscle stretch reflexes of biceps, triceps, brachioradialis,
patellar, and Achilles; inspect posture and look for tremors; test the strength of the
shoulder girdle, upper extremities, abdominal muscles, and lower extremities; test passive
movement of major joints to look for spasticity, clonus, and rigidity
 PHYSICAL EXAMINATION
Signs of cranial nerve dysfunction:
•Ocular dysmotility
•Forehead wrinkling asymmetry
•Incomplete eyelid closure
•Asymmetrical mouth retraction
•Loss of the nasolabial crease
•Swallowing difficulty
•Lateral tongue movement
•Weak shoulder shrugging
•Visual field deficits
Physical examination includes:
•Funduscopy
•Abnormalities of heart and vascular
(auscultation, thoracic scar, carotid bruit
etc)
PROGNOSIS
•On average, the annual risk of future ischemic
stroke after a TIA or initial ischemic stroke is 3–4%
•Incidence is as high as 11% over the next 7 days
•24–29% over the following 5 years
•Risk of stroke following TIA can be predicted by the
ABCD score
 •Thrombolytic therapy
Antiplatelets
The use of aspirin in patients with previous
TIA or stroke has been shown to reduce the
risk of subsequent vascular events by 13%.
Aspirin 300mg as a single dose should be
started while investigations are pending.
Although occasionally TIA can be due to a
small intracerebral haemorrhage, this is
uncommon and it is reasonable to commence
an antiplatelet drug without prior brain
imaging.
TREATMENT

The NICE recommendations for antiplatelet

therapy after stroke are long-term
combination of aspirin 75mg once a day
(or clopidogrel if aspirin not tolerated)
and dipyridamole modified release 200mg
twice a day.
SPECIFIC THERAPY AND PREVENT RECURRENCE
•Antihypertension drugs •Anticoagulants
ACEI, ARB, careful consideration in heart Prevent clots forming, warfarin
diseases
•Intervention of heart diseases and other
•Statins and other hypercholesterolemia possible causes
drugs
•Control blood cholesterol level, reduces
risk of recurrent attack caused by
embolism