A transient ischemic attack (TIA) is a brief episode of neurological dysfunction caused by restricted blood flow. TIAs last less than 24 hours and have an annual incidence of 3 per 10,000 people. Approximately 10% of patients experience a TIA before having a stroke. Management involves identifying risk factors like hypertension and treating the underlying cause, often through antiplatelet agents, anticoagulation, or carotid endarterectomy to prevent future strokes.

1. (TIA)
Harry Haynes
Transient Ischaemic Attack

2. Definition
• A TIA is an acute loss of neurological
function caused by ischaemia with
symptoms lasting minutes – hours (by
definition, <24hrs).
• Annual incidence of 3/10 000.
• Occur in 10% of patients prior to the
development of a stroke.

3. Pathogenesis
• A TIA is caused by artery-to-artery
emboli (ie ulcerated atheromatous
plaque debris from the proximal neck
vessels) or cardiac emboli ………?

4. Pathogenesis
• TIAs are usually the result of microemboli
• TIAs may be caused by a fall in cerebral
perfusion (dysrhythmia, postural hypotension,
decreased flow through vital atheromatous
arteries)
• Rarely, SOL and subdural haematomas cause
episodes indistinguishable from thromboembolic
TIAs
• Increased total red cell volume (polycythaemia)
may also be causative

5. Risk factors
Risk factor Stroke risk
Hypertension x5
High cholesterol x4
Smoking, alcohol x2
Diabetes x2
+ve family history
AF, IHD, Pill
(prog-oes), obesity
Internal carotid
stenosis

6. Clinical Features
• Since episodes are transient, the diagnosis is
made on the basis of the history
• Onset: rapid (seconds – minutes)
• Variable (but full) resolution (<24 hrs)
• Different clinical disturbances can occur
depending on whether the attack involves the
anterior or posterior circulation
• TIA in anterior circulation has a more serious
prognosis

7. Anatomy (we all love JRT)

8. Clinical Features
Anterior Circulation TIAs:
Amaurosis fugax (fleeting blindness) – loss
of vision in 1 eye
• ‘like a shutter coming down’
• Often due to the passage of emboli through
retinal artery
• May be first clinical evidence of internal
carotid artery stenosis

9. Clinical Features
Anterior Circulation TIAs:
Aphasia : loss of ability to use language
(common)
Dominant parietal lobe TIAs (affecting supramarginal
gyrus) may cause difficulty understanding writing
(dyslexia) or impairment of writing ability (dysgraphia)

10. Clinical Features
Posterior Circulation TIAs:
• Homonymous visual field loss
• Dysarthria
• Vertigo, diplopia, dysphagia (rarely TIAs
if in isolation)
• Tetraparesis
• Transient global amnesia (unknown path)

11. Clinical Features
Anterior OR posterior circulation TIAs:
• Unilateral weakness affecting the face, arm or leg
in isolation or combination
• Unilateral sensory loss affecting the face, arm or
leg in isolation or combination
TIAs rarely lead to an alteration of
consciousness. If this occurs, an alternative
diagnosis should be considered

12. Examination
• Usually reveals no neurological
abnormalities post TIA
• CVS exam may elicit relevant signs:
• Hypertension, retinal changes,
arrhythmias, heart murmur, HF signs,
carotid bruits, loss of peripheral pulses

13. Differential Diagnosis
Usually a TIA is clear-cut and a confident
diagnosis can be made. Similar symptoms may
be produced by:
• Migraine: slower progression with positive
symptoms and headache
• Partial seizures: shorter with similar recurrence
• Hypoglycaemia: does produce similar transient
neuro deficits
• Peripheral nerve lesions: have characteristic
symptoms and signs

14. Investigation
• Routine bloods for polycythaemia (FBC), glucose, U&E,
random cholesterol, infection, vasculitis, thrombophilia,
syphilitic serology, clotting studies, autoantibodies
• CXR, ECG
• Carotid Dopplers
• Angiography
• In those patients where the differential diagnosis includes a
SOL or partial seizures, head CT or MRI is indicated

15. Secondary Prevention of TIA
[Primary Prevention of Stroke]
• Control of hypertension reduces stroke rate
by 40%
• Control of diabetes, stopping smoking,
moderating alcohol intake and control of
hypercholesterolaemia all reduce atheroma
progression
• This reduces stroke risk, CAD and MI (the
most common cause of death post stroke)

16. Management
Antiplatelet Therapy
• Aspirin 300mg daily should be given as soon as
the diagnosis of thromboembolic TIA is
confirmed, reducing to 75mg after several days
• Long-term 75mg aspirin daily substantially
reduces the risk of further infarction after
thromboembolic TIA (by 25%)

17. Management
Antiplatelet Therapy
• Combined aspirin 75mg daily and
dipyridamole 200mg twice daily () is
probably the best prophylaxis against
further thromboembolic TIA
• Dipyridamole inhibits platelet phosphodiesterase which
increases cAMP and potentiates the action of PGI2
• Clopidogrel seems to have same benefit as aspirin alone

18. Management
Anticoagulants
• Should be considered if px has AF, mitral
stenosis, recent MI, cardiomyopathies, other
dysrhythmias
• With TIA with AF, the risk of future stroke is
reduced from 12% yr-1
to 4% with anticoagulation
to an INR of 2-3
• The risk of future stroke should be balanced
against the risk of falls, GI bleed risk, compliance
and treatment monitoring

19. Management
Internal Carotid endarterectomy
• Recommended in TIA patients who have
internal carotid stenosis >70%
• Successful surgery reduces the risk of
further TIA/stroke by ~75%
• Surgical mortality is 3%
• Percutaneous transluminal angioplasty
(stenting) is an alternative proceedure

20. Prognosis
• The risk of stroke and MI is ~7% per year
• The risk of stroke is 12% in the first year
and 10% subsequently if carotid stenosis
>70%
• Mortality is ~3x that of a TIA-free
matched population

21. Summary
• Diagnosis of TIAs depends on the history
• ~10% of patients have a TIA before having
a stroke
• Management depends on understanding the
pathophysiology of TIAs
• Management includes the use of
antiplatelet agents, anticoagulation or
carotid endarterectomy