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Transient Ischemic Attack

dr. Ashari Bahar, M.Kes, Sp.S, FINS


Department of Neurology
Faculty of Medicine
University of Hasanuddin
Definition

• TIAs is a brief episode of neurological


dysfunction caused by focal brain or retinal
ischemia, with clinical symptoms typically
lasting less than one hour, and without evidence
of acute infarction on brain imaging.
Epidemiology

• The incidence (United States) 200 000 to


500 000 per year
• Prevalence 2.3% / 5 million individuals
• TIA incidence rates (different study cohorts)-
US &abroad 0.37 to 1.1 / 1000 per year
Etiology

• ≈ ischemic stroke
• Determining the etiology very important as
there are several causes that, if treated
urgently, may prevent a stroke
• E.g. atrial fibrillation and symptomatic carotid
stenosis
Presentation

• TIAs present ≈ acute ischemic stroke


• The only difference is that the symptoms and
signs rapidly and completely resolve, usually
within minutes
• There is not a typical presentation – it
depends on the vascular territory affected
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Differential diagnosis

• Syncope
• Seizure
• Migraine
• Vestibular dysfunction; vertigo.
• Anxiety, panic attack
• Hypoglycemia
• Drug intoxication
• Mass such as tumor or subdural hematoma
• Metabolic encephalopathy
Diagnostic evaluation

The goals of the modern neuroimaging evaluation of


TIA are:
1) To obtain evidence of a vascular origin for the symptoms
either directly (evidence of hypoperfusion and/or acute
infarction) or indirectly (identification of a presumptive
source such as a large-vessel stenosis)
2) To exclude an alternative nonischemic origin
3) To ascertain the underlying vascular mechanism of the
event (eg, large-vessel atherothrombotic, cardioembolic,
small-vessel lacunar), which, in turn, allows selection of
the optimal therapy
4) To identify prognostic outcome categories
Diagnostic evaluation cont.

• Computed Tomography (CT scan)


• Magnetic Resonance Imaging (MRI)
Vessel Imaging

• Extracranial disease:
– Carotid ultrasound/transcranial Doppler (CUS/TCD)
– MRA
– CTA
• Intracranial disease :
– TCD
– MRA
– CTA
– Conventional cerebral angiography/DSA (Gold standard)
Cardiac testing

• ECG
• Transthoracic echocardiography (TTE) &
transesophageal echocardiography (TEE)
• Holter monitoring
Other testing

• Routine blood test :


– Complete blood count
– Chemistry panel
– Basic coagulation studies(prothrombin time,
partial thromboplastin time)
Other testing Cont.

• Specialized coagulation tests can be considered in younger patients with


TIAs
• Particularly when no vascular risk factors exist and no underlying cause is
identified
– Protein C, protein S, antithrombin III activities
– Activated protein C resistance/factor V Leiden
– Fibrinogen
– D-Dimer
– Anticardiolipin antibody
– Lupus anticoagulant
– Homocysteine
– Prothrombin gene G20210A mutation
– Factor VIII
– Von Willebrand factor
– Plasminogen activator inhibitor-1
– Endogenous tissue plasminogen activator activity
Management

• ≈ acute ischemic stroke


• Observe the patient for 24 hours. Remember,
if they develop new neurological symptoms
they could be candidates for TPA if no other
exclusions exist
• Start daily antiplatelets
• Educate the patient about:
– stroke risk factors including smoking, exercise, weight loss,
alcohol
– specific medications prescribed for prevention;
– recurrent symptoms to look for; and
– calling emergency services for acute stroke symptoms.
• Discharge with established follow-up plans.
AHA/ASA Recommendations for the Prevention of Stroke in
Patients With Stroke and Transient Ischemic Attack

Recommendations for Antiplatelet Therapy


Class I Recommendations
1. For patients with noncardioembolic ischemic stroke or TIA, antiplatelet agents
rather than oral anticoagulation are recommended to reduce the risk of recurrent
stroke and other cardiovascular events (Class I, Level of Evidence A).
2. Old recommendation: Aspirin (50 to 325 mg/d), the combination of aspirin and
extended-release dipyridamole, and clopidogrel are all acceptable options for
initial therapy (Class IIa, Level of Evidence A).
New recommendation: Aspirin (50 to 325 mg/d) monotherapy, the combination of
aspirin and extended-release dipyridamole, and clopidogrel monotherapy are all
acceptable options for initial therapy (Class I, Level of Evidence A).*
3. Old recommendation: Compared with aspirin alone, both the combination of
aspirin and extended-release dipyridamole and clopidogrel are safe.
The combination of aspirin and extended-release dipyridamole is suggested over
aspirin alone (Class IIa, Level of Evidence A).
New recommendation: The combination of aspirin and extended-release
dipyridamole is recommended over aspirin alone (Class I, Level of Evidence B).
AHA/ASA Recommendations for the Prevention of Stroke in
Patients With Stroke and Transient Ischemic Attack cont.

Class II Recommendations
1. Clopidogrel may be considered over aspirin alone on the basis of direct-
comparison trials (Class IIb, Level of Evidence B).
2. For patients allergic to aspirin, clopidogrel is reasonable (Class IIa, Level of
Evidence B).
Class III Recommendation
The addition of aspirin to clopidogrel increases the risk of hemorrhage.
Combination therapy of aspirin and clopidogrel is not routinely recommended for
ischemic stroke or TIA patients unless they have a specific indication for this
therapy (ie, coronary stent or acute coronary syndrome) (I).

• *For patients who have an ischemic cerebrovascular event while taking aspirin,
there is no evidence that increasing the dose of aspirin provides additional benefit.
• Although alternative antiplatelet agents are often considered for
noncardioembolic patients, no single agent or combination has been well studied
in patients who have had an event while receiving aspirin.
AHA/ASA Recommendations for the Prevention of Stroke in
Patients With Stroke and Transient Ischemic Attack cont.

Recommendations for Lipid Management


Class I Recommendations
• Ischemic stroke or TIA patients with elevated cholesterol, comorbid coronary artery disease,
or evidence of an atherosclerotic origin should be managed according to NCEP III guidelines,
which include lifestyle modification, dietary guidelines, and medication recommendations
(Class I, Level A)
• Statin agents are recommended, and the target goal for cholesterol lowering for those with
CHD or symptomatic atherosclerotic disease is an LDL-C level of 100 mg/dL. An LDL-C 70
mg/dL is recommended for very high-risk persons with multiple risk factors (Class I, Level A)
New Recommendation
• On the basis of the SPARCL trial, administration of statin therapy with intensive lipid-
lowering effects is recommended for patients with atherosclerotic ischemic stroke or TIA and
without known CHD to reduce the risk of stroke and cardiovascular events (Class I, Level B)
Class II Recommendation
• Ischemic stroke or TIA patients with low HDL cholesterol may be considered for treatment
with niacin or gemfibrozil (Class IIb, Level B)
• NCEP indicates National Cholesterol Education Panel; LDL-C, low-density lipoprotein
cholesterol; and HDL, high-density lipoprotein.
Risk Stratification

• The ABCD2 score was derived to provide a more robust prediction


standard
• Patients with TIA score points (indicated in parentheses) for each of the
following factors:
Age 60 years (1)
Blood pressure 140/ 90 mm Hg on first evaluation (1)
Clinical symptoms of focal weakness with the spell (2) or speech impairment
without weakness (1)
Duration 60 minutes (2) or 10 to 59 minutes (1)
Diabetes (1)
• In combined validation cohorts, the 2-day risk of stroke was :
0% for scores of 0 or 1
1.3% for 2 or 3
4.1% for 4 or 5
8.1% for 6 or 7
The risk of stroke after TIA:
the Diabetes, Duration, Weakness (DDW) score

Three risk factors Number of risk Estimates risk of


for stroke after TIA factors present stroke in 7 days
(Give 1 point each
if present)
Diabetes mellitus 0 1%

Duration of episode 1 4%
≥ 60 minutes
Weakness (focal) 2 9%
with episode
3 10%
Prognosis after TIA

• After an ED visit for TIA:


– 5.3% stroke risk within 2 days
– 10.5% stroke in 90 days (21% fatal, 64% disabling)
• 1 in 9 patients will have a stroke within 3
months
“TIME IS BRAIN”

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