TRANSIENT ISCHEMIC ATTACKS : RECENT DEVELOPMENTS

DR. PIYUSH OJHADM RESIDENT

DEPARTMENT OF NEUROLOGYGOVT MEDICAL COLLEGE, KOTA

• Stroke and TIA are on a spectrum of serious conditions

involving brain ischemia.

• Both are markers of reduced cerebral blood flow and an increased risk of disability and death.

• However, TIAs offer an opportunity to initiate treatment that can prevent the onset of permanently disabling injury.

• The 2014 AHA statistical update – approx 5 million TIAs annually in US.

• Lack of recognition by both the public and healthcare systems of the transitory focal neurological symptoms associated with TIAs lead to gross underestimates.

• A TIA is a prognostic indicator of Stroke, with one-third of untreated TIAs having a stroke within 5 years.

• About 1 in 10 patients with TIA experience stroke in the next 3 months with half occuring within next 48 hours.

• The interval from the last TIA is an important predictor of stroke risk.

• Of all patients who subsequently experience stroke :– 21% do so within 1 month– 51% do so within 1 year of the last TIA.

• In one series, patients with TIA had a 3-month stroke risk of 10.5%, equal to the recurrence rate following a stroke.(Johnson et al, 2000)

• Furthermore, 50% of those strokes occurred within 48 hours of TIA onset.

• The 5-6% annual mortality rate after TIA is mainly caused by MI.

• Among patients who present with stroke, the prevalence of prior TIA has been reported to range from 7% to 40%.

• In 2 population-based studies (Oxford Vascular Study and Oxfordshire Community Stroke Project) and 2 other randomized trials (UK TIA Aspirin Trial and the European Carotid Surgery Trial), the timing of a TIA before stroke was highly consistent, with – 17% occurring on the day of the stroke– 9% on the previous day, and – another 43% at some point during the 7 days before the

stroke.

• Risk of cardiac events also is elevated after TIA.

• In a large study, 2.6% of TIA patients were hospitalized for major cardiovascular events (myocardial infarction, unstable angina, or ventricular arrhythmia) within 90 days.

• Over the course of 5 years, a nearly equal number of patients with TIA will have myocardial infarction or sudden cardiac death as will have a cerebral infarction.

• Cardiac events are the principal cause of death in patients who have had a TIA.

• TIAs are brief episodes of neurological dysfunction resulting from focal cerebral ischemia not associated with permanent cerebral infarction.

• A TIA is a temporary and “nonmarching” neurological deficit of sudden onset; attributed to focal ischemia of the brain, retina or cochlea; and lasting less than 24 hours.

• Most TIAs last only a few minutes.• Episodes that last longer than 1 hour are usually due to small

infarctions.

• The traditional definition of a TIA was a sudden, focal neurological deficit of presumed vascular origin lasting < 24 hours.

• The arbitrary 24-hour threshold used to distinguish TIA from stroke arose in the mid-1960s.

• At that time, it was assumed that transient symptoms disappeared completely because no permanent brain injury had occurred.

• The term TIA was applied to events lasting up to 24 hours, and the term Reversible ischemic neurological deficit was applied to events lasting 24 hours to 7 days.

• Only symptoms enduring 7 days were thought to reliably indicate infarction and received the designation stroke.

• During the 1970s, it became clear that the great preponderance of events lasting 24 hours to 7 days were associated with infarction, rendering the term Reversible ischemic neurological deficit obsolete, and it disappeared from standard nomenclature.

• Various studies - 30% to 50% of classically defined TIAs show brain injury on DWI –MR imaging.

Shah et al : A multicenter pooled, patient-level data analysis of diffusion-weighted MRI in TIA patients. Stroke. 2007;38:463.

• With these observations in mind, a group of Cerebrovascular physicians proposed a Tissue-based, rather than time-based, definition in 2002 :

• Newer operational definition of TIA - “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.”

• AHA-Endorsed Revised Definition of TIA– Transient ischemic attack (TIA): a transient episode of

neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction.

• Points in favour of new definition :– The classic 24-hour definition was misleading in that many

patients with transient <24-hour events actually have associated cerebral infarction.

– The traditional definition can impede the administration of acute stroke therapies.

– A 24-hour limit for transiently symptomatic cerebral ischemic was arbitrary and not reflective of the typical duration of these events.

• Thus a “Tissue-based” modification of TIA definition has been proposed :

– Any transient episode, regardless of duration, associated with a clinically appropriate lesion by MRI be defined as Stroke, and

– That otherwise prolonged events (>1-6 hours in duration) be defined as stroke rather than TIA when otherwise clinically appropriate.(Albers et al. 2002)

• Johnston et al. developed a risk stratification score in patients with TIAs, known as the ABCD2 score.

• The ABCD2 score is based on age, blood pressure (≥140/90 mm Hg), clinical features, TIA duration, and diabetes.

• ABCD2 scores of 4 or greater indicate a moderate to high stroke risk and justify prompt hospital admission

Age 60 or older - 1 point

Blood pressure ≥140/90 - 1 point

Clinical: Unilateral weakness - 2 points Speech impairment - 1 point

Duration: 60 minutes or more - 2 points <60 minutes - 1 point

Diabetes mellitus - 1 point

ABCD 2 SCORE

• In combined validation cohorts, the 2-day risk of stroke was calculated as :– 0% for scores of 0 or 1– 1.3% for 2 or 3– 4.1% for 4 or 5 and – 8.1% for 6 or 7.

• The 2009 American Heart Association and American Stroke Association (AHA/ASA) guidelines for the definition and evaluation of TIA state that it is reasonable to hospitalize patients with TIA who present within 72 hours of symptom onset and meet any of the following criteria :

(Class IIa; Level of Evidence C)– ABCD2 score ≥3– ABCD2 score of 0 to 2 and uncertainty that the diagnostic

workup can be completed within two days as an outpatient

– ABCD2 score of 0 to 2 and other evidence that the event was caused by focal ischemia

• DW-MRI is useful in predicting the risk of early stroke – patients with TIA and DW-MRI lesions are at greater risk of experiencing a subsequent stroke than patients without a lesion.(Coutts et al.,2005)

• Evidence of vessel occlusion on acute brain MRA also has been associated with a 4-fold increased short-term risk of stroke.

• The onset of TIA symptoms is sudden, reaching maximum intensity almost immediately.

• To qualify as a TIA, therefore, an episode should also be followed by complete clinical recovery.

• Symptoms Suggestive of Carotid Transient Ischemic Attacks :

– Transient ipsilateral monocular blindness (amaurosis fugax)

– Contralateral body weakness or clumsiness– Contralateral body sensory loss or paresthesias– Aphasia with dominant hemisphere involvement– Various degrees of contralateral homonymous visual field

defects– Dysarthria (not in isolation)

Symptoms Suggestive of Vertebrobasilar TIAs :

– Usually bilateral weakness or clumsiness but may be unilateral or shifting

– Bilateral, shifting, or crossed (ipsilateral face and contralateral body) sensory loss or paresthesias

– Bilateral or contralateral homonymous visual field defects or binocular vision loss

– Two or more of the following symptoms: vertigo, diplopia, dysphagia, dysarthria, and ataxia

Symptoms Not Acceptable as Evidence of TIAs

• Syncope, dizziness, confusion, urinary or fecal incontinence, and generalized weakness

• Isolated occurrence of vertigo, diplopia, dysphagia, ataxia, tinnitus, amnesia, drop attacks, or dysarthria

• Capsular warning syndrome - characterized by restricted, stereotyped, repeated episodes of capsular ischemia causing contralateral symptoms involving the face, arm, and leg.

• Occasionally, “stuttering TIAs” may be confused with epileptic events.

• When capsular infarction develops, it is usually a lacunar-type stroke and involves a single penetrating vessel.

• Occasionally, striatocapsular or anterior choroidal artery territory infarction occurs.

• These may be lacunar in origin but sometimes are associated with carotid artery steno-occlusive disease.

• Typically these patients are refractory to conventional forms of therapy.

ETIOLOGY• Transient ischemic attacks may result from

atherothromboembolism that originates from :– Ulcerated extracranial arteries– Emboli of cardiac origin– Occlusion of small penetrating arteries that arise from the

large surface arteries of the circle of Willis– Altered local blood flow (perfusion failure) due to severe

arterial stenosis, nonatherosclerotic vasculopathies, or hypercoagulable states

• In a published series, TIAs occurred before :– 25 - 50% of atherothrombotic infarcts– 11 - 30% of cardioembolic infarcts, and – 11 - 14% of lacunar infarcts.

• Lacunar TIAs in general share the same pathogenetic mechanisms of lacunar infarcts and are associated with a substantially better prognosis than nonlacunar TIAs.

• Crescendo episodes of cerebral ischemia that increase in frequency, severity, or duration must be treated as neurological emergencies.

DIAGNOSTIC EVALUATION• Rational treatment of patients with TIAs depends on a careful

history and detailed physical examination.

• The neuro vascular examination may disclose a well-localized cervical bruit.

• However, the presence of a cervical bruit does not necessarily indicate underlying carotid artery atherosclerosis.

• Correlation with angiography or ultrasound studies shows only a 60% concordance with cervical auscultation in predicting the presence of arterial stenosis.

• Radiated cardiac murmurs, hyperdynamic states, nonatherosclerotic carotid arterial lesions, and venous hums can produce cervical murmurs.

• The bruit may disappear when the stenosis is advanced.

• Asymmetrical hypertensive retinal changes noted on funduscopy are suggestive of a high-grade carotid artery stenosis or occlusion on the side of the less severely involved retina.

• Venous stasis retinopathy may occur with high-grade carotid artery stenosis or occlusion and is characterized by diminished or absent venous pulsations, dilated and tortuous retinal veins, peripheral microaneurysms, and blossom-shaped hemorrhages in the midperipheral retina.

• Retinal microvascular abnormalities correlate with an increased incidence of lacunar strokes (Yatsuya et al., 2010).

• Corneal arcus senilis may be less obvious or absent on the side of low perfusion.

• The goals of the modern neuroimaging evaluation of TIA are

– 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)

– To exclude an alternative nonischemic origin– 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 and

– To identify prognostic outcome categories.

• With respect to the frequency of identifying brain infarcts in patients with TIAs, one needs to analyze :

– Whether the infarcts reported are new or old– Whether they are in a clinically relevant vascular territory

or not and – whether the infarcts are cortical or in a perforator

territory.

• Conventional MRI is more sensitive than standard CT in identifying both new and pre-existing ischemic lesions in TIA patients.

• Across various studies, MRI has shown at least 1 infarct somewhere in the cerebrum in 46% to 81% of TIA patients.

• DWI provides a more precise evaluation of ischemic insult in TIA patients compared with standard CT and MRI studies.

• Several studies have analyzed the imaging characteristics of DWI-positive lesions.

• Compared with patients with clinical stroke, DWI-positive lesions tend to be smaller in TIA patients.

• In a multicenter, patient-level analysis of 808 patients in which DWI lesions were present in 33% of TIA patients, predictors of DWI positivity were as follows :

– Presence of motor symptoms – Longer duration of TIA and – MRI within 24 hours of resolution of symptoms

CARDIAC TESTING• The tests that are considered in this setting include – ECG– Transthoracic echocardiography (TTE)– Transesophageal echocardiography (TEE) and– Holter monitoring.

• TEE is more sensitive than TTE for atheroma of the aortic arch and abnormalities of the interatrial septum (eg, atrial septal aneurysm, PFO, atrial septal defect), atrial thrombi, and valvular disease.

• Holter monitoring is abnormal in a minority of patients with TIA.

• Prolonged cardiac monitoring (inpatient telemetry or Holter monitor) is useful in patients with an unclear origin after initial evaluation.

• Patients with a history of palpitations or evidence of structural heart disease by ECG or echocardiogram might reflect abnrmal results.

• In addition, longer monitoring may be expected to yield greater results.

• In a consecutive series of 28 patients with no identified cause of stroke or TIA, including testing with Holter monitoring for 24 hours, 14% had paroxysmal atrial fibrillation on a 4-day automatic cardiac event recorder.

ROUTINE BLOOD TESTS• No systematic studies have been performed to assess the

value of blood tests in patients with TIA. • It is reasonable to perform the same routine blood tests in

patients presenting with TIAs as in patients presenting with ischemic stroke.

• Including a complete blood count, chemistry panel, and basic coagulation studies (PT, aPTT).

• These tests are useful to exclude TIA mimics (eg, hypoglycemia) and can help identify less common causes of thrombotic events (eg, polycythemia vera).

• A fasting lipid profile also is appropriate.

EXTRACRANIAL VESSEL IMAGING

• Tests include :– Carotid ultrasound/transcranial Doppler (CUS/TCD)– MR Angiography and– CT Angipgraphy.

• Carotid Ultrasound detects > 50% stenosis of the extracranial internal carotid artery in 8% to 31% of patients with TIA and very minor stroke.

• CUS also provides reliable assessment of the carotid bifurcation.

• A sensitivity of 88% and specificity of 76% have been reported.

• CUS findings carry prognostic significance. • When 311 consecutive TIA patients underwent CUS/TCD

within 24 hours of symptoms, patients with moderate to severe intracranial stenosis or extracranial stenosis had 3 times the risk for stroke within 90 days of follow-up.

• Supra-aortic MRA and CTA also provide reliable assessment of the carotid bifurcation and of the intracranial circulation.

• MRA sensitivity of 92% and specificity of 76% for extracranial carotid disease has been reported.

• CTA has been reported to have an excellent (100%) negative predictive value for excluding > 70% stenosis compared with catheter angiography, thereby functioning well as a screening test.

• Ultrasound, CTA, or MRA should be performed as the initial screen of the carotid bifurcation.

• In patients with abnormal tests, a common strategy includes a second confirmatory noninvasive test to evaluate the carotid bifurcation before endarterectomy if there is no plan to perform catheter angiography.

• If 2 noninvasive tests are discordant, catheter angiography should be considered before endarterectomy.

• Trans Cranial Doppler (TCD) provides information regarding intracranial stenoses.

• Recent data identify the following predictive values for TCD identification of intracranial stenosis: positive predictive value of 36% and negative predictive value of 86%.

• MRA and CTA had comparable performance for identifying intracranial stenosis.

INTRACRANIAL VESSEL IMAGING

• Conventional cerebral angiography is an important diagnostic tool in the evaluation of patients with cerebrovascular disease, including stroke and TIA.

• Despite recent advances in noninvasive diagnostic neuroimaging, cervicocerebral angiography remains the gold standard for the diagnostic evaluation of patients with a wide range of cervical and intracranial vascular diseases.

• However, if noninvasive imaging provides firm diagnostic findings, cerebral angiography may not be required.

MANAGEMENT GUIDELINES FOR TIA

Guidelines for the Prevention of Stroke in Patients With Stroke and Transient Ischemic Attack : Stroke 2014

• HYPERTENSION

– Initiation of BP therapy is indicated for previously untreated patients with ischemic stroke or TIA who, after the first several days, have an established BP ≥140 mm Hg systolic or ≥90 mm Hg diastolic (Class I; Level of Evidence B).

– Initiation of therapy for patients with BP <140 mm Hg systolic and <90 mm Hg diastolic is of uncertain benefit (Class IIb; Level of Evidence C).

• HYPERTENSION

– Resumption of BP therapy is indicated for previously treated patients with known hypertension for both prevention of recurrent stroke and prevention of other vascular events in those who have had an ischemic stroke or TIA and are beyond the first several days (Class I; Level of Evidence A).

– Several lifestyle modifications have been associated with BP reductions and are a reasonable part of a comprehensive antihypertensive therapy (Class IIa; Level of Evidence C). These modifications include salt restriction; weight loss; the consumption of a diet rich in fruits, vegetables, and low-fat dairy products; regular aerobic physical activity; and limited alcohol consumption.

DYSLIPIDEMIA• Statin therapy with intensive lipid-lowering effects is

recommended to reduce risk of stroke and cardiovascular events among patients with ischemic stroke or TIA presumed to be of atherosclerotic origin and an LDL-C level ≥100 mg/dL with or without evidence for other ASCVD (Class I; Level of Evidence B).

• Statin therapy with intensive lipid-lowering effects is recommended to reduce risk of stroke and cardiovascular events among patients with ischemic stroke or TIA presumed to be of atherosclerotic origin, an LDL-C level <100 mg/dL, and no evidence for other clinical ASCVD (Class I; Level of Evidence C).

GLUCOSE DISORDERS• After a TIA or ischemic stroke, all patients should probably be

screened for DM with testing of fasting plasma glucose, HbA1c , or an oral glucose tolerance test.

• Choice of test and timing should be guided by clinical judgment and recognition that acute illness may temporarily perturb measures of plasma glucose.

• In general, HbA1c may be more accurate than other screening tests in the immediate post event period (Class IIa; Level of Evidence C).

OBESITY

• All patients with TIA or stroke should be screened for obesity with measurement of BMI (Class I; Level of Evidence C).

• Given the demonstrated beneficial effects of weight loss on cardiovascular risk factors, the usefulness of weight loss among patients with a recent TIA or ischemic stroke and obesity is uncertain (Class IIb; Level of Evidence C).

• For patients with a TIA or ischemic stroke within the past 6 months and ipsilateral severe (70%–99%) carotid artery stenosis as documented by noninvasive imaging, CEA is recommended if the perioperative morbidity and mortality risk is estimated to be <6% (Class I; Level of Evidence A).

• For patients with recent TIA or ischemic stroke and ipsilateral moderate (50%–69%) carotid stenosis as documented by catheter-based imaging or noninvasive imaging with corroboration (eg, MRA or CTA), CEA is recommended depending on patient-specific factors, such as age, sex, and comorbidities, if the perioperative morbidity and mortality risk is estimated to be <6% (Class I; Level of Evidence B).

CAROTID DISEASE

CAROTID DISEASE

• When the degree of stenosis is <50%, CEA and CAS are not recommended (Class III; Level of Evidence A).

• When revascularization is indicated for patients with TIA or minor, nondisabling stroke, it is reasonable to perform the procedure within 2 weeks of the index event rather than delay surgery if there are no contraindications to early revascularization (Class IIa; Level of Evidence B).

• CAS is indicated as an alternative to CEA for symptomatic patients at average or low risk of complications associated with endovascular intervention when the diameter of the lumen of the internal carotid artery is reduced by >70% by noninvasive imaging or >50% by catheter-based imaging or noninvasive imaging with corroboration and the anticipated rate of periprocedural stroke or death is <6% (Class IIa; Level of Evidence B).

• It is reasonable to consider patient age in choosing between CAS and CEA.

• For older patients (ie, older than ≈70 years), CEA may be associated with improved outcome compared with CAS, particularly when arterial anatomy is unfavorable for endovascular intervention.

• For younger patients, CAS is equivalent to CEA in terms of risk for periprocedural complication (ie, stroke, MI, or death) and long-term risk for ipsilateral stroke (Class IIa; Level of Evidence B).

CAROTID DISEASE

• Routine, long term follow-up imaging of the extracranial carotid circulation with carotid duplex ultrasonography is not recommended (Class III; Level of Evidence B).

• For patients with recurrent or progressive ischemic symptoms ipsilateral to a stenosis or occlusion of a distal (surgically inaccessible) carotid artery, or occlusion of a midcervical carotid artery after institution of optimal medical therapy, the usefulness of EC/IC bypass is considered investigational (Class IIb; Level of Evidence C).

CAROTID DISEASE

INTRACRANIAL ATHEROSCLEROSIS• For patients with recent stroke or TIA (within 30 days)

attributable to severe stenosis (70%–99%) of a major intracranial artery, the addition of clopidogrel 75 mg/d to aspirin for 90 days might be reasonable (Class IIb; Level of Evidence B).

• For patients with stroke or TIA attributable to 50% to 99% stenosis of a major intracranial artery, the data are insufficient to make a recommendation regarding the usefulness of clopidogrel alone, the combination of aspirin and dipyridamole, or cilostazol alone (Class IIb; Level of Evidence C).

• For patients with a stroke or TIA attributable to 50% to 99% stenosis of a major intracranial artery, maintenance of systolic BP below 140 mm Hg and high-intensity statin therapy are recommended (Class I; Level of Evidence B).

• For patients with a stroke or TIA attributable to moderate stenosis (50%–69%) of a major intracranial artery, angioplasty or stenting is not recommended given the low rate of stroke on medical management and the inherent periprocedural risk of endovascular treatment (Class III; Level of Evidence B).

• For patients who have experienced an acute ischemic stroke or TIA with no other apparent cause, prolonged rhythm monitoring (≈30 days) for AF is reasonable within 6 months of the index event (Class IIa; Level of Evidence C).

• For most patients with a stroke or TIA in the setting of AF, it is reasonable to initiate oral anticoagulation within 14 days after the onset of neurological symptoms (Class IIa; Level of Evidence B).

• For patients with ischemic stroke or TIA and AF who are unable to take oral anticoagulants, aspirin alone is recommended (Class I; Level of Evidence A).

• The addition of clopidogrel to aspirin therapy, compared with aspirin therapy alone, might be reasonable (Class IIb; Level of Evidence B).

CARDIAC MONITORING

• For patients with ischemic stroke or TIA who have rheumatic mitral valve disease and AF, longterm VKA therapy with an INR target of 2.5 (range, 2.0–3.0) is recommended (Class I; Level of Evidence A).

• For patients with ischemic stroke or TIA who have rheumatic mitral valve disease without AF or another likely cause for their symptoms (eg, carotid stenosis), long-term VKA therapy with an INR target of 2.5 (range, 2.0–3.0) may be considered instead of antiplatelet therapy (Class IIb; Level of Evidence C).

• For patients with rheumatic mitral valve disease who have an ischemic stroke or TIA while being treated with adequate VKA therapy, the addition of aspirin might be considered (Class IIb; Level of Evidence C).

• For patients with ischemic stroke or TIA and native aortic or non-rheumatic mitral valve disease who do not have AF or another indication for anticoagulation, antiplatelet therapy is recommended (Class I; Level of Evidence C).

ANTIPLATELET THERAPY• For patients with noncardioembolic ischemic stroke or TIA,

the use of antiplatelet agents rather than oral anticoagulation is recommended to reduce the risk of recurrent stroke and other cardiovascular events (Class I; Level of Evidence A).

• Aspirin (50–325 mg/d) monotherapy (Class I; Level of Evidence A) or the combination of aspirin 25 mg and extended-release dipyridamole 200 mg twice daily (Class I; Level of Evidence B) is indicated as initial therapy after TIA or ischemic stroke for prevention of future stroke.

• Clopidogrel (75 mg) monotherapy is a reasonable option for secondary prevention of stroke in place of aspirin or combination aspirin/dipyridamole (Class IIa; Level of Evidence B). This recommendation also applies to patients who are allergic to aspirin.

• The combination of aspirin and clopidogrel might be considered for initiation within 24 hours of a minor ischemic stroke or TIA and for continuation for 90 days (Class IIb; Level of Evidence B).

ANTIPLATELET THERAPY

• The combination of aspirin and clopidogrel, when initiated days to years after a minor stroke or TIA and continued for 2 to 3 years, increases the risk of hemorrhage relative to either agent alone and is not recommended for routine long-term secondary prevention after ischemic stroke or TIA (Class III; Level of Evidence A).

• For patients who have an ischemic stroke or TIA while taking aspirin, there is no evidence that increasing the dose of aspirin provides additional benefit.

• Although alternative antiplatelet agents are often considered, no single agent or combination has been adequately studied in patients who have had an event while receiving aspirin (Class IIb; Level of Evidence C).

ANTIPLATELET THERAPY

CONCLUSIONS• Tissue-based definition of TIA: a transient episode of

neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction.

• Patients with TIAs are at high risk of early stroke, and their risk may be stratified by clinical scale, vessel imaging, and diffusion magnetic resonance imaging.

• Diagnostic recommendations include:

– TIA patients should undergo neuroimaging evaluation within 24 hours of symptom onset, preferably with magnetic resonance imaging, including diffusion sequences

– Noninvasive imaging of the cervical vessels should be performed and

– Noninvasive imaging of intracranial vessels is reasonable

– Electrocardiography should occur as soon as possible after TIA and prolonged cardiac monitoring and echocardiography are reasonable in patients in whom the vascular etiology is not yet identified

– routine blood tests are reasonable; and

– it is reasonable to hospitalize patients with TIA if they present within 72 hours and have an ABCD 2 score > 3, indicating high risk of early recurrence, or the evaluation cannot be rapidly completed on an outpatient basis.

THANK YOU

REFERENCES• Bradley’s textbook of neurology 6th edition

• Definition and Evaluation of Transient Ischemic Attack : Stroke. 2009;40:2276-2293

• Guidelines for the Prevention of Stroke in Patients With Stroke and Transient Ischemic Attack : Stroke. 2014;45:00-00

• TIA :Practice Essentials : Emedicine.com

• Occlusive disease in the Subclavian arteries or the Innominate artery can give rise to extracranial steal syndromes.

• The most well-defined syndrome - Subclavian Steal syndrome (SSS).

• In SSS, reversal of flow in the vertebral artery due to a high-grade subclavian artery stenosis or occlusion proximal to the origin of the vertebral artery from the aortic arch or innominate artery, with resultant symptoms of brainstem ischemia, usually precipitated by actively exercising the ipsilateral arm.

• The left side is involved most frequently.

• With Innominate artery occlusion, the origin of the right carotid is also subject to reduced perfusion pressure.

• Subclavian artery or Innominate artery stenosis can be suspected by a reduced or delayed radial pulse and diminished blood pressure in the affected arm relative to the contralateral arm.

• A subclavian steal may be symptomatic or asymptomatic.

• Many patients have angiographic evidence of reversed vertebral blood flow without ischemic symptoms.

• Transcranial Doppler ultrasonography may detect transient retrograde basilar blood flow during an ischemic forearm challenge.

• Retrograde vertebral artery flow is a benign entity.

• Brainstem infarction is an uncommon complication of the Subclavian steal syndrome.

• Transient global amnesia (TGA) is characterized by a reversible antegrade and retrograde memory loss, except for a total amnesia of events that occur during the attacks and inability to learn newly acquired information.

• During the attacks, patients remain alert without motor or sensory impairments and often ask the same questions repeatedly.

• Able to retain personal identity and carry on complex activities. • Most commonly affects patients 50 years and older. • Men >> women.

• The attacks begin abruptly without warning. • A typical attack lasts several hours (mean, 3–6 hours) but

seldom longer than 12 hours. • Onset of TGA may follow – Physical exertion– Sudden exposure to cold or heat or – sexual intercourse.

• In most instances, TGA is of primary or unknown cause.

• TGA has been associated with – Epilepsy – Migraine – Intracranial tumors – Overdose of diazepam– Cardiac arrhythmias secondary to digitalis intoxication and – as a complication of cerebral and coronary angiography.

• Many reports have suggested a vascular causal factor.

• Bilateral hippocampal and parahippocampal complex ischemia in the distribution of the posterior cerebral arteries or cortical spreading depression of migrainous origin in these areas are potential mechanisms.

• Others have suggested an epileptic causal factor for a minority of patients.

• Venous hypertension with transient hypoxemia in the context of incompetent internal jugular vein valves has also been suggested as a possible mechanism for TGA.

• Transient amnesias have been divided into :– Pure TGA– Probable epileptic amnesia and – probable transient ischemic amnesia.

• In contrast to patients with TIAs, the prognosis of persons with pure TGA is benign, with no apparent increased risk for vascular endpoints.

• Recurrences are uncommon. • Extensive evaluations are not usually required except to

distinguish TGA from TIA or seizures. • Treatment with platelet antiaggregants is not indicated in

most patients unless there is a suspicion for transient ischemic amnesia.

• The use of prophylactic calcium channel blockers may be justified in patients with a potential migrainous causal factor.

• Drop attacks are characterized by the sudden loss of muscle tone and strength.

• The attacks cause the patients to unexpectedly fall to the ground.

• Consciousness is preserved. • Most attacks occur while standing or walking and often follow

head or neck motion. • Considered a symptom of vertebrobasilar ischemia• Many patients may have other coexistent disorders.

• Rarely may be caused by ischemia of the corticospinal tract or reticular formation.

• However, isolated drop attacks are seldom a manifestation of vertebrobasilar occlusive disease.

• In most instances these attacks are secondary to akinetic seizures, high cervical spine or foramen magnum lesions, postural hypotension, Tumarkin otolithic crises (in Ménière disease), or near syncope of cardiac origin.