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AHA/ASA Scientific Statement Definitionand Evaluation of Transient Ischemic Attack The American Academy of Neurology affirms the value of this statement as an educational tool for neurologists.  Stroke. 2009;40:2276-2293
Traditional Definition  Transient Ischemic Attack (TIA) was a sudden, focal neurologicaldeficit of presumed vascular origin lasting <24 hours. Reversible ischemic neurological deficit was applied to events lasting 24 hours to 7 days. Only symptomsenduring >7 days were thought to reliably indicate infarctionand received the designation stroke.
2002 AHA-Endorsed Revised Definition of TIA Transient ischemic attack (TIA):  a transient episode of neurologicaldysfunction caused by focal brain, spinal cord, or retinal ischemia,without acute infarction. Patients with TIAs are at high risk of earlystroke, and their risk may be stratified by clinical scale,vessel imaging, and diffusion MRI.
Arguments in Favor the New Definition The classic 24-hour definition is misleading in that many patientswith transient <24-hour events actually have associated cerebralinfarction. The traditional definition can impede the administration ofacute stroke therapies. A 24-hour limit for transiently symptomatic cerebral ischemicis arbitrary and not reflective of the typical duration of theseevents. Disease definitions in clinical medicine, including those forischemic injuries, are most useful when tissue based.
Arguments Against the New Definition The new definition requires brain imaging that will vary dependingon the availability of imaging resources. Stroke and TIA incidencerates will differ depending on whether and when detailed imagingstudies are performed. Stroke and TIA rates will not be directly comparable to previouslydefined rates if the new definition is adopted. Primary care physicians may be confused as to whether to designatea presumed transient event of brain ischemia a stroke or TIAif they do not have immediate access to neuroimaging or otherdiagnostic resources.
Risk Stratification Patients with suspectedTIA should be evaluated as soon as possibleafter an event (ClassI, Level of Evidence B). Patients with TIAs are at high risk of earlystroke, and their risk may be stratified by clinical scale,vessel imaging, and diffusion MRI.
The California score and the ABCD 2  scores  Patients with TIA score points (indicatedin parentheses) for each of the following factors:  Age ≥60 years(1) Blood pressure ≥140/90 mmHg on first evaluation (1)  Clinicalsymptoms of focal weakness with the spell (2) or  speech impairmentwithout weakness (1) Duration ≥60 minutes (2) or 10 to 59 minutes(1) Diabetes (1) 	In combined validation cohorts, the 2-dayrisk of stroke was  ABCD 2  scores : 	0 or 1	 0% ABCD 2  scores : 	2 or 3	  1.3% ABCD 2  scores :4 or 5	  4.1% ABCD 2  scores :	6 or 7	  8.1%
Hospitalization It is reasonable tohospitalize patients with TIA if they present within 72 hoursof the event and any of the following criteriaare present:    ABCD 2  scores of 3 (Class IIa,Level of EvidenceC). ABCD 2  scores of0 to 2 and uncertaintythatdiagnostic workup can be completedwithin 2 days as anoutpatient (Class IIa, Level of EvidenceC). ABCD 2  scores of 0 to 2 and other evidencethat indicates thepatient’s event was caused by focalischemia (Class IIa,Level of Evidence C).
Hospitalization Patients with TIA or minor stroke who have DWI lesions,especially when multiple, are at higher risk of recurrent ischemicevents.  The presence of large-vessel occlusion is also a predictorof new events. MRI can help to triage patients with TIA or minorstroke.  In addition, it can help to determine which TIA patientsto admit to hospital, and it may help in identifying patientsto treat with more aggressive therapies.  DWI also can assist with stroke localization and understandingthe mechanism of the stroke.
Frequency of DWI Abnormality in Patients With Transient Neurological Episodes of Different Durations: Pooled Data From 10 MRI Studies Enrolling 818 Patients
Diagnostic Evaluation Goals of modern neuroimaging evaluation of TIA: to obtain evidence of a vascular origin for thesymptoms either directly (evidence of hypoperfusion and/or acuteinfarction) or indirectly (identification of a presumptive sourcesuch as a large-vessel stenosis) to exclude an alternativenonischemic origin to ascertain the underlying vascularmechanism of the event (eg, large-vessel atherothrombotic, cardioembolic,small-vessel lacunar), which allows selection of theoptimal therapy to identify prognostic outcome categories
Patients with TIA should preferably undergo neuroimaging evaluationwithin 24 hours of symptom onset.  MRI, including DWI, is thepreferred brain diagnostic imaging modality.  If MRI is not available,CT should be performed (Class I, Level of Evidence B).
Noninvasive imaging of the cervicocephalic vessels shouldbeperformed routinely as part of the evaluation of patientswithsuspected TIAs (Class I, Level of Evidence A).
Noninvasivetesting of the intracranial vasculature reliablyexcludes thepresence of intracranial stenosis (Class I, Levelof EvidenceA) and is reasonable to obtain when knowledge ofintracranialsteno-occlusive disease will alter management. Reliable diagnosisof the presence and degree of intracranialstenosis requiresthe performance of catheter angiography toconfirm abnormalitiesdetected with noninvasive testing.
Initial assessment of the extracranial vasculature may involveany of the following: carotid ultrasound/ transcranialDoppler (CUS/TCD), MRA, or CTA, depending on localavailability and expertise, and characteristics of the patient(Class IIa, Level of Evidence B).
If only noninvasive testingis performed before endarterectomy,it is reasonable to pursue2 concordant noninvasive findings;otherwise, catheter angiographyshould be considered (ClassIIa, Level of Evidence B).
Therole of plaque characteristics and detection of microembolic signals (MESs) isnotyet defined (Class IIb, Level of Evidence B).
ECG should occuras soon as possible after TIA (Class I, Levelof Evidence B). Prolonged cardiac monitoring (inpatient telemetryor Holtermonitor) is useful in patients with an unclear originafterinitial brain imaging and electrocardiography (Class IIa,Levelof Evidence B).
Echocardiography (at least TTE) is reasonablein the evaluationof patients with suspected TIAs, especiallyin patients in whomno cause has been identified by other elementsof the workup(Class IIa, Level of Evidence B).  TEE is useful in identifyingpatent foramen ovale (PFO), aortic arch atherosclerosis, and valvulardisease and isreasonable when identification of these conditionswill altermanagement (Class IIa, Level of Evidence B).
Routine Blood Tests Routineblood tests (CBC, chemistry panel,PT and aPPT, and fastinglipid panel)are reasonable in the evaluation of patients withsuspectedTIAs (Class IIa, Level of Evidence B).
Optional Coagulation Screening Tests (Consider in Younger Patients With TIAs, Particularly When No VascularRisk 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 Anticardiolipinantibody  Lupus anticoagulant Homocysteine Prothrombingene G20210A mutation  Factor VIII  Von Willebrand factor  Plasminogenactivator inhibitor-1  Endogenous tissue plasminogen activator activity

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Definition and Evaluation of Transient Ischemic Attack

  • 1. AHA/ASA Scientific Statement Definitionand Evaluation of Transient Ischemic Attack The American Academy of Neurology affirms the value of this statement as an educational tool for neurologists. Stroke. 2009;40:2276-2293
  • 2.
  • 3. Traditional Definition Transient Ischemic Attack (TIA) was a sudden, focal neurologicaldeficit of presumed vascular origin lasting <24 hours. Reversible ischemic neurological deficit was applied to events lasting 24 hours to 7 days. Only symptomsenduring >7 days were thought to reliably indicate infarctionand received the designation stroke.
  • 4. 2002 AHA-Endorsed Revised Definition of TIA Transient ischemic attack (TIA): a transient episode of neurologicaldysfunction caused by focal brain, spinal cord, or retinal ischemia,without acute infarction. Patients with TIAs are at high risk of earlystroke, and their risk may be stratified by clinical scale,vessel imaging, and diffusion MRI.
  • 5. Arguments in Favor the New Definition The classic 24-hour definition is misleading in that many patientswith transient <24-hour events actually have associated cerebralinfarction. The traditional definition can impede the administration ofacute stroke therapies. A 24-hour limit for transiently symptomatic cerebral ischemicis arbitrary and not reflective of the typical duration of theseevents. Disease definitions in clinical medicine, including those forischemic injuries, are most useful when tissue based.
  • 6. Arguments Against the New Definition The new definition requires brain imaging that will vary dependingon the availability of imaging resources. Stroke and TIA incidencerates will differ depending on whether and when detailed imagingstudies are performed. Stroke and TIA rates will not be directly comparable to previouslydefined rates if the new definition is adopted. Primary care physicians may be confused as to whether to designatea presumed transient event of brain ischemia a stroke or TIAif they do not have immediate access to neuroimaging or otherdiagnostic resources.
  • 7. Risk Stratification Patients with suspectedTIA should be evaluated as soon as possibleafter an event (ClassI, Level of Evidence B). Patients with TIAs are at high risk of earlystroke, and their risk may be stratified by clinical scale,vessel imaging, and diffusion MRI.
  • 8. The California score and the ABCD 2 scores Patients with TIA score points (indicatedin parentheses) for each of the following factors: Age ≥60 years(1) Blood pressure ≥140/90 mmHg on first evaluation (1) Clinicalsymptoms of focal weakness with the spell (2) or speech impairmentwithout weakness (1) Duration ≥60 minutes (2) or 10 to 59 minutes(1) Diabetes (1) In combined validation cohorts, the 2-dayrisk of stroke was ABCD 2 scores : 0 or 1  0% ABCD 2 scores : 2 or 3  1.3% ABCD 2 scores :4 or 5  4.1% ABCD 2 scores : 6 or 7  8.1%
  • 9. Hospitalization It is reasonable tohospitalize patients with TIA if they present within 72 hoursof the event and any of the following criteriaare present:    ABCD 2 scores of 3 (Class IIa,Level of EvidenceC). ABCD 2 scores of0 to 2 and uncertaintythatdiagnostic workup can be completedwithin 2 days as anoutpatient (Class IIa, Level of EvidenceC). ABCD 2 scores of 0 to 2 and other evidencethat indicates thepatient’s event was caused by focalischemia (Class IIa,Level of Evidence C).
  • 10. Hospitalization Patients with TIA or minor stroke who have DWI lesions,especially when multiple, are at higher risk of recurrent ischemicevents. The presence of large-vessel occlusion is also a predictorof new events. MRI can help to triage patients with TIA or minorstroke. In addition, it can help to determine which TIA patientsto admit to hospital, and it may help in identifying patientsto treat with more aggressive therapies. DWI also can assist with stroke localization and understandingthe mechanism of the stroke.
  • 11. Frequency of DWI Abnormality in Patients With Transient Neurological Episodes of Different Durations: Pooled Data From 10 MRI Studies Enrolling 818 Patients
  • 12. Diagnostic Evaluation Goals of modern neuroimaging evaluation of TIA: to obtain evidence of a vascular origin for thesymptoms either directly (evidence of hypoperfusion and/or acuteinfarction) or indirectly (identification of a presumptive sourcesuch as a large-vessel stenosis) to exclude an alternativenonischemic origin to ascertain the underlying vascularmechanism of the event (eg, large-vessel atherothrombotic, cardioembolic,small-vessel lacunar), which allows selection of theoptimal therapy to identify prognostic outcome categories
  • 13. Patients with TIA should preferably undergo neuroimaging evaluationwithin 24 hours of symptom onset. MRI, including DWI, is thepreferred brain diagnostic imaging modality. If MRI is not available,CT should be performed (Class I, Level of Evidence B).
  • 14. Noninvasive imaging of the cervicocephalic vessels shouldbeperformed routinely as part of the evaluation of patientswithsuspected TIAs (Class I, Level of Evidence A).
  • 15. Noninvasivetesting of the intracranial vasculature reliablyexcludes thepresence of intracranial stenosis (Class I, Levelof EvidenceA) and is reasonable to obtain when knowledge ofintracranialsteno-occlusive disease will alter management. Reliable diagnosisof the presence and degree of intracranialstenosis requiresthe performance of catheter angiography toconfirm abnormalitiesdetected with noninvasive testing.
  • 16. Initial assessment of the extracranial vasculature may involveany of the following: carotid ultrasound/ transcranialDoppler (CUS/TCD), MRA, or CTA, depending on localavailability and expertise, and characteristics of the patient(Class IIa, Level of Evidence B).
  • 17. If only noninvasive testingis performed before endarterectomy,it is reasonable to pursue2 concordant noninvasive findings;otherwise, catheter angiographyshould be considered (ClassIIa, Level of Evidence B).
  • 18. Therole of plaque characteristics and detection of microembolic signals (MESs) isnotyet defined (Class IIb, Level of Evidence B).
  • 19. ECG should occuras soon as possible after TIA (Class I, Levelof Evidence B). Prolonged cardiac monitoring (inpatient telemetryor Holtermonitor) is useful in patients with an unclear originafterinitial brain imaging and electrocardiography (Class IIa,Levelof Evidence B).
  • 20. Echocardiography (at least TTE) is reasonablein the evaluationof patients with suspected TIAs, especiallyin patients in whomno cause has been identified by other elementsof the workup(Class IIa, Level of Evidence B). TEE is useful in identifyingpatent foramen ovale (PFO), aortic arch atherosclerosis, and valvulardisease and isreasonable when identification of these conditionswill altermanagement (Class IIa, Level of Evidence B).
  • 21. Routine Blood Tests Routineblood tests (CBC, chemistry panel,PT and aPPT, and fastinglipid panel)are reasonable in the evaluation of patients withsuspectedTIAs (Class IIa, Level of Evidence B).
  • 22. Optional Coagulation Screening Tests (Consider in Younger Patients With TIAs, Particularly When No VascularRisk 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 Anticardiolipinantibody Lupus anticoagulant Homocysteine Prothrombingene G20210A mutation Factor VIII Von Willebrand factor Plasminogenactivator inhibitor-1 Endogenous tissue plasminogen activator activity