PRACTICAL ISSUES IN ACUTE STROKE Stroke 101

1. PRACTICAL ISSUES IN ACUTE STROKE(Stroke 101) MURRAY FLASTER M.D.,Ph.D. UNIVERSITY OF NEVADA SCHOOL OF MEDICINE 12-1-08 INTERNAL MEDICINE RESIDENT’S CONFERENCE

2. OVERVIEW RAPID STROKE EXAMINATION/PERTINENT HISTORY. SCAN (CT OR MR GRE). IV TPA? LARGE VESSEL ROADMAP. FURTHER TREATMENT OPTIONS: INTRAARTERIAL TPA, MECHANICAL DISRUPTION WITH SPECIAL CATHETERS (“PENUMBRA”, “MERCI RETRIEVER” OR ANGIOPLASTY) OR ?NEUROPROTECTANTS (AS IN HIGH DOSE ALBUMIN IN ALIAS TRIAL). THERAPUTIC ULTRASOUND (AS IN CLOTBUST ALEXANDROV et.al. NEJM 2004 351 2170). CONFIRM STROKE ANATOMY/ FIND ETIOLOGY (DW MRI ETC.) PREVENT FUTURE EVENTS: LARGE VESSEL CERVICAL AND INTRACRANIAL DISEASE, CARDIAC SOURCES, SMALL VESSEL ANGIOPATHY. TIA RISK FACTOR EVALUATION AND MODIFICATION

3. LET’S THINK ABOUT IV TPA.

4. THE MANY Ss OF THE ACUTE STROKE PRESENTATION ISCHEMIC STROKE HEMORRHAGIC STROKE IPH, SAH, SDH SEIZURES AND RECURRENT SPELLS UNWITNESSED SEIZURE POST-SEIZURE PARALYSIS COMPLEX PARTIAL SEIZURES WITH FOCAL FEATURES, ESPECIALLY APHASIA TRANSIENT GLOBAL AMNESIA SEPSIS STUPOR AND DELERIUM METABOLIC COMA, DRUG ASSOCIATED STATES, HYPOGLYCEMIA. THE DOUBLE FAKEOUT OF THALAMIC OR MIDBRAIN STROKE (RAS). SYNCOPE ESPECIALLY IN THE SETTING OF PRIOR NEUROLOGIC DEFICITS SEPHALGIAS, ESPECIALLY COMPLICATED MIGRAINE AND HYPERTENSIVE CRISIS (PRES) SEPHALITIS AND CEREBRAL INFLAMMATORY DISEASES SPACE OCCUPYING LESIONS SEREBRAL VASCULITIS PSEUDO-STROKE (CONVERSION DISORDERS)

5. THE MANY Ss OF THE ACUTE STROKE PRESENTATION ISCHEMIC STROKE HEMORRHAGIC STROKE IPH, SAH, SDH SEIZURES AND RECURRENT SPELLS UNWITNESSED SEIZURE POST-SEIZURE PARALYSIS COMPLEX PARTIAL SEIZURES WITH FOCAL FEATURES, ESPECIALLY APHASIA TRANSIENT GLOBAL AMNESIA SEPSIS STUPOR AND DELERIUM METABOLIC COMA, DRUG ASSOCIATED STATES, HYPOGLYCEMIA. THE DOUBLE FAKEOUT OF THALAMIC OR MIDBRAIN STROKE (RAS). SYNCOPE ESPECIALLY IN THE SETTING OF PRIOR NEUROLOGIC DEFICITS ENCEPHALGIAS, ESPECIALLY COMPLICATED MIGRAINE AND HYPERTENSIVE CRISIS (PRES) ENEPHALITIS AND CEREBRAL INFLAMMATORY DISEASES SPACE OCCUPYING LESIONS CEREBRAL VASCULITIS PSEUDO-STROKE (CONVERSION DISORDERS)

6. CASE A 54 y/o DIABETIC MAN COMES TO THE ED WITH ONE HOUR OF SLURRED SPEECH AND RIGHT FACIAL WEAKNESS. HE REPORTS VAGUELY NOT FEELING WELL WITH DECREASED APPETITE SINCE THE LATE MORNING. HE IS MILDLY HYPERTENSIVE (160s/90s), AFEVRILE AND HIS NIHSS IS 3. CTH SUGGESTS MILD DEEP WHITE MATTER CHANGES ONLY, CBC AND PT/PTT ARE NORMAL, BMP IS DELAYED IN THE LAB AS IS THEREFORE CT ANGIOGRAM. THERE ARE NO RECENT SURGERIES OR OTHER CONTRAINDICATIONS TO ACUTE THROMBOTICS. CAN WE TREAT? FINGERSTICK GLUCOSE IS 56 AND D50 REVERSES THE DEFICIT.

7. IV TPA

8. THE END OF GIVE THEM AN ASPIRIN AND I’LL SEE THEM IN THE MORNING.THE END OF GIVE THEM AN ASPIRIN AND I’LL SEE THEM IN THE MORNING.

9. NINDS Study: rtPAin Acute Ischemic Stroke Double-blind, placebo-controlled, randomized 2-part study1 IV rtPA, 0.9 mg/kg, <3 hrs, 10% bolus, 90% over 1 h1 624 patients treated within 3 hours of stroke onset1 32% more rtPA patients had minimal or no disability (Barthel index)1 Odds ratio of good outcome at 6 and 12 months: 1.72 Intracranial hemorrhage by 36 h: 6.4% rtPA, 0.6% placebo (P<.001)1 Mortality by 3 months: 17% rtPA, 21% placebo1 In 1995, the 2-part NINDS Recombinant Tissue Plasminogen Activator Stroke Study found patients treated with rtPA within 3 hours of stroke onset were at least 30% more likely than patients given placebo to have minimal or no disability according to scores on the modified Rankin scale 3 months after the stroke. The trial had 2 parts: in Part 1, investigators looked for any clinical activity by rtPA as indicated by an improvement of 4 points over baseline values in the score of the National Institutes of Health stroke scale (NIHSS) or resolution of the neurologic deficit within 24 hours of stroke onset. Part 2 used a global test statistic to assess clinical outcome at 3 months, according to scores on the Barthel index, modified Rankin scale, Glasgow outcome scale, and NIHSS. No significant difference was found between the rtPA and the placebo groups in the percentages of patients with neurologic improvement at 24 hours. A benefit was, however, observed for all 4 outcome measures at 3 months and in a combined post-hoc analysis, confirming the long-term clinical benefit of rtPA; global odds ratio for a favorable outcome was 1.7 (95% CI, 1.2 to 2.6; P=.008). Symptomatic intracerebral hemorrhage within 36 hours after stroke onset occurred in 6.4% of patients given rtPA but only in 0.6% of placebo patients (P<.001). Mortality at 3 months was 17% in the rtPA group and 21% in the placebo group (P=.30). In 1995, the 2-part NINDS Recombinant Tissue Plasminogen Activator Stroke Study found patients treated with rtPA within 3 hours of stroke onset were at least 30% more likely than patients given placebo to have minimal or no disability according to scores on the modified Rankin scale 3 months after the stroke. The trial had 2 parts: in Part 1, investigators looked for any clinical activity by rtPA as indicated by an improvement of 4 points over baseline values in the score of the National Institutes of Health stroke scale (NIHSS) or resolution of the neurologic deficit within 24 hours of stroke onset. Part 2 used a global test statistic to assess clinical outcome at 3 months, according to scores on the Barthel index, modified Rankin scale, Glasgow outcome scale, and NIHSS. No significant difference was found between the rtPA and the placebo groups in the percentages of patients with neurologic improvement at 24 hours. A benefit was, however, observed for all 4 outcome measures at 3 months and in a combined post-hoc analysis, confirming the long-term clinical benefit of rtPA; global odds ratio for a favorable outcome was 1.7 (95% CI, 1.2 to 2.6; P=.008). Symptomatic intracerebral hemorrhage within 36 hours after stroke onset occurred in 6.4% of patients given rtPA but only in 0.6% of placebo patients (P<.001). Mortality at 3 months was 17% in the rtPA group and 21% in the placebo group (P=.30).

10. Overall Benefits and Risks of IV tPA for Stroke Benefit: Neurologically normal at 3 months1 55% relative increase; 12% absolute increase Robust effect2: NNT to cure=7 Risk of symptomatic ICH: 6.4%1 Overall benefits in spite of the ICHs Risk of ICH can be reduced by closely following tPA protocol Benefit using nihss at 3 mos.Benefit using nihss at 3 mos.

11. THE EARLIER THE BETTER!

12. WHAT IF IT’S A LITTLE STROKE? WHAT IF IT’S A REALLY BIG STROKE?

13. NINDS Trial: Stroke Subtypes Favorable outcomes at 3 months as measured on the Barthel index (minimal or no disability, scored as 95 or 100) are shown here by stroke subtype. Of rtPA patients with lacunar (small-vessel occlusive) stroke 75% had a favorable outcome at 3 months vs only 50% of placebo patients at 3 months. In those patients who had atherothrombotic (large-vessel occlusive) stroke, 49% of those treated with rtPA had a favorable outcome at 3 months vs only 36% of patients given placebo. Similar results were seen in cardioembolic stroke patients; 46% of rtPA patients had a favorable outcome at 3 months vs only 37% of patients given placebo.1 A follow-up study analyzed data for these patients at 6 and at 12 months and found no interaction between stroke subtype at baseline and treatment, suggesting these rates are stable after the initial 3-month study period.2 Favorable outcomes at 3 months as measured on the Barthel index (minimal or no disability, scored as 95 or 100) are shown here by stroke subtype. Of rtPA patients with lacunar (small-vessel occlusive) stroke 75% had a favorable outcome at 3 months vs only 50% of placebo patients at 3 months. In those patients who had atherothrombotic (large-vessel occlusive) stroke, 49% of those treated with rtPA had a favorable outcome at 3 months vs only 36% of patients given placebo. Similar results were seen in cardioembolic stroke patients; 46% of rtPA patients had a favorable outcome at 3 months vs only 37% of patients given placebo.1 A follow-up study analyzed data for these patients at 6 and at 12 months and found no interaction between stroke subtype at baseline and treatment, suggesting these rates are stable after the initial 3-month study period.2

14. rtPA in Ischemic Stroke: Guidelines Non–tPA-eligible patient characteristics: Rapidly improving or NIHSS <4 or >221-3 Major surgery <14 d1-3 Suspected subarachnoid hemorrhage1-3 Systolic BP >185, diastolic BP >1101-3 Gastrointestinal or urinary tract hemorrhage <21 d, arterial puncture <7 d, use of heparin, seizure at stroke onset1-3 INR ?1.5, platelets ?100K, glucose ?50, >4001-3 These guidelines reflect a consensus among experts from the American Academy of Neurology1 and the Stroke Council of the American Stroke Association.2 The large number of exclusion criteria for tPA precludes treating up to 99% of patients with acute ischemic stroke3; efficacy of thrombolytic therapy when administered >3 hours after stroke onset has not been demonstrated, but studies are ongoing.4These guidelines reflect a consensus among experts from the American Academy of Neurology1 and the Stroke Council of the American Stroke Association.2 The large number of exclusion criteria for tPA precludes treating up to 99% of patients with acute ischemic stroke3; efficacy of thrombolytic therapy when administered >3 hours after stroke onset has not been demonstrated, but studies are ongoing.4

15. rtPA in Ischemic Stroke: Guidelines Non–tPA-eligible patient characteristics: Rapidly improving or NIHSS <4 or >221-3 (BUT UTILITY TO THE PARTICULAR PATIENT IS FIRST CONSIDERATION). Major surgery <14 d1-3 Suspected subarachnoid hemorrhage1-3 (AS IN PICA ANEURYSM, FOR EXAMPLE, CAN YOU GIVE THROMBOLYTIC TO PATIENT WITH A SACCULAR ANEURYSM?) Systolic BP >185, diastolic BP >1101-3 (TREAT!) Gastrointestinal or urinary tract hemorrhage <21 d, arterial puncture <7 d, use of heparin, seizure at stroke onset1-3 INR ?1.5, platelets ?100K, glucose ?50, >4001-3 WHEN IMAGING GUIDES YOU, BLACK BOX RULES CAN BE BENT! These guidelines reflect a consensus among experts from the American Academy of Neurology1 and the Stroke Council of the American Stroke Association.2 The large number of exclusion criteria for tPA precludes treating up to 99% of patients with acute ischemic stroke3; efficacy of thrombolytic therapy when administered >3 hours after stroke onset has not been demonstrated, but studies are ongoing.4These guidelines reflect a consensus among experts from the American Academy of Neurology1 and the Stroke Council of the American Stroke Association.2 The large number of exclusion criteria for tPA precludes treating up to 99% of patients with acute ischemic stroke3; efficacy of thrombolytic therapy when administered >3 hours after stroke onset has not been demonstrated, but studies are ongoing.4

16. CONCLUSIONS TREATMENT WITH IV TPA IS EFFECTIVE. DECISION MAKING SHOULD BE MADE WITH AWARENESS OF THE GUIDELINES. THE EARLIER THE TREATMENT, THE BETTER THE OUTCOME. TREATMENT UNDER 90 MINUTES MAY BE PARTICULARLY EFFICACIOUS. IV TPA COUPLED WITH IA THERAPY, MECHANICAL THERAPIES AND OTHER ADJUVANTS REMAIN WORKS IN PROGRESS, MAY OFFER SIGNIFICANT BENEFITS BUT SHOULD BE RESTRICTED TO EXPERIMENTAL PROTOCOLS.. IV TREATMENT BEYOND THE THREE HOUR WINDOW ALSO REMAINS A WORK IN PROGRESS BUT RECENT WORK SUGGESTS WE MAY EXPAND THE WINDOW TO 4.5 HOURS IN SOME CASES. (WHEN AND IF OFFERED, SHOULD BE CLEARLY DISCUSSED AS OUTSIDE OF GUIDELINES.)

17. LARGE VESSEL ROADMAPS CATHETER CEREBRAL ANGIOGRAPHY ULTRASOUND CAROTID TRANSCRANIAL MR ANGIOGRAPHY CT ANGIOGRAPHY

18. WHY GET LARGE VESSEL ROADMAPS? CUTOFFS INTRACRANIAL OCCLUSIONS DUE TO EMBOLIC THROMBUS OR STENOSIS DUE TO OTHER CAUSE EXTRACRANIAL DISEASE

19. A 36 Y/O LADY DEVELOPED CONFUSED AND HALTING SPEECH WHILE ON THE TELEPHONE. ON ARRIVAL TO THE ED HER SYMPTOMS CLEARED BUT THEN REAPPEARED. BOTH EXPRESSIVE AND AT TIMES GLOBAL APHASIA APPEARED TO BE PRESENT TOGETHER WITH RIGHT UPPER EXTREMITY AND FACIAL WEAKNESS. CT SCAN OF THE HEAD WAS UNREMARKABLE AND CT ANGIOGRAM OF THE HEAD AND NECK WERE NORMAL WITH THE EXCEPTION OF THE LEFT MCA WHERE A DISTAL M1 FILLING DEFECT WAS SUSPECTED. HER INITIAL SYMPTOMS BEGAN AT ABOUT 1:15 PM, SHE WAS ASSYMPTOMATIC AFTER ED ARRIVAL AT 4:30 PM, AND THEN HER SYMPTOMS REAPPEARRED. HER INITIAL EVALUATION WAS COMPLETED BY 5:00 PM.

40. SO FLIUDS AND BLOOD PRESSURE ARE OFTEN CRUCIAL. BASED ON HER EXAM AND HISTORY SHE RECEIVED IV TPA. WHEN SHE CONTINUED TO FLUCTUATE IV FLUIDS WERE INCREASED AND SHE WAS PLACED ON PRESSORS. (SOME WOULD CONSIDER MECHANICAL THROMBOLYSIS AT THIS POINT.). SHE STABILIZED OVER 48 HOURS, MADE A COMPLETE RECOVERY, AND RETURNED TO WORK AS A FLIGHT ATTENDANT ONE MONTH LATER. REPEAT MRA EVENTUALLY SHOWED COMPLETE RESOLUTION OF THE FLOW IRREGULARITY. SMOKING AND BCPs WERE THE ONLY RISK FACTORS FOUND AFTER EXHAUSTIVE WORK-UP.

41. CAROTID STENOSIS RISK ASSESSMENT CEA STENT (SAPPHIRE, CREST)

42. LARGE VESSEL INTRACRANIAL DISEASE ESTIMATES OF ANNUAL INCIDENCE 8% TO 10% OF ISCHEMIC STROKES. STROKE RECURRENCE RATES ARE HIGH IN THIS GROUP OF PATIENTS, PERHAPS UP TO 15% YEARLY. IN WASID (CHIMOWITZ et.al NEJM 2005 325 1305) ISCHEMIC RISK IN THE INDEX TERRITORY WAS 12% FOR ASA AND 11% FOR WARFARIN WHILE OVERALL ISCHEMIC RISK WAS 15% IN THE FIRST YEAR. WASID CLEARLY SHOWED WAFARIN WAS OF NO BENEFIT (HEMORRHAGIC RISK 2.55 FOLD GREATER, P=0.01). INTERESTINGLY, MI WAS MORE FREQUENT IN THE WARFARIN GROUP (RR 2.5, P=0.02). STENTS MAY WORK. CURRENT ESTIMATE OF PERIPROCEDURAL RISK 7% TO 10% WHEN WINGSPAN STENT IS EMPLOYED. SAMMPRIS TRIAL NOW UNDERWAY TO TEST THIS HYPOTHESIS.

43. ATRIAL FIBRILLATION THE SINGLE LARGEST CAUSE OF STROKE IN OLDER PATIENTS, PERHAPS 30% OF STROKE PATIENTS OVER AGE 80. STROKE RISK INCREASES WITH AGE AND MAY REACH AS HIGH AS 10-20% YEARLY IN PATIENTS ABOVE AGE 75 WITH OTHER RISK FACTORS.. EMBOLIC INFARCTS SECONDARY TO ATRIAL FIBRILLATION ARE OFTEN LARGE, CORTICAL AND DEVASTATING. WAFARIN REDUCES STROKE RISK BY AS MUCH AS 80% IN SOME STUDIES. METAANALYSIS OF THE MAJOR CLASS I TRIALS YIELDS A 68% RISK REDUCTION. WAFARIN RISK PROFILE IS HIGH SO IT MUST BE USED VERY CAREFULLY. ESPECIALLY CLOSE MONITORING IS NEEDED IN PATIENTS WITH DEMENTIA OR GAIT DISTRUBANCE BUT OVERWITHOLDING OF TREATMENT IS PROBABLY MORE COMMON THAN OVERTREATMENT IN GENERAL CLINICAL PRACTICE. HISTORIC SIGNIFICANT BLEED RATES UP TO 4% ANNUALLY BUT RECENT TRIALS (TARGET INR 2.5) YIELDED RATES OF 1-2%.

44. TIA

45. Half of 90 day stroke risk is incurred in the first 2 days.(5.3% at 48hrs)Half of 90 day stroke risk is incurred in the first 2 days.(5.3% at 48hrs)

46. STROKE AFTER TIA IN ONTARIO, CANADA

47. IN ONTARIO CANADA, STROKE RISK WAS 4% AT 2 DAYS AND 8% AT 3 MONTHS WHILE HOSPITAL READMIT RATE BY 30 DAYS WAS 32% (CMAJ 2004 170 1099) . OXFORD VASCULAR STUDY FOUND AN 8% STROKE RISK AT 7 DAYS AND A 17% RISK AT 3 MONTHS (BMJ 2004 328, 326). IN SOUTHWEST GERMANY, STROKE RISK WAS 8% AVERAGED OVER 10 DAYS AND 13% OVER 6 MONTHS WITH 38% DEPENDENT (mRS > 2) AT 6 MONTHS (STROKE 2004 35, 2435). GREATER CINCINNATI/NORTHERN KENTUCY STROKE STUDY FOUND A 2 DAY STROKE OR TIA RISK OF 6% AND A 3 MONTH RISK OF 23% (STROKE 2005 36, 1). IN SOUTH TEXAS, STROKE RISK WAS ONLY 1.6% AT 2 DAYS AND 4% AT 90 DAYS (STROKE 2004 35, 1842) , BUT ASCERTAINMENT METHODOLOGY MAY HAVE DIFFERED SIGNIFICANTLY. CONCENSUS NOW IS ATLEAST 10% STROKE RISK AT 3 MONTHS WITH ATLEAST HALF OF THAT RISK IN FIRST 48 HOURS. STROKE RISK AFTER TIA IN OTHER STUDIES

48. CONCLUSIONS (2008) PATIENTS WITH TIA ARE AT HIGH EARLY RISK OF STROKE AND OTHER VASCULAR EVENTS. THE 2 DAY RISK OF STROKE MAY BE AS HIGH AS 5% WHILE THE 90 DAY RISK OF STROKE AS HIGH AS 10%. WE BELIEVE KEEPING THESE PATIENTS IN THE ED AND RAPIDLY EVALUATING AND MODIFYING THEIR STROKE RISKS IS APPROPRIATE. THIS POLICY IS NOW EXPLICITLY SUPPORTED BY EVIDENCE BASED OUTCOME STUDIES. WE BELIEVE STROKE NETWORKS WHERE EASILY DIFFUSABLE TECHNOLGY IS COMBINED WITH CENTERS OF EXCELLENCE WOULD BEST SERVE THE POPULATION AT RISK.

49. RISK FACTOR CONTROL HYPERTENSION HYPERGLYCEMIA TOBACCO ABUSE HYPERLIPIDEMIA and STATIN THERAPY EPIDEMIOLOGICAL STUDIES HAVE NOT SHOWN A DIRECT LINK BETWEEN ELEVATED SERUM CHOLESTEROL AND STROKE COPARABLE TO THE TIGHT LINK TO CAD. BUT NUMEROUS STUDIES OF STATIN THERAPY AND CAD HVE SHOWN REDUCTIONS IN STROKE RISK AS A SECONDARY ENDPOINT. HIGH-DOSE ATORVASTATIN AFTER STROKE OR TIA (SPARCL ) TRIAL (NEJM 2006 355 549) . 4700 RECENT STROKE PATIENTS WITHOUT KNOWN CAD WERE RANDOMIZED TO 8O MG OF STATIN OR PLACEBO AND FOLLOWED FOR 5YEARS. (LDL WAS BETWEEN 100 AND 190 mg/dl.) RELATIVE 5 YEAR STROKE RISK WAS REDUCED BY 16% WHILE COMPOSITE MAJOR CARDIOVASCULAR OR STROKE RELATIVE RISK WAS REDUCED BY 20%. THERE WAS A SMALL INCREASE IN HEMORRHAGIC STROKE RISK.

51. THANK YOU.

52. RISK SUMMARY STUDY MED/SURG RISK ABSOLUTE NNT PERIOP NASCET >70% 26%/9% 17% 6 5.8% ECST >70% 20%/7% 13% 8 5.6% NASCET >50% 22%/16% 6.5% 15 6.9% (2 YEAR CUMULATIVE RISK) ACAS >60% 11%/5% 6% 17 2.6% (5 YEAR CUMULATIVE RISK)

53. Carotid Endarterectomy Three angiographic methods (ECST [European Carotid Surgery Trial], NASCET [North American Symptomatic Carotid Endarterectomy Trial], and CC [common carotid]) were compared for grading of carotid stenosis. The correlation between angiographic and ultrasound findings was also examined. Investigators found that measurements using the CC method were the most reproducible and those using the NASCET method the least. ECST and CC methods yielded almost identical results (97% agreement). Three angiographic methods (ECST [European Carotid Surgery Trial], NASCET [North American Symptomatic Carotid Endarterectomy Trial], and CC [common carotid]) were compared for grading of carotid stenosis. The correlation between angiographic and ultrasound findings was also examined. Investigators found that measurements using the CC method were the most reproducible and those using the NASCET method the least. ECST and CC methods yielded almost identical results (97% agreement).

54. SAPPHIRE AT 1 YEAR PRIMARY ENDPOINT STENTING 12.2% PRIMARY ENDPOINT CEA 20.1% P= 0.004 FOR NONINFERIORITY CONCLUSION STENTING WITH PROTECTION SHOULD BE CONSIDERED IN HIGH RISK SURGICAL PATIENTS.

55. SMALL VESSEL ISCHEMIC ANGIOPATHY CAUSES 20-25% OF ISCHEMIC STROKES. USUALLY INVOLVES DEEP PENETRATING VESSELS, ARTERIOLES IN THE 200 TO 50 MICRON RANGE AND RESULTS IN “LACUNAR” INFARCTS USUALLY LESS THAN 1 CM IN DIAMETER. SMALL VESSEL ANGIOPATHY MAY RESULT IN EITHER ISCHEMIC OR HEMORRHAGIC INJURY, SOMETIMES IN THE SAME PATIENT. DIFFUSE (MORE SUBTLE?) CHRONIC SMALL VESSEL HYPOPERFUSION RESULTS IN PERIVENTRICULAR DEEP WHITE MATTER CHANGES OR LEUKOARIOSIS.

56. EVIDENCE OF TIA RISK FROM OTHER STUDIES GREATER CINCINNATI/NORTHERN KENTUCY STROKE STUDY FOUND A 2 DAY STROKE OR TIA RISK OF 6% AND A 3 MONTH RISK OF 23% (STROKE 2005 36, 1). OXFORD VASCULAR STUDY FOUND AN 8% STROKE RISK AT 7 DAYS AND A 17% RISK AT 3 MONTHS (BMJ 2004 328, 326). IN SOUTHWEST GERMANY, STROKE RISK WAS 8% AVERAGED OVER 10 DAYS AND 13% OVER 6 MONTHS WITH 38% DEPENDENT (mRS > 2) AT 6 MONTHS (STROKE 2004 35, 2435). IN SOUTH TEXAS, STROKE RISK WAS ONLY 1.6% AT 2 DAYS AND 4% AT 90 DAYS (STROKE 2004 35, 1842), BUT ASCERTAINMENT METHODOLOGY MAY HAVE DIFFERED.

57. CONCLUSIONS PATIENTS WITH TIA ARE AT HIGH EARLY RISK OF STROKE AND OTHER VASCULAR EVENTS. THE 2 DAY RISK OF STROKE MAY BE AS HIGH AS 5% WHILE THE 90 DAY RISK OF STROKE AS HIGH AS 10%. WE BELIEVE KEEPING THESE PATIENTS IN THE ED AND RAPIDLY EVALUATING AND MODIFYING THEIR STROKE RISKS IS APPROPRIATE. OTHERS HAVE DEVELOPED TIA CLINIC STRATEGIES. THESE STRATEGIES MAY HAVE “REAL WORLD” DRAWBACKS. THESE POLICY ALTERNATIVES NEED TO BE EXPLICITLY VALIDATED BY EVIDENCE BASED OUTCOME STUDIES.