Are patients with acutely recovered cerebral ischemia more unstable?
OBJECTIVE
Recent studies suggest that the short-term risk of stroke may be greater after transient ischemic attack (TIA) than after stroke.


METHODS
We compared risks of neurological deterioration in those with and without TIA in the National Institute of Neurological Disorders and Stroke (NINDS) tissue plasminogen activator (tPA) trial, a randomized trial of intravenous tPA given within 3 hours of onset of cerebral ischemia, after excluding those with cerebral hemorrhage and those dying before 90 days of causes other than new ischemic stroke. TIA was defined as a National Institutes of Health Stroke Scale (NIHSS) score of zero at 24 hours. We chose subsequent deterioration as our outcome, defined as a worsening on the NIHSS at 90 days compared with 24 hours, so that episodes of new ischemia that may have been attributed to other causes would be included.


RESULTS
Of 498 subjects meeting entry criteria, 40 (8%) had TIA. Subsequent deterioration occurred in 30% of those with TIA and 10% of others (P=0.001, Fisher exact test). In multivariable models with adjustment for age, sex, ethnicity, 24-hour NIHSS score, tPA administration, presumed stroke subtype, and baseline systolic blood pressure, temperature, and glucose, TIA was an independent predictor of subsequent deterioration (odds ratio, 5.0; 95% CI, 2.0 to 12.5; P=0.001). Subsequent deterioration was not associated with tPA treatment, and there was no interaction between tPA administration, TIA, and subsequent deterioration. Lesser degrees of substantial acute recovery were also associated with greater risk of subsequent deterioration.


CONCLUSIONS
Patients with TIA may be a greater risk of subsequent neurological deterioration from causes other than hemorrhage. Substantial acute recovery may be an indicator of greater instability more broadly.
Johnston
S Claiborne
SC
Department of Neurology, Box 0114, University of California at San Francisco, 505 Parnassus Ave, M-798, San Francisco, CA 94143-0114, USA. clay.johnston@ucsfmedctr.org
Easton
J Donald
JD
D000368:Aged; D002545:Brain Ischemia / Q000175:diagnosis* / Q000188:drug therapy / Q000453:epidemiology; D015984:Causality; D015897:Comorbidity; D018450:Disease Progression; D005260:Female; D006801:Humans; D002546:Ischemic Attack, Transient / Q000175:diagnosis* / Q000188:drug therapy / Q000453:epidemiology; D008297:Male; D015999:Multivariate Analysis; D016017:Odds Ratio; D011379:Prognosis; D016032:Randomized Controlled Trials as Topic / Q000706:statistics & numerical data; D020127:Recovery of Function; D018570:Risk Assessment; D012307:Risk Factors; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index; D013997:Time Factors; D010959:Tissue Plasminogen Activator / Q000627:therapeutic use; D014481:United States / Q000453:epidemiology
D010959:Tissue Plasminogen Activator