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NEUROLOGY 1994;44:1379
© 1994 American Academy of Neurology

Neurologic deterioration in noncomatose patients with supratentorial intracerebral hemorrhage

Stephan A. Mayer, MD, Ralph L. Sacco, MS, MD, Tianying Shi, MS and J. P. Mohr, MD

Departments of Neurology (Drs. Mayer, Sacco, and Mohr, and Mr. Shi) and Public Health (Epidemiology) in the Sergievsky Center (Dr. Sacco), Columbia-Presbyterian Medical Center, New York, NY.

Objective: To determine the frequency, time course, and predictors of neurologic deterioration (ND) in noncomatose patients with supratentorial intracerebral hemorrhage (ICH).

Background: Patients with worsening ICH may benefit from therapy aimed at reducing mass effect due to active bleeding or cerebral edema.

Methods: We analyzed 46 noncomatose (Glasgow Coma Scale [GCS] score ≥ 8) patients with ICH in the Stroke Data Bank (SDB). All subjects were examined within 24 hours of onset (mean, 13.6 hours) and were prospectively followed with serial examinations during hospitalization. ND was defined as (1) a ≥ 2-point decrease in the GCS score, (2) a ≥ 1-point increase in the SDB weakness score, or (3) a new deficit, unrelated to medical or surgical complications.

Results: ND occurred in 15 of 46 patients (33%). The frequency of ND was greatest on the first hospital day (eight of 15 patients) and decreased progressively thereafter. Patients with ND had larger hemorrhages (mean volume, 45 ml versus 16 ml, p < 0.01) and more frequently demonstrated marked mass effect (60% versus 19%, p < 0.01) on initial CT than those with stable deficits, but did not differ with regard to mean GCS score, mean blood pressure, or other clinical variables on admission. Hematoma enlargement was judged to be the cause of worsening in four of 15 (27%) patients. Thirty-day case fatality was 47% in those with ND compared with 3% in those with stable deficits (p = 0.001).

Conclusions: ND occurs in one-third of noncomatose patients with supratentorial ICH and carries a poor prognosis. Large hematoma volume on CT, rather than clinical predictors, identifies patients at high risk for subsequent worsening.

Address correspondence and reprint requests to Dr. Stephan A. Mayer, Neurological Institute, 710 West 168th Street, Box 39, New York, NY 10032.

Presented in part at the 45th annual meeting of the American Academy of Neurology, New York, NY, April 1993.

Supported in part by The Horace W. Goldsmith Foundation and by a National Stroke Association Research Fellowship Award (Dr. Mayer).

Received November 30, 1993. Accepted in final form January 28, 1994




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