Cerebrospinal fluid cellular response in uncomplicated acute ischemic stroke.

Because information regarding cerebrospinal fluid (CSF) cellular response in acute ischemic stroke (AIS) is inconclusive, we conducted the following investigation. Cell counts were performed in CSF obtained within 24 h of onset of symptoms in 118 adult patients 86 years or younger with uncomplicated AIS, after hemorrhage and mass effect were ruled out by computed tomography. In 98, CSF examination was repeated on day 7. None of the patients had evidence for systemic infection, inflammatory disease, vasculitis, leukocytosis, anemia or coagulopathy. CSF pleocytosis was defined as white blood cell (WBC) count of five or more mononuclear leukocytes (MNLs) and/or one or more polymorphonuclear leukocytes per cubic milliliter. No cells were found in 78 (66.1%) patients, 25 (21.2%) had one to four MNLs, and 15 (12.7%) had pleocytosis; none had hypoglycorrhachia. Nine patients had traumatic lumbar puncture (LP); in five of them, pleocytosis persisted after correction for red blood cell count. The highest WBC count was 15 cells per cubic milliliter. Only two patients had CSF pleocytosis on day 7; both had had traumatic LP and pleocytosis acutely. We found no correlation between CSF pleocytosis and cardiac source of embolus or type of ischemic stroke. From our data, we conclude that in uncomplicated AIS, CSF pleocytosis is rare and, when present, is mild; it has no correlation with type of stroke and is of no diagnostic value.

Failure of central nervous system serotonin blockage to influence outcome in acute cerebral infarction. A double blind randomized trial.

To determine the effect of blocking central nervous system (CNS) serotonin reuptake in the outcome of acute cerebral infarction (ACI), 49 patients were studied in a double blind, randomized trial. All patients suffered hemispheric ACI, were seen within 24 hours of onset, and were treated with low dose, subcutaneous heparin to prevent venous thrombosis; 25 received 10 mg. of trazodone hydrochloride intravenously every 12 hours for seven days and 24 were given an identically appearing placebo. To monitor trazodone effect, indol derivatives were measured in spinal fluid collected before and after treatment in 38 patients. Treatment and placebo patients had similar demographic characteristics, comparable risk factors, and neurologic deficit at onset. No appreciable difference was seen between treatment and control patients in regard to intercurrent events, degree of neurologic deficit, time of hospitalization, and mortality. Indol derivatives were consistently higher in the spinal fluid of trazodone patients after treatment, confirming serotonin reuptake blockage; however, this seems to have had no beneficial effect on the outcome of ACI.

Confirmatory tests in the diagnosis of brain death: the role of the radioisotope brain scan.

KIE: Brain death can be determined by clinical examination and the diagnosis confirmed by a variety of laboratory studies. While the most widely used has been the EEG, newer tests are playing an increasingly important role in confirming brain death. The authors discuss the role of one of these tests, the radioisotope brain scan (RIBS), which measures cerebral blood flow. Advantages and limitations of this procedure are outlined and compared with those of the EEG.^ieng

Temporal profile of vertebrobasilar territory infarction. Prognostic implications.

To determine the type and prognostic significance of the various temporal profiles of vertebrobasilar territory infarction, 39 consecutive patients were studied. The following profiles were identified: 1) coma from onset, 5 patients; 2) sudden onset followed by stabilization, 12 patients; 3) gradual onset reaching stabilization within 24 hours, 7 patients; 4) gradual onset with progression beyond 24 hours, 2 patients, and; 5) delayed worsening after stabilization, 13 patients. Patients in Group 1 and those with unstable courses, Groups 4 and 5, had poor outcomes with mortality of 100 and 27 percent, respectively. Mortality for Groups 2 and 3 was 5 percent. Overall, hospital mortality was 25.6 percent. Demographic data, risk factors, presenting symptoms and type of neurologic deficit, other than coma, had no correlation with mortality, degree of disability and long term survival. At follow up of 6 to 52 months, median 24, only 7 percent of the survivors had recurrent cerebrovascular events; 2 patients (7%) died due to nonvascular causes and 72 percent of patients re-examined (20 of 28) were either neurologically normal or had only minimal deficits.