Background and Purpose— There is little information about early outcome after intravenous application of tissue-type plasminogen activator (tPA) for stroke patients treated in community-based settings. We investigated the association between tPA therapy and in-hospital mortality in a pooled analysis of German stroke registers. Methods— Ischemic stroke patients admitted to hospitals cooperating within the German Stroke Registers Study Group (ADSR) between January 1, 2000, and December 31, 2000, were analyzed. The ADSR is a network of regional stroke registers, combining data from 104 academic and community hospitals throughout Germany. Patients treated with tPA were matched to patients not receiving tPA on the basis of propensity scores and were analyzed with conditional logistic regression. Analyses were stratified for hospital experience with the administration of tPA. Results— A total of 13 440 ischemic stroke patients were included. Of these, 384 patients (3%) were treated with tPA. In-hospital mortality was significantly higher for patients treated with tPA compared with patients not receiving tPA (11.7% versus 4.5%, respectively; P <0.0001). After matching for propensity score, overall risk of inpatient death was still increased for patients treated with tPA (odds ratio [OR], 1.7; 95% CI, 1.0 to 2.8). Patients receiving tPA in hospitals that administered ≤5 thrombolytic therapies in 2000 had an increased risk of in-hospital mortality (OR, 3.3; 95% CI, 1.1 to 9.9). No significant influence of tPA use for risk of inpatient death was found in hospitals administering >5 thrombolytic treatments per year (OR, 1.3; 95% CI, 0.8 to 2.4). Conclusions— In-hospital mortality of ischemic stroke patients after tPA use varied between hospitals with different experience in tPA treatment in routine clinical practice. Our study suggested that thrombolytic therapy in hospitals with limited experience in its application increase the risk of in-hospital mortality.

Brain CT studies of 35 patients with anorexia nervosa confirmed the observations of other authors: cerebral dystrophic changes correlate with weight loss and the reversibility of these changes also correlates with the normalization of body weight. Other corroborated facts are: the most numerous and most pronounced enlargements are of the cortical sulci and the interhemispheric fissure, moderate widening affects the ventricles and the rarest and most insignificant changes are those of the cerebellum. The reversibility of the changes showed a parallel to the extent of the changes themselves and to the duration of improvement of the body weight. The reversibility of the enlargement of the cortical sulci and of the distances between the frontal horns of the lateral ventricles was more often significant than that of the abnormal measurements of the cella media. This difference is based on minimal early acquired brain damage which occurs in 60% of our patients. This high incidence of early acquired minimal brain disease in patients with anorexia nervosa is here discussed as a nonspecific predisposing factor. Although there is no exact explanation of the etiology of the reversible enlargement of cerebrospinal fluid (CSF) spaces in anorexia nervosa, the changes resemble those in alcoholics. The mechanisms of brain changes in alcoholism, as shown experimentally, seem to us to throw light on the probable mechanism of reversible dystrophic brain changes in anorexia nervosa.

Toxic leukoencephalopathy without involvement of the cerebellum and brainstem is a rare complication of heroin abuse. The pattern of heroin-induced toxic leukoencephalopathy on MRI might not only be related to an unknown adulterant, but also to the mode of drug administration.

Tracheostomy within 7 days of critical care admission is a feasible and safe procedure for patients with poor-grade subarachnoid hemorrhage. Early tracheostomy was not associated with an improvement in mortality or neurologic outcome but associated with fewer respiratory adverse events.