We retrospectively studied 79 patients from three centers who suffered an intracerebral hemorrhage during treatment with anticoagulants and compared them with 84 patients from one center who suffered a spontaneous intracerebral hemorrhage without anticoagulant treatment Mortality after 30 days was slightly higher in patients with anticoagulant treatment (67%) than in those without (55%), and the proportion of patients who attained moderate or complete recovery was slightly smaller in the treated group (22% and 36%, respectively); neither difference was statistically significant. Volume of the supratentorial hematoma was measured from computed tomograms in 70% of the patients in both groups and was significantly greater in the 55 patients treated with anticoagulants than in the 59 patients not so treated. Volume was not related to the degree of anticoagulation. Based on the total number of patients treated with anticoagulants in the Heerlen region, we conclude that for patients older than 50 years of age the risk of intracerebral hemorrhage during anticoagulant treatment is increased approximately eightfold but is unrelated to the degree of anticoagulation. Our results suggest that intracerebral hemorrhage is more frequent and more extensive in patients treated with anticoagulants but that once it has occurred in such patients intracerebral hemorrhage is not significantly more serious than in untreated patients. (Stroke 1990;21:726-730) T he occurrence of intracerebral hemorrhage (ICH) in patients treated with anticoagulants is a serious complication, often fatal. The risk of ICH in patients >50 years of age who have been treated with anticoagulants is estimated to be 10 times that in untreated subjects of the same age.1 In that study, outcome in treated patients was not different from that in untreated patients, but ICH was diagnosed mainly on clinical grounds. Additionally, it is uncertain whether the risk of ICH is related to the duration and degree of anticoagulation. According to some studies the risk is greatest during the first 6 months, 2 whereas other workers have found that most ICHs occur after at least 1 year of anticoagulation.1 Though ICH in patients receiving anticoagulants often results from overtreatment, many authors have reported a therapeutic degree of anticoagulation at the moment of the bleeding. Received June 23, 1989; accepted January 9, 1990. has not yet been studied in relation to the use of anticoagulants.The purpose of our retrospective study, which we believe is the largest of its type, was to examine the influence of anticoagulation treatment on the risk of ICH, the volume of the hematoma, and the clinical course compared with patients suffering an ICH who were not treated with anticoagulants.
Parkinson's disease is characterized not only by tremor, akinesia and rigidity, but also by frontal cognitive dysfunction, that can be understood as a disturbance in the 'Supervisory Attentional System' (SAS). This concept refers to a system, located in the frontal cortex, that regulates attentional processes under novel, non-routine conditions. The hypothesis that cognitive dysfunction in Parkinson's disease results from a disturbance in the SAS was investigated by recording 'processing negativity' in 33 parkinsonian patients and 17 controls. Processing negativity is an event-related potential that reflects neuronal activity during selective attention. The contribution of the frontal cortex to selective attention can be studied directly using processing negativity. Parkinsonian patients were also scored for clinical symptoms and subjected to a neuropsychological test battery. Processing negativity was clearly disturbed in the parkinsonian patients. Moreover, parkinsonian patients with the lowest scores on 'frontal' neuropsychological tests such as Stroop, Trail Making and Word Fluency, also had the lowest processing negativity. Our results support the hypothesis that cognitive dysfunction in Parkinson's disease might be understood as a disturbance in the frontal regulation of attentional processes. Degeneration of the dopaminergic mesocortical innervation of the frontal cortex in Parkinson's disease is a possible neurochemical substrate of these frontal attentional disturbances.
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