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Background and Purpose— Brain hemorrhage after ischemic stroke is a serious complication of treatment; however, its pathology is poorly understood. A classification based on brain imaging may help to better understand and avoid causal factors. Methods— Review of the results of controlled randomized trials and the available literature. Results— Hemorrhagic infarctions have no impact on clinical outcome and are probably not associated with the thrombolytic itself and the type of reperfusion strategy. They are associated with the extent of ischemic damage and most probably to an ischemic vasculopathy. Parenchymal hematomas are often clinically relevant. Their incidence is affected by the thrombolytic itself, the type, and probably the time point of reperfusion strategy. The loss of hemostatic control seems important in their pathogenesis. Extraischemic hematomas (remote from the infarct), unique or multiple, suggest pre-existing brain pathology, especially cerebral amyloid angiopathy. Conclusions— The radiological description of 3 different types of brain hemorrhage is useful to better understand the specific pathology and the impact on clinical outcome. It may help to avoid clinically relevant brain hemorrhages.

Background— Little is known about the coagulation factors as predictors of cerebral bleeding in rt-PA thrombolysis. The aim of this study was to determine what early coagulation parameters could predict early hemorrhagic lesions. Methods— Consecutive patients were included in the Lyon rt-PA protocol. Early hematomas (within 24 hours), diagnosed on an anatomoradiological basis (symptomatic and not symptomatic) were considered for the study. Fibrinogen and fibrin(ogen) degradation products (FDP) were assessed at entry and at 2 and 24 hours after the beginning of thrombolysis. Results— Of 157 patients, 11 had early parenchymal hematomas (7%), 31 had early hemorrhagic infarcts (19.7%), and 115 had no bleeding (73.2%). In logistic regression, FDP at 2 hours was the single predictor of parenchymal hematomas (OR: 2.5; CI: 1.09 to 5.8), whereas an increase of FDP >200 mg/L multiplied the odds of parenchymal hematoma by 4.95 (IC: 1.09 to 22.4). Early parenchymal hematomas were indicative of a poor prognosis at 3 months ( P =0.001). Conclusions— Early parenchymal hematomas appear as both “malignant” and exclusively related to an explosive increase of FDP at 2 hours, ie, an early fibrinogen degradation coagulopathy (EFDC). All patients scheduled to rt-PA thrombolysis should have an assay of FDP 2 hours after the beginning of thrombolysis: patients with an established EFDC (FDP >200 mg/L) should be monitored specifically, with no antithrombotic drug during the first 72 hours. Patients with FDP >100 mg should share the same monitoring.

Background and Purpose Hemodynamic parameters such as regional cerebral blood volume (rCBV), mean transit time (MTT), and regional cerebral blood flow (rCBF) can be assessed by dynamic susceptibility contrast MRI. The aim of the present study was to apply this method in patients who had symptomatic unilateral internal carotid artery occlusion. Methods Relative hemodynamic parameters (rCBV, MTT, and rCBF) were evaluated on the occluded side and thus compared with contralateral hemispheric values. We also attempted to detect any relationship between collateral flow and the hemodynamic parameters. Results Although rCBV was clearly increased in five patients over the whole hemisphere, we did not observe a statistically significant difference regarding the whole sample between sides (mean rCBV, 14.1±4.58 on the occluded side versus 11.8±2.99 on the contralateral side; P >.10). MTT was clearly increased on the occluded side (mean MTT, 4.29±0.83 on the lesion side versus 3.14±0.81 on the contralateral side; P P Conclusions A significant hemodynamic compromise in patients who had unilateral symptomatic carotid occlusion was observed according to CBF and MTT values. This approach might be promising in the understanding of cerebral hemodynamics in patients with vascular disorders.

Background and Purpose The effects of hyperbaric oxygen (HBO) therapy on humans are uncertain. Our study aims first to outline the practical aspects and the safety of HBO treatment and then to evaluate the effect of HBO on long-term disability. Methods Patients who experienced middle cerebral artery occlusion and were seen within 24 hours of onset were randomized to receive either active (HBO) or sham (air) treatment. The HBO patients were exposed daily to 40 minutes at 1.5 atmospheres absolute for a total of 10 dives. We used the Orgogozo scale to establish a pretreatment functional level. Changes in the Orgogozo scale score at 6 months and 1 year after therapy were used to assess the therapeutic efficacy of HBO. In addition, we used the Rankin scale and our own 10-point scale to assess long term-disability at 6 months and 1 year. Two sample t tests and 95% confidence intervals were used to compare the mean differences between the two treatment groups. Student’s two-tailed test was used to compare the differences between pretherapeutic and posttherapeutic scores at 6 months and 1 year in the two treatment groups. Results Over the 3 years of study enrollment, 34 patients were randomized, 17 to hyperbaric treatment with air and 17 to hyperbaric treatment with 100% oxygen. There was no significant difference at inclusion between groups regarding age, time from stroke onset to randomization, and Orgogozo scale scores. Neurological deterioration occurred during the first week in 4 patients in the sham group, 3 of whom died; this worsening was clearly related to the ischemic damage. Treatment was also discontinued for 3 patients in the HBO group who experienced myocardial infarction, a worsening related to the ischemic process, and claustrophobia. Therefore, 27 patients (13 in the sham group and 14 in the HBO group) completed a full course of therapy. The mean score of the HBO group was significantly better on the Orgogozo scale at 1 year ( P P P P Conclusions Although the small number of patients in each group precludes any conclusion regarding the potential deleterious effect of HBO, we did not observe the major side effects usually related to HBO. Accordingly, it can be assumed that hyperbaric oxygen might be safe. We hypothesize that HBO might improve outcome after stroke, as we detected an outcome trend favoring HBO therapy. A large randomized trial might be required to address the efficacy of this therapy.

Article abstract The authors describe the outcomes in 11 patients who had acute ischemic stroke related to internal carotid artery (ICA) dissection and were treated with IV tissue plasminogen activator (tPA). One symptomatic intracerebral hemorrhage occurred 36 hours after tPA was given. The mean day 90 modified Rankin Scale (m-RS) score was 2.4 (±1.6). No death was observed at 3 months. Four patients of 11 (36.4%) made an excellent recovery (day 90 m-RS score: 0 to 1). This study demonstrates the feasibility of IV thrombolysis with tPA (0.8 mg/kg) in ischemic stroke related to ICA dissection within the first 7 hours.

Background Unilateral upper limb asterixis related to cortical infarct is an unusual clinical picture. We found this association in two patients. Magnetic resonance imaging (MRI), somatosensory evoked potentials (SEPs), and electromyographic recording were performed. Case Descriptions Two patients developed an acute upper limb ataxia with asterixis. This consisted of frequent arrhythmic loss of extensor muscle tone on instruction to maintain the wrist and fingers extended. Voluntary electromyographic activity in the left extensor digitorum communis muscle showed abrupt periods of interruption ranging from 90 to 260 milliseconds in duration in the first case and from 60 to 220 milliseconds in the second case. SEPs were normal. MRI disclosed a right cortical infarct within the primary motor cortex in both cases. Conclusions These findings indicate that asterixis was not related to a failure in the processing of proprioceptive input controlling the regulation of postural tone of the distal upper limbs because SEPs were normal. The involvement of primary motor cortex might suggest that asterixis results from an impairment of a centrally generated motor-command signal controlling the postural tone of the distal upper limb.

P34 Background : Several factors are suspected in the occurrence of hemorrhages after rtPA thrombolysis in cerebral infarcts, but little is known about coagulation in these patients. Methods and results : One hundred consecutive patients had rtPA at the dose of 0.8 mg/kg infused for 90 minutes.We studied the values of fibrinogen, FDP, aPTT, INR and thrombocyte count before thrombolysis and at 2 and 24 hours. Results: Cerebral bleeding at 24 hours included 16 hemorrhagic infarcts (HI) and 7 parenchymal hematomas (PH). 1. Cerebral bleeding in general. Univariate analysis comparing patientswith HI+PH vs patients without bleeding detected 2 significant factors : severity at entry (p=0.03) and and increased values of FDP at 2 hours (p=0.05). Each early CT symptom and pooled early CT symptoms did not appear as factors of bleeding. Multivariate analysis showed that values of FDP>150mg/L multiplicate the odds of bleeding by 6.9, being then a more powerful factor than severity at entry. 2. Factors of seriousness of bleeding. FDP values>150 mg/L multiplicate the odds of parenchymal hematoma by 17. Comparison of patients with PH and HI only showed one potential factor, the lack of hypercholesterolemia (p=0.06). Interestingly, age, delay, severity at entry, early CT signs of ischemia were not factors of parenchymal invasion. Heparin in the fist 24 hours was a potential factor, but not reaching statistical significance. In a logistic regression model, the lack of hypercholesterolemia multiplicates the risk of PH by 10. Conclusion : The ”making“ of a parenchymal hematoma involves at least 2 phases : (1) an early ”acquired coagulopathy“ characterized by increased FDP values at 2 hours (ie a particularly intense thrombolysis); and (2) an increased vulnerability of the arteriolar wall, possibly related to the lipid content of the vessels. The observation of the ”coagulopathy“ should contraindicate any antithrombotic drug during the first 24 hours and imply a surveyance of haemostasis and cerebral bleeding with T2* gradient-Echo MRI during the following days.