Journal of neurology
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Journal of neurology · May 2002
Randomized Controlled Trial Clinical TrialTreatment of acute ischaemic stroke with the low-affinity, use-dependent NMDA antagonist AR-R15896AR. A safety and tolerability study.
A low-affinity, use-dependent N-Methyl-D-Aspartate (NMDA) antagonist AR-R15896AR has neuroprotective properties in animal models of ischaemic stroke. The aim of the present study was to examine the safety and tolerability of a new and higher dosage regimen that would enable acute stroke patients to achieve and maintain neuroprotective plasma concentrations. ⋯ In most of the patients with acute stroke receiving AR-R15896AR the intended high plasma levels were reached within a short time period. However, active treatment produced more side effects than placebo, thus indicating safety concerns and tolerability issues for use in high doses in an acute stroke population.
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Journal of neurology · May 2002
Clinical TrialSubthalamic nucleus stimulation in Parkinson's disease: clinical evaluation of 18 patients.
The aim of the present study was to assess the efficacy and safety of chronic subthalamic nucleus deep-brain stimulation (STN-DBS) in patients with Parkinson's disease (PD). 18 consecutive severely affected PD patients were included (mean age, SD: 56.9+/-6 years; mean disease duration: 13.5+/-4.4 years). All the patients were evaluated clinically before and 6 months after the surgical procedure using the Unified Parkinson's Disease Rating Scale (UPDRS). Additionally, a 12 months follow-up was available in 14 patients. ⋯ Side effects comprised lower limb phlebitis (n = 2), pulmonary embolism (n = 1), depression (n = 6), dysarthria and freezing (n = 1), sialorrhea and drooling (n = 1), postural imbalance (n = 1), transient paresthesias and dyskinesias. This study confirms the great value of subthalamic nucleus stimulation in the treatment of intractable PD. Some adverse events such as depression may be taken into account in the inclusion criteria and also in the post-operative outcome.
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Journal of neurology · May 2002
A sudden arterial blood pressure decrease is compensated by an increase in intracranial blood volume.
A sudden decrease in arterial blood pressure (ABP) will cause the intracranial blood volume (IBV) to rise, despite the fact that arterial cerebral blood flow decreases. The aim of this study was to test the hypothesis that the increase in IBV is caused by a relative decrease of intracranial venous outflow. ⋯ In intact CA, a steep decrease of ABP results in an increase of intracranial blood volume. The transformation of our IBV data by means of the human intracranial pressure-volume relationship results in an excellent agreement with previously reported ICP increases of 10 mmHg. The increase in intracranial blood volume might be of clinical relevance in orthostatic dysregulation by increasing the ischemic tolerance of the brain before cerebral autoregulation becomes effective.