Fifty-four acutely manic patients were allocated to treatment on a double-blind basis with either carbamazepine or lithium carbonate. The short-term effects of treatment were studied over a period of six weeks and the longer term, prophylactic, effects over a period of up to a year. Additional 'rescue' medication was allowed when clinically indicated. There was a high drop-out rate from the trial. Despite this, it appeared that valid comparisons between the two treatments could be made. No statistically significant differences were found, but carbamazepine appeared slightly less effective as a treatment for acute mania and more effective as a prophylactic treatment in this group of patients. Possible predictors of individual responsiveness to each treatment are discussed.

The entorhinal cortex is a major relay between the hippocampus and other cortical and subcortical regions. Glutamatergic axons from layer II neurons form the entorhinal cortical projection to the hippocampus via the perforant pathway. We have demonstrated previously that lesion of the perforant pathway causes the death of approximately 30% of entorhinal layer II (ECL2) neurons. To elucidate mechanisms contributing to neuronal death and to investigate strategies preventing it, we identified the phenotype of the vulnerable neuronal population. Sections were immunolabeled with antibodies to the neuronal markers NeuN, glutamate, and calbindin-D28k, and to receptors for fibroblast growth factor-2 (FGFR1) and NMDA (NMDAR1) and were examined using confocal microscopy. Calbindin immunoreactivity was strikingly lamina-specific to ECL2, where one-third of all ECL2 neurons were calbindin-positive. Localization of glutamate revealed that half of the glutamatergic ECL2 neurons coexpressed calbindin. Quantification using unbiased stereology at 9 weeks after lesion of the perforant pathway revealed that the only ECL2 neuronal population that experienced a significant (70%) loss (20% of the total) was the population of glutamatergic ECL2 neurons that did not coexpress calbindin. All ECL2 neurons expressed FGFR1; therefore, we tested the role of FGF-2 in the survival of glutamatergic ECL2 neurons. We grafted fibroblasts genetically engineered to express nerve growth factor or FGF-2 and found that only FGF-2 grafts prevented loss of the vulnerable glutamatergic/calbindin-negative neurons. We present a hypothesis for the selective vulnerability of these glutamatergic/calbindin-negative ECL2 neurons and address the role of FGF-2 in neuronal rescue.

Introduction & aim: Temporary (60-day) percutaneous peripheral nerve stimulation (PNS) has demonstrated effectiveness for the treatment of chronic post-amputation pain, and this pilot study aims to evaluate the feasibility of temporary percutaneous PNS for the treatment of acute post-amputation pain. Patients & methods: Sixteen veterans undergoing lower extremity amputation received PNS and standard medical therapy or standard medical therapy alone. Results: The PNS group reported greater reductions in average phantom limb pain, residual limb pain and daily opioid consumption, and there were fewer participants taking opioids through 3 months post-amputation. Conclusion: This pilot study suggests that PNS is feasible in the acute postoperative period following lower limb amputation and may provide a non-pharmacologic analgesic therapy that lowers pain scores and reduces opioid consumption, and thus warrants further investigation.

Study design: A survey on pain satisfaction was mailed to 300 individuals with spinal cord injury. Eighty-eight completed surveys were returned, and the results were analyzed. Objectives: The survey queried the respondents on characteristics of their pain, treatments received, the impact of pain on multiple, life activities and functions and the satisfaction with treatment received to reduce pain. Setting: Subjects for the study were selected from the Spinal Cord Injury Registry from the Commonwealth of Virginia in the US. Methods: Information was obtained from a survey sent to the subjects who were chosen randomly with respect to age and gender. At least 1 year had elapsed from the time of injury for each individual.

ObjectiveThe purpose of this study was to establish the feasibility of manipulating a prosthetic knee directly by using a brain–computer interface (BCI) system in a transfemoral amputee. Although the other forms of control could be more reliable and quick (e.g., electromyography control), the electroencephalography (EEG)-based BCI may provide amputees an alternative way to control a prosthesis directly from brain.MethodsA transfemoral amputee subject was trained to activate a knee-unlocking switch through motor imagery of the movement of his lower extremity. Surface scalp electrodes transmitted brain wave data to a software program that was keyed to activate the switch when the event-related desynchronization in EEG reached a certain threshold. After achieving more than 90% reliability for switch activation by EEG rhythm-feedback training, the subject then progressed to activating the knee-unlocking switch on a prosthesis that turned on a motor and unlocked a prosthetic knee. The project took place in the prosthetic department of a Veterans Administration medical center. The subject walked back and forth in the parallel bars and unlocked the knee for swing phase and for sitting down. The success of knee unlocking through this system was measured. Additionally, the subject filled out a questionnaire on his experiences.ResultsThe success of unlocking the prosthetic knee mechanism ranged from 50 to 100% in eight test segments.ConclusionThe performance of the subject supports the feasibility for BCI control of a lower extremity prosthesis using surface scalp EEG electrodes. Investigating direct brain control in different types of patients is important to promote real-world BCI applications.

No abstract

No abstract

No abstract