Brain : a journal of neurology
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Complaints of memory difficulties are common among patients with epilepsy, particularly with temporal lobe epilepsy where memory-related brain structures are directly involved by seizure activity. However, the reason for these complaints is often unclear and patients frequently perform normally on standard neuropsychological tests of memory. In this article, we review the literature on three recently described and interrelated forms of memory impairment associated with epilepsy: (i) transient epileptic amnesia, in which the sole or main manifestation of seizures is recurrent episodes of amnesia; (ii) accelerated long-term forgetting, in which newly acquired memories fade over days to weeks and (iii) remote memory impairment, in which there is loss of memories for personal or public facts or events from the distant past. ⋯ Their presence goes undetected by standard memory tests and yet they can have a profound impact on patients' lives. They pose challenges to current theoretical models of memory. We discuss the evidence for each of these phenomena, as well as their possible pathophysiological bases, methodological difficulties in their investigation and their theoretical implications.
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Dystonia is a neurological disorder characterized by excessive involuntary muscle contractions that lead to twisting movements or abnormal posturing. Traditional views place responsibility for dystonia with dysfunction of basal ganglia circuits, yet recent evidence has pointed towards cerebellar circuits as well. In the current studies we used two strategies to explore the hypothesis that the expression of dystonic movements depends on influences from a motor network that includes both the basal ganglia and cerebellum. ⋯ These results demonstrate important functional relationships between cerebellar and basal ganglia circuits in two different animal models of dystonia. They suggest that expression of dystonic movements depends on influences from both basal ganglia and cerebellum in both models. These results support the hypothesis that dystonia may result from disruption of a motor network involving both the basal ganglia and cerebellum, rather than isolated dysfunction of only one motor system.
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Controlled Clinical Trial
Autologous olfactory ensheathing cell transplantation in human paraplegia: a 3-year clinical trial.
Olfactory ensheathing cells show promise in preclinical animal models as a cell transplantation therapy for repair of the injured spinal cord. This is a report of a clinical trial of autologous transplantation of olfactory ensheathing cells into the spinal cord in six patients with complete, thoracic paraplegia. We previously reported on the methods of surgery and transplantation and the safety aspects of the trial 1 year after transplantation. ⋯ There were no significant functional changes in any patients and no neuropathic pain. In one transplant recipient, there was an improvement over 3 segments in light touch and pin prick sensitivity bilaterally, anteriorly and posteriorly. We conclude that transplantation of autologous olfactory ensheathing cells into the injured spinal cord is feasible and is safe up to 3 years of post-implantation, however, this conclusion should be considered preliminary because of the small number of trial patients.
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Central neuropathic pain following lesions within the CNS, such as spinal cord injury, is one of the most excruciating types of chronic pain and one of the most difficult to treat. The role of spinothalamic pathways in this type of pain is not clear. Previous studies suggested that spinothalamic tract lesions are necessary but not sufficient for development of central pain, since deficits of spinothalamic function were equally severe in spinal cord injured people with and without pain. ⋯ These results suggest that intact thermosensitive nociceptive afferents within lesioned spinothalamic tract pathways distinguish people with central pain from those without. The ability to mimic chronic pain sensations by activation of thermosensory nociceptive neurons implies that ongoing activity in these residual spinothalamic pathways plays a crucial role in maintaining central pain. We propose that processes associated with degeneration of neighbouring axons within the tract, such as inflammation, may trigger spontaneous activity in residual intact neurons that act as a 'central pain generator' after spinal cord injury.