Brain : a journal of neurology
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It has been shown that unilateral left neglect can be significantly improved for a short time after a short period of adaptation to a prismatic shift of the visual field to the right. In neuropsychological studies, however, there is no evidence demonstrating long-lasting effects following treatment by prism adaptation (PA). The first aim of the present study was to find out whether the short-term amelioration found after prismatic adaptation could be converted into long-term therapeutic improvement. ⋯ The amelioration of neglect occurred only in patients who showed the adaptation effect and the after-effect in the pointing task. Neglect amelioration did not occur in one patient who did not show the adaptation effect and had an unstable after-effect. In conclusion, these findings show that prism adaptation is a productive way of achieving long-lasting improvements in neglect treatment.
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High-frequency stimulation of the subthalamic nucleus (STN) constitutes one of the most effective treatments for advanced forms of Parkinson's disease. The cost and potential risks of this procedure encourage the determination of clinical characteristics of patients that will have the best postoperative outcome. Forty-one Parkinson's disease patients underwent surgery for bilateral STN stimulation. ⋯ The severity of levodopa-related motor complications was not a predictive factor. The outcome of STN stimulation was excellent in levodopa-responsive forms of Parkinson's disease, i.e. in patients with selective brain dopaminergic lesions, and moderate in patients with axial motor symptoms and cognitive impairment known to be less responsive or unresponsive to levodopa treatment, i.e. when brain non-dopaminergic lesions develop in addition to the degeneration of the nigrostriatal dopaminergic system. The results are consistent with the classical inclusion criteria for STN stimulation, but imply that the decision to operate on the oldest patients and/or patients with gait and postural disorders, who are poorly responsive to levodopa, should be weighed carefully.
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It is still unclear whether the quality of painful thermal sensation is determined only by conduction in specific, dedicated nociceptive channels (i.e. C or Adelta nociceptors) or whether it is a result of integrated activity in both nociceptive and non-nociceptive systems. To evaluate this question, we conducted quantitative and qualitative somatosensory testing in spinal cord injury subjects who suffered from partial or complete loss of thermal sensibility. ⋯ In these areas, both noxious heat and cold elicited a sensation of heat pain. No consistent pattern of heat-elicited pain was observed in areas in which only cold sensation was intact. These data suggest that the integrity of non-noxious thermal systems is essential for the normal perception of thermal pain, and that the subjective sensation of pain depends on the integration of information from nociceptive and non-nociceptive channels.
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In patients suffering from temporal lobe epilepsy (TLE), increased extracellular glutamate levels in the epileptogenic hippocampus both during and after clinical seizures have been reported. These increased glutamate levels could be the result of malfunctioning and/or downregulation of glutamate transporters (also known as EAATs; excitatory amino acid transporters). In this study, the distribution of protein and mRNA of EAAT subtypes was examined in the hippocampus of TLE patients with hippocampal sclerosis (HS group) and without hippocampal sclerosis (non-HS group), and in autopsy controls without neurological disorders. ⋯ The results indicate an upregulation of EAAT2 protein expression in CA1 and CA2 in neurones in the non-HS group. This is in line with decreased EAAT2 protein levels in the HS group, since these hippocampi are characterized by severe neuronal cell loss. The functional consequences (glutamate transport capacity) of the reported changes in EAAT2 and EAAT3 remain to be determined.
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According to the 'neuronal' theory, cortical spreading depression (CSD) is the pathophysiological correlate of migrainous aura. However, the 'vascular' theory has implicated altered vascular function in the induction of aura symptoms. The possibility of a vascular origin of aura symptoms is supported, e.g. by the clinical observation that cerebral angiography frequently provokes migrainous aura. ⋯ Endothelin-1, in contrast to K(+), did not induce CSD in rat brain slices suggesting indirectly that endothelin-1 may require intact perfusion to exert its effects. In conclusion, endothelin-1 was found in the experiment to be the most potent inducer of CSD currently known. We propose endothelin-1 as a possible candidate for the yet enigmatic link between endothelial irritation and migrainous aura.