1,721,059 research outputs found
Effect of electroconvulsive shock treatment on the opioid-mediated inhibition of serotonin release in rat hippocampal slices
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Mapping of functional changes associated with administration of substances of abuse in the rat
No full textDifferential effects of cocaine on local cerebral glucose utilization in the mouse and in the rat
No full textHeterogeneous pathologies associated with dementia in Parkinsonism share a prion-like spreading mechanism
No full textCognitive alterations accompany or follow motor disorders in subjects with Parkinsonism. The canonical phenotype of the Parkinson's disease Dementia (PD-D) or Lewy Body Dementia (LBD) includes deficit of attention, executive and visuospatial functions, and presents often with apathy, hallucinations, delusions, excessive daytime sleepiness, or sleep disorders. However, the clinical expression may overlap with other neurodegenerative diseases associated with cognitive disorders. Thus, while clinicians rely on phenomenological patterns to infer the disease causing the cognitive impairment, the inference is weakened by the heterogeneous clinical expression of the disease. In addition, recent post-mortem studies seem to undermine the supposed pathology-phenotype coherence, making it more and more unreliable the diagnosis based on symptoms. The lack of coherence between phenotype and pathology may support the speculation about a common mechanism underlying the progression of the disease. While it is very likely that a distinct, specific causal event determines the disease itself, the progression might well follow common patterns. A number of observations suggest that progressive diseases, which cause cognitive impairment, share a prion-like mechanism. A seeding process is supposed to account for the spreading of the lesion
Therapeutic hypothermia for acute stroke
No full textOn a theoretical background, hypothermia surmounts pharmacological neuroprotection by providing simultaneous effects on several mechanisms potentially relevant in the postischemic maturation of the damage. Measurements of the infarct size in animal models reveal that mild hypothermia is probably one of the most effective and documented neuroprotective intervention, both in focal and global ischemia models. As expected, hypothermia is more effective, and the results more consistent, when the time window for initiation of treatment is shorter than 6 h, with an apparent correlation between effect size and time window in the range of 0–6 h. There seems to be also an inverse relationship between temperature depth and reduction in infarct size. Mild hypothermia, such as cooling by 1°C or 2°C, is still associated with a noteworthy 20%–30% infarct size reduction. A few controlled studies in patients with ischemic stroke show feasibility and safety of cooling to a target temperature of 33°C–34°C, for 12 or 24 h, associated with antishivering pharmacological treatment. Hypothermia can be safely induced in acute stroke patients by infusion of iced saline, and the target temperature can be obtained and maintained by either surface or endovascular cooling, followed by controlled rewarming. Multicenter, randomized, phase III trials are ongoing to test the efficacy of the procedure
Effects of single and repeated electroconvulsive shock on local cerebral glucose utilization in the conscious rat
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