Rev Neuroscience
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To determine the safety and effectiveness of mild induced hypothermia in children after traumatic or posthypoxic brain injury. Thirteen patients after traumatic or poshypoxic brain injury were involved in the study. Mean age was 11.1 +/- 5.7 years. Median GCS 6 (3-8), PIM2 20.3 +/- 28.2%. ⋯ Mild induced hypothermia can be safely used in pediatric patients after severe traumatic or posthypoxic brain injury. This method may be of benefit while improving outcomes in children.
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The early recognition of comatose patients with a hopeless prognosis--regardless of how aggressively they are managed--is of utmost importance. Median somatosensory evoked potentials (SSEP) supplement and enhance neurological examination findings in anoxic-ischemic coma and are useful as an early guide in predicting outcome. The key finding is that bilateral absence of cortical evoked potentials reliably predicts unfavorable outcome in comatose patients after cardiac arrest. ⋯ The remaining 27 patients with normal or delayed central conduction times had an uncertain prognosis because some died without awakening or entered a persistent vegetative state. The majority of patients with normal central conduction times had a good outcome, whereas a delay in central conduction times increased the likelihood of neurological deficit or death. Greater use of SSEP in anoxic-ischemic coma would identify those patients unlikely to recover and would avoid costly medical care that is to no avail.
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Placebo analgesia is one of the most robust and best-studied placebo effects. With the help of brain imaging tools, such as positron emission tomography (PET) and functional magnetic resonance imaging (fMRI), our understanding of the brain's role in placebo analgesia has been greatly expanded. Previous studies suggest that multiple mechanisms may underlie the phenomenon of placebo analgesia. ⋯ According to this framework, placebo treatment may exert an analgesic effect on at least three stages of pain processing, by 1) influencing pre-stimulus expectation of pain relief, 2) modifying pain perception, and 3) distorting post-stimulus pain rating. Importantly, change in one such stage may hasten change in another, and furthermore, contribution from any or all of the three stages may vary by circumstance, or between individuals. The literature suggests that multiple brain regions, including the anterior cingulate cortex, anterior insula, prefrontal cortex and periaqueductal grey, play a pivotal role in these processes.
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The adult brain retains the capacity to rewire mature neural circuits in response to environmental changes, brain damage or sensory and motor experiences. Two plastic processes, synaptic remodeling and neurogenesis, have been the subject of numerous studies due to their involvement in the maturation of the nervous system, their prevalence and re-activation in adulthood, and therapeutic relevance. However, most of the research looking for the mechanistic and molecular events underlying synaptogenic phenomena has been focused on the extensive synaptic reorganization occurring in the developing brain. ⋯ Several items of evidence support an interrelationship between NO and BDNF in the regulation of synaptic remodeling processes in adulthood: i) BDNF and its receptor TrkB are expressed by motoneurons and upregulated by axonal injury; ii) they promote axon arborization and synaptic formation, and modulate the structural dynamics of excitatory synapses; iii) NO and BDNF each control the production and activity of the other at the level of individual synapses; iv) the NO/cGMP pathway inhibits BDNF secretion; and finally, v) BDNF protects F-actin from depolymerization by NO, thus preventing the collapsing and retracting effects of NO on growth cones. Therefore, we propose a mechanism of action in which the NO/BDNF ratio regulates synapse dynamics after peripheral nerve lesion. This hypothesis also raises the possibility that variations in this NO/BDNF balance constitute a common hallmark leading to synapse loss in the progression of diverse neurodegenerative diseases such as amyotrophic lateral sclerosis, Alzheimer's and Parkinson's diseases.
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The many signs of cognitive processes in the activation pattern of the primary motor cortex or in corticospinal (CS) excitability gave rise to the idea that the motor cortex is a crucial node in the processing of cognitive information related to sensorimotor functions. Moreover, it became clear that the preparatory motor sets offer a privileged window to investigate the interaction between cognitive and sensorimotor function in the motor cortex. In the present review, we examine how the study of the preparatory motor sets anticipating a mechanical movement perturbation contributes to enlightening this question. ⋯ Thus, CS excitability was measured before the movement was perturbed. These studies demonstrated the readiness of the CS tract to be involved in anticipatory compensatory responses to central movement perturbations induced by TMS in relation to the subject's cognitive attitudes. The question of the cerebral regions upstream of the motor cortex that could be responsible for this modulation in CS excitability remains largely open.