Int Rev Neurobiol
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Pain is a common problem of patients with multiple sclerosis (MS) and may be due to central/neuropathic or peripheral/somatic pathology. Rarely MS may present with pain, or pain may herald an MS exacerbation, such as in painful tonic spasms or Lhermitte's sign. In other patients, pain may become chronic as a long-term sequela of damage to nerve root entry zones (trigeminal neuralgia) or structures in central sensory pathways. ⋯ The pathophysiology of pain in MS may be linked to certain plaque locations which disrupt the spinothalamic and quintothalamic pathways, abnormal impulses through motor axons, development of an acquired channelopathy in affected nerves, or involve glial cell inflammatory immune mechanisms. At this time, the treatment of pain in MS employs the use of antiepileptic drugs, muscle relaxers/antispasmodic agents, anti-inflammatory drugs, and nonpharmacological measures. Research concerning cannabis-based treatments shows promising results, and substances which block microglial or astrocytic involvement in pain processing are also under investigation.
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Status epilepticus (SE) is a medical and neurological emergency requiring prompt and aggressive treatment, particularly for elderly individuals in whom comorbid conditions may increase the severity of consequences in SE. Generalized convulsive status epilepticus (GCSE) is the most common and life-threatening type of SE. It may be overt or subtle in its presentation. ⋯ Analysis of data on elderly patients with overt GCSE from a Veterans Affairs cooperative study revealed that success rates of first-line treatment were 71.4% for phenobarbital, 63.0% for lorazepam, 53.3% for diazepam followed by phenytoin, and 41.5% for phenytoin alone. In elderly patients with subtle GCSE, success rates for first-line treatment were 30.8% for phenobarbital, 14.3% for lorazepam, 11.8% for phenytoin, and 5.6% for diazepam followed by phenytoin. Because each drug has advantages and disadvantages, the choice of which agent to use as first-line treatment depends on individual patient characteristics.
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The object of this work was to subject established empirical medical treatment regimens for infantile spasms to evidence-based medicine analysis in order to determine the current best practice for the treatment of infantile spasms in children. Clinical studies of infantile spasms reported during the presteroid era were reviewed critically to define the natural history of the disorder. Treatment trials of infantile spasms conducted since 1958 were rigorously assessed using MEDLINE and hand searches of the English language literature. ⋯ A practice option recommendation for the use of oral corticosteroids in the treatment of infantile spasms is supported by limited and inconclusive class I and III data. Based on the evidence, no recommendation can be made for the use of pyridoxine, benzodiazepines, or the newer antiepileptic drugs in the treatment of infantile spasms. ACTH and vigabatrin are the most effective agents in the treatment of infantile spasms, but concerns remain about the risk/benefit profiles of these drugs.
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This chapter discusses various levels of interactions between the brain and the immune system in sleep. Sleep-wake behavior and the architecture of sleep are influenced by microbial products and cytokines. On the other hand, sleep processes, and perhaps also specific sleep states, appear to promote the production and/or release of certain cytokines. ⋯ Patterns of endocrine activity during sleep are probably essential for the enhancement of IL-2 and T-cell diurnal functions seen in humans: Whereas prolactin and GH release stimulate Th1-derived cytokines such as IL-2, cortisol which is decreased during the beginning of nocturnal sleep inhibits Th1-derived cytokines. The immunological function of neurotrophins, in particular NGF and BDNF, has received great interest. Effects of sleep and sleep deprivation on this cytokine family are particularly relevant in view of the effects these endogenous neurotrophins can have not only on specific immune functions and the development of immunological memories, but also on synaptic reorganization and neuronal memory formation.
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It is clear that the brain has evolved a mechanism for sensing levels of ambient glucose. Teleologically, this is likely to be a function of its requirement for glucose as a primary metabolic substrate. There is no question that the brain can sense and mount a counterregulatory response to restore very low levels of plasma and brain glucose. ⋯ Glucosensing neurons are clearly a distinct class of metabolic sensors with the capacity to respond to a variety of intero- and exteroceptive stimuli. This makes it likely that these glucosensing neurons do participate in physiologically relevant homeostatic mechanisms involving energy balance and the regulation of peripheral glucose levels. It is our challenge to identify the mechanisms by which these neurons sense and respond to these metabolic cues.