Neurology
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Although neurophysiologic doctrine has traditionally referred to "the" voltage-gated sodium channel, it is now clear that there are at least nine genes that encode molecularly and physiologically distinct sodium channels. Mutations of sodium channel genes provide a basis for genetic channelopathies. Dysregulated expression of sodium channels due to alterations in activity of nonmutated channel genes, on the other hand, can produce acquired channelopathies. ⋯ Emerging evidence also suggests that an acquired channelopathy, characterized by abnormal expression of sensory neuron specific sodium channels that can alter impulse trafficking within Purkinje cells, may contribute to the pathophysiology of MS. Subtype-specific drugs that selectively modulate various types of channels probably will soon be developed. The acquired channelopathies associated with nerve injury and MS may thus represent prototype disorders that present therapeutic opportunities.
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The long-term continuation (retention) rate, efficacy, and safety data of the new antiepileptic drug levetiracetam (LEV) was evaluated in all patients with epilepsy exposed to the drug during its developmental program (n = 1,422). The retention rate was estimated to be 60% after 1 year and 32% after 5 years. Thirty-nine percent (512/1,325) of patients had a seizure reduction of > or =50%, and 13% (183/1,422) became seizure-free for at least 6 months. LEV seems an effective and well tolerated new antiepileptic drug.
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Deficient orexin signaling has been shown to cause narcolepsy-like conditions in animals. In human narcolepsy, CSF levels of orexin A (hypocretin-1) were reported to be low in most cases. ⋯ However, plasma orexin A levels did not differ from those observed in controls. These results suggest that orexin deficiency in patients with narcolepsy is a phenomena restricted to the CNS.