This situation is different for two other antidepressants, gabape

This situation is different for two other antidepressants, gabapentin and pregabalin. For gabapentin, two doubleblind

placebo-controlled studies showed positive results in panic disorder and social phobia.67,68 Even more compelling is the evidence for pregabalin. Five positive double-blind, placebo-controlled studies in GAD69-73 and one positive controlled study in social phobia74 make this compound indeed a well-proven anxiolytic medication. For GAD, an optimal dosage of 200 to 450 mg /day had been determined.75 Agitation in dementia Inhibitors,research,lifescience,medical Following up on earlier observations that antiepileptic drugs reduce aggressiveness in behaviorally disturbed epileptic patients, several Inhibitors,research,lifescience,medical antiepileptic drugs were also tested in demented patients with destructive behavior. After several case reports showed efficacy on aggressiveness with valproate, a recent review article by Lindenmayer76 analyzed these case reports of violent, and aggressive demented patients and found an overall response rate of 77.1%, defined as an at least 50% improvement on the applied scale for aggressiveness. However, a combined analysis Inhibitors,research,lifescience,medical of four small controlled studies could not support, valproate’s efficacy.77 Case reports also suggested beneficial effects of lamotrigine,78 gabapentin,79 and levetiracetam80 in agitated and

aggressive demented patients, but, as with other indications there is still an obvious need for more controlled studies. Pain Many neurologists might object, to a section on pain as a psychiatric condition. However, most types of pain cannot be conceptualized as a pure neurological dysfunction, but also involve strong subjective and emotional aspects. The exact mechanisms of how ACs work in pain conditions are far from being understood; however, Inhibitors,research,lifescience,medical it is intuitive that they may be able to

dampen many of the proposed causes of chronic pain, such as peripheral sensitization, central sensitization, wind-up, hyperexcitability, neuronal disinhibition, ectopic impulse formation, Inhibitors,research,lifescience,medical and finally, the subjective impression and emotional handling of pain. For example, abnormal activation of the NM’DA receptor is believed to be an integral part of kindling in epilepsy as well as windup in neuropathic pain; consequently, pharmacologic agents that suppress this excitation may explain their utility in both conditions.81 through In addition, as already detailed in the section on neurobiology, several ACs also have intrinsic, antidepressant-like effects on serotonin and noradrenalin, eg, the long known activating DAPT secretase manufacturer effect of carbamazepine on locus coeruleus neurons,82 the postsynaptic serotonin (5-HT)1A receptor activity of lamotrigine in the forced swimming test,83 the presynaptic enhancement of serotonin transmission by valproate via a subsensitization of 5-HT1A autore ceptors,84 and theories about the close linkage between depression and epilepsy have been evolved.

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