Case 2 The patient is a 58-year-old woman with a lifelong history of GAD and bipolar depression,

with infrequent hypomanic excursions. She has been under the care of the first author for 1 year. She currently takes lithium carbonate 900 mg hs, quetiapine 100 mg in the morning and 400 mg hs, and www.selleckchem.com/products/Erlotinib-Hydrochloride.html gabapentin 600 mg in the morning and 1200 mg hs. Occasionally, when she feels particularly anxious, she takes timolol maleate 10 mg bid, diazepam 10 mg prn (not to exceed two tablets daily) and clonazepam 4 mg hs prn. Recently the patient forgot to take her bedtime dose of gabapentin. She was taking timolol, clonazepam, and diazepam at the time. Nevertheless the consequences of this lapse were severe. Inhibitors,research,lifescience,medical She scored 3 on the Observational Subscale of the Barnes Akathisia Rating Scale and experienced intense anxiety. Her symptoms were relieved when she took 1200 mg of gabapentin, which she had been cautioned Inhibitors,research,lifescience,medical not to omit, based upon our experience with the previous case. Discussion and conclusions This

article has raised several issues that require further investigation. Gabapentin enhances the inhibitory effect of GABA throughout the central nervous system (CNS), so it would not come as a surprise if controlled trials confirmed our preliminary Inhibitors,research,lifescience,medical observations as well as [Pfeffer et al. 2005] that gabapentin controlled the symptoms of neuroleptic-induced Inhibitors,research,lifescience,medical akathisia. However, the mechanism

of action of gabapentin remains to be elucidated, although two models have considerable heuristic value. The first [Hendrich et al. 2008] proposes that gabapentin binds to the calcium ion channel, thereby inhibiting the influx of calcium ions into GABA-ergic neurons. Because the calcium current is inhibitory, its blockage would promote the release of GABA at the presynaptic terminal. A second recent model [Eroglu et al. 2009] maintains that gabapentin binds to the neuronal thrombospondin receptor and thereby Inhibitors,research,lifescience,medical inhibits the formation of excitatory synapses. Either theory appears to account for the reported ability of gabapentin to suppress seizures, support sleep, relieve anxiety and pain, and suppress abnormal involuntary movements such as those seen in neuroleptic-induced akathisia and RLS. Both cases make it clear that the selleck chemical Y-27632 patients experienced neuroleptic-induced akathisia per DSM IV. They evinced symptoms of greater severity than Anacetrapib RLS. An inherent limitation of Case 2 is that case reports are constrained by the possibility of the placebo effect; this is a limitation of all case reports. The literature contains a recent single-case report [See et al. 2011] describing a 76-year-old diabetic woman who presented with severe akathisia after discontinuing gabapentin abruptly. The akathisia resolved when the woman was given a dose of gabapentin.