Review of adjunctive glutamate antagonist therapy in the treatment of catatonic syndromes.

Catatonia is a common neuropsychiatric syndrome which may arise from GABA-A hypoactivity, dopamine (D2) hypoactivity,and possibly glutamate NMDA hyperactivity. Amantadine and memantine have been reported as effective treatments for catatonia in selected cases, and probably mediate the presence of catatonic signs and symptoms through complex pathways involving glutamate antagonism. The authors identified 25 cases of catatonia treated with either agent. This article provides indirect evidence that glutamate antagonists may improve catatonic signs in some patients who fail to respond to established treatment, including lorazepam or electroconvulsive therapy. Further study of glutamate antagonists in the treatment of catatonia is needed.

Topiramate effect in catatonia: a case series.

The authors describe four cases of catatonia in which topiramate treatment was used. Commonly effective therapies, including benzodiazepines and divalproex, were proven refractory. In all four cases, subjects experienced complete remission of catatonic symptoms and tolerated treatment well. In one case, all psychotropic medications were discontinued because the patient became delirious. The delirium resolved after discovery and treatment of a urinary tract infection. Catatonic agitation relapsed when topiramate was withdrawn but remitted again when topiramate and lorazepam therapy was restored. In two cases, continued topiramate therapy was accompanied by sustained remission. These case reports present a novel approach to the treatment of catatonia.

Ketamine appears associated with better word recall than etomidate after a course of 6 electroconvulsive therapies.

Ten patients treated with electroconvulsive therapy (ECT) for depressive illness received anesthesia with either etomidate or ketamine. Three patients received both etomidate and ketamine anesthesia for ECT during separate episodes of depression. Patients anesthetized with ketamine for ECT had significantly less impairment of short-term memory function than did patients who received ECT with etomidate anesthesia. All patients who received both anesthetics for ECT during 2 different episodes had less memory loss during ECT with ketamine than with etomidate. These results show the importance of studying the effects of all anesthetic agents used during ECT on cognitive functions. The results imply that the effect of ECT on memory may be largely caused by effects mediated by glutamate at N-methyl-d-aspartate receptors and suggest that N-methyl-d-aspartate antagonists may offer protection from memory dysfunction during ECT.

Electroconvulsive therapy in complex regional pain syndromes.

Three cases are presented in which electroconvulsive therapy (ECT) for depression led to the relief of comorbid complex regional pain syndrome as well as depression. In one of the cases, concomitant fibromyalgia was not relieved during 2 separate series of ECT. The literature regarding the role of ECT in the management of chronic pain is reviewed and discussed in light of recent findings about ECT and changes in neurotransmission associated with seizures.