ABSTRACT
Major depressive disorder (MDD) is a prevalent and disabling condition, and many patients do not respond to available treatments. Deep transcranial magnetic stimulation (dTMS) is a new technology allowing non-surgical stimulation of relatively deep brain areas. This is the first double-blind randomized controlled multicenter study evaluating the efficacy and safety of dTMS in MDD. We recruited 212 MDD outpatients, aged 22-68 years, who had either failed one to four antidepressant trials or not tolerated at least two antidepressant treatments during the current episode. They were randomly assigned to monotherapy with active or sham dTMS. Twenty sessions of dTMS (18 Hz over the prefrontal cortex) were applied during 4 weeks acutely, and then biweekly for 12 weeks. Primary and secondary efficacy endpoints were the change in the Hamilton Depression Rating Scale (HDRS-21) score and response/remission rates at week 5, respectively. dTMS induced a 6.39 point improvement in HDRS-21 scores, while a 3.28 point improvement was observed in the sham group (p=0.008), resulting in a 0.76 effect size. Response and remission rates were higher in the dTMS than in the sham group (response: 38.4 vs. 21.4%, p=0.013; remission: 32.6 vs. 14.6%, p=0.005). These differences between active and sham treatment were stable during the 12-week maintenance phase. dTMS was associated with few and minor side effects apart from one seizure in a patient where a protocol violation occurred. These results suggest that dTMS constitutes a novel intervention in MDD, which is efficacious and safe in patients not responding to antidepressant medications, and whose effect remains stable over 3 months of maintenance treatment.
ABSTRACT
INTRODUCTION: Transient bradycardia during the stimulation phase of electroconvulsive therapy (ECT) is a well-known clinical observation. The optimal dose of atropine needed to prevent bradycardia has not been determined. This study was designed to investigate the effect of low doses of atropine on heart rate during ECT. METHODS: Patients who received at least 2 different doses of atropine over their series of right unilateral ECT were included in the analysis. The anesthetic consisted of 0, 0.2, 0.3, or 0.4 mg of atropine, methohexital, and succinylcholine. Heart rate was measured by the RR interval, the time between sequential R waves on the electrocardiogram. Analysis was performed using logistic multivariate regression and repeated-measures multivariate analysis of variance. RESULTS: One hundred eighteen ECT sessions were identified from 19 patients. Patients were grouped into 4 groups by atropine dose (0, 0.2, 0.3, or 0.4 mg) with 9, 33, 13, and 63 ECT sessions identified for each dose, respectively. Patients who received atropine had significantly less bradycardia after electrical stimulus and a faster heart rate through the seizure than patients who did not receive atropine. There was no significant difference in heart rate between patients receiving 0.2, 0.3, and 0.4 mg of atropine at any time point. There was no significant difference in heart rate at time points after the seizure conclusion in any group of patients. CONCLUSION: Low-dose atropine results in significantly less bradycardia after electrical stimulus. There was no significant difference in heart rate across low doses of atropine.
Subject(s)
Anti-Arrhythmia Agents/pharmacology , Atropine/pharmacology , Electroconvulsive Therapy , Heart Rate/drug effects , Adult , Aged , Anesthesia , Anti-Arrhythmia Agents/administration & dosage , Atropine/administration & dosage , Bradycardia/etiology , Bradycardia/prevention & control , Dose-Response Relationship, Drug , Electrocardiography/drug effects , Electroconvulsive Therapy/adverse effects , Electroencephalography , Female , Humans , Male , Middle Aged , Retrospective StudiesABSTRACT
We present the case of a patient with treatment-refractory mania. The patient had been tried on numerous medications, to which she either did not respond well or on which she developed severe side effects, However, the patient improved rapidly when treated with unilateral electropercussive therapy (ECT) following a court order. We outline the legal barriers that have been raised against the use of ECT in patients with mania, who often refuse treatment, and the irony that ECT can be safer than medications for some patients. ECT is underutilized in mania but deserves more frequent consideration. (Journal of Psychiatric Practice. 2011;17:61-66).
Subject(s)
Bipolar Disorder/therapy , Electroconvulsive Therapy/methods , Antipsychotic Agents/therapeutic use , Bipolar Disorder/drug therapy , Electroconvulsive Therapy/legislation & jurisprudence , Female , Follow-Up Studies , Humans , Hypoglycemic Agents/therapeutic use , Lithium Compounds/therapeutic use , Metformin/therapeutic use , Middle Aged , Perphenazine/therapeutic use , Treatment Outcome , Weight Gain/drug effectsABSTRACT
Central cholinergic signaling has long been associated with aspects of memory, motivation, and mood, each affected functions in neuropsychiatric disorders such as schizophrenia. In this chapter, we review evidence related to the core hypothesis that dysregulation of central cholinergic signaling contributes to the pathophysiology of schizophrenia. Although central cholinergic circuits are resistant to simplification-particularly when one tries to parse the contributions of various classes of cholinergic receptors to disease related phenomena--the potential role of ACh signaling in Schizophrenia pathophysiology deserves careful consideration for prospective therapeutics. The established role of cholinergic circuits in attentional tuning is considered along with recent work on how the patterning of cholinergic activity may modulate corticostriatal circuits affected in schizophrenia.
