Objective Electroconvulsive therapy (ECT) is an effective option for treatment-resistant bipolar disorder (trBD). However, the mechanisms of its effect are unknown. Oxidative stress is thought to be involved in the underpinnings of BD. Our study is the first, to our knowledge, to report the association between notable oxidative stress parameters (superoxide dismutase [SOD], glutathione peroxidase [GSH-Px], catalase [CAT], and malondialdehyde [MDA]) levels and ECT response in trBD patients. Methods A total 28 trBD patients and 49 controls were recruited. Six-week ECT and naturalistic follow-up were conducted. SOD, GSH-Px, CAT, and MDA levels were measured by enzyme-linked immunosorbent assay, and the 17-item Hamilton Depression Rating Scale and Young Mania Rating Scale were administered at baseline and the end of the 6th week. MANCOVA, ANCOVA, 2 × 2 ANCOVA, and a multiple regression model were conducted. Results SOD levels were lower in both trBD mania and depression (P = .001; P = .001), while GSH-Px (P = .01; P = .001) and MDA (P = .001; P = .001) were higher in both trBD mania and depression compared with controls. CAT levels were positively associated with 17-item Hamilton Depression Rating Scale scores in trBD depression (radjusted  = 0.83, P = .005). MDA levels in trBD decreased after 6 weeks of ECT (P = .001). Interestingly, MDA levels decreased in responders (P = .001) but not in nonresponders (P > .05). Conclusions Our study indicates that decreased SOD could be a trait rather than a state in trBD. Oxidative stress levels are associated with illness severity and ECT response. This suggests that the mechanism of oxidative stress plays a crucial role in the pathophysiology of trBD.

Purpose: Delirium is common in geriatric with Parkinson's disease (PD). Treatments for delirium have generally been neuroleptics; however, antipsychotics have potential effect to block striatal dopamine D2 receptors and worsen symptom of parkinsonism. We explored whether naloxone can alleviate delirium in PD and other forms of parkinsonism.Patients and Methods: Patients with parkinsonism who met the delirium criteria of the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) received naloxone infusions once or twice daily. Treatment effects were evaluated by the delirium rating scale–revised 98 (DRS-R98), including non-cognitive and cognitive subscales; the Richmond agitation–sedation scale (RASS); and the mini mental status examination (MMSE).Results: Two patients with primary parkinsonism, one with vascular PD were observed. The daily dose of naloxone was 2.08 ± 0.64 mg (range: 1–4 mg). Medication time last from 1 h to 7 days without side effects observed. Following with naloxone infusions, DRS-R98 scores decreased within 12 h and MMSE scores increased. The psychotic symptoms, disorientation, and attention deficits were alleviated significantly, while RASS scores decreased with naloxone treatment.Conclusion: Naloxone alleviated psychotic symptoms, improved cognitive dysfunction, and irritability in patients with delirium in the context of PD. The preliminary findings point out that the opioid system may be involved in the pathophysiology of delirium, which may be one of potential treat targets for delirium of PD.

BackgroundAlthough clozapine is an effective option for treatment-resistant schizophrenia (TRS), there are still 1/3 to 1/2 of TRS patients who do not respond to clozapine. The main purposes of this randomized, double-blind, placebo-controlled trial was to explore the amisulpride augmentation efficacy on the psychopathological symptoms and cognitive function of CTRS patients. MethodsA total of 80 patients were recruited and randomly assigned to receive an initial clozapine plus amisulpride or clozapine plus placebo. Positive and Negative Syndrome Scale (PANSS), Scale for the Assessment of Negative Symptoms (SANS), Clinical Global Impression (CGI) scale scores, Repeatable Battery for the Assessment of Neuropsychological Status (RBANS), Treatment Emergent Symptom Scale (TESS), laboratory measurements and electrocardiograms (ECG) were performed at baseline, week 6, and week 12. ResultsCompared with clozapine plus placebo group, clozapine plus amisulpride had lower PANSS total score, positive subscore and general psychopathology subscore at week 6 and week 12 (all p Bonferroni< 0.01). Furthermore, compared with clozapine plus placebo group, clozapine plus amisulpride showed improved RBANS language score at week 12 (p Bonferroni< 0.001). Clozapine plus amisulpride group had a higher treatment response rate (p = 0.04), lower scores of CGI severity (CGI-S) and CGI efficacy (CGI-E) at week 6 and week 12 than clozapine plus placebo (all p Bonferroni< 0.05). There were no differences in BMI, QT intervals or laboratory measurements between the groups. Our results demonstrate that amisulpride augmentation therapy can safely improve the psychiatric symptoms and cognitive performance of CTRS patients. ConclusionsOur study indicates that amisulpride augmentation therapy has important clinical significance for the treatment of CTRS to improve clinical symptoms and cognitive function with tolerability and safety.Trial registrationClinicaltrials.gov identifier- NCT03652974. Registered 31 August 2018, https://clinicaltrials.gov/ct2/show/NCT03652974

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