A Randomized, Double-Blind, Sham-Controlled Study of Transcranial Direct Current Stimulation as an Augmentation Intervention for the Attenuation of Motor Deficits in Patients With Stroke.

INTRODUCTION: Most studies of transcranial direct current stimulation (tDCS) for motor deficits in patients with stroke administered few sessions of tDCS and with low current amplitude. METHODS: During 2015 to 2019, we randomized 60 inpatients with ischemic/hemorrhagic stroke and motor deficits to true or sham tDCS. Transcranial direct current stimulation was administered at 2- to 3-mA current strength, twice daily, 6 days a week, for 2 weeks; anode and cathode were placed over ipsilesional and contralesional motor cortices, respectively. All patients received individualized motor and cognitive rehabilitation. Motor outcomes were assessed 1 day before and 1 day after the tDCS course using the Fugl-Meyer Assessment, the Jebson-Taylor Hand Function Test, and the Barthel index (all coprimary outcomes). Mood and cognition were also assessed. Motor outcomes were compared between groups using age, baseline scores, and latency to treatment as covariates. The study was prospectively registered (CTRI/2017/01/007733). RESULTS: The mean age of the patients was 46.9 years. The sample was 73.3% male. Six patients did not complete the study. The covariates were significantly related to motor outcomes. Although all patients showed motor improvements, after adjusting for covariates, tDCS was not superior to sham treatment on any motor, mood, or cognitive outcome. Laterality of hemispheric lesion influenced spatial but not motor outcomes with tDCS. One true tDCS patient developed blistering under the anode and was withdrawn from the study; 3 more reported transient itching during sessions. CONCLUSIONS: An intensive course of tDCS, as delivered in this study, does not improve motor, mood, and cognitive outcomes in ischemic/hemorrhagic stroke in patients undergoing individualized rehabilitation. The study provides important leads for directions for future research.

ECT and Pronounced Impairment in Spatial Cognition: The Fallacy of Drawing Conclusions From a Single Case.

INTRODUCTION: Electroconvulsive therapy (ECT) is associated with memory deficits on neuropsychological assessment. The association of ECT with nonmemory cognitive deficits has been poorly studied. METHODS: We present a 40-year-old woman who showed a bizarre form of spatial cognition impairment on a subtest of the Tactual Performance Test (TPT) after recovering from depression with 6 alternate day, thrice-weekly, inpatient ECT treatments. This woman was part of a naturalistic, nonblind study that examined nonmemory cognitive deficits in antidepressant-treated depressed patients who did and did not receive ECT. RESULTS: The impairment was in the form of bizarrely drawn reproductions of differently shaped wooden blocks that had been presented to the patient when she was blindfolded. The impairment was still evident when she was retested (3 hours later) under substantially simplified conditions but was much attenuated approximately 2.5 weeks later. CONCLUSIONS: On the surface, it seems that ECT had induced severe impairment in spatial cognition and that the impairment showed the familiar pattern of attenuation with the passage of time. However, another recovered patient in the study, who did not receive ECT, also showed substantial spatial deficits on the same subtest of the TPT, and the attenuation of the deficits across time in the ECT-treated patient was probably a result of repeated exposure to the task. We suggest that not all patients who seem to experience spectacular cognitive impairment after ECT have deficits that are attributable to ECT.

Interferon-Related Depression: A Primer on Mechanisms, Treatment, and Prevention of a Common Clinical Problem.

BACKGROUND: Depression is among the commonest of psychiatric disorders, and inflammatory mechanisms have been suggested to play a role in its pathophysiology. Interferons are a superfamily of proinflammatory cytokines that play a role in host defence mechanisms. Interferons are used in the treatment of a variety of autoimmune (e.g. multiple sclerosis), viral (e.g. chronic hepatitis B and C), and malignant (e.g. malignant melanoma, hairy cell leukemia) disorders; depression, however, is a notable and clinically troublesome adverse effect. OBJECTIVE: This article seeks to present a simple explanation and update for the reader about what interferons are, how interferons are classified, the clinical conditions in which interferons are used, the occurrence of depression as a clinical adverse effect of interferon therapy, possible mechanisms that explain interferon-related depression, the treatment of interferon-related depression, and the prevention of interferon-related depression. METHODS: A qualitative literature review is presented. RESULTS AND CONCLUSIONS: Irrespective of the indication for IFN therapy, IFNs are associated with a 30- 70% risk of treatment-emergent depression. This risk could be due to the IFN, or to an interaction between the IFN and the indication for which it was prescribed. Various neurohormonal, neurochemical, neurohistological, and other mechanisms have been put forth to explain IFN-related depression. Prophylactic treatment with antidepressants reduces the risk of IFN-related depression; antidepressants also effectively treat the condition. Recent alternatives to IFNs have shown to decrease the risk of treatment-emergent depression.