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Background: Loss of control (LOC) is a pervasive feature of binge eating, which contributes significantly to the growing epidemic of obesity; approximately 80 million US adults are obese. Brain-responsive neurostimulation guided by the delta band was previously found to block binge-eating behavior in mice. Following novel preclinical work and a human case study demonstrating an association between the delta band and reward anticipation, the US Food and Drug Administration approved an Investigational Device Exemption for a first-in-human study., Objective: To assess feasibility, safety, and nonfutility of brain-responsive neurostimulation for LOC eating in treatment-refractory obesity., Methods: This is a single-site, early feasibility study with a randomized, single-blinded, staggered-onset design. Six subjects will undergo bilateral brain-responsive neurostimulation of the nucleus accumbens for LOC eating using the RNS® System (NeuroPace Inc). Eligible participants must have treatment-refractory obesity with body mass index ≥ 45 kg/m2. Electrophysiological signals of LOC will be characterized using real-time recording capabilities coupled with synchronized video monitoring. Effects on other eating disorder pathology, mood, neuropsychological profile, metabolic syndrome, and nutrition will also be assessed., Expected Outcomes: Safety/feasibility of brain-responsive neurostimulation of the nucleus accumbens will be examined. The primary success criterion is a decrease of ≥1 LOC eating episode/week based on a 28-d average in ≥50% of subjects after 6 mo of responsive neurostimulation., Discussion: This study is the first to use brain-responsive neurostimulation for obesity; this approach represents a paradigm shift for intractable mental health disorders., (Copyright © 2020 by the Congress of Neurological Surgeons.)

Language is a defining and prominent feature in humans. This faculty is impaired in those with schizophrenia. Individuals with schizophrenia show numerous abnormalities in language function, including symptoms of disorganized speech, auditory hallucinations, thought disorders, and verbal memory impairments. Structural and functional brain imaging with neurocognitive testing shows various aspects of brain structure and function associated with language that also are abnormal in schizophrenia. This article comparatively reviews this research and relates it to understanding the symptoms and pathophysiologic features of schizophrenia. Understanding the neural basis of language and its disruption in schizophrenia provides a guide for diagnosis, subtyping, treatment, and future research.

Background: Repetitive transcranial magnetic stimulation (rTMS) was approved in 2008 in the United States, and there are relatively few studies describing its use in regular clinical practice since approval.Methods: From April 2011 to October 2014, ten sites within the National Network of Depression Centers (NNDC) provided data on 62 evaluable patients with a depressive episode. Treatment was determined naturalistically. Response was assessed by the Quick Inventory of Depressive Symptoms, Self-Report (QIDS-SR) as the primary outcome, and the Patient Health Questionnaire-9 (PHQ-9) and the clinician-rated Clinical Global Impression (CGI) as secondary depression measures.Results: Enrolled patients exhibited significant treatment resistance, with 70.2% reporting more than 4 prior depressive episodes. Most patients received treatment with standard parameters (10Hz over the left dorsolateral prefrontal cortex), although 22.6% of the patients received 1 or 5Hz stimulation at some point. Over 6 weeks of treatment, response and remission rates were 29.4% and 5.9%, respectively, for the QIDS-SR; 39.2% and 15.7%, respectively, for the PHQ-9; and 50.9% and 17.9%, respectively, for the CGI. Moderator analyses revealed no effect of prior depressive episodes, history of ECT or gender, although early life stress predicted a better response to rTMS therapy.Limitations: The study was an open-label, registry trial, with relatively coarse clinical data, reflecting practice only in academic, depression-specialty centers. Because of the relatively small size and heterogeneity of the sample, type 2 errors are possible and positive findings are in need of replication.Conclusion: rTMS demonstrates effectiveness in clinical practice within the NNDC, although remission rates appear slightly lower in comparison with other recent naturalistic studies. [ABSTRACT FROM AUTHOR]

Abstract: Objective: Schizophrenia patients demonstrate impaired emotional processing that may be due, in part, to impaired facial emotion recognition. This study examined event-related potential (ERP) responses to emotional faces in schizophrenia patients and controls to determine when, in the temporal processing stream, patient abnormalities occur. Method: 16 patients and 16 healthy control participants performed a facial emotion recognition task. Very sad, somewhat sad, neutral, somewhat happy, and very happy faces were each presented for 100 ms. Subjects indicated whether each face was “Happy”, “Neutral”, or “Sad”. Evoked potential data were obtained using a 32-channel EEG system. Results: Controls performed better than patients in recognizing facial emotions. In patients, better recognition of happy faces correlated with less severe negative symptoms. Four ERP components corresponding to the P100, N170, N250, and P300 were identified. Group differences were noted for the N170 “face processing” component that underlies the structural encoding of facial features, but not for the subsequent N250 “affect modulation” component. Higher amplitude of the N170 response to sad faces was correlated with less severe delusional symptoms. Although P300 abnormalities were found, the variance of this component was explained by the earlier N170 response. Conclusion: Patients with schizophrenia demonstrate abnormalities in early visual encoding of facial features that precedes the ERP response typically associated with facial affect recognition. This suggests that affect recognition deficits, at least for happy and sad discrimination, are secondary to faulty structural encoding of faces. The association of abnormal face encoding with delusions may denote the physiological basis for clinical misidentification syndromes. [Copyright &y& Elsevier]