Repetitive Transcranial Magnetic Stimulation Treating Impulsivity in Borderline Personality Disorder and Attention Deficit/Hyperactivity Disorder

The need for novel treatment approaches that target impulsivity symptoms in neuropsychiatric disorders is clear. Repetitive transcranial magnetic stimulation (rTMS) allows selective neuromodulation of regions involved in the functional neuroanatomy of neuropsychiatric disorders. This chapter presents impulsivity in psychiatry, especially in borderline personality disorder (BPD) and attention-deficit hyperactivity disorder (ADHD), its neural underpinnings, and its possible treatment by rTMS. We reviewed available studies on rTMS in impulsivity in BPD and ADHD published before August 13, 2017, systematically searching in the PubMed, Web of Science, and Scopus databases. The results are discussed in the context of the latest neuropsychological models of impulsivity and their underlying functional neuroanatomy. rTMS treatment of impulsivity in BPD and ADHD seems to be a plausible approach. The functional neuroanatomy of processes related to impulsive behavior and decision making in these disorders is linked with abnormalities in the fronto-limbic structures that can be targeted and modulated by rTMS. Although limited evidence is available, rTMS seems to be a safe and potentially effective method of impulsivity treatment in patients with BPD and ADHD. However, more studies are needed to determine the most efficient cortical location and design for rTMS treatment of impulsivity

Transcranial Magnetic Stimulation in Schizophrenia

Transcranial magnetic stimulation (TMS) is a method that can be used in neurophysiological research of schizophrenia and in the treatment of some symptoms or syndromes of this mental disorder. The most important indications for TMS (or repetitive TMS—rTMS) are the negative symptoms of schizophrenia and auditory hallucinations. Other less proven indications include cognitive deficit, especially working memory. This text summarizes general knowledge about (r)TMS and its use in schizophrenia. According to recent experiences, TMS is a very promising experimental and therapeutic method, but it needs further research for its optimized use

Methods for Nonlinear Intersubject Registration in Neuroscience

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The mechanisms of movement control and time estimation in cervical dystonia patients

Traditionally, the pathophysiology of cervical dystonia has been regarded mainly in relation to neurochemical abnormities in the basal ganglia. Recently, however, substantial evidence has emerged for cerebellar involvement. While the absence of neurological "cerebellar signs" in most dystonia patients may be considered at least provoking, there are more subtle indications of cerebellar dysfunction in complex, demanding tasks. Specifically, given the role of the cerebellum in the neural representation of time, in the millisecond range, dysfunction to this structure is considered to be of greater importance than dysfunction of the basal ganglia. In the current study, we investigated the performance of cervical dystonia patients on a computer task known to engage the cerebellum, namely, the interception of a moving target with changing parameters (speed, acceleration, and angle) with a simple response (pushing a button). The cervical dystonia patients achieved significantly worse results than a sample of healthy controls. Our results suggest that the cervical dystonia patients are impaired at integrating incoming visual information with motor responses during the prediction of upcoming actions, an impairment we interpret as evidence of cerebellar dysfunction

Cortico-cerebellar functional connectivity and sequencing of movements in schizophrenia

<p>Abstract</p> <p>Background</p> <p>Abnormal execution of several movements in a sequence is a frequent finding in schizophrenia. Successful performance of such motor acts requires correct integration of cortico-subcortical processes, particularly those related to cerebellar functions. Abnormal connectivity between cortical and cerebellar regions with resulting cognitive dysmetria has been proposed as the core dysfunction behind many signs and symptoms of schizophrenia. The aim of the present study was to assess if these proposed abnormalities in connectivity are a unifying feature of schizophrenia, or, rather, reflect a specific symptom domain of a heterogeneous disease. We predicted that abnormal functional connectivity between the motor cortex and cerebellum would be linked with abnormal performance of movement sequencing.</p> <p>Methods</p> <p>We examined 24 schizophrenia patients (SCH) and 24 age-, sex-, and handedness-matched healthy controls (HC) using fMRI during a modified finger-tapping task. The ability to perform movement sequencing was tested using the Neurological Evaluation Scale (NES). The subjects were categorized into two groups, with (SQ+) and without (SQ-) movement sequencing abnormalities, according to the NES-SQ score. The effects of diagnosis and movement sequencing abnormalities on the functional connectivity parameters between the motor cortex and cerebellum (MC-CRBL) and the supplementary motor cortex and cerebellum (SMA-CRBL) activated during the motor task were analyzed.</p> <p>Results</p> <p>We found no effect of diagnosis on the functional connectivity measures. There was, however, a significant effect on the SQ group: SQ + patients showed a lower level of MC-CRBL connectivity than SQ- patients and healthy controls. Moreover, the level of MC-CRBL and SMA-CRBL negatively correlated with the magnitude of NES-SQ abnormalities, but with no other NES domain.</p> <p>Conclusions</p> <p>Abnormal cortico-cerebellar functional connectivity during the execution of a motor task is linked with movement sequencing abnormalities in schizophrenia, but not with the diagnosis of schizophrenia per se. It seems that specific patterns of inter-regional connectivity are linked with corresponding signs and symptoms of clinically heterogeneous conditions such as schizophrenia.</p

Supervised, Multivariate, Whole-Brain Reduction Did Not Help to Achieve High Classification Performance in Schizophrenia Research

We examined how penalized linear discriminant analysis with resampling, which is a supervised, multivariate, whole-brain reduction technique, can help schizophrenia diagnostics and research. In an experiment with magnetic resonance brain images of 52 first-episode schizophrenia patients and 52 healthy controls, this method allowed us to select brain areas relevant to schizophrenia, such as the left prefrontal cortex, the anterior cingulum, the right anterior insula, the thalamus and the hippocampus. Nevertheless, the classification performance based on such reduced data was not significantly better than the classification of data reduced by mass univariate selection using a t-test or unsupervised multivariate reduction using principal component analysis. Moreover, we found no important influence of the type of imaging features, namely local deformations or grey matter volumes, and the classification method, specifically linear discriminant analysis or linear support vector machines, on the classification results. However, we ascertained significant effect of a cross-validation setting on classification performance as classification results were overestimated even though the resampling was performed during the selection of brain imaging features. Therefore, it is critically important to perform cross-validation in all steps of the analysis (not only during classification) in case there is no external validation set to avoid optimistically biasing the results of classification studies

Depression and Anxiety after Acute Myocardial Infarction Treated by Primary PCI.

AIMS:The main objective of the study was to find out prevalence of depression and anxiety symptoms in the population of patients with AMI with ST-segment elevation (STEMI), treated with primary PCI (pPCI). Secondary target indicators included the incidence of sleep disorders and loss of interest in sex. METHODS AND RESULTS:The project enrolled 79 consecutive patients with the first AMI, aged <80 years (median 61 years, 21.5% of women) with a follow-up period of 12 months. Symptoms of depression or anxiety were measured using the Beck Depression Inventory II tests (BDI-II, cut-off value ≥14) and Self-Rating Anxiety Scale (SAS, cut-off ≥ 45) within 24 hours of pPCI, before the discharge, and in 3, 6 and 12 months). Results with the value p<0.05 were considered as statistically significant. The BDI-II positivity was highest within 24 hours after pPCI (21.5%) with a significant decline prior to the discharge (9.2%), but with a gradual increase in 3, 6 and 12 months (10.4%; 15.4%; 13.8% respectively). The incidence of anxiety showed a relatively similar trend: 8.9% after pPCI, and 4.5%, 10.8% and 6.2% in further follow-up. CONCLUSIONS:Patients with STEMI treated by primary PCI have relatively low overall prevalence of symptoms of depression and anxiety. A significant decrease in mental stress was observed before discharge from the hospital, but in a period of one year after pPCI, prevalence of both symptoms was gradually increasing, which should be given medical attention

Derivation and Molecular Characterization of a Morphological Subpopulation of Human iPSC Astrocytes Reveal a Potential Role in Schizophrenia and Clozapine Response

Abstract Astrocytes are the most abundant cell type in the human brain and are important regulators of several critical cellular functions, including synaptic transmission. Although astrocytes are known to play a central role in the etiology and pathophysiology of schizophrenia, little is known about their potential involvement in clinical response to the antipsychotic clozapine. Moreover, astrocytes display a remarkable degree of morphological diversity, but the potential contribution of astrocytic subtypes to disease biology and drug response has received little attention. Here, we used state-of-the-art human induced pluripotent stem cell (hiPSC) technology to derive a morphological subtype of astrocytes from healthy individuals and individuals with schizophrenia, including responders and nonresponders to clozapine. Using functional assays and transcriptional profiling, we identified a distinct gene expression signature highly specific to schizophrenia as shown by disease association analysis of more than 10 000 diseases. We further found reduced levels of both glutamate and the NMDA receptor coagonist d-serine in subtype astrocytes derived from schizophrenia patients, and that exposure to clozapine only rescued this deficiency in cells from clozapine responders, providing further evidence that d-serine in particular, and NMDA receptor-mediated glutamatergic neurotransmission in general, could play an important role in disease pathophysiology and clozapine action. Our study represents a first attempt to explore the potential contribution of astrocyte diversity to schizophrenia pathophysiology using a human cellular model. Our findings suggest that specialized subtypes of astrocytes could be important modulators of disease pathophysiology and clinical drug response, and warrant further investigations