Search

Persistent cognitive, medical and psychiatric complaints have been extensively described after recovery from acute SARS-CoV-2 infection.To describe neuropsychological, medical, psychiatric, and functional correlates of cognitive complaints experienced after recovery from acute COVID-19 infection.Sixty participants underwent neuropsychological, psychiatric, medical, functional, and quality-of-life assessments 6-8 months after acute COVID-19. Those seeking care for cognitive complaints in a post-COVID-19 clinical program for post-acute symptoms of COVID-19 (clinical group, N = 32) were compared with those recruited from the community who were not seeking care (nonclinical, N = 28). A subset of participants underwent serological testing for proinflammatory cytokines C-reactive protein, interleukin-6, and tumor necrosis factor-α to explore correlations with neuropsychological, psychiatric, and medical variables.For the entire sample, 16 (27%) had extremely low test scores (less than second percentile on at least 1 neuropsychological test). The clinical group with cognitive complaints scored lower than age-adjusted population norms in tests of attention, processing speed, memory, and executive function and scored significantly more in the extremely low range than the nonclinical group (38% vs. 14%, P0.04). The clinical group also reported higher levels of depression, anxiety, fatigue, posttraumatic stress disorder, and functional difficulties and lower quality of life. In logistic regression analysis, scoring in the extremely low range was predicted by acute COVID-19 symptoms, current depression score, number of medical comorbidities, and subjective cognitive complaints in the areas of memory, language, and executive functions. Interleukin-6 correlated with acute COVID symptoms, number of medical comorbidities, fatigue, and inversely with measures of executive function. C-reactive protein correlated with current COVID symptoms and depression score but inversely with quality of life.Results suggest the existence of extremely low neuropsychological test performance experienced by some individuals months after acute COVID-19 infection, affecting multiple neurocognitive domains. This extremely low neuropsychological test performance is associated with worse acute COVID-19 symptoms, depression, medical comorbidities, functional complaints, and subjective cognitive complaints. Exploratory correlations with proinflammatory cytokines support further research into inflammatory mechanisms and viable treatments.

Objective Inhalant users may develop toluene leukoencephalopathy, a devastating neuropsychiatric disorder. We present a case of toluene-induced damage to the corticospinal and the corticonuclear tracts, which presented with involuntary emotional expression disorder. Methods Case study of a 20-year-old man with a 3-year history of frequent solvent abuse was admitted to the Neuropsychiatry Unit of the National Institute of Neurology and Neurosurgery because “he could not speak or walk” but would keep “laughing and crying without reason”. Results Neuropsychiatric examination revealed pathological laughter and crying, facial and speech apraxia, a bilateral pyramidal syndrome, and lack of control of urinary sphincter. Magnetic resonance imaging revealed a highly selective bilateral damage to the pyramidal system and the somatosensory pathway. SPECT imaging showed left fronto-parietal hypoperfusion. Conclusions This document provides support for the understanding of involuntary emotional expression disorders as a differential diagnosis in the clinical practice of psychiatrists, as well as the functional anatomy of these conditions.

Psychiatric sequelae of traumatic brain injury (TBI) can cause significant and often chronic impairment in functioning and quality of life; however, their phenomenological and mechanistic complexities continue to present significant treatment challenges. The clinical presentation is often an amalgam of syndromes and co-occurring symptoms that require a highly nuanced and systematic approach to treatment. Although few randomized controlled trials have tested treatments for psychiatric problems after TBI and the synthesis of results continues to be compromised by the heterogeneity of study populations, small samples, and differing inclusion criteria and outcome measures, an increasing body of literature supports evidence-based treatment strategies. We provide a narrative review of pharmacological, psychoeducational/behavioral, and neuromodulation treatments for psychiatric conditions in adults with TBI and discuss known or postulated mechanisms of action for these treatment approaches. Where data are available, we focus on randomized controlled trials and large case series in which a psychiatric condition provides both a selection criterion and a primary or secondary outcome. We conclude by proposing directions for future research, particularly the need for novel neuropharmacological, behavioral, and neurophysiological studies and pragmatic trials of multicomponent and adaptive models that will increase understanding of the mechanisms underlying post-TBI psychiatric disorders and accelerate dissemination and implementation of effective person-centered care.

Synopsis Many patients with COVID-19 will experience acute or longer-term neuropsychiatric complications. The neurobiological mechanisms behind these are beginning to emerge, however the neurotropic hypothesis is not strongly supported by clinical data. The inflammatory response to SARS-CoV-2 is likely to be responsible for delirium and other common acute neuropsychiatric manifestations. Vascular abnormalities such as endotheliopathies contribute to stroke and cerebral microbleeds, with their attendant neuropsychiatric sequelae. Longer-term neuropsychiatric syndromes fall into two broad categories: neuropsychiatric deficits occurring after severe (hospitalised) COVID-19, and ‘long COVID’, which occurs in many patients with a milder acute COVID-19 illness.

Background Brain tumors are one of the most common solid tumors in pediatric populations, with their treatments having significant neuropsychiatric impact. Objective The objective of this study was to review the literature on neuropsychiatric sequelae after surgical resection of brain tumors in children and adolescents. Methods Using a scoping method, we reviewed empirical articles describing pediatric patients with brain tumors who underwent partial or total resection and examined major neuropsychiatric domains postoperatively over time. Results The initial search yielded 15,543 articles. After duplicate removal, abstract screening, and review, 44 articles were included. Cognitive deficits were the most widely studied outcomes and found to be associated with tumor location, operative variables, perioperative complications, treatment types, and psychosocial factors. Cerebellar mutism, or posterior fossa syndrome, commonly co-occurred with emotional and behavioral dysregulation after posterior fossa resections. Depression, anxiety, and somatization were frequently grouped together as “distress,” with higher rates among pediatric patients with brain tumor than among healthy peers. Problematic school behaviors, antisocial, and attention-deficit traits were increased; however, several other behaviors (e.g., risky sexual behaviors, substance use) were equal or lower when compared to peers. Posttraumatic stress disorder was highly prevalent and often interfered with social functioning. Delirium, eating disorders, and longer-term outcomes received inadequate attention. Conclusion Identifying risk factors of neuropsychiatric sequelae and their impact after pediatric brain tumor resection is important for prognostication and the development of tailored management strategies for these children and adolescents.

The outbreak of the pandemic associated with Severe Acute Respiratory Syndrome coronavirus 2 (SARS-CoV-2) led researchers to find new potential treatments, including nonpharmacological molecules such as zinc (Zn2+). Specifically, the use of Zn2+ as a therapy for SARS-CoV-2 infection is based on several findings: 1) the possible role of the anti-inflammatory activity of Zn2+ on the aberrant inflammatory response triggered by COronaVIrus Disease 19 (COVID-19), 2) properties of Zn2+ in modulating the competitive balance between the host and the invading pathogens, and 3) the antiviral activity of Zn2+ on a number of pathogens, including coronaviruses. Furthermore, Zn2+ has been found to play a central role in regulating brain functioning and many disorders have been associated with Zn2+ deficiency, including neurodegenerative diseases, psychiatric disorders, and brain injuries. Within this context, we carried out a narrative review to provide an overview of the evidence relating to the effects of Zn2+ on the immune and nervous systems, and the therapeutic use of such micronutrients in both neurological and infective disorders, with the final goal of elucidating the possible use of Zn2+ as a preventive or therapeutic intervention in COVID-19. Overall, the results from the available evidence showed that, owing to its neuroprotective properties, Zn2+ supplementation could be effective not only on COVID‐19–related symptoms but also on virus replication, as well as on COVID-19–related inflammation and neurological damage. However, further clinical trials evaluating the efficacy of Zn2+ as a nonpharmacological treatment of COVID-19 are required to achieve an overall improvement in outcome and prognosis., Statement of Significance: By summarizing the available literature on, and exploring the possible role of, zinc in SARS-CoV-2 infection, the present review suggests how Zn2+ supplementation may be effective in COVID-19–related neurological complications.

Introduction Phenylketonuria (PKU) is a rare, treatable inborn error of metabolism with frequent neurological and neuropsychiatric complications, especially in undiagnosed or insufficiently treated individuals. Given the wide range of clinical presentations and the importance of treatment implications, we here delineate the neurological and neuropsychiatric symptom spectrum in a large cohort of previously unreported adults with late-treated PKU. Methods We consecutively evaluated late-treated PKU cases and pooled clinical and paraclinical data, including video-material, from three centers with expertise in complex movement disorders, inborn errors of metabolism and pediatrics. Results 26 individuals were included (10 females, median age 52 years). Developmental delay and intellectual disability were omnipresent with severe impairment of expressive communication noted in 50% of cases. Movement disorders were prevalent (77%), including tremor (38%, mostly postural), stereotypies (38%), and tics (19%). One case had neurodegenerative levodopa-responsive parkinsonism. Mild ataxia was noted in 54% of cases and 31% had a history of seizures. Neuropsychiatric characteristics included obsessive-compulsive (35%) and self-injurious behaviors (31%), anxiety (27%), depression (19%) and features compatible with those observed in individuals with autism spectrum disorder (19%). Neuroimaging revealed mild white matter changes. Adherence to dietary treatment was inconsistent in the majority of cases, particularly throughout adolescence. Conclusion A history of movement disorders, particularly tremor, stereotypies and tics, in the presence of developmental delay, intellectual disability and neuropsychiatric features, such as obsessive-compulsive and self-injurious behaviors in adults should prompt the diagnostic consideration of PKU. Initiation and adherence to (dietary) treatment can ameliorate the severity of these symptoms.

Psychiatric education has struggled to move past dualistic notions separating mind from brain, and embrace the field's identity as a clinical neuroscience discipline. To modernize our educational systems, we must integrate neuroscience perspectives into every facet of our clinical work. To do this effectively, neuroscience education should be clinically relevant, informed by adult learning theory, and tailored to the individualized needs of learners. Classic neuropsychiatry skills can help us better understand our patients' brain function at the bedside. Integrating neuroscience perspectives alongside the other rich perspectives in psychiatry will help trainees appreciate the relevance of neuroscience to modern medical practice.

Neuropsychiatric manifestations of Huntington's disease (HD) can present years before motor symptoms. Nurses with specialized training provide superior care for HD patients, but HD exposure in nursing education is limited. Here we aimed to describe the historical neuropsychiatric burden in 50 HD patients and discuss implications for psychiatric nurses. Fifty patients with HD were assessed by a board-certified psychiatrist and completed surveys about symptoms, social history, medication use, and quality of life outcomes. Descriptive statistics were used to summarize patient characteristics, and correlation analyses assessed the relationships between neuropsychiatric symptoms and quality of life outcomes. Most patients (72%) reported a history of neuropsychiatric symptoms prior to their HD diagnosis. Prodromal anger/irritability was most common (52%), though few patients received treatment for this. Anxiety was the most common current symptom (78%), yet 40% of patients had never been prescribed an SSRI. Anxiety was associated with poorer patient-reported quality of life outcomes (p < .01). HD patients in this sample experienced frequent, early-onset neuropsychiatric symptoms. In coming years, psychiatric nurses in community settings will be more likely to encounter gene-positive HD patients before they develop motor symptoms. Psychiatric nurses can address identified gaps through enhanced screening and encouraging early intervention in those at risk.

Susac syndrome is a rare clinical condition, possibly mediated by an autoimmune process; the classic triad is composed of retinopathy, decreased hearing acuity and neuropsychiatric symptoms (encephalopathy). There are few cases reported with neuropsychiatric symptoms as the main manifestation. We present a case of Susac syndrome in a 34-year-old female with a predominance of neuropsychiatric symptoms, characterised by partial Kluver-Bucy syndrome, apathy syndrome, pathological laughter and crying, and cognitive dysfunction predominantly affecting attention, which showed a qualitative improvement with the use of immunological therapy. This case report highlights the importance of neuropsychiatric manifestations as clinical presentation in patients with neurological conditions.

International audience; Autoimmune Limbic Encephalitis (LE) is a relatively new category of immune-mediated diseases with a wide range of neuropsychiatric symptoms. LE associated with Glutamic Acid Decarboxylase (GAD) antibodies is difficult to diagnose due to its possible atypical presentation with neuropsychiatric and behavioral features. We performed a systematic review of literature and retrieved 21 cases of anti GAD-associated LE with neuropsychiatric signs. Median age at onset was 27 years with a female predominance (81.0 %) and median diagnostic delay of 6 months. Clinical presentation included typical LE symptoms such as anterograde amnesia (95.2 %) and temporal lobe or tonico-clonic seizures (95.2 %). Psychiatric symptoms were described in 61.9 % of patients, presenting as anxiety, depressive symptoms, apathy and behavioral changes. Extra-limbic symptoms were present in 14.3 % of patients. No neoplasia associated was found. Some patients had poor epileptic, cognitive and psychiatric outcomes requiring prolonged immunosuppressive treatment. The description of the neuropsychiatric spectrum of anti-GAD LE and its specificities aims to improve our understanding of this entity, and may lead to earlier diagnosis as well as better outcome.

Background Chloroquine and hydroxychloroquine are among several experimental treatments being investigated in the urgent response to the coronavirus disease-2019. With increased use of these medications, physicians need to become knowledgeable of these drugs' neuropsychiatric side effects and interactions with psychiatric medications. Objective: Clarify evidence base regarding the psychiatric side effects and psychiatric drug interactions of chloroquine and hydroxychloroquine. Methods A literature review was performed in PubMed from 1950 to 2020 regarding psychiatric topics and targeted pharmacological properties of chloroquine and hydroxychloroquine. Results First, chloroquine and hydroxychloroquine may mildly inhibit CYP2D6 metabolism of psychiatric medications, and psychiatric medications that interfere with CYP2D6 or CYP3A4 activity could alter chloroquine and hydroxychloroquine levels. Second, they may prolong the QT interval, warranting caution with concomitant prescription of other QT prolonging agents. Finally, neuropsychiatric side effects are very uncommon but possible and include a potentially prolonged phenomenon of “psychosis after chloroquine.” Hydroxychloroquine has less information available about its neuropsychiatric side effects than chloroquine, with psychosis literature limited to several case reports. Weak evidence suggests a possible association of hydroxychloroquine exposure and increased suicidal ideation. It is not clear whether patients with psychiatric illness are more vulnerable to neuropsychiatric sequela of these medications; however, overdose of these medications by suicidal patients has high risk of mortality. Conclusion The risk of neuropsychiatric side effects of chloroquine and hydroxychloroquine when used for coronavirus disease-2019 treatment is not known. Best practice may include suicide risk assessment for patients treated with hydroxychloroquine. However, delirium is expected to be a more likely etiology of neuropsychiatric symptoms in critically ill patients treated for coronavirus disease-2019, and adjustment disorder is a much more likely etiology of anxiety and depression symptoms than the side effects of chloroquine or hydroxychloroquine.

Background The pandemic of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has emerged as one of the biggest health threats of our generation. A significant portion of patients are presenting with delirium and neuropsychiatric sequelae of the disease. Unique examination findings and responses to treatment have been identified. Objective In this article, we seek to provide pharmacologic and treatment recommendations specific to delirium in patients with COVID-19. Methods We performed a literature search reviewing the neuropsychiatric complications and treatments in prior coronavirus epidemics including Middle Eastern respiratory syndrome and severe acute respiratory syndrome coronaviruses, as well as the emerging literature regarding COVID-19. We also convened a work group of consultation-liaison psychiatrists actively managing patients with COVID-19 in our hospital. Finally, we synthesized these findings to provide preliminary pharmacologic recommendations for treating delirium in these patients. Results Delirium is frequently found in patients who test positive for COVID-19, even in the absence of respiratory symptoms. There appears to be a higher rate of agitation, myoclonus, abulia, and alogia. No data are currently available on the treatment of delirium in patients with COVID-19. Extrapolating from general delirium treatment, Middle Eastern respiratory syndrome/severe acute respiratory syndrome case reports, and our experience, preliminary recommendations for pharmacologic management have been assembled. Conclusions COVID-19 is associated with neuropsychiatric symptoms. Low-potency neuroleptics and alpha-2 adrenergic agents may be especially useful in this setting. Further research into the pathophysiology of COVID-19 will be key in developing more targeted treatment guidelines.

Background Psychogenic nonepileptic seizures (PNES) represent one of the most sizable treatment challenges in neuropsychiatry. Although the underlying mechanism is far from being understood, several interventions have been suggested. However, patients with comorbid psychiatric diagnoses and epilepsy are excluded from most intervention studies. Objective To To present a within-group posttreatment vs pretreatment study representing the retrospective clinical results of an integrative psychotherapy model. Methods: We present the clinical results of 22 patients with PNES diagnosed in an epilepsy center and treated in our neuropsychiatry clinic using an integrative rehabilitative psychotherapy. Therapy included presenting the diagnosis, psychoeducation, seizure reduction behavioral techniques, and coping with past and present stressors. Insomuch as integrative biopsychosocial psychotherapy is based on an individualized treatment protocol for each patient, treatment was individualized and case specific. Results By the end of treatment, 36% of patients had become seizure free and a further 54% achieved a major seizure reduction (reduction of more than 70%). Seventy-two percent of patients kept at least 70% seizure reduction at follow-up. Global Assessment of Functioning scores improved from a mean of 43.09 to a mean of 72.81 at the end of treatment and 69.72 at follow-up. In addition, we present 3 case descriptions that emphasize the individualized nature of psychotherapeutic decisions. Conclusions Our results support the feasibility and effectiveness of biopsychosocial based integrative psychotherapy for PNES and set principles for future treatment and prospective clinical trials in the field of individualized psychotherapy.

Neuropsychiatry is an integrative discipline defined by its history, its preferred patients, and its theoretic framework. Dealing with human behavior needs to consider the brain, but such consideration should avoid oversimplification: neurologic understanding is not essential, necessary, or desirable in all conditions encountered in clinical psychiatry. Neuropsychiatric theory is founded on discoveries in the areas of synaptic plasticity and cortical/limbic anatomy (bottom-up), but also evolutionary biology and anthropology (top-down). Going forward, we need to synthesize vital information, distinguish the essential from the trivial or tenuous, and remain open to dialogue with allied disciplines, our patients, and our students.

Background Bipolar Disorder (BD) is a chronic psychiatric disorder characterized by mood disturbances that include depressive, manic, and hypomanic episodes. Despite the severity of the symptoms, there is still a gap in the literature on the precise neurobiology and treatment of BD. The investigations of inflammatory changes in BD has increased in the last decade, evincing the importance of its role in the pathophysiology of the disorder. The present study aimed to investigate the inflammatory role in BD, through the evaluation of biomarkers and their relation to biological rhythms. Methods It was conducted a case-control study that included 36 BD and 46 healthy controls (HC). The Cyclooxygenase 2 (COX-2) enzyme, Arachidonic Acid (AA), interleukins (IL) IL-4, IL-5, IL-6, IL-10, IL-33, and Tumor Necrosis Factor Alpha (TNF-α) in the serum of individuals. It also was administered the Biological Rhythm Interview of Assessment in Neuropsychiatry (BRIAN) to the BD and healthy control groups. Results: The results indicated that the individuals with BD showed increased COX-2, AA, IL-6, and TNF-α levels in comparison to the HC without psychiatric disorders, as well as significant commitments in all domains evaluated by BRIAN. Limitations Uncontrolled pharmacotherapy used by the included bipolar participants, which had important effects on participants’ inflammatory systems and the lack of cases with bipolar manic episodes. Conclusions The results of the present study reaffirm that inflammation has an important role in BD, as well as the significant changes in biological rhythms. It is still necessary to better characterize the inflammatory pathway of AA.

With the exponential development of mobile health technologies over the past ten years, there has been a growing interest in the potential applications in the field of epilepsy, and specifically for seizure detection. Better detection of seizures is probably one of the best ways to improve patient safety. Overall, we are observing an exponential increase in the number of non-EEG based seizure detection systems and a progressive homogenization of their evaluation procedures. Most importantly, the properties of these devices for detection of tonic-clonic seizures are now very interesting, both in terms of sensitivity and in terms of false-alarm rates. Accordingly, we might expect that these be used in clinical practice in the near future, especially in patients at high risk of seizure-related injuries or sudden unexpected death in epilepsy (SUDEP).

Deep brain stimulation (DBS) is considered a promising intervention for treatment-resistant obsessive-compulsive disorder (trOCD). We conducted a systematic search to investigate the efficacy and safety of DBS for OCD. Primary outcomes included the Yale-Brown Obsessive-Compulsive Scale (Y-BOCS), adverse events (AE), and quality of life. We assessed affective state, global functioning, cognition, and tolerability as secondary outcomes. Eight studies comprising 80 patients with trOCD were analysed both individually and collectively. We found a pooled mean reduction in Y-BOCS of 38.68 %, indicating DBS could be considered an effective therapy for trOCD. Most AE were mild and transient, however there were five severe surgery-related AE: intracerebral haemorrhage in three patients and infection in two. Mood-related serious AE were one completed suicide, three suicide attempts in two patients, and suicidal thoughts and depression in four. Despite this, affective state improved following stimulation. Despite being limited by significant heterogeneity across studies, our review has shown DBS to be an effective treatment in otherwise trOCD. There is a need to standardise study methodology in future research.

Background Anti–N-methyl-D-aspartate (NMDA) receptor encephalitis causes substantial neurological disability. Autoantibodies causing encephalitis directed against the neuronal cell surface or synapse are of diagnostic importance giving the possibility of successful immunotherapy. Objective In this study, we aim to provide supporting evidence that brain 18F-FDG-PET may be helpful in identifying likely patterns of regional brain glucose metabolism. Methods Thirty-three patients (18 men and 15 women; age range of 17–55 y) with positive NMDA receptor antibody encephalitis that underwent an 18F-FDG-PET imaging examination were prospectively selected and compared with a reference group of 14 brain 18F-FDG-PET scans from healthy volunteers using voxel-based statistical analysis. Clusters of hyper- and hypo-metabolism were reported for the whole sample of patients (FWE-corrected P Results Mixed metabolic patterns (focal/bilateral hypermetabolism in the temporal lobe, insula, and cerebellum; associated with severe bilateral hypometabolism in the occipital and parietal lobes) were found. Conclusions Our findings suggest that 18F-FDG-PET should be included as an imaging tool when assessing affected patients in the clinical workup to rule out anti-NMDA encephalitis and help determine the most effective treatment.

International audience

Recent research demonstrating that the glutamatergic modulator ketamine has rapid, robust, and sustained antidepressant effects has been a turning point in drug discovery for depression. The recent FDA approval of esketamine for adults with treatment-resistant major depressive disorder (MDD) has further underscored the relevance of this agent in spurring investigation into novel and mechanistically distinct agents for use in depression. Over the past two decades, ketamine research has ushered in a new wave of studies seeking to not only identify its mechanism of action but also to examine the antidepressant potential of novel or repurposed agents. This article reviews the approaches that have proven particularly fruitful for the field of neuropsychiatry.

Affective disorders, cognitive decline, and psychosis have long been recognized as common in Parkinson disease (PD), and other psychiatric disorders include impulse control disorders, anxiety symptoms, disorders of sleep and wakefulness, and apathy. Psychiatric aspects of PD are associated with numerous adverse outcomes, yet in spite of this and their frequent occurrence, there is incomplete understanding of epidemiology, presentation, risk factors, neural substrate, and management strategies. Psychiatric features are typically multimorbid, and there is great intra- and interindividual variability in presentation. The hallmark neuropathophysiological changes that occur in PD, plus the association between exposure to dopaminergic medications and certain psychiatric disorders, suggest a neurobiological basis for many psychiatric symptoms, although psychological factors are involved as well. There is evidence that psychiatric disorders in PD are still under-recognized and undertreated and although psychotropic medication use is common, controlled studies demonstrating efficacy and tolerability are largely lacking. Future research on neuropsychiatric complications in PD should be oriented toward determining modifiable correlates or risk factors and establishing efficacious and well-tolerated treatment strategies.

OBJECTIVE: Epidemiological research in functional somatic disorders such as irritable bowel syndrome, fibromyalgia, chronic fatigue syndrome, and bodily distress syndrome and related conditions such as health (illness) anxiety is often based on self-reported questionnaires or layman interviews. This study presents and describes the Research Interview for Functional somatic Disorders (RIFD) and provides first data regarding RIFD's ability to identify cases with functional somatic disorders and health anxiety in a two-phase design following self-reported symptom questionnaires.METHODS: RIFD was performed by phone by trained family physicians on a stratified subsample of 1590 adults from a Danish general population cohort (n = 7493). Criterion validity was tested in a small preliminary test including 25 RIFD participants using Schedules of Clinical Assessment in Neuropsychiatry (SCAN), performed by a specialist in functional somatic disorders, as gold standard. Interrater reliability between interviewers was tested in 15 participants.RESULTS: Compared with the comprehensive SCAN, preparation and conduction of RIFD were feasible and prompt. RIFD was well accepted by both interviewers and interviewees. RIFD identified cases with significantly more impairment than identified non-cases. Based on small preliminary tests, RIFD showed promising psychometric properties.CONCLUSION: RIFD was a feasible, well-accepted and promising instrument for use in large epidemiological studies. However, larger studies investigating its psychometric properties are needed.

The pharmacological research on the Cannabis sativa-derived compounds has never terminated. Among the phytocannabinoids without psychotropic effects, the prevalent one in Cannabis is cannabidiol (CBD). Although CBD was initially considered a type 2 cannabinoid receptor (CB2R) antagonist, it did not show a good cannabinoidergic activity. Furthermore, heterogeneous results were obtained in experimental animal models of anxiety disorders, psychotic stages and neurodegenerative diseases. Recently, CBD has been authorized by the FDA to treat some rare forms of epilepsy and many trials have begun for the treatment of autism spectrum disorders. This review aims to clarify the pharmacological activity of CBD and its multiple therapeutic applications. Furthermore, critical and conflicting results of the research on CBD are discussed with a focus on promising future prospects.

The development of next-generation therapies for neuropsychiatric illness will likely rely on a precise and accurate understanding of human brain dynamics. Toward this end, researchers have focused on collecting large quantities of neuroimaging data. For simplicity, we will refer to large cross-sectional neuroimaging studies as broad studies and to intensive longitudinal studies as deep studies. Recent progress in identifying illness subtypes and predicting treatment response in neuropsychiatry has been supported by these study designs, along with methods bridging machine learning and network science. Such methods combine analytic power, interpretability, and direct connection to underlying theory in cognitive neuroscience. Ultimately, we propose a general framework for the treatment of neuropsychiatric illness relying on the findings from broad and deep studies combined with basic cognitive and physiologic measurements.

Resting-state functional MRI (rsfMRI) is a useful technique for investigating the functional organization of human gray-matter in neuroscience and neuropsychiatry. Nevertheless, most studies have demonstrated the functional connectivity and/or task-related functional activity in the gray-matter. White-matter functional networks have been investigated in healthy subjects. Schizophrenia has been hypothesized to be a brain disorder involving insufficient or ineffective communication associated with white-matter abnormalities. However, previous studies have mainly examined the structural architecture of white-matter using MRI or diffusion tensor imaging and failed to uncover any dysfunctional connectivity within the white-matter on rsfMRI. The current study used rsfMRI to evaluate white-matter functional connectivity in a large cohort of ninety-seven schizophrenia patients and 126 healthy controls. Ten large-scale white-matter networks were identified by a cluster analysis of voxel-based white-matter functional connectivity and classified into superficial, middle and deep layers of networks. Evaluation of the spontaneous oscillation of white-matter networks and the functional connectivity between them showed that patients with schizophrenia had decreased amplitudes of low-frequency oscillation and increased functional connectivity in the superficial perception-motor networks. Additionally, we examined the interactions between white-matter and gray-matter networks. The superficial perception-motor white-matter network had decreased functional connectivity with the cortical perception-motor gray-matter networks. In contrast, the middle and deep white-matter networks had increased functional connectivity with the superficial perception-motor white-matter network and the cortical perception-motor gray-matter network. Thus, we presumed that the disrupted association between the gray-matter and white-matter networks in the perception-motor system may be compensated for through the middle-deep white-matter networks, which may be the foundation of the extensively disrupted connections in schizophrenia.

Background Apart from inattention, hyperactivity and impulsivity, ADHD in childhood presents with an impairment of motor coordination and balance functions. Until now, literature is scarce about sensorimotor deficits in adult ADHD. This is a pilot study that identifies and quantifies the role of sensory, motor, and central adaptation mechanisms for adult ADHD patients’ sensorimotor deficits in a systematic way, using postural control. Methods We analyzed spontaneous and externally perturbed stance in ten adult patients suffering from ADHD. Findings were compared to data from ten matched healthy subjects. Results Spontaneous sway amplitudes and velocities were larger in ADHD patients compared to healthy subjects. Furthermore, body excursions as a function of platform tilts were abnormally large in ADHD patients, specifically in the low frequency range. Based on simple feedback model simulations, we found that ADHD patients showed a larger time delay between platform tilts and body response, and a lower value of the integral part of the neural controller, which affects the long-term control of their posture. These postural abnormalities correlated well with the hyperactivity and impulsivity dimensions of the individual ADHD symptoms. Conclusion We conclude that adult ADHD patients’ major postural deficit consists of an impairment of a stable, long-term sensorimotor behavior, which fits very well to the concept of impulsivity and hyperactivity.

Highlights • Neurological symptoms are common in the acute and convalescence phases of viral pandemic • Headache and insomnia are prevalent even among uninfected general public • Early detection and appropriate interventions are essential to handle the neuropsychiatric sequelae., Corona virus disease (COVID-19) has been declared as a controllable pandemic by the World Health Organization (WHO). COVID-19 though is a predominantly respiratory illness; it can also affect brain and other organs like kidneys, heart and liver. Neuropsychiatric manifestations are common during viral pandemics but are not effectively addressed. Fever and cough are common symptoms only in infected individuals but headache and sleep disturbances are common even in uninfected general public. In this selective review, the authors report the available evidence of neuropsychiatric morbidity during the current COVID-19 crisis. The authors also discuss the postulated neuronal mechanisms of the corona virus infection sequelae.

This article reviews the most salient neurobiological information available about borderline personality disorder (BPD) and presents a theoretic model for what lies at the heart of BPD that is grounded in those findings. It reviews the heritability, genetics, and the biological models of BPD, including the neurobiology of affective instability, impaired interoception, oxytocin and opiate models of poor attachment or interpersonal dysfunction, and structural brain imaging over the course of development in BPD; and posits that the core characteristic of BPD may be an impairment in emotional interoception or alexithymia.

Based on the intellicage paradigm, we have developed a novel cognitive, emotional and social phenotyping battery that permits comprehensive standardized behavioral characterization of mice in an experimenter-independent social setting. Evaluation of this battery in a large number of male and female C57BL/6 wildtype mice, tested in >20 independent cohorts, revealed high reproducibility of the behavioral readouts and may serve as future reference tool. We noticed robust sex-specific differences in general activity, cognitive and emotional behavior, but not regarding preference for social pheromones. Specifically, female mice revealed higher activity, decreased sucrose preference, impaired reversal and place-time-reward learning. Furthermore, female mice reacted more sensitively than males to reward-withdrawal showing a negative emotional contrast/Crespi-effect. In a series of validation experiments, we tested mice with different pathologies, including neuroligin-3 deficient mice (male Nlgn3y/- and female Nlgn3+/-) for autistic behavior, oligodendrocyte-specific erythropoietin receptor knockout (oEpoR-/-) mice for cognitive impairment, as well as mouse models of renal failure (unilateral ureteral obstruction and 5/6 nephrectomy) and of type 2 diabetes (ApoE-/-) - for delineating potentially confounding effects of motivational factors (thirst, glucose-craving) on learning and memory assessments. As prominent features, we saw in Nlgn3 mutants reduced preference for social pheromones, whereas oEpoR-/- mice showed learning deficits in place or reversal learning tasks. Renal failure led to increased water intake, and diabetic metabolism to enhanced glucose preference, limiting interpretation of hereon based learning and memory performance in these mice. The phenotyping battery presented here may be well-suited as high-throughput multifaceted diagnostic instrument for translational neuropsychiatry and behavioral genetics.

Impairments in social cognition may reflect dysfunction of disorder specific or disorder general mechanisms. Although cross-disorder comparison may prove insightful, few studies have compared social cognition in different neuropsychiatric disorders. Parallel investigation of schizophrenia and Tourette syndrome (TS) is encouraged by similarities including the presence of problematic social behavior, echophenomena, emotional dysregulation and dopamine dysfunction. Focusing on tests of social cognition administered in both disorders, this review aims to summarize behavioral, neurophysiological and neuroimaging findings, before exploring how these may contribute to clinical symptoms. Studies investigating social cognition (imitation, emotion recognition, and understanding of beliefs or intentions) in patients with schizophrenia or TS were identified through Web of Science and PubMed searches. Although findings indicate that social cognitive deficits are more apparent in schizophrenia, adults with TS can exhibit similar task performance to patients with paranoia. In both disorders, behavioral and neuroimaging findings raise the possibility of increased internal simulation of others' actions and emotions, in combination with a relative under-application of mentalizing. More specifically, dysfunction in neurobiological substrates such as temporo-parietal junction and inferior frontal gyrus may underlie problems with self-other distinctions in both schizophrenia and TS. Difficulties in distinguishing between actions and mental states linked to the self and other may contribute to a range of psychiatric symptoms, including emotional dysregulation, paranoia, social anhedonia and socially disruptive urges. Comparing different patient populations could therefore reveal common neuro-cognitive risk factors for the development of problematic social behaviors, in addition to markers of resilience, coping strategies and potential neuro-compensation mechanisms.

Background Major depression after traumatic brain injury (TBI) has devastating consequences as it increases the risk of suicide, impairs overall quality of life, and affects interpersonal, occupational, and social functioning. Although the literature has reported factors associated with depression after TBI, very few studies have examined the prevalence and correlates focused on the development of new-onset depression (NOD) after first-time TBI. Our study aimed to identify TBI- and non–TBI-related factors associated with the development of NOD in the first year after TBI. Methods A total of 103 subjects with first-time TBI were seen within 12 months postinjury and evaluated for the development of NOD at 3, 6, and 12 months. Results Frontal lobe functioning, frontal lesions, and pre-TBI/early post-TBI social impairment were not found to be predictors of development of NOD within the first year after injury. Decreased post-TBI social functioning as perceived by the subject at 3, 6, and 12 months was found to be associated with NOD at each of these time points, respectively. Conclusion The study findings highlight the importance of psychotherapeutic interventions to address the individuals' overall perception of their social impairment in the early-TBI period. This may help decrease the progression of major depression within the first year after injury.

Nonvascular neurological manifestations of antiphospholipid antibodies (aPLAbs) are emerging and, among these, several neuropsychiatric shymptoms. Psychiatric diseases are gradually being considered as organic illnesses of the brain. The role of blood-brain barrier regulation is under scrutiny, and increased permeability is thought to play a precipitating role. Neuropsychiatric manifestations in women with antiphospholipid syndrome (APS) are suspected of being secondary to direct binding and the effect of aPLAbs on neurons and glial cells once the permeability of the blood-brain barrier has been altered. Placental diseases, sometimes mediated by aPLAbs, are risk factors for schizophrenia in the offspring, and babies born from women with aPLAbs can develop learning disabilities and autism spectrum disorders. Women with APS more often develop mood disorders as time goes by, and diffusion tensor imaging has evidenced subtle changes in their white matter. More data are urgently needed and the therapeutic management remains to be properly planned.

The current study examined the validity of conversational analysis (CA) in Russian patients with seizures, using a scoring table for the Simplified Linguistic Evaluation (SLE). The study sample was composed of 12 adult participants suffering either from epilepsy (ES) or psychogenic nonepileptic seizures (PNES) recruited in the Moscow Research and Clinical Center for Neuropsychiatry. Definitive diagnosis was established only after a habitual event was captured onvEEG. All participants with PNES or ES and at least one mental disorder underwent a 20-minute-long interview recorded on video. The interview then was evaluated by the external blinded physician already experienced in CA. Finally, that physician filled the SLE, consisting of 5 items analyzing the main characteristics of patient narrations. A score of ≥12 suggested a diagnosis of ES, while a score of

Notwithstanding major advances in psychotherapeutics, their efficacy and specificity remain limited. The slow onset of beneficial outcomes and numerous adverse effects of widely used medications remain of chief concern, warranting in-depth studies. The majority of frontline therapies are thought to enhance the endogenous monoaminergic drive, to initiate a cascade of molecular events leading to lasting functional and structural plasticity. They also involve alterations in trophic factor signalling, including brain-derived neurotrophic factor (BDNF), VGF (non-acronymic), vascular endothelial growth factor (VEGF), fibroblast growth factor 2 (FGF2), glial cell-derived neurotrophic factor (GDNF), and others. In several major mental disorders, emerging data suggest protective and restorative effects of trophic factors in preclinical models, when applied on their own. Antidepressant outcomes of VGF and FGF2, for instance, were shown in experimental animals, while BDNF and GDNF prove useful in the treatment of addiction, schizophrenia, and autism spectrum disorders. The main challenge with the effective translation of these and other findings in the clinic is the knowledge gap in action mechanisms with potential risks, as well as the lack of effective platforms for validation under clinical settings. Herein, we review the state-of-the-art and advances in the therapeutic use of trophic factors in several major neuropsychiatric disorders.

MiRNAs are emerging as key molecules to study neuropsychiatric diseases. However, despite the large number of methodologies and software for miRNA-seq analyses, there is little supporting literature for researchers in this area. This review focuses on evaluating how miRNA-seq has been used to study neuropsychiatric diseases to date, analyzing both the main findings discovered and the bioinformatics workflows and tools used from a methodological perspective. The objective of this review is two-fold: first, to evaluate current miRNA-seq procedures used in neuropsychiatry; and second, to offer comprehensive information that can serve as a guide to new researchers in bioinformatics. After conducting a systematic search (from 2016 to June 30, 2020) of articles using miRNA-seq in neuropsychiatry, we have seen that it has already been used for different types of studies in three main categories: diagnosis, prognosis, and mechanism. We carefully analyzed the bioinformatics workflows of each study, observing a high degree of variability with respect to the tools and methods used and several methodological complexities that are identified and discussed in this review.

Microbes inhabit different anatomical sites of the human body including oral cavity, gut, and skin. A growing literature highlights how microbiome variation is associated with human health and disease. There is strong evidence of bidirectional communication between gut and brain mediated by neurotransmitters and microbial metabolites. Here, we review the potential involvement of microbes residing in the gut and in other body sites in the pathogenesis of eight neuropsychiatric disorders, discussing findings from animal and human studies. The data reported provide a comprehensive overview of the current state of the microbiome research in neuropsychiatry, including hypotheses about the mechanisms underlying the associations reported and the translational potential of probiotics and prebiotics.

Background Recent treatment guidelines support treatment of biological rhythm abnormalities as a part of treatment of bipolar disorder, but still, literature examining various domains (Sleep, Activity, Social, and Eating) of biological rhythm and its clinical predictors are less. Objectives The main aim of our study is to compare various domains of biological rhythm among remitted bipolar I subjects and healthy controls. We also explored for any association between clinical variables and biological rhythm among bipolar subjects. Methods 40 subjects with Bipolar I disorder and 40 healthy controls who met inclusion and exclusion criteria were recruited for the study. Diagnoses were ascertained by a qualified psychiatrist using MINI 5.0. Sociodemographic details, biological rhythm (BRIAN—Biological Rhythm Interview of assessment in Neuropsychiatry) and Sleep functioning (PSQI- Pittsburgh Sleep Quality Index) were assessed in all subjects. Results Mean age of the Bipolar subjects and controls were 41.25 ± 11.84 years and 38.25 ± 11.25 years respectively. Bipolar subjects experienced more biological rhythm disturbance when compared to healthy controls (total BRIAN score being 34.25 ± 9.36 vs 28.2 ± 6.53) (p = 0.002). Subsyndromal depressive symptoms (HDRS) had significant positive correlation with BRIAN global scores(r = 0.368, p = 0.02). Linear regression analysis showed that number of episodes which required hospitalization (β = 0.601, t = 3.106, P = 0.004), PSQI (β = 0.394, t = 2.609, p = 0.014), HDRS (β = 0.376, t = 2.34, t = 0.036) explained 31% of variance in BRIAN scores in remitted bipolar subjects. Conclusion Biological rhythm disturbances seem to persist even after clinical remission of bipolar illness. More studies to look into the impact of subsyndromal depressive symptoms on biological rhythm are needed.

BACKGROUND: Biological rhythms (BR) disturbance has been suggested as a potential mediator of mood episodes in Bipolar Disorder (BD). The Biological Rhythms Interview of Assessment in Neuropsychiatry (BRIAN) was designed as an assessment tool to evaluate BR domains comprehensively. In the context of a trial evaluating a smartphone application delivering personalized psychoeducational contents for BD (SIMPLe 1.0), the main aim of this study is to evaluate the potential impact of SIMPLe 1.0 in BR regulation using the BRIAN scale.METHODS: 51 remitted BD patients were asked to use the application for 3 months. Paired t-test analyses were employed to compare baseline and follow-up BRIAN´s total and domains scores. The sample was divided into completers and non-completers of the study to evaluate differences between groups regarding BRIAN scores using ANCOVA analyses.RESULTS: The BRIAN's mean total score of the whole sample significantly decreased from baseline to post-intervention (35.89 (SD 6.64) vs. 31.18 (SD 6.33), t = 4.29, p = 0.001). At post-intervention, there was a significant difference between groups regarding the total BRIAN mean score (29.47 (SD 6.21) completers vs. 35.92 (SD 3.90) non-completers, t = 2.50, p = 0.02). This difference was maintained after conducting a one-way ANCOVA controlling for pre-intervention BRIAN scores, F (1, 46) = 10.545, p=0.002.LIMITATIONS: A limited sample, pre-post measures, and a short study timeframe could have affected the results. Additional factors affecting BR, such as medication, could not be ruled out.CONCLUSION: Our results suggest that there are potential positive effects of a psychoeducational smartphone application as an adjunctive to treatment as usual on BD patients' BR.

Comorbid behavioral and physical health conditions are accompanied by troubling symptom burden, functional impairment, and treatment complexity. Pediatric subspecialty care clinics offer an opportunity for the implementation of integrated behavioral health (BH) care models that promote resiliency. This article reviews integrated BH care in oncology, palliative care, pain, neuropsychiatry, cystic fibrosis, and transplantation. Examples include integrated care mandates, standards of care, research, and quality improvement by child and adolescent psychiatrists (CAPs) and allied BH clinicians. The role of CAPs in integrated BH care in subspecialty care is explored, focusing on cost, resource use, financial support, and patient and provider satisfaction.

Orbitofrontal syndrome is a neuropsychiatric syndrome composed of cognitive, affective and behavioural symptoms, disrupting some of the traits that define us as a species, like cognitive flexibility and affective regulation. In order to effectively treat the condition, the clinician needs to be familiar with both the functional neuroanatomy and the neuropsychiatric semiology of the syndrome. A review of the literature is presented, emphasising the broad spectrum of clinical manifestations of the syndrome, together with three clinical vignettes showing the many faces of the syndrome. Several factors influencing the heterogeneity of clinical presentation are discussed. Taking a hierarchical model of neural networks, two core concepts, loss of interoceptive/exteroceptive integration and loss of affective regulation, are proposed in looking for invariants in orbitofrontal syndrome.

Obsessive-compulsive disorder (OCD) is a debilitating neuropsychiatric disorder that causes the patient to experience intrusive thoughts and/or to carry out repetitive, ritualized behaviors that are time consuming and impairing. OCD is familial and heritable. The genetic factors responsible for pathogenesis, however, remain largely unknown despite the numerous candidate gene studies conducted. Based on efficacy of serotonin reuptake inhibitors (SRIs) in treating OCD, serotonin system genes have been a dominant focus in OCD candidate gene studies. We review the most commonly studied candidate serotonin system gene variants (specifically in SLC6A4, HTR2A, HTR1B, and HTR2C) and their association with OCD. Although findings to date are mixed, serotonin transporter polymorphism 5-HTTLPR and HTR2A polymorphism rs6311 (or rs6313) are most consistently associated with OCD. Mixed findings may be the result of genetic complexity and phenotypic heterogeneity that future studies should account for. Homogenous patient subgroups reflecting OCD symptom dimensions, OCD subtypes, and sex should be used for gene discovery.

Background In recent decades, psychiatrists have become increasingly involved in the care of patients with cancer. Psychiatrists are often less familiar with the field of radiation oncology than with other medical specialties. Objective Therefore, it is beneficial for consulting psychiatrists to be familiar with the basic principles of radiation therapy (RT) and its potential neuropsychiatric sequelae. Methods We performed a PubMed search to identify articles describing neuropsychiatric symptoms resulting from RT, including anxiety, claustrophobia, posttraumatic stress disorder, and neurocognitive impairment. We also searched for other sequelae of RT that may produce psychiatric symptoms, such as radiation necrosis and endocrinopathies. We provide a basic introduction to the delivery of RT. Results Psychiatrists may be involved in the treatment of patients before, during, or after RT, and each phase of treatment produces unique considerations. Anxiety about the treatment, especially the need for immobilization with a mask, can be treatment-limiting. Adverse effects from treatment, including cognitive impairment and endocrinopathies, can result in psychiatric symptoms. Conclusions Consulting psychiatrists should be familiar with the basic principles of RT and the neuropsychiatric sequelae that may result from the treatment. Further research is needed to identify strategies to help patients tolerate RT and to identify additional preventive and therapeutic options for RT-induced cognitive impairment.

Neurocognitive and psychiatric complications are common following cardiac surgery and impact on patient quality of life, recovery from surgery, participation in rehabilitation and long-term mortality. Postoperative cognitive decline, depressive disorders, post-traumatic stress disorder and neurocognitive impairment related to silent brain infarcts have all been linked to the perioperative period of cardiac surgery, and potentially have serious consequences. The accurate assessment of these conditions, particularly in determining the aetiology, and impact on patients is difficult due to the poorly recognised nature of these complications as well as similarities in presentation with postoperative delirium. This review aims to summarise current understanding surrounding psychiatric disturbances following cardiac surgery including the impact on patient quality of life and long-term outcomes.

The purpose of this study is to identify the top 100-cited articles dedicated to epilepsy and status epilepticus published in journals from January, 1950 through February, 2016 that have made key contributions in the field. We performed a search of journals and selected the top 100-cited articles on epilepsy and status epilepticus, respectively, by utilizing the Institute for Scientific Information database available under the banner of the Web of Science. The top-cited articles on epilepsy and status epilepticus were all published in 24 journals, respectively. In both fields of epilepsy and status epilepticus, the most frequently cited journal was Epilepsia (26 articles on epilepsy and 19 articles on status epilepticus). The 100 most-cited articles in the field of both epilepsy and status epilepticus mainly originated from institutions in the United States of America. The articles on epilepsy included 25 laboratory studies, 15 pharmacotherapy studies, 13 general review studies, 12 surgery studies, 11 neuroimaging studies, eight epidemiology studies, eight neuropsychiatry studies, six genetic studies, and two electrophysiology studies, whereas 41 laboratory studies, 21 epidemiology studies, 16 pharmacotherapy studies, nine electrophysiology studies, nine general review studies, and four neuroimaging studies were included in the field of status epilepticus. We demonstrate that neuroimaging, genetics, and surgery are emerging topics in the field of epilepsy over the past decades. Moreover, we found that the majority of top-cited articles on epilepsy and status epilepticus originated from institutions in the United States of America and most were published in Epilepsia.