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Background Many people are not recovering for months after being infected with COVID-19. Long Covid (LC) is a major public health problem that needs defining, quantifying and describing. We aimed to explore and develop understanding of LC symptoms following mild/moderate COVID-19 infection and describe its impact on daily life. Methods The survey was co-produced with people living with LC. Data was collected through an online social media survey mostly from online support groups using convenience non-probability sampling. The criteria for inclusion were adults with lab-confirmed or suspected COVID-19 infection managed in the community (non-hospitalised) in the first two weeks of illness. We used agglomerative hierarchical clustering to identify specific symptom clusters, and their demographic, and functional correlates. Results Data from 2550 participants with a median duration of illness of 7.7 months (interquartile range (IQR) 7.4–8.0) was analysed. The mean age was 46.5 years (standard deviation 11 years) with 82.8% females and 79.9% UK-based. 90% reported good, very good or excellent health prior to infection. Most participants described fluctuating (57.7%) or relapsing LC symptoms (17.6%). The most common initial symptoms that continued were exhaustion, headache, chest pressure/tightness and breathlessness. Cough, fever and chills were prevalent initial symptoms that became less so as the illness progressed. Cognitive dysfunction and palpitations became more common beyond the acute phase. 26.5% reported lab-confirmation of infection (NAAT or antibody). The biggest difference in symptoms between those who reported testing positive and those who did not was loss of smell/taste. Physical activity, stress and sleep disturbance were the most common symptom triggers. A third (32%) reported they were unable to live alone without any assistance at six weeks from start of illness. 66.4% reported taking time off sick, (median 60 days, IQR 20, 129). 37% reported loss of income due to illness. Eighty four percent of participants reported ongoing symptoms affecting at least three organ systems. There were two main ongoing symptoms clusters; the majority cluster (88.7%) exhibited mainly chest, cognitive symptoms and exhaustion, and the minority cluster (11.3%) exhibited multi-system symptoms which had persisted from the start. The multi-system cluster reported more severe functional impact. Conclusion This is an exploratory survey of LC characteristics. Whilst it is a non-representative sample, it highlights the heterogeneity of persistent symptoms, and the significant functional impact. To better characterise ongoing illness and prognosis, research is needed in a representative population-sample using standardised case definitions (to include those not lab-confirmed in the first pandemic wave).

The neurodegenerative and neurodevelopmental hypotheses represent the basic etiological framework for the origin of schizophrenia. Additionally, the dopamine hypothesis, adopted more than two decades ago, has repeatedly asserted the position of dopamine as a pathobiochemical substrate through the action of psychostimulants and neuroleptics on the mesolimbic and mesocortical systems, giving insight into the origin of positive and negative schizophrenic symptoms. Meanwhile, cognitive impairments in schizophrenia remain incompletely understood but are thought to be present during all stages of the disease, as well as in the prodromal, interictal and residual phases. On the other hand, observations on the effects of NMDA antagonists, such as ketamine and phencyclidine, reveal that hypoglutamatergic neurotransmission causes not only positive and negative but also cognitive schizophrenic symptoms. This review aims to summarize the different hypotheses about the origin of psychoses and to identify the optimal neuroimaging method that can serve to unite them in an integral etiological framework. We systematically searched Google scholar (with no concern to the date published) to identify studies investigating the etiology of schizophrenia, with a focus on impaired central neurotransmission. The complex interaction between the dopamine and glutamate neurotransmitter systems provides the long-needed etiological concept, which combines the neurodegenerative hypothesis with the hypothesis of impaired neurodevelopment in schizophrenia. Pharmaco-magnetic resonance imaging is a neuroimaging method that can provide a translation of scientific knowledge about the neural networks and the disruptions in and between different brain regions, into clinically applicable and effective therapeutic results in the management of severe psychotic disorders.

Psychotic disorders occur as a result of pathobiochemical processes in the brain, which disrupt the central neurotransmission of molecules such as dopamine and glutamate. The dopamine hypothesis, adopted more than 2 decades ago, has repeatedly asserted its position as an etiopathogenetic substrate through the action of psychostimulants and neuroleptics on the mesolimbic and mesocortical systems, giving insight into the origin of positive and negative schizophrenic symptoms. On the other hand, cognitive impairments in schizophrenia remain not fully understood but are thought to be present during all stages of the disease, as well as in the prodromal the interictal and residual phases. Over the last decade, functional magnetic resonance imaging has focused on research of brain networks like the Default mode network, the Salience network and Central executive network, enabling a deeper understanding of cognitive deficits, as well as other phenomena such as disorganization of thought and behavior. The study of the nodes of these networks, such as the precuneus and insula, informs about their complex significant roles as structures responsible for important cognitive domains such as concentration, attention, ability to understand and reproduce information, as well as memory functions. It is suggested that the neurotransmission of dopamine and glutamate play a key role in these processes and their successful modulation in the correct brain regions through psychopharmacological and biomedical instrumental methods may lead to a significant reversal of conventional paradigms. Pharmaco-magnetic resonance imaging is a neuroimaging method that can provide the translation of scientific knowledge about the neural networks and the disruptions in and between different brain regions, into clinically applicable and effective therapeutic results in the management of severe psychotic disorders.

Cognitive reserve is originally an epidemiological concept that encompasses individual abilities to cope with changes. It is considered the result of a balance between processes of cellular damage and repair, and its description raised much interest in predicting and preventing cognitive decline in aging and Alzheimer's disease (AD). In this study, we discussed the concept of cognitive reserve considering the recent definition of AD as a biological continuum and suggest that the protection of cognitive reserve may result from efficient synaptic plasticity mechanisms. Despite pathological changes of AD appearing very early during life, long before the onset of cognitive symptoms, different variables act together to keep repair mechanisms effective guaranteeing successful aging if environmental enrichment is maintained.

Introducción. La medición de la dimensión de síntomas cognitivos en depresión es cada vez más relevante ya que se destaca como un elemento determinante en la remisión y predictor de recaídas. Objetivo. Elaboración y validación de una escala de medición de afectación de síntomas cognitivos en depresión, que sea completa, fácil y práctica de aplicar en pacientes deprimidos mexicanos. Método. Realizamos dos reuniones de consenso expertos en depresión para crear los reactivos a incluir en la escala y obtener la validez de constructo. Se aplicó la Escala de Autoevaluación para Depresión y Funcionalidad (EsADFUN) a un grupo de pacientes afectados por depresión de entre 18 y 65 años de edad y a un grupo control pareado por edad, género y escolaridad. Así como la Entrevista Neuropsiquiátrica Internacional (MINI), la Escala de Depresión de Beck, el Cuestionario Sobre la Salud del Paciente (PHQ- 9) y la Prueba de Sustitución de Dígitos y Símbolos (DSST). Resultados. La EsADFUN tuvo una validez de constructo y discriminante adecuada, así como una adecuada consistencia interna, con sensibilidad del 97% y especificidad del 83%. Se observó una correlación leve a moderada, pero significativa entre la severidad de los síntomas depresivos y la afectación cognitiva. Se obtuvo una correlación positiva entre el ítem 10 del EsADFUN y el DSST siendo una pregunta aceptablemente válida para evaluar la velocidad de procesamiento. Discusión y conclusión. Se demostró que la EsADFUN es una escala válida y completa para evaluar los síntomas cognitivos de pacientes deprimidos para propósitos clínicos y de investigación.

Background Vertebral artery dissection (VAD) may cause cerebral ischemia and impair quality of life (QOL) despite of good functional outcome. The aim of this study was the multimodal analysis of patient characteristics after VAD to identify contributing factors. Methods In an exploratory study, 34 consecutive patients with first-ever spontaneous VAD were prospectively examined in comparison to 38 patients with cerebral ischemia without dissection and 25 stroke mimics as control groups. Multimodal assessment was performed for clinical, neurological, cognitive, psychological and radiological data at baseline and for QOL, functional outcome, and stress symptoms by questionnaire at six months follow-up. Subgroup analysis stratified for QOL by Stroke Specific Quality of Life Scale (SS-QOL) were done for patients with good functional outcome (modified Ranking Scale (mRS) scoring 0–2). Predictors for QOL at follow-up were analyzed by regression model. Results 88.2% of patients with VAD suffered from acute cerebral ischemia. Thirteen of 32 VAD patients (40.6%) rated QOL at follow-up as bad (SS-QOL score ≤ 3.9) despite of good functional outcome (mRS score 0–2). Subgroup analysis yielded significantly higher scores for posttraumatic stress symptoms (p = 0.002) in this subgroup. Posttraumatic stress symptoms, severity of neurological disorders, and impaired neuropsychological baseline performance proved to be independent predictors for reduced QOL at follow-up according to regression analysis. Conclusion VAD leads to impaired QOL at 6 months follow-up due to multiple factors. The data suggest that posttraumatic stress symptoms are of significant importance for the QOL after VAD. Clinical monitoring should address this topic to make timely treatment possible.

We evaluated the performance of CSF biomarkers for predicting risk of clinical decline and conversion to dementia in non-demented patients with cognitive symptoms. CSF samples from patients in two multicentre longitudinal studies (ADNI, n = 619; BioFINDER, n = 431) were analysed. Aβ(1–42), tTau and pTau CSF concentrations were measured using Elecsys CSF immunoassays, and tTau/Aβ(1–42) and pTau/Aβ(1–42) ratios calculated. Patients were classified as biomarker (BM)-positive or BM-negative at baseline. Ability of biomarkers to predict risk of clinical decline and conversion to AD/dementia was assessed using pre-established cut-offs for Aβ(1–42) and ratios; tTau and pTau cut-offs were determined. BM-positive patients showed greater clinical decline than BM-negative patients, demonstrated by greater decreases in MMSE scores (all biomarkers: –2.10 to –0.70). Risk of conversion to AD/dementia was higher in BM-positive patients (HR: 1.67 to 11.48). Performance of Tau/Aβ(1–42) ratios was superior to single biomarkers, and consistent even when using cut-offs derived in a different cohort. Optimal pTau and tTau cut-offs were approximately 27 pg/mL and 300 pg/mL in both BioFINDER and ADNI. Elecsys pTau/Aβ(1–42) and tTau/Aβ(1–42) are robust biomarkers for predicting risk of clinical decline and conversion to dementia in non-demented patients, and may support AD diagnosis in clinical practice.

Pain has well-established effects on attention. At present, parallel literatures exist that have examined the effects of experimentally induced pain and consider cognitive performance in patients with chronic pain states. However, no study to date as attempted to examine the combined or differing effects of these 2 manifestations of pain in a single study. Twenty-four participants with fibromyalgia (aged 43.00 ± 28.28 years) and 26 healthy controls (aged 36.07 ± 11.93 years) completed an n-back task, an attentional switching task, and a divided attention task, once during induced, moderately intense pressure pain, and once without induced pain. Pain induction had selective effects on the n-back task and an overall decrease in accuracy on the attentional switching task. Conversely, patients with fibromyalgia were selectively impaired in performance on the divided attention task. These data therefore suggest that the effects of pain are not summative and rather that the mechanisms that underlie the negative effects of pain on performance in acute and chronic states may differ. More research is needed to examine these mechanisms and how these negative effects can be ameliorated to treat cognitive symptoms in pain. PERSPECTIVE: This article presents a study to examine the effects of an acute, induced pain model on cognitive performance in both patients with fibromyalgia and healthy control populations. We established that the effects of acute and chronic pain on attention are different, suggesting that different models need to be developed to understand these phenomena.

Objective The growing prevalence of chronic conditions requiring changes in lifestyle and at-home self-management has increased interest in and need for supplementing clinic visits with data generated by patients outside the clinic. Patient-generated health data (PGHD) support the ability to diagnose and manage chronic conditions, to improve health outcomes, and have the potential to facilitate more “connected health” between patients and their care teams; however, health systems have been slow to adopt PGHD use in clinical care. Materials and Methods We surveyed current and potential users of PGHD to catalog how PGHD is integrated into clinical care at an academic health center. The survey included questions about data type, method of collection, and clinical uses of PGHD. Current users were asked to provide detailed case studies of PGHD use in research and care delivery. Results Thirty-one respondents completed the survey. Seventeen individuals contributed detailed case studies of PGHD use across diverse areas of care, including behavioral health, metabolic and gastrointestinal conditions, musculoskeletal/progressive functional conditions, cognitive symptoms, and pain management. Sensor devices and mobile technologies were the most commonly reported platforms for collection. Clinicians and researchers involved in PGHD use cited the potential for PGHD to enhance care delivery and outcomes, but also indicated substantial barriers to more widespread PGHD adoption across healthcare systems. Conclusion The results of our survey illustrate how PGHD is used in targeted areas of one healthcare system and provide meaningful insights that can guide health systems in supporting the widespread use of PGHD in care delivery.

New psychopharmacological treatments are needed for affective and nonaffective psychoses, especially for the associated negative and cognitive symptoms. Earlier developments mostly failed, probably partly because of limitations in behavioral models used for validation. Now, deeper understanding of the genetics underlying disease pathogenesis and progress in genetic engineering will generate many rodent models with increased construct validity. To improve these models' translational value, we need complementary data from nonhuman primates. We also have to improve and streamline behavioral test systems to cope with increased demand. Here, we propose a comprehensive neurocognitive test battery that should overcome the disadvantages of single tests and yield cognitive/behavioral profiles for modeling subsets of patient symptoms. Further, we delineate a concept for classifying disease-relevant cognitive endophenotypes to balance between face and construct validity and clinical diagnostics. In summary, this review discusses new concepts and the limitations and future potential of translational research on cognition in psychiatry. .Se requiere de nuevos tratamientos psicofarmacológicos para las psicosis afectivas y no afectivas, especialmente para los síntomas negativos y cognitivos asociados. La mayoría de los desarrollos anteriores fallaron; en parte debido, probablemente, a las limitaciones en los modelos conductuales empleados para la validación. Ahora, una comprensión más profunda de la genética subyacente a la patogénesis de la enfermedad y el progreso en la ingeniería genética generará muchos modelos de roedores con una mayor validez de constructo. Para mejorar el valor de estos modelos translacionales se requiere de datos complementarios de primates no humanos. También hay que mejorar y racionalizar los sistemas de pruebas conductuales para hacer frente a una mayor demanda. En este artículo se propone una batería completa de pruebas neurocognitivas que debería superar las desventajas de las pruebas individuales y generar perfiles cognitivo-conductuales para modelar subconjuntos de síntomas del paciente. Además, se plantea un concepto para clasificar los endofenotipos cognitivos relevantes para la enfermedad a fin de equilibrar la validez aparente y de constructo con el diagnóstico clínico. En resumen, esta revisión analiza nuevos conceptos, y las limitaciones y el potencial futuro de la investigación translacional sobre la cognición en psiquiatría.De nouveaux traitements psychopharmacologiques sont nécessaires pour les psychoses dysthymiques ou non, surtout pour les symptômes associés négatifs et cognitifs. Par le passé, la plupart des développements ont échoué, probablement en partie en raison des limites des modèles comportementaux utilisés pour la validation. Aujourd’hui, une meilleure compréhension de la génétique de la pathogenèse de la maladie et les progrès du génie génétique vont produire de nombreux modèles de rongeurs mieux construits. Des données supplémentaires issues de primates non humains sont nécessaires pour améliorer la valeur traductive de ces modèles. Afin de satisfaire une demande croissante, nous devons aussi améliorer et rationaliser les systèmes de tests comportementaux. Nous proposons ici une batterie complète de tests neurocognitifs susceptible de palier les inconvénients des tests isolés et de fournir des profils cognitifs/comportementaux pour des sous-groupes de modélisation des symptômes des patients. En outre, nous définissons un concept pour classer les endophénotypes cognitifs pertinents pour la maladie afin de trouver un équilibre entre une validité de façade et de construit et les diagnostics cliniques. En résumé, cet article analyse de nouveaux concepts ainsi que les limites et les futures possibilités de la recherche translationnelle sur la cognition en psychiatrie.

Background People with mild hearing loss at age 50 are twice as likely to develop dementia increasing to a five times greater risk for those with severe hearing loss. The prevalence of dementia and hearing impairment increase with age. Intact hearing enables cognition, facilitates social interaction and enhances communication. Hearing loss, social isolation and dementia are commonly interwoven. We recently commenced routine audiology screening in our memory service. Methods Consecutive patients with mild cognitive impairment attending a tertiary memory assessment and support service were referred for full audiology screening. People were routinely referred on basis of cognitive diagnosis, and not on the basis of perceived hearing loss. Assessment included ENT history, otoscopy, tympanometry, pure tone audiometry and speech audiometry to determine the presence, type and amount of any hearing loss present. This included speech discrimination testing – a functional test to determine processing of 10 phonetically balanced words with 100% being an optimal response. Results 20 people (12 women), mean age 72.3 (range 57-87) were assessed. The majority had amnestic MCI 18/20 (90%). 9/20 (45%) patients subjectively complained of hearing loss. 7/20 (35%) had history of occupational noise exposure. 12/20 (60%) had occlusion due to ear wax. Hearing loss identified: Mild 8/20 (40%); Moderate to severe 7/20 (35%); with Normal hearing in 5/20 (25%). High frequency hearing loss was noted in 19/20 (95%). Speech discrimination score was impaired in those with hearing loss: mean 89.4% (range 66-100). 6/20 (30%) received referral for hearing aids. Conclusion This study highlights the importance of incorporating an assessment of auditory acuity as part of memory assessment and post-diagnostic care-pathway for people with mild cognitive complaints given the established impact hearing loss has on the future risk for cognitive decline. Hearing loss is frequently unidentified and is a clear modifiable risk factor to promote brain health.

Background Current evidence strongly implicates the burden of vascular risk factors (VRF) in the development of stroke, cognitive decline and dementia. This effect is mediated through several mechanisms, including amyloidogenesis, chronic neuroinflamation, cerebral perfusion and white-matter changes. Vascular risk profiling is well-embedded in stroke and cardiac services, but less so in memory services. Methods A review of established modifiable VRF (hypercholesterolemia, Body Mass Index (BMI), hypertension, HbA1c, smoking and alcohol habits) of people with mild cognitive complaints (mild cognitive impairment and subjective memory decline) in a memory service was performed. Risk factors measured in clinic were classified as: systolic ≥140mmHg / diastolic ≥90mmHg hypertension; LDL cholesterol >3mmol/l; HbA1c >39mmol/mol; weekly alcohol >21units; smoking and BMI >24.9kg/m2. Data was recorded and analysed using Microsoft Excel. Results Thirty-seven people, including 16 females (mean age 71.4, range of 49-83 years), were reviewed. 13/37 (35%) were aged ≤69 years. A total of 91 VRFs were identified in the study population. 29/37 (78%) had ≥2 VRF present. 3/37 (8%) had five VRF. 18/37 (49%) had prior history of either stroke, vascular or heart disease. Five of thirty-seven, (13.5%) and 13/37 (35%) were current and ex-smokers respectively, 2/37 (5%) consumed excess alcohol, 24/37 (65%) had elevated BMI and 11/37 (30%) had elevated LDL cholesterol. 21/37 (57%) had hypertension. Of these, 11/21 were known but poorly-controlled and 10/21 were identified de novo. All of the 32% (12/37) who had hyperglycaemia were de novo. Conclusion This study highlights the high prevalence of unidentified or poorly controlled VRF in people with mild cognitive symptoms attending a memory service. Given its importance to brain health and mitigation of future cognitive decline, a structured focus on identifying and managing these VRF in this setting is necessary. Exercise-based lifestyle programs should be embedded in post-diagnostic services for this population.

Background Dementia poses a serious threat to the wellbeing of the elderly. In the context of the rapidly ageing population of Vietnam however, little is known about the prevalence of symptoms and other related factors. This study aims to detect the prevalence of cognitive symptoms of dementia in the elderly in Vietnam as well as other associated factors. Methods A cross-sectional study was conducted over a period of six communes at the Northern, Central and Southern region of Vietnam. Prevalence of cognitive symptoms of dementia was the outcome of interest and assessed by Mini Mental State Evaluation (MMSE) questionnaire and was standardized according to the age structure of Vietnam. A total of 3308 adults aged 60 and above were included. Association between having cognitive symptoms of dementia and other factors was assessed with logistic regression. Findings Cognitive symptoms of dementia were perceived in 46.4% of the sample group. The symptoms were more common among participants who were older, female, had a lower educational level, were not physically active or have previously had stroke. Conclusions Prevalence of cognitive symptoms of dementia in adults aged 60 and above was relatively high in Vietnam. Other modifiable associated factors including physical inactivity and social connectedness should also be considered in designing intervention program to prevent dementia in the future.

Many studies have been conducted to investigate the effect of cultural influences on menopausal symptoms; however, associations between immigration transition and cognitive symptoms have rarely been uncovered. This secondary analysis aimed to determine these associations among 1,054 midlife women in the United States using the data from two national Internet surveys. The surveys included multiple questions on immigration transition, health and menopausal status, and the Cognitive Symptom Index for Midlife Women. The data analysis was performed using descriptive and inferential statistics including hierarchical multiple regression analyses. Nonimmigrants had larger numbers and higher severity scores of total cognitive symptoms than immigrants ( p < .001). Immigration status explained 1.28% of the total variances in the total numbers and 1.46% of the total variances in the total severity scores of total cognitive symptoms ( p < .001). The study supported significant associations between immigration transition and cognitive symptoms of women at midlife.

BackgroundFibromyalgia (FM) is a chronic pain syndrome with a controversial etiopathogenesis. Patients with FM usually complain of cognitive symptoms, which are described as “fibrofog.” These cognitive complaints might be caused partially by dissociative disorders (DD). The aim of this research is to determine the association between FM and DD.MethodsThe authors conducted a case-control study for this purpose, integrated by 3 groups: control (C), patients with rheumatic disorders (R), and patients with FM (FM), who were compared through the Dissociative Experiences Scale (DES).The findings are as follows: 42% were taking medications in the FM group, and their differences in scores with those who were not under medications were then considered. In terms of the results, the FM group showed higher scores than both C and R groups (p < 0.05). Patients with FM who were taking antidepressants had lower scores than those who were not (Z-score –8.03; p < 0.05); and finally, 5.71% had a score over 30 (χ2 = 3.73, p = 0.15).ConclusionPatients with FM had higher scores, which might be related to the association of dissociative experiences, lifetime trauma, and victimization. Antidepressants might have some role on dissociative symptoms as well.

Introduction: Myotonic dystrophy (DM) is a chronic, multisystemic, neurological condition. Patients and caregivers are uniquely suited to identify what symptoms are most important and highlight the unmet needs that are most relevant to DM. Methods: We conducted a North American, cross‐sectional study of people with DM type‐1, congenital DM, and DM type‐2 and their family members. We sent patients and caregivers separate surveys to identify and quantitate the issues of greatest importance, examine the differences between groups, and identify the most important challenges experienced by this population. Results: 1,180 people with DM and 402 family members/caregivers responded to the surveys. They reported considerable physical and cognitive symptoms, extensive diagnostic delays, and varying clinical phenotypes on the basis of DM type. Discussion: Marked disease burden and numerous unmet needs exist in DM. These needs vary based on DM type and highlight the complex clinical phenotypes of these neurological disorders. Muscle Nerve 59:457–464, 2019

Background: In this study, we investigated the fusion of texture and morphometric features as a possible diagnostic biomarker for Alzheimer’s Disease (AD). Methods: In particular, we classified subjects with Alzheimer’s disease, Mild Cognitive Impairment (MCI) and Normal Control (NC) based on texture and morphometric features. Currently, neuropsychiatric categorization provides the ground truth for AD and MCI diagnosis. This can then be supported by biological data such as the results of imaging studies. Cerebral atrophy has been shown to correlate strongly with cognitive symptoms. Hence, Magnetic Resonance (MR) images of the brain are important resources for AD diagnosis. In the proposed method, we used three different types of features identified from structural MR images: Gabor, hippocampus morphometric, and Two Dimensional (2D) and Three Dimensional (3D) Gray Level Co-occurrence Matrix (GLCM). The experimental results, obtained using a 5-fold cross-validated Support Vector Machine (SVM) with 2DGLCM and 3DGLCM multi-feature fusion approaches, indicate that we achieved 81.05% ±1.34, 86.61% ±1.25 correct classification rate with 95% Confidence Interval (CI) falls between (80.75-81.35) and (86.33-86.89) respectively, 83.33%±2.15, 84.21%±1.42 sensitivity and 80.95%±1.52, 85.00%±1.24 specificity in our classification of AD against NC subjects, thus outperforming recent works found in the literature. For the classification of MCI against AD, the SVM achieved a 76.31% ± 2.18, 78.95% ±2.26 correct classification rate, 75.00% ±1.34, 76.19%±1.84 sensitivity and 77.78% ±1.14, 82.35% ±1.34 specificity. Results and Conclusion: The results of the third experiment, with MCI against NC, also showed that the multiclass SVM provided highly accurate classification results. These findings suggest that this approach is efficient and may be a promising strategy for obtaining better AD, MCI and NC classification performance.

Background: The prevalence of hypothyroidism in the developed world is about 4-5% and in India is 10.9%. The goal of treating hypothyroidism is to maintain thyrotropin (TSH) levels within the normal reference range. Studies have shown that even within the normal range of TSH, patients with low normal TSH (LNT) have better outcomes when compared to patients with high normal TSH (HNT). Aims and Objectives: Our study aimed to find whether patients treated at a dose of levothyroxine resulting in an LNT had improved clinical outcomes and biochemical parameters, when compared to those on a levothyroxine dose resulting in an HNT. Materials and Methods: 180 patients with hypothyroidism on treatment, who had a TSH of 0.27-4.2mIU/L and had been on treatment with a stable dose of at least 50 micrograms of levothyroxine for at least 6 months were administered the Thyroid Symptom Questionnaire. TSH was assayed. Blood pressure and BMI were measured. Serum lipids were measured by spectrophotometry. Results: We found that patients with LNT and HNT did not differ with respect to cognitive symptoms , feelings of coldness, lethargy and fatigue. However, patients with LNT had a better lipid profile (mean LDL 132.24 in HNT and 115.39 in LNT p= 0.08) and lower BMI (1.045kg/m 2 lower in LNT compared to HNT) compared to HNT. Conclusion: Treating patients with a dose of thyroxine titrated to achieve LNT might decrease the cardiovascular risk by improving the lipid profile and BMI.

Maternal immune activation induced by Poly(I:C) administration is one of the most commonly used animal models of schizophrenia at present. Previous work from our team has demonstrated that some, but not all of the features often reported for maternal immune activation exposure in rodents can be observed in rats exposed to maternal immune activation at mid or late gestation. To determine whether previous findings in our laboratory were due to these time points simply being less sensitive neurodevelopmental periods for rats with regard to maternal immune activation effects, we aimed to investigate whether maternal immune activation at an often-reported sensitive period (mid-late gestation, day 14) resulted in more behavioural features reflective of face validity for schizophrenia. We examined the behavioural outcomes of mid-late maternal immune activation on a battery of behavioural tests aimed at assessing validity for positive, negative and cognitive symptoms of schizophrenia. We found that rats exposed to maternal immune activation, compared to controls, exhibited enhanced sensitivity to the locomotor-stimulating effects of amphetamine and reduced exploration of novel objects. These findings present a unique profile of effects, different to what has already been established for the same time point in rats, and different to what we had found at earlier and later time points. This work, among others in the literature, highlights the varying nature of models of maternal immune activation and we submit that it is essential for laboratories to characterise their models of maternal immune activation on behaviour rather than assuming that the effects from one laboratory apply in their own.

Currently available pharmacological treatments for schizophrenia derive their activity mainly by directly modulating the D2 receptor. This mode of action can alleviate the positive symptoms of schizophrenia but do not address the negative or cognitive symptoms of the disease and carry a heavy side effect burden that leads to high levels of patient non-compliance. Novel mechanisms to treat the positive symptoms of schizophrenia with improved tolerability, as well as medicines to treat negative and cognitive symptoms are urgently required. Recent efforts to identify small molecules for schizophrenia with non-D2 mechanisms will be highlighted, with a focus on those that have reached clinical development. Finally, the potential for disease modifying treatments for schizophrenia will also be discussed.

Background Schizophrenia is a multifactorial disease involving interactions between genetic and environmental factors. Vitamin D has recently been linked to many metabolic diseases and schizophrenia. Vitamin D plays essential roles in the brain in the context of neuroplasticity, neurotransmitter biosynthesis, neuroprotection, and neurotransmission. Vitamin D receptors are demonstrated in most brain regions that are related to schizophrenia. However, very few studies in the literature examine the effects of 25-hydroxyvitamin D (25OHD) on schizophrenia symptoms. Methods This study aimed to examine the effects of vitamin D replacement on positive, negative, and cognitive symptoms of schizophrenia. Serum 25OHD levels of 52 schizophrenia patients were measured. SANS and SAPS were used to evaluate the severity of schizophrenia symptoms, and the Wisconsin Card Sorting Test: CV4 was used for cognitive assessment. The study was completed with 40 patients for various reasons. The patients whose serum 25OHD reached optimal levels after vitamin D replacement were reevaluated with the same scales in terms of symptom severity. The SPSS 25 package program was used for statistical analysis. The Independent-Samples t-test was used to examine the relationship between the variables that may affect vitamin D levels and the vitamin D level and to examine whether vitamin D levels had an initial effect on the scale scores. Results The mean plasma 25OHD levels of the patients was 17.87 ± 5.54. A statistically significant relationship was found only between the duration of sunlight exposure and 25 OHD level (p p p Conclusion The data obtained from our study suggest that eliminating the 25OHD deficiency together with antipsychotic treatment can improve the total attention span and positive and negative symptoms in schizophrenia. The 25OHD levels should be regularly measured, replacement should be started when necessary, and the patients should be encouraged to get sunlight exposure to keep optimal 25OHD levels.

Objectives Cognitive impairment is frequent in multiple sclerosis (MS) as approximately half of the patients manifest some degree of cognitive impairment. The Brief International Cognitive Assessment for Multiple Sclerosis (BICAMS) has been designed for brief cognitive evaluation. The purpose of the study was to validate the BICAMS along with the Finnish versions of one self‐rating questionnaire each for cognition and fatigue. Methods A total of 65 MS patients and 45 healthy controls (HC) were assessed with the BICAMS, the Multiple Sclerosis Neuropsychological Questionnaire (MSNQ), and the Fatigue Scale for Motor and Cognitive Functions (FSMC) twice, approximately within nine days. Results MS patients scored markedly lower than the HCs on each of the three tests of the BICAMS. Of the patients, 60% scored at least 1.5 SD below the mean of the HCs on at least one test; 49% on the SDMT, 26% on the CVLT‐II, and 28% on the BVMT‐R. Correlation coefficients for the repeated measurement were between 0.75 and 0.89 for the three tests in the whole study sample. MS patients reported more cognitive symptoms and more fatigue than the HCs. Cronbach's alpha was 0.94 for the MSNQ and 0.98 for the FSMC. Correlation coefficient for the repeated measurement was 0.91 for the MSNQ and between 0.92 and 0.94 for the FSMC scores for the whole study sample. Conclusions The present study supports the validity of the Finnish version of the BICAMS. The SDMT was the most sensitive of the three BICAMS tests and showed cognitive impairment in half of the patients. The Finnish versions of the MSNQ and the FSMC proved useful tools in approaching concerns related to cognition and fatigue., A total of 65 MS patients and 45 healthy controls (HC) were assessed with the BICAMS, the Multiple Sclerosis Neuropsychological Questionnaire (MSNQ), and the Fatigue Scale for Motor and Cognitive Functions (FSMC) twice, approximately within nine days. The BICAMS validation was performed according to published recommendations. The results supported the validity of the Finnish version of the BICAMS. The Finnish versions of the MSNQ and the FSMC proved useful tools in approaching concerns related to cognition and fatigue.

Brain Derived Neurotrophic Factor (BDNF) has been linked to cognitive symptoms of schizophrenia, which has been documented in previous reviews by several authors. However, a trend has recently emerged in this field moving from studying schizophrenia as a disease to studying psychosis as a group. This review article focuses on recent BDNF studies in relation to cognition in human subjects during different stages of the psychotic process, including subjects at high risk of developing psychosis, patients at their first episode of psychosis, and patients with chronic schizophrenia. We aim to provide an update of BDNF as a biomarker of cognitive function on human subjects with schizophrenia or earlier stages of psychosis, covering new trends, controversies, current research gaps, and suggest potential future developments in the field. We found that most of current research regarding BDNF and cognitive symptoms in psychosis is done around schizophrenia as a disease. Therefore, it is necessary to expand the study of the relationship between BDNF and cognitive symptoms to psychotic illnesses of different stages and origins.

OBJECTIVE: To compare the prevalence of cognitive symptoms and their functional impact by age group accounting for depression and number of other health conditions. METHODS: We analyzed data from the 2011 Behavioral Risk Factor Surveillance System, a population-based, cross-sectional telephone survey of US adults. Twenty-one US states asked participants (n = 131, 273) about cognitive symptoms (worsening confusion or memory loss in the past year) and their functional impact (interference with activities and need for assistance). We analyzed the association between age, depression history and cognitive symptoms and their functional impact using logistic regression and adjusted for demographic characteristics and other health condition count. RESULTS: There was a significant interaction between age and depression (p < 0.0001). In adults reporting depression, the adjusted odds of cognitive symptoms in younger age groups (< 75 years) were comparable or greater to those in the oldest age group (≥ 75 years) with a peak in the middle age (45–54 years) group (OR 1.9 (95% Confidence Interval: 1.4–2.5). In adults without depression, adults < 75 years had a significantly lower adjusted odds of cognitive symptoms compared to the oldest age group with the exception of the middle-aged group where the difference was not statistically significant. Over half of adults under age 65 with depression reported that cognitive symptoms interfered with life activities compared to 35.7% of adults ≥ 65 years. CONCLUSIONS: Cognitive symptoms are not universally higher in older adults; middle-aged adults are also particularly vulnerable. Given the adverse functional impact associated with cognitive symptoms in younger adults, clinicians should assess cognitive symptoms and their functional impact in adults of all ages and consider treatments that impact both cognition and functional domains.