Etiology Of Symptoms Research Articles

Veteran Beliefs About the Causes of Gulf War Illness and Expectations for Improvement.

Individuals' beliefs about the etiology of persistent physical symptoms (PPS) are linked to differences in coping style. However, it is unclear which attributions are related to greater expectations for improvement. A cross-sectional regression analysis (N = 262) indicated that Veterans with Gulf War Illness (GWI)who attributed their GWI to behavior, (e.g., diet and exercise), had greater expectations for improvement (p = .001) than those who attributed their GWI to deployment, physical, or psychological causes (p values > .05). Findings support the possible clinical utility of exploring perceived contributing factors of PPS, which may increase perceptions that improvement of PPS is possible. ClinicalTrials.gov Identifier: NCT02161133.

Ventral cervical spondylophytes as differential diagnosis of neurogenic dysphagia

Ventral cervical spondylophytes can lead to severe dysphagia if they are of sufficient extent and height localization and represent an important differential diagnosis of neurogenic dysphagia, especially in older patients. Presentation of various etiologies of ventral cervical spondylophytes, specific symptoms and abnormalities of the swallowing function caused by spondylophytes, their manifestation in the instrumental swallowing diagnostics and an outlook on treatment options. Summary of the current literature on spondylophyte-related dysphagia and an overview of research results regarding differential diagnostic aspects of neurogenic dysphagia. The manifestation forms of ventral cervical spondylophytes can be very diverse. With respect to dysphagia, disorders of pharyngeal bolus transfer and an increased tendency to aspiration have been observed. The occurrence and severity of the symptoms depend primarily on the extent of the bony attachments and their height localization. In some cases, symptomatic ventral cervical spondylophytes can be arelevant differential diagnosis of neurogenic dysphagia. For amore precise evaluation of the dysphagic symptoms and their association with the spondylophytic outgrowths, avideo fluoroscopy of swallowing (VFS) should be added to the fiber endoscopic evaluation (FEES). In most cases, aresection of the bone spurs leads to asignificant improvement or even to acomplete restitution of the swallowing disorders.

Subfield-specific longitudinal changes of hippocampal volumes in patients with early-stage bipolar disorder.

The hippocampus is a heterogeneous structure composed of biologically and functionally distinct subfields. Hippocampal aberrations are proposed to play a fundamental role in the etiology of psychotic symptoms. Bipolar disorder (BPD) has substantial overlap in symptomatology and genetic liability with schizophrenia (SZ), and reduced hippocampal volumes, particularly at the chronic illness stages, are documented in both disorders. Studies of hippocampal subfields in the early stage of BPD are limited and cross-sectional findings to date report no reduction in hippocampal volumes. To our knowledge, there have been no longitudinal studies of BPD evaluating hippocampal volumes in the early phase of illness. We investigated the longitudinal changes in hippocampal regions and subfields in BPD mainly and in early stage of psychosis (ESP) patients more broadly and compared them to those in controls (HC). Baseline clinical and structural MRI data were acquired from 88 BPD, from a total of 143 ESP patients, and 74 HCs. Of those, 66 participants (23 HC, 43 patients) completed a 12-month follow-up visit. The hippocampus regions and subfields were segmented using Freesurfer automated pipeline. We found general baseline deficits in hippocampal volumes among BPD and ESP cohorts. Both cohorts displayed significant increases in the anterior hippocampal region and dentate gyrus compared with controls. Additionally, antipsychotic medications were positively correlated with the posterior region at baseline. These findings highlight brain plasticity in BPD and in ESP patients providing evidence that deviations in hippocampal volumes are adaptive responses to atypical signaling rather than progressive degeneration.

The Same Day on Repeat: A Unique Case of Persistent Déjà Vu Phenomenon as a Long COVID Symptom in an Older Adult

IntroductionDéjà vu is a condition characterized by the experience of recognizing a current situation as familiar with the awareness that the recognition is inappropriate (Pasic et al. Psychiatria Danubina; 30, 21–25). This phenomenon has been well described in temporal lobe epilepsy, and is thought to be caused by abnormal synchronization in the corticolimbic network. While the etiology of neuropsychiatric symptoms in long COVID is still not well demarcated, studies have found that the virus attacks the temporal lobe and limbic system; therefore, we suggest that the ongoing symptoms of déjà vu, in this case, may be a manifestation of long COVID.ObjectivesTo illustrate a unique case of persistent déjà vu after severe infection with COVID-19 virus.MethodsThe patient is a 79-year-old female with a pertinent past medical history of generalized anxiety disorder, major depressive disorder, and prior hospitalization for delirium who presented with a chief complaint of being tired of living the same day. The patient was hospitalized eight months prior for a severe COVID-19 infection that now requires continuous oxygen therapy. Since leaving the hospital, the patient began to develop episodic confusion, memory impairment, and tinnitus which gradually improved. However, the patient developed severe distress due to a constant feeling of déjà vu characterized by a sense of familiarity with events in her daily life. There was no history of loss of consciousness, abnormal involuntary movements, or other semiology related to seizures. Due to distress caused by the déjà vu symptoms, the patient also endorsed depression, anxiety, and insomnia, with deterioration of quality of life.ResultsMRI showed mild volume loss and multifocal regions, including bilateral temporal lobes, of subcortical and periventricular high T2/FLAIR signal abnormality consistent with chronic white matter microangiopathy. MOCA score was 24/30, and the dissociative experiences scale score was 15.36/100. The patient continues to be treated for her depression, insomnia and anxiety with escitalopram 10mg daily and mirtazapine 7.5mg at night as a neuropsychological assessment and electroencephalogram are done.ConclusionsThe incidence of neurological symptoms is more than 80% in severe cases of COVID-19 (Douaud et al. Nature; 604,697–707). This patient was likely predisposed to developing these symptoms due to her age and psychiatric history. Déjà vu occurs in temporal lobe epilepsy, schizophrenia, and depersonalization disorders, all of which affect the limbic-temporal lobe networks (Pasic et al. Psychiatria Danubina; 30, 21–25). Signal abnormalities in the medial temporal lobe are one of the findings seen on MRI in patients with neuropsychiatric symptoms after severe COVID-19 infection. We propose that the persistent déjà vu phenomenon along with cognitive impairments described in this case are manifestations of long COVID.Disclosure of InterestNone Declared

Isoniazid-induced acute psychotic episode in a child with lymph nodes tuberculosis: case report and literature review

Introduction Tuberculosis (TB) is a bacterial infection caused by Mycobacterium tuberculosis and is a major public health problem in Morocco. The World Health Organization (WHO) recommends a four-drug combination therapy for two months (isoniazid (INH), rifampicin, pyrazinamide and ethambutol), followed by two drugs (INH and rifampicin) for 4 months, as first-line treatment for newly diagnosed pulmonary TB in children and adults. This regimen is generally considered effective, safe, and cost-effective. However, adverse effects and drug interactions often complicate the treatment of TB. Isoniazid is associated with 32% of adverse events, of which 1.9% are psychiatric. Objectives focus on drug-induced etiologies of acute psychotic symptoms make the diagnosis of isoniazid-induced psychosis report the literature on the management of this condition. focus on drug-induced etiologies of acute psychotic symptomsmake the diagnosis of isoniazid-induced psychosis report the literature on the management of this condition. Methods The patient and guardians were interviewed to obtain information after their consent. Data from the patient profile forms and laboratory test reports were evaluated. Causality assessment was done by the WHO scale and the Naranjo scale. Oral informed consent was obtained from the patient and parents. Results We report a case of acute psychosis in a child with a temporal sequence strongly in favor of INH-induced psychosis. Treatment with risperidone at an appropriate dose improved the symptomatology while waiting for the end of the antituberculosis protocol. As soon as the isoniazid was stopped, there was a clear return to the child’s premorbid state. Conclusions The acute onset of psychotic symptoms in a patient taking isoniazid should lead to suspicion of this psychiatric side effect and prompt intervention, involving discontinuation of isoniazid and/or a trial of an antipsychotic. As protective measures, the authors suggest adjusting the dose of isoniazid to weight, possibly performing a genetic test if slow acetylation is suspected, and closely monitoring patients with a favourable background. The acute onset of psychotic symptoms in a patient taking isoniazid should lead to suspicion of this psychiatric side effect and prompt intervention, involving discontinuation of isoniazid and/or a trial of an antipsychotic.As protective measures, the authors suggest adjusting the dose of isoniazid to weight, possibly performing a genetic test if slow acetylation is suspected, and closely monitoring patients with a favourable background. Disclosure of Interest None Declared

Multisystem Inflammatory Syndrome in Children.

Multisystem inflammatory disease in children (MIS-C) is a condition typically seen 3 to 6 weeks after acute infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Believed to be a postinfection hyperinflammatory response, the clinical manifestation of this viral sequelae can vary significantly in severity and symptomatic presentation. Clinical prodrome includes persistent fever and dysfunction of at least two organ systems. Often developing after asymptomatic or mildly symptomatic coronavirus disease 2019 (COVID-19) infection, MIS-C is a diagnosis of exclusion that requires evaluation for other infectious or noninfectious etiology for symptoms. Vital sign instability, including fever, tachycardia, and hypotension; laboratory studies demonstrating elevated inflammatory markers and elevated cardiac markers; and positive SARS-CoV-2 polymerase chain reaction, SARS-CoV-2 antibodies, or exposure to someone with confirmed COVID-19 infection 4 to 6 weeks before clinical presentation are used to diagnose this condition. Skin and mucosal involvement, gastrointestinal symptoms, and neurologic manifestations are also commonly seen. An echocardiogram is indicated to evaluate for cardiac dysfunction, including but not limited to coronary artery enlargement, left ventricular dysfunction, arrythmias, or atrioventricular block. [Pediatr Ann. 2023;52(3):e114-e121.].

Mouse population genetics phenocopies heterogeneity of human Chd8 haploinsufficiency

Preclinical models of neurodevelopmental disorders typically use single inbred mouse strains, which fail to capture the genetic diversity and symptom heterogeneity that is common clinically. We tested whether modeling genetic background diversity in mouse genetic reference panels would recapitulate population and individual differences in responses to a syndromic mutation in the high-confidence autism risk gene, CHD8. We measured clinically relevant phenotypes in >1,000 mice from 33 strains, including brain and body weights and cognition, activity, anxiety, and social behaviors, using 5 behavioral assays: cued fear conditioning, open field tests in dark and bright light, direct social interaction, and social dominance. Trait disruptions mimicked those seen clinically, with robust strain and sex differences. Some strains exhibited large effect-size trait disruptions, sometimes in opposite directions, and-remarkably-others expressed resilience. Therefore, systematically introducing genetic diversity into models of neurodevelopmental disorders provides a better framework for discovering individual differences in symptom etiologies.

Abstract TP64: Characterization Of Stroke Mimics Treated With Thrombolytics

Background: Stroke is a medical emergency. The effectiveness of stroke treatment is time dependent. Due to the urgency of treatment and the challenge of rapidly assessing stroke-like symptoms, patients with stroke mimics (non-stroke etiologies of focal neurologic symptoms) may be treated with thrombolysis. We aimed to understand characteristics of patients treated with IV tPA with a final diagnosis of stroke versus a stroke mimic. Methods: This retrospective cohort study identified patients who received tPA for stroke-like symptoms in the emergency department at a single urban Comprehensive Stroke Center over 26 months. Final diagnosis was based on ICD-10 codes. Demographic data, medical history and presenting symptoms were obtained through electronic medical record review. Characteristics of patients with strokes and mimics were compared using Chi-squared and t-tests. Results: Of 202 patients presenting with stroke-like symptoms who received tPA, final diagnosis was ischemic stroke in 166 (82%) and mimic in 36 (18%). A statistically significant difference was noted between the stroke and mimic groups in age (64 ±16.9 vs 57 ±13.8 years, p=0.015) and neared significance in sex (38% vs 56% female, p=0.052). There was no difference in initial NIHSS (7.8 ±7.2 vs 5.8 ±5.2, p=0.109), Hispanic ethnicity (13% vs 22%, p=0.170), presence of stroke risk factors (79% vs 78%, p=0.880), or race distribution (white 54% vs 61%, Black 28% vs 14%, multiple/other 18% vs 25%, p=0.199). The most common mimic symptoms included unilateral weakness (61%), unilateral numbness (53%), dysarthria (33%), ataxia (28%), vertigo (22%), and gait impairment (17%). The most common clinical diagnoses in mimics were headache, functional neurologic disorder, and toxic/metabolic disturbances (17% each). Conclusion: Of patients receiving tPA at our facility, stroke mimics comprised 18% and were significantly younger than patients with ischemic stroke. Further analysis of demographics within these two groups could identify characteristics that distinguish strokes from mimics, which may lower the rate of tPA administration to non-stroke presentations.

Self-Reported Breast Implant Illness: The Contribution of Systemic Illnesses and Other Factors to Patient Symptoms.

Abstract Patients with self-reported breast implant illness (BII) report a range of systemic symptoms which they attribute to having breast implants. The etiology of self-reported BII is unknown. Some patients have limited resolution of symptoms despite implant removal, and the mechanism of persistent symptoms is unclear. Notably, there are a number of prevalent, chronic systemic illnesses and other factors which present with the most common physical symptoms of self-reported BII. Fibromyalgia, chronic fatigue syndrome, autoimmune disorders, and hypothyroidism often produce fatigue, joint and muscle pain, “brain fog,” anxiety or depression, and hair loss in affected patients who may or may not have breast implants. Other factors such as anxiety with or without depression, perimenopause, aging, cigarette smoking/marijuana use, and prominent side effects from common medications are known to produce similar symptoms as those reported by patients concerned with BII. The possibility that patients with breast implants have an undiagnosed, chronic illness unrelated to breast implants should be considered as well as other factors which may produce similar symptoms. Plastic surgeons should be aware of the range of illnesses and factors which can produce physical symptoms similar to those of patients with self-reported BII. For patients in which a systemic illness or other factor is felt to play a contributory role to self-reported BII symptoms, referral to an internist or rheumatologist for a thorough history and physical examination to rule out conditions may be prudent before explantation. This may reduce the need for explantation if the etiology of systemic symptoms is found to be unrelated to breast implants. Level of Evidence: 3

Impact of membrane lipid polyunsaturation on dopamine D2 receptor ligand binding and signaling.

Increasing evidence supports a relationship between lipid metabolism and mental health. In particular, the biostatus of polyunsaturated fatty acids (PUFAs) correlates with some symptoms of psychiatric disorders, as well as the efficacy of pharmacological treatments. Recent findings highlight a direct association between brain PUFA levels and dopamine transmission, a major neuromodulatory system implicated in the etiology of psychiatric symptoms. However, the mechanisms underlying this relationship are still unknown. Here we demonstrate that membrane enrichment in the n-3 PUFA docosahexaenoic acid (DHA), potentiates ligand binding to the dopamine D2 receptor (D2R), suggesting that DHA acts as an allosteric modulator of this receptor. Molecular dynamics simulations confirm that DHA has a high preference for interaction with the D2R and show that membrane unsaturation selectively enhances the conformational dynamics of the receptor around its second intracellular loop. We find that membrane unsaturation spares G protein activity but potentiates the recruitment of β-arrestin in cells. Furthermore, in vivo n-3 PUFA deficiency blunts the behavioral effects of two D2R ligands, quinpirole and aripiprazole. These results highlight the importance of membrane unsaturation for D2R activity and provide a putative mechanism for the ability of PUFAs to enhance antipsychotic efficacy.

Signaling through the dystrophin glycoprotein complex affects the stress-dependent transcriptome in Drosophila.

Deficiencies in the human dystrophin glycoprotein complex (DGC), which links the extracellular matrix with the intracellular cytoskeleton, cause muscular dystrophies, a group of incurable disorders associated with heterogeneous muscle, brain and eye abnormalities. Stresses such as nutrient deprivation and aging cause muscle wasting, which can be exacerbated by reduced levels of the DGC in membranes, the integrity of which is vital for muscle health and function. Moreover, the DGC operates in multiple signaling pathways, demonstrating an important function in gene expression regulation. To advance disease diagnostics and treatment strategies, we strive to understand the genetic pathways that are perturbed by DGC mutations. Here, we utilized a Drosophila model to investigate the transcriptomic changes in mutants of four DGC components under temperature and metabolic stress. We identified DGC-dependent genes, stress-dependent genes and genes dependent on the DGC for a proper stress response, confirming a novel function of the DGC in stress-response signaling. This perspective yields new insights into the etiology of muscular dystrophy symptoms, possible treatment directions and a better understanding of DGC signaling and regulation under normal and stress conditions.

The change in pediatric subject symptoms during the COVID-19 pandemic in China: an increase in cardiac consultation

BackgroundIt is reported that the adverse impact of nonpharmaceutical interventions (NPIs) on the mental health of children and adolescents may lead to psychologically related disorders during the coronavirus disease 2019 (COVID-19) period. Subject symptoms such as chest pain, chest tightness, and palpitation may be related to increased stress and anxiety in children and adolescents. The present research aimed to determine the number of pediatric consults and etiology of subject symptoms during the COVID-19 pandemic period and compared it with the same timelines in 2019 and 2021 to discuss the impact of different periods on the organic disease onset of children with subject symptoms, especially in cardiac involvement.MethodsChildren who visited Qingdao Women and Children’s Hospital, Qingdao University between January 23 to April 30, 2019 (pre-COVID-19 period), January 23 to April 30, 2020 (COVID-19 period), and January 23 to April 30, 2021 (post-COVID-19 period) presenting chest pain, chest tightness, and palpitation were recruited. Information to determine gender, age, medical history, department for the initial visit, clinical manifestations, time from the latest onset to the visit, and diagnosis were recorded.ResultA total of 891 patients were enrolled in the present study (514 males; median age: 7.72). One hundred twenty-three patients presented during the pre-COVID-19 period while 130 during the COVID-19 period, nevertheless, the number substantially increased during the post-COVID-19 period (n = 638). Cardiac etiology accounted for 1.68% (n = 15) of the patient population, including arrhythmias (n = 10, 1.12%), myocarditis (n = 4, 0.44%), and atrial septal defect (n = 1, 0.11%). There was no significant difference among groups in the distribution of organic etiology. The median time from the latest onset to the visit during the pre-COVID-19 period was 7 days compared to 10 days during the COVID-19 period and 3 days during the post-COVID period.ConclusionDuring the post-COVID-19 period, the median time from the latest onset to the visit was significantly shorter than that in the pre-COVID-19 period or COVID-19 period. The pediatric consult of children with subject symptoms presented increased substantially during the post-COVID-19 period, while there was no significant difference in the number of patients involving the cardiac disease. Clinicians ought to be more careful to screen heart diseases to prevent missed diagnosis and misdiagnosis during special periods.

Cell migration is impaired in XPA-deficient cells.

Xeroderma pigmentosum (XP) is a hereditary disorder characterized by photosensitivity, predisposition to skin cancers, and neurological abnormalities including microcephaly and progressive neurodegeneration. A lack of nucleotide excision repair (NER) in patients with XP can cause hypersensitivity to the sun, leading to skin cancer, whereas the etiology of the neuronal symptoms of XP remains ambiguous. There are various neurological disorders that perturb neuronal migration, causing mislocalization and disorganization of the cortical lamination. Here, we investigated the role of the XP group-A (Xpa) gene in directed cell migration. First, we adopted an in utero electroporation method to transduce shRNA vectors into the murine embryonic cerebral cortex for the in vivo knockdown of Xpa. Xpa-knockdown neurons in the embryonic cerebral cortex showed abnormal cell migration, cell cycle exit, and differentiation. The genotype-phenotype relationship between the lack of XPA and cell migration abnormalities was confirmed using both a scratch assay and time-lapse microscopy in XP-A patient-derived fibroblasts. Unlike healthy cells, these cells showed impairment in overall mobility and the direction of motility. Therefore, abnormal cell migration may explain neural tissue abnormalities in patients with XP-A.

End-Tidal CO2 in Patients with Panic Disorder, Stress-Related or Functional Syndromes, Versus Healthy Controls.

A dysregulated autonomic stress physiology is hypothesized to play an important role in the etiology and perpetuation of somatic symptoms that cannot be (fully) explained by an organic disease. The aim of this study was to focus on the role of the respiratory system. We examined end-tidal CO2 concentration (PetCO2) in healthy controls (n = 30), patients with panic disorder (n = 36), and patients with stress-related (overstrain; n = 35, burnout; n = 44) or functional syndromes [fibromyalgia (FM) and/or chronic fatigue syndrome (CFS); n = 36]. Participants went through a rest period and a respiratory challenge with recovery, whilst PetCO2 was continuously monitored by a capnograph. Taken together, our results suggest: (1) an overactive respiratory system to be a possible transdiagnostic underlying factor of overstrain, burnout, and panic disorder, and (2) the presence of a less active respiratory fight-flight response in the more chronic and severe functional syndromes (FM/CFS).

Expression Study of NDUFS1, NDUFV1, and NDUFV2 in Schizophrenia and Paranoid Personality Disorder

Background: Schizophrenia (SCZ) is a major psychiatric disorder with unclear etiology and biological diagnosis. Paranoid personality disorder (PPD) is a type-A personality disorder characterized by paranoia and generalized mistrust. The etiology and molecular mechanisms of SCZ and PPD are not clarified. The present study aimed to examine the expression alteration of three major genes of mitochondrial complex I in the peripheral blood of patients with SCZ and PPD, and its correlations with clinical features of patients, especially the five major personality traits. Materials and Methods: This case-control study was performed on 735 SCZ, 742 PPD, and 750 non-psychiatric individuals. The mRNAs level of NDUFS1, NDUFV1, and NDUFV2 were assessed using quantitative real-time polymerase chain reaction, and their correlations with psychiatric symptoms were assessed by the positive and negative syndrome scale and the brief psychiatric rating scale tests, as well as personality traits that were evaluated by NEO Five-Factor Inventory. Results: Findings showed significant overexpression of NDUFS1, NDUFV1, and NDUFV2 in patients with SCZ (P=0.001, P=0.002, and P=0.004, respectively) and PPD (P=0.001, P=0.003, and P=0.006, respectively) compared with non-psychiatrists. In addition, these genes were associated with positive psychiatric symptoms and neuroticism in SCZ (P=0.008) and PPD (P=0.01). Conclusion: Overexpression genes that encode subunits of complex I play an important role in SCZ and PPD etiology and severity of symptoms. It may bring evidence about the significant role of bioenergetics dysfunction in psychotic behaviors in different psychiatric situations.

Improved psychotic symptoms following resection of amygdalar low-grade glioma: illustrative case.

Epilepsy-associated psychoses are poorly understood, and management is focused on treating epilepsy. Chronic, interictal psychosis that persists despite seizure control is typically treated with antipsychotics. Whether resection of a mesial temporal lobe lesion may improve interictal psychotic symptoms that persist despite seizure control remains unknown. In a 52-year-old man with well-controlled epilepsy and persistent comorbid psychosis, brain magnetic resonance imaging (MRI) revealed an infiltrative, intraaxial, T2 fluid-attenuated inversion recovery intense mass of the left amygdala. The patient received an amygdalectomy for oncological diagnosis and surgical treatment of a presumed low-grade glioma. Pathology was ganglioglioma, World Health Organization grade I. Postoperatively, the patient reported immediate resolution of auditory hallucinations. Patient has remained seizure-free on 2 antiepileptic drugs and no antipsychotic pharmacotherapy and reported lasting improvement in his psychotic symptoms. This report discusses improvement of psychosis symptoms after resection of an amygdalar glioma, independent of seizure outcome. This case supports a role of the amygdala in psychopathology and suggests that low-grade gliomas of the limbic system may represent, at minimum, partially reversible etiology of psychotic symptoms.

Dyspnea Post Pulmonary Vein Isolation Ablation

Phrenic nerve injury is considered a rare complication of pulmonary vein isolation ablation procedure that is used to treat refractory paroxysmal atrial fibrillation and has been reported in different settings in literature. In this case report, we discuss a case presented with dyspnea, cough, headaches, fatigue, and palpitation five months post pulmonary vein isolation ablation. This case has a medical history of several comorbidities that may contribute to the etiology of the above symptoms. Therefore, the prolonged presentation, late onset of symptoms, and multiple cofactors could be assumed to contribute to patient’s etiology of symptoms attributed to the challenge of the diagnosis. However, one should always keep phrenic nerve injury as a differential when dealing with post pulmonary vein isolation ablation dyspnea or exacerbation of co-existing respiratory symptoms, even when facing delayed presentations of symptoms.

Abstract 14997: Computerized Cognitive Training and 24-Month Mortality in Heart Failure

Introduction: Long-term efficacy has not been widely evaluated for computerized cognitive training (CCT) to improve cognition and reduce mortality. The purpose of this study was to evaluate long-term efficacy of CCT to reduce risk of death and test additional predictors of long-term mortality among patients with heart failure (HF). Methods: In this prospective study, a subset of 142 patients with HF were included from the parent 3-arm RCT testing CCT using BrainHQ to improve memory. Mortality data were collected from electronic health records, family caregivers, physicians or nurses during 24 months after the randomization between Mar 2017 and Dec 2020. Multiple logistic regressions were performed with 2 predictor variables (group and an additional predictor) given the small number of death cases. Predictors tested were age, baseline global cognition, memory, working memory, depressive symptoms, and health-related quality of life (HRQL). Results: The sample was 52% women/48% men; mean age 65 (SD=13) years; and race 13% Black, 1% more than one race, 1% Native Hawaiian/Pacific Islander, and 85% White. Mean left ventricular ejection fraction was 46% (SD=14). Of 142 patients, 16 (11.3%) died; 4 (8.3% of 48) in CCT group and 12 (12.8% of 94) in control groups (p=.429). The patients who died were older by 9 years (p=.002), had more depressive symptoms (p=.022), and poorer global cognition (p=.009), memory (p=.069), and HRQL (p=.080) at baseline. In logistic regression models, CCT group was not a statistically significant predictor of 24-month mortality (OR=0.65, 95% CI=0.28-1.15). Patients with better global cognition and memory were less likely to die over 24 months by 27% (OR=0.73, 95% CI=0.58-0.90) and 19% (OR=0.81, 95% CI=0.67-0.99), respectively. Patients with more depressive symptoms (OR=1.10, 95% CI=1.00-1.21) and older age (OR=1.08, 95% CI=1.01-1.14) were more likely to die over 24 months. Working memory and HRQL did not predict mortality. Conclusions: CCT using BrainHQ did not show long-term efficacy on reducing 24-month mortality in HF. Efficacious interventions are needed that are targeted at underlying etiologies of cognitive dysfunction and depressive symptoms in older patients with HF.

Neural activation, cognitive control, and attention deficit hyperactivity disorder: Evaluating three competing etiological models.

Cognitive control impairments are observed across several psychiatric conditions, highlighting their role as a transdiagnostic marker. Individuals with attention deficit hyperactivity disorder (ADHD) have difficulties with inhibition, working memory, processing speed, and attention regulation. These cognitive control impairments may either mediate or moderate the association between neurobiological vulnerabilities and phenotypic presentation in neurodevelopmental disorders. Alternately, neurocognitive vulnerabilities in ADHD may be additive, akin to a multiple deficit model. We tested the mediation, moderation, and additive models using neurocognitive data in youth with ADHD. 7-11 year-old children diagnosed with ADHD (n = 75) and control children (n = 29) completed EEG recordings and neuropsychological testing (full scale IQ; cognitive control). Caregivers provided ADHD symptom ratings. Correlations and linear regression analyses were completed to examine the associations among cortical functioning (aperiodic slope), cognitive control, and ADHD symptoms. We found support for an additive model wherein vulnerabilities in aperiodic slope, event-related potentials, and cognitive control each explained unique variance in ADHD symptoms. There was some evidence that cognitive control moderates the effect of atypical cortical development on ADHD symptoms. There was no support for the mediation model. The etiology of ADHD symptoms is multifaceted and involves multiple "hits" across neurological and cognitive-behavioral factors.

Impact of Exposure to Indoor Air Chemicals on Health and the Progression of Building-Related Symptoms: A Case Report

The aetiology of building-related symptoms (BRSs) is not well supported by sufficient scientific evidence, and it remains unclear whether BRSs are mediated by psychosocial and personal factors or a genuine physical susceptibility to low-dose chemical exposure. In April 2014, a 40-year-old man consulted the Environmental Medical Clinic at Chiba University complaining of recurring BRSs. Indoor air samples were collected from the patient’s house at 11 time points and subjected to chemical analyses. The patient simultaneously completed a questionnaire about his symptoms at the time of the measurements. Statistical examination of the indoor environmental factors and patient survey revealed that the patient’s symptoms were highly correlated with the indoor air quality. Additionally, ventilation may have mitigated his BRSs, whereas aerial odour did not trigger symptoms. These findings suggest that exposure to specific airborne chemicals in an indoor environment can cause BRSs, and ventilation may be one of the treatment options to mitigate symptoms. Additional investigations on the adverse impacts of airborne environmental chemicals on human health are necessary to develop effective treatments and establish preventive measures for BRSs, and further improvement of ventilation systems is required to ensure clean indoor air.