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Transcriptomic pathology of neocortical microcircuit cell types across psychiatric disorders.

Psychiatric disorders such as major depressive disorder (MDD), bipolar disorder (BD), and schizophrenia (SCZ) are characterized by altered cognition and mood, brain functions that depend on information processing by cortical microcircuits. We hypothesized that psychiatric disorders would display cell type-specific transcriptional alterations in neuronal subpopulations that make up cortical microcircuits: excitatory pyramidal (PYR) neurons and vasoactive intestinal peptide- (VIP), somatostatin- (SST), and parvalbumin- (PVALB) expressing inhibitory interneurons. Using laser capture microdissection followed by RNA sequencing (LCM-seq), we performed cell type-specific molecular profiling of subgenual anterior cingulate cortex, a region implicated in mood and cognitive control. We sequenced libraries from 130 whole cells pooled per neuronal subtype (VIP, SST, PVALB, superficial and deep PYR) in 76 subjects from the University of Pittsburgh Brain Tissue Donation Program, evenly split between MDD, BD and SCZ subjects and healthy controls (totaling 380 bulk transcriptomes from ~50,000 neurons). We identified hundreds of differentially expressed (DE) genes and biological pathways across disorders and neuronal subtypes, with the vast majority in interneurons, particularly PVALB. While DE genes were unique to each cell type, there was a partial overlap across disorders for genes involved in the formation and maintenance of neuronal circuits. We observed coordinated alterations in biological pathways between select pairs of microcircuit cell types, also partially shared across disorders. Finally, DE genes coincided with known risk variants from psychiatric genome-wide association studies, suggesting cell type-specific convergence between genetic and transcriptomic risk for psychiatric disorders. Our study suggests transdiagnostic cortical microcircuit pathology in SCZ, BD, and MDD and sets the stage for larger-scale studies investigating how cell circuit-based changes contribute to shared psychiatric risk.

Humans

Cardiovascular risks in psychiatric disorders and psychiatric risks in cardiovascular disorders: implications for prevention and clinical management - a large-scale umbrella review encompassing 76 meta-analyses.

OBJECTIVE: Psychiatric and cardiovascular disorders often co-occur, complicating their assessment and management. No umbrella review(UR) has summarized the meta-analytic evidence on the co-occurrence of psychiatric and cardiovascular disorders and assessed its credibility. METHODS: Meta-analytic systematic reviews of observational studies documenting the prevalence, risk factors, and outcomes associated with the co-occurrence of cardiovascular and psychiatric disorders, indexed from inception through March.16.2026, and meeting established diagnostic criteria, were included. Meta-analytic association and prevalence estimates were recalculated and graded based on established or adapted criteria. The AMSTAR-2 assessed the quality of the meta-analyses, while several subgroup analyses and meta-regressions aimed to explain the heterogeneity. RESULTS: We included 76 meta-analyses yielding 131 meta-analytic estimates. Based on pre-existing meta-analytic evidence, 22/24 prevalence estimates (91.7%) met moderate/strong credibility criteria. Strong credibility emerged for: orthostatic hypotension in Lewy body(58%;95%C.I. = 50-66%) and Alzheimer's dementias(28.0% = 95%C.I. = 17.0-40.0%); pericardial effusion in anorexia nervosa(25.0%;95%C.I. = 17.0-34.0%); in heart failure(HF): major depressive disorder(MDD)(41.9%;95%C.I. = 36.7-47.1%), mild cognitive impairment(MCI)(41.4%;95%C.I. = 38.3-45.6%), anxiety(32.0%;95%C.I. = 26.5-37.6%), MDD + anxiety(24.7%;95%C.I. = 17.9-34.3%), and dementia(19.8%;95%C.I. = 12.9-27.8%); in atrial fibrillation(AF): MCI(26.0%;95%C.I. = 21.0-30.0%), anxiety in patients undergoing pulmonary vein isolation(PVI)(25.0%;95%C.I. = 12.0-46.0%), MDD in PVI patients (20.0%;95%C.I. = 13.0-29.0%); in coronary artery disease: MDD + anxiety(19.8%;95%C.I. = 16.0-24.6%): in schizophrenia spectrum disorders: clozapine-associated-cardiomyopathy(0.6%;95%C.I. = 0.2-2.3%); clozapine-associated-cardiomyopathy absolute death rates (0.0003;95%C.I. = 0.0001-0.0012); clozapine-associated-cardiomyopathy case fatality rate (0.078;95%C.I. = 0.018-0.285). Several additional disorders were multimorbid in>5% of people, yet with a lower credibility rating. No re-pooled risk factors/outcomes reached strong credibility criteria. CONCLUSIONS: The present study provides an atlas of cardiovascular and psychiatric multimorbidity across varying levels of credibility, reinforcing the need for an integrated, multidisciplinary approach to patient care and for more research on actionable risk/protective factors and outcomes.

Humans

Viral infection and psychiatric disorders.

A psychiatric population of 94 inpatients and 12 outpatients was investigated on referral to a psychiatric unit in a general hospital for serum antibody titres to several viruses by a complement fixation technique. Of the total population studied, only eight were considered to have antibody titres of possible significance. This result would appear to indicate that viral infection does not play a major part in the causation or precipitation of psychiatric disorders.

Adenoviridae

A genome-wide analysis of the shared genetic risk architecture of complex neurological and psychiatric disorders.

Although neurological and psychiatric disorders have historically been considered to reflect distinct pathogenic entities, recent findings suggest shared pathophysiological mechanisms. However, the extent to which these heritable disorders share genetic influences remains unclear. Here we performed a comprehensive analysis of genome-wide association study data, involving nearly 1 million cases across ten neurological diseases and ten psychiatric disorders, to compare their common genetic signal and biological associations. Using complementary statistical tools, we demonstrate that a large set of common genetic variants impacts the risk of multiple neurological and psychiatric disorders, even in the absence of genetic correlations. Furthermore, genome-wide association studies on psychiatric disorders consistently implicate neuronal biology, whereas neurological diseases are associated with diverse neurobiological processes. Together, this study elucidates the genetic relationship between complex neurological and psychiatric disorders, indicating a larger degree of genetic pleiotropy than previously recognized. The findings have implications for disease classification, precision medicine and clinical practice.

Humans

A genome-wide cross-trait analysis characterizes the shared genetic architecture between rheumatoid arthritis and psychiatric disorders.

OBJECTIVES: Patients with RA have a 2- to 3-fold elevated risk of psychiatric disorders, suggesting an underlying genetic link between these phenotypes. However, the shared genetic architectures and pathological mechanisms driving RA-psychiatric disorder comorbidity remain to be fully elucidated. Herein, we performed cross-trait analysis to investigate the shared genetic architecture between RA and psychiatric disorders. METHODS: Leveraging European-ancestry genome-wide association studies (GWASs) datasets of RA (n = 1 026 690) and 10 major psychiatric disorders (n = 14 307-1 222 882), we performed cross-trait pleiotropic analysis to identify the shared pleiotropic loci and genes between RA and psychiatric disorders, followed by functional annotation and Mendelian randomization analysis to explore the pathological mechanisms underlying RA-psychiatric disorder comorbidity. RESULTS: Our analysis revealed significant positive genetic correlations between RA and seven psychiatric disorders, such as major depressive disorder. From these correlations, we identified 61 pleiotropic loci jointly influencing RA and psychiatric disorder risk, along with 208 pleiotropic genes predominantly involved in immune and inflammatory response biological processes. Druggable target exploration identified 21 drug-gene interactions involving pleiotropic genes, with two genes (RHOA and TRAF3) classified in the clinically actionable category, representing potential therapeutic targets for both RA and psychiatric disorders. Mendelian randomization further demonstrated a bidirectional causal relationship between RA and schizophrenia, while supporting the causal roles of attention-deficit/hyperactivity disorder, major depressive disorder and post-traumatic stress disorder in increasing RA risk. CONCLUSION: Our findings elucidate the shared genetic architecture between RA and psychiatric disorders, providing novel insights into the pathological mechanisms underlying their comorbidity and laying the groundwork for improved comorbidity management.

Arthritis, Rheumatoid

A population survey of ischaemic heart disease and minor psychiatric disorder in men.

Associations between ischaemic heart disease and psychiatric morbidity in hospital recruited samples may be confounded by differential referral of patients with co-morbidity. Associations of angina, past history of myocardial infarction, blood pressure, and electrocardiographic evidence of ischaemia with psychiatric disorder can best be examined in community samples as reported here in 2204 middle-aged men from the Caerphilly Collaborative Study. There was a strong association between past history of myocardial infarction, non-specific chest pain, Angina Grade II and psychiatric disorder measured by the 30-item General Health Questionnaire. Electrocardiographic evidence of ischaemia alone was not significantly associated with psychiatric disorder. It is suggested that non-specific chest pain is a symptom of psychiatric disorder; conversely in severe angina psychiatric disorder is secondary to the pain, restricted activity and threat to life which angina implies.

Chest Pain

QEEG profiles of psychiatric disorders.

While reports of EEG correlates of psychiatric disorders date back five decades, clinical sensitivity of the EEG to psychiatric disorders has been greatly enhanced with the advent of quantitative methods of analysis (QEEG). Using a QEEG methodology known as neurometrics we have identified distinctive electrophysiological profiles associated with different psychiatric disorders. With this method quantitative features are extracted from 2 minutes of artifact- free eyes closed resting EEG data, log transformed to obtain Gaussianity, age-regressed, and Z-transformed relative to population norms. Using small subsets of neurometric features, multiple stepwise discriminant analyses were used to construct mathematical classifier functions, the values of which are different for members of different a priori defined diagnostic groups. Using this approach, we have demonstrated high discriminant accuracy in independent replications separating many populations of psychiatric patients from normal as well as from each other, including major affective disorder, schizophrenia, dementia, alcoholism, and learning disabilities, as well as high accuracy of discrimination between known subtypes of depression (unipolar vs bipolar). The use of classification accuracy curves (CACs) which allow one to assess the sensitivity and specificity achieved by the discriminant functions is discussed. In addition, using cluster analysis, neurometric subtypes can be identified in several clinically homogenous populations. Preliminary results suggest that baseline membership in some neurometric subtypes may be highly correlated with response to treatment.

Adolescent

Psychiatric disorder in children with speech and language retardation. A critical review.

This article critically reviews the literature concerning psychiatric disorder in children with speech and language retardation. The data indicate that speech- and language-disordered children are at risk for psychiatric disorder, that there is some correlation between the presence of psychiatric disorder and the type of speech and language disturbance, and that there is a likely correlation between certain types of speech and language problems and the type of psychiatric difficulty. Firm conclusions in this area are hampered by many methodological difficulties. Finally, a review of the nature of the association between psychiatric disorder and speech and language retardation reveals that except in rare instances psychiatric disorder does not cause speech and language retardation, and that in most cases psychiatric disorder is indirectly caused by speech and language retardation.

Anxiety

Social class and minor psychiatric disorder in British Civil Servants: a validated screening survey using the General Health Questionnaire.

Major psychiatric disorder is more common in people of lower rather than higher socioeconomic status. This is less clear for the commoner, so-called minor psychiatric disorders, but these are more affected by tendency to report symptoms. To examine this the distribution of minor psychiatric disorder by employment grade measured by the 30-item General Health Questionnaire is reported from the first cross-sectional phase of the Whitehall II Study of 10,314 London-based civil servants, men and women between 35 and 55 years. Validation of the GHQ in a random subsample stratified by grade and sex (N = 201) suggested that people in lower employment grades tend to under-report minor psychiatric disorder on the GHQ relative to those in higher employment grades. The prevalence of minor psychiatric disorder corrected by the coefficients from the validity study was greater in the lower employment grades than the higher employment grades particularly for men. This was echoed in grade differences in well-being measured by the Affect Balance Scale, and in symptoms and recurrent health problems. Overall, for women there were few clear-cut differences in minor psychiatric disorder by employment grade. The lack of social class gradient in women suggests that further exploration should examine women's role at work and their personal lives for the aetiology of minor psychiatric disorder.

Adult

Constipation and Psychiatric Disorders: A Bidirectional Mendelian Randomization Study.

BACKGROUND: Observational studies have shown a link between constipation (CN) and psychiatric disorders, including Schizophrenia (SP), Bipolar disorder (BD), Schizoaffective disorder (SD), and Parkinson's disease (PD). However, it is still unknown whether CN affects the occurrence and development of psychiatric disorders or whether psychiatric disorders cause the occurrence and development of CN. Therefore, this study used Mendelian randomization (MR) analysis to evaluate the relationship between CN and psychiatric disorders. METHOD: We used genome-wide association studies (GWAS) to assess the relationship between constipation (N = 411, 623) and four psychiatric disorders, including SP ( N = 77, 096), BD (N = 51, 710), SD ( N = 210, 962), PD (N = 482, 730 ), using bidirectional MR analysis. Inverse variance weighting (IVW), MR Egger (ME) and Weighted median (WM) were used as causal analysis methods. Cochran's Q test, funnel plot, MR Egger intercept test and Leave.one.out analysis were used to detect sensitivity. Confounding factors were analyzed and eliminated by LDtrait to avoid influencing the final MR Analysis result. RESULTS: The results of positive MR analysis indicated that there was no evidence of influence of constipation on SP (OR 1.043, 95%CI 0.946 - 1.149, P value = 0.398), BD (OR 1.114, 95%CI 0.995 - 1.248, P value = 0.062), SD (OR 0.934, 95%CI 0.674 - 1.294, P value = 0.682) and PD (OR 1.118, 95%CI 0.918 - 1.361, P value = 0.269) under gene prediction. Reverse MR analysis suggested that SP (OR 1.030, 95% CI 1.001-1.060, P value = 0.042) had a causal relationship with constipation. BD (OR 0.993, 95% CI 0.962-1.025, P value = 0.664), SD (OR 1.021, 95% CI 0.984-1.059, P value = 0.265) and PD (OR 1.004, 95% CI 0.974-1.035, P value = 0.790) were not associated with CN. CONCLUSION: There was a positive association between SP and CN. CN may have no exact causal relationship with BD, SD and PD, and the interaction mechanism between these diseases needs to be further explored.

Constipation

Genetic interconnections between personality-related phenotypes and psychiatric disorders.

BACKGROUND: Personality-related phenotypes are genetically correlated with psychiatric disorders, but whether these relationships reflect shared genetic loci and differ across individual phenotypes remains unclear. We investigated their shared genetic architecture at the level of specific phenotype-disorder pairs. METHODS: We analyzed genome-wide association study summary statistics for 13 personality-related phenotypes and eight psychiatric disorders in populations of European ancestry. Genetic correlations were evaluated separately for 104 phenotype-disorder pairs using linkage disequilibrium score regression and high-definition likelihood. For pairs supported by both methods, MTAG and CPASSOC were applied separately to identify pleiotropic signals, followed by linkage disequilibrium clumping, Bayesian colocalization, gene prioritization, functional enrichment and bidirectional two-sample Mendelian randomization analyses. No composite personality or psychiatric-disorder phenotype was constructed. RESULTS: Among the 104 evaluated pairs, 77 showed significant positive genetic correlations in both analyses. Joint screening of MTAG and CPASSOC results identified pleiotropic signals in 61 pairs, comprising 1088 independent lead SNV-pair associations and 776 unique SNVs. Bayesian colocalization supported 351 signals across 42 pairs and 284 unique lead SNVs. MAGMA identified 1293 unique genes, of which 379 were prioritized by PoPS and 151 were further supported by SMR. These genes were enriched in brain tissues and biological processes involving nervous system development, synaptic organization and intercellular connectivity. Inverse-variance weighted Mendelian randomization identified 41 forward and 32 reverse associations after false-discovery-rate correction, including 21 pairs with bidirectional evidence. CONCLUSION: These item-resolved analyses identify widespread but heterogeneous genetic sharing between personality-related phenotypes and psychiatric disorders. The findings provide a pair-specific map of shared loci and prioritized genes, while the Mendelian randomization results should be interpreted cautiously because of residual heterogeneity and potential horizontal pleiotropy. Further validation in diverse populations and functional studies is required.

Colocalization

The role of the brain-bone axis in skeletal degenerative diseases and psychiatric disorders, A genome-wide pleiotropic analysis.

INTRODUCTION: Skeletal degenerative diseases and psychiatric disorders often coexist clinically. However, the genetic correlations and underlying biological mechanisms between these two types of diseases remain unclear. OBJECTIVES: To investigate the genetic correlations between skeletal degenerative diseases and psychiatric disorders and to identify shared genomic loci, genes, and pathways. METHODS: This comprehensive genome-wide pleiotropic association study utilized summary statistics from publicly available genome-wide association data. Various statistical genetic correlation methods were employed, including LDSC, HDL, PLACO, Coloc, Hyprcoloc, and Mendelian randomization (MR) analysis, along with immune cell colocalization analysis. The study aimed to identify potential shared genetic factors among three skeletal degenerative diseases (osteoarthritis, intervertebral disc degeneration, and osteoporosis) and three psychiatric disorders (schizophrenia, anxiety disorder, and major depressive disorder). RESULTS: Analyses using LDSC, HDL, and Bonferroni corrections revealed significant genetic correlations between intervertebral disc degeneration (IVDD) and anxiety disorder (ANX); fractures, IVDD, and arthritis with major depressive disorder (MDD); and arthritis with schizophrenia (SCZ). Significant genetic correlations were also observed between VDD and ANX, fractures, IVDD, hip osteoarthritis (HipOA), knee osteoarthritis (KneeOA) and MDD, and KneeOA and SCZ. Pleiotropy analysis using PLACO, MAGMA, and multitrait colocalization Hyprcoloc identified 65 pleiotropic loci, 27 shared causal loci, and 9 shared risk loci involving immune cells related to both psychiatric and bone-related diseases. Additionally, tissue-specific enrichment analysis showed that genes mapped to these loci were enriched in brain, cardiovascular, pancreatic, and other tissues. The IVW method demonstrated that MDD increased the risk of IVDD and KneeOA, while IVDD increased the risk of ANX and MDD. Conversely, SCZ was associated with a reduced risk of KneeOA. Multiple sensitivity analyses further supported a positive causal effect of IVDD on MDD. CONCLUSION: These findings suggest significant genetic correlations between skeletal degenerative diseases and psychiatric disorders, highlighting multiple shared comorbid genes and key immune cell types. Importantly, the study supports the role of the brain-bone axis in the regulation of skeletal degenerative diseases and psychiatric disorders, which could provide valuable insights for potential therapeutic targets and interventions for these conditions.

Humans

Identifying novel protein biomarkers with cross-psychiatric disorders effects and potential intervention targets: Evidence from proteomic-Mendelian randomization.

Plasma proteins are the potential therapeutic targets for psychiatric disorders due to their important roles in signal transduction. We aimed to explore the plasma protein biomarkers with cross-psychiatric disorders effects. Proteome-wide Mendelian randomization (MR) and colocalization analyses were performed to investigate the potential causal relationship between plasma protein biomarkers and 12 psychiatric disorders and further identify the potential proteins with cross-effects. To assess the directionality and exclude potential reverse causation, Steiger directionality tests and reverse MR analyses were additionally conducted. Then, validation analysis was performed by employing summary data from cross-psychiatric disorder GWAS to validate the cross-psychiatric effects of proteins. Protein-protein interactions were conducted to evaluate the interaction between candidate proteins and druggability assessment was used to prioritize potential drug targets for psychiatric disorders. We identified novel plasma proteins that possessed cross-psychiatric disorder effects, especially BTN2A1 and BTN3A2 associated with major depressive disorder (MDD), schizophrenia (SCZ), and bipolar disorder (BIP); ITIH1, ITIH3, ITIH4 and FES associated with SCZ and BIP, and the cross-effects of these proteins on SCZ and BIP were confirmed by validation analyses. Steiger tests and reverse MR supported causal directionality. Besides, the protein-protein interactions (PPI) analysis indicated cross-effects proteins had significant interaction, especially ITIH1-ITIH3. The druggability assessment prioritized eight proteins, two of which (ITIH3 and NCAM1) has been targeted by antipsychotic drugs. Our findings provided insights into shared biological mechanisms underlying these conditions.

Humans

Associations of Genetic Liability to Six Psychiatric Disorders With Cardiometabolic Diseases.

IMPORTANCE: Individuals with psychiatric disorders have increased risk of cardiometabolic diseases (CMDs). Evaluating how psychiatric genetic liability relates to CMD may clarify mechanisms. OBJECTIVE: Identify genetic overlap between psychiatric disorders and CMDs independent of cross-disorder pleiotropy, BMI, and smoking. DESIGN SETTING AND PARTICIPANTS: Three Northern European cohorts (the Swedish Twin Registry, the Estonian Biobank, and the Norwegian Mother, Father and Child Cohort Study [MoBa]) totaling 355,159 individuals. Associations with CMDs were estimated as adjusted odds ratios (AORs) from logistic models mutually adjusted for all psychiatric PRSs and in models additionally adjusting for body mass index (BMI) and smoking. Cohort-specific AORs were pooled by inverse-variance weighting. MAIN OUTCOMES AND MEASURES: Exposures were PRSs for attention-deficit/hyperactivity disorder (ADHD), major depressive disorder (MDD), anxiety disorder, posttraumatic stress disorder (PTSD), bipolar disorder, and schizophrenia. Outcomes were diagnoses of CMDs (hyperlipidemia, obesity, type 2 diabetes, hypertensive diseases, arteriosclerosis, ischemic heart disease, heart failure, thromboembolic disease, cerebrovascular disease, and arrhythmias), ascertained from electronic health records. RESULTS: The MDD PRS was associated with increased risk of all CMDs across analyses (AORs ranged from 1.13 [95% CI, 1.10-1.15] for heart failure to 1.02 [95% CI, 1.00-1.05] for arrhythmias). The ADHD PRS was associated with increased risk of all CMDs (AOR ranged from 1.11 [95% CI, 1.09-1.12] for obesity to 1.02 [95% CI, 1.01-1.03] for hyperlipidemia), however associations where attenuated when adjusting for BMI and smoking (lifestyle adjusted AOR for obesity: 1.03 [95% CI, 1.02-1.05]). When not mutually adjusting for all psychiatric PRSs, anxiety disorder and PTSD PRSs were associated with all CMDs; these associations diminished after adjustment. The bipolar and schizophrenia PRSs were inversely associated with most CMDs (AOR for schizophrenia PRS and obesity, 0.93 [95% CI, 0.92-0.94]). CONCLUSIONS AND RELEVANCE: Associations between psychiatric PRSs and CMDs diverged: ADHD, MDD, anxiety disorder, and PTSD PRSs were positively associated with CMDs, whereas bipolar and schizophrenia PRSs were inversely associated. Genetic liability to MDD showed robust associations with CMDs independent of cross-disorder pleiotropy, BMI, and smoking status, whereas associations between the ADHD PRS and CMDs were largely attenuated after adjustment for BMI and smoking.

Journal Article

Substance use and other psychiatric disorders among 100 American Indian patients.

One hundred American Indian patients with a Psychoactive Substance Use Disorder (PSUD) were studied with special reference to associated psychiatric disorders. This clinical sample was divided into three groups: PSUD only, PSUD plus an Organic Mental Disorder (OMD), and PSUD plus any other psychiatric disorder. OMD diagnoses included primarily Delirium Tremens and Alcoholic Hallucinosis; cases of Alcohol Amnestic Disorder, Alcohol Dementia, and trauma-induced OMD were also encountered. Other psychiatric disorders included primarily Major Depression and Anxiety Disorder, with smaller numbers of Schizophrenia, Conduct, Sexual, and other Disorders. Demographic and clinical characteristics were compared among these three groups. Those with PSUD+OMD tended to be older, male, and have more DSM-III Axis 3 disorders (American Psychiatric Association 1980) as compared to other patients; those with PSUD+other diagnoses tended to be single and younger. Education and occupational status were not related to the three diagnostic groups. The data were also subjected to MANOVA analysis. Even when corrected for sex, types of substance being abused, Axis 3 health status, and other factors, the three diagnostic groups still bore a significant relationship to age. Those with PSUD+Other psychiatric diagnoses besides OMD tended to be youngest. Those with PSUD-only were intermediate by age, while those with PSUD+OMD tended to be the oldest.

Adolescent

Noise, noise sensitivity and psychiatric disorder: epidemiological and psychophysiological studies.

Noise, a prototypical environmental stressor, has clear health effects in causing hearing loss but other health effects are less evident. Noise exposure may lead to minor emotional symptoms but the evidence of elevated levels of aircraft noise leading to psychiatric hospital admissions and psychiatric disorder in the community is contradictory. Despite this there are well documented associations between noise exposure and changes in performance, sleep disturbance and emotional reactions such as annoyance. Moreover, annoyance is associated with both environmental noise level and psychological and physical symptoms, psychiatric disorder and use of health services. It seems likely that existing psychiatric disorder contributes to high levels of annoyance. However, there is also the possibility that tendency to annoyance may be a risk factor for psychiatric morbidity. Although noise level explains a significant proportion of the variance in annoyance, the other major factor, confirmed in many studies, is subjective sensitivity to noise. Noise sensitivity is also related to psychiatric disorder. The evidence for noise sensitivity being a risk factor for psychiatric disorder would be greater if it were a stable personality characteristic, and preceded psychiatric morbidity. The stability of noise sensitivity and whether it is merely secondary to psychiatric disorder or is a risk factor for psychiatric disorder as well as annoyance is examined in two studies in this monograph: a six-year follow-up of a group of highly noise sensitive and low noise sensitive women; and a longitudinal study of depressed patients and matched control subjects examining changes in noise sensitivity with recovery from depression. A further dimension of noise effects concerns the impact of noise on the autonomic nervous system. Most physiological responses to noise habituate rapidly but in some people physiological responses persist. It is not clear whether this sub-sample is also subjectively sensitive to noise and whether failure to habituate to environmental noise may also represent a biological indicator of vulnerability to psychiatric disorder. In these studies noise sensitivity was found to be moderately stable and associated with current psychiatric disorder and a disposition to negative affectivity. Noise sensitivity levels did fall with recovery from depression but still remained high, suggesting an underlying high level of noise sensitivity. Noise sensitivity was related to higher tonic skin conductance and heart rate and greater defence/startle responses during noise exposure in the laboratory. Noise sensitive people attend more to noises, discriminate more between noises, find noises more threatening and out of their control, and react to, and adapt to noises more slowly than less noise sensitive people.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent

Noise, noise sensitivity and psychiatric disorder: epidemiological and psychophysiological studies.

Noise, a prototypical environmental stressor, has clear health effects in causing hearing loss but other health effects are less evident. Noise exposure may lead to minor emotional symptoms but the evidence of elevated levels of aircraft noise leading to psychiatric hospital admissions and psychiatric disorder in the community is contradictory. Despite this there are well documented associations between noise exposure and changes in performance, sleep disturbance and emotional reactions such as annoyance. Moreover, annoyance is associated with both environmental noise level and psychological and physical symptoms, psychiatric disorder and use of health services. It seems likely that existing psychiatric disorder contributes to high levels of annoyance. However, there is also the possibility that tendency to annoyance may be a risk factor for psychiatric morbidity. Although noise level explains a significant proportion of the variance in annoyance, the other major factor, confirmed in many studies, is subjective sensitivity to noise. Noise sensitivity is also related to psychiatric disorder. The evidence for noise sensitivity being a risk factor for psychiatric disorder would be greater if it were a stable personality characteristic, and preceded psychiatric morbidity. The stability of noise sensitivity and whether it is merely secondary to psychiatric disorder or is a risk factor for psychiatric disorder as well as annoyance is examined in two studies in this monograph: a six-year follow-up of a group of highly noise sensitive and low noise sensitive women; and a longitudinal study of depressed patients and matched control subjects examining changes in noise sensitivity with recovery from depression. A further dimension of noise effects concerns the impact of noise on the autonomic nervous system. Most physiological responses to noise habituate rapidly but in some people physiological responses persist. It is not clear whether this sub-sample is also subjectively sensitive to noise and whether failure to habituate to environmental noise may also represent a biological indicator of vulnerability to psychiatric disorder. In these studies noise sensitivity was found to be moderately stable and associated with current psychiatric disorder and a disposition to negative affectivity. Noise sensitivity levels did fall with recovery from depression but still remained high, suggesting an underlying high level of noise sensitivity. Noise sensitivity was related to higher tonic skin conductance and heart rate and greater defence/startle responses during noise exposure in the laboratory. Noise sensitive people attend more to noises, discriminate more between noises, find noises more threatening and out of their control, and react to, and adapt to noises more slowly than less noise sensitive people.(ABSTRACT TRUNCATED AT 400 WORDS)

Acoustic Stimulation

Premenstrual affective syndrome and psychiatric disorder.

The relationship between premenstrual affective syndrome and psychiatric disorder was investigated, using 81 women presenting to a Neurology Clinic with functional headache. Premenstrual affective syndrome was significantly associated with a history of depressive syndrome in the population studied. Patients judged to have a non-affective psychiatric disorder reported no greater frequency of definite or probable premenstrual affective syndrome than patients considered psychiatrically normal. The premenstrual occurrence or exacerbation of affective symptoms has been noted. This symptom exacerbation maybe sufficient to require hospitalization. Data presented by Coppen indicate that women with affective disorder are more likely to report the premenstrual symptom of depression than women with other psychiatric disorders. These findings suggest that there may be some relationship between depressive disorder and premenstrual affective symptoms. As part of a larger study on the personality and psychiatric correlates of functional headache, data on the relationship between depressive syndrome and premenstrual affective symptoms were obtained.

Acute Disease