Risk For Other Psychiatric Disorders Research Articles

The relationship of history of psychiatric and substance use disorders on risk of dementia among racial and ethnic groups in the United States.

Dementia is characterized by significant declines in cognitive, physical, social, and behavioral functioning, and includes multiple subtypes that differ in etiology. There is limited evidence of the influence of psychiatric and substance use history on the risk of dementia subtypes among older underrepresented racial/ethnic minorities in the United States. Our study explored the role of psychiatric and substance use history on the risk of etiology-specific dementias: Alzheimer's disease (AD) and vascular dementia (VaD), in the context of a racially and ethnically diverse sample based on national data. We conducted secondary data analyses based on the National Alzheimer's Coordinating Center Uniform Data Set (N = 17,592) which is comprised a large, racially, and ethnically diverse cohort of adult research participants in the network of US Alzheimer Disease Research Centers (ADRCs). From 2005 to 2019, participants were assessed for history of five psychiatric and substance use disorders (depression, traumatic brain injury, other psychiatric disorders, alcohol use, and other substance use). Cox proportional hazard models were used to examine the influence of psychiatric and substance use history on the risk of AD and VaD subtypes, and the interactions between psychiatric and substance use history and race/ethnicity with adjustment for demographic and health-related factors. In addition to other substance use, having any one type of psychiatric and substance use history increased the risk of developing AD by 22-51% and VaD by 22-53%. The risk of other psychiatric disorders on AD and VaD risk varied by race/ethnicity. For non-Hispanic White people, history of other psychiatric disorders increased AD risk by 27%, and VaD risk by 116%. For African Americans, AD risk increased by 28% and VaD risk increased by 108% when other psychiatric disorder history was present. The findings indicate that having psychiatric and substance use history increases the risk of developing AD and VaD in later life. Preventing the onset and recurrence of such disorders may prevent or delay the onset of AD and VaD dementia subtypes. Prevention efforts should pay particular attention to non-Hispanic White and African American older adults who have history of other psychiatric disorders.Future research should address diagnostic shortcomings in the measurement of such disorders in ADRCs, especially with regard to diverse racial and ethnic groups.

The contribution of copy number variants to psychiatric symptoms and cognitive ability.

Copy number variants (CNVs) are deletions and duplications of DNA sequence. The most frequently studied CNVs, which are described in this review, are recurrent CNVs that occur in the same locations on the genome. These CNVs have been strongly implicated in neurodevelopmental disorders, namely autism spectrum disorder (ASD), intellectual disability (ID), and developmental delay (DD), but also in schizophrenia. More recent work has also shown that CNVs increase risk for other psychiatric disorders, namely, depression, bipolar disorder, and post-traumatic stress disorder. Many of the same CNVs are implicated across all of these disorders, and these neuropsychiatric CNVs are also associated with cognitive ability in the general population, as well as with structural and functional brain alterations. Neuropsychiatric CNVs also show incomplete penetrance, such that carriers do not always develop any psychiatric disorder, and may show only mild symptoms, if any. Variable expressivity, whereby the same CNVs are associated with many different phenotypes of varied severity, also points to highly complex mechanisms underlying disease risk in CNV carriers. Comprehensive and longitudinal phenotyping studies of individual CNVs have provided initial insights into these mechanisms. However, more work is needed to estimate and predict the effect of non-recurrent, ultra-rare CNVs, which also contribute to psychiatric and cognitive outcomes. Moreover, delineating the broader phenotypic landscape of neuropsychiatric CNVs in both clinical and general population cohorts may also offer important mechanistic insights.

Unique prediction of developmental psychopathology from genetic and familial risk.

Early detection is critical for easing the rising burden of psychiatric disorders. However, the specificity of psychopathological measurements and genetic predictors is unclear among youth. We measured associations between genetic risk for psychopathology (polygenic risk scores (PRS) and family history (FH) measures) and a wide range of behavioral measures in a large sample (n = 5,204) of early adolescent participants (9-11 years) from the Adolescent Brain and Cognitive Development StudySM . Associations were measured both with and without accounting for shared variance across measures of genetic risk. When controlling for genetic risk for other psychiatric disorders, polygenic risk for problematic opioid use (POU) is uniquely associated with lower behavioral inhibition. Attention deficit hyperactivity disorder (ADHD), depression (DEP), and attempted suicide (SUIC) PRS shared many significant associations with externalizing, internalizing, and psychosis-related behaviors. However, when accounting for all measures of genetic and familial risk, these PRS also showed clear, unique patterns of association. Polygenic risk for ASD, BIP, and SCZ, and attempted suicide uniquely predicted variability in cognitive performance. FH accounted for unique variability in behavior above and beyond PRS and vice versa, with FH measures explaining a greater proportion of unique variability compared to the PRS. Our results indicate that, among youth, many behaviors show shared genetic influences; however, there is also specificity in the profile of emerging psychopathologies for individuals with high genetic risk for particular disorders. This may be useful for quantifying early, differential risk for psychopathology in development.

P410. Discounting Rates and Reward in the ABCD Cohort: Relationship to Social, Familial and Clinical Factors

Adolescence is a period of development marked by the emergence of substance use and increased risk for other psychiatric disorders. Identifying at-risk individuals before the onset of psychopathology would provide opportunities for early clinical interventions that may reduce future severity. Delay discounting has been proposed as a putative risk marker for early substance-use initiation and other forms of psychopathology. However, the extent to which other key factors (e.g., socioeconomic status, cognitive ability, brain areas subserving reward) relate to discounting behavior in adolescents is not well established.

The role of race/ethnicity, psychiatric history, and substance use in the risk of dementia subtypes: Findings from the NACC

AbstractBackgroundDementia is characterized by significant declines in cognitive and physical functioning and includes multiple subtypes that differ in etiology. There is limited evidence of the influence of psychiatric and substance use history on the risk of dementia subtypes among underrepresented racial/ethnic minorities. The study explored the role of psychiatric and substance use history on the risk of etiology‐specific dementias: Alzheimer’s disease (AD) and vascular dementia (VaD), in the context of a racially and ethnically diverse sample based on national data in the US.MethodWe conducted secondary data analyses based on the National Alzheimer’s Coordinating Center Uniform Data Set (N = 17,592). Participants completed at least two visits and were dementia‐free at baseline, and were assessed for history of five psychiatric and substance use disorders (depression, traumatic brain injury, other psychiatric disorders, alcohol use, and other substance use). Cox proportional hazard models were estimated to examine the influence of psychiatric and substance use history on the risk of two dementia subtypes, and the interactions between psychiatric and substance use history and race/ethnicity with adjustment for demographic and health‐related factors.ResultIn addition to other substance use, having any one type of psychiatric and substance use history increased the risk of developing AD by 22‐51% and VaD by 22‐53%. The risk of other psychiatric disorders on AD and VaD risk varied by race/ethnicity. For Non‐Hispanic White, history of other psychiatric disorders increased AD risk by 27% and VaD risk by 116%. For African Americans, AD risk increased by 28% and VaD risk increased by 108% when other psychiatric disorder history was present.ConclusionThe findings indicate that having psychiatric and substance use history increases the risk of developing AD and VaD in later life. Preventing the onset and recurrence of such disorders may prevent or delay the onset AD and VaD dementia subtypes. Prevention efforts should pay particular attention to Non‐Hispanic White and African American older adults who have history of other psychiatric disorders.

Early Detection of Temporal Lobe Epilepsy: Identification of Novel Candidate Genes and Potential Biomarkers Using Integrative Genomics Analysis

Currently afflicting more than 50 million people worldwide, epilepsy is the spectrum disorder characterizing seizures that occur without other plausible medical explanations. Temporal lobe epilepsy (TLE) is one of the most common forms of epilepsy. Current clinical methods; including MRI scans, EEG tests, and doctor visits; can take upwards of several months to confirm a TLE diagnosis; during this time, patients may experience additional seizures and are at an increased risk for other psychiatric disorders. The purpose of this study is to identify candidate genetic biomarkers to facilitate the earlier detection and diagnosis of TLE through gene-based testing (e.g., genomic heatmap analysis or genetic and/or microarray testing). It was hypothesized that potential biomarkers could be identified by analyzing genes that are normally significantly overexpressed in the temporal lobe relative to the gray matter. Statistical and functional analysis was performed on significantly overexpressed genes (≥3.000 fold change) in the gene expression profiles of four donors without epilepsy. The experimental-evidence-based STRING protein interactions analysis showed associations between genes found in DAVID keyword search and other genes facilitating network interconnectivity. After evaluation of the genes’ STRING enriched functions, changes in the expression of the genes CAMK2A, NPY, DLG4, MEF2C, and MAPK7 were concluded to be potential biomarkers for TLE, confirming the original hypothesis. Specifically, the identification of MEF2C and MAPK7 for this purpose is relatively novel in the fields of bioinformatics and neurogenetics. Future work includes investigating the utility of the candidate genes in real-world gene-based diagnostic methods.

Anxiety Disorders in Adolescents

Anxiety disorders are highly prevalent in adolescents and remain significantly undertreated. Appropriate screening, diagnosis, and treatment of adolescent anxiety disorders is important, as early intervention may prevent or reduce risk for other psychiatric disorders and functional impairment in adulthood. Screening should be done by mental health and primary care providers routinely to identify adolescents with anxiety disorders or those at risk of developing anxiety disorders. Several studies have evaluated the utility of therapy and medications in the management of adolescent anxiety disorders, and the most effective treatment continues to be cognitive-behavioral therapy (CBT) in combination with selective serotonin reuptake inhibitors. To provide greater access to care and reduce barriers to treatment, novel interventions including Internet-delivered CBT and applied games have been developed and show promising results in early studies. This article reviews the most common anxiety disorders in the Diagnostic and Statistical Manual of Mental Disorders, fifth edition, with specific attention to how presentation and treatment may differ in adolescents. [ Psychiatr Ann. 2019;49(6):251–255.]

A Review of Heterogeneity in Attention Deficit/Hyperactivity Disorder (ADHD).

Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder that affects approximately 8%–12% of children worldwide. Throughout an individual’s lifetime, ADHD can significantly increase risk for other psychiatric disorders, educational and occupational failure, accidents, criminality, social disability and addictions. No single risk factor is necessary or sufficient to cause ADHD. The multifactorial causation of ADHD is reflected in the heterogeneity of this disorder, as indicated by its diversity of psychiatric comorbidities, varied clinical profiles, patterns of neurocognitive impairment and developmental trajectories, and the wide range of structural and functional brain anomalies. Although evidence-based treatments can reduce ADHD symptoms in a substantial portion of affected individuals, there is yet no curative treatment for ADHD. A number of theoretical models of the emergence and developmental trajectories of ADHD have been proposed, aimed at providing systematic guides for clinical research and practice. We conducted a comprehensive review of the current status of research in understanding the heterogeneity of ADHD in terms of etiology, clinical profiles and trajectories, and neurobiological mechanisms. We suggest that further research focus on investigating the impact of the etiological risk factors and their interactions with developmental neural mechanisms and clinical profiles in ADHD. Such research would have heuristic value for identifying biologically homogeneous subgroups and could facilitate the development of novel and more tailored interventions that target underlying neural anomalies characteristic of more homogeneous subgroups.

White matter – emotion processing activity relationships in youth offspring of bipolar parents

BackgroundEarly detection of Bipolar Disorder (BD) is critical for targeting interventions to delay or prevent illness onset. Yet, the absence of objective BD biomarkers makes accurately identifying at-risk youth difficult. In this study, we examined how relationships between white matter tract (WMT) structure and activity in emotion processing neural circuitry differentiate youth at risk for BD from youth at risk for other psychiatric disorders. MethodsOffspring (ages 8–17) of parents with BD (OBP, n = 32), offspring of comparison parents with non-BD psychopathology (OCP, n = 30), and offspring of healthy parents (OHP, n = 24) underwent diffusion tensor and functional magnetic resonance imaging while performing an emotional face processing task. Penalized and multiple regression analyses included GROUP(OBP,OCP)xWMT interactions as main independent variables, and emotion processing activity as dependent variables, to determine significant group differences in WMT-activity relationships. Results8 GROUPxWMT interaction variables contributed to 16.5% of the variance in amygdala and prefrontal cortical activity to happy faces. Of these, significant group differences in slopes (inverse for OBP, positive for OCP) existed for the relationship between forceps minor radial diffusivity and rostral anterior cingulate activity (p = 0.014). Slopes remained significantly different in unmedicated youth without psychiatric disorders (p = 0.017) and were moderated by affective lability symptoms (F(1,29) = 5.566, p = 0.036). LimitationsRelatively small sample sizes were included. ConclusionsForceps minor radial diffusivity-rostral anterior cingulate activity relationships may reflect underlying neuropathological processes that contribute to affectively labile youth at risk for BD and may help differentiate them from youth at risk for other psychiatric disorders.

Investigating the genetic architecture of general and specific psychopathology in adolescence

Whilst associations between polygenic risk scores (PRSs) for schizophrenia and various phenotypic outcomes have been reported, an understanding of developmental pathways can only be gained by modelling comorbidity across psychopathology. We examine how genetic risk for schizophrenia relates to adolescent psychosis-related and internalizing psychopathology using a latent modelling approach, and compare this to genetic risk for other psychiatric disorders, to gain a more comprehensive understanding of the developmental pathways at this age. PRSs for schizophrenia, major depressive disorder, neuroticism and bipolar disorder were generated for individuals in the Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort. Multivariate linear regression was used to examine the relationships of these PRSs with psychopathology factors modelled within (i) a correlated factors structure and (ii) a bifactor structure. The schizophrenia PRS was associated with an increase in factors describing psychotic experiences, negative dimension, depression and anxiety, but, when modelling a general psychopathology factor based on these measures, specific effects above this persisted only for the negative dimension. Similar factor relationships were observed for the neuroticism PRS, with a (weak) specific effect only for anxiety once modelling general psychopathology. Psychopathology during adolescence can be described by a general psychopathology construct that captures common variance as well as by specific constructs capturing remaining non-shared variance. Schizophrenia risk genetic variants identified through genome-wide association studies mainly index negative rather than positive symptom psychopathology during adolescence. This has potentially important implications both for research and risk prediction in high-risk samples.

S139. INVESTIGATING THE GENETIC ARCHITECTURE OF GENERAL AND SPECIFIC PSYCHOPATHOLOGY IN ADOLESCENCE USING SCHIZOPHRENIA POLYGENIC SCORES

BackgroundWhilst associations between polygenic risk scores (PRSs) for schizophrenia and various phenotypic outcomes have been reported, an understanding of developmental pathways can only be gained by modelling comorbidity across psychopathology, something no studies have done to date. We examine how genetic risk for schizophrenia relates to a broad range of adolescent psychopathology using a latent modelling approach, and compare this to genetic risk for other psychiatric disorders, to gain a more comprehensive understanding of development pathways at this age.MethodsPRSs for schizophrenia, major depressive disorder, neuroticism and bipolar disorder were generated for individuals in the Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort. Multivariate linear regression was used to examine relationships of these PRSs with psychopathology factors modelled within i) a correlated factors structure, and ii) a bifactor structure.ResultsThe schizophrenia PRS was associated with an increase in factors describing psychotic experiences, negative dimension, depression, and anxiety, but once modelling a general psychopathology factor specific effects above this persisted only for the negative dimension. Similar factor relationships were observed for the neuroticism PRS, with a (weak) specific effect only for anxiety once modelling general psychopathology.DiscussionPsychopathology during adolescence can be described by a general psychopathology construct that captures common variance as well as by specific constructs capturing remaining non-shared variance. Schizophrenia risk genetic variants identified through genome-wide association studies mainly index negative rather than positive symptom psychopathology during adolescence. This has potentially important implications both for research and risk prediction in high-risk samples.

Traditional marijuana, high-potency cannabis and synthetic cannabinoids: increasing risk for psychosis.

Epidemiological evidence demonstrates that cannabis use is associated with an increased risk of psychotic outcomes, and confirms a dose-response relationship between the level of use and the risk of later psychosis. High-potency cannabis and synthetic cannabinoids carry the greatest risk. Experimental administration of tetrahydrocannabinol, the active ingredient of cannabis, induces transient psychosis in normal subjects, but this effect can be ameliorated by co-administration of cannabidiol. This latter is a constituent of traditional hashish, but is largely absent from modern high-potency forms of cannabis. Argument continues over the extent to which genetic predisposition is correlated to, or interacts with, cannabis use, and what proportion of psychosis could be prevented by minimizing heavy use. As yet, there is not convincing evidence that cannabis use increases risk of other psychiatric disorders, but there are no such doubts concerning its detrimental effect on cognitive function. All of the negative aspects are magnified if use starts in early adolescence. Irrespective of whether use of cannabis is decriminalized or legalized, the evidence that it is a component cause of psychosis is now sufficient for public health messages outlining the risk, especially of regular use of high-potency cannabis and synthetic cannabinoids.

Attention-deficit/hyperactivity disorder.

Attention-deficit/hyperactivity disorder (ADHD) is a persistent neurodevelopmental disorder that affects 5% of children and adolescents and 2.5% of adults worldwide. Throughout an individual's lifetime, ADHD can increase the risk of other psychiatric disorders, educational and occupational failure, accidents, criminality, social disability and addictions. No single risk factor is necessary or sufficient to cause ADHD. In most cases ADHD arises from several genetic and environmental risk factors that each have a small individual effect and act together to increase susceptibility. The multifactorial causation of ADHD is consistent with the heterogeneity of the disorder, which is shown by its extensive psychiatric co-morbidity, its multiple domains of neurocognitive impairment and the wide range of structural and functional brain anomalies associated with it. The diagnosis of ADHD is reliable and valid when evaluated with standard criteria for psychiatric disorders. Rating scales and clinical interviews facilitate diagnosis and aid screening. The expression of symptoms varies as a function of patient developmental stage and social and academic contexts. Although there are no curative treatments for ADHD, evidenced-based treatments can markedly reduce its symptoms and associated impairments. For example, medications are efficacious and normally well tolerated, and various non-pharmacological approaches are also valuable. Ongoing clinical and neurobiological research holds the promise of advancing diagnostic and therapeutic approaches to ADHD. For an illustrated summary of this Primer, visit: http://go.nature.com/J6jiwl.

Autistic spectrum disorder, attention deficit hyperactivity disorder, and psychiatric comorbidities: A nationwide study

Attention deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) are both frequently comorbid with other psychiatric disorders, but the comorbid effect of ASD and ADHD relative to the comorbid risk of other psychiatric disorders is still unknown. Using the Taiwan National Health Insurance Research Database, 725 patients with ASD-alone, 5694 with ADHD-alone, 466 with ASD+ADHD, and 27,540 (1:4) age-/gender-matched controls were enrolled in our study. The risk of psychiatric comorbidities was investigated. The ADHD+ASD group had the greatest risk of developing schizophrenia (hazard ratio [HR]: 95.89; HR: 13.73; HR: 174.61), bipolar disorder (HR: 74.93; HR: 19.42; HR: 36.71), depressive disorder (HR: 17.66; HR: 12.29; HR: 9.05), anxiety disorder (HR: 49.49; HR: 50.92; HR: 14.12), disruptive behavior disorder (HR: 113.89; HR: 93.87; HR: 26.50), and tic disorder (HR: 8.95; HR: 7.46; HR: 4.87) compared to the ADHD-alone, ASD-alone, and control groups. Patients with ADHD+ASD were associated with the greatest risk of having comorbid bipolar disorder, depressive disorder, anxiety disorder, disruptive behavior disorder, and tic disorder. The diagnoses of ASD and ADHD preceded the diagnoses of other psychiatric comorbidities. A comprehensive interview scrutinizing the psychiatric comorbidities would be suggested when encountering and following patients with both ASD and ADHD in clinical practice.

Adult Attention Deficit Hyperactivity Disorder (ADHD): public health implications

In 2008 NICE guidance recommended the identification and treatment of Attention Deficit Hyperactivity Disorder (ADHD) in adults. Previously, diagnosis and treatment of this condition had mainly been confined to children and young people. Dr Tamsin Newlove-Delgado and Professor Ken Stein from University of Exeter explain why adult ADHD is important and what the implications are for health improvement, commissioning and providing evidence based services Attention Deficit Hyperactivity Disorder (ADHD) is a neurodevelopmental disorder, with symptoms of inattention, hyperactivity and impulsivity causing significant impairment in functioning. The diagnostic criteria for ADHD currently require that symptoms must have been present before the age of seven years, and be apparent in more than one setting. There is no single cause; instead the condition appears to result from a complex interaction of genetic and environmental factors.1 ADHD is estimated to affect 3-5% of children of school age in the UK.1,2 Does ADHD exist in adults? Few studies have followed up young people with ADHD beyond the age of 25. A meta-analysis of data from follow-up studies suggested that although the rate of persistence of ADHD meeting the full diagnostic criteria at age 25 was only 15%, the persistence of symptoms was much higher at around 40-60%.3 Therefore, although the prevalence of ADHD certainly declines with age, a significant proportion of adults have still been found to be affected. ADHD in adults remains the subject of some debate, given the high rate of co-morbidities and the difficulty in distinguishing normal symptoms from pathological ones. However, in 2008 the National Institute for Health and Clinical Excellence (NICE) reviewed the evidence on adult ADHD, recommending recognition of the condition and establishment of services for assessment and management, with stimulant medication as the first-line treatment for adults with either moderate or severe levels of impairment.2 How many adults might suffer with ADHD? A meta-analysis of world literature produced a pooled prevalence estimate of 2.5%.4 The UK 2007 Adult Psychiatric Morbidity Survey5 used the six item Adult ADHD Self Report Scale (ASRS) to screen the sample for ADHD symptoms. Using this scale 8.2% of adults scored four or more, which was considered to warrant clinical assessment, and 0.6% scored all six, indicating a high likelihood of a positive diagnosis. NICE have estimated the number of men with ADHD at over 300,000 in England, and the number of women at over 80,000,6 indicating that there is a considerable population likely to be affected. Impact of adult ADHD Higher risk of other psychiatric disorders Adults with ADHD are at increased risk for other psychiatric disorders. Over a lifetime, it is estimated that over threequarters of those with ADHD will have a psychiatric co-morbidity;7 with depression and anxiety being most common. Substance misuse and smoking Substance misuse affects up to half of adults with ADHD.7 A significant proportion of those in contact with substance misuse services also have ADHD symptoms. High rates of smoking (up to 40%) in ADHD8 may be explained by genetic influences or self-medication with nicotine: the condition is also linked with earlier initiation of smoking and difficulty in quitting.9 Accidents Studies have reported that adolescents and adults with ADHD are more likely to be involved in road traffic collisions, to be stopped for speeding, and to report losses of concentration and control whilst driving.10 Similarly, both children and adults with ADHD appear to have more accidents and injuries in general, possibly due to impulsivity and risktaking behaviours.11 Educational and occupational underachievement Adults with ADHD experience higher job turnover and more periods of unemployment. A recent European study found they were twice as likely to be unemployed. …

Continuity of Depressive Disorders From Childhood and Adolescence to Adulthood

To determine and compare rates of homotypic continuity of childhood- and adolescent-onset depression into adulthood. This was a naturalistic, prospective cohort study of children and adolescents receiving psychiatric care at all community mental health centers in Madrid, Spain, from January 1986 to December 2007. Data were obtained from a regional registry wherein all psychiatric visits to public mental health centers are recorded. Patients received their first diagnosis of an ICD-10 F32 or F33 depressive disorder between 6 and 17 years of age and were at least 20 years old at the time of their last visit. Subjects whose first diagnosis was in childhood (aged 6-12 years: depressed-child group) and subjects whose first diagnosis was in adolescence (aged 13-17 years: depressed-adolescent group) were compared in terms of demographic characteristics, psychiatric comorbidity, and rates of homotypic continuity in adulthood. Five hundred twenty-eight patients with depressive disorders met inclusion criteria. The depressed-adolescent group had a higher proportion of girls (60.3%) compared to the depressed-child group, but did not differ on other demographic or clinical variables. Most subjects who later received treatment in adult mental health facilities (n = 243; 57.2%; 95% CI, 50.9-57.2) continued to be diagnosed with a depressive disorder. High rates of anxiety disorders, bipolar disorder, personality disorders, and psychotic disorders in adulthood were observed among subjects from both groups. The absence of psychiatric comorbidity prior to age 18 years was associated with homotypic continuity of depressive disorder into adulthood. Subjects with adolescent-onset depression and subjects without comorbid psychiatric disorders in youth appear to have a higher level of homotypic continuity into adulthood. Both children and adolescents with depressive disorders are at risk for other psychiatric disorders in adulthood.

Deficient Emotional Self-Regulation and Adult Attention Deficit Hyperactivity Disorder: A Family Risk Analysis

A growing body of research suggests that deficient emotional self-regulation (DESR) is prevalent and morbid among patients with attention deficit hyperactivity disorder (ADHD). Family studies provide a method of clarifying the co-occurrence of clinical features, but no family studies have yet addressed ADHD and DESR. Participants were 83 probands with and without ADHD and 128 siblings. All were assessed for axis I DSM-IV conditions with structured diagnostic interviews. The authors defined DESR in adult probands and siblings using items from the Barkley Current Behavior Scale. Analyses tested hypotheses about the familial relationship between ADHD and DESR. Siblings of ADHD probands were at elevated risk of having ADHD, irrespective of the presence or absence of DESR in the proband. The risk for DESR was elevated in siblings of ADHD plus DESR probands but not in siblings of ADHD probands. ADHD and DESR cosegregated in siblings. The risk for other psychiatric disorders was similar in siblings of the ADHD proband groups. The pattern of inheritance of ADHD with DESR preliminarily suggests that DESR may be a familial subtype of ADHD. Our data suggest that DESR is not an expression of other axis I DSM-IV disorders or of nonfamilial environmental factors. The authors cannot exclude contribution of non-axis-I DSM-IV disorders to risk for DESR and cannot determine whether the cosegregation of ADHD in DESR within families is a result of genes or familial environmental risk factors. Further investigation of DESR and its correlates and treatment both in and outside the context of ADHD is warranted.

A controlled family study of children with DSM-IV bipolar-I disorder and psychiatric co-morbidity

To estimate the spectrum of familial risk for psychopathology in first-degree relatives of children with unabridged DSM-IV bipolar-I disorder (BP-I). We conducted a blinded, controlled family study using structured diagnostic interviews of 157 children with BP-I probands (n=487 first-degree relatives), 162 attention deficit hyperactivity disorder (ADHD) (without BP-I) probands (n=511 first-degree relatives), and 136 healthy control (without ADHD or BP-I) probands (n=411 first-degree relatives). The morbid risk (MR) of BP-I disorder in relatives of BP-I probands (MR=0.18) was increased 4-fold [95% confidence interval (CI) 2.3-6.9, p<0.001] over the risk to relatives of control probands (MR=0.05) and 3.5-fold (95% CI 2.1-5.8, p<0.001) over the risk to relatives of ADHD probands (MR=0.06). In addition, relatives of children with BP-I disorder had high rates of psychosis, major depression, multiple anxiety disorders, substance use disorders, ADHD and antisocial disorders compared with relatives of control probands. Only the effect for antisocial disorders lost significance after accounted for by the corresponding diagnosis in the proband. Familial rates of ADHD did not differ between ADHD and BP-I probands. Our results document an increased familial risk for BP-I disorder in relatives of pediatric probands with DSM-IV BP-I. Relatives of probands with BP-I were also at increased risk for other psychiatric disorders frequently associated with pediatric BP-I. These results support the validity of the diagnosis of BP-I in children as defined by DSM-IV. More work is needed to better understand the nature of the association between these disorders in probands and relatives.

Recognition and Treatment of Panic Disorder

Panic disorder is a common, disabling condition that affects 3% to 5% of the world's population. Although it is treatable, panic disorder goes unrecognized and untreated in many patients. Patients with panic disorder have an increased risk for other psychiatric disorders, especially other anxiety disorders, and panic disorder is associated with other medical conditions such as migraines, fibromyalgia, and irritable bowel syndrome. Clinicians treating panic disorder must be able to recognize the disorder, differentiate it from other disorders in which panic attacks are part of the symptomatology, and map out an individualized treatment plan for each patient. This presentation discusses the importance of collaboration between doctor and patient and details available treatment options, including antidepressants, benzodiazepines, and cognitive-behavioral therapy.

Perinatal risk factors for schizophrenia: how specific are they?

The association between exposure to perinatal risk factors and increased vulnerability for schizophrenia is now documented by a large body of epidemiologic studies. However, the diagnostic specificity of this association may be questioned, because subjects with a history of exposure to early environmental risk factors are at an increased risk for other psychiatric disorders with childhood or adult onset, such as autism, anorexia nervosa, or affective disorders. Because a given risk factor may be associated with several adverse health outcomes, these findings do not preclude the existence of a causal relationship between perinatal risk factors and schizophrenia. This lack of diagnostic specificity suggests that the clinical expression of the vulnerability induced by early risk factors depends on gene-environment interactions or interaction between this prenatally determined vulnerability and exposure to later environmental risk factors.