Inattention, but not OCD, predicts the core features of hoarding disorder

Hoarding Disorder (HD), defined as the acquisition of and failure to discard large volumes of possessions, resulting in clutter that precludes normal use of living spaces, is a common and debilitating condition. Although hoarding has historically been conceptualized as a variant of obsessive-compulsive disorder (OCD), increasing evidence suggests that hoarding might be more closely associated with the symptoms of attention deficit-hyperactivity disorder (ADHD). The aim of the present study was to clarify the relationship between the core features of hoarding (clutter, difficulty discarding, acquiring), OCD symptoms, and ADHD symptoms. HD (N = 39), non-hoarding OCD (N = 26), and healthy control (N = 36) participants underwent careful diagnostic interviewing and completed standardized self-report measures of the core features of hoarding (clutter, difficulty discarding, acquiring), OCD symptoms, negative affect, and the inattentive and hyperactive/impulsive symptoms of ADHD. Multiple linear regressions demonstrated that after controlling for global negative affect, OCD symptoms did not significantly predict any of the core features of HD. Conversely, the inattentive (but not hyperactive/impulsive) symptoms of ADHD significantly predicted severity of clutter, difficulty discarding, and acquiring. These results challenge current conceptualizations of hoarding as a subtype of OCD, and suggest an association with neurocognitive impairment.     

Emotion Regulation and Parenting in AD/HD and Comparison Boys: Linkages with Social Behaviors and Peer Preference

Children's emotion regulation strategies and parenting responses in a family task that elicited frustration are investigated by, comparing core attention-deficit/hyperactivity disorder (AD/HD) symptomatology, emotional reactivity, and emotional regulation in the prediction of social behaviors and peer social preference. Participants were boys, ages 6–12 years, either with AD/HD (n = 45) or without problem behaviors (comparison; n = 34). A high-aggressive subgroup of AD/HD boys showed a significantly less constructive pattern of emotional coping than did both a low-aggressive AD/HD subgroup of boys and nondiagnosed comparison boys, who did not differ. With statistical control of core AD/HD symptomatology, noncompliance in a naturalistic summer camp was predicted by boys' overall emotion regulation and three specific strategies (emotional accommodation, problem solving, negative responses) during the parent–child interaction. Emotional accommodation and negative responses to the frustration task also marginally predicted social preference at the camp. These emotion regulation variables outperformed emotional reactivity in predicting such outcomes. Some emotion-related parenting behaviors were associated with child coping in the task. We discuss the relationship of emotion regulation to core AD/HD symptomatology and emotional reactivity, and the role of parents' behaviors in influencing children's emotional responses.     

The Role of Harsh Discipline in Explaining Sex Differences in Conduct Disorder: a Study of Opposite-Sex Twin Pairs

In the current study, two hypotheses about the role of harsh discipline (HD) in explaining the sex difference in the prevalence of conduct disorder (CD) were evaluated: that boys exhibit more CD than girls because (1) they are exposed to more HD and/or (2) there is a greater association between HD and CD in boys. These hypotheses were evaluated in a sample of male and female adult twins from different families (N = 3,502) as well as a sample of adult twin brothers and sisters (N = 655) in order to examine the extent to which sex differences remained after controlling for between-family differences. Retrospective reports of HD experienced between ages 6–13 and DSM-IV CD symptoms experienced before age 18 were obtained via structured psychiatric telephone interviews. Boys reported higher mean levels of HD and CD than girls, both between and within families, and the results of model-fitting analyses suggested that differences in the use of harsh disciplinary practices for sons versus daughters may partially explain the sex difference in the prevalence of CD. Between families, the relation between HD and CD was greater for girls than boys, but within families, there was no evidence of a sex difference in the relation between HD and CD. Inconsistent between-family and within-family results suggest that factors that differ between families are confounded with sex differences in the relation between HD and CD. A more stringent test of sex differences involves eliminating these between-family differences by studying boys and girls within the same family.     

Which Executive Functioning Deficits Are Associated With AD/HD,ODD/CD and Comorbid AD/HD+ODD/CD?

This study investigated (1) whether attention deficit/hyperactivity disorder (AD/HD) is associated with executive functioning (EF) deficits while controlling for oppositional defiant disorder/conduct disorder (ODD/CD), (2) whether ODD/CD is associated with EF deficits while controlling for AD/HD, and (3)~whether a combination of AD/HD and ODD/CD is associated with EF deficits (and the possibility that there is no association between EF deficits and AD/HD or ODD/CD in isolation). Subjects were 99~children ages 6–12 years. Three putative domains of EF were investigated using well-validated tests: verbal fluency, working memory, and planning. Independent of ODD/CD, AD/HD was associated with deficits in planning and working memory, but not in verbal fluency. Only teacher rated AD/HD, but not parent rated AD/HD, significantly contributed to the prediction of EF task performance. No EF deficits were associated with ODD/CD. The presence of comorbid AD/HD accounts for the EF deficits in children with comorbid AD/HD+ODD/CD. These results suggest that EF deficits are unique to AD/HD and support the model proposed by R. A. Barkley (1997).     

Biological markers of cognition in prodromal Huntington's disease: a review

Huntington’s disease (HD), an autosomal-dominant genetic disorder, has historically been viewed as a degenerative movement disorder but it also includes psychiatric symptoms and progressive cognitive decline. There has been a lack of consensus in the literature about whether or not cognitive signs can be detected in carriers before clinical (motor) onset of the disease, i.e., prodromal HD. However, recently validated mathematical formulas to estimate age of clinical onset, refined over the past 5–7 years, have allowed researchers to overcome the methodological limitation of treating all prodromal carriers as a homogenous high-risk group (i.e., whether they may be 2 or 15 years from diagnosis). Here we review 23 articles on the HD prodrome, all of which related cognition to a biological marker of disease burden (i.e., genetic load, neuroimaging). All studies found at least one cognitive domain was associated with disease burden in prodromal HD participants. There was greater variability in both the detection and cognitive domain affected in those farther from onset (or those with less pathology) while most studies reliably found declines in visuomotor performance and working memory in those closer to onset. These findings indicate that cognitive signs can be reliably detected in the HD prodrome when comparing cognition to additional disease markers, however, there continues to be significant variability on cognitive findings among large and methodologically rigorous studies. This may reflect true heterogeneity in the prodromal HD phenotype which must be further explored by analyzing intra-individual variance, determining demographic risk factors associated with decline/protection, and examining if particular HD families exhibit distinct cognitive profiles. These and additional future directions are discussed.     

Effects of Reward and Response Cost on Response Inhibition in AD/HD, Disruptive, Anxious, and Normal Children

In previous research, children with attention deficit/hyperactivity disorder (AD/HD) have demonstrated impaired response inhibition on the stop paradigm. In this study we examined whether this impairment in fact reflects a motivational deficit. Four groups of children (age range 7–13 years) participated in the study: 14 AD/HD children, 21 normal controls, 14 disruptive children, and 14 anxious children. The psychopathological groups were recruited from special educational services and mental health outpatient clinics. Parent, teacher, and child questionnaires were used to select children with pervasive disorders. Normal controls attended regular classes and scored low on all questionnaires. Children were tested once with reward contingencies and once with response cost contingencies in a randomized cross-over design. We hypothesized that if a motivational deficit underlies poor response inhibition in AD/HD children, this deficit will be remedied by response contingencies. Despite the presence of response contingencies, AD/HD children showed poor response inhibition compared with normal controls. Findings argue against a motivational explanation for the response inhibition deficit in AD/HD children     

Evolutionary versus prototype analyses of the concept of disorder.

The harmful dysfunction (HD) analysis of the concept of disorder (J. C. Wakefield, 1992a) holds that disorders are harmful failures of internal mechanisms to perform their naturally selected functions. S. O. Lilienfeld and L. Marino (1995) proposed instead that disorder is a Roschian prototype concept without defining properties. Against the HD analysis, they argued that many disorders are not failures of naturally selected functions because they are either designed reactions (e.g., fever) or failures of functions that are not naturally selected (e.g., reading disorder). The HD analysis is defended here against these and other objections and compared with the Roschian account. It is argued that the objections are based on conceptual confusions and can be turned around to provide strong new support for the HD analysis. A series of conceptual experiments demonstrates the superior explanatory power of the HD analysis and disconfirms the Roschian account.     

Illness representations,knowledge and motivation to perform presymptomatic testing for late-onset genetic diseases

This study addresses the relation between illness representations, knowledge and motivation to perform the presymptomatic testing (PST) of subjects at-risk for Familial Amyloydotic Polyneuropathy (FAP), Huntington’s disease (HD) and Machado–Joseph disease (MJD), compared with subjects at-risk for Hereditary Hemochromatosis (HH). The sample comprised a clinical group of 213 subjects at genetic risk for FAP, HD and MJD, and a comparison group of 31 subjects at genetic risk for HH, that answered three open-ended questions relating illness representations, knowledge about the disease, and motivation to perform PST. People at-risk for FAP, HD and MJD use more metaphors, make more references to the family, are more concerned with the future and feel more out of curiosity and to learn, than for HH. These subjects at-risk correspond to the profile of somatic individual or personhood, wherein the unsubjectivation of the disease can function as a coping mechanism.     

Presymptomatic testing for huntington diseases: Recommendations for counseling

The discovery of a genetic marker linked to the Huntington disease (HD) gene made it possible to perform presymptomatic genetic testing for this late onset disorder. The first two pilot research programs in the United States, at Massachusetts General Hospital and Johns Hopkins Hospital, began offering testing in the Fall of 1986. Twenty-three centers are now offering this testing as part of their clinical service. As testing for this and other late onset diseases becomes more widespread, it is important to assess what we have learned about offering this test to those at risk. This article presents recommendations based on the author's 5 years of experience offering presymptomatic testing for HD in order to alert counselors to the complexities of offering this type of service.     

Dysfunction as a factual component of disorder

The harmful dysfunction (HD) analysis holds that disorder, mental or physical, requires harm, a value criterion, and dysfunction, a factual criterion referring to failure of a mechanism to perform a naturally selected function. Houts' arguments that the HD analysis does not offer an adequate factual account of dysfunction are examined and shown to be invalid. For example, his claim that the HD analysis confuses function with purpose, a value concept, ignores the analysis'account of function in terms of the value-free notion of effect-explanation; and his argument that functions imply norms (e.g., what mechanisms are 'supposed to' do) falsely assumes that such norms are evaluative. The HD analysis of function is analogous in logical structure to the functional analyst's factual behavioral notion of function. Houts' value account of disorder is inconsistent with people's classificatory judgments, as his own examples demonstrate.     

Harmful dysfunction and the DSM definition of mental disorder.

Physicians, including psychiatrists, give a lot of thought in their everyday work to answer the question of whether or not a particular patient has a disorder; they rarely give much thought to the broader issue of what constitutes a disorder. Remarkably, and consistent with the harmful dysfunction (HD) analysis, there is a broad consensus in both the general public and the medical and health professions as to what conditions are disorders--even though there is no consensus definition of disorder. The HD analysis is a substantial advance over previous attempts to define disorder in specifying the nature of what is not working in the individual (the dysfunction). The adoption of the HD analysis in DSM-V (Diagnostic and Statistical Manual of Mental Disorders, 5th ed.) would probably have little if any effect on the list of categories of mental disorders. Its main value would be in helping make revisions in the diagnostic criteria more valid as true indicators of disorder.     

Untangling Intelligence,Psychopathy, Antisocial Personality Disorder,and Conduct Problems: A Meta‐analytic Review

Substantial research has investigated the association between intelligence and psychopathic traits. The findings to date have been inconsistent and have not always considered the multidimensional nature of psychopathic traits. Moreover, there has been a tendency to confuse psychopathy with other closely related, clinically significant disorders. The current study represents a meta‐analysis conducted to evaluate the direction and magnitude of the association of intelligence with global psychopathy, as well as its factors and facets, and related disorders (i.e. antisocial personality disorder, conduct disorder, and oppositional defiant disorder). Our analyses revealed a small, significant, negative relationship between intelligence and total psychopathy (r = ?.07, p = .001). Analysis of factors and facets found differential associations, including both significant positive (e.g. interpersonal facet) and negative (e.g. affective facet) associations, further affirming that psychopathy is a multidimensional construct. Additionally, intelligence was negatively associated with antisocial personality disorder (r = ?.13, p = .001) and conduct disorder (r = ?.13, p = .001) but positively with oppositional defiant disorder (r = .06, p = .001). There was significant heterogeneity across studies for most effects, but the results of moderator analyses were inconsistent. Finally, bias analyses did not find significant evidence for publication bias or outsized effects of outliers. © 2019 European Association of Personality Psychology     

Evolutionary history versus current causal role in the definition of disorder: reply to McNally

The harmful dysfunction (HD) analysis (Wakefield, American Psychologist 47 (1992a) 373) asserts that "disorder" means "harmful dysfunction", where "harm" is a value concept anchored in social values and "dysfunction" is a factual concept referring to failure of a mechanism to perform a natural function. Additionally, the HD analysis claims that a mechanism's natural functions are its naturally selected effects. McNally (Behaviour Research and Therapy (2000) pp. 309-314) argues to the contrary that "dysfunction" is a value concept referring to negative failures of function, that "function" refers to current causal roles and not evolutionarily designed causal roles, and that "disorder" consequently means "harmful failure of a mechanism to perform a valued current causal role." I reply by showing that McNally's proposals lack the HD analysis's power to explain common judgments about function, dysfunction, and disorder. "Dysfunction" cannot be a negative value concept because many dysfunctions are positive or neutral; "function" cannot refer to current causal roles because many current causal roles are not functions and some functions are not current causal roles; and "disorder" cannot refer to harmful failures of current causal roles because that definition allows almost any negative condition whatever to be a disorder and thus fails to explain the distinctions we make between disorder and non-disorder.     

Juvenile onset Huntington's disease--clinical and research perspectives

Huntington's disease (HD) is an inherited neurodegenerative disorder. The mutation which causes the disease is an expansion in the number of repetitions of three nucleotides, C, A, and G in exon 1 of the huntingtin gene. The gene normally has 15 to 30 repeats and an expansion to 40 or more is associated with HD. HD usually has a mid-life onset, but a juvenile form, defined by onset of symptoms before the age of 21 years, is present in about 7% of HD cases. Juvenile HD is characterized by (1) transmission from an HD affected father, (2) an unusually large repeat size, usually of 60 or more units, and (3) unique clinical features, including rigidity and seizure disorder. Although juvenile onset is associated with a more severe neuropathological involvement, the neuropathological characteristics of juvenile HD are similar to those seen in the adult form in that the striatum bears the brunt of the illness. Clumps of protein, termed inclusion bodies, which stain positive for huntingtin and ubiquitin, are found primarily in the nucleus but also in the cytoplasm and axons in HD neurons. Research suggests that these inclusion bodies sequester a deleterious protein fragment and prolong cell life during the degenerative process of the disease.     

Nonparticipation in Huntington's Disease Predictive Testing: Reasons for Caution in Interpreting Findings

When given the opportunity to clarify their genetic status, most individuals at risk for Huntington's disease (HD) currently show a preference not to know. Our understanding of the characteristics of those who do not request HD predictive testing, and the factors influencing their decision, lags behind our knowledge of test applicants. In the light of our experience with interviewing a random sample of nonparticipants in an ongoing study, we critically analyze research concerning the differences between participants and nonparticipants in HD predictive testing programs and the interpretive characterization of these two groups. The findings concerning nonparticipants are limited to a small sample of the at-risk population, with the problems of biased samples and low response rates. We discuss this and other aspects of research in this area, notably the context and timing of data collection and the predominantly questionnaire-based methodology, that lead us to interpret the conclusions drawn about these two groups with caution.     

Social system responses to Huntington disease

Huntington disease (HD) is an adultonset, genetic disorder with major psychosocial implications. Although many of the psychiatric symptoms of the disorder have been attributed to the HD gene, systems factors may also account for the disorder's manifestations. Three illustrative issues--patient preselection, the denial of symptom onset, and suicide induction--are discussed from the vantage point of family systems thinking. Recently developed capacity for presymptomatic testing of HD despite the current absence of treatment or cure makes it likely that family therapists increasingly will be involved in clinical work with individuals and families in which HD occurs.     

Interval length and time-use by children with AD/HD: a comparison of four models

Predictions made by 4 competing models of time use by children with AD/HD were tested using a computerized version of the Matching Familiar Figures Test in 2 studies. In Study 1 teacher-identified AD/HD children (N = 10) and non-AD/HD controls (N = 10) completed the task under 3 different trial duration conditions (5, 10, and 15 s). In Study 2 the same task was completed by a group of children with a diagnosis of Hyperkinetic Disorder (N = 12) and controls (N = 12). In both studies AD/HD children performed poorly on trials of both 5- and 15-s duration but as well as controls on the 10-s trials. This quadratic function provided support for the State Regulation Deficit model of time use in AD/HD. The value of tailoring the temporal features of learning contexts to the conceptual style of AD/HD children is discussed.     

The relationship among resilience,rumination and posttraumatic growth in hemodialysis patients in North China

Research has indicated that clinical serious disease may lead to posttraumatic growth (PTG). However, little is known about PTG among hemodialysis (HD) patients. The study examined the relationship among resilience, rumination and PTG among Chinese HD patients. 196 HD patients were recruited from a tertiary hospital in a Northern city of China between 1 June 2015 and 30 May 2016. Patients were surveyed using the Posttraumatic Growth Inventory-Chinese version, Connor-Davidson Resilience Scale, and Chinese Event Related Rumination Inventory. Correlation analyses showed that resilience was most highly positively correlated with PTG (r = .70, p < .001), deliberate rumination moderately correlated to PTG (r = .50, p < .001), and intrusive rumination was lower negatively related to PTG (r = –.26, p < .001). Regression analyses showed that age, gender, duration of dialysis, resilience and deliberate rumination had significant associations with PTG (β = ?.31, p ＜ .0001; β = –.14, p = .002; β = .10, p = .032; β = .44, p < .001; β = .20, p < .001). They together explained 65% of the total variance in PTG (F [8,195] = 46.74, p < .001). However, intrusive rumination was not associated with PTG (p > .05). The results suggested that resilience and deliberate rumination may be instrumental for PTG improvement.     

Discrete changes in the frequency and functions of autobiographical reminiscence in Huntington's disease

ABSTRACT

Autobiographical memory is widely posited to serve self, social and directive functions. Recent evidence suggests marked autobiographical memory impairments in Huntington's disease (HD), however, no study to date has determined how the perceived functions of autobiographical reminiscence may be altered in HD. The current study aimed to assess the self-reported frequency and function of autobiographical reminiscence in HD. We assessed autobiographical reminiscence in late premanifest (n?=?16) and early stage HD (n?=?14), relative to healthy controls (n?=?30). Participants completed the Thinking About Life Experiences Scale Revised (TALE-R), which measures three putative functions of autobiographical memory (self, social, directive). People with manifest HD reported talking less frequently about the past compared to controls. In contrast, no group differences were found in terms of thinking about the past. Manifest HD participants further reported using their autobiographical memories for social functions less frequently compared to controls. No other group differences were evident in terms of self or directive functions of autobiographical memory. These self-report findings complement recent reports of autobiographical memory disruption on performance-based tasks in HD. Future studies exploring how changes in autobiographical reminiscence impact a sense of self continuity in HD will be important in this regard.     

Psychological impact of the development of a presymptomatic test for Huntington's disease

For the first time, a genetic probe can provide individuals at risk for Huntington's disease (HD) with diagnostic information regarding this progressive genetic disorder before symptoms are exhibited. This article investigates the effects of such a technology on the at-risk HD population. At-risk HD individuals were informed about the genetic probe, and their level of anxiety was assessed. A group conference format was an effective means of providing information regarding the HD probe to a large number of at-risk families. Findings from the measure of anxiety demonstrate that the at-risk HD population is no different from a normative population or from an at-risk HD population unfamiliar with the new technology.