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.     

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.     

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.     

Buddhist Fictionalism

Questions regarding what exists are central to various forms of Buddhist philosophy, as they are to many traditions of philosophy. Interestingly, there is perhaps a clearer consensus in Buddhist thought regarding what does not exist than there may be regarding precisely what does exist, at least insofar as the doctrine of anātman (no self, absence of self) is taken to be a fundamental Buddhist doctrine. It may be noted that many forms of Mahāyāna Buddhist philosophy in particular are considered to offer a quite austere ontology—a rather ‘empty’ account of what exists. Continuing in this vein of ontological austerity, here I will attempt to lay out a relatively novel approach to Buddhist ontology, viz. Buddhist fictionalism.     

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.     

The Changing Age of Individuals Seeking Presymptomatic Genetic Testing for Huntington Disease

Huntington disease (HD) is a progressive neurodegenerative disorder. Presymptomatic genetic testing allows at-risk individuals to clarify their risk status. Understanding the characteristics and motivations of individuals seeking HD presymptomatic genetic testing better equips genetic counselors and other healthcare professionals to provide comprehensive and personalized care. The aims of this study were to (1) determine whether the average age when individuals seek presymptomatic HD genetic testing has decreased over time, (2) assess motivations for seeking testing, (3) explore whether there is a relationship between age and motivations, and (4) explore genetic counselors’ perceptions of the shift in age. Data from the US HD testing centers (N?=?4) were analyzed. A small but statistically significant decrease in age of individuals seeking presymptomatic testing was observed (p?=?0.045). HD community members (N?=?77) were surveyed regarding presymptomatic testing motivations. Younger individuals were more likely than older individuals to cite “To learn whether or not you would develop HD” and “To make choices about further education or a career” compared to older individuals (p?<?0.05). Conversely, older individuals more frequently cited “To give children a better idea of their risk” (p?<?0.002). Sixteen percent of genetic counselors surveyed (6/37) perceived a change in age of testing. All of these respondents had provided HD testing for ten or more years and anecdotally believed the age at testing has decreased over time. Study results help providers personalize counseling based on patient’s age and serve as a starting point for more research into the relationship between age at testing and motivations for testing.     

The research values of policy analysts

While there is growing consensus that conventional notions of the scientific method do not exhaust the methodological needs of policy analysis (at least applied analysis), there is less agreement as to what an improved method would entail. As a result, policy analysts must choose among often competing notions of what constitutes valid policy inquiry. Data from a content analysis of six policy journal articles together with responses from a survey of authors are used to determine what choices are made and whether these matter. Two sets of research norms are discovered within the policy studies community’one which mirrors traditional social science values and another which reflects recent attempts to adjust that methodology to meet the information needs of policy actors. Equally important, values tend, albeit slightly, to condition the character (e.g., degree of rigor or focus) of policy research. David M. Hedge is an associate professor of political science and director of the graduate program in public policy at West Virginia University. His research interests include regulatory politics, intergovernmental relations, and state politics/policy. Jin W. Mok is an assistant professor of political science at the University of Northern Iowa. His area of interests are public policy and methodology.     

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).     

Horsefeathers: a commentary on "evolutionary versus prototype analyses of the concept of disorder".

J. C. Wakefield's (1999) article further develops his harmful dysfunction (HD) model for disorder concepts. This commentary focuses on three areas. The first notes the imbalance in the debate between the Lilienfeld and Marino (1995) Roschian model and the HD model for disorder concepts. The second claims that Wakefield's purposes for the HD model have changed over the years and progressed toward irrelevance to psychopathology in general and toward irrelevance to actual nosologic, reimbursement, and sociopolitical controversies about disorder status. Further discussion is on how certain structural elements in Wakefield's arguments and current limitations of evolutionary theory permit a superficially attractive model for psychopathology. These arguments and limitations, however, harbor serious problems when confronted with actual disputes about disorders. The conclusion notes some virtues to Wakefield's inquiry, in style and substance.     

Cognitive phenomenology and conscious thought

How does mental content feature in conscious thought? I first argue that for a thought to be conscious the content of that thought must conscious, and that one has to appeal to cognitive phenomenology to give an adequate account of what it is for the content of a thought to be conscious. Sensory phenomenology cannot do the job. If one claims that the content of a conscious thought is unconscious, one is really claiming that there is no such thing as conscious thought. So one must either accept that there is such a thing as cognitive phenomenology, or deny the existence of conscious thought. Once it is clear that conscious thought requires cognitive phenomenology, there is a pressing question about the exact relationship between a thought’s cognitive phenomenological properties and its content. I conclude with a discussion of the nature of this relationship.     

A stop-signal task for sheep: introduction and validation of a direct measure for the stop-signal reaction time

Huntington’s disease (HD) patients show reduced flexibility in inhibiting an already-started response. This can be quantified by the stop-signal task. The aim of this study was to develop and validate a sheep version of the stop-signal task that would be suitable for monitoring the progression of cognitive decline in a transgenic sheep model of HD. Using a semi-automated operant system, sheep were trained to perform in a two-choice discrimination task. In 22% of the trials, a stop-signal was presented. Upon the stop-signal presentation, the sheep had to inhibit their already-started response. The stopping behaviour was captured using an accelerometer mounted on the back of the sheep. This set-up provided a direct read-out of the individual stop-signal reaction time (SSRT). We also estimated the SSRT using the conventional approach of subtracting the stop-signal delay (i.e., time after which the stop-signal is presented) from the ranked reaction time during a trial without a stop-signal. We found that all sheep could inhibit an already-started response in 91% of the stop-trials. The directly measured SSRT (0.974 ± 0.04 s) was not significantly different from the estimated SSRT (0.938 ± 0.04 s). The sheep version of the stop-signal task adds to the repertoire of tests suitable for investigating both cognitive dysfunction and efficacy of therapeutic agents in sheep models of neurodegenerative disease such as HD, as well as neurological conditions such as attention deficit hyperactivity disorder.     

Stress, Coping, and Differentiation of Self: A Test of Bowen Theory

Differentiation of self from the family of origin is thought to be a significant factor in psychological functioning. Bowen contended that the effects of stress are moderated by differentiation of self, such that high levels of stress would have more impact on individuals lower in differentiation as compared to individuals higher in differentiation in predicting dysfunction. We tested this hypothesis and also assessed the relations among stress, coping, differentiation of self, and dysfunction. Results provided support for Bowen's prediction; differentiation indeed moderated the effects of perceived stress in predicting psychological functioning in expected ways. The interaction of differentiation of self and stress predicted variance in functioning beyond what was accounted for by coping styles, suggesting that although coping and differentiation of self are related, they are not synonymous.     

Intentions to use predictive testing by those at risk for Huntington's disease: Implications for prevention

Huntington's disease (HD) is a late onset, genetic disorder that is incurable and undetectable until the onset of symptoms. A marker for the gene that causes HD was recently discovered which will lead to a predictive test. The purpose of this research was to assess the knowledge, attitudes, beliefs, and behavioral intentions concerning the impending predictive test by those at risk for HD. Results indicated that a majority of participants favored using the test presymptomatically and would encourage their adult children to use it as well. Fewer participants favored using the predictive test prenatally or on minors. Characteristics that best differentiated those who intend and do not intend to use predictive testing were identified and discussed. Suggestions for interventions were presented with an emphasis on outreach and prevention programs designed to prepare HD families for the difficult decisions the predictive test will precipitate and the subsequent impact of those decisions.     

The psychological treatment of memory impairment: A review of empirical studies

Memory impairment is a frequent effect of many different forms of brain dysfunction. Memory impairment is also a frequent focus of treatment interventions, and there have been many different treatment methods suggested. The suggested methods include direct retraining, the use of spared skills in compensating for the impairment (alternate functional systems), and the use of behavioral strategies to circumvent the manifest memory dysfunction (behavioral prosthetics). Unfortunately, there are very few studies comparing the various suggested treatment methods. The present paper evaluates the empirical evidence related to the treatment of memory dysfunction and suggests directions for future investigations. Although the evidence is not conclusive, it appears that some forms of treatment may be helpful in remediating certain types of memory impairment. An approach likely to be productive would include some consideration of the impaired neurological and psychological mechanisms responsible for the manifest memory deficit as well as a consideration of the etiology of the injury thought to be causally related to the memory deficit. As yet, there have been no rigorous empirical evaluations of these considerations.     

Causes or Cures: What makes us think of attention issues as disorders?

Are attention issues disorders or not? Philosophers of medicine have tried to address this question by looking for properties that distinguish disorders from non-disorders. Such properties include deviation of a statistical norm, a loss of function or experienced suffering. However, attempts at such conceptual analysis have not led to a consensus on the necessary and sufficient conditions for the application of the concept of disorder. Recently, philosophers have proposed an experimental approach to investigate in which circumstances people think a specific concept is applicable. Here we present a quantitative vignette study investigating whether disorder attribution depends on the perceived cause and the perceived type of treatment for an attention problem. The results of our study indicate that the attribution of a disorder decreased when the attention problem was understood as caused by bullying (social environmental cause) or by an accident (non-social environmental cause) rather than a genetic cause. When prescribed a pill, attention problems were considered a disorder to a larger extent than when the child was prescribed an environmental treatment. Our study also suggests that whereas successful environmental treatments will not necessarily decrease the disorder attribution, successful pharmacological treatments will decrease the likelihood that a person is thought to still suffer from a disorder after receiving the treatment.     

Harm and the concept of medical disorder

According to Jerome Wakefield’s harmful dysfunction analysis (HDA) of medical disorder, the inability of some internal part or mechanism to perform its natural function is necessary, but not sufficient, for disorder. HDA also requires that the part dysfunction be harmful to the individual. I consider several problems for HDA’s harm criterion in this article. Other accounts on which harm is necessary for disorder will suffer from all or almost all of these problems. Comparative accounts of harm imply that one is harmed when one is made worse off, that is, worse off than one otherwise would have been. Non-comparative accounts imply that one is harmed when one is put into some kind of condition or state that is, in some way, bad in itself. I argue that whether harm is construed comparatively or non-comparatively, HDA’s harm criterion is problematic. I tentatively conclude that an analysis of medical disorder should not make use of the concept of harm.     

The Narrative Architecture of Political Forgiveness

Although there is widespread agreement with the argument that Hannah Arendt made more than half a century ago, that forgiveness is “one of the human faculties that make social change possible” (Misztal, 2011, p. 201), beyond this, there is little consensus of what it means. Applying a narrative structure to this discussion, there is a lack of clarity around questions of who, what, where, when, and why to forgive. This article will explore the politics of forgiveness in East Germany, where these issues have been hotly contested for more than 25 years. The data examined in this article suggest that the fraught process of forgiveness embodies not consensus but contest, as people disagree on key questions such as who has the right to forgive whom, for what, how long the window for the opportunity of forgiveness stays open, and even why these questions matter, not only for individuals but for the whole of society.     

I—What is the Normative Role of Logic?

The paper tries to spell out a connection between deductive logic and rationality, against Harman's arguments that there is no such connection, and also against the thought that any such connection would preclude rational change in logic. One might not need to connect logic to rationality if one could view logic as the science of what preserves truth by a certain kind of necessity (or by necessity plus logical form); but the paper points out a serious obstacle to any such view.     

Where’s the problem? Considering Laing and Esterson’s account of schizophrenia,social models of disability,and extended mental disorder

In this article, I compare and evaluate R. D. Laing and A. Esterson’s account of schizophrenia as developed in Sanity, Madness and the Family (1964), social models of disability, and accounts of extended mental disorder. These accounts claim that some putative disorders (schizophrenia, disability, certain mental disorders) should not be thought of as reflecting biological or psychological dysfunction within the afflicted individual, but instead as external problems (to be located in the family, or in the material and social environment). In this article, I consider the grounds on which such claims might be supported. I argue that problems should not be located within an individual putative patient in cases where there is some acceptable test environment in which there is no problem. A number of cases where such an argument can show that there is no internal disorder are discussed. I argue, however, that Laing and Esterson’s argument—that schizophrenia is not within diagnosed patients—does not work. The problem with their argument is that they fail to show that the diagnosed women in their study function adequately in any environment.     

Depression and Huntington's disease: prevalence, clinical manifestations, etiology, and treatment

In order to determine the extent to which depression complicates Huntington's disease (HD), we have analyzed the existing literature on depression in HD in order to report the prevalence, clinical manifestations, and treatment of HD depression. By means of MEDLINE literature searches and reviews of HD articles' bibliographies, we identified for our analysis 16 HD depression studies. Our results indicate that the prevalence of depression is 30% for all HD patients. Clinical manifestations of HD depression include a marked increased risk for suicide. The etiology of HD depression is unclear, but may be due to a number of factors, such as dysfunction in the caudate nucleus, dysfunction in the ventral striatum, and various genetic factors that are discussed in this review. Case reports and case series support the efficacy of standard antidepressant interventions in resolving symptoms of depression. Efficacious treatments reported in the literature include tricyclic antidepressants, monoamine oxidase inhibitors, selective serotonin reuptake inhibitors, and electroconvulsive therapy. In this study, the successful anecdotal treatment of seven consecutive HD depressed patients with sertraline suggests that sertraline may be a safe and efficacious treatment of HD depression.