The pivotal problem of comorbidity research lies in the psychometric foundation it rests on, that is, latent variable theory, in which a mental disorder is viewed as a latent variable that causes a constellation of symptoms. From this perspective, comorbidity is a (bi)directional relationship between multiple latent variables. We argue that such a latent variable perspective encounters serious problems in the study of comorbidity, and offer a radically different conceptualization in terms of a network approach, where (...) class='Hi'>comorbidity is hypothesized to arise from direct relations between symptoms of multiple disorders. We propose a method to visualize comorbidity networks and, based on an empirical network for major depression and generalized anxiety, we argue that this approach generates realistic hypotheses about pathways to comorbidity, overlapping symptoms, and diagnostic boundaries, that are not naturally accommodated by latent variable models: Some pathways to comorbidity through the symptom space are more likely than others; those pathways generally have the same direction (i.e., from symptoms of one disorder to symptoms of the other); overlapping symptoms play an important role in comorbidity; and boundaries between diagnostic categories are necessarily fuzzy. (shrink)

The frequent occurrence of comorbidity has brought about an extensive theoretical debate in psychiatry. Why are the rates of psychiatric comorbidity so high and what are their implications for the ontological and epistemological status of comorbid psychiatric diseases? Current explanations focus either on classification choices or on causal ties between disorders. Based on empirical and philosophical arguments, we propose a conventionalist interpretation of psychiatric comorbidity instead. We argue that a conventionalist approach fits well with research and clinical (...) practice and resolves two problems for psychiatric diseases: experimenter’s regress and arbitrariness. (shrink)

I strongly endorse many of the suggestions made by the authors of the extremely useful reviews in this issue. In particular, the need to identify the complex causal mechanisms underlying the major health risk factors requires urgent attention of the research community. I suggest considering the important role of emotional disturbances as contributors to health risks given the empirically established comorbidity between mental and somatic illness. Better knowledge of these mechanisms is an essential prerequisite to develop tailored personalized prevention (...) and intervention programs, including reliable and valid assessment of deficits. (shrink)

There is a relationship between reading and math skills, as well as comorbidity between reading and math disorders. A mutual foundation for this comorbidity could be that the quality of phonological representations is important for both early reading and arithmetic. In this study, we examine this hypothesis in a sample traced longitudinally from preschool to first grade. The results show that phonological awareness does not explain development in arithmetic, but that there is an indirect effect between phoneme awareness (...) in preschool and arithmetic in first grade via phoneme awareness in first grade. This effect is, however, weak and restricted to verbal arithmetic and not arithmetic fluency. This finding is only partly in line with other studies, and a reason could be that this study more strongly controls for confounders and previous skills than other studies. (shrink)

ObjectivesTo document the auditory processing, visual attention, digit memory, phonological processing, and receptive language abilities of individual children with identified word reading difficulties.DesignTwenty-four children with word reading difficulties and 28 control children with good word reading skills participated. All children were aged between 8 and 11 years, with normal hearing sensitivity and typical non-verbal intelligence. Both groups of children completed a test battery designed to assess their auditory processing, visual attention, digit memory, phonological processing, and receptive language.ResultsWhen compared to children (...) who were good readers, children with word reading difficulties obtained significantly lower average scores on tests of auditory processing, including the frequency pattern test, gaps in noise, frequency discrimination, Dichotic Digit difference Test, and Listening in Spatialized Noise. The two groups did not differ on the discrimination measures of sinusoidal amplitude modulation or iterated rippled noise. The results from children with word reading difficulties showed that 5 children (21%) had comorbid deficits in auditory processing, visual attention, and backward digit memory; whereas 12 children (50%) had comorbid auditory processing and visual attention deficits only, and 2 children (8%) had comorbid deficits in auditory processing and digit memory; the remaining children had only auditory processing, visual attention, or digit memory deficits.ConclusionThe current study highlights the general co-existence of auditory processing, memory, and visual attention deficits in children with word reading difficulties. It is also noteworthy, however, that only one fifth of the current cohort had deficits across all measured tasks. Hence, our results also show the significant individual variability inherent in children with word reading difficulties. (shrink)

In lieu of an abstract, here is a brief excerpt of the content:Psychiatric Comorbidity:More Than a Kuhnian AnomalyPeter Zachar (bio)Keywordscomorbidity, classification, epidemiology, differential diagnosis, personality disorderDr. Aragona's article in this issue of Philosophy, Psychiatry, & Psychology makes some important points regarding the relationship between comorbidity rates and the classification system currently used in psychiatry. Particularly persuasive is his claim that observed patterns of comorbidity are, in important respects, consequences of the structure of the classification system. I am (...) not convinced, however, that comorbidity is best conceptualized as an artifact of the taxonic structure of the Diagnostic and Statistical Manual of Mental Disorders (DSM) and the International Classification of Diseases (ICD). Instead, I suggest that the use of dichotomies such as true versus artifactual should be used with caution when psychiatric classification is being discussed.In contrast with the artifact hypothesis, I argue that the phenomena covered by the term "comorbidity" are real, expectable features of the psychiatric domain. They are not the phlogiston and luminiferous ether of psychiatry. I am skeptical of the notion that high comorbidity rates as a whole can be understood as Kuhnian anomalies, or that there is a crisis, or that after a period of revolutionary science a new paradigm would eliminate these 'anomalies.' In short, high rates of comorbidity in psychiatry will not simply disappear once scientists develop a better nosological paradigm. High levels of comorbidity can, however, be both lowered and provided a better, evidence-based conceptual framework.Many Conditions, One OrganIn general medicine, comorbidity conventionally refers to the simultaneous occurrence of two independent disease processes or distinct clinical entities, such as heart disease and liver cancer (Feinstein, 1970; Jablensky 2004). The presence of one disease is supposed to affect the other in such a way that the co-occurrence of the two has implications for prognosis and treatment.Comorbidity in psychiatry is a broader concept, referring to a variety of conditions that overlap in multiple ways. The different kinds of overlap are amenable to detailed empirical analysis (e. g., Klein and Riso 1993; Neale and Kendler 1995). Depressive reactions to primary disorders, attention deficit symptoms associated with mania, panic attacks in the context of severe borderline personality disorder, substance abuse disorders among psychopaths, histrionic dynamics combined [End Page 13] with narcissistic personality traits, and emergent conditions such as schizoaffective disorder are all distinct types of comorbidity. The kinds of overlapping conditions just listed are sometimes termed psychiatric comorbidity. Also important is comorbidity between psychiatric disorders and general medical conditions as is studied in behavioral medicine and health psychology. The crisis, if there is one, is a crisis of comorbidities.The heart disease and liver cancer type of comorbidity as independent organ systems being affected is ruled out a priori in psychiatric comorbidity proper. In psychiatry, "psychopathological disease processes" can all be expected to affect a single organ, namely the brain or, more likely, affect the different systems that are tightly integrated in the brain. The tight integration can make putative comorbid psychiatric disorders difficult to disentangle.It is a widely held consensus that causes, not organ systems, are what matter in comorbidity. In this tradition, Dr. Aragona claims that in general medicine shared symptoms between two diseases (such as fever and fatigue) are not a problem because the diseases are differentiated with respect to etiology; in psychiatry, however, where syndromes are differentiated by a description of symptoms only, symptomatic overlap is a problem.Is descriptive psychopathology, therefore, a root cause of the "crisis of comorbidity" and should it be abandoned in favor of etiological classification? Unfortunately, forcing psychiatric nosology to conform to an etiological paradigm is unlikely to resolve the problem of psychiatric comorbidity. As noted, the problem is one of distinguishing between the different etiological disease processes that are affecting tightly integrated systems in the brain. The brain as a whole is a multilevel, dynamic, and open system, which has an ecology (Zachar 2000). As argued by Kendler (2005) and Schaffner (2002, 2008), it has not thus far, and may never be fully possible to segregate causes and their associated psychiatric disorders into parsimonious etiological packages. In the ecology of neuroscience, causes and effects tend to merge in a continuous series of common pathways.It would be foolish... (shrink)

In developmental psychopathology, differentiating between the coexistence and the clinical entity of two problem areas is of utmost importance. So far, logistic regression analysis has already provided helpful answers, as shown in studies on comorbidity of tic disorders. While the concept of bridging symptoms may be investigated adequately by both logistic regression and the network approach, the former (latent variable) seems to be of advantage with regard to the problems of multiple comorbidities and development.

In lieu of an abstract, here is a brief excerpt of the content:About and Beyond Comorbidity:Does the Crisis of the DSM Bring on a Radical Rethinking of Descriptive Psychopathology?Massimiliano Aragona (bio)Keywordscomorbidity, nosography, phenomenology, philosophy of scienceThe problem of psychiatric comorbidity is part of a series of difficulties of the current diagnostic system which at once were considered as a consequence of the way the system itself is organized (Aragona 2006). It was then believed that a Kuhnian reformulation of (...) the contemporary debate on the problems of the psychiatric diagnosis was very useful because it allowed clarification in a comprehensive picture of the many rivulets of conceptual research in that field.In their comments Zachar (2009) and Banzato (2009) seem to agree with my analysis of psychiatric comorbidity (Aragona 2009a) when it stresses that abnormally high frequencies of co-occurrence are to be explained, in important respects, as a consequence of the way mental disorders are operationalized in the Diagnostic and Statistical Manual of Mental Disorders (DSM; also showing the importance of conceptual clarification to deal with this sort of only apparently pure factual problems). On the contrary, they are both unconvinced of the appropriateness and/or fruitfulness of the use of the Kuhnian technical terms and theory in this context.It could be said that the major aim of the paper was to let clinicians understand the effect of conceptual decisions on what would otherwise seem as a simple empirical finding (in this case, high levels of comorbidity), and that this result seems to be achieved in any case, thus minimizing the importance of a disagreement about the philosophical terms as a pure terminological dispute. Nevertheless, in my work the Kuhnian model had a significant role in the clarification of this matter and it also suggests to the reader a range of possible consequences that are not trivial (Zachar, for example, says to be skeptical about the possibility of a crisis and also about the possibility that a new paradigm could eliminate what I call the [End Page 29] comorbidity anomaly). As a consequence, some of the Kuhnian concepts that seemed to be at odds in this context have to be considered in detail to justify my analysis and its consequences. For reasons of space, I avoid a point-by-point reply to all the comments and I concentrate my discussion on three main points. First, I discuss the background of Kuhn's definition of terms such as anomaly and paradigm, as well as my own reasons for using them. In doing so the details of the psychiatric items under study that I wanted to highlight through the use of these philosophical concepts should emerge more clearly. Second, I discuss the problem of having distinguished between artifactual and real comorbidity. Third, I reconsider some of these problems, looking for their implications for future psychopathological research.Anomalies and ParadigmsBanzato (2009) stresses that comorbidity cannot be a truly Kuhnian anomaly because it is an anticipated side effect of the initial setup of the DSM, and not some unexpected discovery that violates the paradigm-induced expectation. This is a basically correct account of the most known version of Kuhnian anomalies; that is, the tale of some evident nature's failure to conform to clear paradigm expectations, which immediately forces researchers to recognize its importance as a possible source of crisis. However, as is the case for many other Kuhnian terms, he discussed anomalies in several scripts and there are other possible versions of its meaning. In particular, Kuhn (1977, XVII) highlighted that only in very rare cases are anomalies completely unexpected and come out of blue to announce an imminent crisis that leads to a large revolution. More frequently, scientific revolutions are much more smaller, like the discovery of oxygen, and in these cases the process is so gradual that historians find it difficult to say exactly when a discovery was made and who did it. Even in these much smaller cases the usual prelude to changes of this sort is the awareness of anomaly, but here anomalies are not extraordinary events; rather, they are "countless discrepancies between theory and experiment [that] during the course of his career, every natural scientist again and again notices and passes by" (Kuhn... (shrink)

Despite several criticisms surrounding the DSM classification in psychiatry, a significant bulk of research on mental conditions still operates according to two core assumptions: a) homogeneity, that is the idea that mental conditions are sufficiently homogeneous to justify generalization; b) additive comorbidity, that is the idea that the coexistence of multiple conditions in the same individual can be interpreted as additive. In this paper we take autism research as a case study to show that, despite a plethora of criticism, (...) psychiatric research often continues to operate in accordance with this model. Then we argue that such a model runs into problems once facts about comorbidity are taken into account. Finally, we offer some suggestions on how to tackle the challenge raised by comorbidity and its impact on heterogeneity. To do so, we explore transdiagnostic stratification accounts and network models to show that combining these approaches can move us in the right direction. (shrink)

Applying a necessary condition communication theory formalism roughly similar to that of Dretske, but focused entirely on the statistical properties of long sequences of signals emitted by the interacting cognitive modules of human biology, we explore the regularities apparent in comorbid psychiatric and chronic physical disorders using an extension of recent perspectives on autoimmune disease. We find that structured psychosocial stress can literally write a distorted image of itself onto child development, resulting in a life course trajectory to characteristic forms (...) of comorbid mind/body dysfunction affecting both dominant and subordinate populations within a pathogenic social hierarchy. (shrink)

The “dynamic developmental” theory of attention-deficit/hyperactivity disorder (ADHD) has come full circle from Wender's (1971) reinforcement hypothesis. By specifying the principle of time constraints on reinforcement and extinction, the present theory allows for empirical validation. However, the theory implies, but does not discuss, implications for the neurophysiology of comorbidity in ADHD. The authors' attribution of comorbid oppositional behavior to parental and societal reinforcement leaves out biological factors.

Cramer et al.'s network approach reconceptualizes mental comorbidity on the basis of symptom space originating from psychometric signatures. We argue that the advantages of this approach need to be regarded in the context of the multi-level functional organization of the neural substrate, ranging from neurogenetic to psychometric. Neuroelectric oscillations are proposed as a level-integrating principle.

Despite several criticisms surrounding the DSM classification in psychiatry, a significant bulk of research on mental conditions still operates according to two core assumptions: a) homogeneity, that is the idea that mental conditions are sufficiently homogeneous to justify generalization; b) additive comorbidity, that is the idea that the coexistence of multiple conditions in the same individual can be interpreted as additive. In this paper we take autism research as a case study to show that, despite a plethora of criticism, (...) psychiatric research often continues to operate in accordance with this model. Then we argue that such a model runs into problems once facts about comorbidity are taken into account. Finally, we offer some suggestions on how to tackle the challenge raised by comorbidity and its impact on heterogeneity. To do so, we explore transdiagnostic stratification accounts and network models to show that combining these approaches can move us in the right direction. (shrink)

The results of recent community epidemiological research are reviewed, documenting that major depressive disorder (MDD) is a highly prevalent, persistent, and often seriously impairing disorder, and that bipolar disorder (BPD) is less prevalent but more persistent and more impairing than MDD. The higher persistence and severity of BPD results in a substantial proportion of all seriously impairing depressive episodes being due to threshold or subthreshold BPD rather than to MDD. Although the percentage of people with mood disorders in treatment has (...) increased substantially since the early 1990s, a majority of cases remain either untreated or undertreated. An especially serious concern is the misdiagnosis of depressive episodes due to BPD as due to MDD because the majority of depression treatment involves medication provided by primary care doctors in the absence of psychotherapy. The article closes with a discussion of future directions for research. (shrink)

We agree with Cramer et al. that pure cases of behavioral disorders with no symptom overlaps are rare. However, we argue that disorders do exist and the network idea is limited and limiting. Networks of symptoms are observed mainly at behavioral levels. The core deficit is commonly at the cognitive or brain levels, and there the story is completely different.

Jakovljevic and Crnčevic review the concept of comorbidity in relation to mental disorders, which is timely. Yet they seem to ignore a longstanding and important notion of comorbidity, highlighted in psychiatry particularly by Sigmund Freud. The ignored notion is that of compensatory comorbidity. Compensatory comorbidity is a special case of compensatory phenomena in relation to disrupted health.

The psychopathological profile of patients with medication overuse headache appears to be particularly complex. To better define it, we evaluated their performance on a targeted psychological profile assessment. We designed a case-control study comparing MOH patients and matched healthy controls. Headache frequency, drug consumption, HIT-6, and MIDAS scores were recorded. All participants filled in the following questionnaires: Beck Depression Inventory-II Edition, trait subtest of State-Trait Anxiety Inventory, Difficulties in Emotion Regulation Scale, Barratt Impulsiveness Scale, Toronto Alexithymia Scale. The primary endpoint (...) was to establish if MOH patients have an altered psychopathological profile. The secondary endpoint was to establish whether the worst profile correlates with the worsening of headache and disability measures. We enrolled 48 consecutive MOH patients and 48 HC. MOH patients showed greater difficulty in recognition/regulation of emotions, depression, anxiety, and impulsiveness. We found a positive correlation among DERS, BDI-2, STAI-Y, and BIS scores and MIDAS and HIT-6 scores and among DERS and headache frequency and drug consumption. MOH patients showed a high rate of emotion regulation difficulties, depression, and anxiety, which may negatively affect their headaches. The ability to regulate/recognize emotions may play a central role in sustaining medication overuse. (shrink)

We agree with Cramer et al.'s goal of the discovery of causal relationships, but we argue that the authors' characterization of latent variable models (as deployed for such purposes) overlooks a wealth of extant possibilities. We provide a preliminary analysis of their data, using existing algorithms for causal inference and for the specification of latent variable models.

The comorbidity of chronic pain and opioid addiction is a serious problem that has been growing with the practice of prescribing opioids for chronic pain. Neuroimaging research has shown that chronic pain and opioid dependence both affect brain structure and function, but this is the first study to evaluate the neurophysiological alterations in patients with comorbid chronic pain and addiction. Eighteen participants with chronic low back pain and opioid addiction were compared with eighteen age- and sex-matched healthy individuals in (...) a pain-induction fMRI task. Unified structural equation modeling (SEM) with Lagrange multiplier (LM) testing yielded a network model of pain processing for patient and control groups based on 19 a priori defined regions. Tests of differences between groups on specific regression parameters were determined on a path-by-path basis using z-tests corrected for the number of comparisons. Patients with the chronic pain and addiction comorbidity had increased connection strengths; many of these connections were interhemispheric and spanned regions involved in sensory, affective, and cognitive processes. The affected regions included those that are commonly altered in chronic pain or addiction alone, indicating that this comorbidity manifests with neurological symptoms of both disorders. Understanding the neural mechanisms involved in the comorbidity is crucial to finding a comprehensive treatment, rather than treating the symptoms individually. (shrink)

We suggest that the network approach to comorbidity (Cramer et al.) is best examined by using longitudinal, multi-measurement, intra-individual data. Employment of time-series analysis to the examination of the generalized anxiety disorder and major depressive disorder comorbidity enables a detailed appreciation of fluctuations and causal trajectories in terms of both symptoms and cognitive vulnerability.

Despite that it is commonly accepted that migraine is a disorder of the nervous system with a prominent genetic basis, it is comorbid with a plethora of medical conditions. Several studies have found bidirectional comorbidity between migraine and different disorders including neurological, psychiatric, cardio- and cerebrovascular, gastrointestinal, metaboloendocrine, and immunological conditions. Each of these has its own genetic load and shares some common characteristics with migraine. The bidirectional mechanisms that are likely to underlie this extensive comorbidity between migraine (...) and other diseases are manifold. Comorbid pathologies can induce and promote thalamocortical network dysexcitability, multi-organ transient or persistent pro-inflammatory state, and disproportionate energetic needs in a variable combination, which in turn may be causative mechanisms of the activation of an ample defensive system with includes the trigeminovascular system in conjunction with the neuroendocrine hypothalamic system. This strategy is designed to maintain brain homeostasis by regulating homeostatic needs, such as normal subcortico-cortical excitability, energy balance, osmoregulation, and emotional response. In this light, the treatment of migraine should always involves a multidisciplinary approach, aimed at identifying and, if necessary, eliminating possible risk and comorbidity factors. (shrink)

Social anxiety is highly prevalent in adolescents and is often associated with great individual suffering and functional impairment. Psychiatric comorbidity is common and further adds to this burden. The purposes of this study were: (1) to describe the occurrence of diagnosed and self-reported social anxiety among 8,199 Norwegian adolescents aged 13–19 years who participated in the population-based Young-HUNT3 study (2006–2008); (2) to examine associations between sociodemographic characteristics and different subgroups of social anxiety; and (3) to describe the psychiatric health (...) comorbidities among adolescents diagnosed with social anxiety disorder (SAD). In total, 388 (5.9%) of the adolescents screened positive for SAD and were invited into a diagnostic interview, performed by professional nurses, using Anxiety Disorders Interview Schedule for DSM IV: child version (ADIS-C) (response rate = 54.6%). A SAD diagnosis was indicated in 106 individuals (50% of the interview subjects), and more than two-thirds of the adolescents diagnosed with SAD had one or more comorbid psychiatric disorders. Higher mean scores of self-reported social anxiety symptoms, poor self-rated health, sleep problems, poor family economic situation, low physical activity, and having sought professional help within the last year were associated with higher odds of being in the screening positive subgroup. Screening positive subjects who did not meet for a diagnostic interview did not differ notably from the rest of the screening positive group in terms of these sociodemographic characteristics. Based on our results and the fact that individuals with social anxiety often fear interview situations, the use of ADIS-C, screening questions and self-reports seem to be sufficient when aiming to identify epidemiologically representative cohorts of adolescents at risk of social anxiety. (shrink)

There is a high prevalence of comorbidity between neurodevelopmental disorders. Contemporary research of these comorbidities has led to the development of multifactorial theories of causation, including the multiple deficit model. While several combinations of disorders have been investigated, the nature of association between literacy and motor disorders remains poorly understood. Comorbid literacy and motor disorders were the focus of the two present studies. In Study 1, we examined the prevalence of comorbid literacy and motor difficulties relative to isolated literacy (...) and motor difficulties in a community sample. The prevalence of comorbidity was five times greater than expected by chance alone, implying some relationship between difficulties. In Study 2, we examined the cognitive profiles of children with literacy and motor disorders amongst a subsample of children from Study 1. Children with literacy disorder had deficits in phonological processing, selective attention, and memory whilst children with motor disorder had deficits in visuospatial processing and memory, suggesting the disorders should be considered to have both independent and shared cognitive risk factors. Children with comorbid literacy and motor disorder demonstrated an additive combination of these deficits. Together, these findings are consistent with predictions from the MDM. (shrink)

The literature on brain activity in depression and anxiety is reviewed with an on highlighting discrepancies and inconsistencies. In particular, and posterior asymmetries have been reported for both depression anxiety, but the magnitude and direction of these asymmetries has been We propose that by identifying subtypes of depression and anxiety of these inconsistencies can be explained. In addition, we review suggesting that issues of comorbidity are important to consider in to account for regional brain activity in depression and anxiety.

This article introduces the concept of 'cognitive comorbidity,' which lays emphasis on common cognitive deficits that cut across different disorders. The concept is illustrated with the help of two commonly reported overlapping conditions (autism and epilepsy). It is further explained by concentrating on two important cognitive processes of facial emotional recognition and emotional memory, shown to be compromised in both conditions; and their underlying neural substrates. Cognitive comorbidity is then contrasted with 'comorbidity,' a term which is more (...) commonly used for describing cognitive disorders. The paper closes by providing directions for rehabilitative and theoretical efforts that could be inspired by the newly introduced concept. (shrink)

Opioid use disorder rarely presents as a unitary psychiatric condition, and the comorbid symptoms likely depend upon the diverse risk factors and mechanisms by which OUD can arise. These factors are heterogeneous and include genetic predisposition, exposure to prescription opioids, and environmental risks. Crucially, one key environmental risk factor for OUD is early life adversity. OUD and other substance use disorders are widely considered to derive in part from abnormal reward circuit function, which is likely also implicated in comorbid mental (...) illnesses such as depression, bipolar disorder, and schizophrenia. ELA may disrupt reward circuit development and function in a manner predisposing to these disorders. Here, we describe new findings addressing the effects of ELA on reward circuitry that lead to OUD and comorbid disorders, potentially via shared neural mechanisms. We discuss some of these OUD-related problems in both humans and animals. We also highlight the increasingly apparent, crucial contribution of biological sex in mediating the range of ELA-induced disruptions of reward circuitry which may confer risk for the development of OUD and comorbid neuropsychiatric disorders. (shrink)

Cramer et al. make a good case for reconceptualizing comorbid psychopathologies in terms of complex network theory. We suggest the need for an extension of their network model to include reference to latent causes. We also draw attention to a neglected approach to theory appraisal that might usefully be incorporated into the methodology of network theory.

The comorbidity of personality disorders and mental disorders is commonly understood through three types of theoretical models: either a) personality disorders precede mental disorders, b) mental disorders precede personality disorders, c) mental disorders and personality disorders share common etiological grounds. Although these hypotheses differ with respect to their idea of causal direction, they all imply a latent variable perspective, in which it is assumed that either personality and mental disorders are latent variables that have certain causal relations [models a) (...) and b)]; or that, as in model c), the common etiology is in fact a latent variable that causes symptomatology of both personality and mental disorders. We aim to provide another perspective on the comorbidity between personality and mental disorders, namely a network perspective. To this end, we investigated Major Depression and Borderline Personality Disorder and hypothesized that symptoms of BPD and MD could interact with one another rather than being caused by a latent variable. To illustrate this theoretical network conceptualization of the comorbidity of BPD and MD we analyzed a cross-sectional clinical dataset of 376 patients who were asked to complete the Structured Clinical Interview for DSM-IV Axis II Disorders and the Beck Depression Inventory II. The results identify direct associations between symptoms of MD and BPD. If we take the links in this empirical network to be ‘substantive', this suggests a radical shift of our current conceptualization of the comorbidity of mental disorders and personality disorders. (shrink)

Cramer et al.'s account of comorbidity comes with a substantive philosophical view concerning the nature of psychological disorders. Although the network account is responsive to problems with extant approaches, it faces several practical and conceptual challenges of its own, especially in cases where the individual differences in network structures require the analysis of intra-individual time-series data.

The concept that alterated communications between the gut microbiome and the brain may play an important role in human brain disorders has recently received considerable attention. This is the result of provocative preclinical and some clinical evidence supporting early hypotheses about such communication in health and disease. Gastrointestinal symptoms are a common comorbidity in patients with autism spectrum disorders (ASD), even though the underlying mechanisms are largely unknown. In addition, alteration in the composition and metabolic products of the gut (...) microbiome has long been implicated as a possible causative mechanism contributing to ASD pathophysiology, and this hypothesis has been supported by several recently published evidence from rodent models of autism induced by prenatal insults to the mother. Recent evidence in one such model involving maternal infection, that is characterized by alterations in behavior, gut physiology, microbial composition, and related metabolite profile, suggests a possible benefit of probiotic treatment on several of the observed abnormal behaviors. (shrink)

Patients with insomnia complain of problems with sleep onset or sleep maintenance or early morning awakenings, or a combination of these, despite adequate opportunity and circumstances for sleep. In addition, to fulfill the diagnostic criteria for insomnia the complaints need to be associated with negative daytime consequences. For chronic insomnia, the symptoms are required to be present at least 3 days per week for a duration of at least 3 months. Lastly, for insomnia to be defined as a disorder, the (...) sleep complaints and daytime symptoms should not be better explained by another sleep disorder. This criterion represents a diagnostic challenge, since patients suffering from other sleep disorders often complain of insomnia symptoms. For instance, insomnia symptoms are common in e.g., obstructive sleep apnea and circadian rhythm sleep-wake disorders. It may sometimes be difficult to disentangle whether the patient suffers from insomnia disorder or whether the insomnia symptoms are purely due to another sleep disorder. Furthermore, insomnia disorder may be comorbid with other sleep disorders in some patients, e.g., comorbid insomnia and sleep apnea. In addition, insomnia disorder is often comorbid with psychological or somatic disorders and diseases. Thus, a thorough assessment is necessary for correct diagnostics. For chronic insomnia disorder, treatment-of-choice is cognitive behavioral therapy, and such treatment is also effective when the insomnia disorder appears comorbid with other diagnoses. Furthermore, studies suggest that insomnia is a heterogenic disorder with many different phenotypes or subtypes. Different insomnia subtypes may respond differently to treatment, but more research on this issue is warranted. Also, the role of comorbidity on treatment outcome is understudied. This review is part of a Research Topic on insomnia launched by Frontiers and focuses on diagnostic and treatment challenges of the disorder. The review aims to stimulate to more research into the bidirectional associations and interactions between insomnia disorder and other sleep, psychological, and somatic disorders/diseases. (shrink)

ABSTRACTAnxious individuals report disproportionately negative expectations concerning the future, termed the negative expectancy bias. In contrast, ageing is associated with an inflated expectancy for positive future events. A recent study [Steinman, S. A., Smyth, F. L., Bucks, R. S., MacLeod, C., & Teachman, B. A.. Anxiety-linked expectancy bias across the adult lifespan. Cognition and Emotion, 27, 345–355. doi:10.1080/02699931.2012.711743] found using an interpretation bias task, a negative expectancy bias in young adults and positive expectancy bias in older adults with high trait (...) anxiety. Extending this, the current study examined expectancy bias for positive, negative and ambiguously emotionally toned information in younger and older adults with clinical levels of depression and anxiety to community control groups, thus allowing examination of both disorder status and age on biases. Clinical participants reported a pervasive tendency to expect negative events relative to positive regardless o... (shrink)

Latent variable modeling has revealed important conundrums in the DSM classification system. We agree that the network perspective has potential to inspire new insights and resolve some of these conundrums. We note, however, that alone it cannot really help us understand etiology. Etiology, not comorbidity, is the fundamental question.

People with mental illnesses have higher prevalence and mortality rates with regard to common somatic diseases and causes of death, such as cardio-vascular conditions or cancer. One factor contributing to this excess morbidity and mortality is the sub-standard level of physical healthcare offered to the mentally ill. In particular, they are often subject to diagnostic overshadowing: a tendency to attribute physical symptoms to a pre-existing diagnosis of mental illness. This might be seen as an unfortunate instance of epistemic bad luck, (...) where particular features of a group of patients make a timely and correct diagnosis unlikely. While this can explain some cases of diagnostic overshadowing, I argue that in other cases, epistemic injustice is involved. Analyzing the case of diagnostic overshadowing, I distinguish two kinds of testimonial injustice. For one, there are classic cases of transactional testimonial injustice resulting from prejudices against the mentally ill. In addition, there are cases of structural testimonial injustice resulting from features of health care systems. To overcome diagnostic overshadowing, remedies on the individual as well as structural level are thus needed. (shrink)

Although the network model represents a promising new approach to conceptualizing comorbidity in psychiatric diagnosis, the model applies most directly to Axis I symptom disorders; the degree to which the model generalizes to Axis II disorders remains open to question. This commentary addresses that issue, discussing opportunities and challenges in applying the network model to DSM-diagnosed personality pathology.

BackgroundCognitive Behavioral Therapy is delivered in most of the early intervention services for psychosis in different countries around the world. This approach has been demonstrated to be effective in decreasing or at least delaying the onset of psychosis. However, none of them directly affect the comorbidity of these types of patients that is often the main cause of distress and dysfunctionality. The Unified Protocol for the Transdiagnostic Treatment of Emotional Disorders is a psychological intervention that combines cognitive-behavioral and third-generation (...) techniques that address emotional dysregulation as an underlying mechanism that these disorders have in common. The application of this intervention could improve the comorbid emotional symptoms of these patients.Materials and methodsThe study is a randomized controlled trial in which one group receives immediate UP plus standard intervention and the other is placed on a waiting list to receive UP 7 months later, in addition to standard care in one of our early psychosis programs. The sample will be 42 patients with UHR for psychosis with comorbid emotional symptoms. The assessment is performed at baseline, at the end of treatment, and at 3-months’ follow-up, and includes: general psychopathology, anxiety and depression, positive and negative emotions, emotional dysregulation, personality, functionality, quality of life, cognitive distortions, insight, and satisfaction with the UP intervention.DiscussionThis will be the first study of the efficacy, acceptability, and viability of the UP in a sample of young adults with UHR. The results of this study may have clinical implications, contributing to improving the model of care for young people who consult for underlying psychotic, anxiety, and/or depressive symptoms that can lead to high distress and dysfunctionality.Clinical trial registration[https://clinicaltrials.gov/], identifier [NCT04929938]. (shrink)

The present study examines the comorbidity between specific learning disorders and attention deficit and hyperactivity disorder by comparing the neuropsychological profiles of children with and without this comorbidity. Ninety-seven schoolchildren from 8 to 14 years old were tested: a clinical sample of 49 children with ADHD, SLD or SLD in comorbidity with ADHD, and 48 typically-developing children matched for age and intelligence. Participants were administered tasks and questionnaires to confirm their initial diagnosis, and a battery of executive (...) function tasks testing inhibition, shifting, and verbal and visuospatial updating. Using one-way ANOVAs, our results showed that all children in the clinical samples exhibited impairments on EF measures when compared with TD children. A more specific pattern only emerged for the updating tasks. Only children with SLD had significant impairment in verbal updating, whereas children with ADHD, and those with SLD in comorbidity with ADHD, had the worst performance in visuospatial updating. The clinical and educational implications of these findings are discussed. (shrink)