I much appreciate the honour of being invited to deliver the first Manson lecture, which, its founder has laid down, is to be devoted to the consideration of some subject of common interest to philosophy and medicine. I cannot think of anything which better fulfils that condition than the neurological approach to the problem of perception. The neurologist holds the bridge between body and mind. Every day he meets with examples of disordered perception and he learns from observing the effects (...) of lesions produced by disease, or by the physiologist's experiments, something of how the neural basis of perception is organized. It is possible to study perception as though this was largely irrelevant. How far that view is right will be for you to judge when I have finished. (shrink)

In the past decades, reductionism has dominated both research directions and funding policies in clinical psychology and psychiatry. The intense search for the biological basis of mental disorders, however, has not resulted in conclusive reductionist explanations of psychopathology. Recently, network models have been proposed as an alternative framework for the analysis of mental disorders, in which mental disorders arise from the causal interplay between symptoms. In this target article, we show that this conceptualization can help explain why reductionist approaches in (...) psychiatry and clinical psychology are on the wrong track. First, symptom networks preclude the identification of a common cause of symptomatology with a neurobiological condition; in symptom networks, there is no such common cause. Second, symptom network relations depend on the content of mental states and, as such, feature intentionality. Third, the strength of network relations is highly likely to depend partially on cultural and historical contexts as well as external mechanisms in the environment. Taken together, these properties suggest that, if mental disorders are indeed networks of causally related symptoms, reductionist accounts cannot achieve the level of success associated with reductionist disease models in modern medicine. As an alternative strategy, we propose to interpret network structures in terms of D. C. Dennett's (1987) notion ofreal patterns, and suggest that, instead of being reducible to a biological basis, mental disorders feature biological and psychological factors that are deeply intertwined in feedback loops. This suggests that neither psychological nor biological levels can claim causal or explanatory priority, and that a holistic research strategy is necessary for progress in the study of mental disorders. (shrink)

In this paper, I respond to commentaries on my book “Are Mental Disorders Brain Disorders?”. The topics I discuss are: accounts of function and dysfunction, constraints on the relationship between processes at the level of the brain and the mind, externalism in psychiatry, implications for moral responsibility and the question whether my account is a form of conceptual engineering. I defend my account and argue that the key criterion for whether mental disorders are brain disorders is whether (...) we can map dysfunctional psychological processes onto specific differences in brain function. I also acknowledge that my commentators have identified points where my account needs further development. (shrink)

The contemporary brain disorders debate echoes a century-long conflict between two different approaches to mental suffering: one that relies on natural sciences and another drawing from the arts and humanities. We review contemporary neuroimaging studies and find that neither side has won. The study of mental differences needsboththe sciences and the arts and humanities. To help develop an approach mindful of both, we turn to physician-writer Anton Chekhov’s story “A Nervous Breakdown.” We review the value of the arts and (...) humanities as a coequal partner with natural sciences in the creation of a robust mental health humanities. (shrink)

I argue that despite the merits of Jefferson’s account of a brain disorder, which are many, the notion of function she deploys is unsuitable to the overall goals of that account. In particular, Jefferson accepts Cummins’ causal role theory of function and dysfunction. As the causal role view, in its standard elaborations, is wedded to human interests, goals, and values, it cannot serve as a value-neutral anchor for her hybrid “harm-dysfunction” account of disorder. I argue that the (...) selected effects theory, or some comparably value-neutral account, would serve her purposes better. (shrink)

The question of whether mental disorders are disorders of the brain has led to a long- running and controversial dispute within psychiatry, psychology and philosophy of mind and psychology. While recent work in neuroscience frequently tries to identify underlying brain dysfunction in mental disorders, detractors argue that labelling mental disorders as brain disorders is reductive and can result in harmful social effects. This book brings a much- needed philosophical perspective to bear on this important question.

People hold wildly opposing and very strong views on the question whether mental disorders are brain disorders, and the disagreement is primarily a conceptual one, not one about whether there are,...

This contribution focuses on what type of question “Are mental disorders brain disorders?” is and what task Anneli Jefferson performs in her book with the same title. I distinguish between conceptual engineering and conceptual choice, the former involving the individuation of an adequate concept for a specific goal, and the latter involving the normative problem of whether we should employ the concept at hand. I contend that Anneli Jefferson’s book is a work of conceptual engineering, which is valuable in (...) and of itself, but that this is insufficient to answer an equally essential version of the question, “Are mental disorders brain disorders?”, namely, whether we should adopt the newly engineered concept or not, considering a broader range of goals for mental health research and practice. (shrink)

Non-human animal models of human diseases advance our knowledge of the genetic underpinnings of disease and lead to the development of novel therapies for humans. While mice are the most common model organisms, their usefulness is limited. Larger animals may provide more accurate and valuable disease models, but it has, until recently, been challenging to create large animal disease models. Genome editors, such as Clustered Randomised Interspersed Palindromic Repeat, meet some of these challenges and bring routine genome engineering of larger (...) animals and non-human primates well within reach. There is growing interest in creating NHP models of brain disorders such as autism, depression and Alzheimer’s, which are very difficult to model or study in other organisms, including humans. New treatments are desperately needed for this set of disorders. This paper is novel in asking: Insofar as NHPs are being considered for use as model organisms for brain disorders, can this be done ethically? The paper concludes that it cannot. Notwithstanding ongoing debate about NHPs’ moral status, animal welfare concerns, the availability of alternative methods of studying brain disorders and unmet expectations of benefit justify a stop on the creation of NHP model organisms to study brain disorders. The lure of using new genetic technologies combined with the promise of novel therapeutics presents a formidable challenge to those who call for slow, careful, and only necessary research involving NHPs. But researchers should not create macaques with social deficits or capuchin monkeys with memory deficits just because they can. (shrink)

In this paper, I address the question whether mental disorders should be understood to be brain disorders and what conditions need to be met for a disorder to be rightly described as a brain disorder. I defend the view that mental disorders are autonomous and that a condition can be a mental disorder without at the same time being a brain disorder. I then show the consequences of this view. The most important of (...) these is that brain differences underlying mental disorders derive their status as disordered from the fact that they realize mental dysfunction and are therefore non-autonomous or dependent on the level of the mental. I defend this view of brain disorders against the objection that only conditions whose pathological character can be identified independently of the mental level of description count as brain disorders. The understanding of brain disorders I propose requires a certain amount of conceptual revision and is at odds with approaches which take the notion of brain disorder to be fundamental or look to neuroscience to provide us with a purely physiological understanding of mental illness. It also entails a pluralistic understanding of psychiatric illness, according to which a condition can be both a mental disorder and a brain disorder. (shrink)

A large campaign has sought to destigmatize psychiatric disorders by disseminating the view that they are in fact brain disorders. But when psychiatric disorders are associated with neurobiological correlates, laypeople's attitudes toward patients are harsher, and the prognoses seem poorer. Here, we ask whether these misconceptions could result from the essentialist presumption that brain disorders are innate. To this end, we invited laypeople to reason about psychiatric disorders that are diagnosed by either a brain or a behavioral (...) test that were strictly matched for their informative value. Participants viewed disorders as more likely to be innate and immutable when the diagnosis was supported by a brain test as compared to a behavioral test. These results show for the first time that people spontaneously essentialize psychiatric conditions that are linked to the brain, even when the brain probe offers no additional diagnostic or genetic information. This bias suggests that people consider the biological essence of living things as materially embodied. (shrink)

The publication of DSM-5 has been accompanied by a fair amount of controversy. Amongst DSM’s most vocal ‘insider’ critics has been Thomas Insel, Director of the US National Institute of Mental Health. Insel has publicly criticised DSM’s adherence to a symptom-based classification of mental disorder, and used the weight of the NIMH to back a rival research strategy aimed at a more biology-based diagnostic classification. This strategy is part of Insel’s vision of a future, more preventative psychiatry in which (...) mental disorders are not only understood as biological disorders of the brain, but also as neurodevelopmental disorders. This paper examines the interest and merit of Insel’s views of mental and neurodevelopmental disorder for the philosophy of psychopathology, with a special focus of his neurodevelopmental model of schizophrenia. Pitman’s ‘moderate materialism’ will be used both as a philosophical lens through which to examine Insel’s position, as well as an example of a philosophical framework that may require updating and revision in the light of moves towards a neurodevelopmental conception of mental disorder. (shrink)

Recently there has been a trend of moving towards biological and neurocognitive based classifications of mental disorders that is motivated by a dissatisfaction with the syndrome-based classifications of mental disorders. The Research Domain Criteria (indicated with the acronym RDoC) represents a bold and systematic attempt to foster this advancement. However, RDoC faces theoretical and conceptual issues that need to be addressed. Some of these difficulties emerge when we reflect on the plausible reading of the slogan “mental disorders are brain (...) disorders”, that according to proponents of RDoC constitutes one of its main presuppositions. Some authors think that endorsing this idea commits RDoC to a form of biological reductionism. We offer empirical and theoretical considerations for concluding that the slogan above should not be read as a reductionist thesis. We argue, instead, that the slogan has a pragmatic function whose aim is to direct research in psychopathology. We show how this function might be captured in the framework of a Carnapian explication as a methodological tool for conceptual engineering. Thus, we argue that a charitable interpretation of the aims of the proponents of RDoC should be understood as an attempt at providing an explication of the concept of mental disorder in terms of brain disorder whose main goal is to provide a more precise and fruitful notion that is expected to have a beneficial impact on classification, research, and treatment of psychiatric conditions. (shrink)

In this two-part analysis, I analyze Marc Lewis’s arguments against the brain-disease view of substance addiction and for a developmental-learning approach that demedicalizes addiction. I focus especially on the question of whether addiction is a medical disorder. In Part 1, I argued that, even if one accepts Lewis’s critique of the brain evidence presented for the brain-disease view, his arguments fail to establish that addiction is not a disorder. Relying on my harmful dysfunction analysis of (...) disorder, I defended the view that addiction is a medical disorder and a brain disorder. In Part 2, I consider some broader philosophical issues raised by Lewis’s arguments: I consider a larger puzzle, at the heart of the neo-Kraepelinian program in contemporary psychiatry, that is raised by Lewis’s argument that addiction is not a disorder because the brain displays no damage but only normal learning: must all mental disorders be brain disorders, or can mental disorders occur in normal brains? I argue that mental disorders can occur in normal brains. I critique Lewis’s response to the evolutionary “novel environment” approach to explaining why addiction is a disorder. Lewis agrees with brain-disease proponents that interpreting addiction as brain disorder relieves addicts of moral censure, but I argue that moral defect and brain disease are not exclusive. Finally, I consider Lewis’s “developmental-learning” account of addiction that encourages positive and empowering narrativizing of addiction, but I argue that the developmental-learning view is vacuous due to use of an overly broad notion of “development.”. (shrink)

In this recently published book, Jefferson provides a lucid and detailed examination of, and answer to, its provocative title. In doing so, the focus of Jefferson’s analysis is largely on what a br...

For much of the twentieth century, philosophy and science went their separate ways. In moral philosophy, fear of the so-called naturalistic fallacy kept moral philosophers from incorporating developments in biology and psychology. Since the 1990s, however, many philosophers have drawn on recent advances in cognitive psychology, brain science, and evolutionary psychology to inform their work. This collaborative trend is especially strong in moral philosophy, and these three volumes bring together some of the most innovative work by both philosophers and (...) psychologists in this emerging interdisciplinary field. The neuroscience of morality is in its infancy, with the first brain imaging studies of moral development undertaken only in 2001. The contributors to volume 3 sample the best work in this very new field, discussing a variety of approaches, including functional imaging, lesion studies, abnormal psychology, and developmental neuroscience. Each chapter includes an essay, comments on the essay by other scholars, and a reply by the author of the original essay. Topics include the neural basis of moral emotions and moral judgments as well as comparisons of normal adult moral judgments with those made by children, adolescents, and people with psychopathy, brain damage, and autism. Contributors to Volume 3 Abigail Baird, William Casebeer, Cordelia Fine, Nathan Fox, Uta Frith, Jordan Grafman, Joshua Greene, Catherine Hynes, Fatima Azavedo Ignacio, Richard Joyce, Jerome Kagan, Leonard Katz, Kent Kiehl, Jeanette Kennett, Melanie Killen, Daniel Lapsley, Heidi Maibom, Victoria McGeer, John Mikhail, Jorge Moll, Shaun Nichols, Ricardo de Oliveira-Souza, Adina Roskies, Jana Schaich Borg, Katrina Sifferd, Walter Sinnott-Armstrong, Michael Smith, Mark Timmons, Frederick de Vignemont, Paul Whalen, Roland Zahn. (shrink)

For much of the twentieth century, philosophy and science went their separate ways. In moral philosophy, fear of the so-called naturalistic fallacy kept moral philosophers from incorporating developments in biology and psychology. Since the 1990s, however, many philosophers have drawn on recent advances in cognitive psychology, brain science, and evolutionary psychology to inform their work. This collaborative trend is especially strong in moral philosophy, and these three volumes bring together some of the most innovative work by both philosophers and (...) psychologists in this emerging interdisciplinary field. The neuroscience of morality is in its infancy, with the first brain imaging studies of moral development undertaken only in 2001. The contributors to volume 3 sample the best work in this very new field, discussing a variety of approaches, including functional imaging, lesion studies, abnormal psychology, and developmental neuroscience. Each chapter includes an essay, comments on the essay by other scholars, and a reply by the author of the original essay. Topics include the neural basis of moral emotions and moral judgments as well as comparisons of normal adult moral judgments with those made by children, adolescents, and people with psychopathy, brain damage, and autism. Contributors to volume 3:_ _Abigail Baird, William Casebeer, Cordelia Fine, Nathan Fox, Uta Frith, Jordan Grafman, Joshua Greene, Catherine Hynes, Fatima Azavedo Ignacio, Richard Joyce, Jerome Kagan, Leonard Katz, Kent Kiehl, Jeanette Kennett, Melanie Killen, Daniel Lapsley, Heidi Maibom, Victoria McGeer, John Mikhail, Jorge Moll, Shaun Nichols, Ricardo de Oliveira-Souza, Adina Roskies, Jana Schaich Borg, Katrina Sifferd, Walter Sinnott-Armstrong, Michael Smith, Mark Timmons, Frederick de Vignemont, Paul Whalen, Roland Zahn. (shrink)

Neurobiology-based interventions for mental diseases and searches for useful biomarkers of treatment response have largely failed. Clinical trials should assess interventions related to environmental and social stressors, with long-term follow-up; social rather than biological endpoints; personalized outcomes; and suitable cluster, adaptive, and n-of-1 designs. Labor, education, financial, and other social/political decisions should be evaluated for their impacts on mental disease.

Since the 1990s, many philosophers have drawn on recent advances in cognitive psychology, brain science and evolutionary psychology to inform their work. These three volumes bring together some of the most innovative work by both philosophers and psychologists in this emerging, collaboratory field.

Deep Brain Stimulation (DBS) is a relatively new, experimental treatment for patients suffering from treatment-refractory Obsessive Compulsive Disorder (OCD). The effects of treatment are typically assessed with psychopathological scales that measure the amount of symptoms. However, clinical experience indicates that the effects of DBS are not limited to symptoms only: patients for instance report changes in perception, feeling stronger and more confident, and doing things unreflectively. Our aim is to get a better overview of the whole variety of (...) changes that OCD patients experience during DBS treatment. For that purpose we conducted in-depth, semi-structured interviews with 18 OCD patients. In this paper, we present the results from this qualitative study.We list the changes grouped in four domains: with regard to (a) person, (b) (social) world, (c)characteristics of person-world interactions, and (d) existential stance. We subsequently provide an interpretation of these results. In particular, we suggest that many of these changes can be seen as different expressions of the same process; namely that the experience of anxiety and tension gives way to an increased basic trust and increased reliance on one’s abilities. We then discuss the clinical implications of our findings, especially with regard to properly informing patients of what they can expect from treatment, the usefulness of including CBT in treatment, and the limitations of current measures of treatment success. We end by making several concrete suggestions for further research. (shrink)

People suffering from Obsessive-Compulsive Disorder (OCD) do things they do not want to do, and/or they think things they do not want to think. In about 10 percent of OCD patients, none of the available treatment options is effective. A small group of these patients is currently being treated with deep brain stimulation (DBS). Deep brain stimulation involves the implantation of electrodes in the brain. These electrodes give a continuous electrical pulse to the brain area (...) in which they are implanted. It turns out that patients may experience profound changes as a result of DBS treatment. It is not just the symptoms that change; patients rather seem to experience a different way of being in the world. These global effects are insufficiently captured by traditional psychiatric scales, which mainly consist of behavioural measures of the severity of the symptoms. In this article we aim to capture the changes in the patients’ phenomenology and make sense of the broad range of changes they report. For that we introduce an enactive, affordance-based model that fleshes out the dynamic interactions between person and world in four aspects. The first aspect is the patients’ experience of the world. We propose to specify the patients’ world in terms of a field of affordances, with the three dimensions of broadness of scope (‘width’ of the field), temporal horizon (‘depth’), and relevance of the perceived affordances (‘height’). The second aspect is the person-side of the interaction, that is, the patients’ self-experience, notably their moods and feelings. Thirdly, we point to the different characteristics of the way in which patients relate to the world. And lastly, the existential stance refers to the stance that patients take towards the changes they experience: the second-order evaluative relation to their interactions and themselves. With our model we intend to specify the notion of being in the world in order to do justice to the phenomenological effects of DBS treatment. (shrink)

Externalist theories hold that a comprehensive understanding of mental disorder cannot be achieved unless we attend to factors that lie outside of the head: neural explanations alone will not fully capture the complex dependencies that exist between an individual’s psychiatric condition and her social, cultural, and material environment. Here, we firstly offer a taxonomy of ways in which the externalist viewpoint can be understood, and unpack its commitments concerning the nature and physical realization of mental disorder. Secondly, we (...) apply a strongly externalist approach to the case of Autistic Spectrum Disorder, and argue that this condition can be illuminated by appeal to the hypothesis of extended cognition. We conclude by briefly considering the significance this strongly externalist approach may have for psychiatric practice and pedagogy. (shrink)

In this commentary on Anneli Jefferson’s book “Are Mental Disorders Brain Disorders?,” I offer an overview of her central thesis, and then propose my own modified account of when we are justified in calling mental disorders as “brain disorders.” In doing so, I draw on recent work in neuroscience that understands the relationship between brain and behavior in complex, dynamic, and computational terms. In particular, I disagree with Jefferson’s criterion of sufficiency, that a particular brain process (...) should always realize a psychological dysfunction. I propose that a psychiatric disorder can be said to be a brain disorder if there are empirically identifiable systematic brain differences associated with it and if these associations are contextualized within a scientifically robust theoretical understanding of the relationship between brain and behavior. I conclude by preliminary reflections on whether the issue of “mental disorder” versus “brain disorder” comes down to “the language of psychology” versus “the language of neuroscience,” and the degree to which the former can be expressed in the latter. (shrink)

The DSM-III, DSM-IV, DSM-IV-TR and ICD-10 have judiciously minimized discussion of etiologies to distance clinical psychiatry from Freudian psychoanalysis. With this goal mostly achieved, discussion of etiological factors should be reintroduced into the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. A research agenda for the DSM-V advocated the "development of a pathophysiologically based classification system". The author critically reviews the neuroevolutionary literature on stress-induced and fear circuitry disorders and related amygdala-driven, species-atypical fear behaviors of clinical severity in adult (...) humans. Over 30 empirically testable/falsifiable predictions are presented. It is noted that in DSM-IV-TR and ICD-10, the classification of stress and fear circuitry disorders is neither mode-of-acquisition-based nor brain-evolution-based. For example, snake phobia and dog phobia are clustered together. Similarly, research on blood-injection-injury-type-specific phobia clusters two fears different in their innateness: 1) an arguably ontogenetic memory-trace-overconsolidation-based fear and 2) a hardwired fear of the sight of one's blood or a sharp object penetrating one's skin. Genetic architecture-charting of fear-circuitry-related traits has been challenging. Various, non-phenotype-based architectures can serve as targets for research. In this article, the author will propose one such alternative genetic architecture. This article was inspired by the following: A) Nesse's "Smoke-Detector Principle", B) the increasing suspicion that the "smooth" rather than "lumpy" distribution of complex psychiatric phenotypes may in some cases be accounted for by oligogenic transmission, and C) insights from the initial sequence of the chimpanzee genome and comparison with the human genome by the Chimpanzee Sequencing and Analysis Consortium published in late 2005. Neuroevolutionary insights relevant to fear circuitry symptoms that primarily emerge overconsolidationally are presented. Also introduced is a human-evolution-based principle for clustering innate fear traits. The "Neuroevolutionary Time-depth Principle" of innate fears proposed in this article may be useful in the development of a neuroevolution-based taxonomic re-clustering of stress-triggered and fear-circuitry disorders in DSM-V. Four broad clusters of evolved fear circuits are proposed based on their time-depths: 1) Mesozoic circuits hardwired by wild-type alleles driven to fixation by Mesozoic selective sweeps; 2) Cenozoic circuits relevant to many specific phobias; 3) mid Paleolithic and upper Paleolithic circuits ; 4) Neolithic circuits. More importantly, the author presents evolutionary perspectives on warzone-related PTSD, Combat-Stress Reaction, Combat-related Stress, Operational-Stress, and other deployment-stress-induced symptoms. The Neuroevolutionary Time-depth Principle presented in this article may help explain the dissimilar stress-resilience levels following different types of acute threat to survival of oneself or one's progency. PTSD rates following exposure to lethal inter-group violence are usually 5-10 times higher than rates following large-scale natural disasters such as forest fires, floods, hurricanes, volcanic eruptions, and earthquakes. The author predicts that both intentionally-caused large-scale bioevent-disasters, as well as natural bioevents such as SARS and avian flu pandemics will be an exception and are likely to be followed by PTSD rates approaching those that follow warzone exposure. During bioevents, Amygdala-driven and locus-coeruleus-driven epidemic pseudosomatic symptoms may be an order of magnitude more common than infection-caused cytokine-driven symptoms. Implications for the red cross and FEMA are discussed. It is also argued that hospital phobia as well as dog phobia, bird phobia and bat phobia require re-taxonomization in DSM-V in a new "overconsolidational disorders" category anchored around PTSD. The overconsolidational spectrum category may be conceptualized as straddling the fear circuitry spectrum disorders and the affective spectrum disorders categories, and may be a category for which Pitman's secondary prevention propranolol regimen may be specifically indicated as a "morning after pill" intervention. Predictions are presented regarding obsessive-compulsive disorder and "culture-bound" acute anxiety symptoms. Also discussed are insights relevant to pseudoneurological symptoms and to the forthcoming Dissociative-Conversive disorders category in DSM-V, including what the author terms fright-triggered acute pseudo-localized symptoms. Speculations based on studies of the human abnormal-spindle-like, microcephaly-associated gene, the microcephaly primary autosomal recessive gene, and the forkhead box p2 gene are made and incorporated into what is termed "The pre-FOXP2 Hypothesis of Blood-Injection-Injury Phobia." Finally, the author argues for a non-reductionistic fusion of "distal neurobiology" with clinical "proximal neurobiology," utilizing neurological heuristics. It is noted that the value of re-clustering fear traits based on behavioral ethology, human-phylogenomics-derived endophenotypes and on ontogenomics can be confirmed or disconfirmed using epidemiological or twin studies and psychiatric genomics. (shrink)

Contemporary psychiatry faces serious challenges because it has failed to incorporate accumulated knowledge from basic neuroscience, neurophilosophy, and brain–mind relation studies. As a consequence, it has limited explanatory power, and effective treatment options are hard to come by. A new conceptual framework for understanding mental health based on underlying neurobiological spatial-temporal mechanisms of mental disorders (already gained by the experimental studies) is beginning to emerge.

This is the third of three volumes on moral psychology edited by Walter Sinnott-Armstrong and published by MIT Press in 2008.

ObjectiveTo explore alterations in white matter network topology in de novo Parkinson's disease patients with rapid eye movement sleep behavior disorder.Materials and MethodsThis study included 171 de novo PD patients and 73 healthy controls recruited from the Parkinson's Progression Markers Initiative database. The patients were divided into two groups, PD with probable RBD and PD without probable RBD, according to the RBD screening questionnaire. Individual structural network of brain was constructed based on deterministic fiber tracking and analyses were (...) performed using graph theory. Differences in global and nodal topological properties were analyzed among the three groups. After that, post hoc analyses were performed to explore further differences. Finally, correlations between significant different properties and RBDSQ scores were analyzed in PD-pRBD group.ResultsAll three groups presented small-world organization. PD-pRBD patients exhibited diminished global efficiency and increased shortest path length compared with PD-npRBD patients and HCs. In nodal property analyses, compared with HCs, the brain regions of the PD-pRBD group with changed nodal efficiency were widely distributed mainly in neocortical and paralimbic regions. While compared with PD-npRBD group, only increased Ne in right insula, left middle frontal gyrus, and decreased Ne in left temporal pole were discovered. In addition, significant correlations between Ne in related brain regions and RDBSQ scores were detected in PD-pRBD patients.ConclusionsPD-pRBD patients showed disrupted topological organization of white matter in the whole brain. The altered Ne of right insula, left temporal pole and left middle frontal gyrus may play a key role in the pathogenesis of PD-RBD. (shrink)

Self-compassion is a mechanism of symptom improvement in post-traumatic stress disorder, however, the underlying neurobiological processes are not well understood. High levels of self-compassion are associated with reduced activation of the threat response system. Physiological threat responses to trauma reminders and increased arousal are key symptoms which are maintained by negative appraisals of the self and self-blame. Moreover, PTSD has been consistently associated with functional changes implicated in the brain’s saliency and the default mode networks. In this paper, (...) we explore how trauma exposed individuals respond to a validated self-compassion exercise. We distinguish three groups using the PTSD checklist; those with full PTSD, those without PTSD, and those with subsyndromal PTSD. Subsyndromal PTSD is a clinically relevant subgroup in which individuals meet the criteria for reexperiencing along with one of either avoidance or hyperarousal. We use electroencephalography alpha-asymmetry and EEG microstate analysis to characterize brain activity time series during the self-compassion exercise in the three groups. We contextualize our results with concurrently recorded autonomic measures of physiological arousal, parasympathetic activation and self-reported changes in state mood and self-perception. We find that in all three groups directing self-compassion toward oneself activates the negative self and elicits a threat response during the SC exercise and that individuals with subsyndromal PTSD who have high levels of hyperarousal have the highest threat response. We find impaired activation of the EEG microstate associated with the saliency, attention and self-referential processing brain networks, distinguishes the three PTSD groups. Our findings provide evidence for potential neural biomarkers for quantitatively differentiating PTSD subgroups. (shrink)

The main goal of Brain Death and Disorders of Consciousness is to provide a suitable scientific platform to discuss all topics related to human death and coma.

The tendency to draw mind-brain dichotomies and evaluate mental disorders dualistically arises in both laypeople and mental health professionals, leads to biased judgments, and contributes to mental health stigmatization. This paper offers a theory identifying an underlying source of these evaluations in social practice. According to this theory, dualistic evaluations are rooted in two mechanisms by which we represent and evaluate the beliefs of others in folk psychology and theory of mind: the doxastic conception of mental disorders and doxastic (...) voluntarism. Tracing these origins contributes to our understanding of mental state representation in cognitive science and philosophy of psychiatry, the concept of belief in philosophy of mind, and may help improve patient experience and treatment in light of social stigmatization and bias toward mental illness. (shrink)

ObjectivesAbnormal brain function in ASD patients changes dynamically across developmental stages. However, no one has studied the brain function of prepubertal children with ASD. Prepuberty is an important stage for children’s socialization. This study aimed to investigate alterations in local spontaneous brain activity in prepubertal boys with ASD.Materials and MethodsMeasures of the amplitude of low-frequency fluctuations and regional homogeneity acquired from resting-state functional magnetic resonance imaging database, including 34 boys with ASD and 49 typically developing boys aged (...) 7 to 10 years, were used to detect regional brain activity. Pearson correlation analyses were conducted on the relationship between abnormal ALFF and ReHo values and Autism Diagnostic Observation Schedule and Autism Diagnostic Interview-Revised scores.ResultsIn the ASD group, we found decreased ALFF in the left inferior parietal lobule and decreased ReHo in the left lingual gyrus, left superior temporal gyrus, left middle occipital gyrus, and right cuneus. There were negative correlations between ReHo values in the left LG and left STG and the ADOS social affect score and a negative correlation between ReHo values in the left STG and the calibrated severity total ADOS score.ConclusionBrain regions with functional abnormalities, including the left IPL, left LG, left STG, left MOG, and right cuneus may be crucial in the neuropathology of prepubertal boys with ASD. Furthermore, ReHo abnormalities in the left LG and left STG were correlated with sociality. These results will supplement the study of neural mechanisms in ASD at different developmental stages, and be helpful in exploring the neural mechanisms of prepubertal boys with ASD. (shrink)

Social cognition is a broad term, incorporating all aspects of social functioning from perceiving emotional stimuli to attributional style and theory of mind. Not distinguishing between these different capacities may confound the interpretation of the data deriving from studies of the relationship between psychiatric disorders and the social brain. The distinction between cognitive and affective components of social cognition is clearly exemplified by the abnormalities observed in psychopathy and Williams syndrome.

The present dissertation starts from the general claim that neuroscience is not neutral, with regard to theoretical questions like the nature of consciousness, but it needs to be complemented with dedicated conceptual analysis. Specifically, the argument for this thesis is that the combination of empirical and conceptual work is a necessary step for assessing the significant questions raised by the most recent study of the brain. Results emerging from neuroscience are conceptually very relevant in themselves but, notwithstanding its theoretical (...) sophistication, neuroscience is not sufficient to provide a complete interpretation or an appropriate understanding of their impact. Consequently, the present thesis starts from the need for an interdisciplinary and hybrid field of research, i.e. fundamental neuroethics. Within this framework, the thesis takes consciousness and related disorders and the addicted brain as illustrative cases of the potential fruitful collaboration between empirical and conceptual investigations. The general goal of the thesis is to contribute to the overall development of bridging the gap between empirical and conceptual understandings of consciousness. The first paper sets the theoretical framework, providing an empirically-based description of the brain with significant philosophical implications for an understanding of consciousness. The last three papers of the thesis try to apply the theoretical framework to illustrative cases. Papers II and III analyse the possible application of science and technology for an easier detection and clinical care of patients with disorders of consciousness, with particular attention to communication mediated by neurotechnology and the simulation of the conscious brain, respectively; paper IV provides a potentially new ethical analysis of addiction within the elaborated general conceptual framework. The conclusion of the thesis is that the impact of neuroscientific results needs that a dedicated conceptual approach reveals and investigates their conceptual meaning. This conceptual analysis is not exclusive but integrative and complementary to the empirical science. The case of consciousness, analysed from both an ethical and conceptual point of view, is highly illustrative in this respect. In the end, a conceptual/linguistic work of clarification is urgently needed. (shrink)

It is often assumed that similar domain-specific behavioural impairments found in cases of adult brain damage and developmental disorders correspond to similar underlying causes, and can serve as convergent evidence for the modular structure of the normal adult cognitive system. We argue that this correspondence is contingent on an unsupported assumption that atypical development can produce selective deficits while the rest of the system develops normally (Residual Normality), and that this assumption tends to bias data collection in the field. (...) Based on a review of connectionist models of acquired and developmental disorders in the domains of reading and past tense, as well as on new simulations, we explore the computational viability of Residual Normality and the potential role of development in producing behavioural deficits. Simulations demonstrate that damage to a developmental model can produce very different effects depending on whether it occurs prior to or following the training process. Because developmental disorders typically involve damage prior to learning, we conclude that the developmental process is a key component of the explanation of endstate impairments in such disorders. Further simulations demonstrate that in simple connectionist learning systems, the assumption of Residual Normality is undermined by processes of compensation or alteration elsewhere in the system. We outline the precise computational conditions required for Residual Normality to hold in development, and suggest that in many cases it is an unlikely hypothesis. We conclude that in developmental disorders, inferences from behavioural deficits to underlying structure crucially depend on developmental conditions, and that the process of ontogenetic development cannot be ignored in constructing models of developmental disorders. Key Words: Acquired and developmental disorders; connectionist models; modularity; past tense; reading. (shrink)