The neuropathologies of the self are disorders of the self and identity that occur in association with neuropathology and include perturbations of the bodily, relational, and narrative self. Right, especially medial-frontal and orbitofrontal lesions, are associated with these conditions. The ego disequilibrium theory proposes this brain pathology causes a disturbance of ego boundaries and functions and the emergence of developmentally immature styles of thought, ego functioning, and psychological defenses including denial, projection, splitting, and fantasy that the NPS patient has (...) in common with the child. I hypothesize that during brain development between approximately ages 3 and 7 immature defensive functions and fantasies tend to be replaced by mature defenses and the inhibition of fantasy a process that depends upon maturational processes within the right hemisphere. I propose a four-tiered model of the NPS that emphasizes a multifactorial approach and includes both negative and positive, bottom up and top down, and neuropsychological and psychological factors. (shrink)

By age 85, most adults manifest some degree of motor impairment. However, in most individuals a specific etiology for motor decline and treatment to modify its inexorable progression cannot be identified. Recent clinical-pathologic studies provide evidence that mixed-brain pathologies are commonly associated with late-life motor impairment. Yet, while nearly all older adults show some degree of accumulation of Alzheimer’s disease and related dementias pathologies, the extent to which these pathologies contribute to motor decline varies widely from person to person. Slower (...) or faster than expected motor decline in the presence of brain injury and/or pathology has been conceptualized as more or less “resilience” relative to the average person This suggests that other factors, such as lifestyles or other neurobiologic indices may offset or exacerbate the negative effects of pathologies via other molecular pathways. The mechanisms underlying neural motor resilience are just beginning to be illuminated. Unlike its cousin, cognitive resilience which is restricted to neural mechanisms above the neck, the motor system extends the total length of the CNS and beyond the CNS to reach muscle and musculoskeletal structures, all of which are crucial for motor function. Building on prior work, we propose that by isolating motor decline unrelated to neuropathologies and degeneration, investigators can identify genes and proteins that may provide neural motor resilience. Elucidating these molecular mechanisms will advance our understanding of the heterogeneity of late-life motor impairment. This approach will also provide high value therapeutic targets for drug discovery of therapies that may offset the negative motor consequences of CNS pathologies that are currently untreatable. (shrink)

_Abstract_: In this paper, I will examine the Goldstein-Cassirer approach to neuropathology to determine its current potential for yielding valuable insights. To this end, I will reconstruct the philosophical and theoretical underpinnings of such a standpoint in the first four sections. What will emerge is that it entails a definition of pathology as the loss of balance in the adaption of human beings to the environment, leading to a lack of proclivity to categorical behaviour and symbolic performances. Furthermore, we (...) will see that there are behavioural alterations which are not related to the locus of lesions. In the fifth section, I will compare and contrast the holistic stances with current research in neuropsychology. The sixth section is dedicated to conclusive remarks. _Keywords_: Psychopathology; Neuropathology; Ernst Cassirer; Kurt Goldstein; Holism _ La mente ordinatrice. La concezione di Goldstein e Cassirer della neuropatologia e la sua rilevanza oggi _ _Riassunto_: In questo articolo intendo analizzare l’approccio Goldstein-Cassirer alla neuropatologia per comprendere se esso può rivelarsi ancora utile alla luce delle ricerche attuali. A tal fine, ne ricostruirò le basi filosofiche e teoriche nei primi tre paragrafi. Scopriremo che esso implica una definizione di patologia come perdita di equilibrio nell’adattamento degli esseri umani all’ambiente, a seguito della quale viene a mancare la naturale tendenza verso il “comportamento categoriale” e le prestazioni simboliche. Vedremo, inoltre, che vi sono alterazioni del comportamento non collegabili al sito delle lesioni. Nel quinto paragrafo, metterò a confronto le istanze olistiche con le ricerche contemporanee nel campo della neuropsicologia. Il sesto paragrafo contiene le considerazioni conclusive. _Parole chiave_: Psicopatologia; Neuropatologia; Ernst Cassirer; Kurt Goldstein; Olismo. (shrink)

[We understand by ‘person’] a thinking intelligent being, that has reason and reflection, and can consider itself, as itself, the same thinking thing, in different times and places….There has been a tendency among philosophers ever since Locke to conflate the problem of the self with the problem of personal identity, and since memory is clearly essential to a sense of one's identity through time, it is easy to suppose that having a concept of self requires memory too.

This information-packed volume, without doubt a landmark event in the developing neuroscientific study of consciousness, deserves the attention of anyone interested in this subject. It is a sequel and companion to an earlier collection, The Boundaries of Consciousness: Neurobiology and Neuropathology, also edited by Steven Laureys (2005), which contains the proceedings of a 2004 conference sponsored by the Association for the Scientific Study of Consciousness (ASSC). Published initially as a special issue of Progress in Brain Research (volume 150), Boundaries (...) has been reissued in paperback and appears on the ASSC website as one of its official titles. Both volumes include many prominent figures in contemporary neuroscience, and the two volumes together constitute about as clear, comprehensive, and authoritative a picture as one can find anywhere of the current state of mainstream neuroscientific thinking about consciousness and the brain. Like classical physics of the late 19th century, it is a picture of great power and beauty; nevertheless, just as discordant phenomena such as black-body radiation and the photoelectric effect presaged the rise of quantum mechanics, this book, precisely because of its clarity, reveals signs of trouble ahead. (shrink)

This essay provides an analysis of the clinical problems that arise at the borderline between neurology and psychiatry. We postulate that psychopathological and neuropathological constructs have distinct referents and conceptual fields, but they are not mutually exclusive categories. After establishing criteria for defining neuropsychiatric constructs, we outline rules for identifying cases where a significant relationship exists between neuropathological and psychopathological patterns. We propose three approaches to establishing this relationship: a clinical epidemiology approach, a clinical neuroscience approach offering a mechanistic model, (...) and a longitudinal study of individual cases incorporating idiographic perspectives. We discuss the logic of brain-behavior relationships and emphasize the need for closer academic feedback between neuroscientific research and clinical practice to better understand the causality of psychopathological phenomena in the context of neuropsychiatry. While precise demarcation may be challenging in some cases, we provide two types of examples: first, straightforward cases where neuropathology explains psychopathological patterns; second, complex cases that require studying the causal interactions between neuropathological factors, psychological factors, and sociocultural contexts, leading to intricate clinical patterns that demand cognitive neuropsychiatry resources, and a multidisciplinary approach to clinical care. (shrink)

Consciousness is one of the most significant scientific problems today. Renewed interest in the nature of consciousness - a phenomenon long considered not to be scientifically explorable, as well as increasingly widespread availability of multimodal functional brain imaging techniques (EEG, ERP, MEG, fMRI and PET), now offer the possibility of detailed, integrated exploration of the neural, behavioral, and computational correlates of consciousness. The present volume aims to confront the latest theoretical insights in the scientific study of human consciousness with the (...) most recent behavioral, neuroimaging, electrophysiological, pharmacological and neuropathological data on brain function in altered states of consciousness such as: brain death, coma, vegetative state, minimally conscious state, locked-in syndrome, dementia, epilepsy, schizophrenia, hysteria, general anesthesia, sleep, hypnosis, and hallucinations. The interest of this is threefold. First, patients with altered states of consciousness continue to represent a major clinical problem in terms of clinical assessment of consciousness and daily management. Second, the exploration of brain function in altered states of consciousness represents a unique lesional approach to the scientific study of consciousness and adds to the worldwide effort to identify the "neural correlate of consciousness". Third, new scientific insights in this field have major ethical and social implications regarding our care for these patients. (shrink)

I develop an interpretation of Maurice Merleau-Ponty's concept of motor intentionality, one that emerges out of a reading of his presentation of a now classic case study in neuropathology—patient Johann Schneider—in Phenomenology of Perception. I begin with Merleau-Ponty's prescriptions for how we should use the pathological as a guide to the normal, a method I call triangulation. I then turn to his presentation of Schneider's unusual case. I argue that we should treat all of Schneider's behaviors as pathological, not (...) only his abstract movements, as is commonly acknowledged in the secondary literature, but also crucially his concrete movements. Using these facts of Schneider's illness, I reconstruct a ‘fundamental function’ of consciousness, as Merleau-Ponty called it, in which there are two kinds of bodily agency: the power of the body to be solicited by a situation and the power of the body to project a situation. I propose that these powers became dissociated in Schneider's case, as evidenced by his abstract and concrete movements, while in the normal case, these powers comprise a dynamic unity, enacted as motor intentionality. I also discuss how my interpretation complements Merleau-Ponty's assertion that motor intentions exist between mind and matter. (shrink)

This collection opens a dialogue between process philosophy and contemporary consciousness studies. Approaching consciousness from diverse disciplinary perspectives—philosophy, psychology, neuroscience, neuropathology, psychotherapy, biology, animal ethology, and physics—the contributors offer empirical and philosophical support for a model of consciousness inspired by the process philosophy of Alfred North Whitehead (1861–1947). Whitehead’s model is developed in ways he could not have anticipated to show how it can advance current debates beyond well-known sticking points. This has trenchant consequences for epistemology and suggests fresh (...) and promising new perspectives on such topics as the mind-body problem, the neurobiology of consciousness, animal consciousness, the evolution of consciousness, panpsychism, the unity of consciousness, epiphenomenalism, free will, and causation. Contents: Introduction, Michel Weber & Anderson Weekes I. Setting the Stage 1. Process Thought as a Heuristic for Investigating Consciousness, Michel Weber & Anderson Weekes 2. Whitehead as a Neglected Figure of 20th Century Philosophy, Michel Weber & Anderson Weekes 3. Consciousness as a Topic of Investigation in Western Thought, Anderson Weekes 4. Whitehead’s Unique Approach to the Topic of Consciousness, Anderson Weekes II. Psychology and Philosophy of Mind 5. Consciousness as a Subjective Form, David Ray Griffin 6. The Interpretation and Integration of the Literature on Consciousness from a Process Perspective, Michael W. Katzko 7. Windows on Nonhuman Minds, Donald R. Griffin III. From Metaphysics to (Neuro)Science and Back Again 8. Panexperientialism, Quantum Theory, and Neuroplasticity, George W. Shields 9. The Evolution of Consciousness, Max Velmans 10. The Carrier Theory Of Causation, Gregg H. Rosenberg IV. Clinical Applications: Consciousness as Process 11. The Microgenetic Revolution in Contemporary Neuropsychology and Neurolinguistics, Maria Pachalska and Bruce Duncan MacQueen 12. From Coma to Consciousness, Avraham Schweiger, Michael Frost, Ofer Keren 13. Consciousness and Rationality from a Process Perspective, Michel Weber V. History (and Future?) of Philosophy 14. Consciousness, Memory, and Recollection according to Whitehead, Xavier Verley 15. Consciousness and Causation in Light of Whitehead’s Phenomenology of Becoming, Anderson Weekes. (shrink)

During the Third Reich, state‐sponsored violence was linked to scientific research on many levels. Prisoners were used as involuntary subjects for medical experiments, and body parts from victims were used in anatomy and neuropathology on a massive scale. In many cases, such specimens remained in scientific collections and were used until long after the war. International bioethics, for a long time, had little to say on the issue. Since the late 1980s, with a renewed interest in the Holocaust and (...) other Nazi crimes, a consensus has increasingly taken hold that research on human tissues and body parts from the Nazi era is inadmissible, and that such specimens should be removed from scientific collections and buried. The question of what to do with scientific data obtained from these sources has not received adequate attention, however, and remains unsolved. This paper traces the history of debates about the ethical implications of using human tissue or body parts from the Nazi period for scientific purposes, primarily in the fields of anatomy and neuropathology. It also examines how this issue, from after the war until today, influenced the establishment of legal and bioethical norms on the use of human remains from morally tainted sources, with a particular emphasis on Germany and Austria. It is argued that the use of such specimens and of data derived from them is unethical not only because of potential harms to posthumous rights of the victims, but also because such use constitutes a moral harm to society at large. (shrink)

The clinical and para-clinical examination of residual self-consciousness in non-communicative severely brain damaged patients remains exceptionally challenging. Passive presentation of the patient’s own name and own face are known to be effective attention-grabbing stimuli when clinically assessing consciousness at the patient’s bedside. Event-related potential and functional neuroimaging studies using such self-referential stimuli are currently being used to disentangle the cognitive hierarchy of self-processing. We here review neuropsychological, neuropathological, electrophysiological and neuroimaging studies using the own name and own face paradigm obtained (...) in conscious waking, sleep, pharmacological coma, pathological coma and related disorders of consciousness. Based on these results we discuss what we currently do and do not know about the functional significance of the neural network involved in “automatic” and “conscious” self-referential processing. (shrink)

In recent years, neuroscience has begun to transform itself into a “big data” enterprise with the importation of computational and statistical techniques from machine learning and informatics. In addition to their translational applications such as brain-computer interfaces and early diagnosis of neuropathology, these tools promise to advance new solutions to longstanding theoretical quandaries. Here I critically assess whether these promises will pay off, focusing on the application of multivariate pattern analysis (MVPA) to the problem of reverse inference. I argue (...) that MVPA does not inherently provide a new answer to classical worries about reverse inference, and that the method faces pervasive interpretive problems of its own. Further, the epistemic setting of MVPA and other decoding methods contributes to a potentially worrisome shift towards prediction and away from explanation in fundamental neuroscience. (shrink)

In this article, I review textual evidence demonstrating that James and Dewey incorporated Kant’s ideas, even while criticizing him. I specifically argue that the pragmatic evolution of the Kantian a priori carried out by James and Dewey is a transition from the mental to the bodily. I further argue that the parallels between pragmatists and Kant, along with the transition from the mental to bodily, relate to scientific contexts in which all developed their outlooks. Though historically grounded, my ultimate goal (...) is to show that pragmatism and by extension Kantianism mesh with and indeed contribute to cutting edge ideas in fields ranging from neuropathology to robotics and AI to cognitive science, whether in the form of Gibsonian theory or enactivism. (shrink)

This article proposes a Social Determinants of Health framework as a counter to the prominence of bio-determinist tropes in understandings of the relationship between concussion and later life neurodegenerative conditions in athletic populations. It is argued that debates about concussion (or repetitive head impacts) causing CTE have been particularly influenced by broader social trends towards neuro-essentialism. This paradigm reduces complex social behaviour to brain matter and continues to dominate the field despite the recent diversification of evidence from autopsy-based studies of (...) neuropathology to epidemiological studies comparing recorded causes of death among former elite athletes. In contrast, this article explores the ‘causes of causes’ of neurodegenerative conditions. It outlines the ways in which the distinct dynamics of: a) employment, b) education, income and wealth, c) health systems and services, and d) social environment and public safety relate to the specific occupational conditions of elite sport and likely negatively shape health outcomes of athletic populations. The article concludes by arguing that to more effectively address these particular health harms we must move beyond narrow, mono-causal models and evoke a cultural change that extends beyond making rule changes and adjusting psychological attitudes and behavioural norms, to redress the social structural parameters of elite sports participation. The continuation of narrower, neuro-centric and reductionist paradigms obscures the causes of the causes of neurodegenerative decline and limits the scope for change. (shrink)

In dementia research evidence is mounting that therapeutic strategies that target moderate and even mild Alzheimer's disease may be missing the ‘therapeutic window’. Given that the neuropathology that leads to Alzheimer's disease probably begins somewhere between 10 and 15 years before symptoms manifest, many believe that the optimal therapeutic strategy would target persons in the earliest phases of disease development or even earlier. This would include, for example, persons with prodromal Alzheimer's and even persons who are deemed at risk. (...) Given the nature of research involving the central nervous system, it is conceivable that some therapeutic investigations may involve an increase over minimal risk. This paper examines how, in dementia research, at-risk persons, although healthy, bring multiple and intersecting vulnerabilities to the prospect of research participation even though they are clinically healthy. Current guidelines for research ethics may not provide adequately for the nuances of ‘healthy individuals’ and their possible vulnerabilities. In the context of neurodegenerative disease, the fact of being ‘at risk’ alters the vulnerability profile in significant ways. While healthy persons who are at risk of developing dementia may not appear to warrant placement in the research category of vulnerable participants (alongside prisoners, pregnant women and children) careful regard for the vulnerabilities that arise as a result of the intersecting circumstances of being healthy and at risk of an incurable disease are worthy of increased attention and consideration, particularly as the research effort for the increasingly prevalent disease of Alzheimer's moves forward. (shrink)

This dissertation is a contribution to the contemporary field of phenomenological psychopathology, or the phenomenological study of psychiatric disorders. The work proceeds with two major aims. The first is to show how a phenomenological approach can clarify and illuminate the nature of psychopathology—specifically those conditions typically labeled as major depressive disorder and bipolar disorder. The second is to show how engaging with psychopathological conditions can challenge and undermine many phenomenological presuppositions, especially phenomenology’s status as a transcendental philosophy and its corresponding (...) anti-naturalistic outlook. In the opening chapter, I articulate the three layers of the subject matter of phenomenological research—what I refer to as “existentials,” “modes,” and “prejudices.” As I argue, while each layer contributes to what we might call the “structure” of human existence, they do not do so in the same way, or to the same degree. Because phenomenological psychopathology—and applied phenomenology in general—aims to characterize how the structure of human existence can change and alter, it is paramount that these layers be adequately delineated and defined before investigating these changes. In chapters two through five, I conduct hermeneutic and phenomenological investigations of psychopathological phenomena typically labeled as major depressive disorder or bipolar disorder. These investigations address the affective aspects of depression and mania, and the embodied aspects of depression. In addition to clearly articulating the nature of these phenomena, I show how certain psychopathological conditions involve changes in the deepest or most fundamental layer of human existence—what I refer to as existentials. As I argue, many of the classical phenomenologists (including Husserl and Heidegger) believed that these structural features were necessary, unchanging, and universal. However, this presupposition is challenged through the examination of psychopathological and neuropathological conditions, undermining the status of phenomenology as a transcendental philosophy. While this challenge to classical phenomenology is only sketched in the early chapters, in chapters six and seven I develop it in more detail in order to achieve two distinct ends. In chapter six I argue that psychopathology and neuropathology not only challenge phenomenology’s status as a transcendental philosophy, but also supply a key to developing a phenomenological naturalism (which I contrast with a naturalized phenomenology). Phenomenological naturalism, as I articulate it, is a position in which phenomenology is not subsumed by the metaphysical and methodological framework of the natural sciences, but nonetheless maintains the capacity to investigate how the natural world stands independent of human subjectivity (and how events in the natural world can bring about changes in the most fundamental structures of human existence). In the seventh chapter I argue that a phenomenology in which existentials are contingent and variable rather than necessary and unchanging allows phenomenologists to contribute to new dimensional approaches to psychiatric classification. Rather than begin from distinct categories of disorder, these approaches begin from distinct core features of human existence. These features, referred to as either dimensions or constructs, can vary in degree and are studied in both normal and pathological forms. (shrink)

This book provides a broad survey of many of the major areas in neuroplasticity research by leading investigators in the field. The topics considered range across all levels of nervous system organization from the molecular to behavioral levels for species ranging from _C. elegans_ to humans. In addition, the effects of development and neuropathological events are discussed. A final summary chapter synthesizes the data gathered in this volume in order to provide the basis for a general theory of neuroplasticity.

Dementia is more than a disease. What dementia is, how it is understood, and how it is experienced is influenced by multiple factors including our societal preoccupation with individual identity. This essay introduces empirical and theoretical evidence of alternative ways of understanding dementia that act as a challenge to common assumptions. It proposes that dementia be understood as an experience of systems, particularly networks of people affected by the diagnosis. Taking this step reveals much about the dementia experience, and about (...) what can be learned from persons with dementia and their networks of family, friends, and carers. It also suggests that dementia may be best thought of as an ecology that arises from the interaction between neuropathological change, people, language, and meaning. While challenging, this perspective may provide new ways of responding to dementia and caring for those affected by it. (shrink)

This paper clarifies Merleau-Ponty’s original account of “higher-order” cognition as fundamentally embodied and enacted. Merleau-Ponty’s philosophy inspired theories that deemphasize overlaps between conceptual knowledge and motor intentionality or, on the contrary, focus exclusively on abstract thought. In contrast, this paper explores the link between Merleau-Ponty’s account of motor intentionality and his interpretations of our capacity to understand and interact productively with cultural symbolic systems. I develop my interpretation based on Merleau-Ponty’s analysis of two neuropathological modifications of motor intentionality, the case (...) of the brain-injured war veteran Schneider, and a neurological disorder known as Gerstmann’s syndrome. Building on my analysis of Schneider’s sensorimotor compensatory performances in relation to his limitations in the domains of algebra, geometry, and language usage, I demonstrate a strong continuity between the sense of embodiment and enaction at all these levels. Based on Merleau-Ponty’s interpretations, I argue that “higher-order” cognition is impaired in Schneider insofar as his injury limits his sensorimotor capacity to dynamically produce comparatively more complex differentiations of any given phenomenal structure. I then show how Merleau-Ponty develops and specifies his interpretation of Schneider’s intellectual difficulties in relation to the ambiguous role of the body, and in particular the hand, in Gerstmann’s syndrome. I explain how Merleau-Ponty defends the idea that sensorimotor and quasi-representational cognition are mutually irreducible, while maintaining that symbol-based cognition is a fundamentally enactive and embodied process. (shrink)

Discrediting 'mystical' or 'psychical' interpretations of out-of-body and near-death experiences, Michael Marsh demonstrates how these phenomena are explicable in terms of brain neurophysiology and its neuropathological disturbances, and discusses the theological and philosophical implications of his hypotheses.

Pathological gambling (PG) is a kind of ‘ideal puzzle’ for the economic model of the consumer. The pathological gambler takes pains to engage in activity that transparently has negative expected returns if utility varies positively with money. She also, typically, spends further resources on commitment devices designed to interfere with her gambling. These properties together describe an agent that is a kind of perfect foil for the rationally maximizing consumer. Recently, aspects of the neuropathology underlying the strange economic agency (...) of the pathological gambler are becoming understood. Thus PG is an ideal test bed phenomenon for working out relationships between economic modeling based on constrained optimization of utility and the new neuroscience of behavior. (shrink)

The authors argue that the consciousness debate inhabits the same problem space today as it did in the 17th century. They attribute the lack of progress to a mindset still polarized by Descartes’ real distinction between mind and body, resulting in a standoff between humanistic and scientistic approaches. They suggest that consciousness can be adequately studied only by a multiplicity of disciplines so that the paramount problem is how to integrate diverse disciplinary perspectives into a coherent metatheory. Process philosophy is (...) well qualified to attempt such a synthesis. The rationale for the volume is summed up in the book's unifying thesis: normal, focal-attentive consciousness is not the sui generis phenomenon it is usually taken to be, but part of a wider spectrum of experience (including marginal, deviant, and non-human experience) that can only be studied by approaches as diverse as phenomenology, psycho- and neuropathology, biology, and zoology. (shrink)

Patients with Wilson’s disease suffer from prospective memory impairment, and some of patients develop cognitive impairment. However, very little is known about how brain structure and function changes effect PM in WD. Here, we employed multimodal neuroimaging data acquired from 22 WD patients and 26 healthy controls who underwent three-dimensional T1-weighted, diffusion tensor imaging, and resting state functional magnetic resonance imaging. We investigated gray matter volumes with voxel-based morphometry, DTI metrics using the fiber tractography method, and RS-fMRI using the seed-based (...) functional connectivity method. Compared with HC, WD patients showed GM volume reductions in the basal ganglia and occipital fusiform gyrus, as well as volume increase in the visual association cortex. Moreover, whiter matter tracks of WD were widely impaired in association and limbic fibers. WM tracks in association fibers are significant related to PM in WD patients. Relative to HC, WD patients showed that the visual association cortex functionally connects to the thalamus and hippocampus, which is associated with global cognitive function in patients with WD. Together, these findings suggested that PM impairment in WD may be modulated by aberrant WM in association fibers, and that GM volume changes in the association cortex has no direct effect on cognitive status, but indirectly affect global cognitive function by its aberrant functional connectivity in patients with WD. Our findings may provide a new window to further study how WD develops into cognitive impairment, and deepen our understanding of the cognitive status and neuropathology of WD. (shrink)

In the 1970s, Stella Chess found a high prevalence of autism in children with congenital rubella syndrome (CRS), 200 times that of the general population at the time. Many researchers quote this fact to add proof to the current theory that maternal infection with immune system activation in pregnancy leads to autism in the offspring. This rubella and autism association is presented with the notion that rubella has been eliminated in today’s world. CRS cases are no longer typically seen, yet (...) autistic children often share findings of CRS including deafness, congenital heart defects and to a lesser extent visual changes. Autistic children commonly have hyperactivity and spasticity, as do CRS children. Both autistic and CRS individuals may develop type 1 diabetes as young adults. Neuropathology of CRS infants may reveal cerebral vasculitis with narrowed lumens and cerebral necrosis. Neuroradiologic findings of children with CRS show calcifications, periventricular leukomalacia, and dilated perivascular spaces. Neuroradiology of autism has also demonstrated hyperintensities, leukomalacia and prominent perivascular spaces. PET studies of autistic individuals exhibit decreased perfusion to areas of the brain similarly affected by rubella. In both autism and CRS, certain changes in the brain have implicated the immune system. Several children with autism lack antibodies to rubella, as do children with CRS. These numerous similarities increase the probability of an association between rubella virus and autism. Rubella and autism cross many ethnicities in many countries. Contrary to current belief, rubella has not been eradicated and globally affects up to 5% of pregnant women. Susceptibility continues as vaccines are not given worldwide and are not fully protective. Rubella might still cause autism, even in vaccinated populations. (shrink)

McGovern, Kevin This article reviews three statements from the National Health and Medical Research Council on post-coma unresponsiveness (PCU). One of the functions of the NHMRC is to propose standards and guidelines for health care in Australia. The paper explores the causes and neuropathology of PCU, imaging and other tests and prognosis from unresponsiveness.

The scientific study of consciousness in the late 19th century, which took place in Western countries across disciplines such as neurology, physiology, neuropathology, psychology, psychiatry and philosophy, appears to have striking parallels to current crossdisciplinary developments in the neurosciences. The 19th century period, however, has received little scholarly attention from historians of medicine, psychology, or science. Historians of depth psychology have investigated the area as part of the history of psychiatry, but cleaved most closely to the versions presented by (...) early psychoanalysts- turned-historians, who have consistently portrayed Freud as the only legitimate history of the period, thus marking the territory of the late 19th century as inherently Freudo-centric. More recently a new line of historiography emanating from the work of the late Henri Ellenberger has launched a post-Freudian perspective in which the classical depth psychologies of Freud, Jung, and Adler may now be understood in a wider and deeper historical context defined by the development of a so-called French, Swiss, English, and American psychotherapeutic axis between 1881 and 1918, before the advent of psychoanalysis. Chief among the prime movers of this axis was Frederic William Henry Myers, graduate of Cambridge University, and co-founder of the Society for Psychical Research in England in 1882. Myers' grasp of the literature of the day regarding the scientific study of consciousness was both profound, and highly influential, particularly on such figures as William James. Since the period itself has yet to be fully reconstructed, the identity of Myers and his contribution to the scientific study of consciousness remain obscure, but are also receiving new attention in the area of modern consciousness studies. (shrink)

In lieu of an abstract, here is a brief excerpt of the content:The Misnomer of Freud's "Seduction Theory"Hall TriplettSigmund Freud's theory of 1896 was buried without a name in 1897, less than two years after it appeared. The process by which it acquired a name, "seduction theory," and the role this name played in the history of psychoanalysis are essential parts of the legend-making in Freud's biography. The label, bestowed half a century after publication, reflected two major rhetorical transformations. First, (...) from a theory presented with highly general claims of infant sex abuse, assault, and trauma, the theory was repackaged as a theory of seduction. Second, from a theory reportedly based in actual, traumatic experience, followed by repressed memory, it was transformed into one of fantasy. The name "seduction theory" has therefore operated as a misleading, strategic misnomer for the theory that Freud published in 1896.Freud announced his theory in three publications, referred to here in order of publication as the Paris paper,1 the Berlin paper,2 and "The Aetiology of Hysteria," published in Vienna.3 In his final publication the emphasis on trauma was greatest. In the space of five pages in the Standard Edition of Freud's works he used the word "traumatic" or "traumatically" fifteen times.4 Although he was extending the traumatic memory theory that he had shared with Josef Breuer in 1895,5 he touted his new modification as "the discovery of a caput [End Page 647] Nili [source of the Nile] in neuropathology."6 Sixteen months later he would privately renounce it. The theory was resurrected in the 1980s as support for the recovered memory movement.7It is essential to recall that the issuance of scientific claims is quite different from scientific validation. Getting the name of a theory right more than a century after publication is one matter only; assessing the basis of its underlying claims raises yet another challenge, particularly when the theory has been transformed with such extensive variation as Freud's theory of 1896.Therefore, the early death of the theory, described only in private letters to Wilhelm Fliess, is critical to an understanding of the entire historical episode. It is essential also to note that when Freud published his retrospective revisions of the theory, he did not know that his contemporary letters to his intimate friend would become competing evidence of the actual events of the mid-1890s.8When Freud secretly abandoned his theory on 21 September 1897 he wrote to Fliess, "I no longer believe in my neurotica."9 Implied already is the fact that Freud's belief in his theory was all that had supported it. One of his retrospective comments unwittingly substantiates this fact. In 1914, in his "History of the Psycho-analytic Movement," he conceded that his theory "broke down under the weight of its own improbability."10Furthermore, abandoning a theory in secrecy with no public defense is itself tantamount to a confession that supporting evidence is missing. Freud had acknowledged the absence of supporting data in his Berlin paper when he stated, "In this kind of communication it is not possible to bring forward the evidence needful to support my assertions, but I hope to fulfill this obligation later in a detailed presentation."11 His claim that it was "not possible to bring forward the evidence" must be challenged. Presenting scientific evidence is always possible when one has it. Moreover, in his "later" paper, by far the longest of 1896, he evaded the presentation of "actual material," opting instead to discuss potential objections.12 He did not present a single case history of hysteria, arguing that this would have taken too much time; yet he had closed his Berlin paper with a case history of paranoia that was purportedly based in the female patient's "sexual relationship" with her brother during childhood.13 [End Page 648] This case is not persuasive, but it demonstrates Freud's eagerness in 1896 to share a case when he believed that he had one to share.The style of a live lecture in "The Aetiology of Hysteria," as though Freud were speaking to an audience of potential objectors, is highly misleading, even fictional. As he explained in his letters... (shrink)

This article will reveal how local scientific determination and ambition, in the face of rejection by funders, navigated a path to success and to influence in national policy and international medicine. It will demonstrate that Birmingham, England's ‘second city’, was the key centre for cutting-edge biological psychiatry in Britain in the 1920s and 1930s. The ambitions of Frederick Mott – doyen of biochemistry, neuropathology and neuropsychiatry, until now celebrated as a London figure – to revolutionize psychiatric treatment through science, (...) chimed with those of the City and University of Birmingham's Joint Board of Research for Mental Diseases. Under Mott's direction, shaped by place and inter-professional working, the board's collaborators included psychiatrist Thomas Chivers Graves and world-renowned physiologist J.S. Haldane. However, starved of external money and therefore fresh ideas, as well as oversight, the ‘groupthink’ that emerged created the classic UK focal sepsis theory which, it was widely believed, would yield a cure for mental illness – a cure that never materialized. By tracing the venture's growth, accomplishments and contemporary potential for biochemical, bacterial and therapeutic discoveries – as well as its links with scientist and key government adviser Solly Zuckerman – this article illustrates how ‘failure’ and its ahistorical assessment fundamentally obscure past importance, neglect the early promise offered by later unsuccessful science, and can even hide questionable research. (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)

Objective: Cognitive impairment is a common neurological complication in patients with end-stage renal disease undergoing maintenance hemodialysis. Brain network analysis based on graph theory is a promising tool for studying CI. Therefore, the purpose of this study was to analyze the changes of functional brain networks in patients on MHD with and without CI by using graph theory and further explore the underlying neuropathological mechanism of CI in these patients.Methods: A total of 39 patients on MHD and 25 healthy controls (...) matched for age, sex, and years of education were enrolled in the study. Resting-state functional magnetic resonance imaging and T1-weighted high-resolution anatomical data were obtained, and functional brain networks for each subject were constructed. The brain network parameters at the global and regional levels were calculated, and a one-way analysis of covariance was used to compare the differences across the three groups. The associations between the changed graph-theory parameters and cognitive function scores in patients on MHD were evaluated using Spearman correlation analysis.Results: Compared with HCs, the global parameters [sigma, gamma, and local efficiency ] in both patient groups decreased significantly. The clustering coefficient in patients with CI was significantly lower than that in the other two groups. The regional parameters were significantly lower in the right superior frontal gyrus, dorsolateral and gyrus rectus of patients with CI than those of patients without CI; however the nodal local efficiency in the left amygdala was significantly increased. The global Cp and regional parameters in the three brain regions were significantly correlated with the cognitive function scores.Conclusion: This study confirmed that the topology of the functional brain network was disrupted in patients on MHD with and without CI and the disruption of brain network was more severe in patients with CI. The abnormal brain network parameters are closely related to cognitive function in patients on MHD. (shrink)

The philosopher Byung-Chul Han affirms that the present age reduces the human being to a performance-machine, and that, because of this reduction, the type of disease that characterizes it this age is neuronal. In the present article, I argue that Han’s analysis is correct but incomplete. Behind this reductionism, which leads to neuropathologies of different types, lies another type of pathology that the philosopher Eric Voegelin calls ‘pneumopathology’—disease of the spirit. The transhumanist view of human enhancement deepens this reduction and (...) shows that the pneumopathology that blights today’s society is in a process of unprecedented chronification. To justify this thesis, I first explain the connection between human enhancement and the achievement imperative denounced by Han; I then analyze the Voegelian category of pneumopathology to show its value for an ontological-historical understanding of human enhancement. (shrink)

Is there a theory that explains the essence of consciousness? Or is consciousness itself just an illusion? The "last great mystery of science," consciousness was excluded from serious research for most of the last century but is now a rapidly expanding area of study for students of psychology, philosophy, and neuroscience. Recently the topic has also captured growing popular interest. This groundbreaking book is the first volume to bring together all the major theories of consciousness studies--from those rooted in traditional (...) Western philosophy to those coming out of neuroscience, quantum theory, and Eastern philosophy. Broadly interdisciplinary, Consciousness: An Introduction is divided into nine sections that examine such topics as how subjective experiences arise from objective brain processes, the basic neuroscience and neuropathology of consciousness, altered states of consciousness, mystical experiences and dreams, and the effects of drugs and meditation. It also discusses the nature of self, the possibility of artificial consciousness in robots, and the question of whether or not animals are conscious. Enhanced by numerous illustrations and profiles of important researchers, the book also includes self-assessment questions, further reading suggestions, and practical exercises that help bring the subject to life. (shrink)

Recently it has been hypothesized that apoptotic cell death is involved in several neuropathological conditions including Parkinson's disease (PD). Initial morphological studies assessing the presence of apoptosis in Parkinsonian brain tissues yielded mixed results. Based on more recent studies in human PD brains as well in animal and cell culture models of the disease, a picture is emerging, however, that strongly suggests that many of the molecular players thought to participate in this type of neuronal cell death are active in (...) the disease. The task of researchers in the field is now to deduce how these players may be interacting with one another to bring about cell death in PD and to design effective therapies to interfere with these processes. BioEssays 23:640–646, 2001. © 2001 John Wiley & Sons, Inc. (shrink)

As individuals enter their 80s, they are inevitably confronted with the problem of neuronal loss in the brain. The incidence of the common movement disorder ‘mild parkinsonian signs’ (MPS) is approximately 50% over the age of 85 years. It has long been known that the loss of dopaminergic neurons in the substantia nigra pars compacta is a neuropathological hallmark of Parkinson's disease (PD). Recently, two papers1,2 present clear evidence for a high burden of mitochondrial DNA deletions within substantia nigra neurons (...) in aged individuals and individuals with PD, pointing towards a common pathway inevitably leading to neuronal dysfunction and death. BioEssays 28: 963–967, 2006. © 2006 Wiley Periodicals, Inc. (shrink)

Sigmund Freud was an Austrian neurologist and the founder of psychoanalysis, a clinical method for treating psychopathology through dialogue between a patient and a psychoanalyst. Freud was born to Galician Jewish parents in the Moravian town of Freiberg, in the Austro-Hungarian Empire. He qualified as a doctor of medicine in 1881 at the University of Vienna. Upon completing his habilitation in 1885, he was appointed a docent in neuropathology and became an affiliated professor in 1902. Freud lived and worked (...) in Vienna, having set up his clinical practice there in 1886. In 1938 Freud left Austria to escape the Nazis. He died in exile in the United Kingdom in 1939. (shrink)

In lieu of an abstract, here is a brief excerpt of the content:Ethics CommentaryTamra Lysaght, Senior Research FellowThe case scenario reflects the dilemmas frequently faced by researchers who discover incidental findings in the course of their studies. Indeed, the literature suggests that the prevalence of incidental findings in neuroimaging research is common,1 and a recent meta-analysis found that such findings increase significantly with age.2 Thus, given the age of the study population and increased likelihood of co-morbidities, it is puzzling that (...) the research team did not anticipate the possibility of finding an anomaly. Even more puzzling is that the reviewing IRB did not detect this omission and require that the team build a plan into the research protocol for managing incidental findings. Following international recommendations,3 such a plan would have likely included protocols for obtaining consent in dealing with an incidental finding, a procedure for evaluating the clinical relevance of the finding, and arranging for suitable follow-up care if necessary.Nevertheless, the research team, not having obtained consent to disclose an incidental finding to the participant, or not, must decide whether to break protocol and contact the participant with information that could have serious health implications for his or her health, especially if the observed lesion turns out to be cancer or some other life-threatening neuropathology. Any decision to break the research protocol should be made in consultation with the approving IRB. The principal investigator, Dr. M, who is ultimately responsible for the ethical conduct of this study, has a number of factors to consider when making this decision. First and foremost, Dr. M will need to weigh up the risks and benefits of disclosing the findings to this 72-year-old [End Page 283] research participant who is presumably already experiencing cognitive impairments, if not early stage symptoms of dementia.Numerous international scholars agree that disclosure of incidental findings should rely on the net beneficence to an individual research participant.4 Specifically, Wolf et al. argue that there should be a strong net benefit for disclosing an incidental finding, such that the information reveals a condition that is likely to be either life-threatening or grave and can be avoided or ameliorated through an intervention. In such instances, the researchers have an ethical obligation to disclose the findings and potentially follow up with clinical care. However, if there is only a net possible benefit, such that the condition is not life-threatening but may be grave or serious and cannot be avoided or ameliorated, then investigators may consider other factors, such as the respect that is owed to research participants and their needs and preferences for information about their health and well-being. Where the condition is not likely to be serious, researchers are not compelled to disclose an incidental finding.In determining the seriousness of an incidental finding, a specialist with expertise in assessing the clinical significance of MRI scans is needed to examine the participants’ images.5 In this instance, Dr. M has a neurologist on the research team who has detected the lesion but is unable to ascertain its clinical relevance without further investigation. The reasons why follow-up information is required is not detailed in the case scenario, but may have arisen because the scans were taken for research purposes and may not be clinically validated for diagnostic purposes — a possibility given the aims of the study (i.e., to elucidate the transition of minimal cognitive impairment to dementia, not brain tumours). For whatever reason, the detected lesion is only a suspected incidental finding that may or may not be life-threatening or grave. Thus, the net benefit to the participant in disclosing this unclear finding is harder to judge.Assuming that the lesion is a serious or life-threatening condition, the team may consider whether it can be avoided or ameliorated with an intervention. The cognitively impaired, although still mentally competent, participant is 72 years old and may respond poorly to a neurosurgical intervention if the diagnosis of a tumour or malignancy is confirmed. The physical and emotional distress of such a procedure may exacerbate the existing cognitive impairments, reducing the net benefit ratio of the disclosure. Indeed, the team should consider the impact that the disclosure... (shrink)

Georg Northoff encounters a problem regarding the logical status of “catatonia.” Whereas Parkinson's disease (PD) is a disease on the basis of Virchowian criteria, catatonia is not. PD is associated with pathognomonic neurological lesions. Catatonia does not require any such association. The diagnosis is rendered using social criteria rather than neuropathological ones. Therefore, Northoff is not comparing two disease states at all.

Between James Parkinson's 'shaking palsy' and the first report of the post-encephalitic manifestation — initially not recognizable as a complication of that incipient 'Spanish flu' epidemic — it took over a hundred years to arrive at a clear appreciation and differentiation of its most disabling feature: rigidity. This paper traces the development, step by hesitant or bold step, of the pertinent ideas and terms regarding muscle tone before and after Parkinson, their basis in neuropathological advances as they were made for (...) related syndromes of basal ganglia disorders, toward the eventual clinical correlation. Chief credits, after Sauvages, must go to Charcot for emphasizing the increase in muscle tone, and to Kinnier Wilson for establishing the extrapyramidal connection. (shrink)

Introduction: Cotard delusion—the delusional belief “I am dead”—is named after the French psychiatrist who first described it: Jules Cotard (1880, 1882). Ramachandran and Blakeslee (1998) proposed that the idea “I am dead” comes to mind when a neuropathological condition has resulted in complete abolition of emotional responsivity to the world. The idea would arise as a putative explanation: if “I am dead” were true, there would be no emotional responsivity to the world. Methods: We scrutinised the literature on people who (...) expressed the delusional belief “I am dead”, looking for data on whether such patients are reported as entirely lacking in emotional responsivity. Results: In numerous cases, patients with Cotard delusion are described as experiencing emotions including anxiety, fear, guilt, distress, euphoria and worry. Conclusions: We conclude that complete absence of emotional responsivity cannot be what prompts the delusional idea that one is dead. We propose that, in at least some cases, the idea “I am dead” comes to mind in response to symptoms of depersonalisation or derealisation, often present in cases of Cotard delusion, and give examples of Cotard patients with abnormalities in various neural areas that could be responsible for the presence of such symptoms. (shrink)

Progressive supranuclear palsy is a movement disorder with prominent tau neuropathology. Brain diseases with abnormal tau deposits are called tauopathies, the most common of which is Alzheimer's disease. Environmental causes of tauopathies include repetitive head trauma associated with some sports. To identify common genetic variation contributing to risk for tauopathies, we carried out a genome-wide association study of 1,114 individuals with PSP and 3,247 controls followed by a second stage in which we genotyped 1,051 cases and 3,560 controls for (...) the stage 1 SNPs that yielded P ≤ 10-3. We found significant previously unidentified signals associated with PSP risk at STX6, EIF2AK3 and MOBP. We confirmed two independent variants in MAPT affecting risk for PSP, one of which influences MAPT brain expression. The genes implicated encode proteins for vesicle-membrane fusion at the Golgi-endosomal interface, for the endoplasmic reticulum unfolded protein response and for a myelin structural component. © 2011 Nature America, Inc. All rights reserved. (shrink)

After the unexpected death of Professor Józef Kałuża at the age of 74 on the 26th of July 2003, not only Polish neuropathology but also Polish philosophy of medical investigations lost one of its most renowned minds. Beginning in 1949, Professor Kałuża studied medical sciences for five years at the Medical Faculty of the Jagiellonian University in Cracow. He did his Ph.D. thesis in neuropathology in the Department of Neuropathology of the Polish Academy of Science. In 1962 (...) he received a Rockefeller Foundation scholarship and spent one year at the National Institutes of Health. In 1981 Professor Kaluza was promoted to a tenured professorship in neuropathology. He is the author of more than 110 articles published in medical periodicals and coauthor of many chapters in medical handbooks. (shrink)

The article explores conceptual, intentional, and emotional dimensions of art , drawing on ideas from process theory , clinical neuropathology and phenomenology. The interdependence of emotion and perception are outlined, with emphasis on the more general role of knowledge in guiding perception.