Given the resurgence of scientific studies on the etiology of homosexuality in the wake of the AIDS epidemic, this article considers the effects these studies had on contemporaneous queer filmmakers. By using the subject of criminality as a way to talk about homosexual causality, queer films of the 1990s illustrate that contemporary scientific studies on homosexuality were historically and politically situated in relation to cultural anxieties about other forms of deviance. This article focuses on films that dissect the hetero-normative (...) tendency to amalgamate forms of deviance in order to distinguish between the diseased and the healthy. Such products of New Queer Cinema highlight this amalgamation of criminality and homosexuality in order to challenge demands by the LGBT community of the 1980s and 1990s for “more positive images” in film. This article argues that queer filmmakers have manipulated the image of the queer criminal to usurp the medical tendency to biologize and pathologize the notion of queer transgression. In such a way, queer films that enthusiastically dramatize the queer outlaw perpetuate myths about homosexuality in order to dissect and discredit them. (shrink)
Cummins (1982) argues that etiological considerations are not onlyinsufficient butirrelevant for the determination offunction. I argue that his claim of irrelevance rests on a misrepresentation of the use of functions in evolutionary explanations. I go on to suggest how accepting anetiological constraint on functional analysis might help resolve some problems involving the use of functional explanations.
It can be shown that considerable common ground exists between indigenous or traditional theories of contagious disease in Africa, and modern medicine, whether human or veterinary. Yet this is not recognized because of the generally low regard in which the medically trained – whether African or expatriate – hold African traditional medicine. This attitude seems to result from the assumption that African health beliefs are based on witchcraft and related “supernatural” thinking. I argue that this may not be so in (...) the important domain of diseases biomedically classified as contagious; such diseases tend to be understood naturalistically. An accurate understanding of how Africans traditionally interpret contagious diseases of humans and livestock is the foundation for the design and implementation of more effective health programs. (shrink)
In this paper I offer a theory of what makes certain influences on visual experiences by prior mental states (including desires, beliefs, moods, and fears) reduce the justificatory force of those experiences. The main idea is that experiences, like beliefs, can have rationally assessable etiologies, and when those etiologies are irrational, the experiences are epistemically downgraded.
Formulations of the essential commitment of the etiological theory of functions have varied significantly, with some individual authors' formulations even varying from one place to another. The logical geography of these various formulations is different from what is standardly assumed; for they are not stylistic variants of the same essential commitment, but stylistic variants of two non-equivalent versions of the etiological theory. I distinguish these “strong” and “weak” versions of the etiological theory (which differ with respect to the role of (...) selection in their definitions of function), draw out their respective implications, and argue that the weak version is to be preferred to the strong. (shrink)
The aim of teleosemantics is to give a scientifically respectable, or ‘naturalistic’ theory of mental content. In the debates surrounding the scope and merits of teleosemantics a lot has been said about the concept of indication (or carrying information). The aim of this paper is to focus on the other key concept of teleosemantics: biological function. It has been universally accepted in the teleosemantics literature that the account of biological function one should use to flesh out teleosemantics is that of (...) etiological function. My claim is that if we replace this concept of function with an alternative one (that we have independent reasons to accept) and if we also restrict the scope of teleosemantics, we can arrive at an account of biologizing mental content that is much less problematic than the previous attempts. (shrink)
In 1905 two different etiologic agents for syphilis were proposed in Berlin, one, the Cytorrhyctes luis, by John Siegel, the other, Spirochaete pallida, by Fritz Schaudinn. Both scientists were pupils of Franz Eilhard Schulze, and were outsiders to the Berlin medical establishment. Both belonged to the same thought collective, used the same thought style, and started from the same supposition that the etiologic agent of syphilis must be a protist. Both used the same morphological approach, the same microscopes and the (...) same stains. Both presented their findings in the same societies, used the same rhetoric, published in the same journals, used the same arguments to criticise each other's shortcomings. Both were backed by powerful institutions and enlisted the support of prestigious patrons. Within half a year, the scientific community at large had in its overwhelming majority accepted Schaudinn's results and rejected those of Siegel. Social forces thus cannot be shown to have played any role in deciding the issue. Ludwik Fleck's suggestion that 'appropriate influence' and a 'proper measure of publicity throughout the thought collective' would have been sufficient for Siegel's ideas to win the day is untenable. (shrink)
This article elaborates on Putnam's ''discrete behavioral states'' model of dissociative identity disorder (Putnam, 1997) by proposing the involvement of the orbitalfrontal cortex in the development of DID and suggesting a potential neurodevelopmental mechanism responsible for the development of multiple representations of self. The proposed ''orbitalfrontal'' model integrates and elaborates on theory and research from four domains: the neurobiology of the orbitalfrontal cortex and its protective inhibitory role in the temporal organization of behavior, the development of emotion regulation, the development (...) of the self, and experience-dependent reorganizing neocortical processes. The hypothesis being proposed is that the experience-dependent maturation of the orbitalfrontal cortex in early abusive environments, characterized by discontinuity in dyadic socioaffective interactions between the infant and the caregiver, may be responsible for a pattern of lateral inhibition between conflicting subsets of self-representations which are normally integrated into a unified self. The basic idea is that the discontinuity in the early caretaking environment is manifested in the discontinuity in the organization of the developing child's self. (shrink)
The doctrine of agent-causation has been suggested by many interested in defending libertarian theories of free action to provide the conceptual apparatus necessary to make the notion of incompatibility freedom intelligible. In the present essay the conceptual viability of the doctrine of agent-causation will be assessed. It will be argued that agent-causation is, insofar as it is irreducible to event-causation, mysterious at best, totally unintelligible at worst. First, the arguments for agent-causation made by such eighteenth-century luminaries as Samuel Clarke and (...) Thomas Reid will be considered alongside the defenses of agent-causation proffered in this century by C.A. Campbell, Roderick Chisholm, and Richard Taylor. It will be shown that the case for agent-causation made by these figures is ultimately unconvincing. Two defenses of agent-causation made within the past ten years will then be taken up for examination and critique. First, Timothy O'Connor's attempt at advancing an unrefined and unrepentant doctrine of agent-causation will be shown to suffer from the same maladies as its predecessors. Next, Randolph Clarke's causal agent-causal theory of free action, which seeks a via media between agent-causal theories of free action and causal theories of action, is examined. Clarke's theory is an attempt at providing an account of how both events and agents qua substances can be the codeterminants of free actions. Despite the improvement of Clarke's theory over more conventional agent-causal theories of free action, it will be shown that agent-causation makes his theory more cumbersome than it needs to be. Clarke is able to get as much mileage out of a causal indeterminacy theory of action that does not require him to posit obscure agent-causes. Finally, a sketch of an alternative theory of free action will be offered. While it may suffer from its own conceptual deficiencies, it may not suffer from the same conceptual problems as agent-causal theories of free action. (shrink)
My aim in this paper is two?fold. I start by contrasting three versions of externalist arguments based on etiological considerations, whose differences are not often appreciated. My purpose in doing so is to isolate one of these versions of externalism as most supportive of current anti?individualist attitudes toward the mental. My second aim is to show that this version, which I call (for reasons soon to be clear) Dialectal Etiology , is marred to a greater extent than the other (...) two by an important problem of language individuation.ii.. (shrink)
Examining the language and paradigms of science as rhetorical, that is, arising from the sociocultural forces that shape ideology, reveals androcentric assumptions that tend to thwart democratic public policy as well as effective methodology. This paper applies some recent feminist critiques of the biological sciences to the current research on the possible hormonal and genetic factors contributing to homosexuality, clarifying how this research perpetuates hierarchical binaries and suggesting ways to reconceptualize human sexuality through revised research protocols.
Phillips & Silverstein (P&S, 2003) propose that NMDA-receptor dysfunction may be the fundamental neurobiological mechanism underlying and associating impaired holistic perception and cognitive coordination with schizophrenic psychopathology. We discuss how the P&S hypothesis shares different aspects of the weak central coherence account of autism from both theoretical and experimental perspectives. Specifically, we believe that neither those persons with autism nor those with schizophrenia integrate visuo-perceptual information efficiently, resulting in incongruous internal representations of their external world. However, although NMDA-hypofunction may be (...) responsible for perceptual impairments in schizophrenia and possibly autism, we suggest that it is highly unlikely that NMDA-hypofunction is specifically responsible for the autistic behavioral symptomology, as described by P&S in their target article. (shrink)
In one approach to classifying island phenomena, there is a group that answers to the following description. (1) ADJUNCT ISLAND CONDITION If an XP is in an adjunct position, nothing may move out of it. In the inﬂuential approach to this condition in Huang (1982), “adjunct” position is deﬁned in terms that reference argument structure and its reﬂection in phrasemarker geometry. This deﬁnition groups together subject phrases and modifying phrases, contrasting them with phrases in “complement” position. The subsequent bounding theories (...) in Lasnik and Saito (1984, 1992) and Chomsky (1986) build on this basic idea, but attempt to spread it to a wide variety of island effects, including those characterized by early versions of Chomsky’s Subjacency condition. Central to their approaches is the notion of “lexical governor,” which is responsible for making the complement/non-complement cut — only phrases that are governed by a suitably lexical Xo are “complements,” and the island conditions are deﬁned, then, over all the others. This part of the system has fallen into disuse partly, I suspect, because characterizing the “lexical” versus “non-lexical” distinction never found itself grounded in something more general, and partly because it became unwieldy in the increasing richness of post-Pollock representations of phrase-markers. This paper adopts the view that there is an island condition like that in (1), which groups together subjects and adjuncts, but it does not attempt to deﬁne these phrases on the basis of a “lexical governor.” Instead, let us adopt a characterization of “adjunct” that is wholly geometric: (2) An adjunct is a phrase whose sister is also a phrase and whose mother is not its projection. This will put together “subject” phrases and modiﬁer phrases under the standard assumption that these are both necessarily sisters to phrases rather than heads. Thus it will single out the boxed phrases in (3). (shrink)
Both accessible and definitive, Deleuze and Guattari provides a critical examination of the writing of two notoriously difficult thinkers. This important introduction is divided into three sections--knowledge, power, and desire--and provides a systematic account of the intellectual context as well as an exhaustive analysis of the key themes informing Deleuze and Guattari's work. Providing a framework for reading the important and influential study Capitalism and Schizophrenia, this volume is attentive to the needs of the student by providing a lexicon of (...) the difficult ideas used in Deleuze and Guattari's discussion of philosophy, art, and politics. Deleuze and Guattari is an important addition to the critical literature on some of the most challenging work in recent social theory. It will be the standard introduction to Deleuze and Guattari for students of philosophy and social theory. (shrink)
The paper treats several ontological questions about certain nineteenth-century and contemporary medical and scientific conceptualizations of hereditary relation. In particular, it considers the account of mid-nineteenth century psychiatric thought given by Foucault in Psychiatric Power: Lectures at the Collège de France, 1973–1974 and Abnormal: Lectures at the Collège de France, 1974–1975 . There, Foucault argues that a fantastical conceptual prop, the ‘metabody,’ as he terms it, was implicitly supposed by that period’s psychiatric medicine as a putative ground for psychiatric pathology. (...) After presenting the heart of Foucault’s thought on the ‘metabody,’ the paper investigates the possibility that a contemporary version of a ‘metabody’ may operate today as a conceptual analog of the nineteenth-century psychiatric theory and practice that Foucault began to expose in the texts examined here. It speculates that we might identify a contemporary genetic version of a ‘metabody’ in a particular current conception of the gene as replicator, an item marked by an ambiguous temporal ontology. (shrink)
One common method of criticizing genetically modified organisms (GMOs) is to label them as “magic bullets.” However, this criticism, like many in the debate over GMOs, is not very clear. What exactly is the “magic bullet criticism”? What are its origins? What flaw is it pointing out in GM crops and agricultural biotechnology? What is the scope of the criticism? Does it apply to all GMOs, or just some? Does it point to a fatal flaw, or something that can be (...) fixed? The goal of this paper is to answer these questions and clarify the magic bullet criticism of agricultural biotechnology. It is hoped that the results of this exercise will be helpful in advancing deliberation over the role GMOs and agricultural biotechnology should play in 21st century agriculture. (shrink)
Introduction : the times they are a changin' -- Doing their best -- Values, evidence, conflict -- What counts as evidence? -- The miracle drug -- The battle for acceptance : defining the relationship between medicine and the world of madness and distress -- The ring -- Foregrounding contexts : what kinds of understanding are appropriate in the world of mental illness? -- Losing Peter -- Mind, language, and meaning -- Beetles -- Ethics before technology : is 'treatment' the best (...) way to think about mental health work? -- Narrative and the ethics of representation -- Meaning and recovery -- Citizenship and the politics of identity -- Are you local? : responding to the challenge of globalization in mental health -- The veil. (shrink)
Maladapting Minds discusses a number of reasons why philosophers of psychiatry should take an interest in evolutionary explanations of mental disorders and, more generally, in evolutionary thinking. First of all, there is the nascent field of evolutionary psychiatry. Unlike other psychiatrists, evolutionary psychiatrists engage with ultimate, rather than proximate, questions about mental illnesses. Being a young and youthful new discipline, evolutionary psychiatry allows for a nice case study in the philosophy of science. Secondly, philosophers of psychiatry have engaged with evolutionary (...) theory because evolutionary considerations are often said to play a role in defining the concept of mental disorder. The basic question here is: Can the concept of mental disorder be given an objective definition, or is it rather a normative concept? Thirdly and finally, evolutionary thinking in psychiatry has often been a source of inspiration for a philosophical view on human nature. Thus evolutionary psychiatrists have suggested, for example, that man's vulnerability to mental disorders may well be one of the defining features of our species. -/- Written by leading authors in philosophy, psychiatry, biology and psychology, this volume illustrates that many debates in contemporary philosophy of psychiatry are profoundly influenced by evolutionary approaches to mental disorders. Conversely, it also reveals how philosophers can help contribute to the burgeoning field of evolutionary psychiatry. It is important reading for a wide range of readers interested in mental health care and philosophy. (shrink)
Philosophical ideas about the mind, brain, and behavior can seem theoretical and unimportant when placed alongside the urgent questions of mental distress and disorder. However, there is a need to give direction to attempts to answer these questions. On the one hand, a substantial research effort is going into the investigation of brain processes and the development of drug treatments for psychiatric disorders, and on the other, a wide range of psychotherapies is becoming available to adults and children with mental (...) health problems. These two strands reflect traditional distinctions between mind and body, and causal as opposed to meaningful explanations of behavior. In this book, which has been written for psychiatrists, psychologists, philosophers, and others in related fields, the authors propose a radical re-interpretation of these traditional distinctions. Throughout the discussions philosophical theories are brought to bear on the particular questions of the explanation of behaviors, the nature of mental causation, and eventually the origins of major disorders including depression, anxiety disorders, schizophrenia, and personality disorder. (shrink)
This book is psychiatry's reply to the diverse group of antipsychiatrists, including Laing, Foucault, Goffman, Szasz and Bassaglia, that has made fashionable the view that mental illness is merely socially deviant behaviour and that psychiatrists are agents of the capitalist society seeking to repress such behaviour. It establishes, by the use of evidence from historical and transcultural studies, that mental illness has been recognised in all cultures since the beginning of history and goes on to explore the philosophical and medical (...) basis for psychiatry's diagnosis and treatment of mental illness. Finally, it tackles two issues where psychiatry has recently been seen as at odds with the values prevailing in society: involuntary hospitalization and the insanity defence. The Reality of Mental Illness does not pretend to offer simple answers to the complex problems it discusses, but will leave the reader with a much greater understanding of psychiatry's aims, practices and problems. (shrink)
Celebrated for disproving the traditional view that lack of oxygen at birth (perinatal asphyxia) contributes significantly to cerebral palsy, a 1986 New England Journal of Medicine article by Karin Nelson and Jonas Ellenberg engineered a new consensus in the medical community: that lack of oxygen at birth rarely causes cerebral palsy. We demonstrate that the article's central argument relies on straightforwardly fallacious statistical reasoning, and we discuss significant implications -- e.g. how carefully fetuses are monitored during labor and delivery, expert (...) testimony in malpractice cases, and public policy decisions. (shrink)
The aim of this paper is to evaluate etiological accounts of functions for the domain of technical artefacts. Etiological theories ascribe functions to items on the basis of the causal histories of those items; they apply relatively straightforwardly to the biological domain, in which neo-Darwinian evolutionary theory provides a well-developed and generally accepted background for describing the causal histories of biological items. Yet there is no well-developed and generally accepted theory for describing the causal history of artefacts, so the application (...) of etiological theories to the technical domain is hardly straightforward. In this paper we consider the transposition of etiological theories in general from the biological to the technical domain. We argue that a number of etiological theories that appear defensible for biology become untenable for technology. We illustrate our argument by showing that the standard etiological accounts of Neander and Millikan, and some recent attempts to improve on them, provide examples of such untenable theories. 1 Introduction 2 Desiderata for theories of functions 3 Etiological theories in general 3.1 Common core and divergent aims 3.2 Reproduction versus non-reproduction etiological theories 3.3 Intentionalist versus non-intentionalist etiological theories 4 Problems for etiological theories in the technical domain 5 The failure of existing reproduction theories 6 The failure of existing non-reproduction theories 7 Improving reproduction by hybridisation 8 Conclusions. (shrink)
It is a plain fact that biology makes use of terms and expressions commonly spoken of as teleological. Biologists frequently speak of the function of biological items. They may also say that traits are 'supposed to' perform some of their effects, claim that traits are 'for' specific effects, or that organisms have particular traits 'in order to' engage in specific interactions. There is general agreement that there must be something useful about this linguistic practice but it is controversial whether it (...) is entirely appropriate, and if so why it is.Many theorists have defended the use of seemingly teleological terms by appeal to an etiological notion of function (Wright, 1973; Millikan, 1984, 2002; Neander, 1991; .. (shrink)
Millikan's account of how we acquire our most basic concepts might be clarified by a better ontological taxonomy, especially one that distinguishes between natural kinds on the one hand and wholes composed of parts on the other. The two have a different causal basis, which is important because once classification goes beyond the stage of naive induction, it becomes fundamentally etiological.
This paper examines Nietzsche’s concept of unified agency. A widespread consensus has emerged in the secondary literature on three points: (1) Nietzsche’s notion of unity is meant to be an analysis of freedom; (2) unity refers to a relation between the agent’s drives or motivational states; and (3) unity obtains when one drive predominates and imposes order on the other drives. I argue that these claims are philosophically and textually indefensible. In contrast, I argue that (1′) Nietzschean unity is an (...) account of the distinction between genuine actions and mere behaviors, rather than between free and unfree actions; (2′) unity refers to a relation between drives and conscious thought; and (3′) unity obtains when the agent’s attitude toward her own action is stable under the revelation of further information about the action’s etiology. I show that Nietzsche develops this notion of unity by drawing on Plato’s and Schiller’s accounts of unified agency. (shrink)
So-called evolutionary error theorists, such as Michael Ruse and Richard Joyce, have argued that naturalistic accounts of the moral sentiments lead us to adopt an error theory approach to morality. Roughly, the argument is that an appreciation of the etiology of those sentiments undermines any reason to think that they track moral truth and, furthermore, undermines any reason to think that moral truth actually exists. I argue that this approach offers us a false dichotomy between error theory and some (...) form of moral realism. While accepting the presuppositions of the evolutionary error theorist, I argue that contract-based approaches to morality can be sensitive to those presuppositions while still vindicating morality. Invoking Stephen Darwall’s distinction between contractualism and contractarianism, I go on to offer an evolutionary-based contractarianism. (shrink)
We focus on the recent non-causal theory of reasons explanationsof free action proffered by a proponent of the agency theory, Timothy O'Connor. We argue that the conditions O'Connor offersare neither necessary nor sufficient for a person to act for a reason. Finally, we note that the role O'Connor assigns toreasons in the etiology of actions results in further conceptual difficulties for agent-causalism.
Many philosophers invoke the "wisdom of nature" in arguing for varying degrees of caution in the development and use of genetic enhancement technologies. Because they view natural selection as akin to a master engineer that creates functionally and morally optimal design, these authors tend to regard genetic intervention with suspicion. In Part II, we examine and ultimately reject the evolutionary assumptions that underlie the master engineer analogy (MEA). By highlighting the constraints on ordinary unassisted evolution, we show how intentional genetic (...) modification can overcome many of the natural impediments to the human good. Our contention is that genetic engineering offers a solution that is more eff icient, reliable, versatile, and morally palatable than the lumbering juggernaut of Darwinian evolution. In Part III, we evaluate a recent attempt to ground precautionary enhancement heuristics in adaptive etiology. Our problem with this approach is two-fold: first, it is based on the same "strong adaptationist" interpretation of evolution that motivates the flawed MEA, and second, the etiological concept of function on which it relies provides indirect and potentially misleading information about the likely consequences of genetic intervention. We offer instead enhancement criteria based on causal relationships in ontogeny. We conclude that rather than grounding a presumption against deliberate genetic modification, the causal structure of the living world gives us good moral reason to pursue it. (shrink)
Evolutionary biology – or, more precisely, two (purported) applications of Darwin's theory of evolution by natural selection, namely, evolutionary psychology and what has been called human behavioral biology – is on the cusp of becoming the new rage among legal scholars looking for interdisciplinary insights into the law. We argue that as the actual science stands today, evolutionary biology offers nothing to help with questions about legal regulation of behavior. Only systematic misrepresentations or lack of understanding of the relevant biology, (...) together with far-reaching analytical and philosophical confusions, have led anyone to think otherwise. Evolutionary accounts are etiological accounts of how a trait evolved. We argue that an account of causal etiology could be relevant to law if (1) the account of causal etiology is scientifically well-confirmed, and (2) there is an explanation of how the well-confirmed etiology bears on questions of development (what we call the Environmental Gap Objection). We then show that the accounts of causal etiology that might be relevant are not remotely well-confirmed by scientific standards. We argue, in particular, that (a) evolutionary psychology is not entitled to assume selectionist accounts of human behaviors, (b) the assumptions necessary for the selectionist accounts to be true are not warranted by standard criteria for theory choice, and (c) only confusions about levels of explanation of human behavior create the appearance that understanding the biology of behavior is important. We also note that no response to the Environmental Gap Objection has been proffered. In the concluding section of the article, we turn directly to the work of Owen Jones, a leading proponent of the relevance of evolutionary biology to law, and show that he does not come to terms with any of the fundamental problems identified in this article. (shrink)
Many writers claim that human kinds are significantly different from biological and natural kinds. Some suggest that humans kinds are unique because social structures are essential for the etiology of human kinds. Others argue that human cultural evolution is decidedly different from other forms of evolution. In this paper I suggest that the gulf between humans and our biological relatives is not as wide as some argue. There is a taxonomic difference between human and nonhuman organisms, but such factors (...) as social structure and cultural evolution do not distinguish us from many other organisms. (shrink)
ABSTRACT: Simon Baron-Cohen has argued that autism and related developmental disorders (sometimes called “autism spectrum conditions” or “autism spectrum disorders”) can be usefully thought of as the condition of possessing an “extreme male brain.” The impetus for regarding autism spectrum disorders (ASD) this way has been the accepted science regarding the etiology of autism, as developed over that past several decades. Three important features of this etiology ground the Extreme Male Brain theory. First, ASD is disproportionately male (approximately (...) 10:1 in the case of Asperger’s Syndrome or high-functioning autism (HFA) and approximately 4:1 in the case of autistic disorder). Second, ASD is not psychogenic but biological in origin, and hence is not the product of sexist conditioning or childrearing practices, although these may affect the development of the disorder. Third, ASD is regarded as a spectrum developmental disorder, unlike other disorders such as Down Syndrome that are diagnosed by a (nearly) binary criterion. Down Syndrome, for example, is diagnosed by the presence in all or most cells within a given individual of an extra copy of Chromosome 21. Autism, on the other hand, is diagnosed by the presence of a set of symptoms that vary in their intensity and in their milder forms seem to conform to purported sex differences in cognitive, emotional, and social functioning. -/- In this paper, I do not challenge accepted science regarding the etiology of autism, and I do not challenge the idea of ASD as a disorder. Nor do I wish to offer an alternative account of what autism is. Instead, I focus on the usefulness of thinking of a disorder as an extreme version of ordinary sex differences. Does it follow from the fact that a disorder is more often found in men that we should think of it as an extreme form of maleness? If not, what other conditions must be met in order to warrant this way of thinking about ASD? What does it mean to say that ASD is a form of “extreme male brain”? Feminists are rightly skeptical of theories that make claims about male and female brains, so how should we respond to the clear evidence that the differences between typical and ASD individuals are not caused by childrearing practices? I explain what I take to be Baron-Cohen’s central argument that autism should be seen as the extreme male brain, and critique that argument. I conclude that there is no good argument that autistic symptoms should be regarded as an extreme form of male mental traits, and that Baron-Cohen’s claim does not help us to understand autism, women, or men. His claim is a speculative thesis that is readily mobilized for sexist practices. As such it requires a higher threshold for evidentiary support and rigorous argumentation—support and argumentation that does not exist. -/- KEYWORDS: autism, brain, gender, neuroscience, feminism, male . (shrink)
Background: Differential diagnosis between ischemic (IDCM) and the nonischemic type (NIDCM) of cardiomyopathy constitutes a challenge in the daily medical practice. Carotid and aortic elastic properties deteriorate in patients with coronary artery disease. However, their predictive role in differentiating IDCM from NIDCM has not been addressed so far. Aim of the work: To examine carotid and aortic mechanical functions using conventional and Doppler tissue echocardiography in the distinction between IDCM and NIDCM in patients with clinically undetermined etiology. Methods: 70 (...) patients with dilatation and diffuse impairment of the left ventricular (LV) contraction were studied. All patients underwent carotid duplex for measuring intima-media (IMT) thickness, peak systolic velocity (PSV), and luminal diameters (LD). Aortic distensibility, strain, and aortic wall velocities (systolic (Sa), early diastolic (Ea), late diastolic (Aa) velocities, Sat, and Eat) were measured. According to coronary angiographic results, patients were categorized into IDCM (n = 36) (age 57.9 9.2 years) and NIDCM groups (n = 34) (age 56.0 8.3 years); they were compared to 30 age- and sex-matched healthy individuals as a control group. Results: The aortic pulsatile change, aortic strain, and distensibility were significantly reduced in both patient groups in comparison to control (P 0.8 mm predicted IDCM with 94.4%, 72.7%, and 97.2% sensitivity and 88.2%, 85.3%, and 97.1% specificity, respectively. Conclusion: Both carotid and aortic mechanical functions are more deteriorated in ischemic compared with nonischemic dilated cardiomyopathy. Different functional and structural mechanisms might be responsible for the deterioration of arterial elastic properties in each category. 2009, Wiley Periodicals, Inc. (shrink)