The Evolving Classification of Dementia

Cult Med Psychiatry (2011) 35:417–435 DOI 10.1007/s11013-011-9219-x

OPINION

The Evolving Classiﬁcation of Dementia: Placing the DSM-V in a Meaningful Historical and Cultural Context and Pondering the Future of ‘‘Alzheimer’s’’

Daniel R. George • Peter J. Whitehouse • Jesse Ballenger

Published online: 19 May 2011 Ó Springer Science+Business Media, LLC 2011

Abstract Alzheimer’s disease is a 100-year-old concept. As a diagnostic label, it has evolved over the 20th and 21st centuries from a rare diagnosis in younger patients to a worldwide epidemic common in the elderly, said to affect over 35 million people worldwide. In this opinion piece, we use a constructivist approach to review the early history of the terms ‘‘Alzheimer’s disease’’ and related concepts such as dementia, as well as the more recent nosological changes that have occurred in the four major editions of the Diagnostic and Statistical Manual since 1952. A critical engagement of the history of Alzheimer’s disease and dementia, speciﬁcally the evolution of those concepts in the DSM over the past 100 years, raises a number of questions about how those labels and emergent diagnoses, such as Neurocog- nitive Disorders and Mild Cognitive Impairment, might continue to evolve in the DSM-V, due for release in 2013.

Keywords Alzheimer’s disease Á Dementia Á Diagnostic and Statistical Manual Á Constructivism Á Brain aging

D. R. George (&) Department of Humanities, Penn State College of Medicine, 500 University Drive, Hershey, PA 17033, USA e-mail: [email protected]

P. J. Whitehouse Department of Neurology, Case Western Reserve University, University Hospital Systems, 10900 Euclid Avenue, Cleveland, OH 44106, USA

J. Ballenger Department of Science, Technology and Society, Penn State University, 201 Old Main, State College, PA 16802, USA 123 418 Cult Med Psychiatry (2011) 35:417–435

Introduction

A century ago, Alzheimer’s disease (AD) was formally established as a distinct nosology in an influential German psychiatry textbook. Since then, the concept has undergone various permutations, and its ongoing evolution carries important implications for the clinical treatment and cultural placement of persons who are given the diagnosis (Herskovits 1995; Whitehouse et al. 2000; George 2010). Today, AD is said to affect 35.6 million people worldwide and 5.3 million people in the United States (Prince and Jackson 2009). By 2040, AD is predicted to affect over 80 million people worldwide, 70% of whom will reside in developing countries (Essink-Bot et al. 2002). Alzheimer’s afflicts the genders differently with more women than men being affected (Barnes et al. 2005) and serving as careers for others with the condition (Alzheimer’s Association and National Alliance for Caregiving 2004). A recent meta-analysis (Plassman et al. 2010) of existing data has failed to identify a singular causal or preventive pathway for a condition that emergently appears to be heterogeneous and age related (Whitehouse and George 2008). Such findings cast doubt on the dominant Western biomedical model of AD, which regards the condition as singular and unrelated to aging (Richards and Brayne 2010). This opinion piece provides a general constructivist overview of the multifaceted historical, social and cultural processes through which severe brain aging has been shaped into an internationally known disease category called ‘‘Alzheimer’s disease’’ over the last 100 years, particularly over the past four decades. Constructivism emphasizes the culture, history, meaning and constructed nature of medical phenomena (Gaines 1992a, b) and informs the processual framework for this analysis that views disease development as an ongoing social process without terminus (Turner 1969). First, we place the AD label in a salient historical context by describing the dominance of neurobiological approaches to brain aging that were set in motion by the discoveries of the German psychiatrist Dr. Alois Alzheimer in the early 20th century. Subsequently, we describe the evolution of the classification of Alzheimer’s-type dementia in the DSM. Finally, we consider how the concepts of AD, dementia and other related diagnoses might continue to evolve in the DSM-V, due for release in 2013. Ultimately, this article adds to the growing interpretive literature on AD (Gubrium 1986; Fox 1989; Lyman 1989; Herskovits 1995; Holstein 1997; Whitehouse et al. 2005; Ballenger 2006; Hendrie 2006; Whitehouse and George 2008) while significantly contributing to what others have identified as ‘‘the meager literature on the history of AD’’. It also provides a speculative framework for future critical inquiry on subsequent publications of the DSM, in which AD will continue to evolve.

Early Terminology of Dementia

While the phenomenology of dementia was ﬁrst recorded in various genres of ancient Egyptian writing, a number of publications have credited the ancient Greeks with having recognized and formulated the concept of dementia (Cohen 1983; 123 Cult Med Psychiatry (2011) 35:417–435 419

Torack 1983; Mahendra 1987). Memory loss and general intellectual decline, as early symptoms of the aging process, were recognized through the ages in the writings of Aristotle, Galen, Hippocrates, Lucretius, Cicero and both the Elder Seneca and the Younger Seneca in the early Roman Empire (Berrios 1987; Karenberg and Forstl 2006). The concept of dementia—a term said to have been coined by Celsus in the first century A.D.—has long carried social implications for those so diagnosed and has been associated with reduced civilian and legal competence, as well as with entitlement to support and protection. According to the writings of Solon and Plato, mentally impaired elders were incapable of making a will and were not eligible for official civilian positions but also could not be charged with unlawful acts (Kurz and Lautenschlager 2010). Similarly, in the Roman era, the concept of dementia was used to reduce the abilities of patients to enter contracts, handle their own affairs, hold public office and be criminally responsible (Berrios 1987). Modern legal systems contain similar provisions for those diagnosed with dementia. Literally meaning ‘‘away’’ or ‘‘out’’ of ‘‘mind’’ or ‘‘reason’’ in Latin, the term ‘‘dementia’’ entered the English language from the French ‘‘de´mence’’ via the French psychiatrist Philippe Pinel (Gaines 2006), who made notable contributions to the categorization of mental disorders in the late 18th and early 19th centuries. Over the centuries, the phenomenology of dementia has been causally associated with witchcraft, moral degeneracy, bad blood and a dissipation of vital energy from the brain, among other factors (Gallagher-Thompson et al. 1997). Today’s standard reductionist framework for dementia explicitly associates the condition with individual brain pathology, and the term refers to the progressive loss of cognitive function in multiple areas: memory, attention, language and problem solving. Medical anthropologists have observed that reductionist biomedical taxonomies such as AD conceptualize illnesses as ‘‘internalizing’’ rather than ‘‘externalizing,’’ in that they give primacy to biological or physical signs that can mark a disease’s progression rather than associating etiology with psychosocial or cosmic relations (Gaines 1992a, b; Lock 2005, 2010). Prior to Dr. Alzheimer’s birth in 1864, the dominant European literature of mid- to late-nineteenth-century neuropathology reflected a more ‘‘internalizing’’ conceptual orientation, as researchers were sensitive to the texture of the brains of the apoplectic and demented. ‘‘Cerebral softening’’ was associated with atherosclerosis and described in a language of liquefaction that united physiological, psychological and moral decay, the latter factor representing a vestigial ‘‘externalizing’’ dimension to dementia held by many scientists (Cohen 1998, p. 21). Suffering in old age was largely perceived as inevitable and natural, a fact of existence that was to be ameliorated but not eliminated (Katzman and Bick 2000). However, in the late 19th century, brain aging came to be understood increasingly as an internal biological event, as scientists began using microscopy as well as sectioning and staining techniques to note changes in the brain tissues and blood vessels of the elderly and associated this pathology with the loss of cognitive functioning (Engstrom 2007). By the beginning of the 20th century, the medical literature on dementia had come to focus almost entirely on brain pathology, and the term ‘‘organic’’ was used to demonstrate that psychopathological symptom clusters in mental disorders could be 123 420 Cult Med Psychiatry (2011) 35:417–435 associated with chronic lesions on the brain (Kurz and Lautenschlager 2010). The psychiatrist, E. E. Southard, wrote that his colleagues had begun to eschew the contribution of external factors for dementia, having found ‘‘little convincing evidence that social factors play much part [in dementia]. Whatever the causes of brain atrophy, it seems they cannot be social’’ (in Ballenger 2006, p. 19). As knowledge of brain pathology widened, the cognitive changes in old age that previous generations of researchers had resigned themselves to were now seen as having visible, specific and identifiable (with the aid of a microscope) correlates in the brain that could potentially be eliminated through greater reductionist understanding. Brain aging had crossed the threshold from the normal to the pathological, and there appeared to be good reason to replace the vague concept of ‘‘senility’’ with more scientifically rigorous disease categories. It was within this context that Dr. Alois Alzheimer of Germany received his formal training as a researcher and developed a particular skill in histology—the study of tissue through the use of a microscope. In the 1890s, Alzheimer and colleagues extensively described and emphasized the critical role of atherosclerosis and stroke in the development of brain atrophy and senile dementia (Mast et al. 1995).

Alzheimer, Kraepelin and the Tenuous Construction of ‘‘Alzheimer’s Disease’’

In 1906, Dr. Alzheimer, then a practicing psychiatrist, presented a lecture entitled ‘‘On a Peculiar, Severe Disease Process of the Cerebral Cortex’’ to the 37th Assembly of Southwest German Alienists [psychiatrists] in Tu¨bingen, Germany (Maurer and Maurer 2003, p. 4). In his talk, he detailed his observations of a 51-year-old woman named ‘‘Auguste D,’’ whom we now know was Auguste Deter, a patient whom he first treated in 1901 while serving as the director of the Irrensstalt [asylum] in Frankfurt, Germany. Upon conducting a postmortem investigation using a methyl blue-eosin staining technique and a silver chromate staining technique1 refined by his colleague Franz Nissl, Dr. Alzheimer found high concentrations of plaques and tangles on her brain and a paucity of cells in the cerebral cortex (Tollis 1994, p. 49). The definitive demonstration of these structures and their interpretation as pathology set the medical understanding of dementia firmly on a path that privileged the material and conflated mind with brain (Chillibeck et al. 2011). Dr. Alzheimer remained uncommitted about the nature of the condition he was observing. His nosological dilemma was whether Auguste D’s symptoms represented an atypical, early-onset form of senile dementia or whether they represented a separate disease entity altogether. Interestingly, the second case study recorded by Dr. Alzheimer involved a 56-year-old laborer from Munich named Johann F, who showed only plaque-related pathology, and no tangles (Alzheimer 1911). And thus after only two cases, Dr. Alzheimer had encountered a significant pathological variance in his observations of presenile dementia. However, Alzheimer’s Chief Emil Kraepelin—one of the most influential psychiatrists in the 20th century (Roelcke 1997, p. 384) and a man nicknamed by his peers as the ‘‘Linnaeus of Psychiatry’’ (Maurer and Maurer 2003)—did not share his 123 Cult Med Psychiatry (2011) 35:417–435 421 reluctance. In 1910, Kraepelin officially coined the term ‘‘Alzheimer-Krankheit’’ (Alzheimer’s disease), including it on page 627 of the eighth edition of his authoritative Textbook of Psychiatry. Historians have cited a variety of reasons for Kraepelin’s decision to conceptualize Alzheimer’s as a distinct disease entity (Engstrom 2007), including political motivations in the context of a rivalry between two major academic institutions in Europe (his lab in Munich versus Arnold Pick’s lab in Prague) (Mo¨ller and Graeber 1998; Ballenger 2006) and between psychiatry and the psychoanalytic methods being advanced by Sigmund Freud (Roelcke 1997; Ballenger 2006). For the next several decades after the publication of ‘‘Alzheimer’s disease’’ in Kraepelin’s 1910 textbook, the diagnosis of AD remained obscure and was rarely applied by those in the medical profession (Gubrium 1986). Alzheimer’s disease was considered a rare condition that affected young people exhibiting presenile dementia; ‘‘hardening of the blood vessels’’ was considered to be the main pathology for cognitive decline in the last decades of life. As many critics have pointed out, Alzheimer and Kraepelin’s conception of Alzheimer’s disease was strongly reductionist, exclusively privileging brain pathology in the etiology of dementia. This is not surprising given the institutional context in which they practiced. As Engstrom has written, German psychiatric clinics during this period were not intended to treat incurable patients, thus patients with dementia usually passed quickly through them on their way to institutions providing custodial care. To the extent that patients with dementia were found in the kind of teaching clinics in which Alzheimer and Kraepelin worked, they were there for their usefulness either in providing training material for students or in providing pathological specimens upon autopsy (Engstrom 2007). Thus the institutional arrangement of the psychiatric clinics at which Alzheimer and Kraepelin tended to reinforce a biological reductionism over the type of psychosocial approach that might emerge in settings that allow for the development of a more robust, long-term relationship between doctors and people with dementia. By the 1940s, the inability to correlate AD with a clear and consistent pathological substrate and therapeutic nihilism that the reductionist approach of Alzheimer and Kraepelin fostered led to a gradual shift toward a psychosocial model and methods that would better help aging persons and families cope with the day-to-day challenges of age-related cognitive decline (Ballenger 2006). Pioneers such as the U.S. psychiatrist David Rothschild, who began his career trying to resolve the anomalous findings concerning the pathology of AD, developed a psychodynamic model of dementia care that predominated in Euro-America in the 1940s and 1950s, challenging dominant biomedical models (in Kitwood 1997,p.55; Ballenger 2006). He and his colleagues argued that, since the pathological structures purported to be characteristic of AD and senile dementia in Kraepelin’s nosology (plaques and tangles) had been found in a variety of other conditions (such as spastic paralyses, hyperthyroidism and multiple sclerosis), these structures were not an expression of any particular disease process and should not be construed as such. Since the 1970s, several factors have contributed to a resurgence of a reductionist biomedical model of AD. Over the course of the 20th century, the average life expectancy increased nearly 30 years for persons living in Western countries. At the 123 422 Cult Med Psychiatry (2011) 35:417–435 same time, the emergence of technology such as electron microscopes, neuroimaging devices and laboratory techniques have enabled a more in-depth study of the neurobiological processes in the brains of persons with dementia and the underlying genetic causes of AD-type pathology. The combination of increasingly visible aging populations and technological tools that expanded investigation into the neurode- generative process created the conditions for the emergence of national and international advocacy organizations in the early 1980s that have created the domestic and global research infrastructure that has made reductionist investigation into the etiology of AD a major source of public and private investment worldwide. Parallels between the emergence of ‘‘brain psychiatry’’ at the end of the 1800s and the re-emergence of biological psychiatry at the end of the last century can be drawn, as enthusiasm for neurobiological mechanisms for mental illness tracked the development of new techniques (Whitehouse 1985).

The Rise and Development of Alzheimer’s Disease in the Diagnostic and Statistical Manual of Mental Disorders

The gradual ascent of AD as a worldwide disease category can be observed in successive versions of the DSM, which has functioned as a palimpsest for changing conceptions of brain aging over the last 60 years. The DSM is a symptom-based classification textbook that is published by the American Psychiatric Association (APA) and used worldwide to provide diagnostic criteria for mental disorders. Although dementia subtypes were originally described by psychiatrists, the development of and the modern-day dominance (at least in some countries) of neurology as a field interested in dementia have challenged the use of psychiatric nosology. Even the very notion that dementia is a ‘‘mental illness’’ has been challenged in efforts to minimize the stigma associated with the label. Neurologists have dominated the debate about diagnostic criteria, especially when neuropathological criteria are incorporated (Newell et al. 1999). Despite this, the DSM is an important compendium that has transformed practice in part though influencing health-care reimbursement. Until the days of mental health parity began to emerge (a state of affairs still in flux), neurological diagnoses were better reimbursed than psychiatric ones. The DSM has proven to be a highly mutable document over the six decades of its existence and has been roundly critiqued in scholarship. As Kleinman has written, the psychiatric concepts of the DSM are not givens in the natural world; rather, they are embedded in social systems and are shaped by social, political, economic and cultural forces (1988a, p. 3). Consequently, medical anthropologists view any given disease catalogued in the DSM not as timeless, but as a historical product that is ‘‘glued together by the practices, technologies, and narratives with which it is diagnosed, studied, treated, and represented and by the various interests, institutions, and moral arguments that mobilized these efforts and resources’’ (Young 1995, p. 5). Researchers in medical anthropology have found it fruitful to elucidate the means by which social, political and economic factors have shaped the content of the DSM 123 Cult Med Psychiatry (2011) 35:417–435 423 over the past six decades, challenging the aura of objectivity surrounding the text in favor of a more constructivist approach to psychiatric conditions. For instance, Young’s Harmony of Illusion (1995) has described how posttraumatic stress disorder achieved general acceptance in 1980 when it was included in the DSM-III following a political struggle waged by psychiatric workers and activists on behalf of the scores of Vietnam war veterans who were suffering from an uncategorized psychological condition that was, to their minds, the tragic effects of war-related trauma. Further, McGrattan’s (2006) discussion about the classification of homosexuality as a disease in the DSM-I and DSM-II and its removal from the DSM-III in 1980 serves to demonstrate how the disease concept was attenuated by increasing gay-rights activism, growing social tolerance and the decline of certain religious values in Western culture. More recently, in The Loss of Sadness, Horwitz and Wakefield (2007) have written that while depressive disorder can certainly be a devastating condition warranting medical attention, the apparent epidemic in modern culture reflects the way the psychiatric profession (perhaps under the influence of pharmaceutical companies looking to widen markets) has understood and reclassified normal human sadness in the DSM-IV as a largely abnormal experience. By dissolving the boundary between normal sadness and mental disorder, the authors of the DSM-IV have allowed depression to be diagnosed without consideration of context. Moreover, critical scholarship has focused acutely on the historical role gender differences have played in shaping a greater prevalence of mental disorders among women, such as depression, bipolar disorder, premenopausal syndrome and hysteria (see Brown 1978; Showalter 1985; Davis and Low 1989; Ussher 1991; Martin 2007). Throughout the late 20th century, the DSM has attempted to unite competing national and international classification systems, with the goal of creating a common nomenclature based on a consensus of the contemporary knowledge about psychiatric disorders (Kleinman 1988b). Exploring the successive versions of the DSM as historical documents helps illustrate the process through which the reductionist AD paradigm has gained formal prominence in the medical community over the last three decades. Young (1995, p. 96) has observed that while Kraepelin’s descriptive approach to psychiatry that regarded mental disorders as organic and biochemical was popular early in the century, by the mid-1950s his influence had waned as psychiatrists increasingly embraced a model concerned with biopsychosocial factors such as individuals’ internal psychological states, their relationships with others and the effects of the surrounding environment on their health in the etiology of mental disorders. This paradigmatic shift away from linking symptoms of mental disorders to pathological structures and processes was reflected in the entry for dementia in the first two editions of the DSM in 1952 and 1968. Both the DSM-I, published in 1952, and the DSM-II, published in 1968, reflected the predominant psychodynamic psychiatry of the era (Mayes and Horwitz 2005), although the biological perspectives and concepts from Kraepelin’s definitive system of psychiatric classification were also included. In total, the first manual listed 106 mental disorders, and the second documented 182. Symptoms were not specified in detail 123 424 Cult Med Psychiatry (2011) 35:417–435 for specific disorders; rather, disorders were seen as reflections of broad underlying psychological conflicts or maladaptive reactions to life problems, in the manner that clinicians like Rothschild approached dementia. Regarding age-associated progressive dementia, the DSM-I and DSM-II used the term ‘‘chronic brain syndrome’’ rather than ‘‘dementia’’ and included only a brief, general description that left room for clinicians to include a broad range of causal factors (APA 1952, 1968). The reliability and validity of the first two editions were challenged on the grounds that the diagnostic descriptions were not detailed enough and left ample room for error. Additionally, it was argued that descriptions had been written by a small number of academics rather than being based on specific empirical studies. The APA committed to changing the way it conducted itself and formed a Task Force on Nomenclature and Statistics in 1974 to undertake a massive overhaul of the DSM-II that targeted the vague phraseologies such as ‘‘impaired reality testing,’’ ‘‘mood swing,’’ and ‘‘anxious overconcern’’ (APA Assembly and Board of Trustees 1973). Aided by the emerging technological tools mentioned in the preceding section, the APA’s mission was to create a symptom-based classification system of mental disorders and organize psychiatry around a stricter catalog of reliable diagnoses identified by specific sets of symptoms that indicated discreet illnesses and minimized the psychodynamic aspects of psychiatry (Kleinman 1988b). This ushered in a new era of classifying and studying mental conditions based on delineating disease progression and its specific pathological underpinnings that was more reflective of Kraepelin’s classification system. That is, the ‘‘progress’’ was a return to a biological basis of afflictions to make psychiatry more ‘‘scientific’’ (Gaines 1992a, b). When the DSM-III was published in 1980, it ushered in a ‘‘diagnostic revolution,’’ illustrating that the sweeping transformation in psychiatric knowledge-making had taken place since the 1950s (Young 1995) and propelling the APA as a significant force in psychiatric nosology (Thakker and Ward 1998, p. 502). At 482 pages, the text was nearly three times the length of its predecessor and identified over 80 more disorders than the DSM-II while setting out operationalized inclusion and exclusion criteria for each of the psychiatric conditions. The manual sold more than half a million copies in the United States, was translated into 14 languages and became an indispensable text for residency training programs, insurance companies, which used the text as a guide to reimbursement, social service agencies, which relied on it to assess disabilities, and courts, which turned to it in resolving questions of criminal culpability (Kleinman 1988b). The DSM-III attempted to describe psychopathology without reference to particular theories as were present in the earlier, more psychodynamic DSM texts and explicitly aspired to embody a ‘‘neo- Kraepelinian’’ or biological approach to diagnosis (Gaines 1992a, b; Roelcke 1997; Kupfer et al. 2002:xvii). However, the manual met strong and diverse criticism, and its cross-cultural applicability was brought into question (Stromgren 1983; Wig 1983). Critics have argued that this transition precipitated the biologization of the person in the practice of psychiatry, in other words, moving medical practice toward a ‘‘somatic individuality’’ that couched selfhood entirely in the body, thereby reducing individuals to a set of symptoms that classified them into diagnostic categories and 123 Cult Med Psychiatry (2011) 35:417–435 425

flattening the psychosocial dimensions of personhood (Lyman 1989; Novas and Rose 2000; Leibing 2008; Shabahangi and Szymkiewicz 2008). Challenges were also made to hierarchical diagnostic conventions that precluded a diagnosis of some disorders when a more severe disorder was simultaneously present (e.g., a patient meeting criteria for schizophrenia and dementia would only get the diagnosis of schizophrenia) (Boyd et al. 1984). Responding to this criticism, the APA published a revision to the DSM-III (the DSM-III-R) in 1987 to improve the consistency, clarity and conceptual accuracy of DSM-III criteria (Kupfer et al. 2002); this augmented the listing of mental illness, raising it to 292 disorders. With regard to AD, even though the condition had re-entered the lexicon of researchers, politicians and the lay public during the early 1980s when the DSM-III was released, there was still much disagreement about the classification of mental disorders of old age (Stromgren 1983, p. 74), and the authors of the manual were hesitant to demarcate AD as a discreet disease. They instead recommended that AD be referred to as a ‘‘presenile dementia’’—continuing the conceptualization that had been in put in place by Alzheimer and Kraepelin at the outset of the century—and justified the nonspecificity of the classification by arguing the following: ‘‘Since nearly all cases of these Dementias are associated with Alzheimer’s and the identification of Alzheimer’s and Pick’s diseases is largely or entirely dependent on histopathological data, it seems more useful to have in a clinical classification of mental disorders a single category that encompasses the syndrome of Primary Degenerative Dementia’’ (APA 1980, p. 125). However, in the 1987 DSM-III-R, the classification of AD appeared to more conspicuously reflect the political and social forces that had led to the emergence of AD as an international problem over the course of the decade. Alzheimer’s disease was designated as an ‘‘Organic Mental Disorder’’ and given the subcategorization code ‘‘290.xx’’: ‘‘Primary Degenerative Dementia of the Alzheimer Type’’ (APA 1987, p. 119); this enabled the clinical application of the label and insurance reimbursement in the U.S. health care system. In 1994, the DSM-IV was published after a three-stage empirical review (Kupfer et al. 2002). In total, 374 disorders were documented, though the current publication has scaled its list back to 283. Critics have variously assailed the DSM-IV (and DSM-III) for having a powerful orientation to Western cultural values despite the pretense of neutrality (e.g., a conception of individuals as having single, stable personalities and absolute notions of normality) (Gaines 1992a, b; Kleinman 1996), featuring a largely U.S. agenda (Rounsaville 2002), being neglectful of culture (Lewis-Fernandez and Kleinman 1995; Kleinman 1996, p. 22) as well as deficient in integrating issues of age and gender (Martin 1987), and retaining a theoretical framework that asserts the primacy of the biomedical model despite the stated claim of being atheoretical (Follette and Houts 1996). Informed by a Western, biomedical sensibility, the DSM-IV makes several theoretical assumptions, mainly that mental illnesses are phenomena of biological origin and can be verified through objective observation (Thakker and Ward 1998), which has led to criticism that the system pathologizes ordinary experiences of the human condition and overemphasizes the notion of the universality of its primary syndromes (Fa´brega 1994; 1992a, b). In reality, while the DSM-IV currently operates with an implicit thesis of the universality of psychopathology, the biological correlates of many of its disorders 123 426 Cult Med Psychiatry (2011) 35:417–435 have not been clearly established (Thakker and Ward 1998, p. 505). This has been shown to be the case with AD (Snowdon et al. 1997; Brayne 2007; Schneider et al. 2007, 2009; Hachinski 2008; Whitehouse and George 2008; Castellani et al. 2009; D’Alton and George 2011). With regard to AD, the DSM-IV criteria currently specify that individuals affected with ‘‘dementia of the Alzheimer type’’ must demonstrate cognitive deficits not attributable to causes associated with other forms of dementia and that display an insidious onset and a progressive deteriorating course (APA 1994). The manual outlines a detailed set of criteria for the diagnosis of AD, establishing that multiple cognitive deficits must be present, one of which must be memory impairment. In addition to problems with memory, one or more of the following must be displayed: aphasia (a deterioration of language abilities), apraxia (difficulty executing motor activities), agnosia (an impaired ability to recognize or identify objects) and problems with executive functioning (planning, organizing, etc.). To meet the criteria for AD, the deficits must affect one’s ability to hold a job or volunteer position, must fulfill domestic responsibilities and/or maintain social relationships and must, also, represent a significant decline from the person’s previous level of functioning. The DSM-V is currently being prepared for a 2013 release, and the classification of AD and dementia is poised to undergo further permutation (Sunderland et al. 2007; Petzel 2008).

Anticipating Changes in the DSM-V

In winter 2010, the APA posted a draft of the DSM-V on an online interface to solicit public opinion on its proposed changes (APA 2010). Most prominently, the Neurocognitive Disorders Working Group announced that it proposed replacing the diagnostic category ‘‘Delirium, Dementia, Amnestic, and Other Cognitive Disor- ders’’ with ‘‘Delirium, Major Neurocognitive Disorder, and Minor Neurocognitive Disorder.’’ This move would effectively replace the longstanding concept of ‘‘dementia’’ with ‘‘Neurocognitive Disorders’’ of the Major and Minor types, the latter being distinguished as a state of predementia when a subject is without significant functional impairment in activities of daily living. The boundary between minor and major hinge on assessment of function in daily life, which is influenced by previous (premorbid) skills, the health care professional’s expertise and biases, gender roles and cultural expectations. Ultimately, there is no absolute difference, hence reinforcing the idea that minor and major represent arbitrary labels on a continuum of dysfunction. As occurred with Mild Cognitive Impairment (MCI), an emerging diagnosis discussed further below, one can imagine defining ‘‘minor,’’ ‘‘very minor’’ and ‘‘premajor’’ intermediate states if the clinician researcher were so inclined. It fairly can be asked what the implications are for phasing dementia out of the DSM, if that should be the final outcome. Certainly, in Western cultures the concept is pejorative when applied to persons without ‘‘Neurocognitive Disorders’’ (i.e., ‘‘My boss is really acting demented today’’) and the APA’s (2010) rationale notes that the term dementia has ‘‘acquired a pejorative or stigmatizing connotation.’’ An 123 Cult Med Psychiatry (2011) 35:417–435 427 argument could thus be made that rendering this diagnosis—which carries such disabling connotations—inappropriate for describing persons with memory loss could lessen the stigma on older individuals and signal a more biopsychosocially sensitive tone reminiscent of the DSM in the mid 20th century. The emphasis on ‘‘disorder’’ rather than ‘‘disease’’ may potentially mitigate against the pathologi- zation of memory loss as an aberrant condition and help foster an understanding of brain aging as a more or less heterogeneous condition occurring on a spectrum rather than being reducible to discrete categories. In contrast, it can be argued that if society continues to define the value of persons in terms of productivity, competence and cognitive ability, it is likely that any new terminology used to describe age-associated, progressive cognitive deterioration will quickly acquire the same pejorative connotations. Absent changes in underlying values and social structures surrounding aging and chronic cognitive impairment, the proposed changes in terminology for DSM-V are unlikely to lessen stigmatization over the long term. It is, however, interesting to note more broadly that the APA has also signaled that Asperger’s syndrome and autism may both be subsumed under the term ‘‘autism spectrum disorder,’’ with diagnosed individuals differentiated by levels of severity. There is a growing sense that these changes, as well as alterations to dementia and other diagnoses, may represent a more general overhaul in which the ‘‘You have it or you don’t’’ tone of past DSMs will be replaced with a perspective that increasingly views psychiatric disorders as occurring along a continuum with differing degrees of severity. Indeed, attempts to use biomarkers such as neuroimaging or cerebrospinal fluid assessment to construct absolute categories have largely failed because quantification of brain measurements leads to continuous distributions not discreet divisions among categories (Graham 2008). Increasingly, conditions causing dementia are seen as overlapping, for example, degenerative and vascular causes and Lewy Body and Alzheimer’s disease (Mitnitski 1997; Graham et al. 1999; Schneider et al. 2007, 2009). And even though genes represent quanta (specific patterns of DNA) DNA, the risks that emerge from susceptibility genes (like ApoE4) and other diagnostic criteria are also poorly understood and need to be expressed as a probability, not a clear all-or-none prediction. Rare, early-onset autosomal dominant mutations create a ‘‘You have it or not’’ duality, but even then various environmental risk factors can affect severity and age or onset. This spectrum nature of brain aging raises manifold questions about the distinction between how the categories of major and minor Neurocogntive Disorders will play out clinically and culturally. Will this bifurcation create interpretive problems? How will clinicians adjudicate between these two categories? What thresholds allow one to pass from one category to the other, and does a doctor need to validate this transition? If so, will the phrases ‘‘Minor’’ and ‘‘Major’’ be an affront to those who receive the diagnosis and might perceive the major/minor qualifiers as value-laden or insufficiently representative of the phenomenology of one’s condition? Will ‘‘Major Neurocognitive Disorder’’ simply be a euphemism for AD that carries the same degree of stigma? And inversely, will a condition such as ‘‘Minor Neurocognitive Disorder’’ indeed become what others have critiqued as a ‘‘predisease’’—a growing family of clinically recognized diagnoses that includes: 123 428 Cult Med Psychiatry (2011) 35:417–435 prevascular disease, prediabetes, prehypertension, preosteoporosis and manifold others? (Brownlee 2007). Such conditions are often critiqued for owing their construction in part to the pharmaceutical industry that views predisease conditions as a means of augmenting existing disease drug market share. One of the more controversial ‘‘prediseases’’—the aforementioned MCI—will presumably enter the DSM-V under the categorization ‘‘Minor Neurocognitive Disorder with Memory Impairment.’’ The concept of MCI is being actively socially constructed at the interfaces of science, clinical work and business (Whitehouse and Juengst 2005; Gaines 2006) and has emerged from a long history of recognizing the obvious: that most, if not all, older persons, develop some changes in cognition as they age and that persons who eventually become demented have a period in their illness before which they develop significant functional impairment. ‘‘Benign Senile Forgetfulness’’ (BSF) and ‘‘Chronic Cerebral Insufficiency (CCI) were the first terms popularized in the medical literature to describe this metamor- phosis, although the broadly used concept of ‘‘senility’’ preceded any usage of medical terms (Kral 1962). Following BSF and CCI, Aging-Associated Memory Impairment (AAMI) emerged and remains of interest today (Crook et al. 1986). AAMI was defined as older people who performed 1 standard deviation less well than young people, hence creating a very large number of people potentially so labeled. Attempts to refine AAMI also occurred, changing the referent population and major focus on memory alone, for example, Age-Related Cognitive Decline (Levy 1994). However, while MCI clearly fits with the emerging continuum-based conceptual framework suspected as forming the undergirding of DSM-V, we believe the concept is problematic on multiple levels. Many population studies have shown that well over a quarter of persons labeled with MCI do not progress to dementia over several-year follow-up periods (Ritchie et al. 2004; Bocti et al. 2005) and some remain stable or return to normal (Hachinski 2008; Gauthier et al. 2006), which raises inherent questions about the accuracy, usefulness and ethical soundness of a label that ostensibly represents a precursor to AD and underscores a need for caution (Graham 2006; Graham and Ritchie 2006). Moreover, the psychometric thresholds for diagnosing someone with MCI are unclear, and salient questions include, How many standard deviations lower than referent population norms must a person be in order to receive the label, and what population(s) should be used as a referent? One might also query how relatively preserved should activities of daily living be in order to differentiate MCI from dementia? Should diagnosis require a subjective complaint from the patient or family, or should it be given freely by the physician? (Whitehouse and George 2008). And to what degree should we be skeptical of industry involvement in the formation of a new diagnostic category that expands potential drug consumers by extending the definition of pathology onto those who may be undergoing basic brain aging (perhaps having ‘‘senior moments’’ as we all do) and rendering them candidates for licensed AD drugs? (Whitehouse et al. 2000, p. 304; Petzel 2008). After all, as others have written, if the boundary between MCI and normal cognitive functioning shifts so that they are closer together, MCI becomes a more accessible route for scientists to experiment with drugs in an expanding population located between dementia and normal functioning (Rivas-Vazquez et al. 2004; Jelic et al. 2006; Katz and Peters 2008). Those fascinated with developing 123 Cult Med Psychiatry (2011) 35:417–435 429 drugs to prevent AD and other dementias are demanding earlier and earlier recognition of the predisease states. Hence, the NIA Alzheimer Disease Neuroim- aging Initiative is classifying MCI into ‘‘e’’ (early) and ‘‘l’’ (late) forms. Dr. Barry Reisberg, who was the first to use the expression MCI in staging dementia, is now advocating for identifying Subjective Cognitive Impairment based on subjective complaints alone (Anderson 2010). Of particular concern to those worried about overmedicalization is that some experts are now arguing for treating asymptomatic (‘‘normal’’) people with ‘‘abnormal’’ imaging and cerebrospinal fluid biomarker profiles with long-term preventative therapies (Dubois et al. 2010). In its therapeutic desperation, the field believes that early treatment is key to finally achieving a treatment success of any meaningful magnitude. Recent Alzheimer’s Association ‘‘diagnostic’’ guidelines (2010) include three levels: preclinical, MCI and dementia. So far, the incorporation of biomarkers is not apparent in the construction of DSM-V. With regard to AD, it remains unclear whether the diagnosis will undergo any further permutations in 2013. Despite the putative clarity of its clinical symptoms and pathological correlates, no clear boundary has been established between AD and aging. The cognitive and functional decline that has come to represent AD is experienced, to one degree or another, by every person who ages. Decades of accumulated autopsy evidence has demonstrated that plaques, tangles and all other relevant biomarkers for AD and other major forms of dementia are found to varying degrees in all aging brains (Richards and Brayne 2010). As George Engel (1977) famously wrote, when categorizing disease, society goes from symptoms, to symptom clusters, to syndromes, to diseases with specific pathology. However, as Dr. Alzheimer himself articulated in the early 20th century, AD is a heterogeneous, age-related condition without pathonomonic brain features, and thus it may be appropriate to ask whether the condition ought to be considered a syndrome (like the concept of dementia) rather than a specific disease (Whitehouse and George 2008). Like autism and Asperger’s, a case can be made on evidentiary grounds for viewing AD as the latter stage of a spectrum of cognitive changes associated with normal aging. One wonders whether the DSM-V will emphasize the age-related, syndromal aspects of AD or acknowledge its multifactorial nature: the fact that most forms of the ‘‘disease’’ have mixed features of other dementias (i.e., vascular changes, inflammation, Lewy Body deposition, etc.) (Mitnitski et al. 1997; Graham et al. 1999). In contrast, there is increasing pressure in the field to focus on biomarkers and define the conditions on the basis of neuroimaging and spinal fluid measurements. However, despite the hundreds of millions of dollars invested in this quest, no such markers have been validated against clinical features. With drug development slowing, it seems fair to wonder whether a greater emphasis on psychosocial approaches to clinical and societal care will emerge (Whitehouse 1993; Whitehouse and George 2009; George and Whitehouse 2010; Whitehouse et al. 2011).

The Way Forward

This article has provided a general overview of the complex cultural processes through which severe brain aging has been shaped into an internationally known 123 430 Cult Med Psychiatry (2011) 35:417–435 disease category called ‘‘Alzheimer’s-type dementia’’ and tracked the evolution of the AD and related classifications in the DSM. If the history of AD tells us anything, it is that the quest for scientific truth is an ongoing process that is surely subject to the vicissitudes of historical and cultural circumstance. With the DSM-V due for publication in two years, the culturally salient question remains: To what extent ought Western culture continue medicalizing the continuum of brain aging and creating specific thresholds of disease given both the heterogeneity and the attendant social meanings of conditions such as AD and other forms of cognitive and functional loss? The publication of the DSM-V in 2013 will be revealing not only of the evolution of our psychiatric classifications, but also of our values as a culture. Once again, we will bear witness to how the Western biomedical system reflects Western society at large. Although we have described the history of the evolution of terms for dementia with one eye to objectivity, we ourselves end up rather fundamental critics. It is not at all clear to us that the medicalization of brain aging is serving society well today or in the future, particularly if biologization continues. The demographic and economic pressures described above are driving many countries to develop national dementia strategies. We can hope for a more enlightened view of health and cognitive health as more than the product of genes and biomarkers and the province of drug therapies. Embedded in the history and conceptual evolution of dementia terminology are seeds of humility about the power of science and lessons about the power of caring. Dementia challenges us to understand more deeply what it means to age and eventually die as a human being in community and exposes the limits of our understanding of our own embodied brains and individual autonomy.

Note

1. The silver precipitation technique, in which individual nerve and cell structures were ﬁxed and preserved for histopathological inquiry, was originated by the Italian scientist Camillo Golgi in 1873 and modiﬁed by the Spanish neurologist and photographer Santiago Ramon y Cajal. Both scientists shared the Nobel Prize for medicine in 1906 for their work on the structure of the nervous system.

References

Alzheimer, Alois 1911 U¨ ber eigenartige Krankheitsfa¨lle des spa¨teren Alters. Zbl Ges Neurol Psych 4:356–385 (translated and with an introduction by H. Fo¨rstl and R. Levy, 1991). Alzheimer’s Association 2010 Proposed Revisions to Diagnostic Criteria for Alzheimer’s Disease: Backgrounder/FAQ. Electronic document, http://www.alz.org/documents_custom/Alz_Diag_Criteria_FAQ.pdf Alzheimer’s Association and National Alliance for Caregiving 2004 Families Care: Caregiving in the United States. Electronic document, http://www.alz.org/ national/documents/report_familiescare.pdf, accessed October 15, 2010. American Psychiatric Association 1952 DSM-I, Diagnostic and Statistical Manual Mental Disorders. Washington, DC: American Psychiatric Association. 123 Cult Med Psychiatry (2011) 35:417–435 431

1968 DSM-II, Diagnostic and Statistical Manual Mental Disorders. 2nd Edition. Washington, DC: American Psychiatric Association. 1980 DSM-III, Diagnostic and Statistical Manual Mental Disorders. 3rd Edition. Washington, DC: American Psychiatric Association. 1987 DSM-III-R, Diagnostic and Statistical Manual Mental Disorders, 3rd Edition (rev.). Washington, DC: American Psychiatric Association. 1994 DSM-IV Diagnostic and Statistical Manual of Mental Disorders. 4th Edition. Washington, DC: American Psychiatric Association. 2010 DSM-5 Development. Delirium, Dementia, Amnestic, and Other Cognitive Disorders. Electronic document, http://www.dsm5.org/ProposedRevisions/Pages/Delirium,Dementia,Amnestic,Other Cognitive.aspx, accessed September 22, 2010. American Psychiatric Association Board of Trustees 1973 Homosexuality and Sexual Orientation Disturbance: Proposed Change in DSM-II, 6th printing, p. 44. Position Statement. APA Document Reference No. 730008. Electronic document, http:// www.psychiatryonline.com/DSMPDF/DSM-II_Homosexuality_Revision.pdf Anderson, Pauline 2010 Subjective Cognitive Impairment Early Indicator of Further Cognitive Deﬁcits. Alzheimers Dement 6: 11–24. Ballenger, Jesse 2006 Self, Senility, and Alzheimer’s Disease in Modern America: A. History. Baltimore, Maryland: Johns Hopkins University Press. Barnes, Lisa L., Robert Wilson, Julia Bienias, et al. 2005 Sex Differences in the Clinical Manifestations of Alzheimer Disease Pathology. Archives of General Psychiatry 62(6): 685–691. Berrios, German E. 1987 Dementia During the Seventeenth and Eighteenth Centuries: A Conceptual History. Psychological Medicine 17: 829–837. Bocti, Christian, John Whitehead, Lisa Fellow, et al. 2005 Characteristics of Patients with Mild Cognitive Impairment Who Do Not Progress to Dementia. Neurology 64: A365. Boyd, Jeffrey H., Jack D. Burke, Ernest Gruenberg, et al. 1984 Exclusion Ccriteria for the DSM-III: A Study of Co-occurrence of Hierarchy-Free Syndromes. Archives of General Psychiatry 41: 983–989. Brayne, Carol 2007 The Elephant in the Room—Healthy Brains in Later Life, Epidemiology and Public Health. Nature Neuroscience 8: 233–239. Brown, George W. 1978 Social Origins of Depression. New York: Free Press. Brownlee, Shannon 2007 Overtreated: Why Too Much Medicine Is Making Us Sicker and Poorer. New York: Bloomsbury. Castellani, Rudy, Hyoung-gon Lee, Sandra L. Siedlak, et al. 2009 Reexamining Alzheimer’s Disease: Evidence for a Protective Role for Amyloid-Beta Protein Precursor and Amyloid-Beta. Journal of Alzheimer’s Disease 18(2): 447–452. Chilibeck, Gillian, Margaret Lock, and Megha Sehdev 2011 Postgenomics, Uncertain Futures, and the Familiarization of Susceptibility Genes. Social Science and Medicine (in press). Cohen, Gene D. 1983 Historical Views and Evolution of Concepts. In Alzheimer’s Disease. B. Reisberg, ed., pp. 29– 33. New York: Free Press. Cohen, Lawrence 1998 No Ageing in India: Alzheimer’s, the Bad Family, and Other Modern Things. Berkeley: University of California Press. Crook, Thomas H., Richard T. Bartus, and Steven H. Ferris 1986 Age-Associated Memory Impairment: Proposed Diagnostic Criteria and Measures of Clinical Change report of a National Institute of Mental Health Work Group. Developmental Neuropsychology 2: 261–276.

123 432 Cult Med Psychiatry (2011) 35:417–435

D’Alton, S., and Daniel R. George 2011 Changing Perspectives on Alzheimer’s Disease: Thinking Outside the Amyloid Box. Journal of Alzheimer’s Disease. doi: 10.3233/JAD-2011-110089. Davis, Dona L., and Setha M. Low, eds. 1989 Gender, Health and Illness: The Case of Nerves. New York: Wiley. Dubois, Bruno, Howard H. Feldman, Claudia Jacova, et al. 2010 Revising the Definition of Alzheimer’s Disease: A New Lexicon. Lancet Neurology 9(11): 1118–1127. Engel, George L. 1977 The Need for a New Medical Model: A Challenge for Biomedicine. Science 196: 129–136. Engstrom, Eric J. 2007 Researching Dementia in Imperial Germany: Alois Alzheimer and the Economies of Psychiatric Practice. Culture, Medicine and Psychiatry 31: 405–413. Essink-Bot, Marie-Louise, Joaquin Pereria, Claire Packer, et al. 2002 Cross-National Comparability of Burden of Disease Estimates: The European Disablity Weights Project. Bulletin of the World Health Organization 80: 644–652. Fa´brega, Horacio 1994 International Systems of Diagnosis in Psychiatry. Journal of Nervous and Mental Disease 182: 256–259. Follette, W.C., and A.C. Houts 1996 Models of Scientific Progress and the Role of Theory in Taxonomy Development: A Case Study of the DSM. Journal of Consulting and Clinical Psychology 64: 1120–1132. Fox, Patrick 1989 From Senility to Alzheimer’s Disease: The Rise of the Alzheimer’s Disease Movement. Milbank Quarterly 67: 58–102. Gaines, Atwood D., ed. 1992a Ethnopsychiatry: The Cuhural Construction of Folk and Professional Psychiatries. Albany, NY: SUNY Press. 1992b From DSM-I to III-R; Voices of Self, Mastery and the Other: A Cultural Constructivist Reading of U.S. Psychiatric Classification. Social Science and Medicine 35(1):3–24. Gaines, Atwood D. 2006 Dementia. In Encyclopedia of Anthropology, Vol. 2. H. James Birx, ed., pp. 725–726. Thousand Oaks, CA: Sage. Gallagher-Thompson, Dolores, Megan C. Leary, Celine Ossinalde, et al. 1997 Hispanic Caregivers of Older Adults with Dementia: Cultural Issues in Outreach and Intervention. Group: Journal of the Eastern Group Psychotherapy 21(3): 211–232. Gauthier, Serge, Barry Reisberg, Michael Zaudig, et al. 2006 Mild Cognitive Impairment. Lancet 367(9518): 1262–1270. George, Daniel R. 2010 Overcoming the Social Death of Dementia through Language. Lancet 376(9741): 586–587. George, Daniel R., and Peter Whitehouse 2010 The Psychosocial Environment: An Intergenerational Approach. National Academy on an Aging Society: Public Policy Aging Report 20(3): 27–35. Graham, Janice 2006 Reifying Relevance in Mild Cognitive Impairment: An Appeal for Care and Caution. Response to Commentaries. Philosophy, Psychiatry, and Psychology 13(1): 57–60. 2008 Facilitating Regulation: The Dance of Statistical Significance and Clinical Meaningfulness in Standardizing Technologies for Dementia. BioSocieties 3(3): 241–263. Graham, Janice, and Karen Ritchie 2006 Mild Cognitive Impairment: Ethical Considerations for Nosological Flexibility in Human Kinds. Philosophy, Psychiatry, and Psychology 13(2): 31–43. Graham, Janice, Arnold B. Mitnitski, Alexander J. Mogilner, and Kenneth Rockwood 1999 The Dynamics of Cognitive Aging: Distinguishing Functional Age and Disease from chronological age in a population. American Journal of Epidemiology 150(10): 1045–1054. Gubrium, Jaber F. 1986 Oldtimers and Alzheimer’s: The Descriptive Organization of Senility. Greenwich, CT: JAI Press. Hachinski, Vladimir 2008 Shifts in Thinking About Dementia. JAMA 300(18): 2172–2173. 123 Cult Med Psychiatry (2011) 35:417–435 433

Hendrie, Hugh C. 2006 Lessons Learned from International Comparative Cross-cultural Studies on Dementia. American Journal of Geriatric Psychiatry 14: 480–488. Herskovits, Elizabeth 1995 Struggling Over Subjectivity: Debates About the ‘‘Self’’ and Alzheimer’s Disease. Medical Anthropology Quarterly 9(2): 146–164. Holstein, Martha 1997 Alzheimer’s Disease and Senile Dementia, 1885–1920: An Interpretive History of Disease Negotiation. Journal of Aging Studies 11: 1–13. Horwitz, Alan V., and Jerome C. Wakeﬁeld 2007 The Loss of Sadness: How Psychiatry Transformed Normal Sorrow into Depressive Disorder. Oxford: Oxford University Press. Jelic, Vesna, Miia Kivipelto, and Bengt Winblad 2006 Clinical Trials in Mild Cognitive Impairment: Lessons for the Future. Journal of Neurology, Neurosurgery and Psychiatry 77(4): 429–438. Karenberg, Axel, and Hans Forstl 2006 Dementia in the Greco-Roman World. Journal of the Neurological Sciences 244(1–2): 5–9. Katz, Stephen, and Kevin R. Peters 2008 Enhancing the Mind? Memory Medicine, Dementia, and the Ageing Brain. Journal of Aging Studies 22: 348–355. Katzman, Robert, and Katherine Bick 2000 Alzheimer Disease: The Changing View. San Diego, CA: Academic Press. Kitwood, Tom 1997 Dementia Reconsidered: The Person Comes First. Philadelphia: Open University Press. Kleinman, Arthur 1988a The Illness Narratives. New York: Basic Books. 1988b Rethinking Psychiatry: From Cultural Category to Personal Experience. New York: Free Press. 1996 How Is Culture Important for DSM-IV? In Culture and Psychiatric Diagnosis: A DSM-IV Perspective. J.E. Mezzich, A. Kleinman, H. Fabrega Jr., and D.L. Parron, eds., pp. 15–25. Washington, DC: American Psychiatric Press. Kral, Voijtech A. 1962 Senescent Forgetfulness: Benign and Malignant. Canadian Medical Association Journal 86(6): 257–260. Kupfer, David J., Michael B. First, and Darrel A. Regier, eds. 2002 A Research Agenda for DSM-V. Washington, DC: American Psychiatric Association. Kurz, Alexander F., and Nicola T. Lautenschlager 2010 The Concept of Dementia: Retain, Reframe, Rename, or Replace? International Psychogeriatrics 22(1): 37–42. Leibing, Annette 2008 Entangled Matters—Alzheimer’s, Interiority, and the ‘Unﬂattening’ of the World. Culture, Medicine and Psychiatry 32(2): 177–193. Levy, Raymond 1994 Aging-Associated Cognitive Decline. International Psychogeriatrics 6: 63–68. Lewis-Fernandez, Roberto, and Arthur Kleinman 1995 Cultural Psychiatry. Theoretical, Clinical, and Research Issues. Psychiatric Clinics of North America 18: 433–448. Lock, Margaret 2005 Alzheimer’s Disease: A Tangled Concept. In Complexities: Beyond Nature and Nurture. Susan McKinnon and Sydel Silverman, eds., pp. 196–222. Chicago: University of Chicago Press. 2010 Dementia Entanglements in a Postgenomic Era. Science, Technology & Human Values. November 17, 2010. Lyman, Karen A. 1989 Bringing the Social Back in: A Critique of the Biomedicalization of Dementia. Gerontologist 29: 597–605. Mahendra, Nidhi 1987 Dementia. A Brief History of the Concept. In Dementia. A Survey of the Syndrome of Dementia. 2nd Edition. B. Mahendra, ed., pp. 1–18. Lancaster, UK: MTP Press.

123 434 Cult Med Psychiatry (2011) 35:417–435

Martin, Emily 1987 The Woman in the Body. Boston: Beacon. 2007 Bipolar Expeditions. Mania and Depression in American Culture Princeton, NJ: Princeton University Press. Mast, Henning, Thomas K. Tatemichi, and J.P. Mohr 1995 Chronic Brain Ischemia: The Contributions of Otto Binswanger and Alois Alzheimer to the Mechanisms of Vascular Dementia. Journal of the Neurological Sciences 132: 4–10. Maurer, Konrad, and Ulrike Maurer 2003 Alzheimer: The Life of a Physicians and the Career of a Disease. New York: Columbia University Press. Mayes, Rick, and Allan V. Horwitz 2005 DSM-III and the Revolution in the Classiﬁcation of Mental Illness. Journal of the History of the Behavioral Sciences 41(3): 249–267. McGrattan, M. 2006 The Social Construction of Disease: Why Homosexuality Isn’t Like Cancer. In Bordering Biomedicine. V. Kalitzkus and P. Twohig, eds. New York: Rodophi. Mitnitski, Arnold, Janice E. Graham, Alexander J. Mogilner, and Kenneth Rockwood 1997 Vector Diagnostics in Dementia Derived from Bayes’ Theorem. American Journal of Epidemiology 146: 665–671. Mo¨ller, Hans J., and M.B. Graeber 1998 The Case Described by Alois Alzheimer in 1911. Historical and Conceptual Perspectives Based on the Clinical Record and Neurohistological Sections. European Archives of Psychiatry and Clinical Neuroscience 248: 111–122. Newell, K.L., B.T. Hyman, J.H. Growdon, and E.T. Hedley-Whyte 1999 Application of the National Institute on Aging (NIA)—Reagan Institute Criteria for the Neuropathological Diagnosis of Alzheimer Disease. Journal of Neuropathology and Experi- mental Neurology 58: 1147–1155. Novas, Carlos, and Nikolas Rose 2000 Genetic Risk and the Birth of the Somatic Individual. Economy and Society 29(4): 483–513. Petzel, Janis 2008 Diagnostic Issues in Dementia: Advancing the Research Agenda for DSM-V: A Review. Psychiatric Services 59: 333–334. Prince, Martin, and Jim Jackson 2009 World Alzheimer Report. Alzheimer’s Disease International. Electronic document, http://www. alz.co.uk/research/ﬁles/World%20Alzheimer%20Report.pdf, accessed October 22, 2010. Plassman, Brenda L., John W. Williams, James R. Burke, et al. 2010 Systematic Review: Factors Associated With Risk for and Possible Prevention of Cognitive Decline in Later Life. Annals of Internal Medicine 153(3): 182–193. Richards, Marcus, and Carol Brayne 2010 What Do We Mean by Alzheimer’s Disease? BMJ 341: 865–867. Ritchie, Karen 2004 Mild Cognitive Impairment: An Epidemiological Perspective. Dialogues in Clinical Neurosci- ence 6: 401–408. Rivas-Vazquez, Rafeal A., Cecilia Mendez, Gustavo Rey, and Enrique J. Carrazana 2004 Mild Cognitive Impairment: New Neuropsychological and Pharmacological Target. Archives of Clinical Neuropsychology 19(1): 11–27. Roelcke, Volker 1997 Biologizing Social Facts: An Early 20th Century Debate on Kraepelin’s Concepts of Culture, Neurasthenia, and Degeneration. Culture, Medicine and Psychiatry 21: 383–403. Rounsaville, Bruce J. 2002 Experience with ICD-10/DSM-IV substance use disorders. Psychopathology 35(2–3): 82–88. Schneider, Julia A., Zoe Arvanitakis, W. Beng, et al. 2007 Mixed Brain Pathologies Account for Most Dementia Cases in Community-Dwelling Older Persons. Neurology 69: 2197–2204. Schneider, Julie A., Neelum T. Aggarwal, Lisa Barnes, et al. 2009 The Neuropathology of Older Persons with and without Dementia from Community Versus Clinic Cohorts. Journal of Alzheimer’s Disease 18: 691–701.

123 Cult Med Psychiatry (2011) 35:417–435 435

Shabahangi, Nader, and Bogna Szymkiewicz 2008 Deeper into the Soul: Beyond Dementia and Alzheimer’s towards Forgetfulness Care. San Francisco: Elders Academy Press. Showalter, Elaine 1985 The Female Malady: Women, Madness and English Culture, 1830–1980. New York: Penguin Books. Snowdon, David A., Lydia Greiner, James A. Mortimer, et al. 1997 Brain Infarction and the Clinical Expression of Alzheimer’s Disease. The Nun Study. JAMA 277: 813–817. Stromgren, Eric 1983 The Strengths and Weaknesses of DSM-III. In International Prespectives on DSM-III. R.L. Spitzer, J.B.W. Williams, and A.E. Skodol, eds., pp. 69–77. Washington, DC: American Psychiatry Press. Sunderland, Trey, Dilip V. Jeste, and Baiyewu Olusegun, eds., et al. 2007 Diagnostic Issues in Dementia: Advancing the Research Agenda for DSM-V. Arlington, VA: American Psychiatric. Thakker, Joanne, and Tony Ward 1998 Culture and Classiﬁcation. Clinical Psychology Review 18: 501–529. Tollis, D. 1994 Who Was Alzheimer? Nursing Times 90(34):49. Torack, Robert M. 1983 The Early History of Senile Dementia. In Alzheimer’s Disease. B. Reisberg, ed., pp. 23–28. New York: Free Press. Turner, Victor W. 1969 The Ritual Process: Structure and Anti-structure. Ithaca, NY: Cornell University Press. Ussher, Jane M. 1991 Women’s Madness: Misogyny or Mental Illness? Amherst: University of Massachusetts Press. Whitehouse, Peter J. 1985 Theodor Meynert: Foreshadowing Modern Concepts of Neuropsychiatric Pathophysiology. Neurology 35: 389–391. 1993 Dementia. Philadelphia: F. A. Davis. Whitehouse, Peter J., and Daniel R. George 2007 Is the Concept of Alzheimer’s Disease Outmoded? Alzheimer’s Dementia 4(4): 331. 2008 The Myth of Alzheimer’s: What You Aren’t Being Told about Today’s Most Dreaded Diagnosis. New York: St. Martin’s Press. 2009 Banking on Stories for Healthier Cognitive Ageing. Lancet 373: 1166–1167. Whitehouse, Peter J., and Eric T. Juengst 2005 Antiaging Medicine and Mild Cognitive Impairment: Practice and Policy Issues for Geriatrics. Journal of the American Geriatrics Society 53(8): 1417–1422. Whitehouse, Peter J., Konrad Maurer, and Jesse F. Ballenger 2000 Aging, Culture, and the Framing of Alzheimer Disease. In Concepts of Alzheimer Disease: Biological Clinical and Cultural Baltimore: Johns Hopkins University Press. Whitehouse, Peter J., Atwood D. Gaines, Heather Lindstrom, et al. 2005 Anthropological Contributions to the Understanding of Age-Related Cognitive Impairment. Lancet Neurology 4: 320–326. Whitehouse, Peter J., Daniel R. George, and Simon D’Alton 2011 Describing the Dying Days of ‘‘Alzheimer’s Disease’’. Journal of Alzheimer’s Disease 24(1): 11–13. Wig, N.N. 1983 DSM-III: A Perspective from the Third World. In International Prespectives on DSM-III. R.L. Spitzer, J.B.W. Williams, and A.E. Skodol, eds., pp. 79–89. Washington, DC: American Psychiatry Press. Young, Allan 1995 The Harmony of Illusions: Inventing Post-Traumatic Stress Disorder. Princeton, NJ: Princeton University Press.

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