While sufferers of major depression to the present day sometimes describe their experience as "mental pain," limited attention has been given to one of the major etiologic theories of 19th century ...psychiatry: melancholia as psychalgia. I illustrate the development of this theory, which arose in the context of the early phases of the application of psychophysiology to mental illness, through German, French, and English psychiatric texts from the 1830-1870s. As clinical pathological correlation became a dominant paradigm in early 19th medicine, nervous diseases stood out as potential exceptions, sometimes demonstrating "pain without lesions" or neuralgia. Tic Douloureux was a paradigmatic example. The first descriptions of reflex actions in the spinal cord in the early 19th century resulted in a range of theories of reflexes in brain that expanded to include "ganglia" that could react to diverse complex social and mental stimuli, and whose actions could impact key mental functions including mood. Theories of neuralgia included a constitutional predisposition and an acute physical trauma producing a hypersensitivity so that normal stimuli (e.g., touch) were misinterpreted as excruciating pain. A parallel framework was conceptualized in the brain to produce psychalgia. A predisposition combined with a mental trauma could produce hypersensitivity in key brain ganglia. This psychophysiological framework explained how normal social and introspective experiences would, in melancholic patients, be interpreted in a distorted manner, reinforcing themes of inadequacy, failure, and worthlessness, and produce a sustained mood state of intense mental pain or psychalgia. I illustrate the development of this theory, which integrated brain and mind-based perspectives on mental illness, through the writings of four major 19th alienists: Guislain, Griesinger, Maudsley, and Krafft-Ebing.
Personality and failures in interpersonal relationships play a stronger etiologic role in major depression for women, but childhood sexual abuse, externalizing psychopathology, prior depression, and ...acute financial, occupational, or legal stress were stronger etiologic pathways to depression for men. The sex differences in these pathways offer a road map for clinicians in addressing psychological issues important to their patients.
ObjectiveThe authors sought to clarify the nature of sex differences in the etiologic pathways to major depression.MethodRetrospective and prospective assessments of 20 developmentally organized risk factors and the occurrence of past-year major depression were conducted at two waves of personal interviews at least 12 months apart in 1,057 opposite-sex dizygotic twin pairs from a population-based register. Analyses were conducted by structural modeling, examining within-pair differences.ResultsSixty percent of all paths in the best-fit model exhibited sex differences. Eleven of the 20 risk factors differed across sexes in their impact on liability to major depression. Five had a greater impact in women: parental warmth, neuroticism, divorce, social support, and marital satisfaction. Six had a greater impact in men: childhood sexual abuse, conduct disorder, drug abuse, prior history of major depression, and distal and dependent proximal stressful life events. The life event categories responsible for the stronger effect in males were financial, occupational, and legal in nature.ConclusionsIn a co-twin control design, which matches sisters and brothers on genetic and familial-environmental background, personality and failures in interpersonal relationships played a stronger etiologic role in major depression for women than for men. Externalizing psychopathology, prior depression, and specific “instrumental” classes of acute stressors were more important in the etiologic pathway to major depression for men. The results are consistent with previously proposed typologies of major depression that suggest two subtypes that differ in prevalence in women (deficiencies in caring relationships and interpersonal loss) and men (failures to achieve expected goals, with lowered self-worth).
The nature of psychiatric disorders Kendler, Kenneth S.
World psychiatry,
February 2016, 2016-Feb, 2016-02-00, 20160201, Letnik:
15, Številka:
1
Journal Article
Recenzirano
Odprti dostop
A foundational question for the discipline of psychiatry is the nature of psychiatric disorders. What kinds of things are they? In this paper, I review and critique three major relevant theories: ...realism, pragmatism and constructivism. Realism assumes that the content of science is real and independent of human activities. I distinguish two “flavors” of realism: chemistry‐based, for which the paradigmatic example is elements of the periodic table, and biology‐based, for which the paradigm is species. The latter is a much better fit for psychiatry. Pragmatism articulates a sensible approach to psychiatric disorders just seeking categories that perform well in the world. But it makes no claim about the reality of those disorders. This is problematic, because we have a duty to advocate for our profession and our patients against other physicians who never doubt the reality of the disorders they treat. Constructivism has been associated with anti‐psychiatry activists, but we should admit that social forces play a role in the creation of our diagnoses, as they do in many sciences. However, truly socially constructed psychiatric disorders are rare. I then describe powerful arguments against a realist theory of psychiatric disorders. Because so many prior psychiatric diagnoses have been proposed and then abandoned, can we really claim that our current nosologies have it right? Much of our current nosology arose from a series of historical figures and events which could have gone differently. If we re‐run the tape of history over and over again, the DSM and ICD would not likely have the same categories on every iteration. Therefore, we should argue more confidently for the reality of broader constructs of psychiatric illness rather than our current diagnostic categories, which remain tentative. Finally, instead of thinking that our disorders are true because they correspond to clear entities in the world, we should consider a coherence theory of truth by which disorders become more true when they fit better into what else we know about the world. In our ongoing project to study and justify the nature of psychiatric disorders, we ought to be broadly pragmatic but not lose sight of an underlying commitment, despite the associated difficulties, to the reality of psychiatric illness.
Histories of the diathesis-stress model trace its origins to the 1950s. However, of 26 psychiatric texts published between 1800 and 1910, 17 noted that causes of insanity could be usefully divided ...into those that predispose to illness and those that excite onset. In this “predisposition-excitation framework” (PEF) for the etiology of insanity, hereditary or constitutional factors were critical predisposing causes, but education, occupation, sex, and marital status were typically included as well. Psychological traumas were key exciting causes, but so were somatic diseases, pregnancy, and substance abuse. The PEF was often used to explain the diversity of individual responses to adversity. While single dramatic events often excited onset, daily repetition of lesser shocks could also bring on insanity. Matching could occur between predisposing and exciting causes in individuals who had “special susceptibilities.” Predispositions could lead to “affects, passions, and perverse manner of life,” which became exciting causes. Authors emphasized that it was easier to prevent exposures to exciting causes than to reverse predispositions. A thought experiment of an individual “transplanted early into new and different social conditions” anticipated models of primary prevention. Ratings of predisposing and exciting causes were mandated in the United Kingdom from 1878 to 1887 and at several U.S. psychiatric hospitals in the early 20th century. The PEF was far more stable over place and time in the 19th century than any psychiatric nosologic system. Contrary to the doctrinaire schools of psychoanalytic and biological psychiatry that dominated much of 20th-century psychiatry, the PEF proposed a flexible, developmental, and pluralistic view of etiologic pathways to psychiatric illness.
In 1893 and 1896, in his fourth and fifth textbook editions, Emil Kraepelin brought together 3 syndromes to form the first and second of his 2 prequels to dementia praecox (DP), a definitive version ...of which he would propose in his 1899 sixth textbook edition. These syndromes, which would become hebephrenic DP, catatonic DP, and paranoid DP, each had distinct histories. Hebephrenic DP was derived from syndromes first proposed by Hecker, and catatonic DP was derived from syndromes first proposed by Kahlbaum, and then both were substantially revised. Kraepelin created paranoid DP de novo from a division of his early broad delusional syndrome Verrücktheit, distinguishing it from paranoia. Two of these syndromes (catatonic DP and paranoid DP) were present in different forms in his earlier textbook editions, and 1 syndrome (hebephrenic DP) was not. In his 2 prequels, the 3 syndromes were listed together with a brief preface. In the sixth textbook edition, they became “clinical forms” of DP with a lengthy integrative introduction. Much more than in his prequels, in his sixth edition, Kraepelin stitched these 3 syndromes together, emphasizing their shared signs, symptoms, and course. Hebephrenia was the core of Kraepelin’s DP concept, while the paranoid subtype fitted least comfortably within his framework. His term dementia was meant in a broad sense consistent with both short-term and rare long-term recoveries. Kraepelin was a pragmatist, not a purist, in his nosologic work and focused both on clinical features and course and outcome. He experimented with various nosologic categories, willing to revise earlier formulations in the light of new data. He was more tentative about his conclusions than many who followed him.
While the evolution of our modern concepts of mania and melancholia over the 19th century is relatively well-understood, no such clear narrative exists for the nonaffective psychotic syndromes that ...culminated in Kraepelin’s concept of dementia praecox in 1899. These narratives were relatively distinct in Germany and France. An important milestone in the French literature is the 1852 essay by the alienist and polymath Charles Lasègue which contained the first detailed modern description of a persecutory delusional syndrome. Lasègue was a careful clinical observer who emphasized a symptomatic approach to psychiatric nosology and was less concerned with course and outcome. He details the evolution of persecutory delusions from increasing referential observations of real events, to the resulting anxious confusion and then the emergence of explanatory delusional beliefs. Once formed, these beliefs, he notes, are relatively impervious to correction. Lasègue was unusual for his time in emphasizing a “first-person perspective” on psychotic experiences, and quotes from his patients in his case history, of which he presents 15. Of these, 12 had auditory hallucinations and 4 passivity phenomena. While conceptualized differently than mid-19th century pre-Kraepelinian German writing on delusional syndromes, and unique on its focus on persecutory delusions, Lasègue’s important essay shared a common view on the key features of a broad nonaffective delusional-hallucinatory syndrome. It was this syndrome that Kraepelin, over multiple drafts in the first 6 editions of his textbook from 1883 to 1899, was to divide into his mature concepts of paranoia and the paranoid subtype of dementia praecox.
Abstract
In 1921, at the age of 65, 6 years after completing the final edition of his textbook, 22 years after first proposing the concept of dementia praecox (DP), and 1 year before retiring from ...clinical work, Emil Kraepelin completed the last edition of his “Introduction to Clinical Psychiatry,” which contained a mini-textbook for students, 10 pages of which were devoted to DP. This work also included a series of new detailed case histories, 3 of which examined DP. This neglected text represents a distillation of what Kraepelin judged, near the end of his long career, to be the essential features of DP. The relevant text and case histories are translated into English for the first time. Kraepelin did not define DP solely by its chronic course and poor prognosis, acknowledging that remissions and even full recovery might be possible. His clinical description emphasized the frequency of bizarre delusions and passivity symptoms. He recognized the heterogeneity of the clinical presentations, outlining 6 subtypes of DP, including dementia simplex, depressive and stuporous dementia, and an agitated and circular DP. Kraepelin’s original concept of DP was not impervious to change and expanded somewhat, especially with the inclusion of Diem’s concept of simple DP. He also reviews several contributions of Bleuler, including his concept “latent schizophrenia.” He writes poignantly of the psychological consequences of DP. His 3 DP cases, for advanced students, included simple DP, “periodic catatonic,” and “speech confusion.”
This essay explores the etiology of psychiatric disorders across biological, psychological, and environmental risk factors, and outlines three central paradigms for risk analysis, mechanisms of ...illness, and first-person approaches to patient empathy.
This essay addresses two interrelated questions: What is the structure of current psychiatric science and what should its goals be? The author analyzed all studies addressing the etiology of psychiatric disorders in the first four 2013 issues of 12 psychiatry and psychology journals. He classified the resulting 197 articles by the risk factors examined using five biological, four psychological, and three environmental levels. The risk factors were widely dispersed across levels, suggesting that our field is inherently multilevel and already practicing empirically based pluralism. However, over two-thirds of the studies had a within-level focus. Two cross-level patterns emerged between 1) systems neuroscience and neuropsychology and 2) molecular or latent genetic factors and environmental risks. The author suggests three fundamental goals for etiological psychiatric research. The first is an eclectic effort to clarify risk factors regardless of level, including those assessed using imaginative understanding, with careful attention to causal inference. An interventionist framework focusing on isolating causal effects is recommended for this effort. The second goal is to clarify mechanisms of illness that will require tracing causal pathways across levels downward to biological neuroscience and upward to social factors, thereby elucidating the important cross-level interactions. Here the philosophy of biology literature on mechanisms can be a useful guide. Third, we have to trace the effects of these causal pathways back up into the mental realm, moving from the Jasperian level of explanation to that of understanding. This final effort will help us expand our empathic abilities to better understand how symptoms are experienced in the minds of our patients.
PDF
