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The Development of Kraepelin’s Mature Diagnostic Concept of Catatonic Dementia Praecox: A Close Reading of Relevant Texts
Through a close reading of texts, this essay traces the development of catatonia from its origination in Kahlbaum’s 1874 monograph to Kraepelin’s catatonic subtype of his new category of Dementia Praecox (DP) in 1899. In addition to Kraepelin’s second to sixth textbook editions, I examine the six articles referenced by Kraepelin: Kahlbaum 1874, Brosius 1877, Neisser 1887, Behr 1891, Schüle 1897, and Aschaffenburg 1897 (Behr and Aschaffenburg worked under Kraepelin). While Brosius and Neisser confirmed Kahlbaum’s descriptions, Behr, Schüle, and Aschaffenburg concluded that his catatonic syndrome was nonspecific and only more narrowly defined forms, especially those with deteriorating course, might be diagnostically valid. Catatonia is first described by Kraepelin as a subform of Verrücktheit (chronic nonaffective delusional insanity) in his second to fourth editions. In his third edition, he adds a catatonic form of Wahnsinn (acute delusional-affective insanity). His fourth and fifth editions contain, respectively, catatonic forms of his two proto-DP concepts: Psychischen Entartungsprocesse and Die Verblödungsprocesse. Kahlbaum’s catatonia required a sequential phasic course. Positive psychotic symptoms were rarely noted, and outcome was frequently good. While agreeing on the importance of key catatonic signs (stupor, muteness, posturing, verbigeration, and excitement), Kraepelin narrowed Kahlbaum’s concept, dropping the phasic course, emphasizing positive psychotic symptoms and poor outcome. In his fourth to sixth editions, as he tried to integrate his three DP subtypes, he stressed, as suggested by Aschaffenburg and Schüle, the close clinical relationship between catatonia and hebephrenia and emphasized the bizarre and passivity delusions seen in catatonia, typical of paranoid DP.
Journal Article
What psychiatric genetics has taught us about the nature of psychiatric illness and what is left to learn
Psychiatric genetics has taught us a great deal about the nature of psychiatric disorders. Traditional family, twin and adoption studies have demonstrated the substantial role of genetic factors in their etiology, clarified the role of genetic factors in comorbidity, elucidated development pathways, and documented the importance of gene–environment correlation and interaction. We have also received some hard lessons when we were unable to detect replicable genes of large effect size and found that our much-valued candidate genes did not live up to their expected promise. With more mature molecular and statistical methods, we are entering now a different era. Statistical analyses of aggregate molecular signals are validating earlier heritability estimates. Replicated findings from genome-wide association studies are beginning to emerge, as are discoveries of large-effect size rare genomic variants. The number of such findings is likely to soon grow dramatically. The most pressing question facing the field is what biological picture these results will reveal. I articulate four possible scenarios that reflect (i) no, (ii) minimal, (iii) moderate and (iv) high biological coherence in the replicated molecular variant findings, which are soon likely to emerge. I discuss the factors that will likely influence these patterns, including the problems of etiological heterogeneity and multiple realizability. These findings could provide critical insights into the underlying biology of our psychiatric syndromes and potentially permit us to perceive, ‘through a glass darkly,’ the levels of the mind–brain system that are disordered.
Journal Article
Melancholia as psychalgia: the integration of psychophysiological theory and psychopathologic observation in the mid-19th century
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.
Journal Article
Psychiatric genetics and the structure of psychopathology
For over a century, psychiatric disorders have been defined by expert opinion and clinical observation. The modern DSM has relied on a consensus of experts to define categorical syndromes based on clusters of symptoms and signs, and, to some extent, external validators, such as longitudinal course and response to treatment. In the absence of an established etiology, psychiatry has struggled to validate these descriptive syndromes, and to define the boundaries between disorders and between normal and pathologic variation. Recent advances in genomic research, coupled with large-scale collaborative efforts like the Psychiatric Genomics Consortium, have identified hundreds of common and rare genetic variations that contribute to a range of neuropsychiatric disorders. At the same time, they have begun to address deeper questions about the structure and classification of mental disorders: To what extent do genetic findings support or challenge our clinical nosology? Are there genetic boundaries between psychiatric and neurologic illness? Do the data support a boundary between disorder and normal variation? Is it possible to envision a nosology based on genetically informed disease mechanisms? This review provides an overview of conceptual issues and genetic findings that bear on the relationships among and boundaries between psychiatric disorders and other conditions. We highlight implications for the evolving classification of psychopathology and the challenges for clinical translation.
Journal Article
Common adult psychiatric disorders in Swedish primary care where most mental health patients are treated
Background
The overall aim of this study is to present descriptive data regarding the treated prevalence of nine common psychiatric and substance use disorders in the first Primary Care Registry (PCR) in Sweden: Major Depression (MD), Anxiety Disorders (AD), Obsessive-Compulsive Disorder (OCD), Adjustment Disorder (AdjD), Eating Disorders (ED), Personality Disorder (PD), Attention Deficit Hyperactivity Disorder (ADHD), Alcohol Use Disorder (AUD) and Drug Abuse (DA).
Method
We selected 5,397,675 individuals aged ≥18. We examined patterns of comorbidity among these disorders and explored the association between diagnoses in the PCR and diagnoses obtained from Hospital and Specialist care. We explored the proportion of patients with these nine disorders that are only treated in primary health care.
Results
For four of our disorders, 80% or more of the cases were present
only
in the PCR: AdjD, DA, AD and MD. For two disorders (OCD and ED), 65–70% of cases were only found in the PCR. For three disorders (PD, AUD, and ADHD), 45–55% of the patients were only present in the PCR.
Conclusion
The PCR will, in the future, likely prove to be an important tool for studies in psychiatric epidemiology.
Journal Article
Socioeconomic status and alcohol use disorders across the lifespan: A co-relative control study
Alcohol use disorders (AUD) is well known to aggregate in families and is associated with socioeconomic status (SES). The objective was to study the effect of education, income and neighborhood SES in adulthood on AUD, and to explore whether the potential associations were confounded by shared familial factors, by using a co-relative control design.
Data on AUD was drawn from the Swedish inpatient and outpatient care registers; prescription drug register; and crime data. Through national population registers we collected information on income, education and neighborhood SES at age 25, 30, 35 and 40 years in all individuals born in Sweden between 1950 and 1980. Each sex-specific stratum consisted of approximately 750,000-1,200,000 individuals, who were followed for AUD for a mean follow-up time ranging between 10 and 15 years until the end of 2013. Cox proportional hazards models were used to investigate the risk of AUD as a function of income, education and neighborhood SES in the general population and in pairs of first cousins and full siblings within the same sex, who differed in their exposure to the SES measure.
Higher educational level, higher income and higher neighborhood SES were all associated with a reduced risk for AUD for both males and females in all ages. The potentially protective effect remained but was attenuated when comparing pairs of first cousins and full siblings.
High educational level and income in adulthood, as well as high neighborhood socioeconomic status, may represent protective factors against alcohol use disorders, even when shared familial factors, e.g. childhood socioeconomic status and genetic factors, have been taken into account.
Journal Article
Marriage and reductions in men's alcohol, tobacco, and cannabis use
Psychoactive substance use is lower among married compared to divorced or unmarried men; yet, the nature of this effect remains unclear because becoming and staying married is potentially confounded with substance-related background familial and individual factors, like parental divorce and personality. The authors investigated the associations between marital status and substance use; how substance use changed across the transition to marriage; and whether marriage effects were likely to be causal.
The sample included 1790 adults from male-male twin pairs from a population-based registry. Measures of marital status and alcohol, tobacco, and cannabis use came from Life History Calendars. Data were analyzed using regression, co-twin comparison, and within-person models. The latter models are tools for quasi-causal inference that control for familial and individual-level confounders.
Married men used less alcohol, tobacco, and cannabis than men who were divorced/separated or single. In analyses of substance use across the transition to marriage, men reduced their alcohol and cannabis use both before and after marriage, but their tobacco use only after marriage. These effects were largely robust in co-twin and within-person analyses.
Marriage was associated with substantial reductions in substance use compared to being divorced/separated or single, and these reductions began prior to marriage. The co-twin comparison and within-person models ruled out the alternative explanation that marriage effects were due to confounding background familial and individual factors. These results provide strong evidence that the social role expectations associated with marriage reduce psychoactive substance use.
Journal Article
The Prehistory of Schneider’s First-Rank Symptoms: Texts From 1810 to 1932
First-rank symptoms (FRS), proposed by Kurt Schneider in 1939, subsequently became influential in schizophrenia diagnosis. We know little of their prehistory. How often were FRS described before 1939 and in which countries and time periods? Which FRS was most frequently noted?
Forty psychiatric texts from 37 authors, published 1810-1932, were identified that described FRS. In a systematic subsample, half of the textbooks examined contained such descriptions with little differences between countries or over time. Somatic passivity was most commonly noted, followed by thought insertion, thought withdrawal, and made actions. This pattern resembled that reported in recent studies of schizophrenia. A novel term-delusions of unseen agency-was seen in psychiatric texts and then found, from 1842 to 1905, in a range of official reports, and psychiatric, medical, and general audience publications. The Early Heidelberg School (Gruhle, Mayer-Gross, Beringer) first systematically described \"self-disturbances\" (Ichstörungen), many of which Schneider incorporated into FRS.
From the beginning of Western descriptive psychopathology in the early 19th century, symptoms have been observed later described as first-rank by Schneider. A term \"delusion of unseen agency\"-closely related to Schneider's first-rank concept-was popular in the second half of the 19th century and described in publications as prominent as the Encyclopedia Britannica and New England Journal of Medicine. The descriptions of these specific symptoms, with substantial continuity, over more than 2 centuries and many countries, suggest that an understanding of their etiology would teach us something foundational about the psychotic illness.
Journal Article
The impact of sex, age at onset, recurrence, mode of ascertainment and medical complications on the family genetic risk score profiles for alcohol use disorder
Alcohol use disorder (AUD) is clinically heterogeneous. We examine its potential genetic heterogeneity as a function of sex, age, clinical features and mode of ascertainment.
In the Swedish population born 1932-1995 (
= 5 829 952), we examined the genetic risk profiles for AUD, major depression (MD), anxiety disorders, bipolar disorder, drug use disorder (DUD), attention deficit-hyperactivity disorder (ADHD) and criminal behavior (CB) in 361 124 cases of AUD subdivided by sex, age at onset (AAO), recurrence, mode of ascertainment and medical complications. Family genetic risk scores (FGRS), calculated from 1st to 5th-degree relatives controlling of cohabitation, assesses genetic risk from phenotypes in the family, not from DNA variants.
FGRS profiles differed modestly across sex with all scores higher in females. Differences were more pronounced for AAO and recurrence with the FGRS for AUD, DUD, ADHD and CB substantially higher in cases with early AAO or high recurrence rates. Genetic profiles differed considerably by mode of ascertainment, with higher FGRS for AUD and most other disorders in patients seen in hospital
primary care settings. Cases of AUD with medical complications had higher FGRS for AUD. AUD cases comorbid with MD and DUD had higher FGRS risk for AUD, but this genetic may be less specific given increases in FGRS for multiple other disorders.
From a genetic perspective, AUD differs substantially as a function of AAO, recurrence, mode of ascertainment and patterns of comorbidity, suggesting caution in cross-sample comparisons of AUD cohorts that differ in these features.
Journal Article