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E Zerbin-Rüdin

Publications and source records attributed to E Zerbin-Rüdin.

At least 19 recordsLinked to original sources
PubMed1996

Ernst Rüdin (1874-1952) and his genealogic-demographic department in Munich (1917-1986): an introduction to their family studies of schizophrenia.

This historical review introduces a series of papers abstracting, reanalyzing and commenting upon family studies of schizophrenia conducted by Ernst Rüdin and his geneologic-demographic department in Munich. These studies, which pioneered many of the methods still critical to psychiatric genetics, are little known in the anglophonic world. Starting with a study of schizophrenia in siblings, members of the Rüdin school expanded to study a wide range of relationships (including grandchildren and nieces/nephews) and disorders (including affective illness, obsessive-compulsive disorder, epilepsy and personality disorders). They examined many methodologic issues in psychiatric genetics including i) ascertainment correction, ii) anticipation, iii) age correction, iv) assortative mating, v) reduced fertility, vi) spectrum disorders, and vii) familial transmission of age at onset. After the rise of Hitler in Germany, Rüdin and his institute became involved in the eugenic policies of the Nazis, raising important questions about possible political abuse of scientific findings in general and those from the field of psychiatric genetics in particular.

Demography↗
PubMed1996

Abstract and review of "Studien Uber Vererbung und Entstehung Geistiger Störungen. I. Zur Vererbung und Neuentstehung der Dementia praecox." (Studies on the inheritance and origin of mental illness: I. To the problem of the inheritance and primary origin of dementia praecox). 1916.

The first major family study of schizophrenia, reported by Ernst Rüdin in 1916, examined 2,732 siblings of 755 probands, diagnosed according to the teachings of Kraepelin. This study, the goal of which was to see whether the segregation pattern of schizophrenia in siblings conformed to simple mendelian expectations, was the first in psychiatry to use systematic ascertainment, proband correction and calculation of an age corrected risk of illness--the morbid risk (MR). The MR for narrowly and broadly defined schizophrenia in this sample can be calculated to equal 5.4 and 7.7%. "Other psychoses"--a heterogeneous category--were also common in these siblings (a MR of 5.1%). In a small sample of half-siblings, the MR for narrowly defined schizophrenia was quite low (0.6%). The risk for schizophrenia in siblings was significantly increased by a parental diagnosis of alcoholism, a history of schizophrenia in second or third degree relatives, and, particularly, by a parental diagnosis of "other psychoses." No evidence was found for sex-specific transmission of schizophrenia in these sibships. The MR for narrowly and broadly definite schizophrenia in parents of these probands can be estimated to be 2.3% and 3.9%, respectively. In accord with more recent studies, Rüdin found i) a familial relationship between schizophrenia and other psychoses ii) a substantially lower risk for schizophrenia in parents vs. siblings and iii) a segregation pattern of schizophrenia in siblings that did not conform to that expected for a simple mendelian disorder.

Female↗
PubMed1996

Abstract and review of "Zur Erbpathologie der Schizophrenie" (Contribution to the genetics of schizophrenia). 1916.

Starting from the 722 probands originally studied by Rüdin, Bruno Schulz re-examined them and their relatives confirming the diagnosis in 660. While Rüdin sought for mendelian ratios in siblings, Schulz, anticipating modern methods, focused on the family study method as an approach to clarifying possible etiologic heterogeneity within the schizophrenia syndrome. Using a Kraepelian approach to diagnosis, Schulz reports a MR for narrowly and broadly defined schizophrenia of 6.7 and 8.2% in siblings and 2.6 and 3.7% in parents. He found no evidence for a difference in risk of illness in siblings as a function of either the gender or outcome of the proband. The risk for schizophrenia was significantly increased in siblings of hebephrenic probands. Compared to siblings of probands with no identified factor which precipitated their schizophrenia, the risk for schizophrenia was significantly decreased in probands with a physical etiologic factor but did not differ in siblings of probands with a psychological etiologic factor. The risk for schizophrenia was particularly low in siblings of probands whose onset of illness occurred within a year of major head trauma.

Female↗
PubMed1995

A review and reanalysis of Bruno Schulz's "Erkrankungsalter schizophrener Eltern und Kinder [Age at onset of illness in schizophrenic parents and offspring]:" Zeitschrift für die gesamte Neurologie und Psychiatrie, 168, 709-721, 1940.

Nearly all previous evidence of the familial transmission of age at onset of schizophrenia has been in siblings and twins. In his paper, Bruno Schulz examined the age at onset distribution of schizophrenia in affected parent and offspring pairs, using a systematic series of ascertained cases (n = 106), as well as a second series of chronic in-patients (n = 36). The parent-offspring correlation in age at onset, for cases with a definite diagnosis in the systematically ascertained series, was estimated at 0.346 (95% confidence interval 0.134, 0.528). Schulz did not test for differences between the two series and between males and females, but our reanalysis, using correlational methods and a mixed linear model, did not detect any significant differences. These results are consistent with previous findings that age at onset of schizophrenia is influenced by familial factors which may be genetic.

Adult↗
PubMed1987

Psychiatric genetics and psychiatric nosology.

At the present time, family and twin data are used in psychiatry to test clinical concepts at issue, and, in particular, to validate or reject diagnostic classifications. The dichotomy between the schizophrenias and the effective disorders, as suggested by Kraepelin, has been supported by contemporary family and twin studies and also is corroborated by modern family and adoption studies. In the atypical psychoses it is demonstrated impressively how family data vary with different sampling procedures and diagnostic practices. In the affective disorders, the family findings at first favored the separation of unipolar and bipolar disorders but, subsequently, this concept was questioned and revised. Currently, psychiatric genetics attempts to contribute to the understanding of the affective disorders, in particular the depressions, by delineating subgroups and by looking for possible genetic relations between depression and frequently associated disorders, such as anxiety or anorexia.

Affective Disorders, Psychotic↗
PubMed1979

[Genetics of endogenous psychoses].

As the endogeneous psychoses do not show a Mendelian mode of inheritance, empirical risk figures have to be calculated. They are heterogeneous and nurture as well as nature have a share in the manifestation of illness. The genetic basis of the schizophrenias is demonstrated by twin and adoption studies. The concordance rate in monozygotic twins is four times the rate in dizygotic twins. Schizophrenia is to be found in the biological families of schizophrenic adoptees but not in the adoptive families. However, despite their genetic identity, monozygotic twins do not show 100% concordance but 60% only. Nongenetic factors must be considered. Obviously they are nonspecific and vary between individuals. The same principles apply to the affective psychoses. At present research is most interested in the problem of heterogeneity. Do pure depressive and manic-depressive disease form one genetic entity, or two different ones, or have they in common part of their genetic basis? Some remarks on genetic counselling are made.

Adoption↗
PubMed1976

[Psychiatry, morphology and behaviour genetics (author's transl)].

No organic substrate is known for endogenous psychoses, neuroses and behaviour disorders. Therefore genetic studies have to depart from the behavioural level. This approach has yielded the empirical risk figures which depend on genetic and environmental factors. Beyond this level behaviour genetics endeavours to clarify the genetic mechanisms underlying normal and abnormal behaviour. In the schizophrenias f.i. several stretegies have been developed to approach the genetic basis: Mathematial models as to the mode of inheritance; use of modified classificatory and diagnostic criteria for genetic analysis; search for phenomena representing steps between genotype and phenotype and showing a clear mode of inheritance, f.i. biochemical or electrophysiological characters. In case the neurotransmitters are not changed in quality or total quantity but in compartmentation in the genetic defect might be localized in the pre- or postsynaptic membranes or receptors. Genetic factors are also involved in nonpsychotic behaviour disorders but to a lesser degree. They can be demonstrated even in psychoses with somatic background.

Catecholamines↗