Manic-Depressive Illness: A Comparative Study of Patients with and Without a Family History

1972 ◽  
Vol 120 (558) ◽  
pp. 523-530 ◽  
Author(s):  
J. Mendlewicz ◽  
R. R. Fieve ◽  
J. D. Rainer ◽  
J. L. Fleiss

Early studies (21, 22, 25, 12) have pointed to a genetic component in the aetiology of manic-depressive disorders. More recently, careful clinical observation has suggested the division of the affective disorders into two distinct groups: the so-called bipolar or manic-depressive group and the unipolar type with recurrent depressions only (14, 27, 1). Although genetic differences in terms of family risk have been demonstrated between the so-called bipolar and unipolar psychoses, it is not yet evident whether each group constitutes a homogeneous entity. Moreover, the diagnosis of unipolar depressive disease for the authors cited above includes such syndromes as involutional psychotic reactions, psychotic depressive reactions, and probably also psychoneurotic depressions.

1973 ◽  
Vol 122 (570) ◽  
pp. 601-602 ◽  
Author(s):  
A. Venkoba Rao

Manic-depressive illness is believed to comprise two different clinical entities: Bipolar and Monopolar. This paper aims to study any differences there may be between monopolar and bipolar depressions in respect of three factors: occurrence of affective disorder (including suicide) in first degree relatives; parental death before the patients' twelfth birthday and the extent of ‘jointness' (Khatri, 1970) of the patients' family.


1985 ◽  
Vol 15 (2) ◽  
pp. 297-309 ◽  
Author(s):  
Graham Robertson ◽  
Pamela J. Taylor

SynopsisSeventy-one men completed a battery of cognitive tests which were designed to reflect verbal analytic and non-verbal holistic functioning. Interest centred around pattern of response. Thirty men were suffering from an affective disorder and forty-one were well. All the men were in prison, the majority awaiting trial. The affective disorder group was subdivided into three categories: men who had a history of manic-depressive illness; a group of unipolar, psychotically depressed men; and men who were regarded as being depressed in reaction to circumstances. All three groups showed specific difficulty in dealing with spatial/holistic tasks, other factors being held constant. They were also found to differ in a number of other respects. The possible significance of these differences is discussed.


1987 ◽  
Vol 2 (3) ◽  
pp. 163-173
Author(s):  
Mario Maj ◽  
Dargut Kemali

SummaryThe question of the nosological status of schizoaffective disorders remains one of the most controversial issues of clinical psychiatry. There are, in fact, at least five different hypotheses about the nature of these disorders: • that they are always variants of schizophrenia, • that they are always variants of major affective disorders, • that they represent a “third psychosis” distinct from both schizophrenia and manic-depressive illness, • that they find their place in the intermediate position of a “continuum” whose poles are represented by the typical forms of schizophrenia and manic-depressive illness, • that they result from the simultaneous occurrence of a true schizophrenia and a true manic-depressive illness in the same patient. The last of these hypotheses can hardly be accepted, since it would predict an annual frequency of schizoaffective disorders of about 2 per 108, compared to the actual frequency of 2 per 105. Of the remaining four hypotheses, the first two are consistent with the Kraepelinian “dichotomic” paradigm, whereas the third and the fourth contradict this paradigm. The results of empirical investigations (that is, of family studies, outcome studies and studies on response to drug treatments in schizoaffective patients) do not provide a full support to any of the above hypotheses. What empirical evidence seems to show, instead, is that schizoaffective disorders represent a heterogeneous group of syndromes. Part of these disorders can be interpreted, upon close scrutiny, as variants of either of the major psychoses (for instance, bipolar schizoaffective States appear to be closely allied to major affective disorders). There seems to be, however, a subpopulation of schizoaffective patients which escapes the Kraepelinian dichotomic model.


1987 ◽  
Vol 151 (4) ◽  
pp. 554-555 ◽  
Author(s):  
C. M. Linter

Diagnosis of classic psychiatric illness in mentally handicapped individuals remains difficult. Manic-depressive illness has previously been reported in both pre-pubertal and pubertal children with a mental handicap and with a family history. This paper reports a case of manic-depressive psychosis in childhood, with no family history, short-cycle mood swings and good response to lithium therapy.


1995 ◽  
Vol 7 (2) ◽  
pp. 67-69
Author(s):  
F. Flentge ◽  
C.J. Slooff

In manic-depressive patients treated with lithium salts the transport of choline over the erythrocyte membrane is strongly inhibited, resulting in dramatically increased erythrocyte choline levels (for review see ref. 1). Whether or not there is a relationship between this effect and treatment response is not clear. Data on this issue are scarce possibly because the measurement of treatment response in lithium prophylaxis is very difficult and time consuming. Also the effect on erythrocyte choline is specific for lithium and not for manic-depressive illness. We will address here the question of a possible relation between erythrocyte choline and clinical effects of lithium.


1989 ◽  
Vol 155 (3) ◽  
pp. 294-304 ◽  
Author(s):  
Peter McGuffin ◽  
Randy Katz

Depressive disorders are more common in the relatives of depressed probands than in the population at large, and there is compelling evidence that the familial aggregation of bipolar disorder and severe unipolar depression is at least partly due to genetic factors. However, the evidence concerning ‘non-endogenous' depression is less clear, and family environment probably plays a stronger role. Much current research is focused on two areas: firstly, the mode of inheritance of manic-depressive illness, with the use of molecular biological techniques to detect and localise major genes; and secondly, the ways in which familial predisposition and environmental insults combine to produce depressive disorder.


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