Vanilmandelicaciduria in the Different Clinical Phases of Manic Depressive Psychosis

1970 ◽  
Vol 116 (533) ◽  
pp. 435-436 ◽  
Author(s):  
Tito Campanini ◽  
Alberto Catalano ◽  
Carlo De Risio ◽  
Giacomo Mardighian
Keyword(s):  
Affective Disorders ◽  
Adrenergic Receptor ◽  
Manic Depressive Psychosis ◽  
Relative Decrease ◽  
Manic Depressive ◽  
Receptor Sites

The catecholamine hypothesis of affective disorders proposes that 'some-if not all-depressions are associated with an absolute or relative decrease in catecholamines, particularly norepinephrine, available at central adrenergic receptor sites. Elation, conversely, may be associated with an excess of such amines' (Schildkraut, 1965).

Normothymotics, “Mood-Normalizers”

1963 ◽  
Vol 109 (463) ◽  
pp. 803-809 ◽  
Author(s):  
Mogens Schou
Keyword(s):  
Clinical Psychiatry ◽  
Affective Disorders ◽  
Psychopathological Symptoms ◽  
Manic Depressive Psychosis ◽  
Manic Depressive ◽  
Mental Diseases ◽  
Drug Compounds ◽  
Almost All

The action of almost all drugs used so far in psychiatric pharmacotherapy has been directed against psychopathological symptoms or syndromes and not against mental diseases as such, the nosological entities defined by classical clinical psychiatry. In this paper the attention will be drawn towards a different type of drug: compounds with an action specific to a disease rather than to a symptom, and evidence will be presented for the existence within this class of a group that is characterized by being active against affective disorders (manic-depressive psychosis).Normothymotics, “mood-normalizers”, is proposed as a collective name for drugs belonging to this group.

Genetical Analysis of Unipolar and Bipolar Endogenous Affective Psychoses

1977 ◽  
Vol 131 (5) ◽  
pp. 478-485 ◽  
Author(s):  
Olga Trzebiatowska-Trzeciak
Keyword(s):  
Affective Disorders ◽  
Unipolar Depression ◽  
Genetical Analysis ◽  
Polygenic Inheritance ◽  
Affective Psychoses ◽  
Manic Depressive Psychosis ◽  
Manic Depressive ◽  
Morbidity Risk ◽  
Second Degree

The mode of inheritance of affective psychoses was studied in 800 first degree and 582 second degree relatives of 122 probands. Morbidity risk for unipolar depression was 12·0±3·2 and 11·4±2·7 per cent respectively for parents and siblings of probands suffering from unipolar depression. Morbidity risk for manic-depressive psychosis for the respective groups of first degree relatives of manic-depressive probands was 15·1±3·2 and 16·9±3·2 per cent. In second degree relatives the morbidity risk was 3·4±1·0 and 5·3±1·4 per cent for unipolar depression and manic-depressive psychosis respectively.The results indicate the role of genetical factors in the etiology of both types of affective disorder and show that unipolar depression and manic-depressive psychosis are distinct entities. The hypothesis of X-linked dominant transmission was not confirmed in either of these affective disorders. By means of the computational model of Slater, no results compatible with a polygenic inheritance of unipolar depression or manic-depressive psychosis were found.

Urinary Excretion of Cyclic Amp and Manic-Depressive Psychosis

1972 ◽  
Vol 120 (557) ◽  
pp. 405-408 ◽  
Author(s):  
B. L. Brown ◽  
J. G. Salway ◽  
J. D. M. Albano ◽  
R. P. Hullin ◽  
R. P. Ekins
Keyword(s):  
Cyclic Amp ◽  
Urinary Excretion ◽  
Affective Disorders ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Normal Subjects ◽  
Manic Depressive Psychosis ◽  
Manic Depressive ◽  
Mental Symptoms ◽  
Manic Patients

Recently several communications have been published implicating impaired 3′5′ cyclic adenosine monophosphate (cyclic AMP) metabolism as a causal factor in affective disorders (1, 3, 7, 8, 9, 11). In particular, the urinary excretion of cyclic AMP in manic patients is reported to be increased compared with that of normal subjects, whereas in depressed patients a decreased excretion has been observed (1, 7, 8, 9). These findings form the basis of a theory explaining the systemic and mental symptoms of affective disorders (1).

Activation of Hageman Factor by α-Adrenergic Stimulation

1970 ◽  
Vol 23 (03) ◽  
pp. 417-422 ◽  
Author(s):  
D. G McKay ◽  
J.-G Latour ◽  
Mary H. Parrish
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Adrenergic Receptor ◽  
Adrenergic Stimulation ◽  
Hageman Factor ◽  
Intravascular Coagulation ◽  
Receptor Sites ◽  
High Doses ◽  
Stimulation Of

SummaryThe infusion of epinephrine in high doses produces disseminated intravascular coagulation by activation of Hageman factor. The effect is blocked by phenoxybenz-amine and is therefore due to stimulation of α-adrenergic receptor sites.

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