A Comparison of Two Drug Treatments in Depressive Illness

1969 ◽  
Vol 115 (523) ◽  
pp. 693-696 ◽  
Author(s):  
M. W. Browne
Keyword(s):  
Depressive Illness ◽  
Drug Treatments ◽  
Amitriptyline Hydrochloride

This paper describes a comparison of two therapeutic regimes for depressive illness: (a) imipramine, and (b) a preparation containing amitriptyline hydrochloride and perphenazine in the ratio 25:2 (Triptafen-DA).

Amitriptyline and Perphenazine in Depressive Illness a Controlled Trial

1967 ◽  
Vol 113 (495) ◽  
pp. 195-199 ◽  
Author(s):  
Ijaz Haider
Keyword(s):  
Controlled Trial ◽  
Depressive Illness ◽  
Double Blind Trial ◽  
Double Blind ◽  
Matching Placebo ◽  
Blind Trial ◽  
Amitriptyline Hydrochloride

This paper describes a “double-blind” trial comparing ‘Triptafen’ tablets—each containing amitriptyline hydrochloride 25 mg. and perphenazine 2 mg.—with a matching placebo in the treatment of depressive illness.

Nosological status of schizoaffective disorders: Theoretical models and empirical evidence

1987 ◽  
Vol 2 (3) ◽  
pp. 163-173
Author(s):  
Mario Maj ◽  
Dargut Kemali
Keyword(s):  
Empirical Evidence ◽  
Affective Disorders ◽  
Theoretical Models ◽  
Depressive Illness ◽  
Simultaneous Occurrence ◽  
Manic Depressive Illness ◽  
Schizoaffective Disorders ◽  
Manic Depressive ◽  
Drug Treatments ◽  
Annual Frequency

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.

Serotonergic Genes and Suicidality

Crisis ◽  
2001 ◽  
Vol 22 (2) ◽  
pp. 54-60 ◽  
Author(s):  
Lisheng Du ◽  
Gabor Faludi ◽  
Miklos Palkovits ◽  
David Bakish ◽  
Pavel D. Hrdina
Keyword(s):  
Suicidal Ideation ◽  
Suicidal Behavior ◽  
Tryptophan Hydroxylase ◽  
Association Studies ◽  
Receptor Gene ◽  
Brain Regions ◽  
Depressive Illness ◽  
Control Group ◽  
Serotonergic Activity ◽  
Completed Suicide

Summary: Several lines of evidence indicate that abnormalities in the functioning of the central serotonergic system are involved in the pathogenesis of depressive illness and suicidal behavior. Studies have shown that the number of brain and platelet serotonin transporter binding sites are reduced in patients with depression and in suicide victims, and that the density of 5-HT2A receptors is increased in brain regions of depressed in suicide victims and in platelets of depressed suicidal patients. Genes that code for proteins, such as tryptophan hydroxylase, 5-HT transporter, and 5-HT2A receptor, involved in regulating serotonergic neurotransmission, have thus been major candidate genes for association studies of suicide and suicidal behavior. Recent studies by our group and by others have shown that genetic variations in the serotonin-system-related genes might be associated with suicidal ideation and completed suicide. We have shown that the 102 C allele in 5-HT2A receptor gene was significantly associated with suicidal ideation (χ2 = 8.5, p < .005) in depressed patients. Patients with a 102 C/C genotype had a significantly higher mean HAMD item #3 score (indication of suicidal ideation) than T/C or T/T genotype patients. Our results suggest that the 102T/C polymorphism in 5-HT2A receptor gene is primarily associated with suicidal ideation in patients with major depression and not with depression itself. We also found that the 5-HT transporter gene S/L polymorphism was significantly associated with completed suicide. The frequency of the L/L genotype in depressed suicide victims was almost double of that found in control group (48.6% vs. 26.2%). The odds ratio for the L allele was 2.1 (95% CI 1.2-3.7). The association between polymorphism in serotonergic genes and suicidality supports the hypothesis that genetic factors can modulate suicide risk by influencing serotonergic activity.

Mitochondrion-Specific Antioxidants as Drug Treatments for Alzheimer Disease

2011 ◽  
Vol 10 (2) ◽  
pp. 149-162 ◽  
Author(s):  
Hector H. Palacios ◽  
Bharat B. Yendluri ◽  
Kalpana Parvathaneni ◽  
Vagif B. Shadlinski ◽  
Mark E. Obrenovich ◽  
...  
Keyword(s):  
Alzheimer Disease ◽  
Drug Treatments

Conditioning and Sensitisation in the Longitudinal Course of Affective Illness

1986 ◽  
Vol 149 (2) ◽  
pp. 191-201 ◽  
Author(s):  
Robert M. Post ◽  
David R. Rubinow ◽  
James C. Ballenger
Keyword(s):  
Depressive Illness ◽  
Manic Depressive Illness ◽  
Conceptual Approach ◽  
Longitudinal Course ◽  
Behavioural Sensitisation ◽  
Affective Illness ◽  
Biological Variables ◽  
Manic Depressive ◽  
Progressive Course

Few biological theories of manic-depressive illness have focused on the longitudinal course of affective dysfunction and the mechanisms underlying its often recurrent and progressive course. The authors discuss two models for the development of progressive behavioural dysfunction—behavioural sensitisation and electrophysiological kindling—as they provide clues to important clinical and biological variables relevant to sensitisation in affective illness. The role of environmental context and conditioning in mediating behavioural and biochemical aspects of this sensitisation is emphasised. The sensitisation models provide a conceptual approach to previously inexplicable clinical phenomena in the longitudinal course of affective illness and may provide a bridge between psychoanalytic/psychosocial and neurobiological formulations of manic-depressive illness.

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