Circadian variations in response to protirelin test in major depressive episode

1991 ◽  
Vol 6 (2) ◽  
pp. 79-88 ◽  
Author(s):  
F Duval ◽  
MC Mokrani ◽  
MA Crocq ◽  
S Rosenberg ◽  
J Oliveira Castro ◽  
...  

SummaryWe studied circadian thyrotropin (TSH) and prolactin (PRL) response to synthetic thyrotropin-releasing-hormone (protirelin) infusion (200μg IV) at 8 am and 11 pm in 35 drug-free inpatients with DSM III-R Major Depressive Episode and in 22 hospitalized controls. In each group, maximum TSH and PRL responses were lower at 8 am than at 11 pm. The difference between 11 pm-ΔTSH and 8 am-ΔJTSH (ΔΔTSH) was significantly lower in depressed patients compared to controls. No such blunting was observed in PRL responses to protirelin in depressed patients. In the overall population, TSH response to protirelin (ie8 am-ΔTSH, 11 pm-ΔTSH, ΔΔTSH) correlated significantly with TSH circadian parameters (ie mesor and amplitude). These correlations were also observed with PRL (except for ΔΔPRL). TSH mesor and amplitude were lower in depressives than in controls. In contrast, PRL mesor and amplitude were not significantly different between diagnostic groups. ΔΔTSH is thus a chronobiological refinement to the measure of thyroid axis dysfunction in major depression. The blunted TSH response to protirelin suggests that the TRH receptors of the pituitary thyrotrophs are hyposensitive in major depression.

2004 ◽  
Vol 35 (6) ◽  
pp. 865-871 ◽  
Author(s):  
JIANLI WANG

Background. Major depression is a prevalent mental disorder in the general population, with a multi-factorial etiology. However, work stress as a risk factor for major depression has not been well studied.Method. Using a longitudinal study design, this analysis investigated the association between the levels of work stress and major depressive episode(s) in the Canadian working population, aged 18 to 64 years. Data from the longitudinal cohort of the Canadian National Population Health Survey (NPHS) were used (n=6663). The NPHS participants who did not have major depressive episodes (MDE) at baseline (1994–1995 NPHS) were classified into four groups by the quartile values of the baseline work stress scores. The proportion of MDE of each group was calculated using the 1996–1997 NPHS data.Results. The first three quartile groups had a similar risk of MDE. Those who had a work stress score above the 75th percentile had an elevated risk of MDE (7·1%). Using the 75th percentile as a cut-off, work stress was significantly associated with the risk of MDE in multivariate analysis (odds ratio=2·35, 95% confidence interval 1·54–3·77). Other factors associated with MDE in multivariate analysis included educational level, number of chronic medical illnesses and child and adulthood traumatic events. There was no evidence of effect modification between work stress and selected sociodemographic, clinical and psychosocial variables.Conclusions. Work stress is an independent risk factor for the development of MDE in the working population. Strategies to improve working environment are needed to keep workers mentally healthy and productive.


1999 ◽  
Vol 24 (7) ◽  
pp. 695-712 ◽  
Author(s):  
Fabrice Duval ◽  
Marie-Claude Mokrani ◽  
Paul Bailey ◽  
Humberto Correa ◽  
Than-Son Diep ◽  
...  

1986 ◽  
Vol 16 (3) ◽  
pp. 541-546 ◽  
Author(s):  
Alec Roy ◽  
David Pickar ◽  
Patrice Douillet ◽  
Farouk Karoum ◽  
Markku Linnoila

SynopsisAn examination was made of urinary catecholamine and metabolite outputs in 28 unipolar depressed patients and 25 normal controls. The total group of depressed patients had significantly higher urinary outputs of norepinephrine (NE) and its metabolite normetanephrine (NM), and significantly lower urinary outputs of the dopamine metabolite dihydroxyphenylacetic acid (DOPAC), than controls. Patients who met DSM-III criteria for a major depressive episode with melancholia (N = 8) had significantly higher urinary outputs of normetanephrine than controls, whereas patients with a major depressive episode without melancholia (N = 7) and dysthymic disorder patients (N = 8) had levels comparable with controls. We postulate that the higher urinary outputs of norepinephrine and its metabolite, normetanephrine, reflect dysregulation of the sympathetic nervous system in depression.


1994 ◽  
Vol 9 (6) ◽  
pp. 307-308
Author(s):  
F Okada ◽  
M Daiguji

Keller and Shapiro (1982) reported that 26% of the first 101 patients who entered the National Institute of Mental Health (NIMH)-Clinical Research Branch Collaborative Program on the Psychobiology of Depression (Katz and Klerman, 1979; Katz et al, 1979) with a major depressive episode were found to have a pre-existing chronic minor depression of at least 2 years’ duration. They labeled this Phenomenon “double depression„ (Keller and Shapiro, 1982). Furthermore, patients with panic disorder almost universally suffer from major depression at some time in the course of their disorder (Coryell et al, 1988; Stein and Uhde, 1988; Vollrath et al, 1990). “Double diagnosis„, or identification of psychotic or related syndromes, co-existing with personality disorders, have received much attention in the literature in recent years (Sanderson et al, 1990; Torgersen, 1990; Barsky et al, 1992). Much of the research on comorbidity between depressive and anxiety disorders has been summarized in two edited volumes (Kendall and Watson, 1989; Maser and Cloninger, 1990).


1999 ◽  
Vol 29 (6) ◽  
pp. 1323-1333 ◽  
Author(s):  
CHRISTINE KUEHNER ◽  
IRIS WEBER

Background. The response styles theory suggests that rumination in response to depressed mood exacerbates and prolongs depression, while distraction ameliorates and shortens it. Gender differences in response styles are said to contribute to the observed gender differences in the prevalence of unipolar depression. While empirical support for the theory has been found from a variety of non-clinical studies, its generalizability to clinically depressed patient populations remains unclear.Methods. A cohort of 52 unipolar depressed in-patients was assessed with the Response Styles Questionnaire during in-patient stay (T1) and 4 weeks after discharge (T2). The patients were followed up 4 months after discharge (T3). Clinical assessment included the SCAN-PSE-10.Results. Moderate and statistically significant retest-stabilities for rumination and distraction were found, comparable for patients with stable and changing depression status from T1 to T2. A cross-sectional diagnosis of a major depressive episode was associated with rumination, while gender was not. Post-discharge baseline rumination (T2), adjusted for concurrent depression, predicted follow-up levels of depression (T3), and, in patients who were non-remitted at post-discharge baseline, it predicted presence of a major depressive episode at follow-up (T3). Results on distraction were more ambiguous.Conclusions. Our results suggest that rumination is likely to have a deteriorating impact on the course of clinical episodes of depression in unipolar depressed patients. Larger longitudinal patient studies are needed to validate these findings.


1997 ◽  
Vol 42 (10) ◽  
pp. 859-870 ◽  
Author(s):  
J. John Mann ◽  
James P. Halper ◽  
Philip J. Wilner ◽  
John A. Sweeney ◽  
Tammy A. Mieczkowski ◽  
...  

1995 ◽  
Vol 10 (S3) ◽  
pp. 167s-172s
Author(s):  
M Van Moffaert ◽  
C Pilate

SummaryDuring the early treatment of a major depressive episode with amitryptiline, insomnia was treated in 81 patients in a double-blind comparative trial comparing zopiclone and flunitrazepam. The study showed no major differences in the efficacy profile and showed better tolerability for zopiclone than for flunitrazepam.


2011 ◽  
Vol 26 (S2) ◽  
pp. 2025-2025
Author(s):  
Z. Rihmer

Antidepressant-resistant major depression (AD-RD) is a great challenge for the treating clinician. The most widely accepted definition of AD-RD refers that the depressed patient does not show a clinically significant response after at least two adequate trials of different classes of antidepressants. In spite of the fact that there are several causes of AD-RD in general, there is increasing evidence that one of the most common sources of it is the unrecognized bipolar nature of the “unipolar” major depressive episode, when the patients receive antidepressant monotherapy - unprotected by mood stabilizers/atypical antipsychotics. While it is well documented that the optimal clinical response to antidepressants is much rare in bipolar I and II than in unipolar major depression, only the most recent clinical studies have focused on the boundaries between treatment-resistant unipolar major depressive disorder and bipolar disorder. The most widely noted conclusion of the prior studies on AD-RD is that if noncompliance, hypothyreosis, use of “depressiogenic” drugs and pharmacokinetic causes etc, can be excluded, antidepressant-resistance reflects the heterogeneity of depressive disorders and different subgroups of depressed patients respond (or do not respond) to different drugs. However, current psychopathological research on the complex relationship between unipolar depression and bipolar disorders show that the most common source of antidepressant-resistance in DSM-IV diagnosed unipolar major depression is the result of the subthreshold or unrecognized bipolar nature of the depressive episode and antidepressant-induced (hypo)manic switches, antidepressant-resistance and “suicide-inducing” potential of antidepressants seem to be related to the underlying bipolarity of the major depressive episode.


2021 ◽  
Vol 3 (4) ◽  
pp. 106-108
Author(s):  
Tatiana Zydb ◽  
MIchael Hart

Background: Treatment resistant depression (TRD) is defined as a major depressive episode that does not improve in response to at least two trials, each of a different class, of antidepressant medication. Pharmacotherapy of TRD with low dose ketamines has been shown as relatively successful in recent studies. Effects of such pharmacotherapy can be augmented by combining ketamine with psychotherapeutic interventions such as Zdyb’s Therapeutic Reset of Internal Processes (TRIP) protocol. Method: 10 adult TRD patients (4 men, 6 women) were treated with low dose ketamines and were also receiving psychotherapeutic intervention as per TRIP protocol. All patients were administered the Patient Health Questionnaire, module 9 (PHQ9) which is a measure of a major depressive episode. The PHQ9 was administered twice: on baseline (i.e., prior to treatment) and after the treatment. Results: On average, our patients fell in the moderate range of severity with respect to symptoms of TRD at baseline (pre-TRIP) as by their mean PHQ9 score of 17.9, (SD = 5.1). Their mean PHQ9 score decreased post TRIP treatment to 9.5 (SD = 6.6): the difference is significant in a t-test, t(10) = 4.3172, p = 0002 (two-tailed). The magnitude of the decrease amounts to 46.9% of the average baseline score. Discussion and Conclusions: Our patients experienced significant reductions in symptoms of TRD in this pilot study. Research studies are now needed with control groups of TRD patients on a waiting list or also of those receiving only the ketamine pharmacotherapy. 


CNS Spectrums ◽  
2010 ◽  
Vol 15 (2) ◽  
pp. 79-94 ◽  
Author(s):  
Stephen M. Stahl

Traditional guidelines call for treatment of major depression with a sequence of single antidepressants. Augmentation with a second agent generally only occurs when the first agent is well tolerated and when it also provides at least some symptomatic improvement on its own. Since this standard approach leads to low rates of attaining and sustaining remission by the first agent, with diminishing returns for each subsequent agent, there is growing dissatisfaction with this approach to the treatment of major depression. One new trend is to attempt to enhance the rates of sustained remission from a major depressive episode by combining two therapeutic agents from the very initiation of treatment of a major depressive episode.Traditional treatment of major depression begins with a single “first line” antidepressant, and if it does not work or is not tolerated, trying another and then another. Unfortunately, this strategy results in disappointing remission rates for the first antidepressant (Figure 1), and disappointing rates of maintaining any improvement that is attained by this first agent because of high relapse rates over the next year despite continuing treatment with the first antidepressant (Figure 2A). And that is the good news. The bad news is that with each subsequent antidepressant treatment administered remission rates are progressively reduced (Figure 1). For those patients who do improve, they are progressively less likely to sustain their therapeutic gains despite continuing to take the drug that led to their initial improvement (Figure 2).


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