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Biomedical subjects

M Ansseau

Publications and source records attributed to M Ansseau.

At least 91 records · Page 5Linked to original sources
PubMed1995

Growth hormone response to apomorphine in panic disorder: comparison with major depression and normal controls.

Several lines of evidence suggest that dopamine might be involved in anxiety states. In the present study we assessed the growth hormone (GH) response to 0.5 mg apomorphine (a dopaminergic agonist) in 10 male drug-free inpatients meeting Research Diagnostic Criteria for panic disorder who were compared with 10 male major depressive inpatients and 10 male normal controls. The three groups differed significantly in the GH peak response (mean +/- SD): 27.8 +/- 12.5 ng/ml in panics, 5.4 +/- 4.0 ng/ml in major depressives, and 25.8 +/- 11.3 ng/ml in normal controls (F(2,27) = 15.3; P = 0.00003). Although there were significant differences between panics and major depressives (P = 0.00004), and between major depressives and controls (P = 0.00004), panics did not significantly differ from controls. These results do not support the hypothesis of an overlap between panic and affective disorders, and suggest that the hypothalamo-GH-somatomedin axis could be intact in panic disorder.

Adult↗
PubMed1995

Catecholaminergic function and P300 amplitude in major depressive disorder (P300 and catecholamines).

The neurobiology of P300 is still a subject of controversy. P300 amplitude appears to be modulated by multiple neurotransmitter systems, especially dopaminergic, noradrenergic as well as cholinergic and GABAergic. In this study, we investigated the relationship between P300 amplitude and catecholaminergic neurotransmission as assessed by the growth hormone (GH) response to clonidine and apomorphine challenges in 20 major depressive patients. Results showed a correlation of P300 amplitude with the apomorphine test (r = 0.54; P = 0.01), but not with the clonidine test (r = 0.22; NS). This study supports a role for dopamine in the neurobiological modulation of P300 amplitude.

Adult↗
PubMed1995

[The influence of suicide risk and despondency on the amplitude of P300 in major depression].

P300 amplitude represents a useful tool to assess information processing in normal and psychopathological subjects. In depressive disorders, many studies have shown a decrease of P300 amplitude and an increase of its latency. However, functional significance of the P300 modifications remain unclear. The aim of the study was to assess the influence of suicidal risk and hopelessness on P300 amplitude among 40 depressive inpatients. The results showed significant relationships between P300 amplitude and suicidal risk (r = -0.68, p < 0.001) and with hopelessness (r = -0.76, p < 0.001). From a clinical point of view, P300 amplitude should be considered as a psychophysiological index of suicidal risk in major depressive disorder.

Adult↗
PubMed1995

The flesinoxan 5-HT1A receptor challenge in major depression and suicidal behavior.

The prevailing neurochemical theory about biological correlates of suicidal behavior focuses on the serotonergic system. In this study, we assessed the cortisol, ACTH, GH, prolactin and temperature responses to flesinoxan, a5-HT1A agonist, in 30 DSM-III-R major depressed inpatients subgrouped into suicide attempters (n = 15) and nonattempters (n = 15). The patients were assessed after a drug-free period of at least 3 weeks. A subsample of 16 patients completed the Buss-Durkee Hostility Inventory as a measure of impulsive aggressive behavior. Mean delta cortisol responses to flesinoxan were significantly lower in the group of depressed patients with a history of suicide attempts than in the group without history of suicidal behavior: for the delta cortisol values 14.5 +/- 16.3 micrograms/l vs 101 +/- 94 micrograms/l (F = 8.9, df = 5.25, p = 0.006). There was also a very significant difference between suicide attempters and nonattempters for the temperature (delta T degrees) responses to flesinoxan: 0.20 +/- 0.24 degrees C vs. 0.60 +/- 0.24 degrees C (F = 18.1, df = 5.25, p = 0.0003). Hormonal and temperature responses to flesinoxan were not correlated with BDHI irritability or assault subscale scores. The results of the present study support the implication of the serotonergic system, particularly 5-HT1A receptors, in the control of self-directed aggressive behavior. Moreover, in depressed patients, serotonergic abnormalities do not appear to be related to aggressive behavior.

Adult↗
PubMed1995

Effect of previous antidepressant therapy on the growth hormone response to apomorphine.

Several lines of evidence suggest a role for dopamine in the pathophysiology of depression. In 1988, we reported a blunted response of growth hormone (GH) to apomorphine, a dopaminergic agonist, in endogenous depression. However, an antidepressant washout period is a major confounding factor in studies assessing the GH response to apomorphine. Indeed, whereas the influence of tricyclic antidepressants on the GH response to apomorphine is presently unknown, several reports have suggested that tricyclics may impair the GH response to clonidine for periods longer than 3 weeks following their discontinuation. In the present study, we hypothesized that a blunted GH response to apomorphine in depressed patients could be related to the recent administration of antidepressants. Therefore, the GH response to apomorphine (0.5 mg) was studied in 11 male DSM-III-R major depressive inpatients who had never received antidepressant therapy (group 1) compared to 11 normal controls and 11 major depressive inpatients drug free for at least 2 weeks (group 2). The three groups differed significantly in the GH peak response to apomorphine: mean (SD) 5.4 (4.0) ng/ml in group 1, 25.5 (10.7) in normal controls, and 5.5 (5.1) in group 2 (F = 15.5, df = 3, 30, p = 0.00001). While group 1 and normal controls (F = 21.8, p = 0.0002) as well as group 2 and controls (F = 5.6, p = 0.03) differed significantly, group 1 and group 2 did not (F = 0.18, p = 0.68). These results suggest that a washout period of 2 weeks could be sufficient in studies assessing the GH response to apomorphine.

Adult↗
PubMed1995

P300 in posttraumatic stress disorder.

In the present study, P300 has been recorded in 26 subjects (15 women) 1 month after an aggression without organic complications. Among our sample, 16 subjects fulfilled DSM-III-R criteria for posttraumatic stress disorder (PTSD) and 10 did not. P300 amplitude was significantly lower in the 16 PTSD subjects as compared to the 10 subjects without PTSD. This study supports information processing disturbances in PTSD.

Adult↗
PubMed1994

Drug utilization review of oral forms of benzodiazepines in a Belgian 635-bed teaching hospital.

A retrospective study based on 4,307 drug patient records was designed to establish a chart of the consumption of benzodiazepines administered orally in a 635-bed teaching hospital, and to determine the influence of patient-related parameters (age, sex) and hospital-related parameters (type of services, prescription habits, etc.) on benzodiazepine utilization. Another objective was to evaluate to which extent benzodiazepine consumption can be induced by hospitalization. A minor but statistically significant difference (p < 0.05) was observed between the proportion of male (42.7%) and female (46.5%) users. Besides, when evaluating the consumption in number of defined daily doses per 100 beddays, there was little difference between the consumption of male (51.2 defined daily doses per 100 beddays) and female (52.8 defined daily doses per 100 beddays) patients. A significant influence of age was also observed with an increase of benzodiazepine use for patients aged from 15-20 to 40-45, followed by a progressive decrease for higher ages. With hypnotics, no peak of consumption related to age was observed but an increase of consumption from age 15-20 to 30-35. For higher ages the consumption of hypnotics was nearly stable or rising slowly. High variations in benzodiazepine utilization were recorded between hospital wards (median: 50.77 defined daily doses per 100 beddays, range 0.23-263.9). Finally, it was found that 6.8% of patients with a benzodiazepine treatment initiated during hospitalization may be considered as potential benzodiazepine consumers after discharge.

Administration, Oral↗
PubMed1994

Controlled comparison of nefazodone and amitriptyline in major depressive inpatients.

Nefazodone, a phenylpiperazine antidepressant, exhibits novel dual activity on serotonin (5-HT) neurons; it binds to 5-HT2 receptors and inhibits 5-HT reuptake. Flexible doses of nefazodone (100-400 mg/day) and amitriptyline (50-200 mg/day) were compared in 106 major depressive inpatients in a 6-week double-blind study. Results showed significant superiority of amitriptyline over nefazodone on all rating instruments: Montgomery and Asberg depression rating scale (P < 0.0001), Hamilton depression scale (P < 0.0006), Clinical Global Impressions (P < 0.0001) and Patient Global Assessment (P < 0.01). A total of 65% of patients under amitriptyline and 56% of patients under nefazodone reported adverse events during the study, with significantly more dry mouth in the amitriptyline group (39% versus 11%, P = 0.001). Modal daily doses within the last treatment week reached 242 mg with nefazodone and 124 mg with amitriptyline. The lower efficacy of nefazodone, which contradicts comparative trials with imipramine in US patients, is discussed with regard to the dose of nefazodone, probably below the optimal therapeutic range for melancholic patients, and to the clinical differences between the patient samples.

Adolescent↗
PubMed1994

Controlled comparison of milnacipran and fluoxetine in major depression.

The efficacy and the tolerance of milnacipran (100 mg/day), a second generation antidepressant which equipotently inhibits both noradrenaline and serotonin reuptake, was compared to fluoxetine (20 mg/day), a selective serotonin reuptake inhibitor, in two parallel groups of, respectively, 97 and 93 major depressive outpatients. The duration of the study was 6 weeks, with assessments every 2 weeks by means of the Montgomery and Asberg depression scale (MADRS), the Hamilton depression scale, the clinical global impressions (CGI), and a checklist of symptoms and side-effects. Results showed significant superiority of fluoxetine over milnacipran on most rating instruments: MADRS (P = 0.01) including five individual items, Hamilton depression scale (P = 0.002) including ten individual items, CGI of severity (P = 0.01) and therapeutical index (P = 0.002). On visual analogue scales assessing the clinical profile of the compounds, fluoxetine was rated as exhibiting more psychostimulating activity than milnacipran (P = 0.0008). The tolerance of the two antidepressants was very similar, with the exception of symptoms of dizziness which were more frequently reported with milnacipran (P = 0.01). These differences in efficacy favoring fluoxetine could result from the selection of a dose of milnacipran below the optimal therapeutic dose for this type of psychiatric patients or to the administration of the compounds in single daily intakes, whereas milnacipran possesses a plasma elimination half-life of only 7 h.

Adult↗
PubMed1994

Relationship between alpha 2-adrenergic function and suicidal behavior in depressed patients.

The current main neurochemical theories of the biological correlates of suicidal behavior involve serotonergic and, to a lesser extent, dopaminergic systems. Few data are available about the possible implication of the noradrenergic function. In the present study, we assessed the growth hormone response to clonidine, a selective alpha 2-adrenergic agonist, in 15 DSM-III-R major depressive inpatients with a history of suicide attempts, compared with 15 age- and gender-matched major depressive inpatients without a history of suicidal behavior. Mean (+/- SD) growth hormone peak responses to clonidine were significantly lower in the group of suicide attempters than in the control group: 2.93 +/- 3.01 ng/ml vs. 8.28 +/- 8.15 ng/ml. Therefore, these results suggest that a blunted growth hormone response to clonidine could be a biological correlate of suicidal behavior.

Adult↗
PubMed1994

Psychophysiological correlates of suicidal behavior in depression. A preliminary study.

P300 and contingent negative variation (CNV) were recorded in depressive inpatients with and without history of suicide attempt. The results show a significant reduction of both P300 and CNV in patients who had attempted suicide as compared with patients who had not. Moreover, a significant correlation was found between the suicidal risk scale and CNV amplitude. Psychophysiological and biochemical implications are discussed.

Adult↗
PubMed1994

Effects of gender and diagnosis on growth hormone response to clonidine for major depression: a large-scale multicenter study.

OBJECTIVE: The authors' goal was to establish, in a large multicenter sample of patients classified according to gender and menopausal status, if the growth hormone (GH) response to clonidine discriminated patients with episodes of major depression from patients with episodes of minor depression. METHOD: The GH response to intravenous clonidine administration (150 micrograms) was compared in 71 male and 140 female patients with major depressive episodes and 47 male and 53 female patients with minor depressive episodes. These patients were diagnosed according to Research Diagnostic Criteria. RESULTS: Differences in the GH response to clonidine between diagnostic groups occurred only between male patients. These results were found in the group as a whole and in each center. The GH responses to clonidine of premenopausal women differed significantly from those of postmenopausal women in each diagnostic group. CONCLUSIONS: These results confirm that gender and menopausal status are of the utmost importance in the interpretation of the clonidine GH test.

Adult↗
PubMed1993

Pressure-induced disorders in neurotransmission and spontaneous behavior in rats: an animal model of psychosis.

Disorders in neurotransmission and spontaneous behavior in rats exposed to a high pressure helium-oxygen mixture that shows interesting parallels with the dopaminergic hypothesis of schizophrenia at both the biochemical and the therapeutic responding levels are reviewed. Furthermore, as human subjects exposed to a very high pressure have shown psychotic episodes, we conclude that the pressure-induced disorders in neurotransmission and spontaneous behavior in rats could constitute a valid animal model of schizophreniform psychosis and a useful tool for both the investigation of the biological mechanisms underlying schizophrenia and the development of new antipsychotic drugs.

Animals↗