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Biomedical subjects

M Hansenne

Publications and source records attributed to M Hansenne.

At least 37 records · Page 2Linked to original sources
PubMed1999

P300 event-related potential and serotonin-1A activity in depression.

The identification of the brain structures and neurotransmitters responsible for the generation and/or modulation of P300 could lead to important clinical implications. Since serotonin disturbances seem to play a critical role in depression, the aim of the study was to assess the possible relationships between the P300 event-related brain potential and serotonergic activity in depression. The study was conducted among 45 major depressive inpatients, and serotonergic activity was assessed by prolactin (PRL) response to flesinoxan (a 5-HT1A agonist). Results showed a significant negative correlation between P300 amplitude and PRL response to flesinoxan (r = -0.40, P = 0.007 at Cz; r = -0.47, P = 0.001 at Pz). In contrast, both P300 latency and reaction time were not related to endocrine response. This study supports a role for serotonin-1A in the neurobiological modulation of P300 amplitude.

Adult↗
PubMed1998

Catecholaminergic function and temperament in major depressive disorder: a negative report.

In the biosocial model of Cloninger, the three personality dimensions are related to different central neurotransmission systems. In agreement with this model, a recent study (Wiesbeck et al., 1995) showed an association between growth hormone response to apomorphine, an indirect assessment of the dopaminergic system, and novelty seeking score in alcohol-dependent men. In the present study we investigated the same methodology in a sample of major depressive patients. In addition, we assessed the relationship between noradrenergic function and Cloninger's dimensions using the clonidine test, an indirect assessment of the noradrenergic system. Growth hormone responses to apomorphine and clonidine were not associated with novelty seeking, reward dependence or harm avoidance dimension scores. This study therefore does not confirm the results of Wiesbeck et al. (1995), and does not support an association between noradrenergic activity and reward dependence dimension. However, given the complexity of central neurotransmission systems and the limitations of neuroendocrine challenges for the assessment of those processes, this study could not be considered as definitive evidence against the association between personality dimensions and their hypothesized central substrates.

Adolescent↗
PubMed1998

[Clinical case of the month. A case of Munchausen syndrome (factitious disorder)].

Factitious disorders are characterized by physical or psychological symptoms that are intentionally produced or feigned in order to assume the sick role. In the particularly severe type presented by Munchausen syndrome, the person's entire life may consist of either trying to get admitted to or staying in hospitals. From the case of a 47 year old patient exhibiting symptoms of neurological aspect associated with psychological complaints, the issue of differential diagnosis of a factitious disorder is addressed. The integration of the reported symptomatology to the subject's personal history seems indispensable to the understanding and the global therapy of the patient.

Diagnosis, Differential↗
PubMed1996

Suicidal behavior in depressive disorder: an event-related potential study.

P300 and contingent negative variation (CNV) were recorded in depressive inpatients with and without history of suicide attempt. The results showed a significant reduction of P200, P300, and CNV and a significant increase of postimperative negative variation (PINV) in patients who had attempted suicide compared to patients with a negative history. Moreover, P300 amplitude was negatively related with the Suicidal Risk and the Hopelessness but not with the Hamilton scales. These results stress the need to differentiate clinical subgroups of patients to assess the psychophysiology of depression, and indicate that patients who attempted suicide exhibit lower cortical resources and poorer cortical performance than patients without history of suicide attempt.

Adult↗
PubMed1996

Growth hormone response to apomorphine in obsessive-compulsive disorder.

Several lines of evidence suggest that dopamine plays a role in the pathophysiology of obsessive-compulsive disorder (OCD). Indeed, some trials have shown the efficacy of neuroleptic addition in the treatment of OCD patients. In this study, we assessed the growth hormone (GH) response to 0.5 mg apomorphine(sc) in 8 drug-free inpatients (6 male, 2 female; mean age +/- SD = 34.7 +/- 12.6) meeting DSM-III-R criteria for OCD without major depression and compared their responses with those of 8 healthy male volunteers (mean age = 27.1 +/- 8.5). The groups did not differ in their mean GH peak response: 12.4 +/- 9.7 ng/mL in OCD patients versus 21.1 +/- 14.2 ng/mL in normal controls (F = 0.9, df1, 14, P = 0.37). These results do not support the hypothesis of dopaminergic overactivity in OCD. In fact, the completely blunted GH response to apomorphine in 2 OCD patients suggests the biological heterogeneity of OCD. Some dopaminergic disturbances could be observed in patients with comorbid diagnoses or patients unresponsive to serotonin reuptake inhibitors, but the results of this study require confirmation from a larger sample with a precise assessment of comorbidity.

Adult↗
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

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↗
PubMed1993

[Role of the dopaminergic system in depression: clinical correlates of the apomorphine test].

Disturbances in dopaminergic neurotransmission seem to play an important role in biochemical mechanisms involved in depressive disorders. The study of the growth hormone (GH) response to apomorphine, a dopaminergic agonist, provides an indirect index of dopaminergic neurotransmission at the postsynaptic level. In the present study, we assessed the role of the dopaminergic system in some psychopathological dimensions in depression: personality dimensions, suicidal behavior, psychomotor disturbances and dichotomy unipolar/bipolar. Our studies included major depressed inpatients matched for gender, age and, in the case of women, menopausal status. Our results show that dopaminergic disturbances are related to social introversion and anxiety according to dopaminergic hypothesis of schizophrenic disorders and dopaminergic hyperactivity hypothesis of anxiety disorders. A blunted GH response to apomorphine could be considered as a biological marker of suicidal behavior. Moreover motor retardation appeared to be in relationship with dopaminergic disturbances. Finally, the dopaminergic system did not appear to play a significant role in the dichotomy unipolar/bipolar. The results show the interest of the apomorphine test in the assessment of the relationship between biochemical disturbances and clinical correlates.

Adult↗