Additional intranasal oxytocin to escitalopram improves depressive symptoms in resistant depression: an open trial.

The aim of this open trial was to assess the antidepressant/anxiolytic effects of oxytocin used as an adjunct to antidepressant in treatment-resistant depression. Fourteen patients, who have not responded to 40mg of escitalopram, received intranasal synthetic oxytocin during 4 weeks, in association with antidepressant. This is the first open trial study suggesting OT in association with escitalopram significantly reduced scores on Hamilton Depression Rating Scale.

Autonomic aspect of emotional response in depressed patients: relationships with personality.

STUDY AIM: Affective symptoms are major descriptors of depression; therefore, a lot of studies investigated emotional-responsiveness modulation in depression, and reported either a potentiation of negative affects, a reduction of positive affects, or a reduction of both positive and negative affects. On the other hand, personality was classically found to be modulated in depression, with behavioral inhibition system (BIS)-related dimensions (namely harm avoidance (HA), neuroticism) showing higher scores in depressed subjects. The aim of this study was to investigate the relationships between emotional responsiveness (as measured by skin conductance response [SCR]) and personality in depression. METHODS: SCR was recorded following the presentation of neutral, pleasant, and unpleasant pictures in 20 depressed subjects and 20 controls. RESULTS: Pleasant pictures elicited more and larger responses than unpleasant ones in control but not in depressed subjects. This effect was not modulated by personality. Moreover, depressed subjects were found to show generally faster half-recovery times and to rate emotional pictures as less arousing than control subjects and these effects disappeared when BIS-related dimensions were controlled. CONCLUSIONS: These results suggest that BIS-related dimensions are independent from the specifically reduced responses to pleasant pictures, but are involved in the observed general affect reducing.

Personality modulation of P300 wave recorded within an emotional oddball protocol.

OBJECTIVES: Several studies reported that personality modulates responses to emotional stimuli, including cognitive and attentional aspects of the emotional response. The aim of this study was to refine these results while using visual event-related potentials (ERPs) and referring to Cloninger's personality model. METHODS: ERPs were recorded in 46 normal subjects within a visual oddball protocol with checkerboards as the standard stimuli and pictures selected as neutral, pleasant or unpleasant from the International Affective Picture System as the target stimuli. RESULTS: N200 amplitude was smaller and P300 amplitude was larger following the presentation of pleasant pictures in low-harm avoidance but not high-harm avoidance subjects. CONCLUSIONS: These results support the idea that both automatic and selective cognitive processing of emotional pictures is modulated by personality.

[Impact of personality on the alcohol withdrawal syndrome intensity: a preliminary study with the Cloninger's model]. / Impact de la personnalité sur l'intensité du syndrome de sevrage alcoolique: une étude préliminaire avec le modèle de Cloninger.

INTRODUCTION: The personality of alcohol dependant patients as a factor influencing the intensity of the alcohol withdrawal syndrome has been seldom examined. Cloninger's biosocial model of personality describes four temperaments (novelty seeking, harm avoidance, reward dependence, persistence) which, except for persistence, are admittedly linked to specific central neurotransmitters, and three characters. Novelty seeking is linked with low levels of mesencephalic dopamine, harm avoidance with high levels of serotonin in the septo-hippocampic system and reward dependence with low levels of noradrenaline in the ascending pathways from the locus coeruleus to the limbic system. The same neurotransmitters pathways are known to be involved in alcohol withdrawal, with a decrease of dopaminergic activity in the mesolimbic system, a decrease of serotonergic activity in the nucleus accumbens and an increase of the noradrenergic system. In view of the similarities between the neurobiological systems involved in Cloninger's model and in the neurobiological changes occurring during the withdrawal period, one would expect to observe severe withdrawal symptoms more frequently for patients with high novelty seeking, low harm avoidance and low reward dependence. METHODS: To test this hypothesis, alcohol dependent patients according to DSM IV classification criteria who have drunk in the last twenty four hours were included in the study and received a standardized withdrawal treatment. The withdrawal syndrome intensity was examined with repeated measures of CIWA-Ar, the scores of which were correlated with TCI-R. RESULTS: Twenty eight patients, between 30 et 65 years old and drinking 22,2 +/- 12 standard drinks per day were included. Antidepressant drugs, benzodiazepines and neuroleptics treatment introduced before hospitalisation were stopped or decreased as much as possible. A correlation matrix was carried out between all the variables which could influence withdrawal intensity (age at the hospitalisation, age at the begining of the dependance, ratio between the time of the dependance and the patients' age, the number of alcohol withdrawals carried out and the number of standard drinks per day), and showed a positive correlation between the number of standard drinks per day and withdrawal intensity at day 3 (r=0.7, p<0.000), at day 4 (r=0.52, p<0.005), at day 7 (r=0.41, p<0.036) and at day 8 (r=0.44, p<0.02); as between the ratio between the time of the dependance and the patients' age and withdrawal intensity at day 2 (r=0.43, p<0.03) and at day 5 (r=0.5, p<0.01). Therefore, partial correlations were calculated between the dimensions of personality and withdrawal intensity. The study showed a positive correlation between withdrawal intensity and harm avoidance from day 5 onwards (r=0.6 and P<0.003 at day 5, r=0.59 and P<0.004 at day 6, r=0.56 and P<0.006 at day 7, r=0.66 and P<0.001 at day 8), a negative correlation between withdrawal intensity and reward dependence at day 7 and 8 (r=- 0.45 and P<0.037 at day 7, r=- 0.49 and P<0.02 at day 8) and a negative correlation between withdrawal intensity and persistence from day 6 onwards (r=- 0.5 and P<0.017 at day 6, r=- 0.5 and P<0.019 at day 7, r=- 0.51 and P<0.014 at day 8). No correlation was found between withdrawal intensity and novelty seeking. The same relevant results were found again with the 22 patients without anti-depressant drugs' population. DISCUSSION: Personality dimensions seem to influence alcohol withdrawal intensity once the severe symptomatology is over, while high doses of anti withdrawal treatment in the first days of abstinence may decrease the influence of personality on withdrawal symptoms. The positive correlation between harm avoidance and withdrawal intensity seems to invalidate our neurobiological hypotheses, but can be explained by clinical observations and corroborate studies assessing the influence of personality in benzodiazepine withdrawal intensity and in pain perception. This result encourages the introduction of support therapy during withdrawal and a cognitive-behavioural therapy before withdrawal in order to decrease patients' sensitivity to anxiety. The negative correlation between reward dependence and withdrawal intensity confirms the neurobiological hypotheses, but the weak correlation demands to be cautious in the interpretation of the results. The negative correlation between persistence and withdrawal intensity was expected. CONCLUSION: The characteristics associated with persistence seem to act as protective factors during alcohol withdrawal, whereas those associated with harm avoidance appear to increase the symptoms of alcohol withdrawal. In contrast, the neurobiological hypotheses are only partially confirmed.

Plasma oxytocin levels and anxiety in patients with major depression.

Cerebrospinal fluid and plasmatic levels of oxytocin (OT) have been found to change in mood disorders. In post-mortem studies, the numbers of OT-expressing neurons in the paraventricular nucleus have been reported to be increased. Moreover, OT is considered as an endogenous antistress hormone. It has also revealed antidepressive effects. OT may contribute to the dysregulation of the HPA system in major depression. The aim of the study was to assess a possible relationship between anxiety and plasma oxytocin (OT) levels in depressive patients. Severity of depression was estimated with the Hamilton Depression Rating Scale and anxiety by using the Spielberger State-Anxiety Inventory. Results showed a significant negative correlation between oxytocin and the scored symptoms depression (r=-0.58, p=0.003) and anxiety (r=-0.61, p=0.005).

AVP- and OT-neurophysins response to apomorphine and clonidine in major depression.

A number of studies have reported abnormalities of neurohypophyseal secretions in major depressive disorder. The purpose of the present study was to test the influence of apomorphine and clonidine injections on plasma vasopressin (AVP)-neurophysins and oxytocin(OT)-neurophysins levels, as direct index of posterior pituitary activation in major depression. Apomorphine and clonidine tests were carried out in 25 medication-free depressive patients and 25 age and gender-matched healthy controls. Blood for neurophysins analysis was drawn by venipuncture at t0, t + 20, t + 40, t + 60 and t + 120. Baseline AVP-neurophysins concentrations were significantly lower in depressives (0.12 +/- 0.14 ng/ml) than in healthy subjects (0.24 +/- 2.15 ng/ml) (p < 0.04). The response to apomorphine test revealed a significant reduced response at 20 (p = 0.01), 40 (p = 0.007) and 60 (p = 0.02) and 120 (p = 0.02)min. Following clonidine test, post hoc tests also revealed a significant decrease at 0 (p = 0.04), 20 (p = 0.01), 40 (p = 0.007) and 60 (p = 0.02) and 120 (p = 0.006)min. Concerning OT-neurophysins, no significant differences were found between depressed and controls in response to clonidine or apomorphine injections. Following clonidine and apomorphine, major depressives exhibited a significantly lower peak GH response than controls. The study supports partially the hypothesis of a reduced vasopressinergic activity in depression. Moreover, we did not find any influence of acute apomorphine or clonidine injections on vasopressin-neurophysin or oxytocin-neurophysin in depressive patients.

Personality profile and drug of choice; a multivariate analysis using Cloninger's TCI on heroin addicts, alcoholics, and a random population group.

As personality may predispose, precipitate or perpetuate substance abuse and/or dependence, and as it is considered to remain stable across the years in a given subject, potential links with the drug of choice may help screen future patients before drug consumption. The present study compared three groups: 42 patients with heroin dependence (mean age: 31.2; standard deviation (SD): 5.5; 10 females), 37 patients with alcohol dependence (mean age 44.2; SD: 9.1; 9 females) and 83 subjects from a random population sample (mean age: 38.8; SD: 6.9; 20 females). Personality was measured by Cloninger's Temperament and Character Inventory (TCI). Pillai's MANCOVA with age as a covariate and gender as a cofactor was highly significant. Univariate ANOVA analyses using TCI dimensions as dependent variable showed most variables to vary in parallel for the two patient groups in comparison with controls. Post-hoc tests showed heroin patients to score higher in Novelty-Seeking and Self-Directedness than alcohol patients. Sub-dimensions Exploratory Excitability, Fear of the Uncertain, Responsibility, Congruent Second Nature and Transpersonal Identification were also significantly different in the two patient samples. Logistic regression showed Exploratory Excitability to segregate up to 76% of heroin patients from alcohol patients. In conclusion, personality profiles were linked to some preferential choice of drug and personality screening might be tested in preventive strategies.

[Testosterone and depression in men aged over 50 years. Andropause and psychopathology: minimal systemic work-up]. / Testostérone et dépression chez l'homme de plus de 50 ans. Andropause et psychopathologie: bilan symptomatique mineur.

A reduced feeling of well being with unusual anxiety and irritability, nervousness, mood swings and a depressive state are often mentioned as the psychological symptoms of the age-related hypogonadism. However, psychological aspect of andropause has not yet been specifically studied and most data on psychological symptoms come from researchers' clinical impressions rather than from systematic studies. Therefore, it seems premature to assign them to the age-associated decline in testosterone levels. The implication of testosterone in psychological state has yielded mixed results. Among elderly men, lower testosterone levels were associated with depressive or dysthymic symptoms. Moreover, lower testosterone levels were reported in men with depression, independently of age. In contrast, some studies did not observe any significant difference in testosterone levels between depressed men and controls. Furthermore, several studies have suggested that testosterone replacement improved mood in hypogonadal men, but others did not, as in studies on eugonadal men. Several researchers have also suggested the potential use of testosterone as an antidepressant or adjuvant to current treatments in depressed hypogonadal men. The relationship between andropause and psychological symptoms such as depression is far from clear. Andropause may be associated with "minor depressive symptoms" that are not considered as pathological. Psychological manifestations do not appear specific to andropause and probably have a multifactorial origin.

Mismatch negativity is not correlated with neuroendocrine indicators of catecholaminergic activity in healthy subjects.

The identification of the brain structures and neurotransmitters responsible for the generation and/or modulation of the mismatch negativity (MMN) may contribute to a clearer understanding of its functional significance, and may have clinical implications. In this context, some findings suggest that the scalp-recorded MMN reflects activity from multiple neuronal ensembles within or in the immediate vicinity of the primary auditory cortex and with possible contribution from the frontal cortex. However, few data are available concerning the influence of neurotransmitter systems on the MMN. In this study, the relationship between both noradrenergic and dopaminergic systems and the MMN were investigated in 34 healthy volunteers. Noradrenergic and dopaminergic activities were assessed with the apomorphine and clonidine challenge tests. The results showed no significant relationship between either growth hormone (GH) responses to apomorphine or clonidine and the MMN amplitude or latency. Therefore, this study does not demonstrate the implication of dopaminergic and noradrenergic activities as assessed by GH response to apomorphine and clonidine for the generation and/or the modulation of the MMN. However, given the complexity of the central neurotransmitter systems, these results cannot be considered as definitive evidence against a relationship between dopaminergic and noradrenergic activity and the MMN.

Neuroendocrine evaluation of 5-HT1A function in male alcoholic patients.

BACKGROUND: Preclinical evidences support the hypothesis of a serotonergic dysfunction in alcohol preference. In human, studies have demonstrated a serotonergic hypoactivity in alcoholism. However, little is known about the role of 5-HT1A receptors. METHODS: We assessed the hormonal (prolactin and cortisol) responses to flesinoxan (a highly potent and selective 5-HT1A agonist) in 12 male inpatients meeting DSM-IV criteria for alcohol dependence, 3 weeks after the last reported use of alcohol and antidepressants. These patients were compared to 10 male controls. RESULTS: There was a highly significant difference between alcoholic patients and controls for the area under the curve relative (AUCr) values of prolactin responses. AUCr values of cortisol responses to flesinoxan showed a trend towards lower values in alcoholics compared to controls. CONCLUSION: These results support the implication of the serotonergic system, and particularly a decreased sensitivity of post-synaptic 5-HT1A receptors, in alcoholism.

5-HT1A dysfunction in borderline personality disorder.

BACKGROUND: A number of challenge studies have reported abnormalities of serotonergic function in borderline personality disorder (BPD). There are, however, problems with the pharmacological probes used in these studies since fenfluramine and m-CPP are not only serotonergic agents but also induce release of catecholamines, particularly dopamine. Therefore, we tested whether subjects with BPD showed a blunted prolactin (PRL) response to flesinoxan, a highly potent and selective 5-HT1A agonist. METHODS: Flesinoxan challenge test was carried out in 20 BPD in-patients and 20 healthy controls matched for gender but not for age. Since 16 BPD in-patients exhibited major depressive co-morbidity, a group of 20 depressed in-patients matched for gender but not for age was also included. RESULTS: BPD in-patients exhibited blunted PRL responses as compared to controls, whereas depressed in-patients did not differ from controls. Moreover, PRL responses were lower among BPD in-patients than among depressed in-patients. Among the BPD in-patients, PRL responses to flesinoxan were lower in patients with past history of suicide attempts (N = 8) than in those with a negative history. CONCLUSIONS: The results show major involvement of serotonergic function in BPD and are consistent with previous studies linking lower serotonergic activity with impulsivity. More particularly, our data suggest that BPD is characterized by lower 5-HT1A receptor sensitivity. Moreover, the data support the involvement of 5-HT1A activity in suicidal behaviour. However, this conclusion is limited because other hormonal responses such as ACTH and cortisol were not assessed, and because BPD was assessed by a self-report questionnaire and not a structured clinical interview.

Serotonin, personality and borderline personality disorder.

Serotonin is one of the neurotransmitters implicated in normal personality. Many psychobiological models of personality include some dimensions related to serotonin. For instance, the harm avoidance dimension of the biosocial model developed by Cloninger is related to serotonergic activity. Higher scores on the harm avoidance dimension should theoretically reflect increased serotonergic activity. However, correlation studies related serotonin activity to harm avoidance dimension have not yielded consistent findings. These controversial results are probably related to the complexity of the neurotransmitter systems, and the different assessment techniques used in these studies. Finally, recent genetic studies have examined the association between personality dimensions and serotonergic receptor polymorphisms with mixed results. Serotonin is not only related to some dimensions of normal personality. Several psychopathological disorders are associated with serotonergic dysfunction. More particularly, borderline personality disorder (BPD) can be defined by many of the symptoms associated with serotonergic dysregulation, including affective lability, suicidal behaviours, impulsivity and loss of impulse control. Indeed, several reports have demonstrated the efficacy of selective serotonin re-uptake drugs in treating the depressive and impulsive symptoms of patients with BPD. Moreover, some challenge studies have reported a lower serotonergic activity in BPD. Because these challenges are not specific, we have assessed the serotonergic activity in BPD with the flesinoxan challenge. Preliminary results showed that the prolactine responses to flesinoxan were significantly lower in BPD patients compared to those observed in controls.

Role of dopamine in non-depressed patients with a history of suicide attempts.

Several data are available about the implication of the dopaminergic system in the control of inward-directed aggression. Previously, we suggested an involvement of D2-dopaminergic function in the expression of suicidal behavior by demonstrating a smaller growth hormone (GH) response to apomorphine, a dopaminergic agonist, in depressed patients with a history of suicide attempts in comparison to non-attempters. In the present study, in order to test this hypothesis, GH responses to intravenous apomorphine were measured in non-depressed patients with a history of suicide attempts. The study was performed in 17 non-depressed male patients with a score less than 12 on the 17-item HAMD. The patients were subgrouped into suicide attempters (N = 7) and non-attempters (N = 10). Mean GH peak responses to apomorphine differed significantly between suicide attempters and non-attempters: (mean +/- SD) for GH peak, 10.4 +/- 8.2 ng/mL vs 27.3 +/- 13.1 ng/ml, F = 9.0, P = 0.009. In conclusion, dopaminergic disturbances seem to play a role in the biology of inward-directed aggression in non-depressed patients.

Reduced dopamine function in depressed patients is related to suicidal behavior but not its lethality.

Several lines of evidence suggest a role for dopamine in the control of suicidal behaviour. Previously, we suggested an involvement of D2-dopaminergic function in the biology of suicide by demonstrating a smaller growth hormone (GH) response to apomorphine, a dopaminergic agonist, in depressed patients who later died by suicide. The purpose of the present study was to assess GH response to apomorphine in major depressed in-patients with a history of highly lethal suicide attempt compared to depressed patients with a low lethal lifetime suicide attempt history and non-attempters. The study was performed in a sample of 26 male depressed in-patients with a history of suicide attempt compared to 26 male depressed non-attempters. We observed a significant difference between suicide attempters and non-attempters (for GH peak, 6.3+/-5.1 ng/ml vs 15.8+/-14.2 ng/ml, F=10.3, df=1, 50, P=0.002). Moreover, GH peak responses to apomorphine did not differ between depressed patients with a high lethal lifetime suicide attempt history and patients who made low lethal lifetime suicide attempt. In conclusion, the results of the present study support a role for dopamine in the biology of suicidal behaviour. More specifically, an impaired GH response to apomorphine could be a marker of suicide risk.

Alpha-2-adrenoreceptors in depressed suicide attempters: relationship with medical lethality of the attempt.

Several lines of evidence tend to suggest a role for noradrenaline, and more specifically alpha-2-adrenoreceptors, in the biology of suicidal behavior. The purpose of this study was to assess the growth hormone (GH) response to clonidine, an alpha-2-adrenergic agonist, in majorly depressed inpatients with a history of highly lethal suicide attempt compared to depressed patients with a history of low lethal suicide attempt and nonattempters. Our sample included 20 male depressed inpatients with a history of suicide attempt compared to 20 male depressed nonattempters. We did not observe any significant difference between suicide attempters and nonattempters for GH peak values (2.4 +/- 2.9 vs. 4.1 +/- 3.7 ng/ml; F = 2.52, d.f. = 1, 38, p = 0.12). Moreover, GH peak responses to clonidine were not related to the degree of lethality of the attempt. The results of the present study do not support a major role for noradrenaline in the biology of suicidal behavior.

Contingent negative variation and personality in depression.

Contingent negative variation (CNV) has been applied in depression with controversial results. A major source for these controversial results could result from the diversity of depressed patients included in the different studies. Supporting this assumption, impulsivity, blunted affect and suicidal behavior significantly influence CNV amplitude. However, no data are available on the possible influences of personality of depressed patients on CNV. Since personality is related to CNV in normal subjects, the aim of the present study was to investigate the relationship between CNV and personality as assessed by the Temperament and Character Inventory (TCI) in 52 depressed patients. A group of 76 healthy volunteers was included in the study. Among depressed patients, the main results of the study shows that CNV amplitude is positively correlated with self-transcendence dimension. In healthy volunteers, results show that CNV amplitude is negatively correlated with novelty seeking and persistence dimensions. The other dimensions are not related to CNV amplitude either in depressed patients or in healthy volunteers. The findings among depressed subjects suggest that lower CNV amplitude may be associated with psychotic traits (high self-transcendence scores), and those observed in healthy subjects are consistent with previous studies and support energetical models of slow potentials. However, the preliminary nature of the present results with respect to the weak statistical significance should be underlined.

Reduced dopaminergic activity in depressed suicides.

Several data are available about the implication of the dopaminergic system in the control of inward-directed aggression. Previously, we suggested an involvement of D2-dopaminergic function in the expression of suicidal behavior by demonstrating a smaller growth hormone (GH) response to apomorphine, a dopaminergic agonist, in depressed patients with a history of suicide attempts in comparison to nonattempters. In the present study, the purpose was to analyze GH responses to apomorphine in depressive patients who later died by suicide. Our sample comprised eight male depressive inpatients who died by suicide within one year after hospitalisation. These patients were compared to 18 male major depressed inpatients who never attempted suicide. Mean GH peak responses to apomorphine differed significantly between suicide completers and controls (mean +/- SD): for GH peak, 7.6 +/- 4.1 ng/ml vs 18.9 +/- 14.2 ng/ml, U = 30, Z = -2.33, P = 0.02. Our results tend to confirm the role of dopamine in the biology of suicide in depression.

[The p300 cognitive event-related potential. I. Theoretical and psychobiologic perspectives]. / Le potentiel évoqué cognitif P300 (I): aspects théorique et psychobiologique.

The P300 is a positive wave which arises when an attended stimulus is detected. Its parameters depend on a number of variables, in particular the subject's mental state, the task that has to be accomplished, the significance of the stimulus, and the degree of attention. It can be recorded with accuracy, and the different stages of information processing can therefore be analyzed. The P300 wave shows the modifications in neuronal activity which take place during the cognitive process: P300 latency provides an indirect indication of the duration of the processes involved in stimulus discrimination while its amplitude, which is influenced by a number of variables, provides an index of the intensity of the energetic activation or arousal involved. The P300 wave consists of several components which reflect distinct information-processing events (P3a, P3b, P3e, P-SR, P-CR). According to the theoretical models, it is hypothesized that P300 could either represent the adaptation of the working memory to further environmental input ('context updating'), or indicate a closing process ('context closure') in information processing. As regards the physiological aspect of P300 and its association with cortical networks, various studies have suggested that several cortical generators of P300 may co-exist: the medial temporal lobe, the temporo-parietal junction, and the medial and lateral frontal lobe. Psychopharmacological studies have shown that different neurotransmitter systems are involved in the generation and modulation of P300, namely the cholinergic, noradrenergic, dopaminergic, serotoninergic and gabaergic systems. It appears that the noradrenergic agonists increase the amplitude of P300, dopaminergic agonists may have a biphasic effect (increase/reduction), while cholinergic antagonists and gabaergic agonists reduce P300 amplitude and prolong its latency.

[The p300 cognitive event-related potential. II. Individual variability and clinical application in psychopathology]. / Le potentiel évoqué cognitif P300 (II): variabilité interindividuelle et application clinique en psychopathologie.

The P300 wave is one of the cognitive components of the event-related potential (ERP) that is used to investigate the cognitive processes, and which can be used to study patient populations with a variety of psychiatric disorders. Its clinical utility has been increased by the identification of factors that contribute to the variability in its amplitude and latency. However, its value as a diagnostic index has not been entirely established. It can provide a useful recording of patients' information processing, and indicate the severity of the clinical state and its possible evolution. It can also assist in determining what therapeutic approach to adopt. In the present review, the findings in the literature concerning interindividual variation in the P300 wave are first described; several variables significantly influence the amplitude and latency of this wave, such as age, gender, intelligence and personality. Following this, the relevance of the data in the literature on the clinical applications of P300 in psychopathology is examined, including the studies undertaken to obtain an objective diagnostic index for mental disorders and also those carried out to assess the problems concerning the interpretation of information connected with the mental pathologies examined. P300-associated findings on dementia, schizophrenia, depression, alcoholism, drug addiction, anxiety disorders (panic disorder, obsessive-compulsive disorder, and post-traumatic stress syndrome) and on personality disorders (schizoid, antisocial or borderline personality disorder) have been examined in detail.

P300 event-related brain potential and personality in depression.

P300 is an event-related brain potential (ERP) particularly interesting to the study of cognitive processes in normal subjects and in psychopathology. P300 has been applied in depression with controversial results. A major source for these controversial results could result from the diversity of depressed patients included in the different studies. Supporting this assumption, impulsivity, blunted affect, suicidal behavior and psychotic features significantly influence P300 amplitude. However, no data are available on the possible influences of the personality of depressed patients on P300. Since personality is related to P300 in normal subjects, the aim of the present study is to investigate the relationship between ERPs (P200, N200, and P300) and the Temperament and Character Inventory (TCI) in 54 depressed patients. The main results of the study concern the absence of major correlations between personality dimensions as assessed by the TCI and ERP parameters among depressed patients. Only weak partial positive correlations relate N200 latency with harm avoidance, and P300 amplitude (Pz) with the self-directedness dimension. N200 amplitude is also negatively correlated to persistence. However, the preliminary nature of the presented results with respect to the weak statistical significance should be underlined.