PubMed Health⌕ Search

Biomedical subjects

O Cottencin

Publications and source records attributed to O Cottencin.

10 recordsLinked to original sources
PubMed2006

Directed forgetting in PTSD: a comparative study versus normal controls.

The most characteristic feature of Post-Traumatic Stress Disorder (PTSD) is the reexperiencing syndrome. The patient's memory seems to be fixed on the traumatic event, which may be due to disturbance of the autobiographic memory. To retrieve memories, others have to be inhibited. These inhibition mechanisms have been studied using the Directed Forgetting Paradigm, which measures the capacity to forget recently processed information and to retain the relevant information. Our hypothesis is that during PTSD, the memory is saturated with traumatic memories, so that the patients are no longer able to use the inhibitory processes. Therefore, during a Directed Forgetting Task (DFT) in which words "to remember" and words "to forget" are given, PTSD patients cannot inhibit the words "to forget", and so recall more words than the controls. We studied 30 patients with PTSD and compared them with 30 healthy controls, using DFT. The results show that the patients remembered significantly fewer words overall, and fewer of the words "to remember" than the controls, both for immediate and final recall. Our results are in favor of a reduction in directed forgetting in patients suffering from PTSD, resulting in difficulty in inhibiting irrelevant information from the overall information. There seems to be a deficit in the inhibitory processes in the memory in PTSD.

Adult↗
PubMed1999

A case of agitated catatonia.

Agitation is one of the diagnostic features of catatonia in the DSM IV classification, but permanent forms of agitated catatonia have occasionally been described. We report the case of a 43-year-old man who had already suffered from undifferentiated schizophrenia for 7 years, and in whom we diagnosed agitated catatonia. While our patient was being treated with a neuroleptic during a second episode of paranoia, a state of agitation was observed which persisted for a further 8 months. During this period, he was treated with several different neuroleptics and benzodiazepines, either alone or in association, without any improvement. No organic cause was found. He was then transferred to our electroconvulsive therapy (ECT) unit, with a diagnosis of schizophrenic agitation resistant to drug therapy. ECT was begun, and he was only given droperidol in case of agitation and alimemazine for insomnia, neither of which had any effect. In view of his persistent agitation without any purpose, echolalia and echopraxia, stereotyped movements with mannerisms and marked mimicking and grimacing, we diagnosed him as having agitated catatonia. After the fourth session of ECT, we decided to stop all treatment and gave him lorazepam at a dose of 12.5 mg daily. Twenty-four hours later, all symptoms of agitation had disappeared. In our opinion, permanent catatonic agitation is not rare. In our case, the neuroleptic treatment maintained and may even have worsened the symptomatology. Lorazepam can be used as a therapeutic test for this type of agitation, especially if it does not respond to neuroleptics. This also allows the patient to be sedated rapidly and effectively, thus preventing him from injuring himself further.

Adult↗
PubMed1998

Carbamazepine in the treatment of neuroleptic malignant syndrome.

BACKGROUND: Neuroleptic malignant syndrome (NMS) is a potentially lethal adverse effect to neuroleptic drugs. METHODS: We report on 2 cases where NMS dramatically improved with carbamazepine. Incidental removal and reapplication of carbamazepine attests to its effectiveness for this condition. RESULTS: A 34-year-old woman treated for a major depressive disorder experienced NMS with a phenothiazine. Her condition dramatically improved in 8 hours after she was administered carbamazepine. Since carbamazepine was discontinued, NMS recurred in 10 hours and remitted anew within less than 24 hours after reintroduction. A 31-year-old woman experiencing a schizoaffective disorder displayed NMS with aphenothiazine and a butyrophenone. NMS completely resolved within 8 hours after she was administered carbamazepine. NMS recurred within 12 hours after carbamazepine discontinuation. CONCLUSIONS: These data thus account for a cause-effect relationship between carbamazepine administration and NMS relief, and argue against the neuroleptic withdrawal to be responsible by itself for NMS relief.

Adult↗
PubMedDate not supplied

[Study on psychiatric disorders and defensive process assessed by the "defense style questionnaire" in sterile males SAMPLE consulting in andrology].

BACKGROUND: The literature about artificial insemination and the associated psychological, psychiatric and sexual disorders is relatively rich. But the majority of these studies is made in gynaecology, with a feminine approach of the disorder. There are very few works led in andrology. This justified the investigation of new trails in order to understand better the clinical context of the sterile man. We undertake a study about the psychiatric disorders among sterile men and about the defense styles. These are a clinical entity recently introduced in the quantitative psychopathology research. The defense style questionnaire (DSQ) is a psychometric scale used in common practice in order to measure the defense styles. OBJECTIVES: We made this study in order to examine the psychiatric state of a sterile males sample consulting in andrology; to assess the defense style by means of the Bond and al DSQ-88 ; to look into a difference between the defensive process according to their clinical situation of azoospermic males or as the oligoazoospermic males and finally, to reveal a correlation between the psychiatric disorders developed in this sample of sterile males and the defensive process they used. METHOD: There were 42 people (22 azoospermic males and 20 oligoazoospermic males) aged between 23 and 49 years old in the analysed sample. These have been selected at the surgery of andrology at the RUHC of Lille, depending on their arrival order for 6 months. There was no significant difference between the two groups as far as the age and the education standard are concerned. The selection criteria were medical and somatic. Our sample population were divided into two groups: azoospermia (no spermatozoon found in the semen analysis) and oligoasthenospermia (decrease of the number and the mobility of the spermatozoa and an increase of the percentage of atypical forms). The method first consisted in the DSQ, followed by the analysis of the psychiatric state according to the DSM IV, a hetero questionnaire to collect some general information about infertility and a self questionnaire about the sexual, conjugal and social effects of infertility. The DSQ and the interviews took place in the andrology department with the same investigator trained for this job. RESULTS: We found in our sample 26.2% of psychiatric disorders according to the DSM IV with a significant over-representation of generalized anxious disorder and somatization disorder. The comparison between azoospermic males and oligoazoospermic males patients showed the absence of significative difference as far as psychiatric morbidity rate and the use of defense styles are concerned. DISCUSSION: Our sample defended himself in accordance with modalities similar to the general population and used defense mechanisms preferentially belonging to the mature defense style, such as humor, repression and anticipation. The psychiatric pathology was significantly correlated to the preferential use of withdrawal, consumption, reaction formation and lack of humor use. We also confirm in our study the fact that the subjects using especially neurotic defense styles are more likely to develop a psychiatric disorder than the others. Our male sample is a waiting population and threatened by failure. The situation of wait creates anxiety. We also know that infertility is one of the most stressful situations a couple might face. However, our study did not enable us to know the precise relations between generalized anxious disorder and infertility, especially whether the generalized anxious disorder preceded this pathology or not. The over-representation of a somatization disorder only allows us to acknowledge its existence. We can also deduce from that a possible link between infertility and psychic disorder, even if no research permitted to affirm to date the existence of interrelations linking infertility and psychic life. On the whole, this population was suffering despite 73.8% of the patients had no confirmed psychiatric disorder. It is the reason why a liaison psychiatry more inserted into highly specialized teams is interesting, especially because it includes a medical and psychological approach of such disorders. The defense mechanisms preferentially used by this population were humor, repression and anticipation. Humor can only be considered as a defense mechanism when it is applied to oneself. The population who has no psychiatric disorder more uses humor. Does humor protect against the development of a psychiatric pathology, as certain authors proved it ? On the other hand, is repression really protective? It didn't interfere in our study about the development of a psychiatric pathology. So we can suppose that repression was protective for our whole sample, but we can not prove it. However, we wonder if this mechanism works after the failure of an artificial insemination is announced. In which measure such a stress can be repressed out of the conscience field? As for anticipation, it is used by our population who is for the most part in good health. But the question is to know if our sample really envisaged all the different possible solutions or only the success of artificial insemination. As some other works, we confirm that the, psychiatric, people significantly use the neurotic style. Our psychiatric patients used less humor and more consumption, withdrawal and reaction formation than the sane people. Consumption is rarely considered as a defense mechanism by some other authors. And yet, consumption and the existence of psychiatric disorders were very closely linked. This association is found again with anxiety in other studies. The correlation between psychiatric disorder and withdrawal was veryimportant too. The DSM lV defines withdrawal as an apathetic withdrawal. It is not an apathetic withdrawal in our population because the average scores for the ,, activity >, defense mechanism remained high. In our sample, the use of this defense mechanism would encourage the expression of psychiatric troubles. The reaction formation quoted by Freud and Bergeret are both valorised in our society. What kinds of reaction formations use these men ? Are they pathological ? Our study can not answer to these questions. However, the DSQ items examining the reaction formation present its "socially promoted" aspect and forget the pathological one. It has been showed that the evaluation of the defense modalities in a certain type of population can allow the emergence of specific defense mechanisms. This can be considered as predictive factors of development of a mental pathology. The evaluation of specific mental defenses could permit to define vulnerability and affinity for given affections instead of simple personality traits or profiles. Most part of the works shows results in favour of the capacity of DSQ to assess the different defense mechanisms according to the diagnosis groups. But the insufficient numbers of studies moderate on the whole the hypothesis of the existence of specific defense mechanisms--protective factors and factors of vulnerability--linked to a given psychiatric disorder. CONCLUSION: There is not a difference of psychological effect in terms of degree of sterility. On the other hand, the existence of over-represented psychiatric disorders with sterile males compared with a control group force Consultation-Liaison psychiatrists and andrologists would be able to understand the pain beyond the need of acting by the artificial insemination. In our opinion, this justifies the fact that the patients should have the opportunity of expressing, in the department where they are treated, all the feelings inherent to their personal and conjugal drama as part of a specialized treatment. Our study confirms the difficulty to know whether some defense mechanisms are vulnerability factors for a certain psychiatric disorder or whether the defense mechanisms are an epiphenomenon of a particular psychiatric disorder. This is the reason why a lot of authors having worked with DSQ agree to conclude that additional prospective studies, which would permit to make a link between the defense mechanisms anda certain psychiatric pathology, are necessary. In the case we study, it is important to explore the defensive modalities before the infertility diagnosis and after the birth of a child, with a more important sample population. A better knowledge of the defensive modalities of such a population, used in a psychotherapeutic context could help to prevent the appearance of psychiatric disorders or, if not, to anticipate them.

Adaptation, Psychological↗
PubMedDate not supplied

[Post-traumatic stress, post-traumatic depression and major depressive episode: literature].

Although they are likely to add their effects, physical and psychic traumata (or traumas) can provoke in different ways the appearance of depressive symptoms sometimes common. Post-traumatic depression, reactional depression, major depressive disorder and post-traumatic stress disorder represent different clinical and nosographic disorders in despite of their occasionally common symptomatic core. Historically, it is interesting to note during the XXth century the true semantic change of the terms of trauma from the somatic field to the psychic sphere. Physical traumatism is often represented by a material shock for the subject and by its organic consequences. It is defined as an event that leaves its mark which itself inflicts and handicaps the vital trajectory of the subject. It primarily comprises brain and rachis injuries, whose evolution is frequently characterized by the occurrence/appearance of a depressive disorder, whose genesis rests on psychological but also neurobiologic and physical arguments. Thus major depressive disorders are often present in the course of various physical traumatisms mainly related to nervous system. In accordance with several studies, the prevalence of major depressive disorders ranges from 25% to 50%. These mood disorders occur in the year which follows the accidental event. Their average time of revelation is estimated at four months and their average duration lies between three and six months. Lastly, although these depressive illnesses present clinical symptoms comparable with those observed in other contexts, some nuances can be raised. Nonetheless, they confine sometimes with true clinical forms depending on the intensity, the form, the circumstances or the consequences of the trauma. Psychic traumatism doesn't have the same profile and rests for much dedicated with the reexperiencing. Thus for some authors, depression illness represents a disorder that occurs after a traumatic event whereas others see a differential diagnosis which exludes or which represents a comorbidity with post-traumatic stress disorder. The review of the literature allows us to emphasize the complexity of the links as well as the clinical and epidemiologic differences between stress disorder and major depressive disorder. From the clinical point of view, the major features of PTSD are articulated around a triad of symptoms. They include the reexperiencing symptoms of the traumatic event such as intrusive memories and recurrent nightmares, the protective reactions such as avoidance of the stimuli associated with the trauma and emotional numbing, and the arousal symptoms such as the startled response and hypervigilance. The complexity of this syndrom is due to the frequent combination of these symptoms with other nonspecific ones. As far as the mood is concerned (the mood symptoms are concerned), the regrouping of some of these symptoms allows the clinician to sometimes releave a depressive symptomatology without being able to assess the DSM diagnosis of major depressive disorder. Epidemiologic studies dealing with the risk of installation of a PTSD after a traumatic event reveal differences in the prevalence depending on the nature of the traumatic events: ranging from 1% in general population to 80% following some situations of extreme and durable psychic suffering. Between both poles, one finds a prevalence ranging between 20 and 50% following other events such as serious accidents, natural disasters or criminal assaults. The clinical features of depressive episodes comorbid or associated with PTSD have some characteristics making it possible to individualize various clinical forms as a function of traumatic event type: asthenic, characterial or with somatic symptoms. According to the majority of authors, the co-occurrence of post-traumatic stress disorder and major depressive disorder is high although differential diagnosis is sometimes difficult. However, conceptual differences remain and two conceptions are distinguished. For some authors, like Bleich and Shalev, there would not be true chronological evolution from PTSD to MDD. Moreover the presence of symptoms considered as pertaining to the mood register within the criteria of PTSD would be clearly predictive of the occurrence and the severity of the diagnosis but not of the chronicity. For others, there would be a continuity between post-traumatic stress disorder and major depressive disorder. It is the case in many studies of veterans but also for civilian traumatic events. It is also the case for the American national study of comorbidity in which Kessler concludes that for 78% of the subjects who present a comorbidity PTSD/MDD (comorbidity raised for 48% of the 5,877 subjects included), the mood disorder is secondary to PTSD. (ABSTRACT TRUNCATED)

Comorbidity↗
PubMedDate not supplied

[Carbamazepine-fluvoxamine interaction. Consequences for the carbamazepine plasma level].

The current practices concerning psychotropic drugs use plasma levels for the therapeutic adaptation and for the prevention of overdose and side effects. We observed, among two patients treated with constant dosages of carbamazepine (CBZ), that the addition of fluvoxamine (FLV) has increased significantly plasma levels of CBZ. The first patient, suffering of an affective bipolar trouble (ICD-10), was hospitalized for major depression. His admission treatment was CBZ (800 mg/day) and cyamemazine (75 mg/day). The introduction of the FLV (200 mg/day) was justified by the symptomatology. Then, plasma levels of CBZ increased progressively. No clinic or biological side effect was observed. Rapidly, CBZ oral dosages were decreased, but the plasma levels of CBZ reached the therapeutic window only when the FLV prescription was definitively stopped. The other patient was hospitalized for an acute exacerbation of a paranoiac disorder. He was treated with haloperidol for this episode. For five years, he received CBZ for neuralgia of the Trigeminus. The emergence of a depressive disorder justified a FLV treatment. From the introduction of FLV, plasma levels of CBZ were significantly increased. The reduction, then the stop of the FLV treatment, has allowed the standardization of plasma concentrations of CBZ. Three similar studies were found in the literature. The danger of this interaction was notified in two studies (one case each). Furthermore, in the third study (three cases) was put forward the hypothesis of a new therapeutic pathway. this hypothesis was suggested by the fact that these two medications were proposed independently to treat impulsive behaviors.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

[Erythrocyte superoxide dismutase (eSOD) determination in positive moments of psychosis].

Dysregulation of free radical metabolism has been supposed to be involved in schizophrenia etiopathogeny. Recently, Wang et al. showed a red blood cell super oxide dismutase increase in positive schizophrenia (Crow's type I), but neither in negative schizophrenia (Crow's type II) nor in controls. The study included 28 in-patients suffering from acute positive psychosis who were compared with 15 controls. We confirmed the results of Wang. We found a significantly red blood cell Super oxide dismutase increase in positive psychosis, in comparison to negative psychosis and controls (p = 0.0001). This SOD increase was in relationship with the degree of clinical psychomotor excitement. After 21 days of neuroleptic treatment, SOD activity decreased and reached standard values. These results support the hypothesis of striking relationships between catecholaminergic hyper-metabolism and SOD increase, in positive psychosis. These could account for psychotic positive symptoms improvement with neuroleptic treatment, which blocks dopamine pathways.

Adult↗
PubMedDate not supplied

[Erythrocyte ketone reductase activity, total plasma haloperidol and acute psychoses].

Haloperidol (HAL) is a widely used and clinically effective neuroleptic. Its metabolism differs in various animal species. In humans, reduced haloperidol (RHAL), a hydroxy metabolite of HAL, is produced by a cytosolic ketone reductase. Interconversion is known to occur whereby HAL is found in the plasma after administration of RHAL in vivo. Interconversion of HAL and RHAL has been observed in man. However, the capacity for reductive HAL is greater than its oxidation back from RHAL. RHAL, the resulting metabolite of HAL, is reported to be about 10-25% as active as HAL in an animal model. Large intersubject variation has been observed in the pharmacokinetics of HAL and RHAL. A wide variation in reductive drug-metabolizing has been observed in schizophrenic patients treated with HAL. Both high and low RHAL/HAL ratios or RHAL levels were reported to be linked to poor response in HAL-treated patients and might be correlated with the therapeutic window effect of HAL treatment. It is conceivable, therefore, that subjects with high reductive capacity relative to oxidative capacity may have less therapeutic response from the same dose of HAL than those with a low reductive capacity relative to oxidative capacity. This aim of this study was to investigate the HAL reduction among a sample of HAL-treated schizophrenic patients. Because ketone reductases are generally not tissue specific, we investigate the reductase activity in Red blood cells (as described by Inaba), before and during the treatment. Steady-state plasma drug levels during 2 weeks of treatment were quantified. We examined the relationships between fixed doses of HAL treatment, Red blood cells ketone reductase activity, plasma HAL and RHAL levels and the percentage of change of the Positive and Negative Syndrome Scale for Schizophrenia. The participants in this study were 15 inpatients consecutively being treated in the adult psychiatric wards of the University of Lille. All subjects met DSM III-R criteria for schizophrenia (paranoid form). Upon induction subjects were evaluated clinically by trained raters using the Positive and Negative Syndrome Scale for Schizophrenia (PANSS). Subjects were required to score 40 or higher on the general psychopathology subscale of the PANSS to continue participation. All subjects were drug free. Haloperidol was administered orally at three times daily dose. Patients were randomized to treatment at three orally fixed doses: 6 mg per day, 10 mg per day and 15 mg per day. Patients were treated for 2 periods of one week. At the end of each period, dosages could be modified according to the clinic evolution of the patient. PANSS was repeated by the same raters blinded to the haloperidol dosage, plasma concentration and Rbc haloperidol ketone reductase activity, at the beginning and at the end of each period. Blood samples were collected on the same day that clinical assessment were made. Multiple regression analysis (forward stepwise) revealed that Red blood cells reductase activity at D0 is an important variable predicting haloperidol plasma levels at week 2. Similarly Red blood cells reductase activity at D0 and D7 predicted Reduced haloperidol plasma concentrations at week 2. In this sample, no parameter was found to be consistency predicted the percentage change in the PANSS positive subscale from baseline, at week 2. Nevertheless, Red blood cells reductase activity at D0, Reduced haloperidol/haloperidol ratio at week 2, haloperidol plasma levels at week 2 and the dose of haloperidol at week 1 were important variables predicting the percentage change in the PANSS general subscale from baseline at week 2. These results suggest that the knowledge of reductase activity could predict the treatment response in acute schizophrenic patients.

Acute Disease↗