[Interest of the use of the "MYDEFI" smartphone application to help reduce alcohol consumption in the involvement of pharmacists in the prevention of at-risk consumption: Results of a survey in the Hauts-de-France]. / Intérêt de l'utilisation de l'application smartphone « MYDEFI ¼ d'aide à la réduction de la consommation d'alcool dans l'implication des pharmaciens dans la prévention de la consommation à risque : résultats d'une enquête dans les Hauts-de-France.

OBJECTIVES: Evaluate the interest in the MyDéfi application as a tool to help pharmacists identify and manage excessive alcohol consumption, as well as their perception and knowledge of alcohol and their possible role in its management. METHODS: Prospective mixed qualitative and quantitative study, based on face-to-face semi-directive interviews. RESULTS: The 101 pharmacists interviewed in Hauts-de-France region considered that the detection of alcohol consumption was part of their mission, even if it is a difficult subject, and that they had received specific training in alcohology during their university training. Only 12% were aware of early screening and brief intervention on alcohol. Several obstacles were mentioned, such as the lack of training and confidentiality, and difficulties related to patient specificities. Forty-one percent said that the pharmacy was not suitable and almost 72% said that the MyDéfi application could be useful for screening and 91% would recommend the application as one of the best supports, easy to advise with a personalised follow-up. For 32%, the application is accessible to patients (40% think that the main drawback of the application is inaccessibility and 27% its cost). CONCLUSION: Pharmacists consider that excessive alcohol use is a major problem that should mobilise them but many do not feel ready to offer brief interventions. After seeing how the MyDéfi application worked, the majority considered that it could help them in their prevention mission.

[Abuse of alcohol and benzodiazepine during substitution therapy in heroin addicts: a review of the literature]. / Abus d'alcool et de benzodiazépines lors des traitements de substitution chez l'héroïnomane : une revue de la littérature.

INTRODUCTION: In spite of its seriousness, dependence on alcohol and benzodiazepines during substitution treatment are poorly documented. Its frequency is nonetheless significant. According to studies, between one and two thirds of patients are affected. This consumption is under verbalized by patients and underestimated by carers. In one study, where the average diazepam doses were from 40 to 45 mg per day, 30% of the patients were taking 70 to 300 mg per day, two thirds having experimented with a fixed dose of 100mg. Benzodiazepines, especially diazepam and flunitrazepam, were studied versus placebo. Thus, 10 to 20mg of diazepam gave rise to euphoria, a sensation of being drugged, sedation and lessening of cognitive performance. The aim of this consumption is to potentiate the euphoria induced by opioids, a "boost" effect during the hour after taking it, or the calming of the outward signs of withdrawal. The most sought after molecules are the most sedative, those with pronounced plasmatic peaks, and the most accessible. LITERATURE FINDINGS: In multidependant subjects, opioid dependence had been earlier in adolescence, with a number of therapeutic failures. They had been faced with repetitive rejection and separation during childhood, medicolegal and social problems. Somatization, depression, anxiety and psychotic disorders are frequent in this subgroup. Heavy drinkers under methadone treatment are highly vulnerable to cocaine. Their behaviour is at risk, with exchange of syringes; their survival rate is 10 years less than that of moderate consumers of alcohol. Most are single, with a previous prison, psychiatric or addictive cursus and they present significant psychological vulnerability. For some authors, benzodiazepines indicate a psychiatric comorbidity. Methadone significantly reduces the consumption of alcohol by nonalcoholic heroin addicts. Although alcohol is an enzymatic inductor of methadone catabolism, with bell-shaped methadone plasma curves over 24 hours, a substitution treatment is recommended. It has a minimum impact on care, in spite of efficiency and retention in therapeutical programs, allowing the subject's inclusion in the framework of a more regular and sustained medical follow-up. Treatment of benzodiazepine dependence by a progressive regression of doses has little efficacy in subjects which cannot control how much medication they are taking. Certain authors have suggested maintenance treatments of clonezepam. The most appropriate therapeutic propositions are: (1) maintenance of therapeutic links though a framework of deliverance from flexible substitution treatment; (2) prevention by cautious prescribing and control of dispensing medication; (3) parallel treatment of psychiatric comorbidities and related personality disorders; (4) individual psychiatric treatment, either institutional or in consistent networks.

[Smoking and schizophrenia: epidemiological and clinical features]. / Tabac et schizophrénie: aspects épidémiologiques et cliniques.

FREQUENCY: The prevalence of cigarette smoking is significantly higher among patients with schizophrenia (60-90%) than in the general population (23-30%). While tobacco smoking decreases in the general population (from 45% in the 1960's to 23-30% in the 2000's), smoking in patients with schizophrenia remains high. Patients with schizophrenia smoke more cigarettes than control subjects. Patients smoke more deeply, thereby increasing their exposure to the harmful elements in tobacco smoke. IMPACT OF SMOKING IN SCHIZOPHRENIC PATIENTS: As in the general population, smoking contributes to the reduced life expectancy in patients with schizophrenia. Patients with schizophrenia are at increased risk for cardiovascular disease due to high rates of cigarette smoking. In the Department of Mental Health of the commonwealth of Massachusetts, cardiovascular disease was the factor the most strongly associated with excess mortality. Cardiac deaths were elevated more than six-fold. Weight gain, insulin resistance, metabolic syndrome and diabetes mellitus are frequent in patients with schizophrenia, and may worsen the risk of cardiovascular diseases. It has been reported that the risk for lung cancer in patients with schizophrenia is lower than that of the general population, despite increased smoking. However, in a study conducted in Finland, a slightly increased cancer risk was found in patients with schizophrenia. Half of the excess cases were attributable to lung cancer. IMPROVEMENT OF COGNITIVE DEFICITS: Patients with schizophrenia may use nicotine to reduce cognitive deficits and negative symptoms or neuroleptic side effects. Smoking may transiently alleviate negative symptoms in schizophrenic patients by increasing dopaminergic and glutamatergic neurotransmission in the prefrontal cortex. In patients with schizophrenia, nicotine improves some cognitive deficits: (1) sensory gating deficits and abnormalities in smooth pursuit eye movements associated with schizophrenia are transiently normalized with the administration of nicotine ; (2) high-dose nicotine transiently normalizes the abnormality in P50 inhibition in patients with schizophrenia and in their relatives; (3) in tasks that tax working memory and selective attention, nicotine may improve performance in schizophrenia patients by enhancing activation of and functional connectivity between brain regions that mediate task performance (Jacobsen et al. 2004; Paktar et al.2002); (4) cigarette smoking may selectively enhance visuospatial working memory and attentional deficits in smokers with schizophrenia. However, Harris et al., found that nicotine affects only the attention without effects of nicotine on learning, memory or visuospatial/constructional abilities. In addition, smoking could facilitate disinhibition in schizophrenic patients.

[Tobacco and schizophrenia: therapeutic aspects]. / Tabac et schizophrénie: aspects thérapeutiques.

Although patients with have low motivations to quit smoking, smoking cessation treatment can be effective for these patients. Patients schizophrenia who achieve significant smoking reduction during a treatment intervention can at least maintain that level of reduction at 2 years. Cigarette smoking by patients with frequently goes unaddressed, contributing to excess mortality in this population. Behavioural interventions improve smoking cessation in schizophrenia patients. Nicotine replacement can substantially reduce withdrawal symptoms. Bupropion enhances smoking abstinence rates. Bupropion is well-tolerated and safe for use in schizophrenia patients: bupropion does not worsen clinical symptoms of schizophrenia. Atypical antipsychotics may reduce smoking consumption in schizophrenia patients, in particular clozapine. Atypical antipsychotic medication, in combination with the nicotine transdermal patch, significantly enhance the rate of smoking cessation. Interactions between smoking and antipsychotic medication - Smoking increases the metabolism of the antipsychotic medications by inducing the cytochrome P450 1A2 isoform. Smoking lowers the blood levels of typical or atypical antipsychotic medication, in particular haloperidol, chlorpromazine, olanzapine and clozapine. -Abstinence can increase many psychotropics' blood levels. Accordingly, smoking appears to reduce neuroleptic-induced parkinsonism. In contrast, smoking is a risk factor for tardive dyskinesia, independent of neuroleptic exposure.

[Schizophrenia and amphetamine dependence. A case report]. / Schizophrénie et dépendance aux amphétamines.

UNLABELLED: Whereas observations of psychotic disorders induced by amphetamines are common, few observations described the impact of chronic amphetamine abuse on schizophrenic patients. We report the case of a schizophrenic patient who presented with amphetamine dependence for several years, without other accompanying addiction. CASE REPORT: During his adolescence, Mr. X. gradually developed delusional beliefs of persecution and telepathy. He believed that the other pupils and teachers spoke about him in malicious terms. At the age of 23, Mr. X began to consume 60-100 mg/week of amphetamines orally. He consumed amphetamines during 7 years. The delusions, in particular the auditory hallucinations worsened after the use of amphetamines. Subsequently, he married and was declared unfit for national service due to the psychotic disorders. Mr. X received neuroleptic treatment with moderate effects on the psychotic symptoms. Between the age of 24 and 30, the patient presented persecutory, megalomanic and physical transformation beliefs, delusions of being controlled as well as auditory, somatic-tactile and visual hallucinations. At the age of 30, while he had stopped his consumption of amphetamines for 9 months, the patient, overwhelmed with the delusions, murdered his wife. He was sent in jail for 13 months, and subsequently hospitalized for one year in a high security psychiatric department and 7 years in our psychiatric department. The neuroleptic treatment was effective, particularly against the hallucinations. Following stabilisation, the symptomatology of the patient was marked by a disorganization syndrome, including prominent thought disorder, disorganized speech, associative loosening, frequent derailments and negative signs of schizophrenia, in particular affective flattening and blunting of emotional expression. When the patient was 43, a trial discharge was authorized owing to improvement of his condition. The neuroleptic treatment was switched with single-drug olanzapine therapy, 10 mg/day which improved the negative symptoms. Mr. X. resumed part-time professional activities and remarried. DISCUSSION: The patient fulfilled the DSM IV criteria for schizophrenia and for amphetamine dependence assessed using the Composite International Diagnostic Interview (CIDI). He presented, in particular, withdrawal syndrome when amphetamines were discontinued. The amphetamine consumption was followed by a marked deterioration in the delusions, particularly the hallucinations. Worsening of the positive symptoms in schizophrenic patients by amphetamines has been established in single dose studies, in particular characterized by persecutory delusions and hallucinations. On the other hand, amphetamines tend to transiently and moderately reduce the negative symptoms. Some stu-dies have shown that amphetamine consumption promoted violent acting out in non-schizophrenic subjects. In our observation, the acting out may be not related to the acute effects of these substances, since it occurred 9 months after stated discontinuation of amphetamine consumption. However, the cerebral toxicity and psycho-behavioural disturbances related to amphetamines might be prolonged after withdrawal. In non-schizophrenic patients, the existence of prolonged neurotoxicity of amphetamines and related psycho-behavioral disturbances has been suggested. The prolonged administration of amphetamines to animals produces neuro-axonal degeneration in the striatum, the frontal cortex, the nucleus accumbens and the amygdala. In human, there are some evidence of persistant deteriorations of the serotoninergic and dopaminergic systems in the caudate nucleus, the putamen and the nucleus accumbens following amphetamine consumption. CONCLUSION: The neurobiological and psycho-behavioural effects of amphetamines may be prolonged following withdrawal in both schizophrenic and non-schizophrenic patients.

[The psychiatric forms of Creutzfeldt-Jakob disease]. / Les aspects psychiatriques de la maladie de Creutzfeldt-Jakob.

CLINICAL FEATURES: Frequent in the new variant of Creutzfeldt-Jakob disease, psychiatric disorders are less common in the sporadic form. The disorders are non-specific: mood disorders, personality changes and psychotic symptoms. DIAGNOSIS: The diagnosis of Creutzfeldt-Jakob disease is evoked on the emergence of the first neurological signs, notably ataxia and myoclonia. The diagnosis is supported by the search for P 14-3-3, EEG in the cerebrospinal liquid as well as electroencephalogram and magnetic imaging that permit distinction between the sporadic and the new variant forms.

[Cannabis and schizophrenia: demographic and clinical correlates]. / Cannabis et schizophrénie: données cliniques et socio-démographiques.

UNLABELLED: The high prevalence of psychoactive substance abuse or dependence among schizophrenic patients has now been well established. Mueser et al. stressed the need to assess the abuse of specific classes of substances and analyse the data accordingly. The objective of this study was to compare the socio-demographic correlates and the clinical features in a group of schizophrenic patients with a lifetime cannabis abuse or dependence according to the DSM III-R with a group of schizophrenic patients who had never presented any abuse or dependence. SUBJECTS AND METHODS: The study included 124 subjects with diagnoses of schizophrenia or schizoaffective disorders according to the DSM III-R. Inclusion criteria for participation in the study were age 18 years or older and willingness to provide consent to participate in the study. The inpatients were evaluated when their condition was stabilised. Assessment tools were the psychoactive substance use disorder section of the Composite International Diagnostic Interview (CIDI), the Positive and Negative Syndrome Scale (PANSS), the Global Assessment of Functioning Scale (GAF). Subjects with cannabis abuse or dependence during their lifetime were compared with subjects without abuse or dependence, using chi(2) test for categorical variables and analyses of covariance (ANCOVA) for quantitative variables. RESULTS: Forty-nine subjects (42,6%) presented lifetime abuse or dependence on one or more substances. Since 19 patients with alcohol, stimulant, sedative or opiate abuse or dependence were excluded, the study finally included 96 subjects including a first group of schizophrenic patients with cannabis abuse (n=6) or dependence (n=24) and a second group without any psychoactive substance abuse (n=66). Thirteen (11.3%) patients presented cannabis abuse or dependence within the 6 months prior to the assessment. The mean SD age of onset of cannabis abuse or dependence was 19.6 +/- 3.0 years. Cannabis abuse/dependence preceded the first psychiatric treatment in 70% of the subjects (n=21). 83.3% of the schizophrenic patients with cannabis abuse or dependence were male (n=25) compared to 62.1% in the group without substance abuse (n=41) (chi(2)=4.32, df=1, p=0.04). Schizophrenic patients with cannabis abuse were significantly younger (mean age: 28.9 +/- 6.3 vs 37.0 +/- 12.7, ANCOVA, F=7.2, df=1,96 p=0.009). There was no significant difference between the two groups for marital status, (chi(2)=5.34, df=2, p=0.07), level of education, (chi(2)=0.93, df=2, p=0.62) professional status, (chi(2)=8.7, df=5, p=0.11), on PANSS total score (ANCOVA, F=0.42, df=1,93, p=0.52), GAF score (ANCOVA, F=0.06, df=1,92, p=0.80), mean number of hospitalizations (ANCOVA, F=3.25, df=1,85, p=0.08), mean age of first psychiatric contact (ANCOVA, F=0.74, df=1,93, p=0.39), and neuroleptic dosages (ANCOVA, F=0.03, df=1,90, p=0.87). In contrast, the total duration of hospitalization was significantly longer for the group with cannabis abuse. Patients with cannabis abuse were more likely to have an history of suicide attempts than subjects without substance abuse (chi(2)=11.52, df=1, p=0.0007). DISCUSSION: The prevalence rates for substance abuse and the socio-demographic characteristics of the population of our study are consistent with findings of previous studies. Male gender and age were significantly related to history of cannabis abuse or dependence. Cannabis abuse frequently preceded the onset of psychiatric treatment. However, both schizophrenia and substance abuse tend to develop gradually, with no clear demarcation for the onset of schizophrenia. The absence of any link between the scores for the subscales of the PANSS and cannabis abuse, both in our study and in some retrospective previous studies, is not suggestive of cannabis abuse as a self-medication of positive or negative symptoms of schizophrenia. Self-medication could concern other symptoms, such as cognitive deficits. In addition, the hypothesis of self-medication has especially been suggested in cocaine abuse or dependence. Some limitations to this study can be discussed. First, although the recruitment was systematic and done in a public mental health service, the patients of our study are not necessarily representative of all schizophrenic patients. Secondly, as in any retrospective study, the prevalence of lifetime substance abuse may have been under-estimated. Urinary toxicology tests may have been able to improve the sensitivity of the diagnosis of recent substance abuse, but structured interviews are more appropriate for the diagnosis of lifetime substance abuse in schizophrenic patients than urinary toxicology tests. CONCLUSION: The socio-demographic characteristics of cannabis abuse or dependence in schizophrenia are similar to those found in general population. Cannabis using schizophrenic patients were more likely to be younger and male than non users. The duration of hospitalization was significantly longer for the group with cannabis abuse. Prevalence of suicide attempts in schizophrenia is closely correlated to cannabis abuse.

[Psychiatric manifestations of a new variant of Creutzfeldt-Jakob disease. Apropos of a case]. / Manifestations psychiatriques du nouveau variant de la maladie de Creutzfeldt-Jakob. A propos d'un cas.

UNLABELLED: The new variant of Creutzfeldt-Jakob disease (nvCJD) was first described in the UK in 1996 (16). The nvCJD differs from sporadic, genetic and iatrogenic CJD. Creutzfeldt-Jakob disease is closely associated with an abnormal isoform PrPSc of a cell-surface glycoprotein, prion protein (14). Molecular analysis suggests that nvCJD is caused by the same prion strain as bovine spongiform encephalopathy (BSE) (4, 10). To the end of September 2000, there have been 82 cases of nvCJD in the UK. We report the second French case of nvCJD to our knowledge (5, 13). CASE REPORT: This 36 year old woman was referred by a local general practitioner with a 6 month history of psychiatric symptoms of major depressive disorder. According to her family, the patient had suffered from personality change for several months before the onset of depression including apathy, emotional lability, infantile affect. There was no history of health problems. As she was admitted to the psychiatric department of our hospital in Paris suburbs, she presented a major depressive disorder. There were no specific psychiatric features allowing distinction from common depressive disorders, except a marked emotional lability. The patient's condition progressed rapidly within the following days. She presented memory impairment and disorientation. Drug treatments, clomipramine (125 mg/day) and venlafaxine (200 mg/day), were used with no benefit. She presented subsequently transient delusions and auditory hallucinations, fleeting for some hours. The predominant delusional themes were somatic type and pregnancy. The delusions were concomitant with delusions of the onset of cognitive impairment. The patient tested negative for the P 14.3.3 protein in the CSF. Computed tomography scan of the brain did not show any relevant abnormality. The electroencephalogram showed non specific slow wave activity. The neurological symptoms developed 7 months after the onset of depressive symptoms including ataxia, myoclonus, excessive daytime drowsiness, headache. After the onset of neurological symptoms, the illness progressed rapidly over the next 2 months with cognitive impairment, particularly memory impairment, myoclonus, ataxia, incontinence of urine and progressive immobility leading to dependency. CSF tests were negative. She was referred to a neurology department where the diagnosis was confirmed by brain biopsy (detailed elsewhere). The patient died in a state of akinetic mutism. DISCUSSION: The clinical features of our patient were consistent with previous descriptions of nvCJD, mainly those of the National CJD Surveillance Unit studies (17): early psychiatric symptoms, prolonged duration of illness (median: 14 months), earlier age at death, compared with sporadic CJD. Psychiatric symptoms occur in the clinical course in about a third of cases of sporadic CJD (3). In contrast, of the 35 cases that have died of nvCJD identified in the study by Will et al. (17), 34 suffered from early and prominent psychiatric symptoms, mainly depression and anxiety. In most of the patients, the first symptoms were psychiatric. Drug treatment was used in most cases, some patients had a transient improvement (18). The patient without psychiatric symptoms reported by the NCJDSU (17) was emotionally labile. Infantile affect and emotional lability, found in our patient, are frequently reported in other studies (1, 18). Schizophreniform disorders have been described during the clinical course, with auditory and visual hallucinations and paranoid delusions (17, 18). The insomnia and excessive daytime drowsiness our patient presented have been described in similar cases (18). Investigations are important to rule out alternative diagnoses. EEG records do not show periodic triphasic complexes as in sporadic CJD. The P 14.3.3 protein in the CSF is positive in half the cases of nvCJD (17). First neurological symptoms developed 6 months after the onset of psychiatric symptoms including ataxia, myoclonus and persistent painful sensory symptoms (17, 18). In most of the cases, MRI brain scans show bilateral pulvinar high signal (17), found subsequently in our patient and detailed elsewhere (13). The terminal stages are progressive cognitive impairment, helplessness and akinetic mutism. CONCLUSION: The first symptoms of this patient were purely psychiatric and difficult to distinguish from common psychiatric disorders. Clinical surveillance of human prion disease is crucial in France, as in UK. The link with BSE has dramatically highlighted the need for neurological and neuropsychological precise investigations.

Substance abuse and suicidality in schizophrenia: a common risk factor linked to impulsivity.

Lifetime substance abuse comorbidity is frequent in schizophrenic patients, but the clinical correlates remain unclear. We have explored the chronological relations between substance abuse and course of schizophrenia, and compared several clinical characteristics and personality dimensions in 50 schizophrenic patients with or without lifetime substance abuse or dependence. Abuse occurred mainly after the first prodromal symptoms and just before the first psychotic episode. Substance-abusing patients were not different from non-substance-abusing patients on the Chapman Physical Anhedonia Scale, PANSS total score, negative subscore or depression item, CGI, treatment response and demographic variables. In contrast, substance-abusing patients had higher scores on the Barratt Impulsivity Scale (total, cognitive and non-planning scores) and had attempted suicide more often. In patients with schizophrenia, as in the general population, substance abuse or dependence appears associated with higher impulsivity and suicidality. High impulsivity could facilitate substance abuse as a maladaptive behavior in response to prodromal symptoms, precipitating the onset of a characterized psychosis.

Is substance abuse in schizophrenia related to impulsivity, sensation seeking, or anhedonia?

OBJECTIVE: The authors compared impulsivity, sensation seeking, and anhedonia in a group of schizophrenic patients with and without lifetime substance abuse or dependence. METHOD: Patients (N=100) with schizophrenia or schizoaffective disorder (per DSM-III-R criteria) were assessed with the Composite International Diagnostic Interview's section on psychoactive substance use disorder, the Positive and Negative Syndrome Scale, the Barratt Impulsivity Scale, the Zuckerman Seeking Sensation Scale, and the Chapman Physical Anhedonia Scale. RESULTS: The mean scores for impulsivity and sensation seeking were higher in the group with substance abuse (N=41) than in the group without substance abuse (N=59). No significant difference between groups was found regarding physical anhedonia. CONCLUSIONS: As in the general population, high levels of impulsivity and sensation seeking are associated with substance abuse in patients with schizophrenia.

Prevalence of hepatitis B virus, delta agent and human immunodeficiency virus infections in drug addicts.

Infections with the hepatitis B (HBV) and delta (HDV) viruses and with the human immunodeficiency virus (HIV) are very common among intravenous drug addicts. The serum of 80 percent of drug addicts contains one of the HBV markers, and 15 percent of them carry an anti-D antibody. Infections with the hepatitis A and non A-non B viruses are also very common among drug abusers. Some of them may harbour several of these pathogens. This can explain the frequency of liver disease (biological anomalies and histological lesions) observed in drug addicts, as does alcohol consumption associated with drug abuse. Fifty to 60 per cent of intravenous drug addicts are seropositive for HIV. This prevalence varies across studies and countries. The high prevalence of infection by HIV in drug addicts may be explained by the use of a shared syringe. This prevalence exposes drug addicts to an increase in AIDS cases in the near future. The high prevalence of infections by HBV, HDV and HIV in drug addicts represents a risk factor for the spread of HBV, HDV and HIV infections among the general population. Preventing the rapid spread of these viruses among drug addicts is of utmost importance for the future.