Bupropion as an add-on therapy in depressed bipolar disorder type I patients with comorbid cocaine dependence.

OBJECTIVES: The treatment of bipolar disorder type I (BD-I) with a comorbid cocaine dependence disorder (CDD) is a challenge in current psychiatric practice. Drugs with proven efficacy in manic/mixed episodes, such as atypical antipsychotics and mood stabilizers, sometimes do not prevent depressive relapses; on the other hand, the use of antidepressants during acute depressive episodes may increase the risk of a manic switch. The aim of the present study was to investigate the short-term efficacy of bupropion augmentation in acutely depressed BD-I patients with co-occurring CDD. METHODS: Twelve depressed BD-I patients, with a comorbid CDD, treated with valproate 1000 to 1500 mg/d and aripiprazole 10 mg/d, were randomly assigned to receive bupropion 150 mg/d as an open-label add-on therapy (n = 5) or to continue their previous treatment (n = 7). RESULTS: After 4 weeks of observation, patients receiving add-on therapy with bupropion have improved in terms of Hamilton Depression Rating Scale scores and Drug Abuse Screening Test scores, with respect to those of the comparison group, whereas no significant increase of Young Mania Rating Scale scores over time was observed. CONCLUSIONS: Our preliminary findings suggest that combining bupropion with mood stabilizers and atypical antipsychotics may be a good therapeutic option in short-term treatment of depressed BD-I patients with comorbid CDD.

Prevalence and intensity of basic symptoms among cannabis users: an observational study.

BACKGROUND: It is difficult to establish whether people who are prone to psychosis are drawn to cannabis use or whether cannabis use truly increases the incidence of psychotic experiences. OBJECTIVES: The aim of our study was to evaluate, in a sample of healthy high school and university students, the presence and level of subjective experiences (SEs) and their relation to cannabis use. METHODS: A total of 502 voluntary subjects were recruited; an anamnestic interview was administered to obtain socio-demographic information, cannabis use data, and psychiatric familial history. SEs were assessed using the Italian version of the Frankfurt Complaint Questionnaire (FCQ). RESULTS: One hundred and fourteen subjects declared the use of cannabis: 20.5% smoked more than 1 joint per week, and 71.9% used cannabis for a period of more than 1 year. Cannabis users did not differ from the cannabis-free group in any of the 10 FCQ dimensions. Higher FCQ total scores were found in cannabis users with a familial history of psychiatric disorders respective to those without a psychiatric load (p<.05). CONCLUSIONS AND SCIENTIFIC SIGNIFICANCE: In our study, SE intensity was not influenced by the use of cannabis. With regard to familial data, this is the first study to explore the relationship between SE and the presence of psychiatric problems in first-degree relatives. The association between FCQ intensity and psychiatric familial load may confirm the independence of these phenomena from the use of cannabis.

Benign intracranial hypertension associated to blood coagulation derangements.

BACKGROUND: Benign Intracranial Hypertension (BIH) may be caused, at least in part, by intracranial sinus thrombosis. Thrombosis is normally due to derangements in blood coagulation cascade which may predispose to abnormal clotting activation or deficiency in natural inhibitors' control. The aim of the study is to examine the strength of the association between risk factors for thrombosis and BIH. PATIENTS AND METHODS: The incidence of prothrombotic abnormalities among a randomly investigated cohort of 17 patients with BIH, was compared with 51 healthy subjects matched for sex, age, body mass index, height and social background. RESULTS: The number of subjects with protein C deficiency was significantly higher in patients than in controls (3 vs 1, p < .001; Fisher Exact Test). Moderate to high titers of anticardiolipin antibodies (beta2-Glycoprotein type I) were found in 8 out of 17 patients. Increased plasma levels of prothrombin fragment 1+2, fibrinopeptide A (FPA), and PAI-1 were demonstrated in patients group (5.7 +/- 1.15 nM vs 0.45 +/- 0.35 nM; 8.7 +/- 2.5 ng/mL vs 2.2 +/- 1.25 ng/mL; 45.7 +/- 12.5 ng/mL vs 8.5 +/- 6.7 ng/mL, respectively; p < .001; Fisher Exact Test). Gene polymorphisms for factor V Leiden mutation, prothrombin mutation 20210 A/G, MTHFR 677 C/T, PAI-1 4G/5G, ACE I/D were detected in 13 patients. DISCUSSION: In agreement with other authors our data suggest a state of hypercoagulability in BIH associated with gene polymorphisms. Our findings also showed that mutations in cardiovascular genes significantly discriminate subjects with a BIH history. The association between coagulation and gene derangements, usually regarded to as cryptogenic, may suggest a possible pathogenetic mechanism in BIH. So, a prothrombotic tendency may exist that would, at least in part, explain some cases of BIH. Although based on a small population, these findings raise the exciting possibility of using these haemostatic factors as markers for selecting high-risk subjects in BIH disease.