To examine the efficacy of lithium and valproate in Bipolar I patients suffering from a manic episode with previous EEG abnormalities.

Fifteen patients of both sexes were included in four weeks, prospective, observational, open-label treatment trial. They met criteria: Bipolar I affective disorder (manic episode) according to ICD-10 and EEG abnormalities (high voltage, 10-13 cps alpha, “iritative”, sharp activity). Patients were divided into two groups: Group I – seven patients (4 male and 3 female) treated with lithium 900 mg/day, haloperidol 10 mg/day and chlorpromazine 150 mg/day and Group II – eight patients (4 male and 4 female) treated with valproate 1000 mg/day, haloperidol 10 ma/day and 150 mg/day. Severity of illness and treatment efficacy were measured with Young Mania Rating Scale (YMRS) at the start point, after 2 and 4 weeks, along with conventional EEG registration.

Throughout observational period, lithium treated patients (Group I) did not expressed any improvement in EEG (continuously showing high voltage, sharp alpha activity). Meanwhile, Group II (valproate) patients, after 2 weeks of treatment expressed clear EEG stabilisation. In addition, after 4 week of lithium appliance (Group I) there is no significant reduction in YMRS-score. Group II (valproate) patients after 2 weeks achieved significant clinical improvement (significance level p<0,05) and after 4 weeks highly significant YMRS-score reduction (p<0,01).

Conventional EEG may be useful in therapeutic prediction in a manner that patients with EEG abnormalities had better respond to anticonvulsant mood stabilizers than lithium.

The aim of this study was to identify risk factors in early postpartum that predict postpartum depression (PPD) at 6-8 weeks.

A prospective cohort of 309 women was studied between the 2nd-3rd days postpartum and at 6-8 weeks postpartum. Initially we administered a general information questionnaire that included obstetrical variables and history of personal and family affective disorders. Between the 2nd and 3rd days postpartum they filled out the Spanish version of the Edinburgh Postnatal Depression Scale (EPDS), Spielberg Anxiety Trait and State Inventory (STAI-R/S), Neuroticism Dimension (EPQ), St Paul Ramsey Questionnaire (life events) and Duke Social Support Scale. At 6-8 weeks postpartum they filled out again the EPDS. Women who scored ≥10 were screened as having PPD.

The incidence of PPD at 6-8 weeks was 14.6%. After Bonferroni correction, univariated analysis showed that previous personal history of depression (p<0.001), high neuroticism (p<0.001), low social support (p<0.002) and high EPDS (p<0.001) in the immediate postpartum were associated with PPD. Logistical regression analysis identified previous personal history of depression and high initial level of depression (OR=14.6; 95%CI=4.8-12.2; p<0.001) as risk factors for PPD. The absence of signification of the Hosmer-Lemersshow test (x2 =9.654; df=8; p=0.290) indicated the goodness-of-fit of the prediction model.

A previous history of depression and EPDS≥10 in the immediate postpartum allow to identify women with high risk of PPD before leaving the Obstetric Ward.

This study has been supported in part by grants: Instituto Carlos III: GO3/184; FIS: PI041783 and FIS 05/2565.

The aim of our study: to evaluate the efficacy of trazodone in the treatment of patients with depression showing marked insomnia.

45 patients, with diagnosis F32.0 -F32.2 (according to ICD -10) with marked insomnia, aged 29- 64 years, were enrolled. Patients received trazodone 15o mg/day, 6 weeks,without concomitant medication.The visits were organized at the beginning of treatment, after 2, and after 6 weeks of treatment for all the patients.The Montgomery Asberg Depression Rating Scale was used as a rating instruments.Gathered data were statistically processed.

There was a significant improvement for trazodone treated patients in the MADRS item 4 scores at weeks 2 and 6 versus baseline (p < 0,05).They also showed significant and clinically relevant improvement in MADRS total scores after trazodone treatment.

Trazodone shows a significant beneficial effect in reducing sleep disturbance in depressed patients.

The most common psychical disorder which occurs with epilepsy is interictal epilepsy which life prevalence is 40%-60%.

To establish the frequency of depressive disorder in epileptic patients taking into account socio-demographic characteristics and the type of epileptic seizures.

The survey comprised randomly chosen 476 patients treated at the Dispensary for epilepsy at the Neurology Clinic, University Clinical Center Sarajevo. All patients were tested with MMSE, Beck and Hamilton depression tests.

In the surveyed sample males were represented with 53.4%, mean age 36.7 years and SD=12.58, while mean age in females was 33.3% and SD=12.58%. 80% of patients had high school education. Male patients had significantly higher rate of marriage and employment than women (p<0.001). Two thirds of patients had partial seizures with or without secondary generalization. Out of that number women had significantly more frequent seizures with partial complex symptoms. Depressive disorder was present in 34% of patients at the Beck scale and 38.8% at the Hamilton scale, significantly more frequent in women.

Depressive disorder was significantly more present in middle-aged women, predominantly in women with high school education, unmarried, unemployed, with significantly more frequent seizures with partial complex symptoms than males.

We evaluated the efficacy of eszopiclone (ESZ) and concurrent escitalopram oxalate (EO) in patients with insomnia and co-morbid GAD.

Patients meeting DSM-IV-TR criteria for GAD and insomnia received 10 weeks of EO 10mg and co-therapy with ESZ 3mg or placebo (PBO) for 8 weeks. For the last 2 weeks, ESZ was replaced with single-blind PBO to evaluate discontinuation effects. Sleep, daytime functioning and anxiety measures were captured during the study.

ESZ+EO improved sleep and daytime functioning at each week and the double-blind period average (p<0.05). At Week 8, significantly more ESZ+EO patients had no clinically meaningful insomnia based on ISI</=7. Significant improvements with ESZ+EO (relative to PBO+EO) were observed in HAM-A total scores each week, and Weeks 4-10 excluding the insomnia item. ESZ+EO was significantly better at every timepoint on CGI-I (p<0.02); CGI-S was not different between treatments after Week 1. Median time to anxiolytic response was reduced with ESZ+EO based on HAM-A and CGI-I. HAM-A response and remission rates at Week 8 were higher with ESZ+EO, and HAM-D17 scores were improved at all timepoints (p<0.004). After eszopiclone discontinuation, there was no evidence of rebound insomnia, and no treatment differences in sleep or daytime function. Significant treatment differences in anxiety and mood were maintained after discontinuation.

In this study, ESZ+EO was well tolerated and associated with improved sleep and daytime function without evidence of tolerance. Improvements in anxiety and mood were observed with ESZ+EO.

Support for this study provided by Sepracor Inc., Marlborough, MA.

Depression occurs in a quarter of general practice attendees, relapse is frequent five to 10 years from first presentation and residual disability is common. Estimating overall risk across a range of putative risk factors is fundamental to prevention of depression.

This is a prospective study. As part of the European Predict study, in Málaga (Spain), 9 general practices were recruited. Consecutive attendees aged 18 to 75 were recruited and undertook a detailed interview. Subjects were administered the Composite International Diagnostic Interview (CIDI) depression subscale allowing diagnoses using ICD-10 criteria for depressive episode. For risk factors the interviews included individual-level risk factors and environmental risk factors. All participants completed baseline and follow up assessments at six and 12 months.

A total of 1276 patients were interviewed in the first assessment of the PREDICT study, in Málaga, (Spain) and the response rate of the study one year later was 88%. Out of 1276, 70.5% of the sample is women whilst only 29.5% were men. The sample's mean age was 49 years (SD=15.3). Depression was common amongst this sample of primary care attendees, although point prevalence values varied slightly according to the diagnostic criteria used. The prevalence of ICD-10 Depressive Episode was 38.2% while ICD-10 depressive episode of mild was 3.4% moderate 12% and severe intensity 22.8%.

The high prevalence we found shows that the depressive disorders are a very common problem with the primary care attendees in our area.

The efficacy of venlafaxine extended-release (XR) at doses between 75 mg/d and 300 mg/d has been demonstrated in patients with recurrent major depressive disorder (MDD) over 2.5 years. This analysis evaluated the long-term efficacy of venlafaxine XR ≤225 mg/d, the approved dosage in many countries.

In the primary multicenter, double-blind trial, outpatients with recurrent MDD (N=1096) were randomized to receive 10-week acute-phase treatment with venlafaxine XR (75 mg/d to 300 mg/d) or fluoxetine (20 mg/d to 60 mg/d), followed by a 6-month continuation phase. Subsequently, at the start of 2 consecutive, double-blind, 12-month maintenance phases, venlafaxine XR responders were randomized to receive venlafaxine XR or placebo. Data from the 24 months of maintenance treatment were analyzed for the combined end point of maintenance of response (ie, no recurrence of depression and no dose increase above 225 mg/d), and each component individually. Time to each outcome was evaluated with Kaplan-Meier methods using log-rank tests for venlafaxine XR-placebo comparisons.

The analysis population included 114 patients who had received venlafaxine XR doses less than or equal to 225 mg/d prior to maintenance phase baseline (venlafaxine XR: n=55; placebo: n=59). Probability estimates for maintaining response were 70% for venlafaxine XR and 38% for placebo (P=0.007), for no dose increase were 76% and 58%, respectively (P=0.019), and for no recurrence were 87% vs 65%, respectively (P=.099).

These data confirm venlafaxine XR is effective maintaining response at doses ≤225 mg/d for up to 2.5 years in patients with MDD.

This pooled analysis evaluated the predictors of clinical outcome in the short-term treatment of panic disorder.

Data were pooled from 4 randomized, placebo-controlled studies of venlafaxine XR in adult outpatients with Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) panic disorder with or without agoraphobia (n=1595). Patients were randomly assigned to 10 to 12 weeks' treatment with either placebo or venlafaxine (fixed or flexible dosing, range from 75 mg/d to 225 mg/d). The primary efficacy measure was the proportion of patients free of full-symptom panic attacks at end point. Predictors included panic severity (<8 or ≥8 full-symptom panic attacks during each 2 week period in the 4 weeks prior to baseline) and gender. Other predictors included panic disorder, clinical global impressions, anxiety, somatic and psychic anxiety, depression, mood, phobias, fear, and avoidance.

In both the active treatment and placebo groups, males (65% and 50%, respectively) and those with low symptom severity (69% and 53%, respectively) were significantly (P<0.05) more likely to be panic-free at end point. For nearly all baseline ratings on clinical measures, greater symptom severity was associated with lower proportions of patients who were free from full-symptom panic attacks at end point. Change scores showing improvement in symptom severity following treatment were associated with higher proportions of patients who were free from full-symptom panic attacks at end point.

Panic-free status at end point was predicted by gender, panic disorder severity, and most baseline and change scores of clinical ratings scales.

This pooled analysis compared the efficacy of venlafaxine extended-release (XR) versus placebo in the treatment of social anxiety disorder (SAD).

Data were pooled from 5 randomized studies of patients with Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) SAD (N=1459) who were treated with venlafaxine XR 75 mg/d to 225 mg/d or placebo for 12 weeks (4 studies) or 28 weeks (1 study). Response and remission rates were calculated for the overall sample, as well as stratified by gender and level of physical symptom severity at baseline. Response was defined as a score of 1 or 2 on the Clinical Global Impressions–Improvement (CGI-I) scale. Remission was defined as a total score of <30 on the Leibowitz Social Anxiety Scale (LSAS).

At baseline the mean LSAS score was 88.1 and 86.6 for the venlafaxine and placebo arms, respectively. Overall response rates at week 12 were 55% for venlafaxine XR and 33% for placebo (P<0.0001); remission rates were 25% and 12%, respectively (P<0.0001). Among patients with less severe physical symptoms, response rates were 52% and 32% for venlafaxine XR and placebo, respectively (P<0.0001); remission rates were 27% and 14%, respectively (P<0.0001). Response rates among patients with more severe physical symptoms were 56% for venlafaxine XR and 33% for placebo (P<0.0001); remission rates were 24% and 11%, respectively (P<0.0001).

Venlafaxine XR is effective in the treatment of SAD, regardless of gender or severity of physical symptoms.

We report the results from the first 12 months of a 2-year maintenance phase of a study evaluating long-term efficacy and safety of venlafaxine extended-release (XR) in preventing recurrence of depression.

Patients with recurrent unipolar depression (N=1096) were randomly assigned in a 3:1 ratio to 10-week treatment with venlafaxine XR (75 mg/d to 300 mg/d) or fluoxetine (20 mg/d to 60 mg/d). Responders (HAM-D17 total score ≤12 and ≥50% decrease from baseline) entered a 6-month, double-blind, continuation phase on the same medication. Continuation phase responders enrolled into the maintenance treatment period consisting of 2 consecutive 12-month phases. At the start of each maintenance phase, venlafaxine XR responders were randomly assigned to double-blind treatment with venlafaxine XR or placebo; fluoxetine responders continued for each period. Time to recurrence (HAM-D17 total score >12 and <50% reduction from acute phase baseline at 2 consecutive visits or the last visit prior to discontinuation) was evaluated using Kaplan-Meier methods and compared between groups using log-rank tests.

At the end of the continuation phase, venlafaxine XR responders were randomly assigned to venlafaxine XR (n=164) or placebo (n=172); 129 patients in each group were evaluated for efficacy. The cumulative probability of recurrence through 12 months was 23.1% (95% CI: 15.3, 30.9) for venlafaxine XR and 42.0% (95% CI: 31.8, 52.2) for placebo (P=0.005).

Twelve months of venlafaxine XR maintenance treatment was effective in preventing recurrence in depressed patients who had been successfully treated with venlafaxine XR during acute and continuation therapy.

This study evaluated the efficacy and safety of venlafaxine extended-release (XR) in preventing recurrence of depression.

Outpatients with recurrent unipolar depression (N=1096) were randomly assigned in a 3:1 ratio to 10-week treatment with venlafaxine XR (75 mg/d to 300 mg/d) or fluoxetine (20 mg/d to 60 mg/d). Responders (HAM-D17 ≤12 and ≥50% decrease from baseline) entered a 6-month, double-blind, continuation phase on the same medication. Continuation phase responders enrolled into maintenance treatment consisting of 2 consecutive 12-month phases. At the start of each maintenance phase, venlafaxine XR responders were randomized to double-blind treatment with venlafaxine XR or placebo; fluoxetine responders continued on fluoxetine. Time to recurrence (HAM-D17 >12 and <50% reduction from acute phase baseline at 2 consecutive visits or the last valid visit prior to discontinuation) was evaluated using Kaplan-Meier methods and compared between groups using log-rank tests.

In the second maintenance phase, the cumulative probabilities of recurrence through 12 months in the venlafaxine XR (n=43) and placebo (n=40) groups were 8.0% (95% CI: 0.0, 16.8) and 44.8% (95% CI: 27.6, 62.0), respectively (P<0.001). The probabilities of recurrence over 24 months for patients assigned to venlafaxine XR (n=129) or placebo (n=129) for the first maintenance phase were 28.5% (95% CI 18.3, 37.8) and 47.3% (95% CI 36.4, 58.2), respectively (P=0.005).

An additional 12 months of venlafaxine XR maintenance therapy was effective in preventing recurrence in depressed patients who had responded to venlafaxine XR after acute, continuation, and 12 months' initial maintenance therapy.

Antiepileptic drugs have been more and more used by psychiatrists in treatment of disorders not related to epilepsy. Valproate and carbamazepine are approved in the treatment of Bipolar Disorder, as mood stabilizers. Lamotrigine also showed efficacy in bipolar depression, and gabapentine is a promising drug in treatment of anxiety disorders. This drugs are also being studied in other psychiatry disorders, as borderline personality, Schizophrenia, and agitation related to dementia.

The authors make a review about the use of antiepileptic drugs in Psychiatry disorders, with focus on mechanisms of action, pharmacokinetics, adverse effects and efficacy.

In the past, Antiepileptic drugs were exclusively for epilepsy. Now-a-days, they are used in a variety of Psychiatry disorders. This is a good example about the connexion between Psychiatry and Neurology.

Venlafaxine (VLF) is an antidepressant drug often used by pregnant women. Its possible adverse effects on fetal CNS development have not been studied. The present study will fill the knowledge gap.

To assess neurodevelopment of children exposed to VLF during gestation.

Cohort study -controlled, matched, and blinded. Assessment of 5 groups of mother-child pairs: exposed to VLF (n=32) or other SRIs (n=29), healthy controls (n=42), and 2 groups of siblings (n=15). Siblings were unexposed relatives of children from the VLF or ‘other SRIs’ groups. Primary outcome: WPPSI-III Scales of Intelligence. VLF exposed children will be compared with those of children in control groups and their non-exposed siblings.

There were no differences in Full Scale IQ, Performance IQ and Verbal IQ between the VLF and SRIs groups (103+10vs105+12; 102+11vs102+15; 103+11vs105+12), VLF group and their siblings (105+12vs100+8; 102+15vs105+7; 105+12vs95+10), or the the SRIs group and their siblings (103+10vs104+8; 102+10vs104+8; 103+11vs106+12). Healthy controls scored significantly higher than the VLF group and the other 3 groups in Full Scale IQ, Performance IQ and Verbal IQ (P= 0.011; 0.041; and 0.028 respectively).

Preliminary results show that factors such as maternal depression, genetics, and environment (not necessarily the antidepressant) are strongly associated with the child's cognitive abilities. Assessment of siblings helps to verify the impact of these factors and is possibly the strongest evidence in drug safety studies.

Wyeth Pharmaceuticals

Due to negative correlation rates with level of depression, anxiety and hopelessness it is possible to apply GAF like measure of assessment of patient's depression and anxiety, and useful follow up tool of patients treatment with psychopharmacotherapy.

The management of treatment-resistant depression remains a major public health problem. Several acute depression trials suggest that only 45% of the patients achieve remission state with antidepressant monotherapy. An increasing body of evidence is emerging suggesting that multi-action antidepressants might be more effective in treatment-resistant depressed patients than single-action agents. In this context, the purpose of the study was to assess the effectiveness of duloxetine in treatment-resistant major depressed outpatients.

We performed a prospective study assessing the efficacy of duloxetine in major depressed outpatients who did not achieve full symptom remission (CGI-S (severity) ≥ 3) after treatment of adequate dose and duration (more than 8 weeks) with at least either one SSRI or the SNRI venlafaxine. We excluded patients with a severe medical illness and a personality disorder. CGI-S was used as a measure of symptom severity and administered before the administration of duloxetine and 6 weeks later. Five patients had been treated with venlafaxine and the others with a SSRI (Fluoxetine, Paroxetine, Citalopram).

The sample included 10 patients (3 M, 7 F). We observed a very significant decrease in CGI-S scores (5 ± 0.45 to 1.2 ± 0.63, p < 0.0001) after treatment with duloxetine (dose between 20 and 60 mg). Remission was achieved in 90% of the patients. The tolerance was excellent.

This study suggests the potential interest of duloxetine in treatment-resistant depressed patients.

To examine the postpartum thyroid dysfunction (PPTD) and positive thyroid antibodies (Ab+) frequency in the Postpartum Depression (PPD) and to investigate if the PPD patients subgroup with PPTD and/or Ab+ have different characteristics.

Eighty one (N=81) patients with PPD, according with DSM-IV criteria, were included. Thyroid function (Free T3, Free T4,TSH), autoimmune status of the thyroid (Thyroperoxidasa antibodies, Thyroglobulin antibodies) and severity of depression (EPDS and 21-item Hamilton scales), were assessed joint with other several demographics, psycho-social and reproductive variables.

Twenty per cent of the patients with PPD had positive thyroid antibodies and 14% present PPTD. Prior history of early stressors in the PPD patients were significantly related with the presence of Ab+: the presence of childhood maltreatments and/or sexual abuse increased thirteen times the probability of Ab+ (OR: 13,01, 95% CI, 2.01-84.02). Greater number of total stressors were associated with Ab+ (p< 0,030), and Ab+ women showed a higher average of total stressors (2,1) than antibody negative women (1,52). Depressed women with PPTD had positive correlation with previous depressive episodes (p< 0,008).

The depressed postpartum women with dysregulation of pituitary-thyroid axis have more early childhood stressors and previous depressive episode. The implication of the inmunitary system and the HPT axis in the etiopathogenesis of the PPD through the activation of the response in front to stress is discussed.