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It has been well documented that acute tryptophan depletion (ATD) induces symptoms in remitted depressed patients treated with an SSRI. ATD also has effects on cognition, both in patients and in healthy samples. The exact nature of ATD-induced cognitive changes in depression remains unclear. It is also unclear whether cognitive effects can be induced through partial ('low-dose') depletion. The aim of this study is to investigate the differential effects of low-dose and high-dose ATD on emotional information processing and mood in remitted depressed patients. Eighteen remitted depressed patients received high-dose and low-dose ATD in a randomized, double-blind, within-subjects crossover design. Mood was assessed before and after administration of the depletion drink. Five hours after administration, patients conducted tests measuring neutral and emotional information processing. High-dose ATD increased depressive symptoms and induced a temporary depressive 'relapse' in half of the patients. High-dose ATD also decreased the recognition of fear and impaired learning and memory retrieval. The impaired learning occurred only in mood-responders. Low-dose ATD had no effects on mood but speeded the recognition of facial expressions of disgust. Accurate recognition of sad faces at baseline was associated with mood response to ATD. High-dose ATD leads to changes in memory and in the recognition of negative facial expressions in SSRI-treated remitted depressed patients. The effect of low-dose ATD on mood and cognition seems to be quite limited. Emotional information processing at baseline predicts moodresponse to ATD. [ABSTRACT FROM AUTHOR]

Background: Despite various studies, supportive evidence for the efficacy of exercise in treatment of mental illness is still weak. Objective: The aim of this study was to compare two forms of exercise, namely running therapy (RT) and physiotraining therapy (PT), on stationary devices. Methods: Patients in a day treatment programme for treatment of affective disorders were randomly allocated to one of the exercise groups or to a control group. Depression scores, self-efficacy, physical conditions and appreciations of the training programme were measured. Results: After 6 weeks, no significant differences were found between both the training groups and the control group; however, after 12 weeks, the physiotraining group showed significant improvement on scores for blind-rated Hamilton Rating Scale for Depression and on scores for self-rated Beck Depression Inventory 21-item version. Conclusions: Our results suggest that PT has advantages over RT. We speculate that an improved feeling of self-efficacy may be a mediating factor. [ABSTRACT FROM AUTHOR]

It has frequently been demonstrated that acute tryptophan depletion (ATD) induces a transient depressed mood in some patients who are in remission from depression. However, the effects of ATD on cognitive processes in remitted depressed patients have not been investigated. The aim of the present study was to investigate the effects of different extents of depletion on mood and cognitive tasks involving neutral and emotional stimuli. Twenty patients in remission or in partial remission from depression received ATD in a double-blind, crossover design. Mood was assessed at both sessions before, at +6.5 h and +24 h after depletion. Cognitive assessment in both sessions started at +4.75 h, and also before and after the whore procedure. The ATD mixtures induced the expected reductions of plasma tryptophan levels. High-dose ATD induced a depressive response in a subsample of patients and impaired the processing of positive information independent of mood change. Attention for neutral stimuli (Stroop interference) improved in a dose-dependent manner. ATD may affect mood and cognition via different pathways: one implicated in mood regulation and the processing of emotional information, and one for the processing of neutral information. The first pathway may be more important for discriminating vulnerability to impaired serotonin function. The comparison of the effects of high-dose and low-dose ATD is useful for those studies aiming to investigate the relationships among 5-HT, mood and cognition. [ABSTRACT FROM AUTHOR]

IntroductionShort-term randomised clinical trials on valproate in distinct types of disturbed behaviour in dementia showed no effects on agressive behaviour. ObjectivesTo assess the course of disturbed behaviour during medium term treatment with sodium valproate for aggressive behaviour. DesignAn open label observational 12-week follow-up study consecutive to a preceding randomised control trial; assessments at 4-week interval. SettingA psychogeriatric medium-stay ward at a psychiatric teaching hospital and psychogeriatric nursing home wards. ParticipantsPatients who completed a preceding randomised placebo controlled clinical trial on sodium valproate in aggressive behaviour in dementia were included. InterventionThe starting dose of sodium valproate was 2×6 ml of a 40 mg/ml suspension (daily defined dose of 480 mg). The patient's regular physicians managed all treatment decisions, including decisions on dosage and plasma level measurements of sodium valproate and decisions regarding discontinuation. Co-medication was allowed and any change in prescription was recorded. MeasurementsThe Social Dysfunction and Aggression Scale-9 (SDAS-9), the Behaviour Observation scales for Intramural Psychogeriatrics (in Dutch: Gedragsobservatieschaal voor Intramurale Psychogeriatrie (GIP) and the Clinical Global Impression of aggressive behaviour (CGI) were performed at the last week of each 4-week interval. ResultsData of 39 patients (F=24 and M=15) were analysed. At week 12 compared to week 0 mean sodium valproate prescriptions were higher; aggressive behaviour as measured by the SDAS-9 improved. Non-social behaviour, apathetic behaviour, disoriented behaviour and distorted memory improved, but rebellious behaviour increased as measured by the GIP. Seven patients died during this study. Limitations of the studyOpen label observational design; absence of placebo/reference prescription; no systematic measurements of sodium valproate plasma levels and the allowance of psychotropic co-medication. ConclusionLow dose sodium valproate may be effective reducing a broad range of types of disturbed behaviours in aggressive demented patients. The high death rate underlines the fragility of demented patients with aggressive behaviour. Copyright © 2004 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

The efficacy and tolerability of sodium valproate 2 x 240 mg compared to placebo were investigated in aggressive behavior in dementia. A randomized, placebo controlled, double-blind cross-over design. The trial included a baseline period (one week); a placebo period (three weeks); a wash-out period with placebo (one week); and a treatment period with sodium valproate (three weeks). A psychogeriatric short-stay ward at a psychiatric teaching hospital. Demented patients who met Patel's criteria for aggressive behavior and had a score of > or =3 on at least one of the items of the Social Dysfunction and Aggression scale-9 (SDAS-9). A fixed dose of sodium valproate 2 x 6 ml of a 40 mg/ml suspension (daily defined dose of 480 mg) was compared to placebo. Primary outcome variables were changes of the score of SDAS-9 and Clinical Global Impression scale (CGI) performed at the last week of each treatment period. Data of 42 patients (F=25 and M=17; age 80.4+/-6.8 years) were analyzed. Treatment with sodium valproate showed no differences compared to placebo on aggressive behavior. The mean plasma level of sodium valproate was 40.9+/-10.8 microg/ml. Regression analysis showed a trend for improvement between the plasma levels of sodium valproate and the SDAS-9 and the CGI scores. Adverse events were not related to the plasma levels of sodium valproate. Secondary outcome measurements showed significant improvement on restless, melancholic and anxious behavior; a trend for improvement was found on suspicious and dependent behavior. Possible limitations of this study are the low dose of sodium valproate, the relatively short treatment period (three weeks), and the absence of statistical corrections for multiple comparisons. This study showed no effect of sodium valproate 2 x 240 mg over placebo on aggressive behavior in dementia. [ABSTRACT FROM AUTHOR]

ObjectiveThe purpose of this study was to evaluate the effects of bright light therapy combined with melatonin on motor restless behaviour in dementia. DesignDouble-blind, placebo-controlled, cross-over trial consisting of four periods. One week wash-out was followed by a 2-week period of light therapy in combination with placebo or melatonin. The second wash-out period of 1 week was followed by 2 weeks of treatment (cross-over). SettingTwenty-four bed medium-stay psychogeriatric ward at a Dutch psychiatric teaching hospital. PatientsTen patients, who met the criteria for dementia (DSM-IV) and motor restless behaviour (subscale 10 of the GIP), were included. Informed consent was obtained by proxy. InterventionAll subjects were exposed during 2×5 consecutive days for 30 minutes to 10,000 lux bright light and randomly administered 2.5 mg melatonin or placebo at 22.00 h. AssessmentsClinical Global Impression (CGI), Dutch version of the geriatric behavioural observation scale (GIP), Social Dysfunction and Aggression Scale (SDAS) were assessed after each wash-out and treatment period. Outcome criteria were CGI, assessing motor restless behaviour, the SDAS, measuring extrovert aggression and the GIP, assessing social, psychomotor and emotional behaviour. ResultsSix demented inpatients completed the trial. Positive effects were found for the treatment combined with placebo. Patients were less restless and more co-operative. The condition with melatonin showed no additional positive effects, additionally, patients became more aggressive and showed the same or more disturbed behaviour. ConclusionsBright light therapy has a positive effect on motor restless behaviour. Light therapy in combination with melatonin has no positive effects. The results might be explained by a possible overshoot of chronobiological synchronisation or the timing of the melatonin intake. Copyright © 2001 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Objective To study the influence of the introduction of a behaviour rating scale on reported incidence and management of aggressive behaviours in patients in a psychogeriatric nursing home. Design An 8-month prospective cohort intervention study. Setting Two wards of a Dutch psychogeriatric nursing home with residents of 65 years and older. Patients All residents of the two wards were included (N =75). Intervention Social Dysfunction and Aggression Scale (SDAS) assessed at weekly intervals during 4 months after a 4 months' baseline period. Assessments During 8 months at 2 months' interval the BOP (ie the validated Dutch version of the Stockton Geriatric Rating Scale); frequency of aggressive behaviour reported at daily nursing staff report; mean prescriptions of psychotropic and somatic drugs; number of days a patient was submitted to physically restrictive measures. Results Eleven patients (N =11) did not complete the study; information on 64 patients was analysed. The frequency of aggressive behaviour reported by the nursing staff increased, while prescriptions of psychotropic drugs decreased. No alteration was found for BOP scores, mean prescriptions of somatic drugs and the use of physically restrictive measures. Conclusions The introduction of a behaviour rating scale does influence the reported incidence and management of aggressive behaviour. Prospective intervention studies should include a stabilization phase for measurements prior to any planned trial. Copyright © 2000 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Objectives: The aims of this study were to describe the characteristics of hyponatremia in elderly users of antidepressants, to determine the prevalence and risk factors for hyponatremia, and to identify the underlying mechanisms., Study Design: Cross-sectional study (March 2007-April 2009) with prospectively collected data. Patients were older than 60 years, used antidepressants, and had a complete geriatric assessment., Main Outcome Measures: Serum sodium and antidiuretic hormone levels, serum osmolality, urine sodium level, and urine osmolality were measured. The prevalence of hyponatremia (serum sodium <135 mM) as an adverse reaction to an antidepressant (AR-AD), defined with Naranjo's algorithm, was calculated. Hyponatremic patients were compared to normonatremic patients with regard to gender, age, weight, history of hyponatremia, hyponatremia-associated medications and disorders, and type and duration of antidepressant use., Results: Of 358 eligible patients, 345 were included. The prevalence of hyponatremia as an AR-AD was 9.3%. Risk factors were a history of hyponatremia (adjusted OR 11.17, 95%CI 2.56-40.41), weight<60 kg (adjusted OR 3.47, 95%CI 1.19-10.13), and psychosis (adjusted OR 3.62, 95%CI 1.12-11.73). Non-suppressed ADH was found in a minority of hyponatremic patients., Conclusions: In elderly patients, the prevalence of hyponatremia as adverse reaction to all types of antidepressants was 9%. Patients with previous hyponatremia, weight <60 kg, and psychosis were at risk. Beside SIADH, the nephrogenic syndrome of inappropriate antidiuresis, in which ADH secretion was normal, is postulated as an underlying mechanism. This has consequences for treatment of antidepressant-induced hyponatremia with vasopressin receptor antagonists., (Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.)

Background: Prediction of treatment outcome has important clinical consequences. Personality factors have rarely been tested as predictors of acute outcome. Personality, demographic and illness-related characteristics were assessed at baseline for prediction of outcome of treatment in depressed out-patients., Methods: One hundred and ninety-three patients with major depressive disorder (MDD) were enrolled in a 12 to 16 week trial. The treatment consisted of nefazodone, nefazodone in combination with interpersonal psychotherapy (IPT), IPT in combination with placebo and IPT alone. Demographic and illness related variables were collected at baseline. Personality was assessed using the NEO-FFI. This instrument measures five dimensions of personality. A hierarchical logistic regression was carried out to test for significant predictors of remittance. Further a multiple regression analysis was used to investigate variables predictive of changes on the Hamilton Depression Rating Scale as dependent variable., Results: Univariate analysis showed a significant relationship of outcome with severity, duration of index episode, and use of medical services (UMS). None of the personality variables was predictive of outcome. Regression analyses showed that these disease related variables each uniquely predicted outcome, but that personality factors did not significantly contribute to the prediction model., Limitations: The study was carried out in secondary and tertiary care centers and may not be generalizable to other populations. Personality dimensions were assessed with a self-report instrument and may be prone to bias., Conclusions: Severity and duration of the index episode, and to a lesser extent, UMS, and not personality factors, predict outcome in the short term treatment of MDD.

Background: Depression is a major risk factor for cardiovascular disease. An important risk factor for cardiovascular disease, low heart rate variability, often has been found in depressed patients and has been associated with impulsivity. The present study investigated whether experimental lowering of serotonin would decrease heart rate variability and increase impulsivity in remitted depressed patients, in particular in those patients with disturbed impulse control., Methods: Nineteen patients in remission from depression received high-dose and low-dose acute tryptophan depletion in a randomized, counterbalanced, double-blind crossover design. Heart rate variability and impulsivity were assessed during each acute tryptophan depletion session and during a baseline session. Suicidal ideation during past depression was used as an index for individual differences in impulse control., Results: High-dose acute tryptophan depletion led to a larger increase in depressive symptoms than did low-dose acute tryptophan depletion. High-dose acute tryptophan depletion decreased heart rate variability and increased impulsivity and anxiety, but only in patients with a history of suicidal ideation. Symptom effects of high-dose acute tryptophan depletion correlated with low heart rate variability at baseline., Conclusions: Depressed patients who have problems with controlling impulsivity might be more at risk for developing cardiovascular disease, possibly related to increased vulnerability to impaired 5-hydroxytryptamine function.

Background: It has frequently been demonstrated that experimental lowering of serotonin (5-HT) neurotransmission by acute tryptophan depletion (ATD) induces a transient depressed mood in 50-60% of patients treated with a selective serotonin reuptake inhibitor (SSRI) who are in remission from depression. In unmedicated depressed patients, ATD has no immediate effect on symptoms. The effects in currently depressed medicated patients have not been investigated., Methods: Fourteen currently depressed patients (seven patients treated with a selective serotonin-noradrenalin reuptake inhibitor (SSNRI); seven other treatment, non-SSNRI) received ATD in a double-blind, crossover design. Different strengths of the ATD mixture (aimed at 50% and 90% reduction of tryptophan) were used on separate days. Psychiatric symptoms were assessed at both sessions prior to, at +6.5 h, and at +24 h after ATD., Results: The ATD mixtures induced the expected reductions of plasma tryptophan levels. Full but not partial depletion improved mood and other psychiatric symptoms at +24 h in patients who received SSNRI treatment, as indicated by clinical ratings and self-report. Subjective sleep quality also improved., Conclusions: The effects of ATD on psychiatric symptoms in currently depressed patients are remarkably different from the results in recently remitted SSRI-treated patients. ATD in currently depressed patients treated with serotonergic antidepressants possibly provides important information about the mechanism of action of SSRIs.