Effects of momentary self-monitoring on empowerment in a randomized controlled trial in patients with depression.

BACKGROUND: Interventions based on the experience sampling method (ESM) are ideally suited to provide insight into personal, contextualized affective patterns in the flow of daily life. Recently, we showed that an ESM-intervention focusing on positive affect was associated with a decrease in symptoms in patients with depression. The aim of the present study was to examine whether ESM-intervention increased patient empowerment. METHODS: Depressed out-patients (n=102) receiving psychopharmacological treatment who had participated in a randomized controlled trial with three arms: (i) an experimental group receiving six weeks of ESM self-monitoring combined with weekly feedback sessions, (ii) a pseudo-experimental group participating in six weeks of ESM self-monitoring without feedback, and (iii) a control group (treatment as usual only). Patients were recruited in the Netherlands between January 2010 and February 2012. Self-report empowerment scores were obtained pre- and post-intervention. RESULTS: There was an effect of group×assessment period, indicating that the experimental (B=7.26, P=0.061, d=0.44, statistically imprecise) and pseudo-experimental group (B=11.19, P=0.003, d=0.76) increased more in reported empowerment compared to the control group. In the pseudo-experimental group, 29% of the participants showed a statistically reliable increase in empowerment score and 0% reliable decrease compared to 17% reliable increase and 21% reliable decrease in the control group. The experimental group showed 19% reliable increase and 4% reliable decrease. CONCLUSIONS: These findings tentatively suggest that self-monitoring to complement standard antidepressant treatment may increase patients' feelings of empowerment. Further research is necessary to investigate long-term empowering effects of self-monitoring in combination with person-tailored feedback.

[Sleep-wake disorders and DSM-5]. / Slaap-waakstoornissen en DSM-5.

BACKGROUND: Most individuals with mental disorders complain about the problems they experience with sleeping and waking. It is becoming evident that careful diagnosis of sleep-wake disorders is of great importance for the prevention and treatment of mental disorders. Since the introduction of the DSM-IV, clinical scientific research has provided important new insights in this field. AIM: To find out whether the new classification of sleep-wake disorders in DSM-5 is likely to improve the diagnosis of disorders of this type. METHOD: We discuss the main changes in the DSM-5 classification of sleep- wake disorders, comparing the new version with the version in DSM-IV. RESULTS: Because considerable attention is being given to the symptom-orientated and dimensional approach, the classification of sleep-wake disorders in the DSM-5 is closer to current psychiatric practice and it does justice to the current scientific insights into the dimensional nature of psychiatric disorders. CONCLUSION: The DSM-5 classification takes recent scientific insights into account and might help to improve the diagnosis of sleep-wake disorders in psychiatry.

[The new curriculum for the University Training Course in Psychiatry in South Limburg and for the Mental Health Services in Eindhoven]. / Het vernieuwde cursorische onderwijs van de universitaire opleiding psychiatrie Zuid-Limburg en GGZ Eindhoven.

BACKGROUND: The curriculum for the Academic Training Course in Psychiatry in South- Limburg (UOP-ZL) needed to be modernised. There were widely differing views about the purpose and function of psychiatry and about the structure of the curriculum. Trainees failed to attend regularly because of their daily duties. AIM: Following discussion about the need for modernisation of the course in Psychiatry (HOOP), the UOP-ZL curriculum was thoroughly revised and updated. METHOD: Further development of HOOP, a careful study of the teaching material and discussion among members of UOP-ZL and the Mental Health Service in Eindhoven, led to the development of more unified views about psychiatry and produced the ingredients for a revised curriculum for training in psychiatry. RESULTS: In the early stages of their course, trainees are introduced to some basic principles; these include understanding the mechanisms for dimensions of affect, motivation, salience and cognition from a biological, cognitive and ecological perspective, and perceiving the relationship between these factors and normal and abnormal behaviour. The course is a mix of problem based learning and interactive classroom teaching and is delivered by clinical and scientific experts. Every two weeks the trainees in each year-group are given a whole day 'free' (i.e. free of normal duties) when they are required to attend classed and lectures. CONCLUSION: The two main results of the new curriculum are: diagnosis-related teaching has been replaced by an approach based on explanatory mechanisms for dimensional psychopathology and dysfunction, and the tuition provided is both problem-based and interactive and is given by expert teachers.

Momentary assessment technology as a tool to help patients with depression help themselves.

OBJECTIVE: Given high relapse rates and residual symptoms in depression, new strategies to increase treatment effectiveness are required. A promising avenue is to investigate how electronic momentary assessment technology may contribute to clinical assessment and interventions in depression. METHOD: A literature search was conducted focusing on the potential contribution of momentary assessments to clinical applications in depression. RESULTS: Momentary assessments are able to reveal subtle, small but repetitive and relevant patterns of emotional expression that predict future course of depression. A momentary assessment tool may expose manageable pieces of daily life behaviour contributing to the depressive experience that patients can influence. The use of this explicit knowledge of daily life experience is understudied with regard to its contribution to diagnostic assessment, monitoring of treatment effects and feedback interventions in depressed patients. The clinical application of momentary assessments may stimulate a shift from passive consumption of treatment to an active role for patients in their recovery and increased patient ownership. CONCLUSION: The precise, prospective and fine-grained information that momentary assessment technology provides may contribute to clinical practice in various ways. Future studies should examine the clinical impact of its use and the feasibility of its implementation in mental health care.

Cognitive functioning in young and middle-aged unmedicated out-patients with major depression: testing the effort and cognitive speed hypotheses.

BACKGROUND: Cognitive deficits are common in major depressive disorder, but their nature is unclear. The effort hypothesis states that performance on effortful tasks is disproportionately impaired compared with the performance on automatic tasks. The cognitive speed hypothesis states that depression is characterized by cognitive slowness, which is a source of cognitive dysfunctioning. The present study investigated both theories in unmedicated adult depressive patients. It was also investigated whether the cognitive deficits can be attributed to more general physical illness-related factors or specifically to depressive disorder. METHOD: Thirty non-psychotic depressive out-patients were compared with 38 healthy control subjects and 25 patients with severe allergic rhinitis. The effects of group on more automatic and more effortful aspects of cognitive tasks measuring cognitive speed (Concept Shifting Task, Stroop Colour Word Test, Memory Scanning Test) and memory retrieval (Visual Verbal Learning Task, Verbal Fluency Test) were evaluated by MANCOVA. Age, sex, education and pre-morbid intelligence were treated as covariates. RESULTS: The depressive group had cognitive deficits in the automatic processing subtask of the Stroop, memory scanning and memory span. Performance on more effortful tasks was not impaired. CONCLUSIONS: Our results are more consistent with the cognitive speed hypothesis. Cognitive functioning in depressive disorder seems to be characterized by a reduced speed of information processing in automatic subtasks.

Salivary cortisol patterns and cognitive speed in major depression: a comparison with allergic rhinitis and healthy control subjects.

Few studies have investigated the relationship between cortisol and cognitive functions other than memory in depression. This study investigated daily salivary cortisol patterns (basal cortisol levels at 08:00, 16:00, and 21:00 h and flatness of the diurnal curve) in relation to cognitive speed and memory. Twenty-seven unmedicated outpatients with major depressive disorder (MDD) were compared with 36 healthy controls and with 20 allergic rhinitis patients, to determine whether effects should be ascribed to MDD or to more general disease-related processes. MDD patients were characterised by a flatter diurnal cortisol curve and by reduced cognitive speed. Flatter cortisol curves were associated with cognitive slowness. However, this relationship is unlikely to be causal; after control for depressive symptoms and group membership, flatness of the diurnal cortisol curve was no longer a significant predictor of cognitive slowness. Thus, MDD and related depressive symptoms appeared to be independently associated with altered cortisol secretory patterns and with decrements in cognitive speed.

The acute effects of the noradrenaline reuptake inhibitor Org 4428 on EEG sleep in healthy volunteers.

Drug-induced improvement of depression may be mediated by changes in sleep physiology. In earlier studies on sleep EEG changes during treatment with antidepressants in depressed patients it could not be excluded that sleep disruptions and changes in the amount and distribution of REM sleep play a role in the changes in the sleep EEG. Therefore knowledge of the effects of antidepressants on the sleep EEG in healthy subjects with non-disturbed baseline sleep is necessary. In a three-way cross-over study in 12 healthy volunteers two single doses of Org 4428 (a highly specific noradrenaline reuptake inhibitor), 25 and 100 mg, were compared with placebo. Sleep EEGs were visually analysed and EEG power of non-REM sleep was measured. The results indicate that sole noradrenaline reuptake inhibiting activity is a potent mechanism to affect sleep polygraphic variables in an antidepressant-like way, i.e. REM sleep suppression and lengthening of REM latency. Despite the increase in the duration of non-REM sleep, i.e. stage 2, no significant changes in EEG power in the range 1-15 Hz were found. Therefore, the acute REM sleep suppression of Org 4428 did not result in a simultaneous reduction of EEG power during non-REM sleep. To date, these and earlier results indicate that most drugs with antidepressant properties affect REM sleep variables consistently, whereas their effect on both sleep polygraphic and EEG power variables in non-REM sleep is unpredictable.

The link between sleep and depression: the effects of antidepressants on EEG sleep.

The assumption that sleep dysregulation is more than a mere epiphenomenon of depression is based on several observations: sleep disturbances are strongly associated with the depressive state; a number of sleep manipulations can alleviate symptoms of depression in some patients; and the majority of antidepressants bring about remarkable changes in sleep polygraphic variables. An obvious question is whether changes in sleep physiological processes are intimately involved in the pathogenesis and recovery from depression. One way to elucidate the link between sleep and depression is to examine whether the influence of antidepressants on sleep is related to clinical improvements in depressives. For that purpose, the effects of antidepressants on EEG sleep and their importance for the treatment of depression are summarized against the background of two existing hypotheses concerning the link between sleep and depression: one hypothesis concerning the role of REM; the other concerning the role of non-REM sleep. EEG sleep studies on the use of antidepressants in depressives have not produced clear evidence of the involvement of REM sleep or non-REM sleep in the mechanisms underlying clinical change. Furthermore, the role of sleep physiological mechanisms during treatment with antidepressants is still unclear. To interpret the effects of antidepressants on EEG sleep in terms of sleep physiological processes more fundamental sleep research is necessary. Also, more comparative studies of antidepressants with similar therapeutic effects but different pharmacological profiles are needed in both healthy and depressed subjects to further quantify the impact of EEG sleep modification in the recovery from depression and to differentiate between pharmacological and sleep-related aspects.

Changes in EEG power density of non-REM sleep in depressed patients during treatment with trazodone.

Recently, it was hypothesized that acute or cumulative suppression of non-REM sleep intensity might be related to the therapeutic effects of antidepressants. This intensity has been proposed to be expressed in the EEG power density in non-REM sleep. In the present study, the relationship was examined between the changes of EEG power density in non-REM sleep and the changes in clinical state in 8 depressed patients during treatment with trazodone. A 1-week wash-out period was followed by 1 week of placebo administration, a medication period of 5 weeks and a 1-week placebo period. To minimize systematic influences of sleep duration and non-REM-REM sleep alterations, EEG power was measured over the longest common amount of non-REM sleep stages 2-4 (168.5 min), accumulated from sleep onset onwards. During trazodone treatment, the 13- and 14-Hz bins showed a significant reduction in EEG power. No clear-cut change, however, was observed in the EEG power of the delta frequency range (1-4 Hz) which is considered to be the principle manifestation of non-REM sleep intensity. Furthermore, no overall significant relationship between EEG power suppression and clinical improvement could be demonstrated.

Changes in sleep polygraphic variables and clinical state in depressed patients during treatment with citalopram.

Drug-induced improvement of depression may be mediated by changes in sleep physiology. The aim of this study was to relate changes in sleep polygraphic variables to clinical state during treatment with citalopram, a highly specific serotonin uptake inhibitor. Sixteen patients took part. The study was single-blind and uncontrolled. A 1-week wash-out period was followed by 1 week of placebo administration, a medication period of 5 weeks, and a 1-week placebo period. For the entire group a significant decrease of rapid eye movement sleep (REMS) and a significant lengthening of REMS latency were observed initially as well as at the end of treatment. No changes in sleep continuity were found, but non-REMS stage 2 (percentage) was significantly increased. On the basis of clinical change, as expressed by the scores of the Hamilton Rating Scale for Depression, at the end of the citalopram treatment the patient group was split in two halves: eight less and eight more improved patients. The groups did not differ with respect to any sleep polygraphic variable.

Effects of trazodone on EEG sleep and clinical state in major depression.

The effects of the antidepressant trazodone on clinical state and on EEG sleep in eight outpatients with a major depressive disorder were investigated in a single blind study. A medication period of 5 weeks was preceded and followed by one week placebo treatment. Five subjects showed a positive treatment response. Trazodone did not influence sleep continuity and slow wave sleep, but did suppress REM sleep significantly. A significant increase of REM sleep latency was also found. These results are in contrast with earlier reports on trazodone's effects on EEG sleep but are in accordance with the general finding that antidepressants influence REM sleep characteristics without necessarily affecting sleep continuity.

Seasonal variation of cortisol plasma levels in depressives.

There is some evidence for a seasonal variation of plasma cortisol levels after administration of dexamethasone in depressed subjects. This variation is suspected to be associated with similar season-related changes in pre-dexamethasone cortisol levels. Therefore, cortisol plasma levels in depressed subjects before and after dexamethasone administration were investigated. No seasonal variation was found in pre- or post-dexamethasone cortisol levels.

The 24-hour pattern of urinary MHPG excretion in depressives and normals.

The 24-h pattern of urinary 3-methoxy-4-hydroxy-phenylglycol (MHPG) was studied in 15 depressives and 15 healthy controls. MHPG was measured at 3-h intervals over two consecutive 24-h periods. The shape of the MHPG excretion pattern of the depressed group was different from that of the control group. However, both the consistency and shape of the individual 24-h MHPG patterns exhibited a high interindividual variability. Therefore it is difficult to speculate on a circadian phase difference between depressives and healthy controls. Major factors that may have influenced our results are discussed.

Maintenance of therapeutic effects of total sleep deprivation by limitation of subsequent sleep. A pilot study.

In a previous study it was shown that in endogenous depression repeated sleep deprivation (SD) during clomipramine treatment resulted in rapid improvement after each SD. However, except after the first night, relapses were observed after all sleep nights following SD (the "recovery nights"). The present pilot study had a therapeutic aim, namely to prevent these relapses. We were interested in whether limitation of sleep during the recovery nights might prevent these relapses and whether different amounts of sleep would have different effects on the course of mood after recovery sleep. Ten endogenously depressed patients were treated with clomipramine and with three SD's. Five patients slept for approximately 2 h, and the other five for about 5 h during the second and third recovery nights. On average, no relapse was shown by these patients and, in fact, there was some additional improvement after these nights, in contrast to the findings in the previous study, where patients were allowed unlimited sleep.