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Contains fulltext : 110312.pdf (publisher's version ) (Open Access), BACKGROUND: Not only is the heterogeneous concept of depression too comprehensive, it is also insufficiently differentiated. This serves as a barrier to scientific research and obscures the symptoms that should indicate what treatment is required. AIM: To describe an accurate model for staging and profiling depression. METHOD: We placed depressive disorders in the context of the entire course of the disorder and we regarded the course as a continuum of psychopathology. RESULTS: First of all we distinguish five stages: (1) the prodromal phase, (2) the first depressive episode, (3) residual symptoms following an episode, (4) the relapse episode and (5) the chronic and/or treatment-resistant depression. The higher the stage, the greater the need for complex and specialised treatment. As characteristics for profiling we distinguish (a) aetiological and pathophysiological variables and (b) clinical factors. The latter are the ones that mainly influence treatment from stage 2 onwards. CONCLUSION: In our article we give a tentative overview of possible characteristics for profiling. At the moment the clinical factors are the ones used most for assessment. Current research into the value of aetiological characteristics for profiling will increase the applicability of a staging and profiling model.

Contains fulltext : 110312.pdf (publisher's version ) (Open Access), BACKGROUND: Not only is the heterogeneous concept of depression too comprehensive, it is also insufficiently differentiated. This serves as a barrier to scientific research and obscures the symptoms that should indicate what treatment is required. AIM: To describe an accurate model for staging and profiling depression. METHOD: We placed depressive disorders in the context of the entire course of the disorder and we regarded the course as a continuum of psychopathology. RESULTS: First of all we distinguish five stages: (1) the prodromal phase, (2) the first depressive episode, (3) residual symptoms following an episode, (4) the relapse episode and (5) the chronic and/or treatment-resistant depression. The higher the stage, the greater the need for complex and specialised treatment. As characteristics for profiling we distinguish (a) aetiological and pathophysiological variables and (b) clinical factors. The latter are the ones that mainly influence treatment from stage 2 onwards. CONCLUSION: In our article we give a tentative overview of possible characteristics for profiling. At the moment the clinical factors are the ones used most for assessment. Current research into the value of aetiological characteristics for profiling will increase the applicability of a staging and profiling model.

Contains fulltext : 110312.pdf (publisher's version ) (Open Access), BACKGROUND: Not only is the heterogeneous concept of depression too comprehensive, it is also insufficiently differentiated. This serves as a barrier to scientific research and obscures the symptoms that should indicate what treatment is required. AIM: To describe an accurate model for staging and profiling depression. METHOD: We placed depressive disorders in the context of the entire course of the disorder and we regarded the course as a continuum of psychopathology. RESULTS: First of all we distinguish five stages: (1) the prodromal phase, (2) the first depressive episode, (3) residual symptoms following an episode, (4) the relapse episode and (5) the chronic and/or treatment-resistant depression. The higher the stage, the greater the need for complex and specialised treatment. As characteristics for profiling we distinguish (a) aetiological and pathophysiological variables and (b) clinical factors. The latter are the ones that mainly influence treatment from stage 2 onwards. CONCLUSION: In our article we give a tentative overview of possible characteristics for profiling. At the moment the clinical factors are the ones used most for assessment. Current research into the value of aetiological characteristics for profiling will increase the applicability of a staging and profiling model.

Major depressive disorder (MDD) is a common complex trait with enormous public health significance. As part of the Genetic Association Information Network initiative of the US Foundation for the National Institutes of Health, we conducted a genome-wide association study of 435 291 single nucleotide polymorphisms (SNPs) genotyped in 1738 MDD cases and 1802 controls selected to be at low liability for MDD. Of the top 200, 11 signals localized to a 167 kb region overlapping the gene piccolo (PCLO, whose protein product localizes to the cytomatrix of the presynaptic active zone and is important in monoaminergic neurotransmission in the brain) with P-values of 7.7 × 10

Major depressive disorder (MDD) is a common complex trait with enormous public health significance. As part of the Genetic Association Information Network initiative of the US Foundation for the National Institutes of Health, we conducted a genome-wide association study of 435 291 single nucleotide polymorphisms (SNPs) genotyped in 1738 MDD cases and 1802 controls selected to be at low liability for MDD. Of the top 200, 11 signals localized to a 167 kb region overlapping the gene piccolo (PCLO, whose protein product localizes to the cytomatrix of the presynaptic active zone and is important in monoaminergic neurotransmission in the brain) with P-values of 7.7 × 10

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Contains fulltext : 28093.pdf (publisher's version ) (Open Access), Changes in psychomotor slowing were studied in 21 inpatients with a Major Depressive Episode. Fine motor retardation was measured and analysed using computer-aided drawing and figure-copying tasks at T0 (the start of 6 weeks treatment with fluoxetine 20 mg/day) and 5 weeks later (T1). The differences in reaction time between the patients and a group of healthy, matched controls at T0 had disappeared at T1. The initial motor deficit, expressed in longer movement times, had not improved at T1. These findings combined with the effect of manipulation of cognitive and motor demands, suggested that only cognitive processes had accelerated.

Contains fulltext : 28096.pdf (publisher's version ) (Open Access), New computerized techniques allow the precise measurement of psychomotor retardation in patients with a major depressive episode (MDE). One such technique is the analysis of writing and drawing behaviour during figure copying tasks. In the present study, 22 inpatients with an MDE were compared to 22 normal controls. Three tasks were used: the drawing of lines and simple figures, the copying of complex figures and a task in which figures had to be rotated. Objectives were to provide support for earlier findings that the patients were slower than the controls and to explore the cognitive and motor processes involved. Two strategies were applied: analysis of the reaction time and movement time and their different components, and manipulation of the cognitive and motor demands. Patients showed considerable retardation with most of the kinematic variables. Motor deficits and cognitive slowing down contributed to this retardation. Cognitive difficulties increased with increasing complexity of the task.

Contains fulltext : 28093.pdf (publisher's version ) (Open Access), Changes in psychomotor slowing were studied in 21 inpatients with a Major Depressive Episode. Fine motor retardation was measured and analysed using computer-aided drawing and figure-copying tasks at T0 (the start of 6 weeks treatment with fluoxetine 20 mg/day) and 5 weeks later (T1). The differences in reaction time between the patients and a group of healthy, matched controls at T0 had disappeared at T1. The initial motor deficit, expressed in longer movement times, had not improved at T1. These findings combined with the effect of manipulation of cognitive and motor demands, suggested that only cognitive processes had accelerated.

Contains fulltext : 28096.pdf (publisher's version ) (Open Access), New computerized techniques allow the precise measurement of psychomotor retardation in patients with a major depressive episode (MDE). One such technique is the analysis of writing and drawing behaviour during figure copying tasks. In the present study, 22 inpatients with an MDE were compared to 22 normal controls. Three tasks were used: the drawing of lines and simple figures, the copying of complex figures and a task in which figures had to be rotated. Objectives were to provide support for earlier findings that the patients were slower than the controls and to explore the cognitive and motor processes involved. Two strategies were applied: analysis of the reaction time and movement time and their different components, and manipulation of the cognitive and motor demands. Patients showed considerable retardation with most of the kinematic variables. Motor deficits and cognitive slowing down contributed to this retardation. Cognitive difficulties increased with increasing complexity of the task.

Contains fulltext : 28093.pdf (publisher's version ) (Open Access), Changes in psychomotor slowing were studied in 21 inpatients with a Major Depressive Episode. Fine motor retardation was measured and analysed using computer-aided drawing and figure-copying tasks at T0 (the start of 6 weeks treatment with fluoxetine 20 mg/day) and 5 weeks later (T1). The differences in reaction time between the patients and a group of healthy, matched controls at T0 had disappeared at T1. The initial motor deficit, expressed in longer movement times, had not improved at T1. These findings combined with the effect of manipulation of cognitive and motor demands, suggested that only cognitive processes had accelerated.

Contains fulltext : 28096.pdf (publisher's version ) (Open Access), New computerized techniques allow the precise measurement of psychomotor retardation in patients with a major depressive episode (MDE). One such technique is the analysis of writing and drawing behaviour during figure copying tasks. In the present study, 22 inpatients with an MDE were compared to 22 normal controls. Three tasks were used: the drawing of lines and simple figures, the copying of complex figures and a task in which figures had to be rotated. Objectives were to provide support for earlier findings that the patients were slower than the controls and to explore the cognitive and motor processes involved. Two strategies were applied: analysis of the reaction time and movement time and their different components, and manipulation of the cognitive and motor demands. Patients showed considerable retardation with most of the kinematic variables. Motor deficits and cognitive slowing down contributed to this retardation. Cognitive difficulties increased with increasing complexity of the task.