Psychomotor Retardation In Depression Research Articles

Motor versus Psychomotor? Deciphering the Neural Source of Psychomotor Retardation in Depression.

Major depressive disorder (MDD) is characterized by psychomotor retardation whose underlying neural source remains unclear. Psychomotor retardation may either be related to a motor source like the motor cortex or, alternatively, to a psychomotor source with neural changes outside motor regions, like input regions such as visual cortex. These two alternative hypotheses in main (n = 41) and replication (n = 18) MDD samples using 7 Tesla MRI are investigated. Analyzing both global and local connectivity in primary motor cortex (BA4), motor network and middle temporal visual cortex complex (MT+), the main findings in MDD are: 1) Reduced local and global synchronization and increased local-to-global output in motor regions, which do not correlate with psychomotor retardation, though. 2) Reduced local-to-local BA4 - MT+ functional connectivity (FC) which correlates with psychomotor retardation. 3) Reduced global synchronization and increased local-to-global output in MT+ which relate to psychomotor retardation. 4) Reduced variability in the psychophysical measures of MT+ based motion perception which relates to psychomotor retardation. Together, it is shown that visual cortex MT+ and its relation to motor cortex play a key role in mediating psychomotor retardation. This supports psychomotor over motor hypothesis about the neural source of psychomotor retardation in MDD.

The Habenula in the Link Between ADHD and Mood Disorder.

Attention-deficit/hyperactivity disorder (ADHD) is a childhood-onset, neurodevelopmental disorder, whereas major depressive disorder (MDD) is a mood disorder that typically emerges in adulthood. Accumulating evidence suggests that these seemingly unrelated psychiatric disorders, whose symptoms even appear antithetical [e.g., psychomotor retardation in depression vs. hyperactivity (psychomotor acceleration) in ADHD], are in fact associated with each other. Thus, individuals with ADHD exhibit high comorbidity with MDD later in life. Moreover, genetic studies have shown substantial overlaps of susceptibility genes between ADHD and MDD. Here, we propose a novel and testable hypothesis that the habenula, the epithalamic brain region important for the regulation of monoamine transmission, may be involved in both ADHD and MDD. The hypothesis suggests that an initially hypoactive habenula during childhood in individuals with ADHD may undergo compensatory changes during development, priming the habenula to be hyperactive in response to stress exposure and thereby increasing vulnerability to MDD in adulthood. Moreover, we propose a new perspective on habenular deficits in psychiatric disorders that consider the habenula a neural substrate that could explain multiple psychiatric disorders.

Transcriptomic Signatures of Inflammation and Metabolic Reprogramming in Peripheral Blood Immune Cells are Implicated in Psychomotor Retardation in Depression

Inflammation affects basal ganglia motor circuits in association with psychomotor retardation, a key symptom of major depression (MD). We previously reported associations between circulating protein inflammatory biomarkers and motor slowing as measured by a battery of neuropsychological tests probing psychomotor speed in medically-stable, unmedicated outpatients with MD.

Cognitive component of psychomotor retardation in unipolar and bipolar depression: Is verbal fluency a relevant marker? Impact of repetitive transcranial stimulation.

In the literature, psychomotor retardation (PMR) is increasingly highlighted as a relevant marker for depression. Currently, we chose to focus on the fluency capacities as an evaluation of the frontal lobes functioning to reach a better understanding of cognitive and neurobiological mechanisms involved in PMR in depression. The aims of this study were: (i) to explore the cognitive component of PMR through the analysis of verbal fluency (VF) performance in unipolar and bipolar depression; and (ii) to examine whether a repetitive transcranial magnetic stimulation treatment could improve concomitantly the PMR and VF capacities, as a relevant marker characteristic of the cognitive component of PMR. Fifteen unipolar and 15 bipolar patients were compared to 15 healthy adults. Before treatment, the results showed VF deficits, particularly marked in the bipolar group. The investigation of the interplay between PMR, VF performance, Montgomery-Åsberg Depression Rating Scale scores, and Montreal Cognitive Assessment scores showed that the deficits in these various dimensions were not homogeneous. The absence of correlation between the psychomotor retardation scale (the French Retardation Rating Scale for Depression) and VF, and the correlation with MoCA raise the hypothesis of a more global cognitive impairment associated with PMR in the BD group. The repetitive transcranial magnetic stimulation treatment had a positive impact on depression, PMR, and fluency scores. Correlations between the Retardation Rating Scale for Depression and VF performances appeared after treatment, showing the cognitive role of psychomotor functioning in depression. Further analyses, including other cognitive measures in an objective evaluation of PMR, are required for a better understanding of these complex relationships.

Psychomotor retardation associated to depression differs from that of normal aging

Psychomotor retardation (PMR) is a main symptom of depressive illness. In the elderly, it is associated with the severity of depression and poor prognosis. However, PMR is also commonly associated with normal aging, Therefore, depressive PMR is frequently misinterpreted as the age-related slowing in the elderly, which contributes to poor recognition of depression. Moreover, neurobiological and neuroanatomical studies on PMR hardly allowed to discriminate geriatric depression from normal aging. Reaction time experiments have rarely been tested in elderly population although they are particularly suited for examining PMR. We performed two reaction time experiments using an additive factor analysis in healthy and depressed old individuals with the hypothesis that PMR associated to depression differed from that of normal aging. Results showed that age-related PMR affected all stages of central nervous system information processing, while PMR associated with depression is limited to the components of response-selection and motor-adjustment. These results clearly show that PMR in geriatric depression differed from the age related slowing. Depression also spares stimulus preprocessing in old individuals as it did in younger adults.

Psychomotor Retardation in Depression: A Systematic Review of Diagnostic, Pathophysiologic, and Therapeutic Implications

Psychomotor retardation is a central feature of depression which includes motor and cognitive impairments. Effective management may be useful to improve the classification of depressive subtypes and treatment selection, as well as prediction of outcome in patients with depression. The aim of this paper was to review the current status of knowledge regarding psychomotor retardation in depression, in order to clarify its role in the diagnostic management of mood disorders. Retardation modifies all the actions of the individual, including motility, mental activity, and speech. Objective assessments can highlight the diagnostic importance of psychomotor retardation, especially in melancholic and bipolar depression. Psychomotor retardation is also related to depression severity and therapeutic change and could be considered a good criterion for the prediction of therapeutic effect. The neurobiological process underlying the inhibition of activity includes functional deficits in the prefrontal cortex and abnormalities in dopamine neurotransmission. Future investigations of psychomotor retardation should help improve the understanding of the pathophysiological mechanisms underlying mood disorders and contribute to improving their therapeutic management.

Psychomotor retardation in depression: biological underpinnings, measurement, and treatment.

Psychomotor retardation is a long established component of depression that can have significant clinical and therapeutic implications for treatment. Due to its negative impact on overall function in depressed patients, we review its biological correlates, optimal methods of measurement, and relevance in the context of therapeutic interventions. The aim of the paper is to provide a synthesis of the literature on psychomotor retardation in depression with the goal of enhanced awareness for clinicians and researchers. Increased knowledge and understanding of psychomotor retardation in major depressive disorder may lead to further research and better informed diagnosis in regards to psychomotor retardation. Manifestations of psychomotor retardation include slowed speech, decreased movement, and impaired cognitive function. It is common in patients with melancholic depression and those with psychotic features. Biological correlates may include abnormalities in the basal ganglia and dopaminergic pathways. Neurophysiologic tools such as neuroimaging and transcranial magnetic stimulation may play a role in the study of this symptom in the future. At present, there are three objective scales to evaluate psychomotor retardation severity. Studies examining the impact of psychomotor retardation on clinical outcome have found differential results. However, available evidence suggests that depressed patients with psychomotor retardation may respond well to electroconvulsive therapy (ECT). Current literature regarding antidepressants is inconclusive, though tricyclic antidepressants may be considered for treatment of patients with psychomotor retardation. Future work examining this objective aspect of major depressive disorder (MDD) is essential. This could further elucidate the biological underpinnings of depression and optimize its treatment.

A study using transcranial magnetic stimulation to investigate motor mechanisms in psychomotor retardation in depression

The pathophysiological basis of psychomotor retardation in depression is unclear. In this study, transcranial magnetic stimulation (TMS) was used to examine the functioning of the motor cortical system in 19 depressed patients and 10 healthy control subjects. Motor-evoked potentials were measured in the biceps brachii muscle during a series of tests with the muscle at rest and during voluntary elbow flexion contractions. Maximal voluntary force, as well as force and electromyographic responses to TMS were also measured during fatiguing maximal contractions. Depressed psychomotor-retarded subjects were less able to produce output from the motor cortex than non-psychomotor-retarded, depressed subjects and healthy controls during maximal exertion and fatigue. This finding was independent of depression severity. In contrast, responses to TMS elicited during relaxation or weak contractions did not differ between healthy and psychomotor-retarded subjects. Our study suggests that although the motor pathway from the motor cortex to the muscle is unimpaired, psychomotor retardation in depression is characterized by a reduced ability to drive the motor cortex.

Forebrain circuitry involved in effort-related choice: Injections of the GABAA agonist muscimol into ventral pallidum alter response allocation in food-seeking behavior

Organisms often make effort-related choices based upon assessments of motivational value and work requirements. Nucleus accumbens dopamine is a critical component of the brain circuitry regulating work output in reinforcement-seeking behavior. Rats with accumbens dopamine depletions reallocate their instrumental behavior away from food-reinforced tasks that have high response requirements, and instead they select a less-effortful type of food-seeking behavior. The ventral pallidum is a brain area that receives substantial GABAergic input from nucleus accumbens. It was hypothesized that stimulation of GABAA receptors in the ventral pallidum would result in behavioral effects that resemble those produced by interference with accumbens dopamine transmission. The present studies employed a concurrent choice lever pressing/chow intake procedure; with this task, interference with accumbens dopamine transmission shifts choice behavior such that lever pressing for food is decreased but chow intake is increased. In the present experiments, infusions of the GABAA agonist muscimol (5.0–10.0 ng) into the ventral pallidum decreased lever pressing for preferred food, but increased consumption of the less preferred chow. In contrast, ventral pallidal infusions of muscimol (10.0 ng) had no significant effect on preference for the palatable food in free-feeding choice tests. Furthermore, injections of muscimol into a control site dorsal to the ventral pallidum produced no significant effects on lever pressing and chow intake. These data indicate that stimulation of GABA receptors in ventral pallidum produces behavioral effects similar to those produced by accumbens dopamine depletions. Ventral pallidum appears to be a component of the brain circuitry regulating response allocation and effort-related choice behavior, and may act to convey information from nucleus accumbens to other parts of this circuitry. This research may have implications for understanding the brain mechanisms involved in energy-related psychiatric dysfunctions such as psychomotor retardation in depression, anergia, and apathy.

S04.05 Psychomotor retardation in depression during treatment with SSRI's

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Retardation in depression: assessment by means of simple motor tasks

Background: psychomotor retardation in depression has mostly been assessed with tasks requiring both cognitive and motor processes. This study tested whether retardation could be measured if the cognitive demands of the task were minimal. Methods: 30 inpatients with a major depressive episode were compared one week after the start of antidepressant treatment, to 30 healthy control persons, matched for age, sex and educational level. Tests consisted of ten simple drawing tasks. The kinematics of drawing movements were recorded using a specially designed pen, a graphics tablet and a personal computer. Results: patients showed marked motor slowing on all the tasks: longer movement durations, longer pauses and lower velocities. Conclusions: psychomotor retardation in depressed patients treated with antidepressants occurs during drawing tasks, in which the cognitive demands are minimal and less than those required in the figure copying tasks used in our previous studies. Limitations: the use of co-medication can have influenced the results, although no correlations were found between the use of medication and the kinematic variables. Clinical relevance: detailed registration and analysis of drawing movements enable a more precise diagnosis of psychomotor disturbances in depressed patients.

Psychomotor retardation and anhedonia in depression.

Anhedonia, the inability to experience pleasure, and observed changes in psychomotor performance are frequent psychopathological phenomena in major depression with possible common neurobiological mechanisms. Interest, pleasure and reactivity to pleasurable stimuli contribute to movement generation and observable behaviour. Therefore the relationship between anhedonia and psychomotor retardation was studied in 48 depressed patients. Subjectively experienced anhedonia correlated with self-rated but not with observer-rated global severity of depression. There was a significant correlation between anhedonia and psychomotor retardation assessed with the Widöcher Retardation Scale. The results suggest the existence of an empirical relationship between reduced ability to experience pleasure and observable psychomotor retardation in depression. Specific measures of psychomotor phenomena may provide further insights into the relationship between observable behaviour and self-experienced symptoms in depression.

Can digit symbol-verbal fluency comparisons facilitate detection of pseudodementia? A preliminary study.

Depressive psychomotor retardation may impair performance on timed tests. By comparison word association measures of verbal fluency are reportedly unaffected by depression. Comparisons of a brief psychomotor test with a measure of verbal fluency may therefore prove useful when there is a concern that depression may be undermining adaptive functioning, assuming both measures display: (1) broad-spectrum sensitivity to brain impairment, (2) differential vulnerability to depression, and (3) moderate correlation in nondepressed persons. Digit Symbol (DS) and the "FAS" measure of verbal fluency are sensitive to genuine dementia, satisfying the first criterion. We found that depressed schizophrenics performed at significantly lower levels on DS, but not on FAS, than nondepressed schizophrenics. The two groups differed significantly on a discrepancy score derived by subtracting FAS from DS scores; normals obtained discrepancy scores highly similar to those of nondepressed schizophrenics. As the normals had higher DS and FAS scores, this discrepancy-score similarity suggests that this index may have wide application. The third criterion is satisfied by the findings of a 0.64 correlation between DS and FAS scores adjusted for age (DS and FAS) as well as gender and educational attainment (FAS) in nondepressed samples. Implications for further research and clinical applications are discussed.

Psychomotor retardation in depression, a pilot study.

Several studies have demonstrated that psychomotor retardation is an important sign of the major depressive episode, both from a diagnostic point of view and as a predictor of treatment outcome. However, it is uncertain to what extent psychomotor retardation is specific for the major depressive episode. A heterogeneous group of psychiatric patients (n=26) was studied using a rating scale developed specifically to assess psychomotor retardation (RRS). The 13 patients suffering from a major depressive episode had a significantly higher RRS score than patients with another diagnosis. Furthermore, in the depressive subjects the severity of the depression (measured by means of Hamilton's depression rating scale) appeared to correlate with the severity of the psychomotor retardation. Cognitive features of psychomotor retardation were mainly responsible for the more severe psychomotor retardation in the depressive patients. Surprisingly. Hamilton's depression scale which was used in this study does not pay much attention to these aspects.

Temporal segmentation of response speed in depression: Neuro-electrophysiological approaches

1. 1. Depressive psychomotor retardation, as observed by delayed reaction times (RT), may be related to a slowing in information processing speed. 2. 2. Two separate studies compared indices of information processing speed in depressed patients and non-clinical controls by segmenting behavioral RT with brain eventrelated potentials (ERPs) and electromyographic (EMG) responses. 3. 3. In Study I, slower behavioral RTs in depression were concomitant with slower central processing times (CPT) but not motor execution times (MET). 4. 4. In Study II, P165, a putative early cognitive ERP related to ‘stimulus evaluation time’, was found to be slower but within normal range in depressed patients.

Slow brain potentials and psychomotor retardation in depression

Event-related cortical potentials were recorded in 11 patients with primary depression and 11 healthy control subjects during a serial choice reaction task. Each new trial was voluntarily initiated when the subject pressed a microswitch; an acoustic go or no-go signal followed after a fixed interval. This elicited a bereitschaftspotential (BP), a contingent negative variation (CNV), acoustically evoked potentials (N1, P2, P3), and a post-imperative negative variation (PINV) in direct succession. These were evaluated conventionally and by principal component analysis (PCA). Patients exhibited significantly longer reaction times and more negative PINVs. BP and CNV did not differ between groups. In conventional amplitude measurement small P3 amplitudes in depressives may be feigned by markedly negative PINVs.