Psychomotor slowing is a key feature of depressive disorders. Despite its great clinical importance, the pathophysiology and prevalence across different diagnoses and mood states are still poorly understood. Actigraphy allows unbiased, objective, and naturalistic assessment of physical activity as a marker of psychomotor slowing. Yet, the true effect-sizes remain unclear as recent, large systematic reviews are missing. We conducted a novel meta-analysis on actigraphically measured slowing in depression with strict inclusion and exclusion criteria for diagnosis ascertainment and sample duplications. Medline/PubMed and Web-of-Science were searched with terms combining mood-keywords and actigraphy-keywords until September 2021. Original research measuring actigraphy for ⩾24 h in at least two groups of depressed, remitted, or healthy participants and applying operationalized diagnosis was included. Studies in somatically ill patients, N < 10 participants/group, and studies using consumer-devices were excluded. Activity-levels between groups were compared using random-effects models with standardized-mean-differences and several moderators were examined. In total, 34 studies (n = 1804 patients) were included. Patients had lower activity than controls [standardized mean difference (s.m.d.) = −0.78, 95% confidence interval (CI) −0.99 to −0.57]. Compared to controls, patients with unipolar and bipolar disorder had lower activity than controls whether in depressed (unipolar: s.m.d. = −0.82, 95% CI −1.07 to −0.56; bipolar: s.m.d. = −0.94, 95% CI −1.41 to −0.46), or remitted/euthymic mood (unipolar: s.m.d. = −0.28, 95% CI −0.56 to 0.0; bipolar: s.m.d. = −0.92, 95% CI −1.36 to −0.47). None of the examined moderators had any significant effect. To date, this is the largest meta-analysis on actigraphically measured slowing in mood disorders. They are associated with lower activity, even in the remitted/euthymic mood-state. Studying objective motor behavior via actigraphy holds promise for informing screening and staging of affective disorders.

Psychomotor activity is one of the traits we most immediately perceive in others. Psychomotor slowing, which can be easily noticed on a first medical examination, is a symptom which may be prodromal of psychic disturbances.

Historically, psychomotor retardation is a characteristic attached to depression, especially melancholia. Some studies show that psychomotor retardation is associated with good therapeutic prognosis, including positive response to electro-convulsivo-therapy. The cluster of non-verbal symptoms includes both basic aspects related to motor behavior such as attitudes and movements and more complex aspects such as goal-directed behaviors. We will see that this intuitive and fundamental dimension of clinical depression is not homogeneous. From a motor point of view, hypo-bradykinesia in depression may be compared to the one found in cortico-subcortical syndromes such as Parkinson's disease. This comparison suggests that key brain structures such as the basal ganglia could be involved in depression.

Moreover, the loss of vital energy is the dominant psychopathological explanation linked to psychomotor retardation. From a phenomenological point of view, this interpretation seems to be relevant but appears disappointing as an experimental variable. However, motivation, understood as the factor that energizes the behavior seems to be an interesting and promising concept.

Experimentally, it is possible to measure how much an individual is able to invest energy in order to achieve a goal.

The impact of depression on the process of incentive motivation will be analyzed before turning to a description of therapeutic interventions related to psychomotor field such as sports or sensorimotor stimulations that appear to be promising tracks for clinical improvement.

This study was designed to evaluate the effect of semantic priming with a lexical decision task in 22 depressed patients (DSM-III-R, 1987) and 30 control subjects. These patients were evaluated twice: first when they arrived at the hospital, and secondly, after clinical improvement. Clinical improvement was evaluated using standard depression rating scales. A lexical decision task involving semantic relations (related vs. unrelated, e.g., apple-pear) was used to evaluate the processing of semantic information. The results showed that, for the first evaluation, the depressives presented similar semantic priming to control subjects. When we compared semantic priming in the first and the second passes, we observed that its amplitude was identical. The sole difference between the two passes concerns the global reaction time in the depressive group. This last result suggested that, with clinical improvement, the characteristic psychomotor retardation declines. One of the major results concerns the fact that severe depressive patients (first pass) exhibit normal semantic priming in a lexical decision task. These results indicate, in this clinical population, the preservation of controlled processes implicated in this lexical decision task.

The contribution of EEG to theory as well as to psychiatric practice of depression is negligible. The prevailing view is that no ‘abnormal’ characteristic can be demonstrated in affective disorders. Since ‘abnormal’ is generally taken in a neurological sense, all those EEG characteristics are faded out which cannot be regarded as neurologically abnormal but which nevertheless may be useful for psychiatric concerns. Thus, early observations concerning the spatio-temporal aspect of the EEG have essentially gone unnoticed, thereby evading systematic scrutiny. It has been maintained that periodically melancholic patients more often exhibited a dynamically rigid EEG than patients with neurotic forms. Our retrospective study involved 314 inpatients with depressive disorders who were subdivided into an ‘endogenous’ and a ‘non-endogenous’ subgroup using both IC'D 9 diagnoses as well as RDC criteria. The EEGs were designated to one of the three categories, rigid, labile, or physiomorphic. Forty-two percent of the patients in the ‘endogenous’ subgroup exhibited a dynamically rigid EEG (DR) compared to 20% of those from the ‘non-endogenous’ subgroup. Symptoms of psychomotor retardation positively correlated with DR, whereas ‘anxiety’ positively correlated with non-DR (labile or physiomorphic EEG dynamics). In addition, there was a positive correlation between DR and both the number of manifestations of depressive disorders and the number of previous hospitalizations. We interpret DR as a personality-bound characteristic which, far from being pathognomonic of a certain syndrome or even diagnosis, instead indicates a higher degree of vulnerability towards manifestation of melancholic syndromes with psychomotor retardation. This does not exclude the possibility of a state-dependent intensification of DR.

In previous reports, we have observed that blood magnesium was significantly higher in drug-free patients with major depression when compared to healthy controls. This was especially true for erythrocyte magnesium. Furthermore, the most severely depressed patients had the highest intracellular magnesium content, showing that intracellular magnesium rate was related to the intensity of symptoms. We report here the results of blood magnesium measured in 88 major depressed patients as compared to 61 controls. We show that the mean erythrocyte and also plasma magnesium contents are both increased in these patients. We observe that about 40% of male and female patients have a very significant increase (25%) in intracellular magnesium content as compared to controls. However, about 60% of the hospitalised depressed patients have normal values. None of the controls has high erythrocyte magnesium. This is less evident concerning the plasma magnesium. No differences are observed between patients when classified according to the intensity of moral pain or anxiety. In contrast, the patients with mild to high psychomotor retardation score, which is an index of hypoexcitability, have significant higher erythrocyte magnesium values compared with other patients. The results of male patients without psychomotor retardation do not differ from control values. Our study suggests that central hypoexcitability might be related to an increase in intracellular magnesium observed at the peripheral level, keeping in mind that hyperexcitability, as observed in various conditions such as stress and cardiovascular disorders, is frequently associated, in contrast, with a decrease in blood magnesium.

Aim: Translation of a specific instrument to measure psychomotor retardation, the “Widlöcher Retardation Rating Scale” and validation of this Dutch translation (Widlöcher remmingsschaal, WRS). Method: In three separate studies, we studied reliability (n = 26), concurrent and divergent validity (n = 25) and predictive validity (n = 28) of the WRS. In- and outpatients with a depressive disorder or schizophrenia participated, and scores on the WRS were compared with those on the Montgomery Asberg Depression Rating Scale (MADRS) and retardation items of the Comprehensive Psychopathological Rating Scale (CPRS).

Results: The internal consistency was good (Cronbach alpha = 0.86), interrater reliability was sufficient to good, the correlation between the sumscores of both raters was r = 0.84, n = 23, p <0.01 and the kappa's were between 0.23 and 0.80. Convergent and divergent validity showed in comparing the correlation between the sum scores on the WRS and the CPRS retardation items (r = 0.91, n = 25, p < 0.01 ) with the correlation between the sumscores on the WRS and the MADRS (r = 0.40, n = 25, p = 0.1). The decrease of the sum scores on the WRS after two weeks of treatment with antide-pressants predicted remission after six weeks. A subgroup of the patients who were not in remission after six weeks, showed a predominance of retardation signs over mood disturbances. The same clinical picture was seen in a group of patients with a chronic disorder.

Conclusion: De Widlöcher Retardation Rating Scale in this Dutch translation is a usefull instrument to measure psychomotor retardation. The connection between remaining retardation symptoms and longterm prognosis deserves further investigation.