Psychomotor retardation in depression: Biological underpinnings, measurement, and treatment

Abstract

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.

Inflammation Effects on Motivation and Motor Activity: Role of Dopamine

“…Moreover, greater severity of motor impairments has been associated with increased depression severity and with treatment outcomes (Bennabi et al, 2013;Caligiuri and Ellwanger, 2000). Although findings have been mixed due to differences in the definition and measurement of psychomotor symptoms, as well as the use of different drugs and variable doses within a class, evidence suggests that agents with broad pharmacologic actions (eg, tricyclics, combined serotonin-norepinephrine or norepinephrine-DA reuptake inhibitors) may be more efficacious in the treatment of psychomotor retardation than SSRIs (Buyukdura et al, 2011;Parker et al, 2010). Finally, patients with severe depression and psychomotor retardation are at increased risk for the development of neurological disorders such as PD (Leentjens et al, 2003;Walter et al, 2015), which is also thought to involve inflammation effects on DA neurons (Lotharius et al, 2005).…”

Cross-Cutting Advancements Usher in a New Era for Motor Research in Psychosis

“…[46][47][48][49][50] We are just now beginning to investigate diagnostic boundaries of these core behaviors, but it is clear that because specific movement domains are closely tied to underlying brain circuits, motor markers lend well to cross-diagnostic approaches. Within the context of RDoC, this type of progress will inevitably encourage motor researchers to consider new units of analysis and groups of other research experts to incorporate motor variables into their proposals.…”

S32212, a Novel Serotonin Type 2C Receptor Inverse Agonist/α2-Adrenoceptor Antagonist and Potential Antidepressant: II. A Behavioral, Neurochemical, and Electrophysiological Characterization

“…Its effects were also evaluated in marble burying and isolation-induced aggression tests in mice, two empirical procedures responsive to currently available antidepressants Kobayashi et al, 2008). Psychomotor retardation can be pharmacologically mimicked by the administration of ␣ 2 -AR agonists, which provokes a loss of righting reflex (LRR) abolished not only by drugs possessing antagonist actions at ␣ 2 -ARs, but also by most clinically active antidepressants (Millan et al, , 2001Buyukdura et al, 2011). The prototypical model of chronic mild stress (CMS)-induced reduction in sucrose consumption, considered to reflect anhedonia, is responsive to antidepressants such as imipramine, which restore sucrose consumption to nonstressed levels, albeit with variable delays reflecting differences in mechanisms of action (Millan et al, 2001;Willner, 2005;.…”