Post-stroke Mood and Emotional Disturbances: Pharmacological Therapy Based on Mechanisms

Abstract

Post-stroke mood and emotional disturbances are frequent and diverse in their manifestations. Out of the many post-stroke disturbances, post-stroke depression, post-stroke anxiety, post-stroke emotional incontinence, post-stroke anger proneness, and post-stroke fatigue are frequent and important symptoms. These symptoms are distressing for both the patients and their caregivers, and negatively influence the patient’s quality of life. Unfortunately, these emotional disturbances are not apparent and are therefore often unnoticed by busy clinicians. Their phenomenology, predicting factors, and pathophysiology have been under-studied, and are under-recognized. In addition, well-designed clinical trials regarding these symptoms are rare. Fortunately, these mood and emotional disturbances may be treated or prevented by various methods, including pharmacological therapy. To administer the appropriate therapy, we have to understand the phenomenology and the similarities and differences in the pathophysiological mechanisms associated with these emotional symptoms. This narrative review will describe some of the most common or relevant post-stroke mood and emotional disturbances. The phenomenology, factors or predictors, and relevant lesion locations will be described, and pharmacological treatment of these emotional disturbances will be discussed based on presumable pathophysiological mechanisms.

Post-Stroke Fatigue May Be Associated with the Promoter Region of a <b><i>Monoamine Oxidase A </i></b>Gene Polymorphism

“…On the contrary, we did not find an association between polymorphisms associated with serotonin metabolism and PSF. Our results are in line with the previous study that reported no effect of selective serotonin reuptake inhibitors on PSF [21,22] . Our results, however, could not completely exclude the possibility of an association between 5-HTTLPR and PSF because we did not evaluate the 5-HT receptor subtype HTR2A gene, which is known to be associated with CFS [16] .…”

Serotonin transporter gene polymorphisms may be associated with poststroke neurological recovery after escitalopram use

“…This is in line with previous studies that showed that improvement of motor dysfunction by SSRI therapy occurred regardless of poststroke depressive symptoms 10. Given that serotonin is involved in the pathogenesis of depression,37 this dissociative effect of SERT gene polymorphisms needs discussion. SSRIs are known to be involved in complex signalling cascades, which result in increased expression of neurotrophic factors, enhanced hippocampal neurogenesis, the inhibition of inflammatory cytokines and subsequent augmentation of neurogenesis, increased axonal sprouting and the development of new synapses 1–3 38 39.…”

Poststroke emotional disturbances and a tryptophan hydroxylase 2 gene polymorphism

“…Because the TPH2 gene is associated with depression in subjects without stroke (Gao et al., ) one may argue that our findings are not specific to PSD. It has been shown that PSD is associated with a complex etio‐pathogenesis that includes psychologic responses secondary to sudden functional disability, neurochemical changes due to brain damage, and difficult familial, social, or environmental situations (Kim, ). On top of these, certain genetic traits for depression may be related to the development of PSD, and our results may provide some evidence to support this argument.…”