Basal Ganglia Volumes and Psychomotor Symptoms: Data From the MODECT Study

Out on PubMed, from researchers in Belgium and the Netherlands, is this study:

A longitudinal study of the association between basal ganglia volumes and psychomotor symptoms in subjects with late life depression undergoing ECT.

Van Cauwenberge MGA, Bouckaert F, Vansteelandt K, Adamson C, De Winter FL, Sienaert P, Van den Stock J, Dols A, Rhebergen D, Stek ML, Emsell L, Vandenbulcke M.Transl Psychiatry. 2021 Apr 1;11(1):199. doi: 10.1038/s41398-021-01314-w.PMID: 33795659

The abstract is copied below:
Psychomotor dysfunction (PMD) is a core element and key contributor to disability in late life depression (LLD), which responds well to electroconvulsive therapy (ECT). The neurobiology of PMD and its response to ECT are not well understood. We hypothesized that PMD in LLD is associated with lower striatal volume, and that striatal volume increase following ECT explains PMD improvement. We analyzed data from a two-center prospective cohort study of 110 LLD subjects (>55 years) receiving ECT. Brain MRI and assessment of mood, cognition, and PMD was performed 1 week before, 1 week after, and 6 months after ECT. Volumetry of the caudate nucleus, putamen, globus pallidus, and nucleus accumbens was derived from automatically segmented brain MRIs using Freesurfer®. Linear multiple regression analyses were used to study associations between basal ganglia volume and PMD. Brain MRI was available for 66 patients 1 week post ECT and in 22 patients also six months post ECT. Baseline PMD was associated with a smaller left caudate nucleus. One week after ECT, PMD improved and volume increases were detected bilaterally in the caudate nucleus and putamen, and in the right nucleus accumbens. Improved PMD after ECT did not relate to the significant volume increases in these structures, but was predicted by a nonsignificant volume change in the right globus pallidus. No volume differences were detected 6 months after ECT, compared to baseline. Although PMD is related to lower striatal volume in LLD, ECT-induced increase of striatal volume does not explain PMD improvement.

The pdf is here.







and from the text:

Discussion 
n a large cohort of LLD patients, we found (1) that PMD was related to lower gray matter volume in the striatum, (2) that ECT induced a transient increase in striatal gray matter volume, and (3) that this volume increase was not related to PMD improvement after ECT.
Focusing on GMV differences between LLD patients with varying severity of PMD, our study showed that patients with more PMD have reduced GMV of the left caudate nucleus, independent of the severity of the depression. Focusing only on psychomotor retardation, both left and right caudate nucleus volumes were reduced in patients with a high CORE retardation subscale score. Healthy aging studies have demonstrated that smaller volumes of the striatum and globus pallidus are directly related to slowing of gait (for review see ref. 53) and that age-related reduced functional connectivity in the striatum impairs motor function. However, atrophy of the dorsal striatum has also been linked to neurodegenerative movement disorders such as Parkinson’s disease and Huntington’s disease. Structural alterations of the basal ganglia in MDD have been observed in several studies, most consistently a lower volume of the caudate nucleus and putamen. Nuclear imaging studies have demonstrated reduced presynaptic dopamine transporter (DAT)39,62 and postsynaptic dopamine 1 receptor (D1-R) binding as well as reduced dopaminergic signaling38 in the basal ganglia of MDD patients.

This is another excellent paper from the MODECT study. It investigates the "mood-motor" relationship in late life depression. The three main findings are highlighted above. It is now proven beyond doubt that ECT transiently increases gray matter volume (here, focused on the basal ganglia), but both the exact neurophysiological basis for this and its correlation with clinical improvement remain to be elucidated. 
"Psychomotor dysfunction (PMD)", as described by these authors, leads to considerations of ECT in Parkinson's Disease and catatonia. Catatonia, of course, may be the ultimate expression of psychomotor retardation.
This paper is worth a full read (~25 mins), with the thoughtful "Discussion" being particularly useful in placing the study findings into the context of current knowledge and strategies for future research.

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