Open AccessGrey matter abnormalities in methcathinone abusers with a Parkinsonian syndrome
Author(s) -
Juurmaa Julius,
Menke Ricarda A. L.,
Vila Pierre,
Müürsepp Andreas,
Tomberg Tiiu,
Ilves Pilvi,
Nigul Mait,
JohansenBerg Heidi,
Donaghy Michael,
Stagg Charlotte J.,
Stepens Ainārs,
Taba Pille
Publication year - 2016
Publication title -
brain and behavior
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.915
H-Index - 41
ISSN - 2162-3279
DOI - 10.1002/brb3.539
Subject(s) - putamen , globus pallidus , grey matter , basal ganglia , caudate nucleus , psychology , hyperintensity , thalamus , voxel based morphometry , white matter , neuroscience , medicine , magnetic resonance imaging , central nervous system , radiology
Background A permanent Parkinsonian syndrome occurs in intravenous abusers of the designer psychostimulant methcathinone (ephedrone). It is attributed to deposition of contaminant manganese, as reflected by characteristic globus pallidus hyperintensity on T1‐weighted MRI . Methods We have investigated brain structure and function in methcathinone abusers ( n = 12) compared to matched control subjects ( n = 12) using T1‐weighted structural and resting‐state functional MRI . Results Segmentation analysis revealed significant ( p < .05) subcortical grey matter atrophy in methcathinone abusers within putamen and thalamus bilaterally, and the left caudate nucleus. The volume of the caudate nuclei correlated inversely with duration of methcathinone abuse. Voxel‐based morphometry showed patients to have significant grey matter loss ( p < .05) bilaterally in the putamina and caudate nucleus. Surface‐based analysis demonstrated nine clusters of cerebral cortical thinning in methcathinone abusers, with relative sparing of prefrontal, parieto‐occipital, and temporal regions. Resting‐state functional MRI analysis showed increased functional connectivity within the motor network of patients ( p < .05), particularly within the right primary motor cortex. Conclusion Taken together, these results suggest that the manganese exposure associated with prolonged methcathinone abuse results in widespread structural and functional changes affecting both subcortical and cortical grey matter and their connections. Underlying the distinctive movement disorder caused by methcathinone abuse, there is a more widespread pattern of brain involvement than is evident from the hyperintensity restricted to the basal ganglia as shown by T1‐weighted structural MRI .