Abstract
BackgroundA 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.MethodsWe 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.ResultsSegmentation 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.ConclusionTaken 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.
Highlights
Due to the ease of synthesis from readily available components methcathinone still presents a continuing public health hazard in many Eastern European countries
We studied the motor network, using the default-mode network (DMN) as an anatomical control
This finding would suggest that the cortical thinning observed in our patients may be a result of neurodegeneration secondary to the subcortical damage caused by manganese toxicity rather than the direct effect of methcathinone per se, a histopathological study would be required to confirm or refute these hypotheses
Summary
Due to the ease of synthesis from readily available components methcathinone (ephedrone) still presents a continuing public health hazard in many Eastern European countries Intravenous abuse of this designer psychostimulant results in a levodopa-unresponsive Parkinsonian syndrome (Stepens et al, 2014). The movement disorder closely resembles that of chronic manganism, involving combinations of hypokinesia, dysarthria, dystonia, and postural instability which manifest as facial impassivity, slowed movements, low volume speech, micrographia, lurching gait with absent arm swing, and falls (Stepens et al, 2008) This methcathinone/manganese-associated movement disorder can be severely disabling, is permanent, and shows no improvement despite abstinence (Selikhova et al, 2008; Sikk et al, 2007; Stepens et al, 2008). This MRI study investigates subcortical and cortical grey matter integrity in intravenous methcathinone abusers
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