Increased reflection impulsivity in patients with ephedrone-induced Parkinsonism
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Published on: March 17, 2019
Atbin Djamshidian1, Yanosh Sanotsky, Yuriy Matviyenko
1Department of Molecular Neuroscience and Reta Lila Weston Institute for Neurological Studies, University of London, London, UK.
Aims:
To examine a syndrome of chronic manganism that occurs in drug addicts in eastern Europe who use intravenous methcathinone (ephedrone) contaminated with potassium permanganate. In many cases the basal ganglia, especially the globus pallidus and the putamen, are damaged irreversibly. Routine neuropsychological assessment has revealed no cognitive deficits, despite widespread abnormalities on brain imaging studies and severe extrapyramidal motor handicap on clinical examination.
Design:
Case-control study.
Setting:
Ephedrone patients and patients with opioid dependence were recruited from Lviv, Ukraine.
Participants:
We tested 15 patients with ephedrone-induced toxicity, 13 opiate-dependent patients who were receiving opioid replacement therapy and 18 matched healthy volunteers.
Measurements:
The 'beads task', an information-gathering task to assess reflection impulsivity, was used and feedback learning, working memory and risk-taking were also assessed.
Findings:
Opiate-dependent patients differed from controls on three of four tasks, whereas ephedrone patients differed from controls on only one task. More specifically, both patient groups were more impulsive and made more irrational choices on the beads task than controls (P < 0.001). However, ephedrone patients had no deficits in working memory (P > 0.1) or risk-taking (P > 0.1) compared with controls. Opioid-dependent patients had significantly worse working memory (P < 0.001) and were significantly more risk-prone than controls (P = 0.002).
Conclusions:
Ephedrone patients may have similar deficits in information-gathering and decision-making to opiate-dependent patients, with preservation of working memory and risk-taking. This may reflect specific damage to anterior cingulate- basal ganglia loops.
Insights
Chronic manganism from intravenous methcathinone (ephedrone) use causes basal ganglia damage. Ephedrone users showed impulsivity but preserved working memory, unlike opioid users.
Area of Science:
- Neuroscience
- Toxicology
- Psychiatry
Background:
- Intravenous methcathinone (ephedrone) use, often contaminated with potassium permanganate, is linked to chronic manganism.
- This condition can cause irreversible basal ganglia damage, particularly in the globus pallidus and putamen.
- Despite neuroimaging abnormalities and motor deficits, routine neuropsychological assessments have shown no cognitive deficits in affected individuals.
Purpose of the Study:
- To investigate the cognitive and decision-making profiles of individuals with ephedrone-induced chronic manganism.
- To compare these profiles with those of opiate-dependent patients and healthy volunteers.
- To explore potential neurobiological underpinnings of observed deficits.
Main Methods:
- A case-control study was conducted in Lviv, Ukraine.
- Participants included 15 patients with ephedrone-induced toxicity, 13 opiate-dependent patients on replacement therapy, and 18 matched healthy controls.
- Neuropsychological assessments included the 'beads task' for reflection impulsivity, feedback learning, working memory, and risk-taking.
Main Results:
- Both ephedrone and opiate-dependent patients exhibited increased impulsivity and irrational choices on the beads task compared to controls.
- Ephedrone patients showed no significant deficits in working memory or risk-taking compared to controls.
- Opioid-dependent patients demonstrated significantly worse working memory and higher risk-proneness than controls.
Conclusions:
- Ephedrone-induced manganism may lead to information-gathering and decision-making deficits comparable to those in opiate-dependent patients.
- Preserved working memory and risk-taking in ephedrone users suggest specific neurotoxic effects.
- These findings may indicate damage to anterior cingulate-basal ganglia circuits.
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