Hammilton
Bluelighter
- Joined
- Sep 2, 2008
- Messages
- 3,435
I wanted to post this here to warn people before they inject or smoke methcathinone / ephedrone made with KMnO4. It is an extremely bad idea. Manganese poisoning cannot be reversed once it happens, and symptoms will often continue to get worse slowly and may not stop progressing. I have probably poisoned myself with manganese but it's too soon to know how bad it'll be (I'm keeping my fingers crossed, while I was exposed to very high levels, it was over a *fairly* short period of time). I did not do so with ephedrone, however, but via another route.
If there is anyone here who has developed manganism from using ephedrone, please send me a PM, I have questions for someone who developed the condition by using this drug.
The last study looks interesting, if nothing else it's probably loaded with excellent ref's.
Ham
Mov Disord. 2008 Nov 15;23(15):2224-31. doi: 10.1002/mds.22290.
Parkinsonism and dystonia caused by the illicit use of ephedrone--a longitudinal study.
Selikhova M, Fedoryshyn L, Matviyenko Y, Komnatska I, Kyrylchuk M, Krolicki L, Friedman A, Taylor A, Jäger HR, Lees A, Sanotsky Y.
Source
Institute of Neurology, Reta Lila Weston Institute of Neurological Studies, UCL, United Kingdom.
Abstract
A neurological syndrome characterized by levodopa unresponsive bradykinesia, retropulsion with falls backwards, dysarthria, gait disturbance, dystonia, and emotional lability was identified in 13 male opiate addicts following the prolonged intravenous use of ephedrone (methcathinone), a central nervous stimulant prepared from pseudoephedrine, potassium permanganate, and vinegar. The natural history, response to treatment, and clinical features has been studied, and MR and dopamine transporter SPECT brain imaging were carried out. Pubic hair was sampled for manganese. The clinical and radiological picture closely resembled previous reports of chronic manganese poisoning and increased mean manganese level in pubic hair observed for at least 1 year after cessation of ephedrone. Odor identification was intact. Cognitive assessment showed a mild executive dysfunction and a mild depression. DaTSCANs were all normal. The neurological syndrome bears some similarities to PSP but differs from Parkinson's disease. Delayed neurological progression despite discontinuation of ephedrone occurred in one-third of cases. Ephedrone poisoning should be considered as a possible cause of secondary Parkinsonism in young adults, particularly from Eastern Europe.
PMID: 18785245 [PubMed - indexed for MEDLINE]
If there is anyone here who has developed manganism from using ephedrone, please send me a PM, I have questions for someone who developed the condition by using this drug.
The last study looks interesting, if nothing else it's probably loaded with excellent ref's.
Ham
Acta Neurol Scand. 2007 Jun;115(6):385-9.
Irreversible motor impairment in young addicts--ephedrone, manganism or both?
Sikk K, Taba P, Haldre S, Bergquist J, Nyholm D, Zjablov G, Asser T, Aquilonius SM.
Source
Department of Neurology and Neurosurgery, University of Tartu, L. Puusepa 2, Tartu 51014, Estonia. [email protected]
Abstract
BACKGROUND:
Parkinsonian syndrome related to intravenous use of a "designer" psychostimulant, derived from pseudoephedrine using potassium permanganate as the oxidant, has been observed in drug addicts in Estonia.
OBJECTIVE:
To describe the symptomatology of four young patients, history of drug administration and chemical analysis of a drug batch.
METHODS:
Mental and motor function and quality of life were scored and ephedrone was analyzed using electrospray mass spectrometry. Manganese content of the final synthetic mixture was analyzed using Inductively Coupled Plasma-Atomic Emission Spectrometry.
RESULTS:
None of the four cases scored below the dementia threshold in MMSE, while other ratings (UPDRS, H&Y, PDQ-39) corresponded to disabilities seen in relatively advanced Parkinson's disease. The ephedrone yield of the reaction was approximately 44% and the mixture was found to contain 0.6 g/l of manganese.
CONCLUSIONS:
The cases were exposed to extreme manganese load. Their symptomatology is probably identical to manganism. The role of ephedrone is presently unknown. Physicians must be aware of early signs of manganism in patients within social risk groups.
Mov Disord. 2008 Nov 15;23(15):2224-31. doi: 10.1002/mds.22290.
Parkinsonism and dystonia caused by the illicit use of ephedrone--a longitudinal study.
Selikhova M, Fedoryshyn L, Matviyenko Y, Komnatska I, Kyrylchuk M, Krolicki L, Friedman A, Taylor A, Jäger HR, Lees A, Sanotsky Y.
Source
Institute of Neurology, Reta Lila Weston Institute of Neurological Studies, UCL, United Kingdom.
Abstract
A neurological syndrome characterized by levodopa unresponsive bradykinesia, retropulsion with falls backwards, dysarthria, gait disturbance, dystonia, and emotional lability was identified in 13 male opiate addicts following the prolonged intravenous use of ephedrone (methcathinone), a central nervous stimulant prepared from pseudoephedrine, potassium permanganate, and vinegar. The natural history, response to treatment, and clinical features has been studied, and MR and dopamine transporter SPECT brain imaging were carried out. Pubic hair was sampled for manganese. The clinical and radiological picture closely resembled previous reports of chronic manganese poisoning and increased mean manganese level in pubic hair observed for at least 1 year after cessation of ephedrone. Odor identification was intact. Cognitive assessment showed a mild executive dysfunction and a mild depression. DaTSCANs were all normal. The neurological syndrome bears some similarities to PSP but differs from Parkinson's disease. Delayed neurological progression despite discontinuation of ephedrone occurred in one-third of cases. Ephedrone poisoning should be considered as a possible cause of secondary Parkinsonism in young adults, particularly from Eastern Europe.
PMID: 18785245 [PubMed - indexed for MEDLINE]
Environ Health Perspect. 2010 Aug;118(8):1071-80. doi: 10.1289/ehp.0901748. Epub 2010 Apr 19.
Manganese and Parkinson's disease: a critical review and new findings.
Guilarte TR.
Source
Neurotoxicology and Molecular Imaging Laboratory, Department of Environmental Health Sciences, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, USA. [email protected]
Abstract
BACKGROUND:
Excess accumulation of manganese (Mn) in the brain results in a neurological syndrome with cognitive, psychiatric, and movement abnormalities. The highest concentrations of Mn in the brain are achieved in the basal ganglia, which may precipitate a form of parkinsonism with some clinical features that are similar and some that are different to those in Parkinson's disease (PD). Recently, scientists have debated the possibility that Mn may have an etiological role in PD or that it may accelerate the expression of PD.
OBJECTIVE:
The goal of this review was to examine whether chronic Mn exposure produces dopamine neuron degeneration and PD or whether it has a distinct neuropathology and clinical presentation.
DATA SOURCE:
I reviewed available clinical, neuroimaging, and neuropathological studies in humans and nonhuman primates exposed to Mn or other human conditions that result in elevated brain Mn concentrations.
DATA EXTRACTION:
Human and nonhuman primate literature was examined to compare clinical, neuroimaging, and neuropathological changes associated with Mn-induced parkinsonism.
DATA SYNTHESIS:
Clinical, neuroimaging, and neuropathological evidence was used to examine whether Mn-induced parkinsonism involves degeneration of the nigrostriatal dopaminergic system as is the case in PD.
CONCLUSIONS:
The overwhelming evidence shows that Mn-induced parkinsonism does not involve degeneration of midbrain dopamine neurons and that l-dopa is not an effective therapy. New evidence is presented on a putative mechanism by which Mn may produce movement abnormalities. Confirmation of this hypothesis in humans is essential to make rational decisions about treatment, devise effective therapeutic strategies, and set regulatory guidelines.