Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The indole alkaloids ibogaine and harmaline are beta-carboline derivatives that cause both hallucinations and tremor. Reports that ibogaine may have potent anti-addictive properties have led to initiatives that it be tested for the treatment of opiate and cocaine addiction. In this study, ibogaine-treated rats were analysed for evidence of neurotoxic effects because human clinical trials of ibogaine have been proposed. We recently found that ibogaine induces a marked glial reaction in the cerebellum with activated astrocytes and microglia aligned in parasagittal stripes within the vermis. Based on those findings, the present study was conducted to investigate whether ibogaine may cause neuronal injury or degeneration. The results demonstrate that, after treatment with ibogaine or harmaline, a subset of Purkinje cells in the vermis degenerates. We observed a loss of the neuronal proteins microtubule-associated protein 2 and calbindin co-extensive with loss of Nissl-stained Purkinje cell bodies. Argyrophilic staining of Purkinje cell bodies, dendrites and axons was obtained with the Gallyas reduced silver method for degenerating neurons. Degenerating neurons were confined to narrow parasagittal stripes within the vermis. We conclude that both ibogaine and harmaline have selective neurotoxic effects which lead to degeneration of Purkinje cells in the cerebellar vermis. The longitudinal stripes of neuronal damage may be related to the parasagittal organization of the olivocerebellar climbing fiber projection. Since these drugs produce sustained activation of inferior olivary neurons, we hypothesize that release of an excitatory amino acid from climbing fiber synaptic terminals may lead to excitotoxic degeneration of Purkinje cells.
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PMID:Degeneration of Purkinje cells in parasagittal zones of the cerebellar vermis after treatment with ibogaine or harmaline. 837 27

In this study, a cocaine abstinence syndrome is confirmed. Moreover, the cocaine withdrawal syndrome was found to be medically and psychiatrically benign and required no medication for detoxification in this inpatient setting. The 150 patients who underwent cocaine withdrawal did not show the three distinct phases of the abstinence symptomatology previously described. No patients required pharmacological intervention for cocaine withdrawal, and the dropout rate was 8% of the 150 cocaine dependents. The common symptoms of acute cessation of cocaine were transient craving, hyperactivity, slight tremor, insomnia and apprehension. The diagnosis of cocaine dependence alone without an additional drug or alcohol diagnosis was unusual in this study at 5%, as is the solitary use of cocaine also uncommon according to other studies. Studies clearly document that the concurrent and simultaneous use and dependence on multiple drugs and alcohol is present in the majority of treatment populations and common in the general population. As many as 54% of cocaine dependents qualified for alcohol dependence in this study, and many were dependent on alcohol prior to their cocaine dependence. Cocaine dependence appears to be yet another diagnosis in the spectrum of the multiple drug and alcohol dependent.
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PMID:Cocaine dependence: alcohol and other drug dependence and withdrawal characteristics. 838 Oct 28