Tramadol hydrochloride use and acute deterioration in Parkinson's disease tremor

Mellor, Katy; Ahmed, Anis; Thomson, Alexander

doi:10.1002/mds.22449

Cited by 6 publications

(1 citation statement)

References 3 publications

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“…Accordingly, morphine, a l receptor agonist, has been shown to inhibit the release of striatal dopamine in vitro [13] and experiments using superfused rat brain tissue have shown that the inhibitory effects of opioids on the release of dopamine from nigral neurons is mediated by presynaptic j receptors [14]. Finally, in Parkinson's disease, taken as an example of altered basal dopaminergic transmission, drugs such as fentanyl acting on opioid receptors may trigger severe worsening of tremor, rigidity and bradykinesia [6,15,16] and induce dystonia [7].…”

Section: Discussionmentioning

confidence: 99%

Naloxone‐responsive acute dystonia and parkinsonism following general anaesthesia

Iselin-Chaves

Grötzsch²,

Besson

et al. 2009

Anaesthesia

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Various movement disorders such as dystonia may acutely develop during or at emergence from general anaesthesia in patients with or without pre-existing Parkinson disease. These movements are triggered by a variety of drugs including propofol, sevoflurane, anti-emetics, antipsychotics and opioids. The postulated mechanism involves an imbalance between dopaminergic and cholinergic neurotransmitters in the basal ganglia. We report an acute, severe and generalised dystonic reaction in an otherwise healthy woman at emergence from general anaesthesia, dramatically reversed by the administration of naloxone, pointing to a potential role of the fentanyl and morphine that the patient had received. Recent literature on the mechanisms of abnormal movements induced by opioids are discussed. The severity of the reaction with usual doses of opioids, in a patient with no prior history of parkinsonism, led to further investigation that demonstrated the possibility of an enhanced susceptibility to opioids, involving a genetically determined abnormal function of glycoproteine-P and catechol-O-methyltransferase

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