Abstract
Pain is a common complication of cancer. As a result of educational efforts, there has been an appropriate increase in the use of opioids. The increase has resulted in a greater detection of a spectrum of neuro-psychiatric adverse effects that include cognitive failure, hallucinations, delirium, severe sedation, generalized myoclonus, hyperalgesia, allodynia and seizures. Various putative mechanisms have been postulated including the neuro-sensitizing effects of opioid metabolites. Numerous metabolites including morphine-3-glu-curonide, morphine-6-glucuronide, hydromorphone 3-glucuronide, and normeperidine have been implicated. Morphine-3-glucuronide appears to cause hyperexcitability via non-opioid receptor mechanisms which are not yet well defined. Renal impairment, high opioid doses, prolonged opioid administration, borderline cognition, dehydration, neuropathic pain and the presence of other psycho-active drugs have consistently been reported to be correlates of opioid associated CNS irritability. Var...
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More From: Journal of Pharmaceutical Care in Pain & Symptom Control
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