Articles: analgesics.
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J Pain Symptom Manage · Apr 1995
Severe undertreatment of cancer pain: a 3-year survey of the German situation.
The aim of this survey was to determine the prescribing patterns of German physicians in the treatment of cancer pain. The computerized patient records of 330 practices, which treated a total number of 1,104,435 patients over a 3-year period, were analyzed. "Strong" opioids, widely accepted in the management of severe cancer pain, were prescribed to just 322 of 16,630 cancer patients (1.9%). ⋯ Germany is still a developing country in terms of pain therapy. This situation is symptomatic of many countries and reflects the continuing prejudice against opioids.
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Clinical Trial
Transdermal fentanyl in combination with initial intravenous dose titration by patient-controlled analgesia.
Two studies including a total of 70 patients evaluated the efficacy and side effects of a combination of initial patient-controlled analgesia (PCA) for dose finding with transdermal fentanyl administration. Patients, requiring strong opioids for severe cancer pain, received intravenous (i.v.) fentanyl on an on-demand basis over a 24 h period. The amount of fentanyl administered was then used for selecting a suitable transdermal therapeutic system (TTS), which remained in place for 72 h. ⋯ A respiratory rate below 8 per minute was observed in three patients. Due to adequate symptomatic treatment, other moderate and severe symptoms were relatively rare. TTS fentanyl was shown to be an effective, safe and simple method for long-term pain relief in cancer patients and presents an interesting novel option in the treatment of cancer pain.
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The analgesic and sedative-hypnotic utility of the alpha 2 agonists clonidine and dexmedetomidine are currently being investigated. Both compounds exert their behavioral responses by activating central alpha 2 adrenoceptors, albeit with different selectivities and efficacies. Furthermore, the analgesic and hypnotic behavioral responses are produced at different sites and may be affected independently of one another. A series of studies was conducted in rats to determine (1) whether tolerance and cross-tolerance develop to the analgesic actions of clonidine or dexmedetomidine; (2) how the number of available alpha 2 adrenoceptors affects the analgesic response to dexmedetomidine and clonidine; and (3) how the number of available alpha 2 adrenoceptor affects the hypnotic response to dexmedetomidine. ⋯ Fewer alpha 2 adrenoceptors need to be available for analgesia to be produced by dexmedetomidine compared with the number required for analgesia by clonidine. This difference should result in less tolerance in the analgesic response to dexmedetomidine than to clonidine with chronic use. Dexmedetomidine requires fewer alpha 2 adrenoceptors to elicit an analgesic response than it does to elicit a hypnotic response. Thus the analgesic properties of alpha 2-adrenergic agonists persist after the hypnotic response has been attenuated after chronic alpha 2 agonist administration.
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Studies in mice and rats have shown that antinociception produced by intrathecal (i.t.) administration of opioids can be partially inhibited by intracerebroventricular (i.c.v.) administration of naloxone. In this study we tested the hypothesis that this inhibition by i.c.v. naloxone results from antagonism of supraspinal endogenous opioid-mediated antinociception produced by the action of i.t. opioids on an ascending antinociceptive pathway. In rats lightly anesthetized with urethane/alpha-chloralose, i.t. ⋯ Microinjection of naloxone methiodide into nucleus accumbens but not into the rostral ventral medulla (RVM) or the periaqueductal gray matter (PAG) antagonized the suppression of the JOR produced by i.t. DAMGO or lidocaine. The possibility that this ascending pathway may represent a source of spinal input to mesolimbic circuitry involved in setting the state of sensorimotor reactivity to noxious stimuli is discussed.