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In reply to Letter to the Editor
Letters to the Editor
produced by combining multiple interventions likely exceeds what would be expected from either intervention alone. Additional research is needed to further validate the use of comprehensive techniques.
References Edwards CL, Sudhakar S, Scales MT, Applegate K, Webster W, Dunn R. Electromyographic (EMG) Biofeedback in the comprehensive treatment of central pain with ataxic tremor following thalamic stroke. Appl Psychophys Biofeedback 2000;25(4):229–240. Fordyce WE, Fowler Jr. RS, Lehmann JF, Delateur BJ, Sand PL, Trieshmann RB. Operant conditioning in the treatment of chronic pain. Arch Phys Medication Rehab 1973;54(9):399–408. Keefe FJ, Jacobs M, Edwards CL. Persistent pain: cognitive-behavioral approaches to assessment and treatment. Semin Anesthes 1997;16(2):117–126. Vick P, Lamer T. Treatment of central post-stroke pain with oral ketamine. Pain 2001;92:311–313.
Wendy L. Webster*, Christopher L. Edwards Chronic Pain Management Program, Box 3842, Duke University Medical Center, Durham, NC 27710, USA * Corresponding author. Tel.: 11-919-6682820. E-mail address: [email protected] (W. L. Webster)
PII: S 0304-395 9(01)00448-1
In reply to Letter to the Editor We agree with a comprehensive approach to the treatment of central post-stroke pain. Our patient had a history of depression that predated her central post stroke pain syndrome. Her complex pain problem exacerbated this depression. We initiated additional psychological evaluation and treatment. Patients with central pain syndromes will benefit from a multidisciplinary evaluation and treatment plan. Psychological support is very important, particularly in a patient population refractory to most pharmacologic and interventional medical therapies.
Pamela Vick* Department of Anesthesiology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7010 USA
* Tel.: 11-919-966-5136. E-mail address: [email protected] (P. Vick) PII: S 0304-395 9(01)00449-3
289
Central antinociceptive-analgesic effect of diclofenac Grace et al. (2001) reported that subcutaneous injection of diclofenac abolished the hyperalgesic response elicited in rats by ischemic stimulation of the tail and suppressed the increased prostaglandin formation in the brain of the animals. The prostaglandin concentration in the spinal cord remained unchanged, although it has been observed by other authors that activation of nociceptive afferents by electrical stimulation of the sciatic nerve (Ramwell et al., 1966) or injection of formalin into the paw (Malmberg and Yaksh, 1995; Scheuren et al., 1997) increased spinal prostaglandin formation. In addition, it has been reported that intrathecal injection of prostaglandin E2 (PGE2) dose-dependently enhanced the nociceptive response of thalamic neurons to electrical stimulation of afferent C fibers (Jurna, 1993); PGE2 was more effective in this respect than PGE1, PGD2, PGI2 and PG1a. In accordance with the concept that non-steroidal antiinflammatory drugs (NSAIDs) inhibit prostaglandin formation, intrathecal injection of NSAIDs reduced the release of PGE2 from the spinal cord (Malmberg and Yaksh, 1992, 1995). It is therefore not surprising that intravenous injection of diclofenac and indometacin, as well as intraperitoneal injection of ibuprofen, depressed nociceptive activity evoked in thalamic neurons of the rat (Jurna and Brune, 1990). Since nociceptive activity was elicited in those experiments by electrical stimulation of afferent C fibers in the sural nerve cut distally to the stimulating electrodes, it had been concluded that the depressant effect of diclofenac and the other NSAIDs was due to a central action of the drugs. Direct evidence for a spinal antinociceptive action of NSAIDs derives from animal experiments and from observations made in patients. Intrathecal injection of acetylsalicylic acid, salicylic acid and indometacin was found to depress the nociceptive activity that was evoked in thalamic neurons of rats by electrical stimulation of afferent C fibers in the sural nerve (Jurna et al., 1992). In addition, it has been reported that intrathecal injection of acetylsalicylic acid in relatively low doses produced marked relief in many patients suffering from intractable cancer pain (Pellerin et al., 1987; Devoghel, 1983, 1993). Grace et al. (2001) failed to detect an increase in prostaglandin production in the spinal cord associated with the nociceptive behavior caused by ischemia of the rat tail, although there was an increase in prostaglandin concentration of the brain. These authors propose that “spinal cord processing may not be involved in the nociceptive processing of hyperalgesia following this particular injury of the tail, either because of its (brief) time course or nature of the stimulus”. In the experiments in which PGE2 facilitated (Jurna, 1993) and NSAIDs depressed (Jurna et al., 1992) nociceptive activity evoked in thalamic neurons of the rat, the time course of the stimulus was very brief (duration of electrical impulse, 0.5 ms; stimulation frequency, 1 impulse/s) and the duration of the response was relatively short (approximately 1 s or less). In these experiments, the
produced by combining multiple interventions likely exceeds what would be expected from either intervention alone. Additional research is needed to further validate the use of comprehensive techniques.
References Edwards CL, Sudhakar S, Scales MT, Applegate K, Webster W, Dunn R. Electromyographic (EMG) Biofeedback in the comprehensive treatment of central pain with ataxic tremor following thalamic stroke. Appl Psychophys Biofeedback 2000;25(4):229–240. Fordyce WE, Fowler Jr. RS, Lehmann JF, Delateur BJ, Sand PL, Trieshmann RB. Operant conditioning in the treatment of chronic pain. Arch Phys Medication Rehab 1973;54(9):399–408. Keefe FJ, Jacobs M, Edwards CL. Persistent pain: cognitive-behavioral approaches to assessment and treatment. Semin Anesthes 1997;16(2):117–126. Vick P, Lamer T. Treatment of central post-stroke pain with oral ketamine. Pain 2001;92:311–313.
Wendy L. Webster*, Christopher L. Edwards Chronic Pain Management Program, Box 3842, Duke University Medical Center, Durham, NC 27710, USA * Corresponding author. Tel.: 11-919-6682820. E-mail address: [email protected] (W. L. Webster)
PII: S 0304-395 9(01)00448-1
In reply to Letter to the Editor We agree with a comprehensive approach to the treatment of central post-stroke pain. Our patient had a history of depression that predated her central post stroke pain syndrome. Her complex pain problem exacerbated this depression. We initiated additional psychological evaluation and treatment. Patients with central pain syndromes will benefit from a multidisciplinary evaluation and treatment plan. Psychological support is very important, particularly in a patient population refractory to most pharmacologic and interventional medical therapies.
Pamela Vick* Department of Anesthesiology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7010 USA
* Tel.: 11-919-966-5136. E-mail address: [email protected] (P. Vick) PII: S 0304-395 9(01)00449-3
289
Central antinociceptive-analgesic effect of diclofenac Grace et al. (2001) reported that subcutaneous injection of diclofenac abolished the hyperalgesic response elicited in rats by ischemic stimulation of the tail and suppressed the increased prostaglandin formation in the brain of the animals. The prostaglandin concentration in the spinal cord remained unchanged, although it has been observed by other authors that activation of nociceptive afferents by electrical stimulation of the sciatic nerve (Ramwell et al., 1966) or injection of formalin into the paw (Malmberg and Yaksh, 1995; Scheuren et al., 1997) increased spinal prostaglandin formation. In addition, it has been reported that intrathecal injection of prostaglandin E2 (PGE2) dose-dependently enhanced the nociceptive response of thalamic neurons to electrical stimulation of afferent C fibers (Jurna, 1993); PGE2 was more effective in this respect than PGE1, PGD2, PGI2 and PG1a. In accordance with the concept that non-steroidal antiinflammatory drugs (NSAIDs) inhibit prostaglandin formation, intrathecal injection of NSAIDs reduced the release of PGE2 from the spinal cord (Malmberg and Yaksh, 1992, 1995). It is therefore not surprising that intravenous injection of diclofenac and indometacin, as well as intraperitoneal injection of ibuprofen, depressed nociceptive activity evoked in thalamic neurons of the rat (Jurna and Brune, 1990). Since nociceptive activity was elicited in those experiments by electrical stimulation of afferent C fibers in the sural nerve cut distally to the stimulating electrodes, it had been concluded that the depressant effect of diclofenac and the other NSAIDs was due to a central action of the drugs. Direct evidence for a spinal antinociceptive action of NSAIDs derives from animal experiments and from observations made in patients. Intrathecal injection of acetylsalicylic acid, salicylic acid and indometacin was found to depress the nociceptive activity that was evoked in thalamic neurons of rats by electrical stimulation of afferent C fibers in the sural nerve (Jurna et al., 1992). In addition, it has been reported that intrathecal injection of acetylsalicylic acid in relatively low doses produced marked relief in many patients suffering from intractable cancer pain (Pellerin et al., 1987; Devoghel, 1983, 1993). Grace et al. (2001) failed to detect an increase in prostaglandin production in the spinal cord associated with the nociceptive behavior caused by ischemia of the rat tail, although there was an increase in prostaglandin concentration of the brain. These authors propose that “spinal cord processing may not be involved in the nociceptive processing of hyperalgesia following this particular injury of the tail, either because of its (brief) time course or nature of the stimulus”. In the experiments in which PGE2 facilitated (Jurna, 1993) and NSAIDs depressed (Jurna et al., 1992) nociceptive activity evoked in thalamic neurons of the rat, the time course of the stimulus was very brief (duration of electrical impulse, 0.5 ms; stimulation frequency, 1 impulse/s) and the duration of the response was relatively short (approximately 1 s or less). In these experiments, the