Twenty-one patients with pancreatic cancer pain were studied to evaluate the effectiveness of celiac plexus block (CPB) on pain relief and quality of life (QOL), compared to the traditional NSAID-morphine treatment. The criteria were morphine consumption, visual analogue pain scale (VAS), performance status (PS) determined by medical and nursing staffs, and answers to QOL questionnaires. Morphine consumption, VAS, PS, and self-assessed QOL scores were taken when the administration of morphine was necessary for pain relief and those scores were used as control. Morphine consumption and the VAS score were recorded at regular weekly intervals and the PS and QOL scores were measured every 2 weeks thereafter. CPB was performed within 2-3 days after the control measurement. The VAS scores of the patients receiving CPB (n = 10) were statistically lower for the first 4 weeks after the procedure than those of the patients receiving the standard NSAID-morphine treatment (n = 11) during the same time period after the control measurement. Morphine consumption was significantly lower in weeks 4-7 (inclusive) following the procedure in the CPB group and continued to be lower thereafter, though not significantly so. Although the PS score slightly improved at the 2nd week after CPB, it was not improved by the start of the NSAID-morphine treatment. Self-assessed QOL scores did not ameliorate statistically after CPB; however, they did deteriorate remarkably in the patients treated only with morphine-NSAID during their survival periods, while they deteriorated only slightly in the CPB group. There were fewer side effects after CPB. These results indicate CPB does not directly improve QOL in patients with pancreatic cancer pain, but it may prevent deterioration in QOL by the long-lasting analgesic effect, limitation of side effects and the reduction of morphine consumption, compared to treatment only with NSAID-morphine.
Neuropathic pain following nerve injury is believed to involve excitatory amino acids (EAAs) and Ca2+-mediated neuronal plastic changes in the central nervous system (CNS). This study was designed to investigate the changes in glutamate and aspartate contents in the dorsal half of the spinal cord following chronic constrictive injury (CCI) of the rat common sciatic nerve. We also examined the changes in intracellular calcium ion concentration ([Ca2+]i) of the spinal dorsal horn in transverse spinal slices in the same animal model. Thermal and mechanical hyperalgesia were observed on day 2 and thereafter following CCI (P < 0.0001). In the CCI rats to which 0.5 mg/kg of i.p. MK-801 was given 30 min prior to CCI and subsequently three daily treatments with 0.5 mg/kg of i.p. MK-801, the development of thermal and mechanical hyperalgesia was suppressed for a period of up to 7 days; however, hyperalgesia appeared on day 10 and day 14 (P < 0.001). In CCI rats, significant increases were observed in glutamate and aspartate contents on the ipsilateral side of the dorsal horn to nerve ligation on days 4, 7 and 14 (P < 0.001). Moreover, significant increases in [Ca2+]i in the spinal dorsal horn were also observed in the superficial (lamina I-II) and deep layers (lamina V-VI) on the ipsilateral side to nerve ligation on days 4, 7 and 14 after nerve ligation in the spinal slices (P < 0.0001). The treatment with i.p. MK-801 suppressed the increases in the contents of glutamate and aspartate and in [Ca2+]i on days 4 and 7. However, the ipsilateral contents of glutamate and aspartate significantly increased on day 14 (P < 0.001 and 0.003, respectively); the increased [Ca2+]i was also observed on day 14 (P < 0.001), and the spatial pattern of the increased regions was similar to untreated CCI rats. We interpret these results to indicate that neuropathic hyperalgesia induced by CCI in the rat is associated with an increase in glutamate and aspartate contents and the subsequent activation of NMDA receptors, followed by an increase in [Ca2+]i within dorsal horn of the spinal cord.
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