Neuropathic pain increased immunological reactivity and pregabalin treatment modulated this reactivity. Increased NK cell activity and splenocyte proliferation were inhibited by pregabalin treatment.

Oxcarbazepine (OCBZ) is a keto analog of carbamazepine (CBZ) and may have similar analgesic properties to CBZ, but studies on its effects in neuropathic pain conditions are rare. In this study, we evaluated the analgesic effects of OCBZ in a rat neuropathic pain model. Male Sprague-Dawley rats were prepared by tightly ligating the left L5 and L6 spinal nerves to produce neuropathic pain. Sixty neuropathic rats were randomly assigned into six groups, and normal saline, a vehicle (polyethylene glycol 400), and OCBZ (10 mg/kg, 20 mg/kg, 30 mg/kg, and 50 mg/kg) were intraperitoneally administered to these individual groups. Mechanical and cold allodynia were observed at preadministration and 15, 30, 60, 90, 120, 150, and 180 min after drug administration and were quantified by measuring withdrawal frequencies to stimuli with von Frey filaments and 100% acetone, respectively. Rotarod performance was measured to detect drug-induced adverse motor effects. In the OCBZ-treated groups, withdrawal frequencies to mechanical and cold stimuli were significantly reduced in a dose-dependent manner (P < 0.05). Only at the largest dose did OCBZ reduce rotarod performance time. These results suggest that OCBZ may be a possible therapeutic consideration in neuropathic pain conditions associated with allodynia and hyperalgesia.

Segmental zoster paresis is a rare complication of herpes zoster, characterized by focal motor weakness that does not always present simultaneously with skin lesions. Zoster paresis can be easily confused with other neuromuscular or spinal diseases. This case report describes the case of a 72-year-old woman with herpes zoster and cervical spinal stenosis at the same spinal level, where it was difficult to distinguish segmental zoster paresis from cervical radiculopathy combined with motor neuropathy. Although segmental zoster paresis in the upper extremity is rare, it should be included in the differential diagnosis of segmental pain and weakness in the extremities, especially in older or immunocompromised patients. Correct diagnosis is required, to avoid unnecessary surgery and allow timely antiviral treatment.

Background: Pain plays roles in both the nervous system and immune system. Changes in the neuroendocrine pathway under pain conditions give rise to sympathetic outflow with increased plasma catecholamines and activate immune reactions. Dexmedetomidine exerts sedative, analgesic, and anesthetic-sparing effects and is known to diminish pro-inflammatory processes by central sympatholytic effects. To investigate the influence of the analgesic effect of dexmedetomidine on immunomodulation under pain conditions, splenic natural killer (NK) tumoricidal cytotoxic activity, proliferative ability of T lymphocytes, and cytokine changes were assessed.Methods: After evaluation of the analgesic efficacy of dexmedetomidine in C57BL mice that were subjected to formalin-induced pain, dexmedetomidine (30 µg/kg) or saline was injected intraperitoneally (ip) 30 min before formalin (20 µL of 2% formalin in 0.9% saline) injection. NK cell activity against NK-sensitive YAC-1 lymphoma cells was evaluated by the percentage of specific lactate dehydrogenase (LDH) release. Various numbers of effector cells (NK cells) were added to the wells of a microtiter plate containing 2 × 104 target YAC-1 cells in 100 μL, to achieve final effector-to-target cell ratios of 80:1, 40:1, and 20:1. The level of lymphocyte proliferation in response to phytohemagglutinin (PHA) was detected by bromodeoxyuridine (BrdU) incorporation assay. TNF-α, IL-1β, and IL-10 levels were determined in blood samples and supernatants of splenocyte preparations.Results: IP administration of dexmedetomidine significantly decreased the time of licking and biting during the first and second phases of the formalin test (p <0.001). Formalin-induced pain led to higher activity of NK cells than in sham-treated mice (p <0.05), but NK activity was not increased significantly by ip dexmedetomidine treatment. Formalin-induced pain significantly increased splenic lymphocyte proliferation (p <0.05), but dexmedetomidine did not alter this response. There was a significant increase in plasma TNF-α (p = 0.048) and IL-6 (p = 0.014) levels after formalin-induced pain. However, the differences between the responses after ip dexmedetomidine did not change significantly.Conclusions: Dexmedetomidine showed antinociceptive effect on both of acute pain phase 1 and hyperalgesic phase 2 of formalin pain model. Formalin-induced pain alters cellular immunity of spleen in mice. Dexmedetomidine attenuates the activation of NK cells under pain condition, but neither the proliferative response of the splenic lymphocytes nor the cytokine production was affected by dexmedetomidine.