Peripheral Nerve Stimulation for Painful Mononeuropathy Secondary to Leprosy: A 12-Month Follow-Up Study.

OBJECTIVE: Leprosy affects approximately 10-15 million patients worldwide and remains a relevant public health issue. Chronic pain secondary to leprosy is a primary cause of morbidity, and its treatment remains a challenge. We evaluated the feasibility and safety of peripheral nerve stimulation (PNS) for painful mononeuropathy secondary to leprosy that is refractory to pharmacological therapy and surgical intervention (decompression). METHODS: Between 2011 and 2013 twenty-three patients with painful mononeuropathy secondary to leprosy were recruited to this prospective case series. All patients were considered to be refractory to optimized conservative treatment and neurosurgical decompression. Pain was evaluated over the course of the study using the neuropathic pain scale and the visual analog scale for pain. In the first stage, patients were implanted with a temporary electrode that was connected to an external stimulator, and were treated with PNS for seven days. Patients with 50% or greater pain relief received a definitive implantation in the second stage. Follow-ups in the second stage were conducted at 1, 3, 6, and 12 months. RESULTS: After seven days of trial in the first stage, 10 patients showed a pain reduction of 50% or greater. At 12-month follow-up in the second stage, 6 of the 10 patients who underwent permanent device implantation showed a pain reduction of 50% or greater (75% reduction on average), and two patients showed a 30% reduction in pain. Two patients presented with electrode migration that required repositioning during the 12-month follow-up period. CONCLUSIONS: Our data suggest that PNS might have significant long-term utility for the treatment of painful mononeuropathy secondary to leprosy. Future studies should be performed in order to corroborate our findings in a larger population and encourage the clinical implementation of this technique.

[Effects of lycium barbarum polysaccharide on formation of traumatic neuroma and pain after transection of sciatic nerve in rats].

OBJECTIVE: To investigate the effects of lycium barbarum polysaccharide (LBP) on the formation of traumatic neuroma and pain after transection of sciatic nerve in rats. METHODS: Forty Sprague-Dawley (SD) rats, weighing 200-220 g, half male and half female, were allocated into 2 groups randomly: LBP group and control group (n = 20 per group). The right sciatic nerves were transected and 2 cm sciatic nerve were removed in all rats of the 2 groups. LBP were intraperitoneally injected in a volume of 10 mg/(kgd) in the LBP group, while the same volume normal saline (NS) in the control group for 28 days. The deficiency of toenail and toe were observed to estimate the autophagy of the operated limb. Light microscope and transmission electron microscope were used to observe the formation of traumatic neuroma after transection of sciatic nerve. RESULTS: Autophagy was observed in 5 rats (25%) of LBP group and in 12 rats (60%) of control group at 4 weeks, showing significant difference (P < 0.05). Neuroma formed in 8 rats (40%) of LBP group and in 16 rats (80%) of control group, showing significant difference (P < 0.05). The observation of light microscope showed that there were unorganized growth cells in the neuroma, infiltrated muscle cells, the regeneration of axons and ensheathing cells to form small patch and funicular structure in the control group, while in the LBP group there were less proliferation of nerve fibers with a regular arrangement. Transmission electron microscope showed that there were lots of axons in nerve tumour, more fusoid fibroblasts, more collagen fiber, and hyperplasia and degenerated myelin sheath in the control group, while in the LBP group there were less myelin sheath in the proximal end of injuring nerves, less Schwann cells and fibroblasts, and sparsed collagen fibers. CONCLUSION: LBP can inhibit autophagy and the formation of traumatic neuroma after transection of sciatic nerve in rats.

Activity of new NOP receptor ligands in a rat peripheral mononeuropathy model: potentiation of morphine anti-allodynic activity by NOP receptor antagonists.

The effect of new NOP receptor agonists and antagonists in the rat chronic constriction injury model was investigated. Intraperitoneally administered NOP receptor agonist SR14150 and antagonists SR16430 and SR14148, had no effect on mechanical allodynia when given alone. The nonselective NOP/mu-opioid receptor agonist SR16435, however, produced an anti-allodynic response, similar to morphine and reversible by naloxone. Notably, co-administration of the NOP receptor antagonists potentiated the anti-allodynic activity of both morphine and SR16435. Increased levels of the NOP receptor are implicated in the reduced efficacy of morphine in neuropathic pain. Our results suggest the utility of NOP receptor antagonists for potentiating opioid efficacy in chronic pain.

Microvasculitic paraproteinaemic polyneuropathy and B-cell lymphoma.

Microvasculitis may play a greater part in the pathogenesis of paraproteinaemic neuropathies than is generally recognised, producing tissue destruction by convergent immune and physical mechanisms. We present a patient with a clinical syndrome of mononeuritis multiplex and a circulating IgM lambda paraprotein, in whom bone marrow aspiration revealed a lymphoplasmacytoid lymphoma. Microvasculitic changes were present in the first nerve biopsy, and the second showed extensive destruction of neural architecture and deposition of IgM-related material. A 2-stage pathogenic cascade is postulated and explored with a review of the relevant literature.