Journal of the peripheral nervous system : JPNS
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J. Peripher. Nerv. Syst. · Jun 2012
Suppression of neurokinin-1 receptor in trigeminal ganglia attenuates central sensitization following inflammation.
This study examined whether local application of a neurokinin-1 (NK1) receptor antagonist into the trigeminal ganglia (TRGs) modulates hyperexcitability of trigeminal spinal nucleus caudalis (SpVc) wide-dynamic range (WDR) neuron activity innervating both the temporomandibular joint (TMJ) region and facial skin following TMJ inflammation. Extracellular single unit recording combined with multibarrel electrodes was used. TMJ inflammation was induced by the injection of complete Freund's adjuvant (CFA). ⋯ The spontaneous WDR activities were current-dependently decreased by local iontophoretic application of an NK1 receptor antagonist into the TRGs after 1 and 2 days of inflammation. The firing frequency of WDR neurons and threshold evoked by mechanical stimulation of facial skin returned to control levels by application of the NK1 receptor antagonist into TRGs after 1 day, but not 2 days, of inflammation. These results suggest that in the early stages of inflammation suppression of the NK1 receptor mechanism in TRGs may prevent central sensitization of SpVc nociceptive neurons.
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Diabetic neuropathy comprises disorders of peripheral nerve in diabetes patients after exclusion of other disorders and can be focal or diffuse. The focal diabetic neuropathies tend to resolve spontaneously and are treated by reassurance, physiotherapy and analgesia for painful symptoms. ⋯ In contrast, a recent evidence-based guideline shows that effective treatments for painful DSP include: pregabalin, amitriptyline, duloxetine, venlafaxine, gabapentin, opioids, nitrate sprays, capsaicin, and transcutaneous electrical nerve stimulation. The choice of treatment is guided by the clinical status of the individual patient.
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J. Peripher. Nerv. Syst. · Dec 2011
Small fibers in Fabry disease: baseline and follow-up data under enzyme replacement therapy.
Fabry disease (FD) is an X-linked lysosomal storage disorder which may lead to impaired peripheral nerve function, mostly affecting small nerve fibers, and to neuropathic pain. Characteristics of the neuropathy associated with FD and the covariates for its development and temporal course have not been described in a large cohort. We studied small fiber function and morphology in 120 Fabry patients at baseline and in subgroups of these until 4-year follow-up. ⋯ Group means for IENFD did not improve under enzyme replacement therapy (ERT), but IENFD in the back increased under ERT in 4/15 patients with good renal function and clinical improvement. Cutaneous cytokine gene expression did not differ from controls. We conclude that ERT may improve proximal skin innervation in patients with good renal function, but does not protect small fiber function in men with impaired renal function.
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J. Peripher. Nerv. Syst. · Dec 2011
The ology of neuropathy: an integrative review of the role of neuroinflammation and TNF-α axonal transport in neuropathic pain.
This 2011 Peripheral Nerve Society plenary lecture reviews the role of axonal transport in neuroimmune communication following peripheral nerve injury, linking focal changes in Schwann cell activation and release of the proinflammatory cytokine tumor necrosis factor-alpha (TNF-α) with subsequent activation and sensitization of ascending sensory neurons and glia which culminate in the neuropathic pain state. New data demonstrate that axonally transported (biotinylated) TNF-α activates and localizes with dorsal horn astrocytes within 96 h after injection into sciatic nerve, and that glial fibrillary acidic protein (GFAP) activation in these glial cells is diminished in TNF receptor 1 knockout mice. The pathophysiology, neuropathology and molecular biology of Wallerian degeneration are also reviewed from a perspective that links it to upregulation of proinflammatory cytokines and the development of neuropathic pain states. Finally, insights into neuroimmune communication provide rationale for new therapy based on interference with the processes of Wallerian degeneration, cytokine signaling and TNF-α protein sequestration.