Articles: neuralgia.
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Benefits of phototherapy were characterized in multiple diseases including depression, circadian rhythm disruptions, and neurodegeneration. Studies on migraine and fibromyalgia patients revealed that green light-emitting diodes (GLED) exposure provides a pragmatic and safe therapy to manage chronic pain. In rodents, GLED reversed hypersensitivity related to neuropathic pain. ⋯ PERSPECTIVE: Development of new pain management therapies, especially for HIV patients, is crucial as long-term opioid prescription is not recommended due to adverse side effects. Green light addresses this necessity. Characterizing the underlying mechanisms of this potentially groundbreaking and safe antinociceptive therapy will advance its clinical translation.
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Curr Opin Anaesthesiol · Dec 2021
ReviewScrambler therapy for noncancer neuropathic pain: a focused review.
Therapeutic methods for neuropathic are limited; available drugs can be inadequate or have adverse effects that compromise quality of life. Interest has grown in alternatives to pharmacologic therapy for neuropathic pain. We present a focused review of the literature about the relatively novel noninvasive, nonpharmacologic electrocutaneous nerve stimulation technique called scrambler therapy for treating noncancer neuropathic pain. ⋯ We present the historical perspective, mechanism of action and trial outcomes of scrambler therapy, representing an avenue for managing neuropathic pain without drugs. Well designed phase II/III clinical trials must be conducted to confirm the positive findings reported using scrambler therapy technology. If validated, scrambler therapy could be a game changer.
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Observational Study
The responsiveness of quantitative sensory testing-derived sensory phenotype to disease-modifying intervention in patients with entrapment neuropathy: a longitudinal study.
The German Research Network on Neuropathic Pain (DFNS) quantitative sensory testing (QST) method for sensory phenotyping is used to stratify patients by mechanism-associated sensory phenotype, theorised to be predictive of intervention efficacy. We hypothesised that change in pain and sensory dysfunction would relate to change in sensory phenotype. We investigated the responsiveness of sensory phenotype to surgery in patients with an entrapment neuropathy. ⋯ Quantitative sensory testing-derived sensory phenotype is sensitive to clinically important change. In an entrapment neuropathy model, sensory phenotype was associated with patient-reported symptoms and demonstrated statistically significant, clinically relevant change after disease-modifying intervention. Sensory phenotype was independent of disease severity and may reflect underlying neuropathophysiology.
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Dorsal root ganglion field stimulation (GFS) relieves evoked and spontaneous neuropathic pain by use-dependent blockade of impulse trains through the sensory neuron T-junction, which becomes complete within less than 1 minute for C-type units, also with partial blockade of Aδ units. We used this tool in the spinal nerve ligation (SNL) rat model to selectively block sensory neuron spontaneous activity (SA) of axotomized neurons at the fifth lumbar (L5) level vs blockade of units at the L4 level that remain uninjured but exposed to inflammation. In vivo dorsal root single-unit recordings after SNL showed increased SA in L5 units but not L4 units. ⋯ In addition, L5 GFS, but not L4 GFS, increased mechanical threshold of DH units during cutaneous mechanical stimulation, while L5 GFS exceeded L4 GFS in reducing evoked firing rates. Our results indicate that SA in injured neurons supports increased firing of DH wide-dynamic-range neurons, contributing to hyperalgesia, allodynia, and ongoing pain. Ganglion field stimulation analgesic effects after nerve injury are at least partly attributable to blocking propagation of this SA.
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Accumulating evidence suggests hippocampal impairment under the chronic pain phenotype. However, it is unknown whether neuropathic behaviors are related to dysfunction of the hippocampal circuitry. Here, we enhanced hippocampal activity by pharmacological, optogenetic, and chemogenetic techniques to determine hippocampal influence on neuropathic pain behaviors. ⋯ Altogether, these results imply that downregulation of the DH circuitry during chronic neuropathic pain aggravates pain-related behaviors. Conversely, activation of the DH reverses pain-related behaviors through local excitatory and opioidergic mechanisms affecting DH functional connectivity. Thus, this study exhibits a novel causal role for the DH but not the VH in controlling neuropathic pain-related behaviors.