Articles: neuralgia.
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Injury can lead to devastating and often untreatable chronic pain. While acute pain perception (nociception) evolved more than 500 million years ago, virtually nothing is known about the molecular origin of chronic pain. Here we provide the first evidence that nerve injury leads to chronic neuropathic sensitization in insects. ⋯ Conversely, disruption of GABA signaling was sufficient to trigger allodynia without injury. Last, we identified the conserved transcription factor twist as a critical downstream regulator driving GABAergic cell death and neuropathic allodynia. Together, we define how injury leads to allodynia in insects, and describe a primordial precursor to neuropathic pain may have been advantageous, protecting animals after serious injury.
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The complex neuroimmunological interactions mediated by chemokines are suggested to be responsible for the development of neuropathic pain. The lack of knowledge regarding the detailed pathomechanism of neuropathy is one reason for the lack of optimally efficient therapies. Recently, several lines of evidence indicated that expression of CCR2 is increased in spinal cord neurons and microglial cells after peripheral nerve injury. ⋯ Additionally, we showed for the first time that intrathecal injection of CCL2 and CCL7 neutralizing antibodies not only attenuated CCI-induced pain-related behaviors in mice but also augmented the analgesia induced by morphine and buprenorphine. In vitro studies suggest that both microglia and astrocytes are an important cellular sources of the examined chemokines. Our results revealed the crucial roles of CCL2 and CCL7, but not CCL12, in neuropathic pain development and indicated that pharmacological modulation of these factors may serve as a potential therapeutic target for new (co)analgesics.
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Randomized Controlled Trial
Repetitive Transcranial Magnetic Stimulation at Different Frequencies for Postherpetic Neuralgia: A Double-Blind, Sham-Controlled, Randomized Trial.
Repetitive transcranial magnetic stimulation (rTMS) at 5 Hz and 10 Hz is effective in improving pain, sleep quality, and anxiety among patients with postherpetic neuralgia (PHN). But it has not been reported which frequency is more effective and which frequency is safer. ⋯ Repetitive transcranial magnetic stimulation, postherpetic neuralgia, pain evaluation.
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Randomized Controlled Trial
High-Voltage, Long-Duration Pulsed Radiofrequency on Gasserian Ganglion Improves Acute/Subacute Zoster-Related Trigeminal Neuralgia: A Randomized, Double-Blinded, Controlled Trial.
Trigeminal postherpetic neuralgia is a severe neuropathic pain and often refractory to existing treatment, it develops secondary to herpes zoster-infected Gasserian ganglion. Therefore, it is important to prevent the transition of acute/subacute zoster-related pain to trigeminal postherpetic neuralgia. Despite numerous studies, the optimal intervention that reduces trigeminal postherpetic neuralgia incidence is still unknown. ⋯ Pulsed radiofrequency, zoster-related trigeminal neuralgia, visual analog scale, 36-Item Short Form Health Survey.
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The conceptualization of placebo has changed from inactive pills to a detailed understanding of how patients' perception of receiving a treatment influences pain processing and overall treatment outcome. Large placebo effects were recently demonstrated in chronic neuropathic pain, thereby opening the question of whether placebo effects also apply to orofacial neuropathic pain. ⋯ Orofacial neuropathic pain is a new research area, and we review the status on definition, diagnosis, mechanisms, and pharmacologic treatment of neuropathic pain after trigeminal nerve injury, as this condition may be especially influenced by placebo factors. Finally, we have a detailed discussion of how knowledge of placebo mechanisms may help improve the understanding, diagnosis, and treatment of orofacial neuropathic pain, and we illustrate pitfalls and opportunities of applying this knowledge to the test of dental treatments.