Articles: neuralgia.
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The apparent failure of pudendal nerve surgery in some patients has led us to suggest the possibility of entrapment of other adjacent nerve structures, leading to the concept of inferior cluneal neuralgia. Via its numerous collateral branches, the posterior femoral cutaneous nerve innervates a very extensive territory including the posterior surface of the thigh, the infragluteal fold, the skin over the ischial tuberosity, but also the lateral anal region, scrotum or labium majus via its perineal branch. ⋯ Cluneal neuralgia constitutes a distinct entity of perineal pain, which must be identified and distinguished from pudendal neuralgia. Surgery should be performed via a transgluteal approach. A lateral ischial obstacle must be investigated, in the form of a constant fibrous expansion, which, like a retinaculum, can cause nerve entrapment.
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The number of studies on trigeminal nerve injury using animal models remains limited. A rodent model of trigeminal neuropathic pain was first developed in 1994, in which chronic constriction injury (CCI) is induced by ligation of the infraorbital nerve (IoN). This animal model has served as a major tool to study trigeminal neuropathic pain. Unfortunately, the surgical procedure in this model is complicated and far more difficult than ligation of peripheral nerves (eg, sciatic nerve). The aim of this study was to improve on the current surgical procedure of IoN ligation to induce trigeminal neuropathic pain in rats. We show that the IoN can be readily accessed through a small facial incision. CCI can be induced by ligation of a segment at the distal IoN (dIoN). This dIoN-CCI procedure is simple, minimally invasive, and time-saving. Our data show that the dIoN-CCI procedure consistently induced acute as well as chronic nociceptive behaviors in rats. Daily gabapentin treatment attenuated mechanical allodynia and reduced face-grooming episodes in dIoN-CCI rats. ⋯ The orofacial pain caused by trigeminal nerve damage is severe and perhaps more debilitating than other types of neuropathic pain. However, studies on trigeminal neuropathic pain remain limited. This is largely because of the lack of proper animal models because of the complexity of the existing surgical procedures required to induce trigeminal nerve injury. Our improved dIoN-CCI model is likely to make it more accessible to study the cellular and molecular mechanisms of neuropathic pain caused by trigeminal nerve damage.
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Pain is a common complication of herpes zoster (HZ) infection which results from reactivation of a latent varicella zoster virus (VZV). A third of HZ patients' progress to a chronic pain state known as post herpetic neuralgia (PHN), and about a quarter of these patients' have orofacial pain. The mechanisms controlling the pain responses are not understood. ⋯ VZV-induced nociception was significantly decreased after administering CNO in male rats. Nociception significantly increased concomitant with increased thalamic c-fos expression after attenuating thalamic VGAT expression. These data establish that the lateral thalamus (posterior, ventral posteromedial, ventral posterolateral and/or reticular thalamic nucleus) controls VZV-induced nociception in the orofacial region, and that GABA in this region appears to reduce the response to VZV-induced nociception possibly by gating facial pain input.
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Case Reports
Microvascular Decompression for a Patient with a Glossopharyngeal Neuralgia: A Technical Note.
The glossopharyngeal neuralgia (GPN) constitutes approximately 0.2-1.3% of all facial pain syndromes. The GPN is a syndrome of neuropathic pain characterized by paroxysmal pain episodes localized in the posterior tongue, tonsil, throat, or external ear canal. The first-line treatment is pharmacological. Patients who are refractory to medical therapy can be treated surgically with microvascular decompression (MVD) or sectioning the IX nerve and the upper rootlets of the X nerve. We aim to describe the technical nuances of MVD of the IX cranial nerve with a targeted inferior mini-craniotomy in a patient with a neurovascular compression.
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Antagonism of the P2X3 receptor is one of the potential therapeutic strategies for the management of neuropathic pain because P2X3 receptors are predominantly localized on small to medium diameter C- and Aδ-fiber primary afferent neurons, which are related to the pain-sensing system. In this study, 5-hydroxy pyridine derivatives were designed, synthesized, and evaluated for their in vitro biological activities by two-electrode voltage clamp assay at hP2X3 receptors. ⋯ However, because compound 29 was inactive by intraperitoneal administration in neuropathic pain animal models due to low cell permeability, the corresponding methyl ester analogue, 28, which could be converted to compound 29 in vivo, was investigated as a prodrug concept. Intravenous injection of compound 28 resulted in potent antiallodynic effects, with ED50 values of 2.62 and 2.93 mg/kg in spinal nerve ligation and chemotherapy-induced peripheral neuropathy rats, respectively, indicating that new drug development targeting the P2X3 receptor could be promising for neuropathic pain, a disease with high unmet medical needs.