Articles: neuralgia.
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External nasal neuralgia is a rare syndrome of atypical facial pain for which there is limited reports in the scientific literature. We aim to review diagnosis and provide an update on treatments for this rare condition. ⋯ Etiology has been documented as post-traumatic due to direct trauma to the nose area and in few case reports, idiopathic. Sensory innervation of the nose arises from the ophthalmic and maxillary divisions of the trigeminal nerve. Direct injury to the nerve appears to be the etiology of post-traumatic external nasal neuralgia. Pathophysiology for idiopathic nasal neuralgia is poorly understood but it appears to be of a central etiology given lack of response to intranasal anesthetics. Pain can be episodic with episodes of tingling sensation lasting up to 30 min, two to three times per day, but for some patients it can be constant bruised sensation of mild to moderate pain. Diagnostic workup including magnetic resonance imaging of brain and computerized tomography of the sinuses are usually negative, but there have been few cases of a nasal contact point. Routine blood work including erythrocyte sedimentation rate is negative. Treatment for this rare condition is varied with very few patients responding to tricyclic antidepressants, specifically amitriptyline. Another medication used as prevention is pregabalin with good results as well. Most patients respond to nerve blockade with local anesthetic to the external nasal nerve and sphenopalatine ganglion block and radiofrequency ablation. More reports of this condition need to be published in the scientific literature to assist with proper diagnosis and treatment of this condition.
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More evidence suggests that dorsal spinal cord microglia is an important site contributing to CB2 receptor-mediated analgesia. The upregulation of P2Y12 and P2Y13 purinoceptors in spinal dorsal horn microglia is involved in the development of pain behavior caused by peripheral nerve injury. However, it is not known whether the expression of P2Y12 and P2Y13 receptors at spinal dorsal horn will be influenced after CB2 receptor activation in neuropathic pain rats. ⋯ In CCI- and ADPbetaS-treated rats, AM1241 pretreatment could efficiently activate CB2 receptor, while inhibiting p38MAPK and NF-kappaB activation in the dorsal spinal cord. CB2 receptor stimulation decreased P2Y13 receptor expression via p38MAPK/NF-kappaB signaling. On the other hand, CB2 receptor activation decreased P2Y12 receptor expression via p38MAPK-independent NF-kappaB signaling pathway.
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Individuals experiencing neuropathic pain (NP) after spinal cord injury (SCI) present with a variety of pain descriptors in different combinations and at different intensities. These sensory features form distinct patterns, known as sensory symptom profiles. ⋯ Classification of SCI-NP patients into the 5 groups identified in the present study based on their distinct sensory symptom profiles may allow identification of those most likely to respond to a specific analgesic approach.
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Experimental neurology · Sep 2017
Exploring acute-to-chronic neuropathic pain in rats after contusion spinal cord injury.
Spinal cord injury (SCI) causes chronic pain in 65% of individuals. Unfortunately, current pain management is inadequate for many SCI patients. Rodent models could help identify how SCI pain develops, explore new treatment strategies, and reveal whether acute post-SCI morphine worsens chronic pain. ⋯ Our data show that specific rat contusion SCI models cause neuropathic pain. Further, chronic neuropathic pain elicited by these contusion SCIs was not amplified by our course of early post-trauma morphine. Using clinically relevant rat models of SCI could help identify novel pain management strategies.
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To evaluate how closely neuropathic-like ocular pain (NOP) symptoms align with a metric of central sensitisation (ie, the presence of persistent ocular pain after topical anaesthetic placement) in individuals with dry eye (DE) symptoms. ⋯ Individuals with DE symptoms and persistent ocular pain after topical proparacaine (a marker of central sensitisation to pain) more frequently report NOP-like symptoms and demonstrate increased sensitivity to evoked pain.