Postherpetic neuralgia (PHN) is a chronic neuropathic pain syndrome that persists for more than three months after the resolution of herpes zoster rash. This condition affects approximately 30% of the population, primarily the elderly and immunocompromised individuals. PHN can be severely debilitating and often proves challenging to treat effectively. Recent advances in prevention and treatment have improved the management of PHN. The introduction of herpes zoster vaccines has shown promise in reducing the incidence of both herpes zoster and PHN. Current treatment guidelines recommend a multimodal approach, with effective therapies including tricyclic antidepressants, topical lidocaine, gabapentin, pregabalin, opioids, and topical capsaicin. This review focuses on optimizing treatment strategies and developing novel therapies to further enhance PHN management.
Trigeminal neuralgia (TN) is a highly disabling disorder characterized by very severe, brief, electric shocks, like recurrent episodes of facial pain. New diagnostic criteria classifying TN on the basis of the presence of trigeminal neurovascular conflict or an underlying neurological disorder can help better characterize patients and determine treatments. Magnetic resonance imaging using specific sequences should be a part of the diagnostic workup to detect a possible neurovascular contact and exclude secondary causes. Carbamazepine and oxcarbazepine are drugs of first choice for long-term treatment, whereas microvascular decompression is the first-line surgical management of medically refractory patients. This review aimed to review the classification, clinical features, pathophysiology, diagnostic approaches, and management of TN.
Background We aimed to investigate candidates for serological biomarkers of neuropathic pain in individuals with neuromyelitis optica spectrum disorder (NMOSD).
Methods We analyzed 38 sera samples from 38 participants with NMOSD in National Cancer Center. Neuropathic pain was evaluated using the painDETECT questionnaire. Pain with neuropathic components (painDETECT score ≥ 13) was observed in 22 participants, among whom 17 had definite neuropathic pain (painDETECT score ≥ 19). The remaining 16 participants had non-neuropathic pain (painDETECT score < 13). Serum glial fibrillary acidic protein (GFAP) levels were assessed using a single-molecule array assay. Several cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin (IL)-6, IL-10, and IL-17A, were measured by a multiplex bead-based immunoassay.
Results In comparison of NMOSD participants with neuropathic pain components (or definite neuropathic pain) and those with non-neuropathic pain, the absolute values of serum GFAP, TNF-α, IL-6, and IL-10 levels were higher in participants with neuropathic pain components (or definite neuropathic pain), but these findings did not reach statistical significance.
Conclusions Further larger-scale investigations to find reliable serological biomarkers for neuropathic pain in NMOSD are warranted.
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The etiology of neuralgia amyotrophy remains unclear. Herpes zoster induced neuralgia amyotrphy has been reported in extremely rare cases. In this case report, we describe the clinical features and electrophysiologic findings in a 68-years-old patient with neuralgia amyotrophy associated with herpes zoster infection. We suggest that brachial plexus inflammation due to viral infection may be a direct cause of reversible neuralgia amyotrophy.
Ossification of the ligamentum flavum(OLF) is not infrequent in the cervical and lumbar regions but is very rare inthe thoracic spine. We reported a 62-year-old women with left thoracic intercostal neuralgia due to an OLF. Physicaland neurological examination were normal. MRI showed an OLF with compression of the thecal sac in the posterolateralaspect of the T9-T10 level. Laminectomy and removal of the ligament resulted in marked clinical improvement. OLFis known to cause thoracic radiculomyelopathy, but presentation with intercostal neuralgia only is very rare.
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