Erythromelalgia is a rare neurovascular pain syndrome characterized by a triad of redness, increased temperature, and burning pain primarily in the extremities. Erythromelalgia can present as a primary or secondary form, and secondary erythromelalgia associated with a myeloproliferative disease such as essential thrombocythemia often responds dramatically to aspirin therapy, as in the present case. Herein, we describe a typical case of a 48-year-old woman with secondary erythromelalgia linked to essential thrombocythemia in the unilateral hand. As this case demonstrates, detecting and visualizing the hyperthermal area through infrared thermography of an erythromelalgic patient can assist in diagnosing the patient, assessing the therapeutic results, and understanding the disease course of erythromelalgia.
BackgroundAccumulating evidence on the causal role of spinal cord microglia activation in the development of neuropathic pain after peripheral nerve injury suggests that microglial activation inhibitors might be useful analgesics for neuropathic pain. Studies also have shown that polyamidoamine dendrimer may function as a drug delivery vehicle to microglia in the central nervous system. In this regard, we developed polyamidoamine dendrimer-conjugated triamcinolone acetonide, a previously identified microglial activation inhibitor, and tested its analgesic efficacy in a mouse peripheral nerve injury model.ResultPolyamidoamine dendrimer was delivered selectively to spinal cord microglia upon intrathecal administration. Dendrimer-conjugated triamcinolone acetonide inhibited lipoteichoic acid-induced proinflammatory gene expression in primary glial cells. In addition, dendrimer-conjugated triamcinolone acetonide administration (intrathecal) inhibited peripheral nerve injury-induced spinal cord microglial activation and the expression of pain-related genes in the spinal cord, including Nox2, IL-1β, TNF-α, and IL-6. Dendrimer-conjugated triamcinolone acetonide administration right after nerve injury almost completely reversed peripheral nerve injury-induced mechanical allodynia for up to three days. Meanwhile, dendrimer-conjugated triamcinolone acetonide administration 1.5 days post injury significantly attenuated mechanical allodynia.ConclusionOur data demonstrate that dendrimer-conjugated triamcinolone acetonide inhibits spinal cord microglia activation and attenuates neuropathic pain after peripheral nerve injury, which has therapeutic implications for the treatment of neuropathic pain.
Background: Herpetic disorders cause pain and skin lesion. So, asymmetric temperature of both sides of the involving dermatome has been reported in thermogram. This study examined the usefulness of infrared thermography for a predictor of post-herpetic neuralgia (PHN).Methods: Patients with acute herpes zoster who underwent nerve block were randomly selected. Biographic data, including age, gender and times of onset of the skin lesions, development of PHN, combined diseases were recorded. Infrared thermography was performed and subjective pain severity, dysesthesia and allodynia, skin lesion size were assessed.Results: The temperature differences between the lesion site and the contralateral site at lateral and posterior were significantly correlated with lesion size (P < 0.01) and the temperature differences at anterior and lateral site were correlated with duration of disease (ant: P < 0.01, lat: P < 0.05). The temperature differences were not correlated with the pain severity, dysesthesia and allodynia (P > 0.05). PHN was correlated with skin lesion size and infrared thermal imaging (P < 0.01).Conclusions: Infrared thermal imaging cannot demonstrate subjective pain objectively in herpes zoster. Short duration showed high temperature on the lesion sites compared to the contralateral sites. The patients with big skin lesions developed PHN more. The PHN can be predicted by the infrared thermal imaging as low temperature on the lesion site compared to the contralateral site.
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