Articles: neuralgia.
-
The voltage-gated calcium channels CaV3.1-3.3 constitute the T-type subfamily, whose dysfunctions are associated with epilepsy, psychiatric disorders, and chronic pain. The unique properties of low-voltage-activation, faster inactivation, and slower deactivation of these channels support their role in modulation of cellular excitability and low-threshold firing. Thus, selective T-type calcium channel antagonists are highly sought after. ⋯ High voltage-gated calcium, as well as tetrodotoxin-sensitive and -resistant sodium, channels were unaffected by 5bk. 5bk inhibited spontaneous excitatory postsynaptic currents and depolarization-evoked release of calcitonin gene-related peptide from lumbar spinal cord slices. Notably, 5bk did not bind human mu, delta, or kappa opioid receptors. 5bk reversed mechanical allodynia in rat models of HIV-associated neuropathy, chemotherapy-induced peripheral neuropathy, and spinal nerve ligation-induced neuropathy, without effects on locomotion or anxiety. Thus, 5bk represents a novel T-type modulator that could be used to develop nonaddictive pain therapeutics.
-
Postherpetic neuralgia (PHN) is a neuropathic pain that causes a reduction in patients' quality of life. There are many topical drugs for PHN, including topical lidocaine patch, topical application of capsaicin, and others. ⋯ Compared with other topical drugs, lidocaine was the most effective and most tolerable drug to be recommended for PHN.
-
Low-back pain (LBP) pathophysiological conditions include nociceptive back pain, somatic referred pain, radicular pain (RP), and radiculopathy. Differential diagnosis is challenging; guidance may come from patients' thorough clinical history and physical examination and, particularly for lumbar RP, from the evaluation of subjective responses of injured lumbar nerves to a strain applied at the buttock (buttock applied strain [BUAS] test). ⋯ Among patients with LBP, the BUAS test showed satisfactory sensitivity, specificity, prior probability, and inter-rater reliability; thus, it may be considered a useful adjunctive tool to diagnose RP in patients with LBP. For more generalized results, more research, in clinical settings other than pain clinics, is needed.
-
Little is known about the epidemiology of neuropathic pain in primary care patients consulting with low back-related leg pain. We aimed to describe prevalence, characteristics, and clinical course of low back-related leg pain patients with and without neuropathic pain, consulting with their family doctor in the United Kingdom. ⋯ This research provides new information on the clinical course of neuropathic pain and a better understanding of neuropathic pain in low back-related leg pain patients consulting in primary care.
-
The sodium channel Nav1.7 is a master regulator of nociceptive input into the central nervous system. Mutations in this channel can result in painful conditions and produce insensitivity to pain. Despite being recognized as a "poster child" for nociceptive signaling and human pain, targeting Nav1.7 has not yet produced a clinical drug. ⋯ No changes were observed in CRMP2 mice to inflammatory, acute, or visceral pain. By contrast, in a neuropathic model, CRMP2 mice failed to develop persistent mechanical allodynia. Our study suggests that CRMP2 SUMOylation-dependent control of peripheral Nav1.7 is a hallmark of chronic, but not physiological, neuropathic pain.