Articles: neuralgia.
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We provide an up-to-date review of the pharmacological treatment of neuropathic pain with emphasis on the latest evidence-based recommendations for its pharmacological treatment. Drugs proposed as first line include tricyclic antidepressants (particularly amitriptyline), serotonin-norepinephrine reuptake inhibitors (particularly duloxetine), pregabalin and gabapentin. ⋯ Third line treatments include strong opioids and botulinum toxin A (for peripheral neuropathic pain). Perspectives include the development of new compounds and a more personalized therapeutic approach, which is made possible by recent progress in the assessment and understanding of neuropathic pain.
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Our aim was to investigate the differences in pressure sensitivity over musculoskeletal and nerve symptomatic and distant areas between individuals with plantar heel pain and healthy subjects and to determine the relationship between sensitivity to pressure pain, foot pain, and fascia thickness. Thirty-five patients with unilateral chronic plantar heel pain and 35 matched healthy controls participated. Pressure pain thresholds (PPTs) were assessed bilaterally over several nerve trunks (median, radial, ulnar, common peroneal, tibial, and sural nerve trunks) and musculoskeletal structures (calcaneus, medial gastrocnemius, tibialis anterior, and second metacarpal) by an assessor blinded to the subject's condition. ⋯ This study found widespread pressure pain hypersensitivity over both nerve trunks and musculoskeletal structures in individuals with unilateral chronic plantar heel pain, suggesting the presence of a central altered central nociceptive pain processing. Pressure hypersensitivity over nerve trunks on the lower extremity was associated with higher pain intensity and related disability. PERSPECTIVES: This study found widespread pressure hypersensitivity over both nerve trunks and musculoskeletal structures in individuals with unilateral chronic plantar heel pain, as a manifestation of a centrally altered central nociceptive pain processing.
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Clinical studies indicate that cannabidiol (CBD), the primary nonaddictive component of cannabis that interacts with the serotonin (5-HT)1A receptor, may possess analgesic and anxiolytic effects. However, its effects on 5-HT neuronal activity, as well as its impact on models of neuropathic pain are unknown. First, using in vivo single-unit extracellular recordings in rats, we demonstrated that acute intravenous (i.v.) increasing doses of CBD (0.1-1.0 mg/kg) decreased the firing rate of 5-HT neurons in the dorsal raphe nucleus, which was prevented by administration of the 5-HT1A antagonist WAY 100635 (0.3 mg/kg, i.v.) and the TRPV1 antagonist capsazepine (1 mg/kg, i.v.) but not by the CB1 receptor antagonist AM 251 (1 mg/kg, i.v.). ⋯ Seven days of treatment with CBD reduced mechanical allodynia, decreased anxiety-like behavior, and normalized 5-HT activity. Antiallodynic effects of CBD were fully prevented by capsazepine (10 mg/kg/day, s.c., for 7 days) and partially prevented by WAY 100635 (2 mg/kg/day, s.c., for 7 days), whereas the anxiolytic effect was blocked only by WAY. Overall, repeated treatment with low-dose CBD induces analgesia predominantly through TRPV1 activation, reduces anxiety through 5-HT1A receptor activation, and rescues impaired 5-HT neurotransmission under neuropathic pain conditions.