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Cited by 39 publications
(27 citation statements)
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“…Results showed that BoNT-A improved pain intensity for a long period of time in patients with mechanical allodynia although peripheral neuropeptides levels did not modify3. BoNT-A might act preferentially through central mechanisms of action, possibly through retrograde axonal transport [6]. In addition, recent data demonstrated axonal transport for BoNT-A antinociceptive action [7] and evidence of toxin enzymatic activity in brainstem and spinal cord sensory regions suggesting that BoNT-A inhibits central pain transmission [8], mechanism that could explain the possitive results obtained in this case report.…”
Section: Discussionmentioning
confidence: 69%
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“…Results showed that BoNT-A improved pain intensity for a long period of time in patients with mechanical allodynia although peripheral neuropeptides levels did not modify3. BoNT-A might act preferentially through central mechanisms of action, possibly through retrograde axonal transport [6]. In addition, recent data demonstrated axonal transport for BoNT-A antinociceptive action [7] and evidence of toxin enzymatic activity in brainstem and spinal cord sensory regions suggesting that BoNT-A inhibits central pain transmission [8], mechanism that could explain the possitive results obtained in this case report.…”
Section: Discussionmentioning
confidence: 69%
“…Currently, preclinical models showed that local injections of BoNT-A exert its antinociceptive activity by preventing the sensory transmitter release in periphery; inhibing the release of various nociceptive mediators, such as substance P, glutamate, CGRP and the expression TRPV1 [6,7], which would justify its used for peripheral neuropatic pain. Notwithstanding, a recent double-blind randomized placebocontrolled trial assessed the sustained efficacy and neurogenic inflammation response of 2 subcutaneous administrations of BoNT-A by measuring neuropeptide levels (calcitonin generelated peptide and substance P) from skin biopsy and quantitative sensory test (QST) in patients with peripheral neuropathic pain including posttraumatic nerve lesion.…”
Section: Discussionmentioning
confidence: 99%
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“…Periarticular tissues from the arthritic TMJs released increased amounts of interleukin 1-β (IL-1β) and tumor necrosis factor α (TNFα). Treatment with botulinum toxin reduced IL-1β release but had no effect on TNFα [35]. In another study of rats with adjuvant-induced arthritis induced in the tibial-tarsal joint, mechanical and thermal hyperalgesia and TRPV1 expression in the L4-5 dorsal root ganglia (DRG) were measured.…”
Section: Botulinum Toxin Studies In Preclinical Models Of Joint Painmentioning
confidence: 99%
“…Increased c-Fos expression may indicate increased neuronal activation through harmful stimuli. In addition, data from other investigations showed that BoNT-A might have an anti-nociceptive effect by down-regulating the voltage-gated Na + -channel expression on the rat trigeminal neuralgia (30), or by reducing the peripheral release of neurotransmitters (substance P, CGRP) and pro-inflammatory cytokine IL-1β in rat temporomandibular arthritis (31). Based on this information, a possible explanation of paininhibition by BoNT-A is that it reduces the release of neurotransmitters, such as substance P and others, thus blocking the pain signal pathway.…”
Section: Mechanism Of Effect Of Bont-a and Hyaluronatementioning
confidence: 99%