Pain
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We performed a prospective study in 32 patients with Guillain-Barré syndrome (GBS) or its variants to correlate intraepidermal nerve fiber density (IENFD) at the distal leg and lumbar region with pain, autonomic dysfunction, and outcome. In the acute phase, IENFD was reduced in 60% and 61.9% of patients at the distal leg and lumbar region, respectively. In the acute phase, 43.7% of patients complained of neuropathic pain. ⋯ Double and triple staining confocal microscope studies showed diffuse damage of myelinated dermal nerves along with axonal degeneration, and mononuclear cell infiltration. Unmyelinated and myelinated skin nerves are diffusely affected in GBS and its variants, including the pure motor form. IENFD declines early, remains low over time, correlates with pain severity in the acute phase, and may predict long-term disability.
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The facial expression of pain plays a crucial role in pain communication and pain diagnostics. Despite its importance, it has remained unknown which dimensions of pain (sensory and/or affective) are encoded in the face. To answer this question, we used a well-established cognitive strategy (suggestions) to differentially modulate the sensory and affective dimensions of pain and investigate the effect of this manipulation on facial responses to experimental pain. ⋯ Furthermore, suggestions for either increased pain affect or pain sensation produced selective modulations in facial response patterns, with facial movements around the eyes mostly encoding sensory aspects, whereas movements of the eyebrows and of the upper lip were closely associated with the affective pain dimension. The facial expression of pain is a multidimensional response system that differentially encodes affective and sensory pain qualities. This differential encoding might have evolved to guarantee that the specific characteristics of one's pain experience are facially communicated, thereby ensuring adequate help and support from others.
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Menthol is a natural compound of plant origin known to produce cool sensation via the activation of the TRPM8 channel. It is also frequently part of topical analgesic drugs available in a pharmacy, although its mechanism of action is still unknown. Compelling evidence indicates that voltage-gated Na(+) channels are critical for experiencing pain sensation. ⋯ In current clamp recordings, menthol inhibited firing at high-frequency stimulation with minimal effects on normal neuronal activity. We found that low concentrations of menthol cause analgesia in mice, relieving pain produced by a Na(+) channel-targeting toxin. We conclude that menthol is a state-selective blocker of Nav1.8, Nav1.9, and TTX-sensitive Na(+) channels, indicating a role for Na(+) channel blockade in the efficacy of menthol as topical analgesic compound.
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Murine models of osteoarthritis (OA) provide a potentially powerful tool to elucidate mechanisms responsible for OA pain. However, few studies have examined pain behaviours in relevant OA models in mice. We have therefore characterized the time course and pharmacological sensitivities of pain-related behaviours in a model of OA in C57Bl/6 mice induced by partial medial meniscectomy. ⋯ In contrast, other analgesic drugs (paracetamol, gabapentin, and tramadol) had selective effects on only 1 or 2 modalities. Pain levels fluctuated during the second phase, with transient periods of reduced pain. At these times, underlying hypersensitivities could be unmasked by administration of naloxone, indicating that reduced pain was due to endogenous opioids.