| 1. |
- Bohm-Starke, Nina, et al.
(author)
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Decreased mechanical pain threshold in the vestibular mucosa of women using oral contraceptives : a contributing factor in vulvar vestibulitis?
- 2004
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In: Journal of reproductive medicine. - Chicago : The Journal. - 0024-7758 .- 1943-3565. ; 49:11, s. 888-892
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Journal article (peer-reviewed)abstract
- Objective:To analyze possible differences in somatosensory perception in the vestibular mucosa in healthy women associated with the use of oral contraceptives.Study design:Quantitative sensory tests were performed on the vestibular mucosa in 39 healthy women. Twenty women were using oral contraceptives containing 30-40 µg ethinyl estradiol combined with various progestins; 19 women with regular menstrual periods not using oral contraceptives served as controls. The testing included mechanical and heat pain thresholds and detection thresholds of warmth and cold in the anterior and posterior part of the vestibule.Results:Significant lower mechanical pain thresholds were observed in both areas tested in women using oral contraceptives. The most sensitive area was the posterior vestibule in the group using oral contraceptives with a mechanical pain threshold of 72±10 (±SEM) mN as compared to 161±3 mN (p<0.01), in the controls. The result of the thermotest showed no significant differences between the groups.Conclusion:Oral contraceptives may induce increased sensitivity in the vestibular mucosa in healthy women and might be one contributing factor in the development of vulvar vestibulitis.
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| 2. |
- Jörum, E., et al.
(author)
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Catecholamine-induced excitation of nociceptors in sympathetically maintained pain
- 2007
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In: Pain. - : Ovid Technologies (Wolters Kluwer Health). - 0304-3959 .- 1872-6623. ; 127:3, s. 296-301
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Journal article (peer-reviewed)abstract
- Sympathetically maintained pain could either be mediated by ephaptic interactions between sympathetic efferent and afferent nociceptive fibers or by catecholamine-induced activation of nociceptive nerve endings. We report here single fiber recordings from C nociceptors in a patient with sympathetically maintained pain, in whom sympathetic blockade had repeatedly eliminated the ongoing pain in both legs. We classified eight C-fibers as mechano-responsive and six as mechano-insensitive nociceptors according to their mechanical responsiveness and activity-dependent slowing of conduction velocity (latency increase of 0.5±1.1 vs. 7.1±2.0ms for 20 pulses at 0.125Hz). Two C-fibers were activated with a delay of several seconds following strong endogenous sympathetic bursts; they were also excited for about 3min following the injection of norepinephrine (10μl, 0.05%) into their innervation territory. In these two fibers, a prolonged activation by injection of low pH solution (phosphate buffer, pH 6.0, 10μl) and sensitization of their heat response following prostaglandin E2 injection were recorded, evidencing their afferent nature. Moreover, their activity-dependent slowing was typical for mechano-insensitive nociceptors. We conclude that sensitized mechano-insensitive nociceptors can be activated by endogenously released catecholamines and thereby may contribute to sympathetically maintained pain. No evidence for ephaptic interaction between sympathetic efferent and nociceptive afferent fibers was found.
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| 3. |
- Namer, Barbara, et al.
(author)
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Endothelin1 activates and sensitizes human C-nociceptors
- 2007
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In: Pain. - Amsterdam : Elsevier. - 0304-3959 .- 1872-6623. ; 137:1, s. 41-49
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Journal article (peer-reviewed)abstract
- Microneurography was used to record action potentials from afferent C-fibers in cutaneous fascicles of the peroneal nerve in healthy volunteers. Afferent fibers were classified according to their mechanical responsiveness to von Frey stimulation (75 g) into mechano-responsive and mechano-insensitive nociceptors. Various concentrations of Endothelin1 (ET1) and Histamine were injected into the receptive fields of C-fibers. Activation and heat sensitization were monitored. Axon reflex flare and psychophysical ratings were assessed after injection of ET1 and codeine into the forearms after pre-treatment with an H1 blocker or sodium chloride. 65% of mechanosensitive nociceptors were activated by ET1. One-third showed long lasting responses (>15 min). In contrast, none of thirteen mechano-insensitive fibers were activated. Sensitization to heat was observed in 62% of mechanosensitive and in 46% of mechano-insensitive fibers. Injection of ET1 produced a widespread axon reflex flare, which was suppressed by pre-treatment with an H1 receptor blocker. In addition, pain sensations were induced more often than itching by ET1 in contrast to codeine. No wheal was observed after injection of ET1. Both itching and pain were decreased after H1 blocker treatment. In summary: (1) In humans ET1 activates mechanosensitive, but not mechano-insensitive, nociceptors. (2) Histamine released from mast cells is not responsible for all effects of ET1 on C-nociceptors. (3) ET1 could have a differential role in pain compared to other chemical algogens which activate additionally or even predominantly mechano-insensitive fibers.
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| 4. |
- Namer, Barbara, et al.
(author)
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Specific changes in conduction velocity recovery cycles of single nociceptors in a patient with erythromelalgia with the I848T gain-of-function mutation of Na(v)1.7
- 2015
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In: Pain. - : Ovid Technologies (Wolters Kluwer Health). - 0304-3959 .- 1872-6623. ; 156:9, s. 1637-1646
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Journal article (peer-reviewed)abstract
- Seven patients diagnosed with erythromelalgia (EM) were investigated by microneurography to record from unmyelinated nerve fibers in the peroneal nerve. Two patients had characterized variants of sodium channel Na(v)1.7 (I848T, I228M), whereas no mutations of coding regions of Na(v)s were found in 5 patients with EM. Irrespective of Na(v)1.7 mutations, more than 50% of the silent nociceptors in the patients with EM showed spontaneous activity. In the patient with mutation I848T, all nociceptors, but not sympathetic efferents, displayed enhanced early subnormal conduction in the velocity recovery cycles and the expected late subnormality was reversed to supranormal conduction. The larger hyperpolarizing shift of activation might explain the difference to the I228M mutation. Sympathetic fibers that lack Na(v)1.8 did not show supranormal conduction in the patient carrying the I848T mutation, confirming in human subjects that the presence of Na(v)1.8 crucially modulates conduction in cells expressing EM mutant channels. The characteristic pattern of changes in conduction velocity observed in the patient with the I848T gain-of function mutation in Na(v)1.7 could be explained by axonal depolarization and concomitant inactivation of Na(v)1.7. If this were true, activity-dependent hyperpolarization would reverse inactivation of Na(v)1.7 and account for the supranormal CV. This mechanism might explain normal pain thresholds under resting conditions.
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