The effect of botulinum neurotoxin type A (BoNTA) on glutamate-evoked temporalis muscle pain and vasomotor responses was investigated in healthy men and women over a 60 day time course. Subjects participated in a pre-BoNTA session where their responses to injection of glutamate (1 M, 0.2 mL) and saline (0.2 mL) into the temporalis muscles were assessed. On Day 1, BoNTA (5 U) was injected into one temporalis muscle and saline into the contralateral temporalis muscle, in a randomized order. Subjects then received intramuscular injections of glutamate (1 M, 0.2 mL) into the left and right temporalis muscles at 3 h and subsequently 7, 30 and 60 days post-injection of BoNTA. Pain intensity, pain area, and neurogenic inflammation (skin temperature and skin blood perfusion) were recorded. Prior to BoNTA treatment, glutamate evoked significantly greater pain and vasomotor reactions (P < 0.001) than saline. BoNTA significantly reduced glutamate-evoked pain intensity (P < 0.05), pain area (P < 0.01), skin blood perfusion (P < 0.05), and skin temperature (P < 0.001). The inhibitory effect of BoNTA was present at 3 h after injection, peaked after 7 days and returned to baseline by 60 days. Findings from the present study demonstrated a rapid action of BoNTA on glutamate-evoked pain and neurogenic inflammation, which is in line with animal studies.
BACKGROUND: The analgesic action of botulinum neurotoxin type A (BoNTA) has been linked to the blockade of peripheral release of neuropeptides and neurotransmitters in animal models; however, there is no direct evidence of this in humans.OBJECTIVES: To investigate the effect of BoNTA on glutamate release in humans, using an experimental model of pain and sensitization provoked by capsaicin plus mild heat.METHODS: Twelve healthy volunteers (six men, six women) were pretreated with BoNTA (10 U) on the volar forearm and with a saline control on the contralateral side. Dermal microdialysis was applied one week later to collect interstitial samples before and after the application of a capsaicin patch (8%) plus mild heat (40°C/60 min) to provoke glutamate release, pain and vasodilation. Samples were collected every hour for 3 h using linear microdialysis probes (10 mm, 100 kD). Dialysate was analyzed for glutamate concentration. Pain intensity and skin vasomotor reactions (temperature and blood flow changes) were also recorded.RESULTS: BoNTA significantly reduced glutamate release compared with saline (P<0.05). The provoked pain intensity was lower in the BoNTA-pretreated arm (P<0.01). The reduction in pain scores was not correlated with glutamate level. Cutaneous blood flow (P<0.05), but not cutaneous temperature (P≥0.05), was significantly reduced by BoNTA. There was a correlation between glutamate level and skin blood flow (r=0.58/P<0.05) but not skin temperature (P≥0.05). No differences according to sex were observed in any response.CONCLUSIONS: The present study provided the first direct evidence supporting the inhibitory effect of BoNTA on glutamate release in human skin, which is potentially responsible for some of the analgesic action of BoNTA.
Background/aims Data on mechanical sensitivity and cutaneous allodynia in different types and phases of migraine headaches are limited. Existence and pattern of such symptoms may advance the understanding of neurophysiological mechanisms, assist clinical evaluation of the patients, and further improve management. Hence, in a large controlled study on migraine patients, mechanical sensitivity and cutaneous allodynia were assessed together with clinical markers. Methods Sensitivity to mechanical stimuli was measured in migraine patients during attack (within 2 h of headache onset), within remission phase (48–72 h after headache onset), and in pain-free periods (>5 days pain-free) in comparison with sex-and age-matched healthy controls. Pin-prick stimulation was performed in the temple region in the pain-referred side using weight-calibrated pins (8, 16, 32, 64, 128, 256 mN) in a randomized order (3 stimuli lasting 2 s), with the patient rating the sensation on a 10-point numerical scale. Pressure Pain Threshold (PPT) was assessed using a handheld algometer (1 cm2 rubber probe) over the anterior aspect of the temporal muscle (30 kPa/s, 3 times). Results Preliminary analysis revealed increased mechanical sensitivity to Pin-prick during all phases in migraine patients (n = 4) compared to healthy controls (n = 5), and likewise increased during attack and remission phases compared to pain-free periods within patients. PPT, assessing mainly muscle nociception, showed a tendency to decline during attack and remission phases (89 ± 13% and 82 ± 6%, respectively) compared to pain-free periods, with even higher sensitivity during attack and remission phases (80 ± 12% and 75 ± 11.1%, respectively) compared to healthy controls. Conclusions The current preliminary observed tendencies imply the presence of mechanical hypersensitivity in migraine patients with a notable change during attack and remission phases. This study is ongoing and no firm conclusion can be stated. In addition, alteration of mechanical sensitivity in different phases will be correlated to objective assessments of biological markers in serum specimens of the study population.
Introduction: Serum levels of several biomarkers along with sensory responsiveness were investigated in juvenile myoclonic epilepsy patients in comparison with healthy controls. Methods: Ten epileptic patients (36.1 ± 3.4 years) and ten gender- and age-matched healthy controls were recruited. Mechanical sensitivity, cold pressor tolerance and serum levels of BDNF, CGRP, PGE2, S100B and TNF-α were investigated. Results: Mechanical sensitivity to pinprick was lower in patients (p < 0.05) while cold pain tolerance threshold was higher. Serum level of BDNF was higher in patients compared with controls (p < 0.01). The same pattern was evident for CGRP (p < 0.05). Serum level of PGE2 was lower in patients (p < 0.01). Conclusion: Juvenile myoclonic epilepsy patients had an altered serum biomarker pattern and sensory perception in comparison with controls.
Background/aims:To test whether patients with Parkinsons disease (PD) have an altered sensory perception in response to painful and nonpainful stimuli and if the PD medications can influence the responses.Methods:PD patients (12) and healthy subjects (12) were recruited. Sensory perception was examined in forearms, low back, and hands by light brush, pinprick, cold pressure test (CPT), and pressure algometry.Results:A significant difference was found in PD patients in response to brush (p<0.05) and pinprick (p<0.001). Lower back and forearms were found to be more sensitive. Tolerance time in CPT was shorter in PD patients (p=0.016). Pressure pain threshold (PPT) before (p=0.011) and after (p=0.050) the CPT showed a higher sensitivity in the patients regardless of the site. No association was found between the sensory perception and the medications.Conclusion:PD patients demonstrated an altered perception to touch and pain stimuli with a general increased in pain intensity and independent of the PD medications.
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