Effects of The Remote C Fibres Stimulation Induced by Capsaicin on the Blink Reflex in Chronic Migraine

Tommaso, Marina de; Sardaro, Michele; Pecoraro, Carla; fruscolo, Olimpia Di; Serpino, Claudia; Lamberti, Paolo; Livrea, Paolo

doi:10.1111/j.1468-2982.2007.01357.x

Cited by 48 publications

(64 citation statements)

References 28 publications

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“…The controls and migraineurs without aura did not exhibit any reflex alterations. These results may suggest a failure of the diffuse noxious inhibitory control system and a disturbed control of the trigeminal reflex at the central level, linked with migraine frequency (De Tommaso et al 2007). …”

Section: Blink Reflexmentioning

confidence: 96%

Where does a migraine attack originate? In the brainstem

et al. 2012

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Migraine is a common, paroxysmal, highly disabling primary headache disorder. The origin of migraine attacks is enigmatic. Numerous clinical and experimental results suggest that the activation of distinct brainstem nuclei is crucial in its pathogenesis, but the primary cause of this activation is not fully understood. We conclude that the initialization of a migraine attack can be explained as an altered function of the neuronal elements of the brainstem nuclei. In light of our findings and the literature data, we can assume that migraine is a subcortical disorder of a specific brainstem area.

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Section: Blink Reflexmentioning

confidence: 96%

Where does a migraine attack originate? In the brainstem

et al. 2012

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“…In line with this, Sandrini et al (2006) found CPM dysfunction in patients suffering from migraine. Likewise, Tommaso et al (2007) also found CPM dysfunction in chronic migraineurs; however, patients with more episodic migraine without aura did not show this deficit. Interestingly, Perrotta et al (2010) also found no CPM dysfunction in patients with episodic migraine compared with healthy controls (CPM deficits were apparent only in patients with medication-overuse headache).…”

Section: Introductionmentioning

confidence: 96%

Endogenous pain inhibition during menstrual cycle in migraine

Teepker

Kunz

Peters

et al. 2014

European Journal of Pain

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Background: Migraine is a common headache disorder that can vary menstrually in women and has been linked to an impairment of endogenous pain inhibitory systems. One of these endogenous pain inhibitory systems, namely conditioned pain modulation (CPM; formerly diffuse noxious inhibitory controls-like), has been shown to be affected by the menstrual cycle. The aim of this study was to examine CPM over the menstrual cycle in migraineurs and healthy controls. Methods: Twenty healthy women and 32 female migraineurs were examined on days 1, 4, 14 and 22 of the menstrual cycle. Detection and pain thresholds for electrocutaneous stimuli were first assessed at baseline. Second, tonic heat stimuli were applied concurrently to the electrical stimuli, and the difference in electrical thresholds to baseline were analysed as indicating CPM inhibition. Results: Migraineurs revealed higher detection thresholds than the control group but similar pain thresholds for the electrical current. Likewise, pain sensitivity for tonic heat stimulation also did not differ between groups. With regard to our main hypotheses, we found that CPM inhibition neither differed between migraineurs and healthy volunteers nor varied over the menstrual cycle. Conclusions: Our findings suggest that CPM inhibition is not altered in female migraineurs; thus, it is questionable whether CPM really plays a role in the development of migraine or whether migraine leads to a dysfunctional CPM inhibition.

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“…TRPV1 is expressed by keratinocytes in the epidermis as well as by fibroblasts, endothelial cells and immunocompetent cells in the dermis [7,14]. However, of main relevance in the context of analgesic effects is the anatomic fitting of the skin layers especially with C and Aδ pain fibres, which are established in the dermis but grow into the vital epidermis [59,60]. With regard to an optimized bioavailability of capsaicin, the mean effect concentration (EC 50 ) at mechanoheat-sensitive C fibres of approximately 350 nmol/l as well as toxicological in vitro data about apoptosis induction at >5 µmol/l over 6 h for keratinocytes and >5 µmol/l over 24 h for cutaneous fibroblasts need to be considered [10,61,62].…”

Section: Discussionmentioning

confidence: 99%

Cutaneous Drug Delivery of Capsaicin after in vitro Administration of the 8% Capsaicin Dermal Patch System

Wohlrab

Neubert²,

Heskamp³

et al. 2014

Skin Pharmacol Physiol

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Objective: Epicutaneous application of capsaicin causes a long-lasting analgesic effect by binding to the membrane transient receptor potential vanilloid 1 (TRPV1) on mechanoheat-sensitive C and Aδ fibres, changing axonal integrity and inhibiting neurogenic inflammatory processes. To date, no information is available regarding the cutaneous drug delivery of capsaicin following patch application. Methods: Using a Franz diffusion cell, the cutaneous concentration-time profiles 30, 60 and 90 min after application of a patch containing 8% capsaicin (640 µg/cm²) on ex vivo thin (mamma) and thick (plantar) human skin were investigated at 32°C, and additionally at 42°C for thin skin and 10°C for thick skin. An HPLC-MS method was used for the analytic detection of capsaicin. Results: The results show that already after a 30-min application of the 8% capsaicin patch, an equilibrium reservoir can be found in the stratum corneum in both thick and thin skin. Under physiological temperature conditions, a sufficient bioavailability of capsaicin in the cutaneous target compartments can be found. Raising the temperature to 42°C has no relevant impact on the concentration-time profile, while reducing the temperature to 10°C leads to a significantly lower bioavailability. Conclusion: After 30 min of application, a sufficient cutaneous bioavailability of capsaicin is reached in thick as well as thin skin. Whether shorter application times may suffice to achieve therapeutic effectiveness requires further investigation. © 2014 S. Karger AG, Basel

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Effects of The Remote C Fibres Stimulation Induced by Capsaicin on the Blink Reflex in Chronic Migraine

Cited by 48 publications

References 28 publications

Where does a migraine attack originate? In the brainstem

Where does a migraine attack originate? In the brainstem

Endogenous pain inhibition during menstrual cycle in migraine

Cutaneous Drug Delivery of Capsaicin after in vitro Administration of the 8% Capsaicin Dermal Patch System

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