Abstract
BackgroundThe physiology and pharmacology of activation or perception of activation of pain-coding trigeminovascular afferents in humans is fundamental to understanding the biology of headache and developing new treatments.MethodsThe blink reflex was elicited using a concentric electrode and recorded in four separate sessions, at baseline and two minutes after administration of ramped doses of diazepam (final dose 0.07 mg/kg), fentanyl (final dose 1.11 μg/kg), ketamine (final dose 0.084 mg/kg) and 0.9 % saline solution. The AUC (area under the curve, μV*ms) and the latency (ms) of the ipsi- and contralateral R2 component of the blink reflex were calculated by PC-based offline analysis. Immediately after each block of blink reflex recordings certain psychometric parameters were assessed.ResultsThere was an effect due to DRUG on the ipsilateral (F3,60 = 7.3, P < 0.001) AUC as well as on the contralateral (F3,60 = 6.02, P < 0.001) AUC across the study.A significant decrement in comparison to placebo was observed only for diazepam, affecting the ipsilateral AUC. The scores of alertness, calmness, contentedness, reaction time and precision were not affected by the DRUG across the sessions.ConclusionPrevious studies suggest central, rather than peripheral changes in nociceptive trigeminal transmission in migraine. This study demonstrates a robust effect of benzodiazepine receptor modulation of the nociception specific blink reflex (nBR) without any μ-opiate or glutamate NMDA receptor component. The nociception specific blink reflex offers a reproducible, quantifiable method of assessment of trigeminal nociceptive system in humans that can be used to dissect pharmacology relevant to primary headache disorders.
Highlights
The physiology and pharmacology of activation or perception of activation of pain-coding trigeminovascular afferents in humans is fundamental to understanding the biology of headache and developing new treatments
In clinical practice the blink reflex (BR) can be elicited when the skin innervated by the supraorbital nerve is electrically stimulated and a compound muscle action potential (CMAP) from the surface of the orbicularis
The study demonstrates an effect of benzodiazepine receptor modulation on the nociception-specific blink reflex without a detectable μ-opioid receptor or ketamine component in this model
Summary
The physiology and pharmacology of activation or perception of activation of pain-coding trigeminovascular afferents in humans is fundamental to understanding the biology of headache and developing new treatments. The physiology and pharmacology of head pain underpins understanding of the various syndromes and development of new therapies for conditions such as migraine and cluster headache. R1 is mediated by exteroceptive A-beta fibers that project to low-threshold mechanoreceptive neurons in the pons [11, 13]. This response has an ipsilateral oligosynaptic reflex arc connecting the Gasserian ganglion to the pontine sensory nucleus of the trigeminal nerve and subsequently to the ipsilateral facial nucleus [14]. Kaube and colleagues [9] developed a novel concentric electrode to allow specific study of nociceptive components of the R2 component of the reflex, the nociception-specific blink reflex (nBR)
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