Nociceptive Quality of the Laser-Evoked Blink Reflex in Humans

Abstract

Laser radiant-heat pulses selectively excite the free nerve endings in the superficial layers of the skin and activate mechano-thermal nociceptive afferents; when directed to the perioral or supraorbital skin, high-intensity laser pulses evoke a blink-like response in the orbicularis oculi muscle (the laser blink reflex, LBR). We investigated the functional properties (startle or nociceptive origin) of the LBR and sought to characterize its central pathways. Using high-intensity CO(2)-laser stimulation of the perioral or supraorbital regions and electromyographic (EMG) recordings from the orbicularis oculi muscles, we did five experiments in 20 healthy volunteers. First, to investigate whether the LBR is a startle response, we studied its habituation to expected rhythmic stimuli and to unexpected arrhythmic stimuli. To assess its possible nociceptive quality, we studied changes in the LBR and the R2 component of the electrical blink reflex after a lidocaine-induced supraorbital nerve block and after intramuscular injection of the opiate fentanyl and the opiate-antagonist naloxone. To characterize the central pathways for the LBR, we investigated the interaction between the LBR and the three components of the blink reflex (R1, R2, and R3) by delivering laser pulses to the perioral or supraorbital regions before or after electrical stimulation of the supraorbital nerve at various interstimulus intervals. Finally, to gain further information on the central LBR pathways, using two identical CO(2)-laser stimulators, we studied the LBR recovery curves with paired laser pulses delivered to adjacent forehead points at interstimulus intervals from 250 ms to 1.5 s. The LBR withstood relatively high-frequency rhythmic stimulations, and unexpected laser pulses failed to evoke larger responses. When lidocaine began to induce hypoalgesia (about 5 min after the injection), the LBR was abolished, whereas R2 was only partly suppressed 10 min after the injection. Fentanyl injection induced strong, naloxone-reversible, LBR suppression (the response decreased to 25.3% of predrug values at 10 min and to 4% at 20 min), whereas R2 remained appreciably unchanged. Whether directed to the perioral or supraorbital regions, preceding laser pulses strongly suppressed R2 and R3 though not R1. Conversely, preceding electrical stimuli to the supraorbital nerve suppressed the LBR. In response to paired stimuli, the LBR recovered significantly faster than R2. These findings indicate that the LBR is a nociceptive reflex, which shares part of the interneuron chain mediating the nonnociceptive R2 blink reflex, probably in the medullary reticular formation. The LBR may prove useful for studying the pathophysiology of orofacial pain syndromes.

Is the cutaneous silent period an opiate‐sensitive nociceptive reflex?

“…The prolonged inhibitory effect of finger stimulation on FDI motoneurons cannot be explained by an insufficient dose of fentanyl, because in earlier studies the same therapeutic dose suppressed the corneal reflex and the laser-evoked blink reflex. 5,26 Moreover, in our healthy volunteers, fentanyl also suppressed the R III flexion reflex. Because the risk of fentanyl-induced respiratory depression prevented us from studying dose-response curves, whether higher doses diminish the CSP remains unknown.…”

“…5,7,26 These differential effects of a narcotic-analgesic drug provide evidence that the cutaneous silent periodunlike the corneal reflex and R III flexion reflex-is not an opiate-sensitive nociceptive reflex.…”

Evidence of a Specific Spinal Pathway for the Sense of Warmth in Humans

“…In preliminary experiments, we observed that laser pulses of low intensity (4.5-7.5 mJ/mm 2 ), relatively long duration (30 -50 ms), and a large irradiated area (spot diameter: 5 mm) were optimal to elicit purely warmth sensations (C warmth input); the mean temperature was 39°C. In contrast, laser pulses of higher intensity (9 -18 mJ/mm 2 ), short duration (5-5 ms), and a small irradiated area (spot diameter: 2.5 mm) were optimal to elicit pinprick sensation (A␦ input) (Romaniello et al 2002); the mean temperature was 48°C. Stimulation sites were marked on the skin and cutaneous temperature was regulated at 30 -32°C.…”

“…In this study, A␦ fibers (type II AMH receptors) were activated with pulses of comparatively high-intensity (mean 9 -18 mJ/mm 2 ), brief duration (15 ms), and a small irradiated area (about 5 mm 2 ). Laser pulses of this kind increased the skin temperature from baseline to 48°C, i.e., above the heat threshold of the type II A␦ nociceptors (Treede et al 1995) and were perceived as a sharp pinprick, a sensation conveyed by A␦ nociceptive fibers (Arendt-Nielsen and Bjerring 1988;Romaniello et al 2002). The peak latency of the N-wave (195-210 ms) came between the latencies of the corresponding components after stimuli delivered to the face (170 ms) and hand (240 ms) with the same laser and recording apparatus (Cruccu et al 1999).…”

Differences of blink-reflex abnormalities in patients suffering from idiopathic and symptomatic trigeminal neuralgia

“…The R3 component of the reflex is not always recorded and has been described only recently [22,23]; it can be reproducibly evoked by noxious stimulation, but can probably also be elicited by innocuous stimuli [24]. Prolonged painful stimulation normally leads to suppression of the R3 component of the reflex [25]. Further structural damage to the trigeminal nerve is also associated with decreased or absent reflex activity.…”