scholarly journals The Effect of Trigeminal Nociceptive Stimulation on Blink Reflexes and Pain Evoked by Stimulation of the Supraorbital Nerve

Cephalalgia ◽  
2003 ◽  
Vol 23 (7) ◽  
pp. 534-540 ◽  
Author(s):  
PD Drummond

The aim of this study was to investigate the effect of painful conditioning stimuli on pain and blink reflexes to supraorbital nerve stimulation. Electromyograph activity was recorded bilaterally from the orbicularis oculi muscles in 13 normal participants in response to low (2.3 mA) and high-intensity (18.6 mA) electrical stimulation of the left supraorbital nerve before, during and after the application of ice to the left or right temple or immersion of the left hand in ice-water for 60 s. The pain evoked by the high-intensity electrical stimulus was greater during painful conditioning stimulation of the ipsilateral temple than during the recovery period afterwards, and was greater than during painful conditioning stimulation of the contralateral temple. These findings imply that spatial summation of nociceptive signals across different divisions of the trigeminal nerve can heighten pain. However, painful conditioning stimulation, particularly to the right temple, strongly suppressed the R2 component of the blink reflex to the low-intensity stimulus, and also suppressed R2 to the high-intensity stimulus. Thus, an inhibitory influence (e.g. diffuse noxious inhibitory controls) appeared to mask ipsilateral segmental facilitation of R2 during ice-induced headache. This finding contrasts with recent electrophysiological evidence of trigeminal sensitization in migraine.

2002 ◽  
Vol 87 (3) ◽  
pp. 1386-1394 ◽  
Author(s):  
A. Romaniello ◽  
J. Valls-Solé ◽  
G. D. Iannetti ◽  
A. Truini ◽  
M. Manfredi ◽  
...  

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 CO2-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 CO2-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.


PLoS ONE ◽  
2010 ◽  
Vol 5 (10) ◽  
pp. e13602 ◽  
Author(s):  
Kirsten E. Zeuner ◽  
Arne Knutzen ◽  
Asmaa Al-Ali ◽  
Mark Hallett ◽  
Günther Deuschl ◽  
...  

Cephalalgia ◽  
2014 ◽  
Vol 34 (11) ◽  
pp. 920-926 ◽  
Author(s):  
Danielle YP Haane ◽  
Peter J Koehler

Background In cluster headache, neuromodulation is offered when patients are refractory to pharmacological prophylaxis. Non-invasive peripheral neuromodulatory approaches are of interest. We will focus on these and particularly on nociception specific, transcutaneous supraorbital nerve stimulation. Methods In a study using the nociception specific blink reflex, we made a serendipitous discovery, notably the potential prophylactic effect of bilateral, time contingent, nociception specific, transcutaneous stimulation of the supraorbital nerve. Results We report on a case series of seven cluster headache patients, in whom attacks seemed to disappear during repeated stimulation of the supraorbital nerves. Three patients stopped experiencing attacks since study participation. Conclusions Bilateral, time contingent, nociception specific, transcutaneous supraorbital nerve stimulation may have a prophylactic effect in episodic and chronic cluster headache. Given its limited side effects and its non-invasive nature, further studies to investigate this potential peripheral neuromodulatory approach for both episodic and chronic cluster headache are warranted.


2002 ◽  
Vol 60 (3A) ◽  
pp. 563-565 ◽  
Author(s):  
Paulo Andre Teixeira Kimaid ◽  
Luiz Antonio Lima Resende ◽  
Heloisa Amélia de Lima Castro ◽  
Fausto Bérzin ◽  
Amilton Antunes Barreira

The blink reflex latencies and cephalometric indexes were analysed in 30 male volunteers from three different races, 10 white, 10 black, and 10 Oriental. Ages ranged from 15 to 59 years, height from 1,60 to 1,80 m, and weight from 60 to 80 kg. Blink reflexes were obtained after unilateral electric stimulation of the supraorbital nerve for quantitative analysis of 3 responses, early ipsilateral (R1), late ipsilateral (R2i) and late contralateral (R2c), obtained from the orbicularis oculi muscle. Cephalometric indexes were calculated by multiplying the ratio between the longer transverse and the longer sagital head diameters by 100. The R1, R2i and R2c latencies were consistent with other published papers revealing no differences between the different racial groups. The mean of the cephalometric indexes of each group were consistent with respective racial characteristics. This study revealed that there are no differences between R1, R2i and R2c latencies in the 3 different studied races.


Author(s):  
Gabriel M. Ronen ◽  
Jeffery R. Donat ◽  
Alan Hill

ABSTRACT:A nine-year-old girl presented with right hemifacial spasm (HFS) of 27 months duration. Stimulation of the right supraorbital nerve produced synkinesis of the ipsilateral facial muscles. Latency and amplitude of the blink reflex were equal bilaterally. Other investigations including computerized tomography (CT) were negative. Treatment with carbamazepine was not helpful. This is the third reported case of HFS in childhood.


1991 ◽  
Vol 65 (1) ◽  
pp. 20-32 ◽  
Author(s):  
Y. Komatsu ◽  
S. Nakajima ◽  
K. Toyama

1. Intracellular recording was made from layer II-III cells in slice preparations of kitten (30-40 days old) visual cortex. Low-frequency (0.1 Hz) stimulation of white matter (WM) usually evoked an excitatory postsynaptic potential (EPSP) followed by an inhibitory postsynaptic potential (IPSP). The postsynaptic potentials (PSPs) showed strong dependence on stimulus frequency. Early component of EPSP and IPSP evoked by weak stimulation both decreased monotonically at frequencies greater than 0.5-1 Hz. Strong stimulation similarly depressed the early EPSP at higher frequencies (greater than 2 Hz) and replaced the IPSP with a late EPSP, which had a maximum amplitude in the stimulus frequency range of 2-5 Hz. 2. Very weak WM stimulation sometimes evoked EPSPs in isolation from IPSPs. The falling phase of the EPSP revealed voltage dependence characteristic to the responses mediated by N-methyl-D-aspartate (NMDA) receptors and was depressed by application of an NMDA antagonist DL-2-amino-5-phosphonovalerate (APV), whereas the rising phase of the EPSP was insensitive to APV. 3. The early EPSPs followed by IPSPs were insensitive to APV but were replaced with a slow depolarizing potential by application of a non-NMDA antagonist 6,7-dinitro-quinoxaline-2,3-dione (DNQX), indicating that the early EPSP is mediated by non-NMDA receptors. The slow depolarization was mediated by NMDA receptors because it was depressed by membrane hyperpolarization or addition of APV. 4. The late EPSP evoked by higher-frequency stimulation was abolished by APV, indicating that it is mediated by NMDA receptors, which are located either on the recorded cell or on presynaptic cells to the recorded cells. 5. Long-term potentiation (LTP) of EPSPs was examined in cells perfused with solutions containing 1 microM bicuculline methiodide (BIM), a gamma-aminobutyric acid (GABA) antagonist. WM was stimulated at 2 Hz for 15 min as a conditioning stimulus to induce LTP, and the resultant changes were tested by low-frequency (0.1 Hz) stimulation of WM. 6. LTP of early EPSPs occurred in more than one-half of the cells (8/13) after strong conditioning stimulation. The rising slope of the EPSP was increased 1.6 times on average. 7. To test involvement of NMDA receptors in the induction of LTP in the early EPSP, the effect of conditioning stimulation was studied in a solution containing 100 microM APV, which was sufficient to block completely synaptic transmission mediated by NMDA receptors. LTP occurred in the same frequency and magnitude as in control solution.


1980 ◽  
Vol 239 (1) ◽  
pp. R137-R142 ◽  
Author(s):  
J. Ciriello ◽  
F. R. Calaresu

To investigate the role of the paraventricular (PAH) and supraoptic (SON) nuclei in regulation of the cardiovascular system experiments were done in 26 cats anesthetized with alpha-chloralose, paralyzed, and artificially ventilated. Electrical stimulation of histologically verified sites in the region of the PAH and SON elicited increases in arterial pressure in bilaterally vagotomized animals and increases in heart rate both in spinal (C2) animals and in animals bilaterally vagotomized, In addition, stimulation of either the PAH or SON inhibited the reflex vagal bradycardia elicited by stimulation of the carotid sinus nerve (CSN) and bilateral lesions of these areas increased the magnitude of the response. On the other hand, stimulation and lesions of these hypothalamic regions did not alter the magnitude of the cardiovascular responses to stimulation of the aortic depressor nerve. These results demonstrate that stimulation of the PAH and SON elicit cardiovascular responses due to reciprocal changes in activity of the parasympathetic and sympathetic nervous systems and that these structures maintain a tonic inhibitory influence on the heart rate component of the CSN reflex.


1982 ◽  
Vol 60 (6) ◽  
pp. 850-855 ◽  
Author(s):  
Radan Čapek ◽  
Barbara Esplin

Effects of taurine and homotaurine (3-aminopropancsuIfonic acid), on excitability of primary afferents were compared with effects of γ-aminobutyric acid (GABA) in spinal unanaesthesized cats. Homotaurine and GABA, administered intravenously or topically, produced a marked increase in afferent excitability. Homotaurine was about 10 times more potent than GABA. Taurine (up to 2 mmol/kg i.v., or 10 mM topically) did not produce a consistent change in afferent excitability. The effect of homotaurine was antagonized by bicuculline or picrotoxin in doses which suppressed the primary afferent depolarization, as indicated by an increase of afferent excitability, evoked by conditioning stimulation of an antagonistic muscle nerve. Semicarbazidc, an inhibitor of GABA synthesis, did not attenuate the homotaurine-induced excitability changes of afferents while suppressing entirely the primary afferent depolarization. These findings suggest that homotaurine exerts a direct GABA-like action on feline primary afferents.


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