Effects of Symptomatic Treatments on Cutaneous Hyperalgesia and Laser Evoked Potentials During Migraine Attack

Abstract

Previously an amplitude enhancement of laser evoked potentials (LEPs) was detected during migraine attack: we further examined pain threshold to CO2 laser stimuli and LEPs during attacks, evaluating the effect of almotriptan, lysine-acetylsalicylate and placebo treatment on cutaneous hyperalgesia to thermal stimuli delivered by CO2 laser and on LEP components. Eighteen patients suffering from migraine without aura were analysed. They were divided into three groups of six patients each, randomly assigned to lysine acetyl-salicylate, almotriptan or placebo treatments. The supraorbital zones and the dorsum of the hand were stimulated on both the symptomatic and not symptomatic side in all patients. The LEPs were recorded by 25 scalp electrodes. During attacks, the P2 wave was significantly enhanced; the amplitude of the P2 component obtained by the stimulation of the supraorbital zone during the attack on the side of the headache was significantly correlated with the intensity of pain and the frequency of headache. Both almotriptan and lysine acetyl-salicylate significantly reduced the P2 amplitude but they showed no effects on hyperalgesia to laser stimulation; headache relief following therapy was correlated with the reduction of the P2 amplitude. The cortical elaboration of laser-induced experimental pain seemed increased during migraine attack, and the severity of headache was mainly related to the increase of the later LEPs components expressing the attentive and emotive compounds of suffering. Reversion of this process appeared to be primarily responsible for the efficacy of drugs in treating migraine, though both almotriptan and lysine-acetil salicilate seemed to have no effect in reducing sensitization at second and third order nociceptive neurons.

Effects of high-frequency repetitive transcranial magnetic stimulation of primary motor cortex on laser-evoked potentials in migraine

“…Similarly, in a study on acute therapies for migraine attack, we observed no drug-induced effects on laser pain concomitant with the clear inhibition of laser-evoked responses [23]. This apparent contrast may be supported by the principle that LEPs reflect more the status of sensory pathways than the perception of subjective pain [8], despite a linear correlation between the intensity of pain perception and the amplitude of vertex LEPs is often present [24].…”

Neurophysiologic study of central pain in patients with Parkinson disease

“…16,20 All of them could contribute to central pain in patients with PD in the context of enhanced LEPs, although higher attention toward the stimulated limb usually leads to asymmetric LEPS, which seems not to be the case of our patients. 20 The decrement of LEP amplitude caused by L-dopa intake in our PD-PCP patients is not a definitive proof for the involvement of dopamine in pain perception, as suggested by previous studies, 5,31 because similar effects have been described for analgesic drugs, 32,33 or even placebo. 34 However, our patients showed higher pain thresholds and lower subjective perception of ongoing pain in "on" condition.…”

Habituation and sensitization in primary headaches

“…During migraine attacks, the area-under-the-curve of the nociceptive blink reflex R2 component is temporary increased on the affected side in comparison with the non-affected side was observed [106]. Similar results were obtained using another noxious stimulation, the radiant laser CO2: amplitude of the N2–P2 complex at the vertex was increased on the affected side compared to the non-affected side [107-109]. Interestingly, in episodic migraine LEPs did not habituate not only interictally, but also during the attacks, underscoring the different cerebral processing of noxious versus innocuous stimuli.…”