Brain, Vol. 125, No. 12, 2766-2781,
December 2002
© 2002 Oxford University Press
Laser-evoked potential abnormalities in central pain patients: the influence of spontaneous and provoked pain
1 INSERM and Laboratoire de neurophysiologie humaine du CERMEP, 2 Équipe d’Accueil EA1880, Université Claude Bernard, 3 Service de Neurologie fonctionnelle, Hôpital Neurologique, Lyon, 4 Centre Stéphanois de la douleur et Service de Neurologie, Hôpital Bellevue, St Étienne, France
Correspondence to: L. Garcia-Larrea, INSERM/Laboratoire de neurophysiologie humaine du CERMEP and Équipe d’Accueil EA1880, Université Claude Bernard, 59 Bd Pinel, 69003 Lyon, France E-mail: larrea{at}univ-lyon1.frPart of these data were presented to the Tenth International Congress of Clinical Neurophysiology, Lyon, France, August 2000.
We recorded laser-evoked cortical potentials (LEPs) in 54 consecutive patients presenting with unilateral neuropathic central pain (n = 42) or with lateralized pain of non-organic origin (n = 12). A number of cases in each group had superimposed hyperalgesia or allodynia. In patients with central pain, LEPs were significantly attenuated after stimulation over the painful territory, relative to stimulation of the homologous normal territory. LEP attenuation concerned not only patients with decreased pain/heat sensation, but also those with allodynia or hyperalgesia to laser pulses. In contrast, LEPs were never attenuated in patients with non-organic forms of pain, in whom LEPs could even be enhanced to stimulation of the painful territory. Increased responses in non-organic pain were a reminder of the cognitive modulation observed in normal subjects who direct attention to a laser stimulus. Enhanced LEPs never accompanied truly neuropathic hyperalgesia or allodynia. In central pain patients with exclusively spontaneous pain, LEP attenuation was more pronounced than that observed in those with allodynia and hyperalgesia. Patients with allodynia also presented occasionally ultra-late responses (>700 ms) to stimulation of the painful side. The hypothesis that such responses may reflect activation of a slow conducting ‘medial’ pain system is discussed. We conclude that, as currently recorded, LEPs essentially reflect the activity of a ‘lateral’ pain system subserved at the periphery by rapidly conducting A-
fibres. They are useful to document the sensorial deficits (deafferentation) leading to neuropathic pain syndromes. Conversely, in the case of deafferentation, they fail to index adequately the affective aspects of pain sensation. On practical grounds, chronic pain coupled with reduced LEPs substantiates the diagnosis of neuropathic pain, whereas the finding of normal or enhanced LEPs to stimulation of a painful territory suggests the integrity of pain pathways, and does not support a neuropathic pathophysiology. In neuropathic cases, partial LEP preservation might increase the probability of developing provoked pain (allodynia/hyperalgesia). The possible predictive value of this phenomenon, when observed before the development of pain, remains to be demonstrated. In selected contexts (pain sine materia, non-organic anaesthesia), normal or enhanced LEPs may support a psychogenic participation in the syndrome.
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