Michel Magnin

Bio: Michel Magnin is an academic researcher from French Institute of Health and Medical Research. The author has contributed to research in topics: Thalamus & Neuropathic pain. The author has an hindex of 35, co-authored 82 publications receiving 4709 citations. Previous affiliations of Michel Magnin include Claude Bernard University Lyon 1 & Saint Joseph's University.

Representation of Pain and Somatic Sensation in the Human Insula: a Study of Responses to Direct Electrical Cortical Stimulation

Abstract: We studied painful and non-painful somaesthetic sensations elicited by direct electrical stimulations of the insular cortex performed in 43 patients with drug refractory temporal lobe epilepsy, using stereotactically implanted depth electrodes. Painful sensations were evoked in the upper posterior part of the insular cortex in 14 patients, mostly in the right hemisphere. Non-painful sensations were elicited in the posterior part of the insular cortex in 16 patients, in both hemispheres. Thus, painful and non-painful somaesthetic representations in the human insula overlap. Both types of responses showed a trend toward a somatotopic organization. These results agree with previous anatomical and unit recording studies in monkeys indicating a participation of the posterior part of the insular cortex in processing both noxious and innocuous somaesthetic stimuli. In humans, both a posterior and an anterior pain-related cortical area have been described within the insular cortex using functional imaging. Our results help to define the respective functional roles of these two insular areas. Finally, lateralization in the right hemisphere of sites where painful sensations were evoked is coherent with the hypothesis of a preponderant role of this hemisphere in species survival.

Low-threshold calcium spike bursts in the human thalamus. Common physiopathology for sensory, motor and limbic positive symptoms.

Abstract: Positive symptoms arise after lesions of the nervous system. They include neurogenic pain, tinnitus, abnormal movements, epilepsy and certain neuropsychiatric disorders. Stereotactic medial thalamotomies were performed on 104 patients with chronic therapy-resistant positive symptoms. Peroperative recordings of 2012 single units revealed an overwhelming unresponsiveness (99%) to sensory stimuli or motor activation. Among these unresponsive cells, 45.1% presented a rhythmic or random bursting activity. Rhythmic bursting activities had an average interburst interval of 263±46 ms corresponding to a frequency of 3.8±0.7 Hz. Frequency variations among the different symptoms were not statistically different. Intraburst characteristics such as the highest frequency encountered in the burst (480±80 Hz) or the mean frequency of the burst (206±44 Hz) were also similar in all patients. All bursts, rhythmic or random, fulfilled the extracellular criteria of low-threshold calcium spike (LTS) bursts. After medial thalamotomy and depending on the symptom, 43–67% of the patients reached a 50–100% relief, with sparing of all neurological functions. On the basis of these electrophysiological and clinical results, we propose a unified concept for all positive symptoms centred on a self-perpetuating thalamic cell membrane hyperpolarization, similar to the one seen in slow-wave sleep.

Motor cortex stimulation for pain control induces changes in the endogenous opioid system.

Abstract: Background: Motor cortex stimulation (MCS) for neuropathic pain control induces focal cerebral blood flow changes involving regions with high density of opioid receptors. We studied the possible contribution of the endogenous opioid system to MCS-related pain relief. Methods: Changes in opioid receptor availability induced by MCS were studied with PET scan and [ 11 C]diprenorphine in eight patients with refractory neuropathic pain. Each patient underwent two preoperative (test–retest) PET scans and one postoperative PET scan acquired after 7 months of chronic MCS. Results: The two preoperative scans, performed at 2 weeks interval, did not show significant differences. Conversely, postoperative compared with preoperative PET scans revealed significant decreases of [ 11 C]diprenorphine binding in the anterior middle cingulate cortex (aMCC), periaqueductal gray (PAG), prefrontal cortex, and cerebellum. Binding changes in aMCC and PAG were significantly correlated with pain relief. Conclusion: The decrease in binding of the exogenous ligand was most likely explained by receptor occupancy due to enhanced secretion of endogenous opioids. Motor cortex stimulation (MCS) may thus induce release of endogenous opioids in brain structures involved in the processing of acute and chronic pain. Correlation of this effect with pain relief in at least two of these structures supports the role of the endogenous opioid system in pain control induced by MCS.

Laser-evoked potential abnormalities in central pain patients: the influence of spontaneous and provoked pain.

Abstract: 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-delta 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.