IFCN-endorsed practical guidelines for clinical magnetoencephalography (MEG)

Magnetoencephalography (MEG) records weak magnetic fields outside the human head and thereby provides millisecond-accurate information about neuronal currents supporting human brain function. MEG and electroencephalography (EEG) are closely related complementary methods and should be interpreted together whenever possible. This manuscript covers the basic physical and physiological principles of MEG and discusses the main aspects of state-of-the-art MEG data analysis. We provide guidelines for best practices of patient preparation, stimulus presentation, MEG data collection and analysis, as well as for MEG interpretation in routine clinical examinations. In 2017, about 200 whole-scalp MEG devices were in operation worldwide, many of them located in clinical environments. Yet, the established clinical indications for MEG examinations remain few, mainly restricted to the diagnostics of epilepsy and to preoperative functional evaluation of neurosurgical patients. We are confident that the extensive ongoing basic MEG research indicates potential for the evaluation of neurological and psychiatric syndromes, developmental disorders, and the integrity of cortical brain networks after stroke. Basic and clinical research is, thus, paving way for new clinical applications to be identified by an increasing number of practitioners of MEG. (C) 2018 International Federation of Clinical Neurophysiology. Published by Elsevier B.V.Peer reviewe

Focal capsular vascular lesions can selectively deafferent the prerolandic or the parietal cortex: Somatosensory evoked potentials evidence

Four patients with a unilateral focal vascular accident involving the internal capsule (but not the cortex) were studied electrophysiologically. Averaged somatosensory evoked potentials (SEPs) to electrical stimulation of the median nerve on the left or the right side were analyzed. In the 3 patients with hemiparesis and normal somatic sensation, the precentral P22 and N30 SEP components were lost, whereas the parietal components were preserved. In another patient with clinical somatosensory loss unaccompanied by any central motor impairment, the precentral SEP components were preserved, whereas the parietal SEP components were lost. Thus, a small capsular lesion can eliminate distinct cortical SEP components by selectively involving either the axons of the thalamic VPLc nucleus going to parietal receiving cortex or the axons of thalamic VPLo going to motor area 4. These findings extend to subcortical lesions the diagnostic value of SEPS in patients with dissociated clinical motor and sensory signs. Copyright © 1991 American Neurological AssociationSCOPUS: ar.jFLWNAinfo:eu-repo/semantics/publishe

Independent somatosensory projection to motor cortex in man

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Bilateral somatosensory evoked potentials in four patients with long‐standing surgical hemispherectomy

Four patients were studied electrophysiologically 8 to 24 years after surgical removal of one cerebral hemisphere without damage to the striatum or diencephalon. Somatosensory evoked potentials(SEPs)to electrical stimulation of the median nerve on the left or right side were averaged and mapped out over the scalp. Stimulation on the side opposite to the missing hemisphere evoked brief P9 and P14 farfields and a slow N18 negative potential of 15‐to 25‐msec duration bilaterally. No additional focal response was detected over the remaining (ipsilateral) hemisphere for 60 msec after the stimulus. Because long‐standing hemispherectomy entails massive retrograde degeneration of thalamocortical neurons, the preserved P14 and N18 responses must reflect neural activities generated below the thalamus that are volume conducted to the scalp bilaterally. The data clarify several current issues in the evaluation of SEP components. Copyright © 1989 American Neurological AssociationSCOPUS: ar.jFLWNAinfo:eu-repo/semantics/publishe

Thalamic Pain Syndrome of Dejérine-Roussy: Differentiation of Four Subtypes Assisted by Somatosensory Evoked Potentials Data

In 30 patients with a thalamic vascular lesion and clinical somatosensory disturbances in the opposite hemibody without hemiplegia, four nosological groups were identified: group 1 had no central pain but complete hemianesthesia and loss of cortical somatosensory evoked potentials (SEPs) on the affected side (analgic thalamic syndrome). Group 2 had central pain, severe hypoesthesia, and loss of cortical SEPs. Group 3 had central pain and hypoesthesia, with cortical SEPs present, although reduced or delayed on the affected side. Group 4 had central pain with preserved touch and joint sensations and normal SEPs (pure algetic thalamic syndrome). Clinical signs and SEP titration of the actual involvement of lemniscal pathways in these four groups of patients with thalamic syndrome are discussed in relation to current pathophysiology of central pain. © 1988 American Medical Association All rights reserved.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Insular Dichotomy in the Implicit Detection of Emotions in Human Faces

International audienceAbstract The functional roles of the insula diverge between its posterior portion (PI), mainly connected with somato-sensory and motor areas, and its anterior section (AI) connected with the frontal, limbic, and cingulate regions. We report intracranial recordings of local field evoked potentials from PI, AI, and the visual fusiform gyrus to a full array of emotional faces including pain while the individuals’ attention was diverted from emotions. The fusiform gyrus and PI responded equally to all types of faces, including neutrals. Conversely, the AI responded only to emotional faces, maximally to pain and fear, while remaining insensitive to neutrals. The two insular sectors reacted with almost identical latency suggesting their parallel initial activation via distinct functional routes. The consistent responses to all emotions, together with the absence of response to neutral faces, suggest that early responses in the AI reflect the immediate arousal value and behavioral relevance of emotional stimuli, which may be subserved by “fast track” routes conveying coarse-spatial-frequency information via the superior colliculus and dorsal pulvinar. Such responses precede the conscious detection of the stimulus’ precise signification and valence, which need network interaction and information exchange with other brain areas, for which the AI is an essentialhub

Neural generators of N18 and P14 far-field somatosensory evoked potentials studied in patients with lesion of thalamus or thalamo-cortical radiations

Somatosensory evoked potentials (SEPs) to electrical stimulation of the right or left median nerve were studied in 4 patients with hemianesthesia and a severe thalamic or suprathalamic vascular lesion on one side. The SEPs were recorded with a non-cephalic reference. The normal side of each patient served as his or her own control. The lesion consistently abolished the parietal N20-P27-P45 and the prerolandic P22-N30 SEP components. It did not significantly affect the P9-P11-P14 positive far fields, nor the widespread bilateral N18 SEP component. This allowed N18 features to be studied without interference from cortical components. It is proposed that N18 reflects several deeply located generators in brain stem and/or thalamus whereas N20 represents the earliest cortical response of the contralateral post- central receiving areas.info:eu-repo/semantics/publishe

Astereognosis and dissociated loss of frontal or parietal components of somatosensory evoked potentials in hemispheric lesions: Detailed correlations with clinical signs and computerized tomographic scanning

Detailed clinical sensory and motor signs were correlated case by case with somatosensory evoked potentials (SEP) in 22 selected patients with a single circumscribed hemisphere lesion. The lesions collectively mapped out a variety of cerebral sites from the anterior frontal to the posterior parietal regions. SEPs were averaged from 8 standard scalp sites with an earlobe reference electrode, so that parietal N20-P27-P45 were differentiated from prerolandic P22-N30 SEP components. SEP wave forms to stimulation on the unaffected side served as the patient's own control.A complete parietal lesion produced contralateral hemianaesthesia without upper motor neuron signs and eliminated the parietal N20-P27-P45 while the prerolandic P22-N30 persisted at usual latencies. The neural generators for the N20 and the P22 components are thus distinct. It is also proposed that direct, short latency pathways convey somatosensory inputs to the motor cortex, independently of connections via parietal areas 2 and 5. Enhancement of P22-N30 after chronic parietal lesions suggests collateral reinnervation by residual inputs after partial deafferentiation of prerolandic cortex.Small postcentral lesions produced astereognosis (with preserved tactile and deep sensation) and reduced or eliminated the N20 and P27 SEP components, but did not affect the P22-N30 components. Precentral lesions with severe hemiplegia (but not prefrontal lesions) eliminated the prerolandic P22-N30 SEP components and did not alter the parietal N20-P27-P45 components. The data are pertinent to the understanding of the pathophysiology of somatosensory deficits and for the diagnostic use of SEPs in cerebral lesions. © 1983 Oxford University Press.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

The neural dynamics of reward value and risk coding in the human orbitofrontal cortex

International audienceThe orbitofrontal cortex is known to carry information regarding expected reward, risk and experienced outcome. Yet, due to inherent limitations in lesion and neuroimaging methods, the neural dynamics of these computations has remained elusive in humans. Here, taking advantage of the high temporal definition of intracranial recordings, we characterize the neurophysiological signatures of the intact orbitofrontal cortex in processing information relevant for risky decisions. Local field potentials were recorded from the intact orbitofrontal cortex of patients suffering from drug-refractory partial epilepsy with implanted depth electrodes as they performed a probabilistic reward learning task that required them to associate visual cues with distinct reward probabilities. We observed three successive signals: (i) around 400 ms after cue presentation, the amplitudes of the local field potentials increased with reward probability; (ii) a risk signal emerged during the late phase of reward anticipation and during the outcome phase; and (iii) an experienced value signal appeared at the time of reward delivery. Both the medial and lateral orbitofrontal cortex encoded risk and reward probability while the lateral orbitofrontal cortex played a dominant role in coding experienced value. The present study provides the first evidence from intracranial recordings that the human orbitofrontal cortex codes reward risk both during late reward anticipation and during the outcome phase at a time scale of milliseconds. Our findings offer insights into the rapid mechanisms underlying the ability to learn structural relationships from the environment