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We studied alpha and beta EEG oscillatory changes in healthy volunteers during two different auditory go/no-go paradigms, in order to investigate their relationship with different components of the motor process. In the first paradigm (S2-centered), the initial tone (S1) was constant (warning), and the second tone (S2) indicated the subject whether to move or not. In the second paradigm (S1-centered), S1 indicated whether to move or not, while S2 just indicated the timing of the movement. A medial frontal beta energy increase was found in all conditions after the stimulus that forces the subject to decide whether to move or not (S1 or S2 depending on the paradigm). In both go conditions, a central alpha and beta energy decrease began after the go decision, reaching minimum values during the movement; it was followed by a beta post-movement increase, limited to the central contralateral area. In the no-go conditions, a marked fronto-central beta synchronization appeared after the decision not to move. In conclusion, our study was able to dissociate the beta oscillatory changes related to movement preparation and execution (central decrease/increase) from those associated with decision-making (medial frontal increase) and motor inhibition (fronto-central increase).

We studied the effect of stimulus predictability on the alpha and beta changes observed in central regions during stimulus-induced movement paradigms. Six young volunteers were instructed to extend briskly their dominant wrist as soon as possible after hearing a 2000 Hz sound. Two sequences of stimuli were presented to each subject, the first rhythmic at 1/6 s and the second with random intervals between 5 and 13s. A time-frequency analysis of nonphase-locked activity in the 7-37 Hz range was performed on stimulus-centred EEG sweeps using wavelet filters and Gabor transforms. During the sequence of predictable rhythmic stimuli, stimulus-induced movements were accompanied by a decrease in beta activity that began contralaterally about 1 s prior to the stimulus and extended to both sides later on. This decrease was followed by a rebound after the end of the movement. In the alpha band, the decrease observed started just after the sound. During the sequence of non-predictable, random stimuli, stimulus-induced movements were accompanied by a shorter and smaller alpha and beta-ERD, that started after the stimulus. The presence of a pre-stimulus beta ERD only in the rhythmic predictable paradigm suggests that central pre-movement beta ERD may be an indicator of motor preparation, and could be used for objective evaluation of time estimation and motor timing. The minimal differences observed in the alpha changes in both paradigms suggest that alpha-ERD may not be linked to motor preparation.

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Objective: We studied movement-related electroencephalographic oscillatory changes in the alpha and beta range during a sequence of two movements in 7 healthy volunteers, in order to investigate the relationship between these changes and each component in the sequence.Methods: The sequence consisted of a wrist active extension-passive flexion followed by a first and second finger pincer. A total of 10.5 s sweeps were recorded using the level of surface electromyographic (EMG) activity in wrist extensors as trigger, including a 7.5 s prestimulus. The sweeps were also realigned manually offline using as trigger the end of the first EMG burst, or the beginning of the second movement. An index of the changes in non-phase-locked energy in the 7 -37 Hz range was obtained by averaging single-sweep timefrequency transforms.Results: The duration of each of the movements in the sequence and the relationship between them were compatible with the use of two different motor programmes in the sequence. In the beta band, a decrease in energy (event-related desynchronisation, ERD) began 1.5 s before the onset of the first movement, and was sustained until the end of the second movement. No energy increases were observed until the end of the second movement. In the alpha band, the ERD began 0.5 seconds before the first movement and was sustained throughout the recording.Conclusion: These findings suggest that the beta-event-related synchronisation is related to the end of the whole motor process, and not to the end of each motor programme.

Our findings support a credible role of cortical and juxtacortical involvement in the development of epileptic seizures in MS.

ObjectiveTo describe the neuropathologic features and the molecular data of phosphorylated tau (pTau) in a new case of anti-IgLON5 disease.MethodsReview of clinical data, postmortem neuropathologic examination. Biochemical analyses of pTau were performed in brain samples from the present case and from a previously described patient with anti-IgLON5 with the characteristic brainstem tauopathy.ResultsThe patient was a 71-year-old man with a clinical syndrome consisting of sleep disturbance and bulbar symptoms. IgLON5 antibodies of predominant IgG4 subtype were detected in serum and CSF. He carried the HLA DRB1*10:01-DQB1*05:01 haplotype. Despite treatment with IV immunoglobulins, he unexpectedly died during sleep 2 years after disease onset. Histology showed neurofibrillary pathology and β-amyloid deposits consistent with Alzheimer disease (AD) of intermediate severity. pTau deposits were absent in the brainstem. There were few perivascular CD8+ T-cell infiltrates in the posterior hypothalamus, amygdala, and brainstem with microglial activation. The pTau immunoblot showed a pattern of bands consistent with AD, which was different from that observed in the patient with anti-IgLON5 with brainstem tauopathy who presented a differential band around 56 KDa.ConclusionThe absence of pTau deposits in the brainstem of the present patient suggests that the tauopathy of patients with anti-IgLON5 disease may be a late, secondary event. The anti-IgLON5 brainstem tauopathy has a specific molecular signature different from primary tauopathies. pTau deposits restricted to the hippocampus/limbic regions of patients with anti-IgLON5 may represent an age-related comorbidity.

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