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Simultaneous Scalp Electroencephalography (EEG), Electromyography (EMG), and Whole-body Segmental Inertial Recording for Multi-modal Neural Decoding
Published on: July 26, 2013
Movement preparation is affected by tissue damage in multiple sclerosis: evidence from EEG event-related
L Leocani1, M Rovaris, F Martinelli-Boneschi
1Department of Neurology, Clinical Neurophysiology and Neurorehabilitation, Scientific Institute, Hospital San Raffaele, University Vita-Salute, Via Olgettina 60, 20132 Milan, Italy. leocani.letizia@hsr.it
Objective:
To investigate the impact of brain tissue damage in Multiple Sclerosis (MS) on the efficiency of programming of voluntary movement, assessed using event-related desynchronization of the EEG.
Methods:
The onset latency of mu ERD (percent desyncronization of the mu rhythm preceding movement onset) to hand movement was studied in 34 MS patients. ERD onset was compared with normative data and correlated with T1 and T2 total lesion volume (TLV) at magnetic resonance imaging (MRI).
Results:
ERD onset latency was significantly correlated with T1-TLV (r = 0.53, P = 0.001) and T2 lesion load (r = 0.5, P = 0.003), even after correcting for disability. Patients with higher T1-TLV had significantly delayed ERD onset compared with normal subjects and with patients with lower T1-TLV; patients with higher T2-TLV had significantly delayed ERD compared with normal subjects only. ERD onset latency was not correlated to clinical disability.
Conclusions:
Our finding of delayed ERD onset in patients with more severe measures of brain damage, independently from clinical disability, suggests that functional cortico-cortical and cortico-subcortical connections underlying the expression of ERD during programming of voluntary movement are disrupted by the MS related pathological process. Further, studies are needed to evaluate the role of specific anatomical cortico-subcortical circuits in determining this abnormality.
Significance:
The extent of brain lesion load in multiple sclerosis affects cortical changes related to motor preparation, detected by analysis of onset latency of event-related desynchronization (ERD) of the mu rhythm to self-paced movement.
Insights
Brain lesion load in multiple sclerosis (MS) impacts motor preparation efficiency. Delayed event-related desynchronization (ERD) onset indicates disrupted neural connections, independent of clinical disability.
Area of Science:
- Neuroscience
- Neurology
- Neurophysiology
Background:
- Multiple Sclerosis (MS) is a demyelinating disease affecting the central nervous system.
- Brain tissue damage in MS can impair motor function and neural processing.
- Event-related desynchronization (ERD) of the mu rhythm is a neurophysiological marker of motor preparation.
Purpose of the Study:
- To investigate the relationship between brain lesion volume in MS and the efficiency of voluntary movement programming.
- To assess motor preparation using electroencephalography (EEG) and event-related desynchronization (ERD).
- To determine if lesion load correlates with delayed ERD onset, indicating disrupted neural pathways.
Main Methods:
- Studied 34 MS patients, measuring the onset latency of mu ERD preceding hand movement.
- Correlated ERD onset latency with T1 and T2 total lesion volume (TLV) from MRI scans.
- Compared ERD onset latency with normative data and adjusted for clinical disability scores.
Main Results:
- ERD onset latency showed significant correlations with both T1-TLV (r = 0.53) and T2 lesion load (r = 0.5).
- Higher T1-TLV was associated with significantly delayed ERD onset compared to controls and lower T1-TLV groups.
- Higher T2-TLV was linked to delayed ERD onset compared to controls, but ERD onset was not correlated with clinical disability.
Conclusions:
- Increased brain lesion load in MS is associated with delayed ERD onset, reflecting impaired motor preparation.
- The findings suggest MS-related pathology disrupts cortico-cortical and cortico-subcortical connections involved in voluntary movement.
- Further research is needed to elucidate the role of specific anatomical circuits in these motor preparation abnormalities.
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