Fasciculation electromechanical latency is prolonged in amyotrophic lateral sclerosis

TY - JOUR

T1 - Fasciculation electromechanical latency is prolonged in amyotrophic lateral sclerosis

AU - Planinc, D

AU - Muhamood, N

AU - Cabassi, C

AU - Iniesta, R

AU - Shaw, C E

AU - Hodson-Tole, E

AU - Bashford, J

N1 - Funding Information: JB acknowledges funding from the Medical Research Council and Motor Neurone Disease Assocation (Lady Edith Wolfson Clinical Research Training Fellowship; MR/P000983/1), Sattaripour Charitable Foundation, UK Dementia Research Institute and the National Institute for Health Research (Academic Clinical Lectureship program). DP, NM and CC contributed during their MSc qualifications in Clinical Neuroscience. R.I.’s input represents independent research supported by the NIHR BioResource Centre Maudsley at South London and Maudsley NHS Foundation Trust (SLaM) & Institute of Psychiatry, Psychology and Neuroscience (IoPPN), King's College London. We would like to thank all the patients involved in this study for their willingness and determination to participate. We thank TMSi for supplying the amplifier and sensors. Funding Information: JB acknowledges funding from the Medical Research Council and Motor Neurone Disease Assocation (Lady Edith Wolfson Clinical Research Training Fellowship; MR/P000983/1), Sattaripour Charitable Foundation , UK Dementia Research Institute and the National Institute for Health Research (Academic Clinical Lectureship program). DP, NM and CC contributed during their MSc qualifications in Clinical Neuroscience. R.I.’s input represents independent research supported by the NIHR BioResource Centre Maudsley at South London and Maudsley NHS Foundation Trust (SLaM) & Institute of Psychiatry, Psychology and Neuroscience (IoPPN), King’s College London. We would like to thank all the patients involved in this study for their willingness and determination to participate. We thank TMSi for supplying the amplifier and sensors. Publisher Copyright: © 2022 International Federation of Clinical Neurophysiology

PY - 2023/1

Y1 - 2023/1

N2 - OBJECTIVE: In amyotrophic lateral sclerosis (ALS), motor neurons become hyperexcitable and spontaneously discharge electrical impulses causing fasciculations. These can be detected by two noninvasive methods: high-density surface electromyography (HDSEMG) and muscle ultrasonography (MUS). We combined these methods simultaneously to explore the electromechanical properties of fasciculations, seeking a novel biomarker of disease.METHODS: Twelve ALS patients and thirteen healthy participants each provided up to 24 minutes of recordings from the right biceps brachii (BB) and gastrocnemius medialis (GM). Two automated algorithms (Surface Potential Quantification Engine and a Gaussian mixture model) were applied to HDSEMG and MUS data to identify correlated electromechanical fasciculation events.RESULTS: We identified 4,197 correlated electromechanical fasciculation events. HDSEMG reliably detected electromechanical events up to 30 mm below the skin surface with an inverse correlation between amplitude and depth in ALS muscles. Compared to Healthy-GM muscles (mean = 79.8 ms), electromechanical latency was prolonged in ALS-GM (mean = 108.8 ms; p = 0.0458) and ALS-BB (mean = 112.0 ms; p = 0.0128) muscles. Electromechanical latency did not correlate with disease duration, symptom burden, sum muscle power score or fasciculation frequency.CONCLUSIONS: Prolonged fasciculation electromechanical latency indicates impairment of the excitation-contraction coupling mechanism, warranting further exploration as a potential novel biomarker of disease in ALS.SIGNIFICANCE: This study points to an electromechanical defect within the muscles of ALS patients.

AB - OBJECTIVE: In amyotrophic lateral sclerosis (ALS), motor neurons become hyperexcitable and spontaneously discharge electrical impulses causing fasciculations. These can be detected by two noninvasive methods: high-density surface electromyography (HDSEMG) and muscle ultrasonography (MUS). We combined these methods simultaneously to explore the electromechanical properties of fasciculations, seeking a novel biomarker of disease.METHODS: Twelve ALS patients and thirteen healthy participants each provided up to 24 minutes of recordings from the right biceps brachii (BB) and gastrocnemius medialis (GM). Two automated algorithms (Surface Potential Quantification Engine and a Gaussian mixture model) were applied to HDSEMG and MUS data to identify correlated electromechanical fasciculation events.RESULTS: We identified 4,197 correlated electromechanical fasciculation events. HDSEMG reliably detected electromechanical events up to 30 mm below the skin surface with an inverse correlation between amplitude and depth in ALS muscles. Compared to Healthy-GM muscles (mean = 79.8 ms), electromechanical latency was prolonged in ALS-GM (mean = 108.8 ms; p = 0.0458) and ALS-BB (mean = 112.0 ms; p = 0.0128) muscles. Electromechanical latency did not correlate with disease duration, symptom burden, sum muscle power score or fasciculation frequency.CONCLUSIONS: Prolonged fasciculation electromechanical latency indicates impairment of the excitation-contraction coupling mechanism, warranting further exploration as a potential novel biomarker of disease in ALS.SIGNIFICANCE: This study points to an electromechanical defect within the muscles of ALS patients.

KW - Humans

KW - Fasciculation/diagnosis

KW - Amyotrophic Lateral Sclerosis/diagnostic imaging

KW - Electromyography/methods

KW - Motor Neurons/physiology

KW - Muscle, Skeletal/diagnostic imaging

UR - http://www.scopus.com/inward/record.url?scp=85144588952&partnerID=8YFLogxK

U2 - 10.1016/j.clinph.2022.11.005

DO - 10.1016/j.clinph.2022.11.005

M3 - Article

C2 - 36442378

SN - 1388-2457

VL - 145

SP - 71

EP - 80

JO - Clinical Neurophysiology

JF - Clinical Neurophysiology

ER -