Motor Unit Properties of the First Dorsal Interosseous in Chronic Stroke Subjects: Concentric Needle and Single Fiber EMG Analysis

Abstract

The purpose of this study was to better understand changes in motor unit electrophysiological properties in people with chronic stroke based on concentric needle electromyography (EMG) and single fiber EMG recordings. The first dorsal interosseous (FDI) muscle was studied bilaterally in eleven hemiparetic stroke subjects. A significant increase in mean fiber density (FD) was found in the paretic muscle compared with the contralateral side based on single fiber EMG (1.6 ± 0.2 vs. 1.3 ± 0.1, respectively, P = 0.003). There was no statistically significant difference between the paretic and contralateral sides in most concentric needle motor unit action potential (MUAP) parameters, such as amplitude (768.7 ± 441.7 vs. 855.0 ± 289.9 μV), duration (8.9 ± 1.8 vs. 8.68 ± 0.9 ms) and size index (1.2 ± 0.5 vs. 1.1 ± 0.3) (P > 0.18), nor was there a significant difference in single fiber EMG recorded jitter (37.0 ± 9.6 vs. 39.9 ± 10.6 μs, P = 0.45). The increase in FD suggests motor units of the paretic FDI have enlarged due to collateral reinnervation. However, sprouting might be insufficient to result in a statistically significant change in the concentric needle MUAP parameters. Single fiber EMG appears more sensitive than concentric needle EMG to reflect electrophysiological changes in motor units after stroke. Both single fiber and concentric needle EMG recordings may be necessary to better understand muscle changes after stroke, which is important for development of appropriate rehabilitation strategies. The results provide further evidence that motor units are remodeled after stroke, possibly in response to a loss of motoneurons.

Model-Based Analysis of Muscle Strength and EMG-Force Relation with respect to Different Patterns of Motor Unit Loss

“…Neurological disorders can influence motor unit properties, contributing to muscle atrophy, contracture, weakness, unstable force output, and altered electromyogram-(EMG-) force relationship. For example, previous studies have revealed various changes in motor unit properties of poststroke patients, such as loss of functional motor units [1][2][3][4][5][6], impaired motor unit control properties (reduced motor unit peak firing rates and compressed ranges of motor unit recruitment) [7][8][9][10], and altered motor unit morphological features [11][12][13]. These factors significantly impair muscle force generation and the EMG-force relation.…”

Probing the Brain–Body Connection Using Transcranial Magnetic Stimulation (TMS): Validating a Promising Tool to Provide Biomarkers of Neuroplasticity and Central Nervous System Function

“…Although the target muscle varies between studies, we chose the first dorsal interosseous (FDI) muscle to measure TMS-evoked MEPs because of the muscle’s large motor cortex representation and smaller motor unit-to-muscle fiber innervation ratio [ 61 , 62 ]. This is especially important and practical when testing participants with greater levels of neurological disability, who may have high motor thresholds [ 63 , 64 , 65 ] and low, difficult-to-measure, MEP amplitudes [ 50 , 58 , 59 ].…”

Hip Fractures in Elderly Stroke Patients - The Role of Sarcopenia and Osteoporosis

“…Following a stroke, loss of central control of the alpha motor neurone leads to denervation and loss of motor units [15]. It is thought that remodelling occurs as re-innervation from surrounding neurones attempts to restore neuromuscular function [15,16].…”

“…Unfortunately re-innervation tends to favour the relative increase in the slow twitch muscle fibre type 1 (which is weaker) compared to the fast twitch type II a and b (x) muscle fibres, which generate greater force of contraction and power, and are lost in much greater numbers [15,16]. The overall effect is reduced muscle mass and muscle weakness [15,16]. In addition poor nutrition due to neurogenic dysphagia following stroke can lead to significant weight loss (cachexia) and generalized loss of muscle mass further contributing to the sarcopenia [17].…”