Motor excitability in painful musculoskeletal shoulder conditions: A scoping review

Abstract

Objective

Altered motor excitability is a proposed mechanism of musculoskeletal shoulder pain. This scoping review aims to summarise studies examining motor excitability in individuals with painful musculoskeletal shoulder conditions, identify research gaps, and suggest clinical and research insights from these studies.

Data Sources

PubMed, EMBASE, CINAHL

Review methods

Databases were searched for studies from January 2004 to April 2026. Studies were included if they assessed motor excitability in participants with painful musculoskeletal shoulder conditions or healthy participants with experimentally induced shoulder pain.

Results

A total of 19 studies were included. Shoulder pain condition, target muscle selection, participant positioning, and measures of motor excitability varied between studies. Moreover, 11 of 16 studies comparing shoulder motor excitability in those with clinical or experimental shoulder pain to controls reported decreases in motor excitability in those with shoulder pain. Two of three studies reporting intervention effects describe increased excitability following interventions in at least one measure.

Conclusion

Shoulder motor excitability appears decreased in those with clinical shoulder pain. Mixed effects of experimental shoulder pain models on motor excitability suggest that more work clarifying the effect of pain on motor excitability changes is warranted. Preliminary studies report increased excitability following interventions, yet the clinical significance of these improvements is unclear. In order to minimise nervous system maladaptations in those with shoulder pain, clinicians may emphasise pain management and consider interventions that enhance motor excitability of the shoulder musculature. Because of heterogeneity in methodology and experimental pain models, further exploration of motor excitability as a mechanism and treatment target in musculoskeletal shoulder pain appears warranted.

Keywords

Rotator cuff neuroscience shoulder exercise physiology upper extremity (arm)

Introduction

Musculoskeletal shoulder pain is prevalent and represents a large focus in rehabilitation practice and research.^1,2 Shoulder muscle weakness, altered muscle activation, and altered pain processing are thought to contribute to musculoskeletal shoulder pain conditions,^3–15 and previous work has started to explore neurophysiological mechanisms underlying these alterations.^13–19

Motor excitability is gaining attention as a potential mechanism contributing to both muscle weakness and altered motor activation, and refers to the excitability of the neural structures involved in motor activation. Motor excitability is measured using either transcranial magnetic stimulation to measure corticospinal excitability,^9,20 or using Hoffman reflexes to measure alpha motor neuron excitability.^20–23 A schematic of transcranial magnetic stimulation and Hoffman reflexes is illustrated in Figure 1 .

Figure 1.

(a) Transcranial magnetic stimulation schematic illustrating a transcranial magnetic stimulation coil magnetically inducing motor cortex stimulation at a target muscle hotspot, which propagates through the corticospinal tract and then through an alpha motoneuron to elicit an electromyographic signal from a target muscle. Recorded by an electromyography recording electrode (square labeled “EMG”), measures of motor excitability are then derived from the recorded electromyographic signal. (b) Hoffman reflex schematic illustrating bidirectional electrical stimulation of a mixed sensory/motor nerve (square labeled “ES”), which elicits simultaneous stimulation of sensory Ia fibres and an alpha motor neuron supplying a target muscle. Initial stimulation of 1a sensory fibres results in a synapse within the ventral horn of the spinal cord onto alpha motor neurons, which result in the propagation of an action potential and ultimately activation of a target muscle. The electromyographic signal of a target muscle following this sequence is the Hoffman reflex and is recorded using an electromyography recording electrode (square labeled “EMG”). Initial stimulation of the alpha motor neuron results in activation of a target muscle, and the resulting electromyographic signal is the M-wave. The M-wave is a measure of peripheral nerve excitability and is often used as a method to normalise Hoffman reflex measurement. Note the larger duration of time (increased latency) preceding the Hoffman reflex, as compared to the M-wave, which reflects the longer length of neurons through which action potentials propagate to elicit a Hoffman reflex (through 1a sensory fibres and the full length of an alpha motor neuron).

Motor excitability may influence the motor alterations seen in those with clinical shoulder pain.^24–26 Furthermore, measures of motor excitability overcome significant limitations of electromyographic measurements because they are taken during rest or light muscle activation and therefore do not require maximal contraction during assessment, which can be altered in the presence of pain. Furthermore, the measures are thought to reflect excitability of neural pathways which may generalise across all tasks, whereas electromyographic activity reflects muscle activation during specific tasks, and likely varies between tasks.

While motor excitability is known to influence motor performance, emerging evidence suggests that motor excitability may also be related to the neurophysiological processing of pain, with preliminary evidence from studies examining repetitive motor cortex stimulation, which have shown improved pain and quality of life in individuals with fibromyalgia following stimulation.^27–30

Since motor excitability of the shoulder muscle is a factor thought to underlie altered shoulder muscle performance and potentially pain processing, it may be an important factor to consider to prevent the development or progression of shoulder pain. A framework describing motor excitability as a potential mechanism of shoulder pain and progression is presented in Figure 2 .

Figure 2.

Framework describing decreased motor excitability as a mechanism of shoulder pain and progression.

The primary aim of this scoping review is to summarise work that has examined motor excitability in individuals with painful musculoskeletal shoulder conditions to answer three questions: First, is motor excitability of shoulder musculature altered in those with clinical shoulder conditions compared to controls? Second, does experimental shoulder pain result in altered motor excitability of local shoulder musculature? Third, what effects of interventions on shoulder muscle motor excitability have been observed?

Methods

Cochrane Database Systematic Reviews and the Joanna Briggs Institute database were searched to confirm that there were not any reviews in progress or to be published that would be redundant in scope. After confirmation, the databases PubMed, EMBASE, and CINAHL were searched for relevant studies from 1 January 2004 to 30th April 2026. Full descriptions of database search queries are located in Supplementary file 1.

During database searches, titles and abstracts of studies were screened, and initial eligibility was determined. Initial eligibility was determined for studies by the primary author if upon abstract screening they included participants with painful musculoskeletal shoulder conditions (rotator cuff tendinopathy, adhesive capsulitis, total shoulder arthroplasty, reverse total shoulder arthroplasty, Bankart repair, superior labrum anterior–posterior repair, glenohumeral osteoarthritis, glenohumeral instability, acromioclavicular joint osteoarthritis) or healthy participants with experimentally induced shoulder pain and examined either the effect of painful musculoskeletal shoulder conditions or experimental pain on motor excitability measured using corticospinal excitability or Hoffman reflex. In addition, studies were included if they examined the effect of intervention on motor excitability in participants with musculoskeletal shoulder conditions. Studies involving participants with nonmusculoskeletal shoulder pain (poststroke shoulder pain, for example) were excluded. Following initial screening, duplicate studies were removed, and the primary author then read full-text articles of potentially eligible studies to determine eligibility for final inclusion. References of included studies were then screened for the presence of additional relevant studies. Variables that were extracted if present in each study included participant demographic information, the shoulder condition of participants, methods for obtaining measurements of motor excitability, and details of the interventions used and effects of interventions on motor excitability. Independent data extraction was completed using standardised, preorganised digital templates by two assessors who subsequently remediated any disagreements until consensus was achieved. Supplementary file 2 includes a blank template of the data extraction spreadsheet used during data extraction. Once consensus was achieved for all disagreements, data were transcribed by the primary author into a final tabulated form. During this data synthesis process, studies were grouped by the aims that they addressed. Specifically, studies were organised into three groups, with the first group consisting of studies comparing motor excitability in those with clinical shoulder pain to controls, the second group consisting of studies comparing motor excitability in participants before and during experimental pain, and the third group consisting of studies reporting intervention effects on motor excitability in those with clinical shoulder pain.

Results

The search yielded 1558 references, which were screened and resulted in 21 unique full-text articles assessed. 19 studies were ultimately included following full-text screening.^{24–26,31–46} Figure 3 illustrates the PRISMA flow chart, and Figure 4 illustrates the publication timeline of included studies.

Figure 3.

PRISMA flowchart.

Figure 4.

Publication timeline of included studies.

Table 1 summarises each included study and describes the aims and methods used during neurophysiological assessment. In the included studies, there is heterogeneity among the ages, diagnoses, chronicity of symptoms, and functional levels of participants in the included studies. Athletic participants were included in one study.³² Moreover, 17 of the 19 studies assessed motor excitability using transcranial magnetic stimulation, whereas two assessed motor excitability using normalised Hoffman reflexes. Measures of motor excitability of the upper trapezius, middle trapezius, lower trapezius, serratus anterior, middle deltoid, anterior deltoid, and infraspinatus muscle groups are reported. Of the 17 studies assessing motor excitability with transcranial magnetic stimulation, one study assessed the resting motor threshold of the target muscle primary motor cortex,³⁴ whereas the remaining studies assessed corticospinal excitability during active contraction of the target muscle. The amount of force and electromyography feedback during assessment of active motor threshold varied from 4% to 25% of maximum voluntary isometric contraction. Three studies assessing active motor threshold did not specify the amount of target muscle contraction during assessment.^33,35 Six studies assessing active motor threshold specified that electromyography biofeedback was used to maintain a target level of muscle contraction,^{26,32,35,37,41} whereas the remaining 11 did not specify whether electromyography or force biofeedback was used during assessment. Arm position during assessment of corticospinal excitability varied, even between studies targeting the measurement of identical muscles.^26,31,35 Neither of the two studies assessing Hoffman reflexes reported on the reliability of such measurements, although two of the 17 studies examining motor excitability using transcranial magnetic stimulation described the reliability of the measures.^32,40 In these two studies reporting on reliability, good reliability was observed for the measurement of active motor threshold for the upper trapezius (Intraclass correlation coefficient = 0.81, minimum detectable change₉₅: 3.89%) and middle deltoid (intraclass correlation coefficient = 0.89, minimum detectable change₉₅: 2.60%),⁴⁰ and excellent reliability was observed for the measurement of motor excitability for lower trapezius and serratus anterior (intraclass correlation coefficient >0.91).³² All included studies measuring corticospinal excitability using transcranial magnetic stimulation used the same stimulator model. Additional measures of motor excitability that were measured in the included studies are listed in Table 1 .

Table 1.

Aims of studies and methods used to characterise motor excitability.

Article	Aim	Motor excitability method	Target muscle	Outcomes assessed	Percentage of maximal voluntary isometric contraction during assessment	Participant position during testing	Reliability analysis
Alexander (2007)	To examine the trapezius reflex and corticospinal excitability of the upper and lower trapezius in participants with non-traumatic shoulder instability, compared to asymptomatic controls	Transcranial magnetic stimulation	Upper trapezius Lower trapezius	Upper trapezius: -Active motor threshold -Motor evoked potential latency at 120% active motor threshold Lower trapezius: -Active motor threshold -Motor evoked potential latency at 120% active motor threshold	20%–30% (force)	Seated with a painful arm held in 70 degrees of shoulder flexion in the plane of the scapula, with the elbow extended and the wrist in neutral position
Berth (Sep. 2009)	To investigate neuromuscular alterations of the middle deltoid in patients with unilateral chronic rotator cuff tear in comparison to asymptomatic participants	Transcranial magnetic stimulation	middle deltoid	-Active motor threshold-Motor evoked potential amplitude-stimulus-response curves	∼5%–10% (force)	Supine with the shoulder abducted 40 degrees
Berth (Dec. 2009)	To investigate the neuromuscular alterations of the middle deltoid in participants with unilateral chronic rotator cuff tears and in participants without shoulder pathology with transcranial magnetic stimulation, to provide a better understanding of adaptive changes in the motor cortex after chronic rotator cuff tears	Transcranial magnetic stimulation	middle deltoid	-Active motor threshold-Motor evoked potential amplitude-stimulus-response curve slope	Not specified	Supine with the shoulder abducted 40 degrees
Vangsgaard (2012)	To determine whether the H reflex in trapezius was altered in the presence of delayed-onset muscle soreness. The reproducibility of the H reflex in the trapezius was also investigated to address methodological issues due to variability in the H reflex between days	Hoffman reflex	Trapezius	-Normalised maximal Hoffman reflex amplitude-Hoffman reflex latency-M-wave amplitude-M-wave latency-Stimulus-response curve slope-Hi-50-Hi-75	15 ± 2% (Electromyography)	Seated with back supported
Ngomo (2015)	To investigate whether rotator cuff tendinopathy leads to changes in central motor representation of a rotator cuff muscle, and to assess whether such changes are related to pain intensity, pain duration, and physical disability	Transcranial magnetic stimulation	Infraspinatus	-Active motor threshold-stimulus-response curve slope	5% ± 1% (Electromyography)	Seated with 40 degrees of shoulder abduction
Bradnam et al. (2016)	To characterise short afferent inhibition and the cortical silent period in the primary motor cortex representations of the infraspinatus muscle in healthy adults and people experiencing chronic shoulder pain, and to determine the impact of a suprascapular nerve block in those with chronic shoulder pain.	Transcranial magnetic stimulation	Infraspinatus	-Active motor threshold-cortical silent period-Motor evoked potential amplitude at 120% active motor threshold	Not specified (Electromyography)	Seated with their dominant or painful upper limb positioned in 5 degrees of shoulder flexion, 10 degrees of abduction, and 45 degrees of external rotation and 120 degrees of elbow flexion and limb supported under the elbow
Belley (2018)	To evaluate the added benefit of anodal transcranial direct current stimulation combined with a rehabilitation programme centred on sensorimotor training for symptoms and functional limitations of individuals with rotator cuff tendinopathy, and to evaluate the immediate effects of these interventions on corticospinal excitability.	Transcranial magnetic stimulation	Infraspinatus	-Motor evoked potential amplitude at 120% active motor threshold	5% ± 1% (Electromyography)	Not described
Stefanelli et al. (2019)	To examine whether application of topical menthol-based analgesic affected measures of corticospinal excitability and spinal excitability, to study the influence of delayed-onset muscle soreness of the elbow flexors on indices of corticospinal excitability and spinal excitability, and to investigate the interactive effect of delayed-onset muscle soreness of the elbow flexors and the topical analgesic on measures of corticospinal excitability and corticospinal inhibition of the biceps brachii	Transcranial magnetic stimulation	Biceps brachii	-Motor evoked potential latency at 120% active motor threshold-Cortical silent period-Motor evoked potential area/maximum M-wave amplitude at 120% active motor threshold	5% (force)	Seated with back and head supported and strapped in place, with hips and knees flexed 90 degrees, shoulder slightly abducted, and elbow flexed 90 degrees and supported on pads with wrists midway between pronation and supination and stabilised by custom-made orthosis.
Laramee (2021)	To assess feasibility of conducting a randomised sham-controlled trial and to collect preliminary data on the effects of infraspinatus dry needling on corticospinal excitability and mechanical pain sensitivity	Transcranial magnetic stimulation	Infraspinatus	-Active motor threshold	7.5% ± 2.5% (force)	Not described
Chung et al (2022)	To assess and compare corticospinal excitability in the upper and lower trapezius and serratus anterior muscles in participants with and without subacromial impingement syndrome	Transcranial magnetic stimulation	Serratus anteriorLower trapeziusUpper trapezius	Serratus anterior:-Active motor threshold -Motor evoked potential amplitude-Motor evoked potential latency-Cortical silent period at 120% active motor thresholdLower trapezius:-Active motor threshold-Motor evoked potential amplitude-Motor evoked potential latency-Cortical silent period at 120% active motor thresholdUpper trapezius:-Active motor threshold-Motor evoked potential amplitude-Motor evoked potential latency-Cortical silent period at 120% active motor threshold	10%–15% (force)	Seated with arm actively elevated 90 degrees in the scapular plane
Takeno (2022)	To compare measures of neuromuscular function in the upper extremity musculature between individuals with glenohumeral labrum repair and uninjured controls	Transcranial magnetic stimulation	Middle deltoidUpper trapezius	Middle deltoid:-Active motor thresholdUpper trapezius:-Active motor threshold	Upper trapezius:-15% (force)Middle deltoid:-20% (force)	Seated upright	Upper Trapezius active motor threshold:-ICC(3,1) = 0.81-SEM: 1.41%, -MDC95: 3.89%Middle deltoid active motor threshold:-ICC(3,1) = 0.89, -SEM: 0.94%, -MDC95: 2.60%
Melo et al. (2023)	To assess the possible differences in trapezius neural excitability between participants with shoulder pain and asymptomatic participants	Hoffman reflex	Upper trapeziusMiddle trapeziusLower trapezius	Upper trapezius:-Maximum Hoffman reflex amplitude/maximum M-wave amplitude-Maximum Hoffman reflex latencyMiddle trapezius:-Maximum Hoffman reflex amplitude/maximum M-wave amplitude-Maximum Hoffman reflex latencyLower trapezius:-Maximum Hoffman reflex amplitude/maximum M-wave amplitude-Maximum Hoffman reflex latency	Not specified	Sitting position with 2/3 of the thigh supported, the knee and hip at 90 deg of flexion, the feet on the floor and with the head, pelvis and trunk in a neutral position. Shoulders held against gravity at 90 deg abduction in the scapular plane, with the forearm in neutral position and the elbow extended. Arms were supported during Mmax assessment
Bouchard et al. (2024)	To describe how participants with subacromial impingement syndrome respond to transcranial magnetic stimulation procedures as well as feasibility issues encountered, and to verify whether transcranial magnetic stimulation outcome measures discriminate between participants with subacromial impingement syndrome and asymptomatic participants, and between painful and non-painful sides in subacromial impingement group	Transcranial magnetic stimulation	Upper trapezius	-Resting motor threshold-Motor evoked potential amplitude at 120% resting motor threshold-Motor evoked potential latency at 120% resting motor threshold	∼0% (resting)	Seated with shoulder resting at side
Duport (2024)	To investigate whether kinesiophobia modulates pain-induced changes in upper limb kinematic parameters and shoulder muscle activation during a precise pointing task, as well as changes in the corticospinal excitability of the anterior deltoid muscle involved in arm flexion	Transcranial magnetic stimulation	Anterior deltoid	-Stimulus-response curve slope	10% ± 2% (Electromyography)	Seated with feet resting on the footrest, head resting on the headrest
Luo (2024)	To examine the changes in the corticospinal mechanisms after a 30-min session of scapular-orientation or strength training in individuals with shoulder impingement syndrome.	Transcranial magnetic stimulation	Lower trapezius Serratus anterior	Lower trapezius:-Active motor threshold-Motor evoked potential amplitude at 120% active motor threshold-Cortical silent period at 150% lower trapezius active motor thresholdSerratus anterior:-Motor evoked potential amplitude at 120% lower trapezius active motor threshold-Cortical silent period at 150% lower trapezius active motor threshold	20%–25% of lower trapezius (Electromyography)	Seated with shoulder elevated 90 degrees in scapular plane	Transcranial magnetic stimulation variables: -ICC: .911- .981
Takeno (2024)	To determine whether common measures of upper extremity neuromuscular function could distinguish between individuals with and without glenohumeral labral repair, and how accurately selected measures could classify injury status.	Transcranial magnetic stimulation	Upper trapezius Middle deltoid	Upper trapezius:-Active motor thresholdMiddle deltoid:-Active moor threshold	Not specified	Seated upright
Duport (2025)	To determine whether kinesiophobia can modulate changes induced by shoulder pain on kinematic parameters and muscle activation during a pointing task, and corticospinal excitability.	Transcranial magnetic stimulation	Anterior deltoid	-Stimulus-response curve slope	10% ± 2%	Seated upright
Duport (2026 March)	To use a non-negative matrix factorisation coordination-based approach to investigate relationships between pain- related changes in muscle coordination and corticospinal excitability during a pointing task.	Transcranial magnetic stimulation	Anterior deltoid	-Stimulus-response curve slope-Stimulus intensity required to elicit 50% of maximum motor evoked potential amplitude	10% ± 2%	Seated with feet and head supported
Duport (2026 April)	To evaluate the interaction between CSE excitability in different muscles and endogenous pain modulation, and to determine whether kinesiophobia and pain catastrophising modulate this interaction	Transcranial magnetic stimulation	Anterior deltoid	-Stimulus-response curve slope-Stimulus intensity required to elicit 50% of maximum motor evoked potential amplitude	10% ± 2%	Seated with arms and head supported

Table 2 summarises the included studies which compare participants with painful shoulder conditions with controls. Ten of the included studies compared the motor excitability of individuals with painful shoulder conditions to that of asymptomatic controls. Clinical painful shoulder conditions in participants were variable and included rotator cuff tear, rotator cuff tendinopathy, subacromial impingement syndrome, non-traumatic glenohumeral joint instability, postoperative glenohumeral labrum repair, and nonspecific shoulder pain. Of these ten studies, nine observed overall decreases in motor excitability in at least one measure of motor excitability compared to asymptomatic controls.^{24–26,33,35,36,38,40,43} One study among these that did not find differences only reported on the resting motor threshold as missing data disallowed comparison of other measures of motor excitability.³⁴

Table 2.

Comparisons of shoulder muscle motor excitability between participants with clinical shoulder pain and controls.

Article	Painful shoulder group	Control	Variables indicating a decrease in the excitability of the shoulder muscles
Alexander (2007)	11 participants with non-traumatic shoulder instability	8 asymptomatic participants	Lower trapezius:-Active motor threshold-Motor evoked potential latency
Berth (Sep. 2009)	10 men with >6 months of shoulder pain and a large, massive rotator cuff tear	13 asymptomatic participants	Middle deltoid:-Stimulus-response curve slope
Berth (Dec. 2009)	6 men with >6 months of shoulder pain and large, massive rotator cuff tear	Contralateral shoulders	Middle deltoid:-Motor evoked potential amplitude
Ngomo 2015	39 participants with unilateral rotator cuff tendinopathy	Contralateral shoulders	Infraspinatus:-Active motor threshold
Bradnam et al. (2016)	8 participants with >1 year of shoulder pain	18 asymptomatic participants	Infraspinatus:-Active motor threshold-Cortical silent period
Chung et al. (2022)	14 participants with subacromial impingement syndrome	14 asymptomatic participants	Lower trapezius:-Active motor threshold-Cortical silent periodSerratus anterior:-Active motor threshold
Takeno (2022)	16 participants with a history of glenohumeral labral repair >6 months prior	14 asymptomatic participants	Upper trapezius:-Active motor threshold
Melo et al. (2023)	12 participants with continuous nonspecific shoulder pain or 2 episodes of shoulder pain within the last 3 months	12 asymptomatic participants	Upper trapezius:-Maximum Hoffman reflex amplitude/maximum M-wave amplitudeLower trapezius:-Maximum Hoffman reflex latency
Bouchard et al. (2024)	15 participants with >3 months of unilateral subacromial impingement syndrome	15 asymptomatic participants	None
Takeno (2024)	16 participants with a history of unilateral glenohumeral labral repair	14 asymptomatic participants	Upper trapezius:-Active motor threshold

Table 3 summarises the included studies which compare participants before and after experimental shoulder pain is induced. Participants with experimental shoulder pain induced by a topical irritant were assessed in four studies,^37,44–46 and participants with experimental pain induced by delayed onset muscle soreness were included in two studies.^39,41 In both studies using delayed-onset muscle soreness as an experimental pain model, decreases in motor excitability in at least one measure of motor excitability were observed.^39,41 In three of four studies using topical irritant (1% topical capsaicin cream) as the experimental pain model, no alterations in motor excitability were observed for any measure of motor excitability^37,44–45 with one study reporting conflicting evidence with one variable indicating a decrease in motor excitability.⁴⁶

Table 3.

Comparisons of motor excitability in participants before and after experimentally induced shoulder pain.

Article	Experimental pain participants and model	Variables indicating a decrease in the excitability of the shoulder muscles
Vangsgaard (2012)	13 asymptomatic and untrained participants with delayed-onset muscle soreness of scapular retractors	Middle trapezius:-Stimulus intensity required to elicit maximum Hoffman reflex amplitude-Maximum Hoffman reflex amplitude/maximum M-wave amplitude at stimulus intensity required to elicit 75% maximum Hoffman reflex amplitude-Maximum Hoffman reflex amplitude/maximum M-wave amplitude at stimulus intensity required to elicit 50% of maximum Hoffman reflex amplitude
Stefanelli et al. (2019)	16 asymptomatic men with delayed-onset muscle soreness of elbow flexors	Biceps brachii:-Motor evoked potential area/Mmax area-Cortical silent period
Duport (2024)	30 asymptomatic participants with experimental pain induced by 1% topical capsaicin cream at the right deltopectoral groove	None
Duport (2025)	35 asymptomatic participants with experimental pain induced by 1% topical capsaicin cream at the right deltopectoral groove	None
Duport (2026 March)	21 asymptomatic participants with experimental pain induced by 1% topical capsaicin cream at the right deltopectoral groove	None
Duport (2026 April)	20 asymptomatic participants with experimental pain induced by 1% topical capsaicin cream at the right deltopectoral groove	-Stimulus intensity required to elicit 50% of maximum motor evoked potential amplitude

Table 4 summarises the included studies which examine intervention effects on shoulder muscle motor excitability. Among the three studies examining intervention effects on motor excitability, increased excitability was observed in two studies in at least one measure of motor excitability.^31,32,42 Increases in motor excitability were observed following dry needling, sham dry needling, and resistance-based exercise with and without feedback.

Table 4.

Effects of interventions on motor excitability in participants with painful shoulder conditions.

Article	Variables indicating increased excitability of shoulder muscles following intervention	Interventions resulting in a change in excitability	Interventions not resulting in a change in excitability
Belley (2018)	None	None	-Sensorimotor training-Anodal transcranial direct current stimulation
Laramee (2021)	Infraspinatus:-Active motor threshold	-Dry needling-Sham dry needling	None
Luo (2024)	Lower trapezius:-Motor evoked potential amplitudeSerratus anterior:-Motor evoked potential amplitude	-Resistance exercise-Scapular-oriented exercise	None

Discussion

This review has identified preliminary research exploring altered motor excitability as a mechanism and treatment target in musculoskeletal shoulder conditions. Frequently, decreases in motor excitability were observed in the studies that compared participants with clinical shoulder conditions to controls. Furthermore, decreased motor excitability was observed in three of six studies examining participants with experimental shoulder pain. These findings collectively suggest that shoulder pain may directly contribute to decreased motor excitability observed in those with clinical shoulder pain. However, the pain models in these studies used topical irritants and delayed-onset muscle soreness as experimental pain models, which may not accurately model pain experienced during many shoulder conditions.^47,48 Furthermore, discordant effects that are observed between each of these models suggest that enhanced pain models that more accurately model pain experienced during clinical shoulder conditions may provide clarification. If pain directly contributes to decreased motor excitability, then adequate and early pain management may be necessary during rehabilitation of those with clinical shoulder conditions so as to minimise maladaptive decreases in motor excitability. While the acute effect of shoulder pain on motor excitability remains contentious, the acute effect of pain may not completely explain motor excitability changes in those with chronic shoulder pain. Other secondary factors apart from pain, such as decreased use⁴⁹ or sleep dysfunction⁵⁰ may also be relevant factors contributing to observed decreases in motor excitability in those with chronic clinical shoulder pain. Preliminary studies exploring the effects of exercise and non-exercise interventions on motor excitability suggest that motor excitability is increased following resistance exercise and both dry needling and sham dry needling.^31,32 These early findings are consistent with previous studies examining the effects of resistance exercise on motor excitability in other body regions.^44,51 Resistance exercise has shown clinical effectiveness in the management of shoulder pain and is recommended for clinical management,⁵² and this review highlights one potential mechanism of effect of resistance exercise. Of note, the effect of resistance exercise on motor excitability of shoulder musculature appears mixed, as one study examining the effect of multimodal intervention, including resistance exercise, did not observe altered motor excitability following intervention.⁴² These mixed results suggest that the effect of resistance exercise on motor excitability may depend on exercise parameters, which may be clarified with future research. In one study,³¹ dry needling and sham dry needling resulted in increased shoulder muscle motor excitability and provided evidence that interventions that provide somatosensory input may play a role in modulating motor excitability in those with chronic shoulder pain. The clinical relevance of these neurophysiological changes following such interventions should be examined, particularly when combined with exercise-based interventions.

One limitation of this scoping review is that no quantitative analysis is provided. Heterogeneity among the included studies limits the feasibility of quantitative analyses and is evident in participant demographics, shoulder pain conditions, and methods used to characterise motor excitability. Future work appears necessary to standardise methods of both transcranial magnetic stimulation and Hoffman reflex assessment when measuring motor excitability in individuals with shoulder pain. Considering the relatively small sample sizes across the included studies, which ranged from 6 to 41 participants, more homogeneous work examining these neurophysiological measures in individuals with shoulder pain would permit pooled analyses, which would enhance the validity of conclusions derived from such work. In addition, only two of the included studies in this review reported on the reliability of the obtained measures.^32,40 Given that there is otherwise limited evidence for high reliability of transcranial magnetic stimulation measurements of many shoulder muscles,⁵³ and that these measurements may be operator dependent, the degree of measurement error relative to the distinct effects of pain or interventions which were reported in the included studies remains unclear. Reliability analyses should be included in future work that uses these measurements. In summary, this review highlights growing acknowledgement of motor excitability as a potential mechanism and treatment target in musculoskeletal shoulder pain, but future work appears necessary to clarify factors influencing motor excitability as well as determine whether targeting of motor excitability leads to clinically significant improvement in individuals with musculoskeletal shoulder disorders.

Clinical messages

Shoulder motor excitability appears decreased in the presence of clinical musculoskeletal shoulder pain.

Experimental pain models suggest pain may contribute to decreased shoulder muscle motor excitability, but further research is warranted.

In order to minimise nervous system maladaptations in those with shoulder pain, clinicians may emphasise pain management and the use of interventions that enhance motor excitability of the shoulder musculature.

Preliminary studies report increases in excitability following interventions, yet the clinical significance of these improvements should be clarified.

Supplemental Material

sj-docx-2-cre-10.1177_02692155261458737 - Supplemental material for Motor excitability in painful musculoskeletal shoulder conditions: A scoping review

Supplemental material, sj-docx-2-cre-10.1177_02692155261458737 for Motor excitability in painful musculoskeletal shoulder conditions: A scoping review by Jeffrey S Paskewitz, Daniel W Safford, Kshamata M Shah and Philip W McClure in Clinical Rehabilitation

Supplemental Material

sj-pdf-3-cre-10.1177_02692155261458737 - Supplemental material for Motor excitability in painful musculoskeletal shoulder conditions: A scoping review

Supplemental material, sj-pdf-3-cre-10.1177_02692155261458737 for Motor excitability in painful musculoskeletal shoulder conditions: A scoping review by Jeffrey S Paskewitz, Daniel W Safford, Kshamata M Shah and Philip W McClure in Clinical Rehabilitation

Footnotes

ORCID iDs

Jeffrey S Paskewitz

Philip W McClure

Ethical considerations

No IRB approval was required to conduct this scoping review.

Consent to participate

Not applicable

Consent for publications

Not applicable

Funding

The authors received no financial support for the research, authorship, and/or publication of this article.

Declaration of conflicting interests

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Data availability statement

Data from this review are available in supplementary materials.

Supplemental material

Supplemental material for this article is available online.

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