Journal of Muscle IQ - Volume 9
May of 2026
 

Central Nervous System Contributions to

Musculoskeletal Pain and Motor Dysfunction

A Research Synthesis of 11 Studies

Chris Knudsen, DPT

Muscle IQ Physical Therapy | Orem, Utah

May 2026

Note on Sources

Verbatim quotes (in italics with quotation marks) are drawn from open-access full text: Mata et al. (2024), Navarro-Santana et al. (2022), and Venezia et al. (2024). For the remaining 8 studies, findings are represented accurately based on the published abstracts and author-reported results.

Introduction

Pain does not live only in the tissues. Decades of neurophysiology research have established that the brain, brainstem, and spinal cord are active participants in the generation, amplification, and suppression of pain — and that in many common musculoskeletal conditions, those central systems become part of the problem. Standard strength testing — the most common measure used to clear patients for return to activity — can miss this dysfunction entirely. A strength test measures final force output: the end result of everything the nervous system did to move the muscle. What it cannot detect is whether the nervous system fully “switched on” the muscle to produce that force, or whether it was quietly compensating. Voluntary activation testing measures how completely the nervous system recruits available muscle fibers during a maximal effort. Motor unit analysis goes deeper still, examining the individual nerve-fiber groups the nervous system uses — how many are firing, at what rates, and in what sequence. A patient can produce a normal force number on a dynamometer while the nervous system is compensating: recruiting fewer motor units at abnormally high firing rates, using substitute muscle patterns, or reorganizing recruitment in ways that pass a force test but represent genuine underlying dysfunction. The research in this synthesis documents exactly this phenomenon: motor unit deficits and voluntary activation failure that persist even after strength symmetry is restored.

What makes this especially relevant clinically is that several common assessment tools — tissue sensitivity, autonomic reactivity, motor output — may all be reading the same underlying brainstem system, suggesting that what a clinician observes across different tests may reflect a single central state rather than isolated local findings.

This synthesis draws together 11 peer-reviewed studies organized around a single clinical question: What does the research tell us about how the central nervous system (CNS) contributes to musculoskeletal pain and motor dysfunction, and what does that mean for how we treat it?

The 11 studies address four interconnected topics: (1) how the motor system fails centrally in common knee conditions; (2) how the brain's pain-inhibition system is impaired in chronic pain; (3) how the autonomic nervous system and pain modulation are connected through the brainstem; and (4) what treatments actually restore central pain processing — and what does not.

The evidence converges on four consistent findings. First, the nervous system is not a passive conductor of signals from injured tissue — it is an active participant in generating, amplifying, and suppressing pain, and its dysfunction cannot be detected by standard force testing alone. Second, multiple clinical measurements that appear to be separate tools — Conditioned Pain Modulation (CPM), Heart Rate Variability (HRV), skin conductance, and local pressure pain sensitivity — are likely reading the same underlying brainstem state through different windows, with meaningful implications for how clinicians interpret treatment responses. Third, restoring central pain processing requires a therapeutic dose: single-session interventions produce real local effects but do not shift the brain’s pain inhibition system; that requires a sustained, multimodal approach over multiple sessions. Fourth, the timing of sensorimotor rehabilitation matters biologically — the window for restoring normal sensory input before the brain reorganizes around a compensatory strategy is early and should not be missed.

Part 1: The Motor System Is Centrally Impaired in Common Musculoskeletal Conditions

1.1 Efferent Pathway Dysfunction Across the Three Most Common Knee Diagnoses

Sherman et al. (2024) conducted a narrative review synthesizing neuroimaging and neurophysiological research across anterior cruciate ligament (ACL) injury, anterior knee pain (patellofemoral pain), and knee osteoarthritis (OA). The review mapped motor system dysfunction from the motor cortex down through the corticospinal tract to the spinal motoneuron pool and final muscle force output — the complete efferent (outgoing motor command) pathway.

The central finding: altered motor system excitability and reduced voluntary muscle activation are present in all three knee pathologies. The impairment is not isolated to one level — dysfunction appears at every step of the motor pathway. Yet the specific mechanisms differ across conditions, meaning no single explanation covers all three diagnoses.

Most critically for clinical practice, the authors found that motor unit deficits — the fine grain of how the nervous system recruits muscle fibers — persist even after conventional strength metrics have normalized. A patient who passes a strength test may still have measurably impaired motor cortex excitability and voluntary activation. The force number on a dynamometer is not the same thing as the nervous system's capacity to drive the muscle.

Key finding: Standard strength testing is insufficient to detect or track central motor system impairment. Neurophysiologic assessment — Transcranial Magnetic Stimulation (TMS), voluntary activation testing, motor unit analysis — is necessary to characterize what is actually happening in the motor pathway.

1.2 ACL Injury Disrupts All Three Levels of the Sensorimotor System Simultaneously

Vitharana et al. (2025, Part 1) provided a clinical framework for understanding sensorimotor dysfunction after ACL injury. The framework organizes impairment into three systems: the afferent pathway (incoming sensory signals from the joint and muscles), the efferent pathway (outgoing motor commands from the brain), and central processing (how the brain integrates and responds to signals).

After ACL injury, all three systems are disrupted at once. On the afferent side: pain and swelling increase the processing demand on the brain, and proprioception (joint position sense) is reduced. On the efferent side: motor cortex excitability is reduced, descending motor drive is impaired, and spinal reflex excitability is acutely suppressed and chronically dysregulated. In the central processing system: the brain compensates for lost proprioceptive feedback by shifting to visual-motor control — athletes begin watching their movements rather than feeling them.

This visual compensation appears to become entrenched over time if not addressed. An athlete who looks "strong" in a strength test may still have impaired descending motor drive, altered motor unit recruitment, and a nervous system that has reorganized around a less accurate sensory input.

Key finding: ACL rehabilitation that focuses only on restoring strength and function misses two-thirds of the problem. The afferent and central processing deficits must be addressed in parallel, beginning early in rehabilitation.

Part 2: Central Sensitization in Chronic Pain — When the Nervous System Becomes the Problem

2.1 Knee Osteoarthritis — The Brain's Pain Off-Switch Is Broken

Conditioned Pain Modulation (CPM) is the clinical test used to measure how well the brain's descending pain inhibitory system is working. In a CPM test, a test pain stimulus is measured before and during a second, remote painful stimulus. In a healthy nervous system, the second stimulus activates brainstem inhibitory pathways that reduce the first pain — the brain turns down the volume on incoming pain signals. A reduced CPM response means this system is not working effectively.

Temporal Summation of Pain (TSP) measures the opposite tendency — how quickly the spinal cord amplifies repeated pain signals. In TSP testing, identical painful stimuli are applied repeatedly; a healthy spinal cord keeps the perceived pain relatively constant, while a sensitized spinal cord allows it to build with each repetition.

Rodríguez-Lagos et al. (2025) conducted a systematic review and meta-analysis of 19 studies comparing CPM and TSP in knee osteoarthritis (KOA) patients versus healthy controls. The results were consistent: KOA patients showed lower CPM efficiency (moderate effect size, SMD = -0.55) and both higher local and remote TSP (small effect sizes). Both findings were statistically significant across hundreds of patients and controls.

This means that knee OA is not just a joint problem. The brain's pain inhibition system is less effective in KOA patients, and the spinal cord is amplifying repeated pain signals more than it should. Both are signatures of central sensitization — a state in which the nervous system itself has become primed to generate and amplify pain, independent of the ongoing tissue damage in the joint.

Key finding: Treating only the knee joint in KOA — through injection, mobilization, or even surgery — leaves the centrally sensitized nervous system untouched. Central sensitization may explain why many patients continue to experience pain after apparently successful joint-level interventions.

2.2 Chronic Knee Pain Decouples Pain Modulation from Autonomic State

Uzawa et al. (2025) studied 90 female patients with knee pain, divided into those with chronic knee pain (pain lasting 3 months or more) and those with non-chronic knee pain (pain less than 3 months). They measured both CPM and autonomic nervous system (ANS) function using Heart Rate Variability (HRV) — beat-to-beat variation in heart rate, a measure of how the autonomic system is functioning.

In non-chronic knee pain patients, the two measures tracked together: autonomic state and CPM were positively associated. This is the expected relationship — the autonomic nervous system and the pain modulatory system share overlapping brainstem circuitry, and in a relatively intact nervous system, they move together.

In chronic knee pain patients, that association disappeared. CPM became decoupled from autonomic state. Instead, sympathetic nervous system activity in the chronic group was driven by pain catastrophizing (unhelpful pain-related thoughts) and the number of body sites experiencing pain — not by the pain modulation system. The normal regulatory relationship had broken down.

Key finding: Chronic pain does not simply amplify the normal pain experience — it reorganizes the underlying regulatory systems. The tools that work for assessing and treating non-chronic pain may operate differently in patients whose chronicity has decoupled the system.

Part 3: The Brain's Pain Off-Switch — How the Autonomic Nervous System and Pain Modulation Are Connected

3.1 Heart Rate Variability and CPM Are Linked Through the Periaqueductal Grey

Makovac et al. (2021) conducted a multi-modal neuroimaging study in 30 healthy adults, simultaneously measuring CPM efficiency, Heart Rate Variability (HRV), and brain activity using functional and structural MRI. Their goal was to identify the neuroanatomical bridge between autonomic state and pain modulation.

The key finding: the Periaqueductal Grey (PAG) — a brainstem region long recognized as the primary hub of descending pain modulation — mediates the relationship between HRV and CPM. Individuals with greater autonomic reactivity during pain had more effective CPM, and this relationship was mediated by connectivity between the PAG and the ventromedial prefrontal cortex. The PAG was also structurally associated with CPM efficiency — people with more grey matter volume in the PAG had better pain inhibition.

This study provides the neuroanatomical explanation for why autonomic state and pain modulation move together. The PAG does not simply modulate pain — it integrates autonomic information to set the gain of the descending pain inhibitory system. An intervention that shifts autonomic state shifts the input to the PAG and therefore, plausibly, the output of the pain modulatory system.

Key finding: The brainstem PAG is the shared hardware for autonomic regulation and pain modulation. Interventions that calm the autonomic system — manual therapy, sensory input, cranial nerve stimulation — may improve descending pain modulation through the same PAG circuitry, not as a separate effect.

3.2 The Baroreflex — A Second Autonomic Gateway to Pain Modulation

Venezia et al. (2024) studied the relationship between baroreflex function and pain modulation in 22 patients with chronic low back pain (CLBP) and 29 pain-free controls. The baroreflex is the body's automatic blood pressure stabilizer — specialized pressure-sensitive receptors in the blood vessel walls that continuously regulate heart rate and blood pressure to maintain homeostasis.

In pain-free participants, activating the baroreflex reduced pain. The body's blood pressure regulation system naturally dampens pain perception. Venezia et al. confirmed this:

"baroreflex stimulation reduced perceived pressure pain in NP participants, whereas the opposite pattern was observed in CLBP participants"

— Venezia et al. (2024), doi:10.1113/JP286375

In chronic low back pain patients, the same baroreflex activation increased pain instead of reducing it. The normal pain-inhibitory effect of baroreflex function had inverted — become pain-facilitatory.

The study also confirmed that baroreflex sensitivity correlated with CPM efficiency in both groups. Even in chronic pain, the structural relationship between baroreflex function and pain modulation capacity was preserved — but the direction of the effect had flipped. The authors described this as a pathological shift:

"the influence of the baroreflex on descending pain modulation pathways may shift towards pain facilitation rather than pain inhibition during stress"

— Venezia et al. (2024), doi:10.1113/JP286375

The clinical and research implications are significant:

"Our data provide evidence that indicates the importance of baroreflex functioning in pain modulatory processes in NP and CLBP participants... We suggest they provide enticing potential as markers of pain severity and movement towards the much needed mechanism-based profiling of individuals with chronic pain."

— Venezia et al. (2024), doi:10.1113/JP286375

Key finding: The cardiovascular system is not separate from the pain system — they share regulatory infrastructure. In chronic pain, normally inhibitory autonomic mechanisms can invert and become pain-facilitatory. This is a second pathway, alongside the HRV-PAG connection documented by Makovac (2021), through which autonomic dysregulation drives persistent pain.

Part 4: What Treatments Actually Restore Central Pain Processing

4.1 Comprehensive Manual Therapy — 4 Sessions Restores CPM and TSP

Mata et al. (2024) recruited 63 patients with chronic neck pain and treated them with 4 weekly sessions of comprehensive manual therapy — approximately 45 minutes per session, combining articular passive mobilization, soft tissue mobilization, and trigger point treatment. CPM and TSP were measured before and after the treatment course.

After 4 sessions, both central pain processing measures normalized:

"The present work provides novel evidence of restoration of normal central pain processing following manual therapy in NSCNP patients, as shown by TSP, CPM and PPT values returning to levels comparable to normative data."

— Mata et al. (2024), doi:10.1371/journal.pone.0294100

The CPM improvement is particularly significant. The authors explain why CPM is a meaningful target:

"An enhanced CPM is considered to reflect greater efficacy of endogenous analgesia mechanisms and thus a more favorable position to control central excitation induced by incoming peripheral nociceptive input."

— Mata et al. (2024), doi:10.1371/journal.pone.0294100

Both clinical outcomes (less pain, less disability, less fear of movement) and central processing measures improved. However, the two were not tightly correlated with each other — suggesting that manual therapy works through multiple mechanisms simultaneously:

"Collectively, the present observed beneficial effects on TSP and CPM responses support the notion that manual therapy may operate, to some extent, by influencing central pain processing to ameliorate pain and improve clinical status. Nonetheless, the fact that no clear association was observed between restoration of normal central pain processing and clinical outcome suggests a plurality of underlying mechanisms... the mechanism of action of manual therapy may be inherently multifactorial."

— Mata et al. (2024), doi:10.1371/journal.pone.0294100

Key finding: 4 weeks of comprehensive manual therapy normalizes both the brain's pain inhibition system (CPM) and the spinal cord's pain amplification tendency (TSP) in chronic neck pain. The treatment dose matters — this was a multi-modal, 45-minute, 4-session protocol, not a single brief intervention.

4.2 Motor Control Exercise — A Specific Exercise Modality That Improves CPM

Chen et al. (2024) conducted a systematic review with meta-analysis examining exercise effects on CPM and TSP across patients with chronic musculoskeletal pain. Thirteen studies were included, covering aerobic exercise, resistance exercise, isometric exercise, and motor control exercise.

The overall finding was that exercise as a category does not significantly change CPM or TSP. Generic aerobic or resistance exercise did not produce consistent improvements in central sensitization measures. However, motor control exercise — exercise that demands active attention to movement pattern, position sense, and neuromuscular coordination — produced a significant enhancing effect on CPM, particularly in patients with chronic neck pain.

This is a critically important distinction. Not all exercise is equivalent in its effect on the central pain processing system. Motor control exercise, which directly engages the neuromuscular system's capacity to generate precise, coordinated output, may engage the same brainstem descending modulatory circuitry that CPM measures. Generic exercise may produce clinical benefits through peripheral, metabolic, or psychological pathways without specifically restoring descending pain inhibition.

Key finding: Modality matters within exercise, just as dose matters in manual therapy. Motor control exercise is the specific exercise category associated with CPM improvement — not generic strengthening or aerobic exercise.

4.3 Single-Session Interventions Do Not Change CPM

Martínez Pozas et al. (2024) conducted a well-designed randomized controlled trial comparing a single session of mobilization with movement versus sham mobilization in 58 patients with chronic low back pain. They measured CPM, Pressure Pain Threshold (PPT), and movement-related pain intensity immediately before and after the intervention.

No significant differences were found between real and sham mobilization on any of the three outcomes. All effect sizes were small. The authors noted that patients had not been pre-screened for CPM dysfunction — meaning some participants with already-normal CPM were included, which would dilute any detectable effect.

This study should be read alongside Mata (2024) as a dose-response contrast, not a contradiction. A single brief mobilization session is not the same intervention as four 45-minute comprehensive manual therapy sessions. The absence of effect here does not mean mobilization is ineffective — it means a single session is unlikely to be sufficient to shift the central pain system.

Key finding: A single manual therapy session does not restore CPM in unselected chronic low back pain patients. Restoring central pain processing appears to require a therapeutic dose — multiple sessions, multimodal treatment, sufficient total contact time.

4.4 Dry Needling — Changes Autonomic State and Local Sensitivity, But Not CPM After One Session

Navarro-Santana et al. (2022) conducted a double-blinded randomized controlled trial comparing real dry needling to sham dry needling in 60 patients with chronic neck pain. They measured skin conductance (a direct readout of sympathetic nervous system activation), local Pressure Pain Thresholds, Temporal Summation, and CPM — before and immediately after the single-session intervention.

The results were specific and informative:

"dry needling had no effect on neural excitability (measured by TS) nor the diffuse noxious inhibitory control (measured by CPM). Maybe one of the most interesting findings is the fact that dry needling seems to induce autonomic nervous system responses (measured by SC), since we identified greater percentages of change (but not absolute values) of skin conductance when compared with sham needling."

— Navarro-Santana et al. (2022), doi:10.3390/jcm11226616

In plain terms: dry needling changed the sympathetic nervous system (measured by skin conductance) and reduced local tissue sensitivity (measured by PPT at the needled site) — but did not change the brain's global pain inhibition system (CPM). The authors' conclusion:

"dry needling applied to patients with chronic nonspecific neck pain produced an immediate decrease in mechanical hyperalgesia at local sites and produced an increase in skin conductance as compared with sham needling."

— Navarro-Santana et al. (2022), doi:10.3390/jcm11226616

This pattern — ANS change and local sensitivity change without CPM change — has direct implications for how we interpret our clinical tools. Skin conductance and Pressure Pain Threshold move together in response to a peripheral intervention; CPM does not. This is consistent with the Uzawa (2025) finding that in chronic pain, CPM has decoupled from autonomic state.

Key finding: Dry needling produces real, measurable effects — sympathetic activation and local desensitization. But these are not the same as restoring the brain's global pain off-switch. The two systems are not identical, and their response to treatment is not identical.

Part 5: Rehabilitation — A Framework for Addressing the Whole System

5.1 Fix the Afferent Pathway Early; Restore Efferent Function Throughout

Vitharana et al. (2025, Part 2) provided the rehabilitation counterpart to the assessment framework in Part 1. Their framework organizes ACL rehabilitation around two parallel priorities, with timing considerations for each:

Priority 1 — Restore somatosensory function and reduce visual-motor reliance. Proprioceptive (joint position sense) training should begin within the first six weeks of injury or surgery, before the brain's compensatory shift to visual-motor control becomes entrenched. If this window is missed, the brain reorganizes around a less accurate input, and that compensation becomes more difficult to undo. Training complexity should progressively challenge the patient by varying task type, available visual information, cognitive load, and perturbations.

Priority 2 — Improve peripheral and central efferent function. This priority runs throughout rehabilitation. In the acute phase, cryotherapy and transcutaneous electrical nerve stimulation (TENS — electrical stimulation through the skin) reduce pain and improve initial muscle recruitment. Throughout rehabilitation, progressive strength training, neuromuscular electrical stimulation (NMES), and surface electromyographic (EMG) biofeedback at high intensity improve both central and peripheral motor output capacity.

Key finding: The rehabilitation timing of sensory input restoration matters. Delaying proprioceptive training allows visual-motor compensation to become dominant — a harder problem to reverse. Sensorimotor rehabilitation must start early, not after strength is re-established.

Synthesis: What the Evidence Tells Us Together

The Central Nervous System Is Not a Bystander in Musculoskeletal Pain

Across all 11 studies, the same theme emerges: the nervous system is an active participant in musculoskeletal pain and motor dysfunction — not a passive conductor of signals from injured tissue. Motor cortex excitability is reduced in ACL injury, anterior knee pain, and knee OA (Sherman, 2024; Vitharana, 2025). The brain's pain inhibitory system is impaired in knee OA (Rodríguez-Lagos, 2025) and chronic neck pain (Mata, 2024). The spinal cord's pain amplification tendency is enhanced across multiple chronic pain conditions (Rodríguez-Lagos, Mata, Chen). And when pain becomes chronic, the regulatory relationship between the autonomic nervous system and pain modulation breaks down entirely (Uzawa, 2025).

Pain Modulation, Autonomic State, and Clinical Measurement Are Reading the Same Substrate

Three studies converge on a single insight: CPM, Heart Rate Variability, baroreflex sensitivity, skin conductance, and local Pressure Pain Threshold are different instruments reading overlapping aspects of the same underlying system — the brainstem's regulation of autonomic state and pain modulation through the Periaqueductal Grey (Makovac, 2021) and related circuits (Venezia, 2024).

This convergence has direct implications for clinical reasoning. When a clinician observes changes in tissue sensitivity, autonomic reactivity, or motor output in response to a treatment, those observations may be reading the same underlying brainstem state through different measurement windows. The fact that Navarro-Santana (2022) found dry needling changed skin conductance and local PPT without changing CPM — and that Uzawa (2025) found chronic pain decouples CPM from ANS state — suggests that these instruments are related but not identical, and their dissociation in chronic pain is itself clinically meaningful.

Treatment Dose and Modality Both Matter for Changing the Central System

The treatment literature in this synthesis produces a coherent dose-response picture:

• A single session of mobilization does not change CPM (Martínez Pozas, 2024).

• A single session of dry needling does not change CPM but does change autonomic state and local sensitivity (Navarro-Santana, 2022).

• Four sessions of comprehensive manual therapy normalizes both CPM and TSP (Mata, 2024).

• Motor control exercise — not generic exercise — specifically improves CPM in chronic neck pain (Chen, 2024).

The clinical implication is direct: if the goal is to restore the brain's pain inhibition system, the treatment must match the scale of the problem. Brief single-session interventions produce real local effects. Restoring central pain processing requires a sustained, multimodal therapeutic approach.

The Rehabilitation Window Has Biological Significance

Vitharana (2025) adds a temporal dimension to the picture: the timing of sensorimotor rehabilitation after ACL injury influences how the nervous system compensates. If proprioceptive input is not restored early, the brain shifts to visual-motor dominance — a compensation strategy that is harder to reverse later. This is not a soft clinical preference; it reflects how the brain's plastic reorganization unfolds in the absence of normal afferent input.

Open Question: What Happens to Clinical Measures in Chronic Pain?

Uzawa (2025) raises the most important unanswered question in this synthesis: if CPM decouples from autonomic state in chronic pain, what does this mean for the interpretation of clinical findings in that population? If skin conductance, local tissue reactivity, and manual muscle test response all read autonomic state — and if in chronic pain that autonomic state no longer tracks with the brain's pain modulation system — then the meaning of those clinical signals in a chronic patient is different from what it is in a non-chronic patient. This is not a reason to abandon clinical observation; it is a reason to reason carefully about what any particular finding means in the context of pain duration.

Conclusions

The eleven studies reviewed in this synthesis collectively establish that musculoskeletal pain conditions involving the knee — including osteoarthritis, ACL injury, and chronic knee pain — are fundamentally disorders of central nervous system function, not merely peripheral tissue pathology. Motor pathway dysfunction persists beyond force recovery, the brain’s descending pain inhibition system is reliably impaired in chronic presentations, and normal pain-protective mechanisms can invert to become pain-amplifying. Autonomic state and descending pain modulation share brainstem circuitry, meaning interventions that restore autonomic regulation carry a direct mechanistic pathway to improving pain processing. Early sensorimotor rehabilitation after injury is ideal — when it is delayed, the brain reorganizes around compensatory movement patterns that are harder to correct later. Taken together, these findings support a clinical framework in which the nervous system is assessed and addressed first, and in which normalization of strength and tissue health is understood as downstream of — not a substitute for — restoration of central motor and pain-modulatory function.

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