Abstract: Equine lameness diagnosis is dominated by a joint- and tendon-centric paradigm. The standard diagnostic algorithm relies on gait observation, perineural and intrasynovial anesthesia, and cross-sectional imaging. It is directed almost exclusively at skeletal and articular structures. Myofascial trigger points (MTrPs) are hypersensitive, hyperirritable loci within taut bands of skeletal muscle. They produce local and referred pain on compression or contraction. In horses, MTrPs are a clinically relevant but systematically overlooked source of primary lameness. This review synthesises evidence from equine and comparative research. We argue that MTrPs can act as the primary-not merely secondary-cause of gait asymmetry, performance deficits, and pain behavior in horses. Key mechanisms include the energy crisis model of MTrP formation, peripheral and central sensitization, referred pain projection mimicking distal limb pathology, and the biomechanical consequences of MTrP-induced muscle inhibition on gait. Electrophysiological studies confirm that equine MTrPs show the same spontaneous electrical activity as human and animal MTrPs. Prevalence studies indicate that MTrPs are present in many sport horses. Dressage horses show particularly high prevalence in the cervical and thoracolumbar musculature. Of clinical importance is the referred pain phenomenon: MTrPs in proximal muscles such as the gluteus medius, longissimus lumborum, and biceps femoris may produce apparent distal limb pain. Such pain can be clinically indistinguishable from joint or tendon pathology. This has direct and underappreciated implications for diagnostic accuracy. We propose that systematic myofascial palpation should be integrated into the routine equine lameness workup as a first-tier diagnostic step. Rapid resolution of gait asymmetry following targeted MTrP treatment should be interpreted as supportive evidence of myofascial origin. We further delineate the clinically relevant trigger point activity spectrum from active to latent states, address differential diagnoses such as Lyme-associated diffuse myalgia and primary myopathies (PSSM2, MIM, IMM), summarise the principal therapeutic modalities used in equine MTrP management, and examine biotensegrity as a mechanobiological framework explaining the multisegmental fascial effects of myofascial dysfunction.
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Overview
This research article reviews the role of myofascial trigger points (MTrPs) as a primary cause of lameness in horses, challenging the traditional focus on joints and tendons.
It synthesizes biomechanical, neurophysiological, and fascial evidence to highlight how MTrPs contribute to gait abnormalities and pain, advocating for their inclusion in standard diagnostic procedures.
Traditional Diagnosis of Equine Lameness
Current diagnostics primarily focus on joints and tendons, often ignoring muscle-related causes.
Standard tools include gait observation, nerve blocks (perineural and intrasynovial anesthesia), and imaging techniques.
These methods are generally directed at skeletal and articular structures rather than muscle issues.
What are Myofascial Trigger Points (MTrPs)?
MTrPs are hypersensitive, hyperirritable spots found within taut bands of skeletal muscle.
They trigger local and referred pain when pressed or when the muscle contracts.
In horses, MTrPs have been overlooked as a potential primary source of lameness rather than a secondary effect.
Key Mechanisms Underpinning MTrP Formation and Effects
Energy Crisis Model: Proposes that local muscular energy failure leads to MTrP formation.
Peripheral and Central Sensitization: Heightened sensitivity in nerves around MTrPs contributes to pain amplification.
Referred Pain: Pain generated by MTrPs can radiate to areas far from the original muscle, mimicking distal limb injuries.
Biomechanical Consequences: MTrPs cause muscle inhibition, disrupting normal gait and leading to asymmetry.
Evidence from Electrophysiological and Prevalence Studies
Electrophysiological studies show that equine MTrPs have spontaneous electrical activity similar to those in humans and other animals.
Many sport horses have MTrPs, with particularly high prevalence in dressage horses, especially in the cervical and thoracolumbar muscle regions.
Clinical Significance of Referred Pain Phenomenon
MTrPs in large proximal muscles (e.g., gluteus medius, longissimus lumborum, biceps femoris) may produce pain perceived in distal limbs.
This “referred pain” can be confused with joint or tendon pathologies.
The misinterpretation has significant implications for the accuracy of lameness diagnosis.
Recommendations for Clinical Practice
The authors propose integrating systematic myofascial palpation into routine lameness examinations as a first step.
Quick improvement in gait after targeted MTrP treatment should be considered evidence supporting myofascial origin of the lameness.
Additional Considerations and Differential Diagnoses
The article clarifies the trigger point activity spectrum, from active (painful) to latent states (inactive but palpable).
Differential diagnoses including Lyme disease-associated myalgia and primary muscle disorders such as PSSM2, MIM, and IMM are addressed.
Therapeutic Approaches for Equine MTrPs
Management strategies include manual therapy, dry needling, stretching, and other modalities tailored to release MTrPs.
These treatments aim to reduce pain, improve muscle function, and restore normal gait biomechanics.
Biotensegrity Framework
The article explores biotensegrity as a mechanobiological model explaining how myofascial dysfunction affects multiple segments of fascial networks.
Biotensegrity refers to the complex tension and compression system within connective tissues that maintains structural integrity.
This model helps explain how localized MTrPs can produce widespread biomechanical effects beyond the muscle where they form.
Cite This Article
APA
Scheibenpflug M, Haussler KK.
(2026).
Myofascial trigger points as a primary cause of equine lameness: a biomechanical, neurophysiological, and fascial review.
Front Vet Sci, 13, 1852775.
https://doi.org/10.3389/fvets.2026.1852775
College of Veterinary Medicine, Lincoln Memorial University, Harrogate, TN, United States.
Conflict of Interest Statement
The author(s) declared that this work was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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