Recently, we shared a post on social media that stated:
Back pain shuts down the multifidus and tightens the long back muscles, locking the spine.
Rehab isn’t a bonus. It’s essential.
A member of our community came back to us with a genuinely excellent question:
Are we sure the neuromotor inhibition of the multifidus is due to back pain? Or does inhibition happen for other reasons, leading to tightening of the longissimus dorsi, which then gives rise to back pain?
What a BRILLIANT question!
It challenges linear thinking. It questions causality versus association. And it reflects the reality of clinical practice, where back pain rarely follows a neat, one-directional pathway.
We wanted to do this question justice by really diving into the research behind it. Because the answer matters, not just academically, but clinically; for how we assess, treat, and rehabilitate horses with back pain.
Understanding Arthrogenic Muscle Inhibition (AMI)
To understand what happens to the multifidus in back pain, we first need to understand arthrogenic muscle inhibition (AMI).
AMI is a well-described neurophysiological phenomenon where nociceptive input from joints or deep tissues alters motor output. In simple terms, pain changes how muscles are activated; not because the muscle is damaged, but because the nervous system adapts in an attempt to protect the area.
Pain signals from spinal structures influence motor control at both spinal cord and supraspinal levels. The result is a reflexive inhibition of muscles responsible for fine, segmental control, alongside increased activation of larger, global muscles that can provide gross stability.
This pattern has been extensively described in human low back pain literature and is directly applicable to the horse.
Hilary Clayton (2012) describes this clearly when reviewing equine back pain from a motor control perspective: pain disrupts the normal feed-forward activation of the multifidus, resulting in delayed or absent recruitment. When this deep stabilising system fails, the nervous system compensates by increasing reliance on superficial epaxial muscles.
AMI explains why pain relief alone rarely restores normal movement – because the issue is not just tissue pathology, but altered neuromotor control.
Multifidus vs Longissimus: A Motor Control Perspective
The multifidus and the longissimus dorsi are both epaxial muscles, but they play very different roles.
The multifidus is a deep stabiliser. It provides segmental control, contributes to spinal stiffness at a local level, and plays a key role in preparing the spine for movement (Clayton, 2012; Stubbs et al., 2010).
The longissimus dorsi, by contrast, is a global mover. It generates torque, assists with extension, and contributes to larger, more powerful movements of the spine.
When multifidus activation is inhibited, the nervous system still needs stability. The solution it chooses is increased co-contraction of the longissimus dorsi (Clayton, 2012). While this may create a sense of stability, it comes at a cost: reduced segmental mobility, increased stiffness, and a spine that becomes “locked” into extension.
This is not a strength problem – it is a motor control strategy driven by the nervous system.
Why Pattern Matters: Symmetrical vs Asymmetrical Atrophy
One of the strongest arguments for pain-driven multifidus inhibition lies in the pattern of muscle change, not just its presence.
Generalised disuse or deconditioning typically results in bilateral, symmetrical atrophy. If a horse is rested, confined, or under-loaded, muscle mass may reduce – but it does so evenly.
Pain-mediated inhibition, however, produces a very different picture.
Stubbs et al. (2010) demonstrated that multifidus atrophy in Thoroughbred racehorses was segmental and ipsilateral to sites of osseous spinal pathology. Horses with more severe thoracolumbar and pelvic lesions showed marked asymmetry in multifidus cross-sectional area at the affected levels.
This type of localised and lateralised atrophy is difficult to explain without a neural inhibitory mechanism linked to nociception. It strongly supports the idea that pain is not just associated with multifidus atrophy, it plays a causal role.
Evidence That Pain Can Drive Multifidus Atrophy
Several lines of evidence point toward pain as a powerful driver of multifidus inhibition:
Osseous spinal pathology has been shown to correlate with ipsilateral multifidus atrophy and asymmetry (Stubbs et al., 2010). This relationship is location specific – the muscle changes mirror the location of the lesions.
Clayton (2012) explains that back pain alters motor control strategies, inhibiting the multifidus and increasing reliance on longissimus dorsi. This shift reduces spinal mobility and contributes to further dysfunction.
Importantly, these changes do not require dramatic pain behaviours to be present. Low-grade, persistent nociceptive input is sufficient to alter neuromotor control.
Taken together, these findings suggest that pain is not merely coincidental – it is a biologically plausible and well-supported driver of multifidus inhibition.
If Not Pain, What Else Can Contribute to Multifidus Atrophy?
The community question is still absolutely valid. Pain is not the only factor that can influence multifidus activation, and acknowledging this complexity is important.
Reduced spinal movement and disuse – such as prolonged box rest or limited postural variability – can reduce tonic activation of the multifidus. However, this typically results in generalised, symmetrical changes rather than the marked asymmetry seen in painful spines.
Training and postural strategies also play a role. Chronic thoracolumbar extension bias, rigid frames, and reduced spinal articulation can shift muscular demand toward the longissimus and away from segmental stabilisers. This may reduce multifidus engagement over time, particularly if combined with fatigue or overload.
Proprioceptive disruption is another contributor. Facet joints, intervertebral discs, and deep spinal tissues are rich in mechanoreceptors. Injury or degeneration in these tissues alters afferent input, impairing motor planning even before overt pain behaviours are recognised.
Central motor control changes further complicate the picture. Chronic pain can lead to cortical reorganisation, meaning multifidus inhibition may persist even after tissue healing has occurred.
These factors can all contribute – but on their own, they rarely explain the localised, unilateral patterns of atrophy documented in painful backs.
Can Multifidus Inhibition Exist Before Pain?
So which comes first?
The most defensible answer is that both pathways are possible.
Reduced multifidus activation may precede overt pain in some horses, particularly in the presence of poor movement strategies or reduced spinal variability. However, once nociception enters the system, neuromotor inhibition becomes more pronounced, compensation increases, and the system becomes self-reinforcing.
Pain, inhibition, stiffness, and altered movement patterns begin to feed into one another.
This is why waiting for pain to resolve before addressing motor control so often fails.
Why Rehabilitation Changes the Equation
This is where rehabilitation becomes non-negotiable.
Targeted rehabilitation does more than rebuild muscle mass – it retrains the nervous system.
Dynamic mobilisation exercises have been shown to increase multifidus cross-sectional area and improve symmetry over a three-month period (Stubbs et al., 2011). These changes reflect restored motor control, not just hypertrophy.
Similarly, a multimodal rehabilitation approach incorporating therapeutic exercise led to improvements in posture, spinal curvature, muscle symmetry, and performance in horses with thoracolumbar pain (de Melo & Ferreira, 2021).
Rehabilitation works because it addresses the mechanism of dysfunction, not just the structural findings on imaging.
So… Is Multifidus Atrophy a Cause or a Consequence of Back Pain?
The answer is not either–or.
Multifidus inhibition can be influenced by multiple factors, and in some cases may precede pain. But the literature consistently shows that pain is a powerful, reliable driver of neuromotor inhibition, asymmetry, and loss of segmental spinal control.
Once pain is present, inhibition is no longer optional. It is neurological.
And that is why rehabilitation is not a bonus. It is the mechanism by which we restore motor control, break the cycle, and give the spine back its ability to move.
References
- Clayton, H.M. (2012). Equine back pain reviewed from a motor control perspective. Equine Veterinary Journal, 44(1), 114–119.
- de Melo, U.P. & Ferreira, C. (2021). Multimodal therapy for treatment of equine back pain: a report of 15 cases. Journal of Equine Veterinary Science, 103, 103656.
- Stubbs, N.C., Riggs, C.M., Hodges, P.W., Jeffcott, L.B., Hodgson, D.R. & Clayton, H.M. (2010). Osseous spinal pathology and epaxial muscle ultrasonography in Thoroughbred racehorses. Equine Veterinary Journal, 42(8), 654–661.
- Stubbs, N.C., Kaiser, L.J., Hauptman, J. & Clayton, H.M. (2011). Dynamic mobilisation exercises increase cross-sectional area of musculus multifidus. Equine Veterinary Journal, 43(4), 522–529.
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