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Your TPLO was perfect. The dog uses the limb and is recovering— But something is off.

Understanding stifle dysfunction beyond the bone


The surgery went smoothly. Bone is healing as expected.

We are at week 4. The dog is walking and using the operated limb.

But when we observe closely – a significant number of dogs still show subtle but abnormal gait patterns.

 

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Have you ever wondered:

  • Why isn’t the dog fully extending or flexing the stifle?

  • Why do they externally rotate the limb and walk with stifle in flexion?

 

What I see in these dogs

I often see dogs with cruciate ligament disease — both pre- and post-operatively — walking with a consistently flexed stifle, despite having full passive range of motion.

 

This isn’t just something we think we see — it’s been documented.

Tinga et al., BMC Vet Res 2018 used fluoroscopic kinematic analysis to show relatively flexed stifle during gait in dogs with cranial cruciate ligament disease. (And multiple other studies from the same group)

 

Sometimes there’s ongoing pain, synovitis, or sensitivity — but often, there isn’t.

Let’s say everything checks out: no infection, no meniscal injury, no surgical complications.

Even then, the gait still isn’t right.

And it’s not rare — we see this pattern quite regularly.

 

So I had another deep dive to the Literature

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Not just veterinary papers — human orthopedics/sports medicine & rehabilitation literature.

And here’s what we haven’t learned in vet school 👇

 

There are three key concepts in movement dysfunction

These theories are grounded in human research and functional anatomy. We still need more direct evidence in dogs — but they help explain what we see clinically.

 

1. Arthrogenic Muscle Inhibition (AMI)

When a joint is inflamed or injured, the nervous system reflexively inhibits key stabilizing muscles — particularly the quadriceps. Even without overt pain, alpha motor neuron activity is reduced.

 

👉 Without proper quad activation, the dog can’t extend the stifle effectively. So they keep it flexed and it becomes the default !

 

2. Compensatory Motor Patterns

When one muscle isn’t firing, others step in.

 

With quadriceps inhibition, the hamstrings — particularly the biceps femoris — step in to stabilize the limb and, in doing so, contribute to external rotation.

(Well-documented in human ACL studies)

 

At the same time, hip flexors (iliopsoas, rectus femoris) ramp up to help advance the limb during swing phase.

 

The role of the gastrocnemius is more variable — some studies show compensatory activation, but inhibition is also reported, especially in early post-injury or post-op stages.

(Evidence in humans is mixed)

 

This results in a mismatch of activation across all dynamic stabilizers of the stifle — A neuromuscular chaos.

 

What’s the outcome?

A pelvic limb that stays flexed and externally rotated in both stance and swing phases.

 

And that’s not all — over time, this abnormal limb posture leads to secondary compensations, such as: Kyphosis / Pelvic tilt.

 

What begins as a short-term strategy for joint protection can quickly evolve into a chronic movement dysfunction if not addressed.

 

Another note:

External rotation widens the base of support — maybe a subconscious adaptation that helps when proprioception is impaired or the dog doesn’t fully trust the limb.

 

 3. Neuroplasticity in Adaptation

Pain reshapes the brain.The longer a dog compensates, the more that movement becomes their new normal. Even after the tissue heals, the motor system may stay stuck in a dysfunctional pattern.

 

 

Bottom line

That classic “stifle-flexed + externally rotated” pelvic limb gait isn’t just lingering post-op soreness. It’s the result of a deeper neuromuscular response — driven by:

  • Quadriceps inhibition

  • Hamstring and hip flexor dominance

  • A well-intentioned, but maladaptive compensation strategy

👉 AND it doesn’t easily resolve on its own.


This is exactly where targeted rehabilitation makes the difference:

Through neuromuscular re-educationstrategic strengthening, and gait retraining, we can intervene before temporary compensation becomes permanent dysfunction.

 

What can we do?

Next week, we’ll dive into rehab strategies to reverse arthrogenic muscle inhibition (AMI) and retrain proper limb use.

 

Stay tuned — this is where all the fun rehab starts to feel like magic. Because when neurology, movement, and intention come together, the results speak for themselves.

 


** If you want to read more, here you are..

 

Tinga S, et al. Femorotibial kinematics in dogs with cranial cruciate ligament insufficiency: a three-dimensional in-vivo fluoroscopic analysis during walking. BMC veterinary research. 2018 Dec;14:1-9.

 

Tinga S, et al. Femorotibial kinematics in dogs treated with tibial plateau leveling osteotomy for cranial cruciate ligament insufficiency: an in vivo fluoroscopic analysis during walking. Veterinary Surgery. 2020 Jan;49(1):187-99.

 

Sonnery-Cottet B, et al. Prevention of knee stiffness following ligament reconstruction: Understanding the role of Arthrogenic Muscle Inhibition (AMI). Orthopaedics & Traumatology: Surgery & Research. 2024 Feb 1;110(1):103784.

 
 
 

1 Comment


Yulseon Hong
Jul 06

Thank you so much for sharing such an insightful post 🙏

As a new vet, I really appreciate how you’ve explained these unfamiliar concepts so clearly — the content was not only informative but genuinely interesting!

Also, thank you again for the fascinating discussion during the last journal club.


I had a couple of questions from your post, if you don’t mind:


  1. Regarding the diagnosis of Arthrogenic Muscle Inhibition (AMI) — is there a definitive diagnostic method for it? Or is it more of a diagnosis of exclusion, where we rule out infection, meniscal injury, surgical complications, etc.? I’m also wondering how feasible it is to truly rule out all those other causes in real clinical settings.


  1. Also, the part…


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