Canine Cushing’s Myopathy

 Canine Cushing’s disease commonly presents with muscle weakness and atrophy, and occasionally with additional degeneration of the muscle fibers that is best described as a myopathy. Being able to recognise the signs of this myopathy is essential to the correct medical treatment and management of these patients.

Canine Cushing’s myopathy will be evident in a handful of Cushing’s cases, where electromyography will reveal abnormal, high-frequency firing of the muscle, and biopsies will reveal degeneration of the muscle fibers.

As Vetrehabbers, we need to be able to recognize the signs of this myopathy to ensure that the patient receives the best care available to them.

What is Cushing’s Disease?

Many Vetrehabbers may not be as familiar with Cushing’s disease as Veterinarians are. Cushing’s disease can negatively affect our success during rehabilitation, so being able to recognise the clinical signs can help us ensure the best outcome for these patients.

Canine Cushing’s disease, also known as hyperadrenocorticism, occurs when the adrenal glands produce excess cortisol. This serious health condition can be life threatening, and puts the dog at risk of developing additional illnesses such as kidney disease, high blood pressure, blood clots or diabetes mellitus.

Hyperadrenocorticism can be caused by several small benign tumors or a single larger tumor in the pituitary glad, a tumor on the adrenal gland, or can be iatrogenic due to the prolonged use of steroids.

Signs to look out for

Common signs we may see in practice include:

• excessive drinking
• excessive urination
• increased appetite
• a thin skin
• hair loss
• muscle weakness
• an enlarged abdomen with a potbelly appearance
• panting
• lethargy

If there are clinical signs of Cushing’s disease, the patient should be referred to the Veterinarian for diagnosis and to ensure that the proper medical treatment is prescribed.

Treating Cushing’s disease

Cushing’s disease is most commonly medically managed, with the goal of medication being to decrease the amount of cortisol produced by the adrenal glands. To treat Cushing’s disease, the tumor(s) would have to be removed or treated; in most cases this is not a viable option.

The treatment approach also depends on what is causing the Cushing’s disease, and will vary   according to whether the disease is caused by the pituitary gland, the adrenal gland or steroid medication.

Myopathy associate with hyperadrenocorticism

In rare cases, Cushing’s disease is associated with myopathy. A handful of publications have reported on these kinds of myopathies, sharing findings about patients who presented with:

• moderate to significant muscle weakness and atrophy,
• muscle stiffness,
• proximal appendicular muscle enlargement.

Diagnostic findings beyond the initial ones to diagnose Cushing’s disease include:

• normal or abnormal electromyography readings,
• myotonic, high frequency discharges on electromyography readings,
• histologic, electron microscopic, and histochemical findings in the musculature of dogs that were examined, characteristic of non-inflammatory degenerative myopathy,
• mild degenerative changes of fibre size variation, focal necrosis and fibre splitting, as revealed in muscle biopsies.

So what can we do as Vetrehabbers when we are presented with these cases, especially if they are referred to us for a primary orthopedic or neurological condition?

What we can do as Vetrehabbers

The first and most important consideration is to ensure that the condition is correctly diagnosed, treated and managed by the primary or specialist Veterinarian. Without the correct medical management and a comprehensive team approach, we don’t stand much chance of improving quality of life for these patients.

As there is little to no information available on our role in treating the musculoskeletal aspect of this condition, many Vetrehabbers who have been presented with it have treated it as best they could as part of a team. Recently, this topic was discussed in the Small Animal Vetrehabbers Facebook group. Below, I share a few of the points raised by the community on how they have managed this presentation.

What our Vetrehabbers have to say

Dr Tara Edwards, DVM, DACVSMR, CCRT, CVPP, cVMA:

I had a case of Cushing’s myotonia. The dog was 17 and had absolutely crazy muscle tone – such excessive tone that it was creating hyperextension at the level of the stifles. I unfortunately didn’t get a chance to actually treat this guy from a rehab perspective. I was very honest with the clients after my assessment that I didn’t feel I would have a direct impact on his current gait but would have loved to at least address the secondary issues/compensatory areas to help improve his comfort.

Dr David Lane, DVM, ACVSMR, CVSMT, CVA, CCRT:

I had a single case with similar presentation to Tara Edwards’. I improved quality of life somewhat by managing secondary muscle soreness and concurrent OA, but accomplished very little in reducing muscle tone – that was in the hands of the internal medicine person. I don’t know if this case was more refractory than most, but internal medicine had little success. I saw the dog every 6-8 weeks for 2-3 years. He would show a transient decrease in muscle tone for a week or so following treatment, with some commensurate improvement in mobility. I think most of the benefit was in improving the secondary back pain. Owners felt the appointments were worthwhile, but I always was disappointed that I couldn’t accomplish more… the benefits were definitely transient. Treatment consisted of combined acupuncture and manual therapy (CAMT) plus laser.

Dr Sarah Love, DVM, DACVIM (SAIM), DACVSMR, CCRT, CVSMT:

Similar experience here to Dr Lane’s case. Even with good control of the clinical signs of Cushing’s disease, the myopathy minimally improved. I tried many many things.

Dr Britt Barton, DVM, CVA, CCRP:

I had a patient with this. She first came to me as a post-op hemilam. I noted her odd imbalance in muscle size in her rear limbs but thought she had incomplete muscle activation associated with her herniation.

I felt that, despite neuro rehab and acupuncture, her muscle activation imbalance was getting worse. Her owner was noticing her pet being ‘stiff’.

I reassessed her labs and they were fairly boring except for an unexplained CK elevation (not crazy but in the 300s). I had noted a finding of ‘adrenal nodule’ on her prior MRI, so I sent her back to a specialist for reassessment and suspected myopathy. They felt like she was fine so no work up.

Long story short, two more referrals back, and a follow-up MRI, EMG and ACTH stim testing and she was finally diagnosed with metabolic myopathy. Her cholesterol did not elevate and she did not become PU/PD until the third trip back to the specialist.

Her case continued to progress until she herniated another disc. She died of ascending myelomalacia after her second surgery.

I feel her severe muscle hypertrophy and increased persistent contraction was a contributor to her second herniation.

I’ll try to share her gait video in a moment.

Good management of the Cushing’s is imperative. The damage to the muscle physiology may not reverse with treatment but without really good Cushing’s management it can progress.

I recommend assessing flexibility and determining what the pet’s physical limitations are to help get an idea what to focus on in therapy. Myofascial pain management is an important component of care (acupuncture, conservative dry needling, controlled and directed massage) but you don’t have a tool that will change what is happening with the muscle physiology.

Dr Carla Wilkie, DVM, CVA, CSMT and CCRT:

I’ve now seen two, one a dachshund, the other an Aussie shepherd. Sadly, both presented so late in their progression that even treatment of the Cushing’s was precluded. Very sad cases.

Both cases were presented to me for rehab of suspected ‘arthritis’, but on discovering the hypertonicity of appendicular muscles, neuro referral in the first case led to the Cushing’s diagnosis. I don’t recall learning of this bizarre variant of a Cushing’s presentation in vet college.

The second one was ‘easier’ to spot; it’s such an unusual clinical picture.

Dr Amanda Sorensen DVM, CVA:

My own dog had this terrible condition. It was awful. We had great control of the Cushing’s with trilostane, but the myotonia kept getting worse. Nothing really helped except chiropractic to help with the neck pain, but that was very temporary. It was really tough.

The team approach

Thank you to each of the Vetrehabbers who have shared their experiences, so that more of us can recognise these patients should they come across our paths and can give them the best possible help and care.

I want to highlight and add a word of caution: Cushing’s disease, and the myopathy that may accompany it, is a condition that needs to be managed primarily by an internal medicine team/Veterinarian. There are several types of metabolic myopathies that present in a similar manner, and there may be additional diagnostics and treatments necessary. I have not discussed the treatment of the tumors, possible medications, or the complications and considerations that are paired with these techniques.

The role that Vetrehabbers can play will be a supportive one, as we help to reduce the compensatory pain and discomfort and assist the patient to remain as pain free as possible. We have not discussed the different treatment approaches and modalities that may benefit the patient within a rehabilitation setting – trust your clinical reasoning skills to address the needs of the individual patient in front of you, with the tools and modalities that you have available.

Conclusion

A degenerative myopathy can present in certain patients with Cushing’s disease, leading to a degeneration of the muscle fibres and their function in the patient, together with an abnormal firing pattern. Patients are often treated for primary orthopedic or neurological conditions, with the Cushing’s myopathy identified as a result of abnormal progression or presentation. Being able to recognise the signs of this condition is essential if these patients are to have an optimal outcome.

References

• Braund, KG, Dillon, AR, Mikeal RL & August, JR (1980). Subclinical myopathy associated with hyperadrenocorticism in the dog, Pathol, 17: 134-148.
• Greene, CE, Lorenz, MD, Munnell, JF, Prasse, KW, White & NA, Bowen, JM (1979). Myopathy associated with hyperadrenocorticism in the dog, J Am Vet Med Assoc, June 15: 174(12):1310-5.
• Small Animal Vetrehabbers’ Facebook Group.