A multifaceted treatment protocol can slow, halt or even temporarily reverse the progression of degenerative myelopathy.

Degenerative myelopathy (DM) is a progressive disease of the spinal cord. It’s found mainly in large breed dogs, with the onset of symptoms typically occurring between seven and 14 years of age. It begins with a wobbly gait (ataxia) in the hind limbs. Affected dogs will sway, cross over, knuckle, stumble up curbs and drag their feet. DM can begin in one hind limb and later affect the other. The clinical course can range from six months to one year, during which the limbs become progressively weaker, with buckling and eventual paraplegia. In later stages, urinary and fecal incontinence can occur, with progression to the front limbs. DM is not associated with pain.

Causes of degenerative myelopathy

During the 80s and early 90s, Roger Clemmons, DVM, PhD, professor of Neurology at the University of Florida, suspected DM was an autoimmune process, resulting in demyelination of the affected spinal cord segments, as in multiple sclerosis (MS) (Clemmons, 1992). We now know that DM is not simply “doggie MS”, but more closely related to amyotrophic lateral sclerosis (ALS). The lesions invariably start between T3 and L3, presumably because this cord segment is supplied by smaller arteries, making it more subject to ischemia and oxidative stress. Super oxide dismutase (SOD-1) is a free radical scavenger, abundantly present in the CNS cytoplasm. Dogs affected with DM have a mutation in the SOD-1 enzyme. Oxidative stress upregulates the synthesis of the mutated SOD-1 enzyme. The mutation results in the mis-folding of proteins, which potentially alters cellular function, substrate selection, and ultimately results in an accumulation of toxic by-products in the axon. It is these toxic by–products that lead to the disruption of axoplasmic flow – “excitotoxicity”. Destruction of myelin and replacement of normal axons with astrogliosis (sclerosis) follows later (Coates and Wininger, 2010).

Diagnosing degenerative myelopathy

Degenerative myelopathy is a diagnosis of elimination. Radiography, myelography and MRI are used to rule out other causes of weakness, such as intervertebral disc disease, fibrocartilagenous infarct, tumors, cysts and infection.

A definitive diagnosis can only be made by an examination of post-mortem tissues. A DNA test has been developed at the University of Missouri-Columbia and is available through the Orthopedic Foundation for Animals. It clearly identifies dogs that have two normal copies of the SOD-1 enzyme gene; those that are carriers (one normal copy and one mutated copy); and those at high risk of developing DM (two copies of the mutated gene) (Coates and Wininger, 2010). Sixty percent of homozygous affected dogs will eventually express the disease, while 40% remain unaffected. There must be other factors, in addition to the SOD-1 mutation, that lead to the clinical development DM in dogs. (Zeng et al, 2014)

Hallmark clinical traits considered uniquely characteristic of DM include:

• Disease progression
• Asymmetric UMN weakness at onset
• Pelvic limb proprioceptive ataxia
• Lack of pain

These findings are considered sufficient to rule out other disorders, although DM is often paired with other orthopedic or neurological problems that are considered incidental (Coates and Wininger, 2010). Common examples of co-morbidities include:

• Disc disease
• Degenerative joint disease
• Cruciate ligament laxity

The evolution of DM therapy

The only treatment protocol currently in the literature was formulated by veterinary neurologist Roger Clemmons (see below).

Clemmons found that dogs placed on an unprocessed diet, supplements and a structured, regular exercise program experienced the slowest progression of the disease, and in some cases stabilized and even improved. An independent study in the UK tested only the supplement regimen. No diet or physiotherapy was implemented. In this case, 70% of the dogs progressed to complete paraplegia within six months.

In 2006, a physiotherapy efficacy test showed that animals receiving intensive (n=9) physiotherapy had longer (P=< .05) survival times (mean 255 days), compared to those with moderate (n=6; mean 130 days) or no (n=7; mean 55 days) physiotherapy (Kathmann et al, 2006). Physiotherapy, in addition to strengthening the legs, would likely promote general spinal flexibility and circulation, helping to avoid induction of defective SOD-1. Therefore, diet and exercise appear to play key roles in slowing or halting the progression of degenerative myelopathy (Marsden, 2014).

Degenerative myelopathy is a multifactorial disease in traditional Chinese veterinary medicine; making a diagnosis depends on assessing the animal’s personality as well as what body systems are affected. In TCVM, muscles are associated with the Spleen/Earth element and the tendons and ligaments with the Liver/Wood element. Since degenerative myelopathy causes weakness, ataxia and muscle wasting, it is most commonly diagnosed in TCVM as Spleen Qi deficiency with Liver Yin deficiency. Other systems may also be simultaneously out of balance.

Acupuncture and herbal therapies may help slow the progression of the disease, while improving quality of life and relieving GI symptoms. Points are chosen for the disease pattern (i.e. Spleen Qi deficiency) as well as the animal’s constitution and secondary symptoms (Xie, 2013).

1. Cord injury: begins as thoracic cord illness

• Starts in same cord location T3-L3/highest cord:canal ratio
• Disc disease/spondylosis
• Slip and fall
• Autoimmune
• Aging of the spine
• Surgery

Treatment goal

• Gently restore spinal mobility to distribute motion across all vertebral segments
• Break down ligamentous calcification that promotes spondylosis and rigidity
• Preserve muscle tone and strength with early intervention
• Start while dogs are still walking

Methods

• Chiropractic adjustments to address vertebral fixations from cervical to lumbosacral spine
• Massage for circulation, tone and static range of motion/ breaks down calcification
• Swimming: alternate day sessions recommended
• Walking: can be alternated with swimming
• Underwater treadmill
• Stretches

2. Oxidative stress: the role of processed foods

• Starchy foods promote inflammatory cyokine production
• Inflammation is promoted by excessive increases in insulin
• Increased protein kinase C => decreased nitric oxide => failure of inflammation to resolve
• Cyclo-oxygenase damage impairs repair cascade
• Smouldering inflammation promotes more oxidative stress

Treatment goal

• Stop stoking the fire/maintain pliability in tissue

Methods

• Avoid overfeeding
• Reduce gycemic index: unprocessed, non-starch based.
• Homemade diets
• Raw diets
• Fresh food is more nutritionally complex and higher in antioxidants

3. SOD-1 and excitotoxicity

Treatment goals

• Control inappropriate enzyme upregulation and the production of toxic by-products that “clog up” cord
• Buildup of toxins in cord should eventually degrade and be removed if process is slowed and/or halted • Reduce inflammation
• Improve function

Methods

• Acupuncture: reduce Heat/release Blood Stasis (Marsden, 2014)
• Sedate: BL 13, BL 17, ST 37 (below ST 36 on cranial tibialis m. area) (T3 and T7)
• Tonify: BL 40 and GV 14
• Sedate Stomach 36 and Gallbladder points 17, 19, 25
• GB 41 regulates the T-L junction dermatomes (treats paralysis)
• Treatments may be needed for spring/fall flare-ups that are due to stuck seasonal energy movement
• TVCM/Western herbs– Chinese Diagnosis: Blood Stasis
• Minor Bleuperum Combination – drives blood flow out yet icepack -like function

Xiao Chen Hu Tang – Natural Path Herb Company Opens peripheral circulation Benefits limb function

• Minor Invigorate the Collaterals (curcumin-containing)

Xiao Huo Luo Dan – Natural Path Herb Company Curcumin crosses blood/brain barrier Inhibits inflammatory mediators

• Major Bleuplerum Combination (original use for acute abdomen)

Dai Chai Hu Tang – Natural Path Herb Company Removes heat, improves blood flow Anti-inflammatory for gut Relapses can be associated with gut stasis

• Curcumin – alone or in Minor Invigorate The Collaterals
• Inhibits cytokine production in the cord
• Inhibits NFkB which leads to proteolysis and gliosis
• Milk Thistle (Silybum marianum)
• Inhibits gliosis/powerful antioxidant
• Prevents final stage of sclerosing in cord
• Nerve Tonic Tincture (Pet Health and Nutrition Center)
• Blend containing St. John’s wort, oat straw, licorice root, ginger, ginkgo leaf, skullcap, gotu kola and cayenne.
• Supports healing of damaged nerve tissue o Improves circulation
• Reduces Inflammation
• Cold laser (Marsden, 2014)
• Daily to twice weekly
• Acute anti-inflammatory settings for T3-T7 and St 37
• Chronic anti-inflammatory settings for BL 40 and GV14
• Essential oils
• Homeopathy
• Omega-3 fatty acids
• Myelin sheath (bovine spinal cord glandular)

Conclusion

A multifaceted treatment protocol is required for this multifaceted disease model. The greatest benefit is seen with early intervention. Case reports suggest that the progress of DM can be consistently slowed, halted or even temporarily reversed.

Case studies

Bronko

Bronko, an award-winning German shepherd police dog, presented in late 2011 with a several-month history of loose stools and crashing when turning at a run. He was knuckling and had a delayed righting response in the hind feet.

His radiographs were normal and no improvement was noted with chiropractic adjustments. A presumptive diagnosis of DM was made.

The attending veterinarian consulted Dr. Marsden and implemented acupuncture and Chinese herbal medicine treatments (Bupleurum/Curcumincontaining blends). The goal was to reach the year’s end and an early forced retirement.

At the end of the year, Bronko was stable. After a few months of therapy, he was no longer falling and his proprioception was normal. He returned to active duty collaring criminals in early 2012, and in September of that year was still on the job. He was happy, active, with a normal gait and able to jump tough obstacles.  Bronko was on schedule for his normal retirement date in November of 2012.

Dancer

Dancer, a 12-year-old F/S Lab mix, presented in September 2014 for lethargy, hind leg weakness, tripping up curbs and exercise fatigue. Her radiographs showed mild arthritis in L5-L6; blood work identified over-supplementation with thyroid medication.

Carprofen and Cosequin therapy were initiated for arthritis and her Levothyroxine dose was decreased. Dancer showed no improvement.

In December, Dr. Tom saw Dancer and initiated essential oil therapy, Myelin Sheath and Nerve Tonic (Western herbs), Omega-3 FA, homeopathy, chiropractic, and a raw diet. Physiotherapy includes regular walks and neuro reflex postural stimulation exercises at home.

Over the next seven months, Dancer had a waxing and waning course, then in August of 2015, her symptoms decreased dramatically. She now has normal energy, is back to full walks with her owners, and has only mild ataxia in her hind limbs.

References

Clemmons RM. “Degenerative Myelopathy”. Vet Clin North Am Small Anim Pract, July, 2010.

Coates JR, Wininger FA. “Canine Degerative Myelopathy”. Vet Clin North Am Small Anim Pract., September 2010.

Kathmann I, Cizinauskas S, Doherr MG, Steffen F, Jaggy A. “Daily controlled physiotherapy increases survival time in dogs with suspected degenerative myelopathy”. J Vet Intern Med., July 2006.

Marsden S. “Degenerative Myelopathy – A Clinical Model and Strategy”. CIVT, 2014.

Zeng R, Coates JR, Johnson GC, Hansen L, Awano T, Kollchenski A, Ivansson E, Perloski M, Lindbald-Toh K, O’Brien DP, Guo J, Katz ML, Johnson GS. “Breed distribution of SOD 1 alleles previously associated with canine degenerative myelopathy”.  Journal of Vet Intern Med, March 2014.