Current Research into the Diagnosis and Treatment …...4 Introduction On 25th May 2018 my 12-year-old Golden Retriever, Dixie, was given a presumptive diagnosis of Degenerative Myelopathy.

Current Research into the Diagnosis and Treatment of Canine Degenerative

Myelopathy

Submitted for The College of Animal Physiotherapy Diploma in Animal Physiotherapy

Student identification number: 100513 (Juliet Emery)

31st October 2018

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Contents Acknowledgements .................................................................................................................... 3

Introduction ................................................................................................................................ 4

History, Signalment and Epidemiology ..................................................................................... 5

Causes......................................................................................................................................... 6

Clinical Signs and Symptoms .................................................................................................... 7

Pathophysiology ......................................................................................................................... 9

Diagnosis .................................................................................................................................. 10

Biomarker Study .................................................................................................................. 11

Diffusion Tensor Imaging Study .......................................................................................... 12

Treatment ................................................................................................................................. 14

Physiotherapy ....................................................................................................................... 14

Therapeutic Exercises ...................................................................................................... 15

Treatment Modalities ....................................................................................................... 17

Alternative Therapies ........................................................................................................... 21

Hydrotherapy .................................................................................................................... 21

Acupuncture ..................................................................................................................... 22

Nutrition and Diet................................................................................................................. 23

Comfort Aids ........................................................................................................................ 25

Boots/Socks ...................................................................................................................... 25

Bedding ............................................................................................................................ 26

Movement Aids .................................................................................................................... 27

Assistive Harnesses and Slings ........................................................................................ 27

Wheelchairs and carts....................................................................................................... 28

Home Modifications ............................................................................................................. 29

Indoor Traction ................................................................................................................. 29

Ramps ............................................................................................................................... 29

Supportive Care .................................................................................................................... 29

Case Study ................................................................................................................................ 31

Conclusion ................................................................................................................................ 32

Bibliography ............................................................................................................................. 33

References ................................................................................................................................ 34

Appendix 1 ............................................................................................................................... 37

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Acknowledgements

I would like to thank Fred and Sherry, the tutors and the support staff at The College of Animal

Physiotherapy for their knowledge, patience and positive support during my years of study for

the Postgraduate Diploma in Animal Physiotherapy.

Thanks also go to Peter A. Jenkins, Director of Education and Technology at Spectravet

Therapeutic Lasers, and Chip Godine, Owner/Veterinarian at Ruckersville Animal Hospital,

Virginia USA for their advice regarding therapeutic laser treatment protocols for canine

degenerative myelopathy.

Heather Halton, who I met on my first practical day, has become a valued friend and has never

faltered in her support and encouragement throughout the duration of my studies.

Xanthe Randall has been Dixie’s hydrotherapist for the last 10 years. She is also a wonderful

friend who has encouraged me endlessly, regularly boosted my confidence, looked after Dixie

when I was away on practical days and proof-read all my assignments.

I would like to thank my wonderful parents for their unfailing support in everything I do and

for being proud of even my smallest achievements.

And last, but not least, to my beloved Dixie. You are the brightest light in my life, my sanity

and my inspiration. I am thankful for you every day. This is for you.

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Introduction

On 25th May 2018 my 12-year-old Golden Retriever, Dixie, was given a presumptive diagnosis

of Degenerative Myelopathy. The news was utterly devastating and I had so many questions

which no one seemed to be able to answer. I decided I wanted to understand everything about

the disease that was slowly going to take her dignity away from her, and her life away from me.

I wanted to know what was happening inside her body and what effect that was going to have

on her physically and mentally. I wanted to find the most recent knowledge from scientific

studies and clinical trials that were aiming to find a cure, a definitive diagnosis and an effective

treatment. Mostly, I wanted to know what I could do to make both our lives easier and happier.

I wasn’t prepared to sit back and let it happen.

Dixie is the reason I wanted to train as a physiotherapist, so I wanted to use the skills she

inspired me to acquire, in order to keep her with me as long as possible. The topic of my final

dissertation was staring me in the face: Current Research into the Diagnosis and Treatment of

Canine Degenerative Myelopathy.

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History, Signalment and Epidemiology

Canine Degenerative Myelopathy (DM) was originally described in 1973 as a specific

degenerative neurological disease of the spinal cord affecting dogs, specifically German

Shepherds, presenting with progressive general proprioceptive ataxia and upper motor neuron

(UMN) spastic paresis of the pelvic limbs (Averill, 1973). In 1975, Griffiths and Duncan

published papers describing cases with similar clinical signs but with additional

histopathological features of nerve root involvement. They named the condition chronic

degenerative radiculomelopathy (CDRM). In their case studies, breeds other than German

Shepherds were represented. Further studies have shown that over 43 breeds have been found

to be affected by DM with an overall disease prevalence of 0.19%. In addition to German

Shepherds, Rhodesian Ridgebacks, Pembroke and Cardigan Welsh Corgis, Boxers and

Chesapeake Bay Retrievers seem to be over-represented, although this is not an exhaustive list

(Zink and Van Dyke, 2013).

DM is an adult onset disease, with clinical signs rarely presenting before 8 years of age and

there is no gender predilection (Coates, 2010). The clinical spectrum of the disease has been

broadened beyond the UMN in the spinal cord, as dogs progressing to later stages of the disease

were found to eventually develop lower motor neuron (LMN) paraparesis which leads to the

involvement of the thoracic limbs and the brainstem. There is currently no cure for DM and it

is ultimately fatal. The average survival time from presumptive diagnosis is 6 – 12 months as

many owners elect for euthanasia when their dogs can no longer support their own weight (Zink

and Van Dyke, 2013).

Most rehabilitation practitioners will encounter dogs with DM during the course of their careers.

The disease itself is not painful, but there may be compensatory issues due to altered

biomechanics and overused tissues which may become painful. As the disease affects older

dogs, there are likely to be arthritic changes in joints, so this will present challenges to the

treatment of the primary disease whilst also maintaining comfort for the dog. The dog may

become mentally distressed as the disease progresses due to an inability to carry out normal

maintenance behaviours such as scratching, comfort shifting of the body, urinating and

defecating. Pressure sores and ulcers, and urine scalding may occur secondary to hindlimb

paralysis and must be dealt with by advanced nursing care by the owner. Quality of life for the

dog and the owner must always be a primary consideration.

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Causes

The cause of DM is still unknown. Research conducted during the 1980s and early 1990s by

Roger Clemmons, Professor of Neurology at the University of Florida, lead him to suspect DM

of being an autoimmune disease. Evidence from recent research would seem to support the

claim that this is an inflammatory autoimmune caused by the dogs own immune systems

attacking the spinal cord. This process creates an accumulation of inflammatory cells and it is

these inflammatory cells over time which result in the degeneration of the myelin sheath leading

to progressive axonal nerve tissue damage and excitotoxicity. If degeneration is very severe,

deficits in the spinal cord lead to an abnormal increase in astrocytes (astrogliosis), causing

sclerotic lesions to form (Marsden, 2015). The damage eventually disrupts nerve signals

resulting in the loss of voluntary and involuntary motor control. Lesions are first noted in the

spinal cord segment T3 to L3, which are supplied by smaller arteries, therefore making it more

susceptible to ischemia and oxidative stress (Pfafman, 2017).

In non-DM affected dogs, an enzyme called super oxide dismutase (SOD) is abundantly present

in the cytoplasm of the central nervous system (CNS) where it scavenges the oxygen free

radicals produced during periods of oxidative stress before they can damage nerve cells. In DM

affected dogs, there is a mutation in this enzyme which results in abnormal folding of the protein

rendering it ineffective. Toxic by-products then accumulate in the axons of the nerve cells

causing destruction of the myelin and increasing the number of reactive astrocytes which causes

scarring and disruption to axonal regeneration, and thus affects the homeostasis of nerve signal

transmission (Coates, 2010).

Since DM appears to have a genetic predisposition, given the disease has a delayed onset, only

affecting dogs approximately 8 years or older, something must precipitate the accumulation of

defective SOD-1 enzymes. Could the inflammation be secondary to mechanical trauma or from

an orthopaedic lesion adjacent to the spinal cord? Could it be associated with other concurrent

conditions such as disc disease? Could this be why the disease always starts in the same region

of the spine? In the dog, the ratio between the spinal cord and the vertebral foramen increases

in the thoracic spinal column, which could imply a greater potential risk for micro-trauma and

cord impingement (Marsden, 2015). These questions are yet to be answered.

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Clinical Signs and Symptoms

Symptoms of DM can be divided into two distinct phases depending on whether it is just the

Upper Motor Neuron (Early disease) which is affected, or whether the disease has progressed

to include both the Upper and Lower Motor Neurons (Late disease) (See Table 1). Symptoms

start gradually but often owners will seek veterinary assistance during the early phase of the

disease when there is a noticeable deficit to the functioning of the pelvic limbs. Affected dogs

will present with a swaying, or staggering spastic/long-strided hind limb gait, often

accompanied by scuffing and dragging of the rear limbs. The two middle toenails may show

signs of abnormal wear. Initially, this tends to be worse on one side but will eventually progress

to both hind limbs (Millis and Levine, 2014). The dog may have difficulty rising from a down

position, walking, running and jumping. The tail may become limp, and owners may notice

their dogs knuckling over onto the dorsal aspect of their hind paws where sores may have

developed. They will likely fail a dorsiflexion neurological test performed by the vet where

they are unable to correct a postural challenge due to loss of conscious proprioception (Figure

1). Full pelvic paralysis usually occurs within 6 – 12 months of diagnosis.

Figure 1: Knuckling onto dorsal aspect of the hind paw

As the disease progresses to affect the Lower Motor Neuron, the dog will likely show signs of

ataxia in the forelimbs, which, as with the hind legs, if allowed to progress, will eventually also

become completely paralysed. There will be widespread muscle atrophy due to disuse as well

as denervation. When all 4 legs are affected, the animal will be considered tetraplegic and will

be non-ambulatory. There will be associated urinary and/or faecal incontinence of varying

degrees which may cause urine scalding. The dog will be totally reliant on the owner for

comfort shifting and may develop bed sores and skin ulcers (Zink and Van Dyke, 2013).

Brainstem involvement may leave the dog with inability to bark, swallow and cough, also

known as dysphagia (Millis and Levine, 2015).

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Table 1: Classification scheme for disease stages of degenerative myelopathy.

Stage of

Disease Neurological Signs Symptoms

Upper Motor Neuron (UMN) affected

1 Asymmetric, general

proprioceptive ataxia and

spastic paresis in pelvic

limbs. Loss of conscious

proprioception.

Rear limb weakness and muscle loss,

decreased co-ordination, loss of balance,

difficulty with positional changes, climb

stairs, jump into the car or onto furniture.

2 Non-ambulatory

paraparesis, paraplegia.

Pelvic limb muscle atrophy

+/- urinary/faecal

incontinence.

Limp tail, crossing of hindlimbs under the

body (“drunken gait”), rear leg drag.

Unusual toe nail wear. May progress to

dragging themselves with the front limbs

due to loss of mobility in the rear. Faecal

and/or urinary incontinence may occur. Bark

may be hoarse. Urinary tract infections may

occur, pressure sores may develop. Anxiety

increases. Twitching of rear limbs as

misfiring of nerves occur.

Lower Motor Neuron (LMN) affected

3 Flaccid paraplegia, thoracic

limb paresis. Severe pelvic

limb muscle atrophy.

Urinary/faecal incontinence.

Weakness advances through the core

muscles and then affects the front limbs.

Muscle mass loss to the shoulders. Dog will

eventually be unable to stand or walk, and

may also be unable to remain in sternal

recumbency without assistance. Pressure

sores, systemic infections, urinary tract

infections due to urine retention.

4 Flaccid tetraplegia. Severe

generalised muscle atrophy.

Urinary/faecal incontinence.

Dysphagia, dysphonia,

respiratory difficulty.

Disease progresses to the brain stem and the

cranial nerves which may affect vital organs

such as the diaphragm and intercostals –

asphyxiation may occur. May lead to

multisystem failure including kidney, lung

and heart. Euthanasia should be considered

prior to this stage if the animal is distressed.

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Pathophysiology

Histopathological studies of spinal sections of dogs that have died of DM, have shown notable

degenerative changes in the white matter, including nerve fibre loss of ascending sensory and

descending motor pathways as a result of axonal degeneration and secondary demyelination

(See Figures 2 and 3). The area’s most severely affected include the mid- to caudal thoracic

spinal cord segments (T3 – L3) (Coates and Wininger, 2010). There is an associated

proliferation of reactive astrocytes which leads to the formation of sclerotic lesions and scar

tissue formation in the myelin sheath of all spinal cord funiculi (axon bundles) but this is

consistently more severe in the dorsal horn of the spinal cord at the mid- to lower thoracic

region (Zink and Van Dyke, 2013). The scar tissue inhibits axon regeneration.

The degeneration of the spinal cord tissue is caused by the action of excessive amounts of

damaging reactive oxygen species (ROS) molecules leading to a chronic inflammatory state.

Neuronal cell body degeneration is rarely noted in the ventral horn.

Figure 2: Section of spinal cord from a

dog that died of DM (left) compared to a

section from the spinal cord of a normal

dog (right). Axonal degeneration in the

white matter is seen as a loss of the blue

colour at the edges of the cord (arrows).

Image from: https://www.holisticpetcentre.com/rehab-medical-conditions/degenerative-myelopathy-pets-dogs-

cats/

Figure 3: Spinal cord histopathology

A – thoracic cord cross-section from

DM-affected 13 yo Pembroke Welsh

Corgi

B - Unaffected 13 yo Labrador

retriever. (Awano, 2008).

Image from: http://www.pnas.org/content/pnas/106/8/2794.full.pdf

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Originally, neurologists compared DM in dogs to Multiple Sclerosis in humans as this too is an

autoimmune disease where parts of the nervous system are recognised as foreign leading to

progressive deterioration of the spinal cord and ultimately results in paralysis. Latterly, genetic

studies have shown that DM is more closely related to the rarer disease familial amyotrophic

lateral sclerosis (ALS) due to the presence of SOD-1 mutations (Awano et al., 2009). Human

ALS, also known as Lou Gehrig’s disease, has an almost identical clinical presentation as an

adult onset fatal paralytic neurodegenerative disease with both upper and lower motor neuron

involvement.

In 2009, Awano et al., sequenced the SOD1 gene in normal and DM affected dogs which

revealed a G to A nucleotide transition, resulting in an E40K missense mutation (Zink and Van

Dyke, 2013). In 2011, Wininger et al., discovered another point mutation in the SOD1 gene; an

A to T nucleotide transition specific to Bernese Mountain Dogs (Kobatake et al., 2017). The

mutation alters the tertiary structure of the SOD protein causing a conformational change,

altering its three-dimensional shape and therefore inhibiting its biological function. The

mutation renders the superoxide dismutase enzyme ineffective at scavenging oxygen free

radicals leading to an accumulation of ROS which results in a chronic state of inflammation.

Additionally, the substrate of the enzyme may be altered leading to the accumulation of toxic

by-products in the axons of the nerve cells in the white matter of the spinal cord thereby causing

degeneration and demyelination as detailed above. This progressive disruption of nerve fibres

that transmit movement commands from the brain to the limbs and then the sensory feedback

from the limbs to the brain, results in the classic symptoms seen in DM and ALS. (Marsden,

2015).

Diagnosis

True diagnosis can only be determined post-mortem by histology of a cross section of the spinal

cord. Currently, DM can only be diagnosed in living animals by elimination of other similarly

presenting diseases based on a lack of clinically relevant compressive myelopathy (Coates and

Wininger, 2010). Other diseases that may mimic the signs and symptoms of DM, include

intervertebral disc disease (IVDD), myelitis, degenerative lumbosacral stenosis, spinal cord

neoplasia (tumour), hip dysplasia and certain parasitic diseases which also cause inflammation

of the spinal cord (Millis and Levine, 2014). These other causes of hind limb weakness must

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be excluded before reaching a presumptive diagnosis of DM, but this can be difficult as some

of them may be concurrent.

A number of investigative procedures can be used to exclude other diseases which have a

similar presentation. Advanced imaging procedures such as electromyography, myelography,

nerve conduction studies, computed tomography (CT) scans and magnetic resonance imaging

(MRI) may be used alone or in combination to rule out other diseases or injury. Disc protrusions

may be present, not necessarily because of IVDD, but as a result of weakness and stresses in

the spine during DM disease progression, and this may confound diagnosis. Conversely, the

position of the dog during the process of imaging can sometimes hide disc protrusions and lead

to a false positive. X-Rays of the chest and thoracolumbar regions of the spine can be used to

screen for primary or metastatic cancerous tumours in close proximity to the spinal cord which

may contribute to the symptoms.

Cerebrospinal fluid (CSF) samples may be collected from a spinal tap and analysed for evidence

of inflammation. Parasitic infections can be diagnosed from CSF panels, however elevated

levels of protein segments in the absence of any parasites may be indicative of DM (Goran,

2010). Blood and urine samples to assess red blood cell cell count, serum chemistry panel,

thyroid panel and urinalysis can indicate other causes of hind limb weakness, but results will

be unremarkable in a dog with DM.

As mentioned previously, genome wide association analysis reveals a SOD-1 mutation in

canine degenerative myelopathy that resembles amyotrophic lateral sclerosis in humans (Coates

et al., 2009). A DNA test for the SOD-1 mutation was developed at the University of Missouri-

Columbia which can identify dogs as either normal (N/N), a carrier of the disease (SOD-1/N),

or those at high risk of developing the disease (SOD-1/SOD-1). About 60% of dogs with two

mutated copies of the gene will go on to develop the disease, whilst the remaining 40% will

not. This means there are other factors at play, in addition to the SOD-1 mutation, that leads to

the clinical development of DM in dogs (Zeng et al., 2014).

Biomarker Study

Recent studies into diagnosing DM have centred around the identification of a biomarker

specific to DM in order to aid early intervention and facilitate appropriate patient management.

In 2017, Toedebusch et al. produced a paper identifying phosphorylated neurofilament heavy

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(pNF-H) as a possible fluid biomarker for canine DM. The protein pNF-H is an abundant

structural protein of myelinated motor axons and can be detected in disease states where axonal

injury is indicated. Increasing levels of this protein in blood serum and cerebrospinal fluid

(CSF) have been shown to have a high correlation with disease progression in human patients

with ALS.

They showed that the biomarker pNF-H was increased in the CSF samples of DM-affected dogs

at all disease stages compared to age-matched control groups, but was not increased in blood

serum. There was no significant difference in the concentration of pNF-H at each of the

different stages of disease progression, therefore levels do not correlate with increasing axonal

degeneration and cannot be used as a measure of axonal damage (Figure 4). Finally, the control

group of ‘mimic’ diseases showed no difference between CSF pNF-H concentrations in DM

dogs versus those with other primary axonal diseases. However, it is still a promising

antemortem diagnostic tool for DM and further study is required (Toedebusch et al., 2017).

Figure 4: pNF-H is increased in CSF of DM-

affected dogs compared with control dogs at all

disease stages (Toedebusch et al., 2017)

Diffusion Tensor Imaging Study

Non-invasive imaging is essential in the management of spinal cord injury. Although

veterinarians regularly use conventional clinical magnetic resonance imaging (MRI) to rule out

‘mimic’ diseases in suspected cases of degenerative myelopathy, the spinal cord lesions

themselves are undetectable and therefore limit the ability to diagnose and monitor the disease

(Hendrix et al., 2015). Diffusion Tensor Imaging (DTI) is an alternative MRI technique that

measures the size and direction of the diffusion of water molecules through various tissues

(Vedantam et al., 2014). In nerve fibres the cell membrane and myelin sheath provide a

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biological barrier to perpendicular diffusion of water molecules instead directing them along

the axon bundles longitudinal axis, therefore DTI can be used to visualise white matter tracts

and can infer the orientation of surrounding axonal fibres (Hendrix et al., 2015).

Quantitative measurements relating to DTI within the spinal cord can provide an assessment of

neural damage in various spinal cord pathologies with a high level of correlation to histological

and functional observations (Figure 5). More data is required, and scanning protocols and

imaging processing need to be further refined and standardised, however, this is a promising

scanning technique for diagnosis and monitoring of patients with spinal cord disease.

(Vedantam et al., 2014)

Figure 5: A human patient with severe myelopathy.

Panel C - conventional MRI was suggestive of only mild

myelopathy. Panel D – DTI shows almost complete loss of fibres at

C5/6 correlating with the patient’s clinical presentation (Hendrix et

al., 2015).

Studies of people with ALS have shown that DTI is able to detect the microscopic changes in

the spinal cord caused by this condition. In August 2017, Dr. Philippa Johnson, an American

Veterinary Surgeon at Cornell University, started a comparative clinical trial with the aim of

determining if DTI is able to detect the spinal cord lesions caused by degenerative myelopathy.

She recruited two groups of dogs: 1) Dogs with a positive SOD-1 test for degenerative

myelopathy that are showing clinical signs consistent with degenerative myelopathy and 2)

Dogs with a normal neurological examination that are over the age of 8 years.

This project aims to determine if this technique is able to identify the spinal cord lesions caused

by DM by comparing imaging results from a group of dogs with the condition with a normal

group. Dr. Johnson hypothesises that DTI can detect white matter lesions, and the extent of the

lesions correlates to the neurological status in DM dogs at the time of imaging. DTI has the

potential to become a non-invasive and reliable imaging method for the diagnosis and

monitoring of degenerative myelopathy. In addition, the ability to track lesion load and location

over time would be a valuable tool to assess response to treatment trials currently being

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undertaken with SOD1 mutant mice aiming to terminate neurological deterioration (Johnson,

2017). Results are pending as the data collection process for the study was due to be concluded

August 2018.

Treatment

Physiotherapy

Managing the symptoms of DM includes ensuring the nervous system is constantly stimulated

to keep the nerve impulses firing. This should prolong the length mobility of the dog. The best-

known treatment to achieve this aim, based on the outcome of a number of case studies, is for

the animal to undergo physiotherapy.

In 2006, Kathmann et al. produced survival data from a study of 22 DM affected dogs that

received varying degrees of physiotherapy. There were three treatment groups in the study:

1. Intensive physiotherapy group (n=9).

• 5 – 20 minutes active gait exercise, 3-5x/day AND

• Massage or Passive ROM, 3x/day OR

• Hydrotherapy daily

2. Moderate physiotherapy group (n=6)

• 5 – 20 minutes active gait exercise, max. 3x/day AND

• Massage 1x/week OR

• Hydrotherapy 1 x/week

3. No physiotherapy group (n=7)

Active exercises were modified depending on the dog’s neurological status, with slings or other

supports used as necessary. The results showed that the dogs in the intensive physiotherapy

group had longer mean survival times (225 days) compared to those on the moderate treatment

plan (130 days) and those on the no treatment plan (55 days) (Kathmann et al., 2006).

Although the study by Kathmann et al., 2006 would imply that physiotherapy has a beneficial

effect on prolonging the survival time of dogs with a presumptive diagnosis of DM, it did not

consider the disease stage or UMN/LMN signs. It also had other limitations such as lack of

randomisation, definitive diagnosis, small group size and owner bias. However, it does warrant

further investigation into the efficacy of disease stage appropriate therapeutic exercises, whilst

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being mindful of not over-exerting these dogs who tire very easily. Over-exertion in many

situations can be counter-productive (Zink and Van Dyke, 2013).

It is clear that physiotherapy has a vital role in the treatment of DM in order to maintain

functional movement in the animal and delay the progression of the disease. Given the poor

prognosis, physiotherapy can also improve the psychological impact on the dog and owner

alike, enhancing the quality of life for the patient and giving the owner a sense of actively

delaying the loss of mobility. Owner support is vital as the dog will become more and more

reliant on them and anxiety may increase as the disease stages progress. Functionally, the aims

of physiotherapy would include:

• Maintaining muscle mass and nerve stimulation

• Maintaining mobility, movement, postural strength and gait patterns

• Prevent tightening of soft tissues such as tendons, muscles and ligaments

• Enhance balance and co-ordination

• Prevent injury that might occur as a result of existing issues

Therapeutic Exercises

One of the known mental and physical stressors for dogs with DM is over-exertion, therefore a

therapeutic exercise program should always begin slowly and at low level and then be modified

regularly by constantly assessing progress and mental state. Ideally, the exercise program

should start while the dogs are still ambulatory, but this is not always possible due to the

difficult nature of diagnosis.

Active exercises should include a variety of core strengthening techniques which will improve

quality of life by targeting trunk musculature (thoracic limb and pelvic stabilisers, vertebral

column stabilising muscles, abdominals) and improving overall movement efficiency. As the

disease progresses, strong core muscles will also aid respiratory movements. Some exercises to

improve core strength include:

• Figure-of-eight around cones.

• Weight shifting (balance pads, wobble cushions) – all 4 legs up

• Rhythmic stabilisations (360°)

• Stepping over Cavaletti rails

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• Sit-stand-sit positional changes

• Stair climbing, incline work

Active and Passive Range of Motion (ROM) exercises will stretch muscle groups in the limbs

in a functional movement pattern therefore aiding efficiency of gait. Spinal flexors and shoulder

flexors will be affected and will restrict movement. Encouraging the stretching of the soft

tissues by focussing on hip extension, spinal extension and shoulder extension will greatly

improve prospects and delay the loss of mobility. It will also help break down ligamentous

calcification that promotes spondylosis and rigidity in the spine. Exercises to improve ROM

include:

• Stepping over Cavaletti rails

• Stair climbing, incline work

• Give-a-paw, extend elbow

• Bowing (elbows extended), forelimb raised, hind limb raised,

• Luring with a treat side-to-side and down between front legs.

Balance and proprioception will be negatively affected by the degeneration of the nerve

impulses, therefore exercises which include increasing the length of time the dog can hold a

standing balance will be beneficial. Offering support by use of a body harness to extend the

amount of time will also encourage improved balance. Encouraging proprioceptive stimulation

can be achieved with light touching, wraps, or gentle tapping of the muscles which will increase

sensory input to the limbs. Exercises to improve balance and proprioception include:

• Stepping over Cavaletti rails

• Weight shifting on balance pads/wobble cushions - forelimbs elevated

• Walking on different surfaces/textures (stones, sand, grass, water etc.)

• Drop-sticks/Obstacle Course

• Lateral stepping

Strengthening and endurance exercises should be modified according to the dog’s baseline

ability. Functional analysis includes ability to walk and efficiency of transitions between

positions.

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Massage will aid circulation, helping to remove toxic inflammatory mediators, which can build

up in the muscles, and therefore will assist maintenance of muscle tone. The increased

circulation will also improve production of white blood cells which will boost the immune

system and decrease cortisol levels reducing stress levels and relaxing the dog.

Treatment Modalities

A physiotherapist will have access to a selection of treatment modalities which can complement

a therapeutic exercise program and benefit the functional aims of treatment. As previously

mentioned, although the degeneration of nerve impulses is not painful in itself, it is

presumptuous to say that some dogs with DM do not suffer pain. Ageing dogs are likely to have

other disease processes which may be painful and exacerbated by lack of co-ordination. There

will also be compensatory effects and concurrent diseases, which may cause some level of pain.

A physiotherapist will be able to identify these areas through massage and palpation techniques.

• Electrotherapy

Electrotherapy involves passing low to medium levels of electrical current through the body in

order to reverse atrophy, improve muscle function and reduce pain signals. At the cellular level,

electrotherapy causes local nerve cell excitation and changes cell membrane permeability which

will stimulate protein synthesis, osteosynthesis and fibroblast formation (Millis, 2017). At the

tissue level, increasing muscular strength by stimulating skeletal muscles can be achieved with

the use of a Neuromuscular Electrical Stimulation (NMES) machine. The device can be used

to stimulate muscle contraction and hence improve muscle bulk and strength by emitting

electrical impulses and stimulating the local motor nerve without the involvement of the central

nervous system (CNS). This device can therefore help reduce the rate of muscle atrophy as a

result of the dog’s inability to actively move their own body. Through the stimulated movement,

the muscle contractions will also result in improved joint mobility as well as circulatory and

lymphatic drainage. Care must be taken to provide an almost imperceptible contraction strength

at the outset, and increase it slowly only when the animal is comfortable and aware of the

procedure so as not to cause any anxiety.

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• Therapeutic Laser Therapy

Photobiomodulation (PMB) is the use of therapeutic lasers in medical treatment, and is intended

to describe the modulation of cellular processes in the body as a result of the application of light

therapy. Class 3 therapeutic lasers emit low power (10mW – 500mW) radiation via photons of

light with wavelengths in the red to near infrared region of the spectrum (660nm – 905nm)

without emitting any heat (non-thermal mechanism). These wavelengths are able to penetrate

the skin to different depths and therefore affect various soft and hard tissue types (Cotler et al.,

2015). These energised cells then have further downstream tissue effects such as pain

modulation, increased local microcirculation for tissue healing and regeneration, stimulation of

the immune system and reduction of the inflammatory process. Depending on the chosen

parameters, PBM can have stimulatory or inhibitory effect on biochemical processes (Downing,

2017).

Biochemical processes are powered by mitochondria, which are the “energy centres” of the cell.

They convert nutrients and oxygen, via a series of chemical reactions, into molecules of energy

(ATP) by a process known as oxidative phosphorylation, or cellular respiration. One of the key

elements of this process, an enzyme called cytochrome c oxidase (CCO), is also a chromophore

and can be activated by photons of light. CCO is the primary photo receptor for red and near

infrared wavelengths of light (Cotler et al., 2015).

In stressed or ischaemic tissues, the level of nitric oxide (NO) increases and can inhibit cellular

respiration by binding to CCO. Unregulated NO production can cause cell death through

oxidative stress, disrupted energy metabolism and DNA damage. This leads to an increase in

the production of reactive oxygen species (ROS) which leads to inflammation. The absorption

of the red and near infrared light photons by CCO, causes NO to dissociate and allows oxygen

back into the electron transport chain, thereby increasing the cellular production of ATP and

reducing ROS. (Hamblin, 2016) (See Figure 6)

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Figure 6: https://eriksenchiropracticlaser.com/storage/app/media/laser_diagram.jpg

Myelin-rich white matter in the nervous system is one of the most sensitive tissues to oxidative

damage in the body – the exact pathology seen in dogs with DM. With these facts, the

application of laser therapy should have a positive effect on dogs with DM. PBM has been used

in a number of studies relating to surgical nerve repair, and it has been shown to support nerve

regeneration, re-innervation of denervated muscle, and functional recovery following

peripheral nerve injury (Anders et al., 2014). A study in 2013 by Anders et al., demonstrated

an increase in neurological activity and angiogenesis on day 14 following a surgically induced

nerve injury treated with a PBM protocol, compared to non-treated controls.

The benefits of PBM include reduction of pain and inflammation, potential nerve regeneration,

increased local circulation and increased axonal growth. This stimulation of neural pathways

should be beneficial for a dog with DM to improve their functional and ambulatory status, and

the reduction of pain and inflammation should ease concurrent and compensatory issues given

the goal to prolong and improve quality of life of the dog. Although there have been some

studies involving mechanical spinal cord damage, there are currently no clinical trials involving

the use of PBM in the treatment of neurodegenerative conditions in a dog, however, as DM is

a naturally occurring canine model of human ALS, anecdotal evidence may lead to funding a

study in the future.

20

In August 2018, there was a presentation by Debbie Torraca at the IAVRPT (International

Association for Veterinary Rehabilitation and Physical Therapy) Rehab Summit where she

reported some benefit to the use of PBM in conjunction with a structured therapeutic exercise

protocol for 24 dogs. At the time of the report, 22 out of the 24 dogs had continued past 12

months, although some were in a cart. The PBM protocol used dosages of 20 – 30 Joules/cm2

“applied to anatomical localised region, and epaxial located in the region”, with most

anatomical regions being “T3 – L3 and L3 – S3”. However, there was no mention of the size

of area treated, the duration of treatment, or the total dose delivered during each treatment

session.

Leading manufacturers of Class 3 and Class 4 lasers are developing some speculative treatment

protocols for various diseases and conditions derived from clinical case reports.

• Spectravet Therapeutic Lasers: Dr. Chip Godine, a US veterinary surgeon and

specialist laser consultant for Spectravet, suggested that he has not seen any positive

benefits to the use of PBM thus far. His theory has been to treat the spinal cord from

mid thoracic area to L4 – L5 using the 810nm-multi-500mW (x4) probe, pulsed at 10Hz

for 80 seconds aimed at 45 degrees to the right and left intervertebral foramen. This

should provide a dose of ~ 3J/cm2 at a depth of 2.5 cm from the skin surface at a

frequency of 3x/week until a clinical effect is seen then can be reduced accordingly

(personal communication, 2018).

• Thor Lasers: A protocol designed by Thor laser systems uses their superficial 69 diode

LED cluster probe (660 and 850nm) giving a total power 1390mW and a dose of

44.6mW/cm. They suggest timings of 1 minute/area with a pulse rate of 2.5Hz. Treat

left and right Paraspinals from C4 – S3, the major muscle groups of hind legs and

pudenal nerve area (See Figure 7).

Figure 7: Green circle indicates

placement of probe. © Thor

21

It is clear there is much work to be done with this treatment option regarding appropriate

treatment location on the body, treatment timings, probe power and accurately measuring the

depth of photon penetration into different tissue types. The treatment doses prescribed above

are in differing units so there needs to be a standardised international dose unit so the results of

case studies and clinical trials can be compared accurately.

Alternative Therapies

Treating DM can be improved by using a multi-modal approach involving a variety of

rehabilitation professionals including hydrotherapy, acupuncture and dietary amendments, in

conjunction with a regular physiotherapy regime. This will help delay the progression of the

disease by keeping the dog mobile for longer and reducing physiological and psychological

stresses.

Hydrotherapy

Hydrotherapy is an excellent form of rehabilitation for dogs with DM. The effects and physical

properties of water, such as density, hydrostatic pressure and buoyancy will benefit the physical

constraints of the condition supporting the weight of the animal and providing low joint impact

during movement to exercise weakened areas of the body. The hydrostatic pressure and

therapeutic temperature of the water stimulates metabolic and neuromuscular systems as well

as decreasing pain and oedema therefore allowing a greater range of joint and muscle motion.

Hydrotherapy is good for any stage of the disease and can be carried out in an underwater

treadmill or in a pool, depending on the stage of the disease. In the early stages of the disease,

while the dog is still able to support its own body weight, a treadmill can be used to encourage

appropriate gait movement. It is best to begin with standing exercises with the water at the level

of the greater trochanter (decreases weight bearing by 73%). Once the dog is comfortable with

standing, progression to slow walking will help maintain muscle strength and joint range of

motion.

Hydrotherapy also provides dogs with mental stimulation, and a sense of freedom and purpose.

The progression of DM can be very distressing for the dog as they are unable to move and

defend themselves, which in turn can make them anxious, depressed and bored. The freedom

22

of moving in water where it is not physically possible on land is hugely beneficial for their

mental wellbeing. It has been reported in some cases that dogs have independently moved

paralysed legs in a hydrotherapy pool! Frequency of hydrotherapy sessions does not have to be

limited except by the fatigue level of the dog.

In conjunction with Hydrotherapy, Ozone Hydro-Massage Therapy in a canine spa has also

shown to be beneficial to dogs with DM. The Ozone has a strong anti-bacterial function and

can help alleviate itching, and other skin conditions which may be concurrent. The tiny and

powerful bubbles and their rhymical impact delivers a full body massage helping to stimulate

and activate body tissues. This relieves tension and fatigue and encourages the production of

red and white blood cells helping to clear inflammatory mediators from stressed muscles. It is

difficult to groom dogs with DM, so the spa has the added benefit of loosening grease and dirt

from the skin as well as loose hairs. Capillaries in the skin are dilated with the warmth of the

water, bringing nourishment to the surface of the skin therefore allowing it to breathe better and

enhancing healing of abrasions and bed sores.

Acupuncture

Acupuncture is one branch of Traditional Chinese Medicine (TCM) that has been used for

thousands of years for the treatment of pain and neurological issues. It has only been since the

1970s that this form of medicine has gained popularity in Western Culture, both clinically and

in research. Acupuncture treatment involves stimulating specific pressure points on the surface

of the body by inserting long, hair thin needles, resulting in a therapeutic or homeostatic effect.

The aim is to ‘realign’ Qi (energy) allowing it to flow harmoniously, which can be equated in

Western practice to stimulation of the parasympathetic and sympathetic components of the

autonomic nervous system. Modern studies have determined that acupuncture points are located

in areas of sensitive neuro-immune modulation, where there is a high density of immune

mediated mast cells, lymphatic vessels and an increased ratio of myelinated nerve fibres

(Roynard et al., 2017).

There are no specific studies using acupuncture in cases of degenerative myelopathy, but there

have been some small randomised trials involving other spinal cord myelopathies with positive

results. A study of acupuncture treatment in rats with spinal cord injuries showed a significantly

improved functional recovery compared to the placebo control groups (Figure 8). The affected

23

group also had a significant reduction in the expression of inflammatory mediators, offering

increased neuroprotection and reducing neuronal cell death and axonal loss (Choi et al., 2010).

Figure 8: Representative footprints obtained from each group of rats with spinal cord

injury at 35 days after SCI. The control group of rats dragged their hind limbs. The

group receiving acupuncture showed advanced functional recovery (Choi et al., 2010).

Nutrition and Diet

In the 1990s a treatment protocol for DM was formulated by a veterinary neurologist Roger

Clemmons, and is known as The Clemmons Protocol. It was formulated around a diet designed

to counter immune-mediated damage as well as a structured and regular exercise program. The

diet centred around unprocessed food with supplements which included sustained use of anti-

oxidants, fibrinolytics and prednisone as and when required. The latter two aimed to limit

inflammation of the cord itself (Marsden, 2015). An independent study testing the supplement

regime in the absence of the diet and physiotherapy showed no improvement in the survival

time of dogs with DM (Pfafman, 2017).

Diet should focus on feeding unprocessed foods as they are naturally higher in anti-oxidants

and will limit oxidative stress in the spinal cord, control acute and chronic inflammation and

help regulate the immune system. Starchy food, as is found in most dog kibble feed, increases

insulin levels and can promote inflammatory cytokine production. This reduces the

bioavailability of nitric oxide (NO) which is a key molecule involved in the resolution of

inflammation. Ongoing inflammation promotes oxidative stress which exacerbates and

accelerates the disease (Pfafman, 2017).

Polyunsaturated fatty acids are one of the most effective anti-inflammatories which should be

included in the diet as they are not produced by the body. The most important is Omega-3 and

it can be found in fish oils. Other antioxidants beneficial to DM affected dogs include vitamin

24

C, vitamin E, vitamin A, carotenoids, selenium, coenzyme Q10 and taurine. Most of these can

be found in fresh fruit and vegetables (Mayer, 2018).

There are some plant extracts which have been shown to protect the spinal cord from

inflammation, these include:

o Bupleurum which helps to moderate white blood cell movement into the

interstitial space of the spinal cord and reduces production of key inflammatory

cytokines.

o Curcumin (found in Turmeric) which inhibits the production of inflammatory

cytokines in the spinal cord and inhibits destruction of damaged tissues and

gliosis (a pathological process in the CNS).

o Milk Thistle which is also a powerful antioxidant and inhibits gliosis (Marsden,

2015.

A canine nutritionist will be able to design a bespoke diet based on the requirement for a low

glycaemic index, high levels of anti-oxidants, and foods with effective anti-inflammatory

properties. With frequent consultation, they will also be able to modify the diet to account for

the diminishing energy requirements of the dog as it starts to lose active mobility and therefore

moderating their weight. This would be an additional benefit to avoid physical and

physiological stress.

Physiotherapy is the most successful and proactive treatment currently available to improve the

quality of life for dogs with DM. Not only is it important for the physical and psychological

welfare of the dog, but also a valuable source of information and support for the owner. A

physiotherapist will be able to advise on alternative treatments to accompany physiotherapy in

a multi-practitioner approach to managing the condition. Although a generalised treatment plan

for physiotherapy and alternative therapies can be devised (See Appendix 1), all dogs are

different and will respond differently to intervention. It is important to modify the plan for each

individual dog as the disease advances, therefore frequent assessment of progress is necessary.

Physiological and psychological stress are accompanied by a decline in neurological function

and one of the major stressors for the dog is a stressed owner (Torraca, 2018). The disease has

a mental and physical impact on owners as they come to terms with the prognosis and managing

a progressively incapacitated dog. A physiotherapist can provide emotional support as well as

25

information and advice on home exercises, comfort aids, assistive devices and home

modifications which will positively impact the welfare of the dog in between treatment sessions.

Comfort Aids

Boots/Socks

Boots and Socks can be used to protect the dog’s paws from abrasions, open sores and wearing

down their nails when they knuckle and drag their hind limbs. There are many varieties of dog

boots available and the correct type will depend on the weight and size of the dog as well as the

stage of the disease. Ruffwear™ Dog Walking Boots and RoyalCare™ Protective dog boots

are both good quality, waterproof and sturdy (Figure 9). It is important to bear in mind that DM

dogs already struggle with hind limb strength and proprioception and so heavy-duty hiking

boots, although durable and good for protection, may not be appropriate for some dogs as they

may be too cumbersome and will throw them off balance causing them to trip.

Figure 9:

Left: https://www.ruffwear.co.uk/dog-gear/dog-boots

Right: https://www.amazon.co.uk/Royalcare-Protective-Boots-Waterproof-Medium/dp/B0776VLQ8S

26

A less cumbersome option is dog socks with grippy soles such as Grippers™ non-slip dog

socks. They are not as protective or durable and will be affected by weather conditions, but the

dog will be less likely to trip while wearing them. Human baby socks with grippy dots for extra

traction could be used as an alternative. PAWZ dog boots are rated well (Figure 10). Although

they look like deflated balloons, they are lightweight, durable and waterproof. They are not

breathable however, so are suitable for outdoors, and then can be swapped for a more breathable

material whilst the dog is indoors. It is important to note that they should be removed overnight

so the dog’s paws and skin can breathe sleeping.

Figure 10:

Left: https://www.dogquality.co.uk/products/grippers

Right: https://www.pawzdogboots.com/

Bedding

A supportive orthopaedic dog bed can alleviate bed sores. If the bed is too soft, it may be

difficult for the dog to get up from it. In addition, because the dog may have lost proprioception,

they may feel unsafe getting on the bed if it is too deep and too soft. A removable washable

cover is beneficial when the dog has become incontinent so it can be cleaned with ease. If the

bed does not have a removable cover, an incontinence sheet or puppy pad can be used and then

covered with blankets. Be cautious of some memory foam beds that compress too easily as this

will unbalance the dog, and they will be less likely to use it. Also consider temperature

regulation as some memory foam mattresses can retain heat and are not breathable. A paraplegic

dog will not be able to alter their recumbent position by themselves, so the owner must be aware

of discomfort. There are many brands of Orthopaedic bed and it is not always possible to try

27

out pet beds before you buy them. The Pet Fusion Ultimate Pet bed and Lounger has received

good reviews.

https://www.amazon.co.uk/PetFusion-Memory-Medium-Large-91x71cmx23cm/dp/B00TQ47CPW

Movement Aids

Assistive Harnesses and Slings

As the symptoms of DM progress, the dog may require assistance walking, going up and down

stairs, getting in and out of the car and even during toileting. This can be quite a physical

challenge for owners with larger breeds. A support harness will enable the dog to remain

mobile, and give them a greater level of perceived independence. The Help ‘Em Up™ Harness

is probably the best known. It is made with high quality materials and with lifting handles over

the front and rear limbs. Not all dogs tolerate the straps around the hind limbs and hips, and

prefer just a thoracic support harness. The GingerLead® Dog Support and Rehabilitation

Harness is a good alternative (Figure 11). There is good sizing advice available by the retailers

of both these harnesses, but additionally, a physiotherapist should be able to help adjust it to fit

comfortably.

Figure 11:

Right: Help ‘Em Up Harness https://www.orthopets.co.uk/mobility-solutions/help-emup/

Left: GingerLead® Harness http://www.gingerlead.com/

A sling is now available to assist dorsiflexion of the hind feet. It prevents paw knuckling by

supporting the two centre digits via an adjustable elastic cord attached to a strap in the hock. It

is not suitable for prolonged use, or where the dog has delicate or sensitive interdigital skin.

28

Another version is available as a Ruffwear boot conversion (Figure 12) so the sling can lift the

paw without directly contacting the skin.

Figure 12: https://www.orthopets.co.uk/mobility-solutions/sciatic-sling/

Wheelchairs and carts

Wheelchairs can be used during the initial stages of the disease when the degeneration only

affects the hind quarters (See Figure 13). They can be expensive and are not always tolerated

by the dog, but for some they bring a new lease of life as the dog enjoys independent locomotion

again. Care must be taken for them to fit correctly, but most reputable suppliers will build a

bespoke wheelchair for each individual dog. Carts can be used at any stage of the disease; as a

respite from fatigue during a walk in the early stages, or just to get the dog out and about for

extended periods of time when they are paraplegic. They are also expensive, but with some

imagination, cheaper options can be found - some owners retrofit a garden trolley!

Figure 13:

Left: Hercules Stroller

https://www.petsownus.co.uk/collections/3-wheelers-dog-strollers-dog-pram/products/hercules-heavy-duty-dog-

buggy-stroller-incl-rain-cover

Right: Eddies Wheels: https://eddieswheels.com/

29

Home Modifications

Indoor Traction

To prevent slips and falls the use of rubber backed mats or non-slip rug netting will give the

dog more traction on slippery floors and stairs. Adhesive anti-slip tape or anti-slip discs are also

available and is an effective solution to provide more grip and enable more stability in the dog’s

movement.

Ramps

Ramps are invaluable when the dog is too large to lift in and out of the car or up and down steps

in the garden. Owners can easily construct a sturdy ramp that will remain permanently in one

position, such as in the garden. Portable ramps for getting in and out of a car are available in

lightweight folding and telescoping configurations.

The provision of any ramp should consider the following recommendations:

• Wide walking surface to make an unstable dog feel more confident to use them.

• Good traction on the surface so the dog doesn’t slip. Reduced proprioception is already

a problem so no slats.

• No bounce – should be built solid so they do not bounce. Uncoordinated dogs will find

a bouncy ramp frightening and will probably refuse to use it.

• Low gradient – should be as long as possible long so the angle of ascent is not too steep.

Always use a harness to guide the dog up and down any ramp.

Supportive Care

Dogs progressing to the second stage of the disease and beyond will be paraplegic and most

likely incontinent. The owner must take on a carer’s role providing support, company and

nursing care. Skin damage can occur as a result of pressure sores and urine scalding, but

frequently turning the dog from one side to the other and providing them with incontinence

pants (Figure 14) can minimise these problems. If skin damage does occur, the owner will need

to provide nursing care to keep the wound clean as it heals – phototherapy devices to aid skin

healing can be rented from a physiotherapist.

30

Figure 14: Washable Wonders™ Dog Pads

https://www.dogquality.co.uk/collections/dog-nappies

Dogs will become very stressed and frustrated as their mobility diminishes. Enrichment games

and toys, such as food puzzles, treat dispensers or snuffle mats (Figure 15) may provide mental

stimulation, but this must be balanced with their total food allowance for the day to ensure there

is no weight gain.

Figure 15: https://www.rufflesnufflemats.com/

31

Case Study

Dixie Emery DOB: 27/06/2006 (Age 12)

Breed: Golden Retriever

Symptoms: Urinary incontinence, urinary infection, scuffing hind toes, reduced weight bearing left

hind limb.

Medical Diagnosis: Degenerative Myelopathy (May 2018)

Investigative Procedures:

• MRI – Unremarkable (severe arthritis L&R tarsal joints)

• CT – Unremarkable (severe arthritis L&R tarsal joints)

• Spinal Tap – Mildly elevated protein concentration

• Neurological examination: delayed conscious proprioception (hind knuckling)

• DNA Test for SOD-1 mutation: N/N (normal – no mutation)

Observations:

• Difficulty rising from recumbency

• Difficulty climbing stairs

• Episodes of vocalising pain concurrent with left limb muscle spasm

Palpation:

• Tightness between scapulas

• Hypotonic gluteals, quadriceps

• Hypertonic hamstrings, gastrocnemius

Treatment since diagnosis (May 2018):

Medication: 100mg Amantadine daily, Metacam daily

Therapeutic Exercises: core conditioning, proprioception, hind limb strengthening

(3-4x/week)

Daily Walk: 1 x 25 minutes, 1 x 45 minutes

Massage: focus on neck, shoulders, pectorals, hamstrings, gastrocnemius (3-4x/week)

PEMF: Treat tarsals on setting F for pain (B:200Hz, P:Constant) 1x/day, 5-7 days/week

PBM*: T3-L5, 10Hz, 40 - 80 seconds (810nm-multi-500mW) probe, 3x/week

Inguinal, popliteal LNs, 2Hz, 20 – 30 seconds, 3x/week

Tarsal Joint (4 points), 5Hz, 20 seconds, 3x/week

Hydrotherapy Pool: Slow ROM 40 minutes, every 2 weeks

Acupuncture: Schedule dictated by acupuncture veterinarian

Supplements: Viacutan Plus (Borage oil gamma linolenic acid, essential fatty acid

combination of plant and fish oil

Dr. Mercola Organic Mushroom Complex (antioxidant)

Dr. Mercola Vitamin B Complex

Dorwest Turmeric Tablets (Curcuminoids + Bioperine)

YuMove

Diet: high quality, grain free kibble - no change from before diagnosis.

*PMB treatment started September 2018

------------------------------------------------------------------------------------------------------------------------

Follow Up: Dixie was assessed again in mid-October 2018, 6 months after diagnosis.

Observations: More alert and playful demeanour. Improved bladder control.

• IMPROVED ability to rise from recumbency

• INCREASED willingness to climb stairs

• NO episodes of vocalising pain, NO left limb muscle spasm

Palpation: No noticeable difference in muscle tone compared to before diagnosis. Improved weight

bearing on left hind, but still not matching right hind.

Conclusion: NO OBVIOUS DEGENERATION SINCE MAY 2018

32

Conclusion

Canine Degenerative Myelopathy is a disease process with many unknowns. The cause is not

completely understood, the pathological processes are complex and haven’t been fully

elucidated and diagnosis cannot yet be confirmed in a living dog. In order to improve treatment

outcomes, it is clear that a definitive diagnosis must be provided at the earliest stage possible.

This paper has described some promising studies measuring biomarkers in CSF and improving

diagnostic imaging of the lesion.

A multifaceted treatment protocol is important to treat this multifaceted disease model

involving a variety of veterinary and rehabilitation professionals. Currently, physiotherapy and

hydrotherapy would appear to be the best treatment options for extending the quality of life of

these patients. Practitioners in both fields should work together in order to create a bespoke

management protocol that best suits each individual dog.

Cumulative oxidative damage starts to appear later in the disease process, therefore better

diagnostic procedures are vital so the disease can be detected earlier. The greatest benefit is

seen with early intervention to slow down progression of the disease. This is also true for home

care and management. It is important to provide the owner with advice for extending and

improving quality of life in and around the home environment.

Current research shows promising results and it can only be of benefit to DM-affected dogs that

the disease closely models the disease process for human ALS. Hope remains that the promising

results of recent studies will warrant successful funding for scientists, veterinarians and

rehabilitation professional to continue the search for answers to the many questions raised by

this complicated degenerative condition. Until there is a cure, minimising the stresses

associated with the physical and emotional impact on the owner and paying close attention to

the welfare of the dog are vital in the management of this ultimately fatal disease.

33

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Intern Med; 28, 515–52

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Appendix 1: Generalised Treatment Plan (Modified from Canine Rehabilitation and Physical Therapy – Millis and Levine, 2014)

Physiotherapy Treatment Home Program Alternative Therapies

Disease Stage 1 General proprioceptive ataxia and asymmetric paraparesis in the pelvic limbs.

Treatment Goals Minimise loss of muscle strength, encourage proprioception, maintain quality of life.

• Assisted standing – balance board, 5 – 10 mins, 2-3x/day

• Weight shifting – balance pad, wobble cushion, 5 – 10 minutes, 2-

3x/day

• Sit to stand – 10-15 reps, 2-3x/day

• Cavalettis – 10-15 reps, 2-3x/day

• Weave poles – 10-15 reps, daily

• Stairs – up and down, 2-3 flights/day

Massage – hind limbs and paraspinal muscles, 1-2x/day

NMES – Quadriceps and Hamstrings, 5–10 minutes, every other day

Laser – T3-L5, 10Hz, 80 seconds (810nm-multi-500mW) probe,

3x/week

• Two-legged standing with weight shifting – 1-2

mins, 2-3 reps, 2x/day

• Slow lead walks – include hill work, 15-20 mins,

2-3x/day – periods of trotting (3-5 mins)

• Walking up and down stairs, 2–4 flights

• Sit-to-stand – 10-15 reps, 2x/day

• Walking/trotting on different surfaces, 5-10 laps,

1-2x/day

Use Paw Protection

UWT – standing, slow walking. 5 – 20

minutes, with breaks

Pool – 10 – 30 minutes with breaks

Acupuncture – frequency as advised by

veterinary practitioner.

Diet – consider changes, include

antioxidants.

Disease Stage 2 Moderate to severe proprioceptive ataxia or non-ambulatory paraparesis/paraplegia in the pelvic limbs. Pelvic limb muscle atrophy +/-

urinary/faecal incontinence.

Treatment Goals Delay loss of muscle strength, continued proprioceptive feedback, maintain quality of life.

• Assisted standing – balance pad, pelvic limb support (as needed)

2 - 5 mins, 2-3x/day

• Weight shifting – balance pad, pelvic limb support (as needed) 2 – 5

minutes, 2-3x/day

• Sit to stand, sling assistance (as needed) – 5 - 10 reps, 2x/day

• Low Cavaletti rails, sling assistance (as needed) – 5 - 10 reps, 2x/day

• Two-legged standing with weight shifting – 1-2

mins, 2-3 reps, 2x/day

• Slow lead walks, pelvic limb support (as needed)

– include hill work, 10-15 mins, 2-3x/day

• Walking up and down stairs, 2–4 flights

UWT – standing, slow walking. 5 – 10

minutes, with breaks

Pool – 10 – 15 minutes with breaks, 3-

4x/week

Acupuncture - frequency as advised by

veterinary00000000 practitioner.

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• Weave poles – 10-15 reps, 2x/day

• Stairs – up and down, pelvic limb support (as needed), 2-3

flights/day

Massage – hind limbs and paraspinal muscles, 1-2x/day

NMES – Quadriceps and Hamstrings, 5–10 minutes, every other day

Laser – T3-L5, 10Hz, 80 seconds (810nm-multi-500mW) probe,

3x/week

• Sit-to-stand, sling assistance (as needed) – 5 - 10

reps, 2x/day

• Walking on different surfaces, 2-8 laps, 1-2x/day

Use paw protection as required.

Use harness and pelvic sling as required.

Use incontinence pants/pads as required.

Diet

Disease Stage 3 Flaccid paraplegia in the pelvic limbs, thoracic limb paresis. Severe pelvic limb muscle atrophy, urinary/faecal incontinence.

Treatment Goals Reduce loss of muscle strength in thoracic limbs, continued proprioceptive feedback, maintain quality of life.

Passive ROM – bicycling movements in all limb joints, 10 – 15 reps,

2-3x/day

Massage – all limbs, neck and paraspinal muscles, 1-2x/day

NMES – Quadriceps and Hamstrings, 10 minutes, once a day

Laser – T3-L5, 10Hz, 80 seconds (810nm-multi-500mW) probe,

3x/week

Passive ROM – bicycling movements in all limb

joints, 10 – 15 reps, 2-3x/day.

Massage – all limbs and neck, 1-2x/day.

Enrichment activities for mental stimulation, daily.

Walking (with cart) on level ground, 2-3x/day.

Nursing care for pressure sores/urine scalding.

Welfare/Quality of life considerations.

UWT – standing, slow walking. 5 – 10

minutes, with breaks, daily. Use floatation

devices as required.

Pool – 10 – 15 minutes, supported standing

during breaks, daily.

Acupuncture - frequency as advised by

veterinary practitioner.

Disease Stage 4 Flaccid tetraplegia. Severe generalised muscle atrophy. Urinary/faecal incontinence. Dysphagia, dysphonia, respiratory difficulty.

Treatment Goals Maintain comfort, welfare considerations, assess quality of life

Passive ROM – bicycling movements in all limb joints, 10 – 15 reps,

2-3x/day

Massage – all limbs, neck and paraspinal muscles, 1-2x/day

Passive ROM – bicycling movements in all limb

joints, 10 – 15 reps, 2-3x/day.

Massage – all limbs and neck, 1-2x/day.

Enrichment activities for mental stimulation, daily.

Nursing care for pressure sores/urine scalding.

Welfare/Quality of life considerations.

Pool – 10 – 15 minutes, floatation devices,

passive ROM, daily.

Acupuncture - frequency as advised by

veterinary practitioner.

*Caution: The above is a guide. Choose only 2 – 4 exercises per session to avoid over exertion. Rate of progression will vary widely among

patients.

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