Equine headshaking and muscle disease Flashcards
What is headshaking in horses + signs
Uncontrollable, repeatable, persistent OR intermittent, vertical OR horizonal movement of the head
Often very subtle at rest but get worse during exercise
[other signs: avoiding airflow onto face, muscle fasciculations/grimacing, lip smacking)
What is the seasonality of headshaking
Most common in spring/summer or spring to autumn
Tend to get remission in winter
What other diseases can mimic headshaking signs
Nuchal crest avulsion fracture
Allergic rhinitis
Guttural pouch disease
Temperohyoid osteopathy
Otitis
Ocular disease
Pemphigus
Mites around nares
What is the pathology of idiopathic headshaking
Functional trigeminal nerve compromise
[there are studies showing lower activation threshold of trigeminal]
Roberts grading of headshaking
1 = signs only whilst exercising and can be ridden
2 = signs only at exercise but unsafe to ride
3 = signs at rest and exercise
What nerve block can be used to help diagnose headshaking
Maxillary nerve block BUT not specific as anything could be causing pain in this region e.g dental disease
+ possible complications
What is a cheap and easy possible treatment of headshaking
Nose nets/face masks
UNclear how
Seems to work better in younger horses
Pharmaceutical control of headshaking
All expensive, not good and many can’t be used in competition
- Cyproheptadine anti-histamine/anti-serotonergic; over 50% improve on this but very expensive and can’t compete
- Carbamezepone to reduce neuron excitability
- Gabapendint
- Dexamethasone; unclear how this could help….
What is the best way to treat idiopathic headhsaking
Percutaneous electrical nerve therapy
Up to 80% get back to normal level of ridden activity
How does percutaneous electrical nerve therapy work for idiopathic headshaking
Sedate heavily with ACP, then detomidine drip + morphine
Place needle through skin and use U/S to check it is just superficial to the nerve
Complete circuit using clipped patch on other side and do electrical therapy
Short withdrawel from competition (2-3days)
How could surgery be done for idiopathic head shaking
Using titanium coils to compress the infraorbital nerve
Can give 50% reduction in sign severity but can make it worse
Three broad categories of muscle disease in horses
Acute muscle injurt
Exertional rhabdomyolysis
Other pyopathies
What two specific muscle enzymes can we measure in serum and what are their peaks like with damage
Creatinine kinease; from skeletal/cardiac muscle so quite muscle specific –> rapid peak in 4-6hrs; cleared in days
Aspartate transferase = less specific, also liver, RBCs; slower peak 12-24hrs and cleared in 2-3 weeks
What counts as a subclinical exertional myopathy
Where there is a more than 200-300% increase in CK levels after gentle exercise
How do we measure post-exercise muscle enzymes activity
Test CK before and then 4hrs after a 15-20 min gentle exercise; normal to see some increase in CK but only 2-3X increase
What are we looking for in urinalysis in myopathy cases
Myoglobinuria; red/brown colour
Need lab analysis to differentiate it from haemaglobinuria
What must we remember with transporting vitamin E assays
Keep on ice in the dark
What may be used to differentiate orthopaedic from neuromuscular atrophy causes
Electromyography; have abnormal EMG in atrophy/weakness
What are type 1 fibre vs type 2 fibre muscle types
Postural muscles are mainly type 1 fibres
Locomotor muscles are mostly type 2 fibres
What are type 1 muscle fibres
Slow contracting fibres; associated with need for fatty acid oxidation for contraction
What are ddx for muscle disorders affecting postural muscles
Equine motor neurone disease
Nutritional myodegeneration
What are ddx for locomotor muscle disease
Recurrent exertional rhabdomyolysis
PSSM
What is sporadic exertional myopathy
Related to increase in work intensity without proper training + exhaustion/overheating
-> Therefore assocaited with racehorses/endurance in hot and humid climates
Signs of sporadic exertional myopathy and tests
Weakness, ataxia, tachypnoea, sweating, muscles may palpate normally
See myoglobinuria + increased CK
What is recurrent exertional rhabdomyolysis
= where we get stiff, firm, painful muscles the day after a rest day
Common in thoroughbreds, esp excitable fillies; likely to be autosomal dominant inheritance
What do we see with tests/biopsy of recurrent exertional rhabdomyolysis
Myoglobinuria, marked elevation in CK and AST
Biopsy used to rule other things out; just see chronic non-specific changes assocaited with muscle regeneration
MAnagement/medication for recurrent exertional rhabdomyolysis
Low starch/sugar diet, access to salt block, vit E
Do not exercise above training scope, avoid rest days, minimise stress
Can use dantrolene a RYR1 antagonist to inhibit calcium release from SR
What is the recommendation on when to return horses with recurrent exertional rhabdomyolysis to work
Recommentation = when CK <3000U/L
But suggested to wait until within reference range <400 to avoid re-triggering it
Which breeds do we see polysaccharide storage myopathy in
Quarter horses
Connemara
Warmbloods
(see PSSM2 esp in these breeds)
What is the pathogenesis of PSSM
Due to accumulation of polysacchardie in the myofibril
Get recurrent episodes often triggered by exercise that can range from mild shifting lameness/laziness to recumbency
How can we diagnose PSSM
Biopsy of muscle; see polysacchardie accumulation in myofibril
Differentiating PSSM1 and PSSM2
PSSM1 = due to GYS1 gene mutation which increases glycogen synthase; abnormal glycogen shape and less effective glycogenolysis
PSSM2 = no GYS1 mutation but altered glycogen staining on biopsy still
What do we expect to happen to CK values after exercise in PSSM case
Increase at least 3X
Management of PSSM horse
Low starch, high fat diet; veg oil making up to 1ml/kg/day
Supplement vit E/se
Lose weight if needed
Minimise stress/change
Keep regular work rhythm as many days as possible but do not exercise beyond training scope
NOT truly reversible but can we well managed
Which horses do we seee equine myofibrillar myopathy
Arabs and warmbloods (some of these may actually be PSSM2 cases)
What do we see on a biopsy with equine myofibrillar myopathy
Disorganised myofibrilas and abnormal desmin accumularion
What signs do we see with equine myofibrillar myopathy
Variable
In arabs stiffness, reluctance to move (like exertional rhabdo)
In warmbloods assocaited with poor performance
Which breeds do we see HYPP in
Quarterhorse, painthorse, appaloose
What is HYPP and how can we diagnose
hyperkalaemic periodic paralysis= where there is a gene mutation that laters the voltage gated Na+ channels in skeletal muscles cells causing persistent depolarisation
Variable clinical signs, can see tremors
Diagnosis = genetic tests + hyperkalaemia
What is post-anaesthetic myopathy
Where there is a localised area of hot, hard swollen muscles
Related to compartment syndrome of increase pressure, ischaemia, swelling etc
Must be careful with the positioning of horses during GA + maintain blood pressure
How can we reduce risk of post-anaesthetic myopathy
If in dorsal ensure animal is symmetrical
If in lateral, extend the lower forelimb forward/lower hindlimb back
Maintain good blood pressure during GA
Which breeds do we get malignant hyperthermia in
Quarterhorses
Painthorses
What is malignant hyperthermia
Where there is a mutation in RYR1 gene causing dramatic increase in intracellular calcium, get contraction, heat in muscles and necrosis
So animal shows marked hyperthermia and acidosis
If we pre-screen a horse as having RYR1 gene mutation what might we bre-treat them with before GA
Dantrolene
What is white muscle disease
Nutritional myodegeneration; affects cardiac and skeletal muscles
Usually foals/youngstock where dam has had selenium/vitE deficiency
Clinical signs of white muscle disease
Dyspnoea, weakness, stiffness, trembling, recumbency, sudden death, irregular tachydysrhythmias
Affects: tongue, gastrocnemius, semimembranosus/tendinosus, biceps femoris, lumbar, gluteals, cardiac muscle
Diagnosis of white muscle disease
Increase in CK/AST
Myoglobinuria
Electrolyte derangements
Low selenium on whole blood, vit E on plasma
Pale oedematous muscle, calcification, hypercontracted fibres
Does cardioresp or skeletal white muscle disease give a better prognosis
Skeletal
Treatment of white muscle disease
Selenium injections IM (NB = irritant so may dilute before injection)
Oral alpha-tocopherol (vit E) supplementation
Supportive nursing
What is alpha-tocopherol
Vit E
General treatment principles for myopathies
Rest; do not exercise in acute phase
NSAIDs
Antioxidants
Analgesia from start
Correct fluid deficit and protect kidneys by staying in isothenuric range
Why do we want to stay in isothenuric range in myopathy case
To avoid pigment nephropathy from myoglobin
Why do we need to be more careful with NSAID use in myopathies
Bceause kidneys already exposed to nephrotoxic myoglobin
What is atypical myopathy
Disease of muscle degeneration due to failure of energy production due to an acquired deficiency in acyl-coA dehydrogenase
What toxin can cause atypical myopathy
Hypoglycin A from sycamore seedlings
–> COnverted to MPCA-CoA which causes irreversible inactivation of dehydrogenases
What is the key with managing an atypical myopathy case
Buying the animal time to produce new dehydrogenases
+ provide B vits and carnitine as building blocks for this
What muscles are affected by atypical myopathy
Type 1 muscle cells; postural muscles
Cardiac muscle
Clinical signs of atypical myopathy
Weakness, stiffness, recumbency, trembling, sweating
Pigmenturia
Dysphagia
Tachycardia
tachypnoea/dyspnoea
What is the key way to differentiate atypical myopathy from colic
Pigmenturia present in atypical myopathy
WHat is it causing pigmenturia in atypical myopathy
Myoglobin
How can we confirm atypical myopathy and what must we consider in terms of how in house machine can cope with this
Measure CK and AST: expect extremely high CK levels in >100,000s
NB: in house machines can struggle with these high numbers so diluting them is a good idea
NB: can get false negatives early in disease process
Why might we see dependent oedema and obstruction of URT in atypical myopathy cases
Due to low head carried from preferential affectation of muscles holding up the head in some cases
This leads to dependent oedema, oes obstruction etc
WHat are the key things to do when managing an atypical myopathy case
Pain relief
Fluid therapy; to replace losses + protect kidneys from myoglobin impact (can do oral and IV)
Oxygen supplementation
Nutritional support; these horses rely on carbohydrate metabolism; can do high fibre, can do parenteral nutrition with lipid part taken out
Anti-odixants and vitamins
What anti-oxidants/vitamins do we give with atypical myopathy
Vit E to prevent lipid peroxidation
Carnitine to bind the toxin hypoglyvin A
Vit B2 to give building blocks to make new acyl dehydrogenase enzymes
What metabolism process is compromised in atypical myopathy
Fatty acid beta-oxidation
Hence why type 1 muscles affected more
Is CK relevant in prognosis for atypical myopathy
NO because not a linear relatioship with muscle damage
What other causes of trigeminal nerve dysfunction should we rule out before getting diagnosis of idiopathic headhsaking
- Fungal disease
- Intranasal mass
- Dental disease
- Headhsaking after surgery causing nerve damage
