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Equine headshaking and muscle disease Flashcards

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1
Q

What is headshaking in horses + signs

A

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)

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2
Q

What is the seasonality of headshaking

A

Most common in spring/summer or spring to autumn
Tend to get remission in winter

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3
Q

What other diseases can mimic headshaking signs

A

Nuchal crest avulsion fracture
Allergic rhinitis
Guttural pouch disease
Temperohyoid osteopathy
Otitis
Ocular disease
Pemphigus
Mites around nares

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4
Q

What is the pathology of idiopathic headshaking

A

Functional trigeminal nerve compromise
[there are studies showing lower activation threshold of trigeminal]

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5
Q

Roberts grading of headshaking

A

1 = signs only whilst exercising and can be ridden
2 = signs only at exercise but unsafe to ride
3 = signs at rest and exercise

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6
Q

What nerve block can be used to help diagnose headshaking

A

Maxillary nerve block BUT not specific as anything could be causing pain in this region e.g dental disease

+ possible complications

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7
Q

What is a cheap and easy possible treatment of headshaking

A

Nose nets/face masks
UNclear how
Seems to work better in younger horses

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8
Q

Pharmaceutical control of headshaking

A

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….
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9
Q

What is the best way to treat idiopathic headhsaking

A

Percutaneous electrical nerve therapy
Up to 80% get back to normal level of ridden activity

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10
Q

How does percutaneous electrical nerve therapy work for idiopathic headshaking

A

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)

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11
Q

How could surgery be done for idiopathic head shaking

A

Using titanium coils to compress the infraorbital nerve
Can give 50% reduction in sign severity but can make it worse

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12
Q

Three broad categories of muscle disease in horses

A

Acute muscle injurt
Exertional rhabdomyolysis
Other pyopathies

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13
Q

What two specific muscle enzymes can we measure in serum and what are their peaks like with damage

A

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

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14
Q

What counts as a subclinical exertional myopathy

A

Where there is a more than 200-300% increase in CK levels after gentle exercise

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15
Q

How do we measure post-exercise muscle enzymes activity

A

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

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16
Q

What are we looking for in urinalysis in myopathy cases

A

Myoglobinuria; red/brown colour
Need lab analysis to differentiate it from haemaglobinuria

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17
Q

What must we remember with transporting vitamin E assays

A

Keep on ice in the dark

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18
Q

What may be used to differentiate orthopaedic from neuromuscular atrophy causes

A

Electromyography; have abnormal EMG in atrophy/weakness

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19
Q

What are type 1 fibre vs type 2 fibre muscle types

A

Postural muscles are mainly type 1 fibres
Locomotor muscles are mostly type 2 fibres

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20
Q

What are type 1 muscle fibres

A

Slow contracting fibres; associated with need for fatty acid oxidation for contraction

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21
Q

What are ddx for muscle disorders affecting postural muscles

A

Equine motor neurone disease
Nutritional myodegeneration

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22
Q

What are ddx for locomotor muscle disease

A

Recurrent exertional rhabdomyolysis
PSSM

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23
Q

What is sporadic exertional myopathy

A

Related to increase in work intensity without proper training + exhaustion/overheating
-> Therefore assocaited with racehorses/endurance in hot and humid climates

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24
Q

Signs of sporadic exertional myopathy and tests

A

Weakness, ataxia, tachypnoea, sweating, muscles may palpate normally
See myoglobinuria + increased CK

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25
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
26
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
27
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
28
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
29
Which breeds do we see polysaccharide storage myopathy in
Quarter horses Connemara Warmbloods (see PSSM2 esp in these breeds)
30
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
31
How can we diagnose PSSM
Biopsy of muscle; see polysacchardie accumulation in myofibril
32
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
33
What do we expect to happen to CK values after exercise in PSSM case
Increase at least 3X
34
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
35
Which horses do we seee equine myofibrillar myopathy
Arabs and warmbloods (some of these may actually be PSSM2 cases)
36
What do we see on a biopsy with equine myofibrillar myopathy
Disorganised myofibrilas and abnormal desmin accumularion
37
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
38
Which breeds do we see HYPP in
Quarterhorse, painthorse, appaloose
39
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
40
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
41
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
42
Which breeds do we get malignant hyperthermia in
Quarterhorses Painthorses
43
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
44
If we pre-screen a horse as having RYR1 gene mutation what might we bre-treat them with before GA
Dantrolene
45
What is white muscle disease
Nutritional myodegeneration; affects cardiac and skeletal muscles Usually foals/youngstock where dam has had selenium/vitE deficiency
46
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
47
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
48
Does cardioresp or skeletal white muscle disease give a better prognosis
Skeletal
49
Treatment of white muscle disease
 Selenium injections IM (NB = irritant so may dilute before injection)  Oral alpha-tocopherol (vit E) supplementation  Supportive nursing
50
What is alpha-tocopherol
Vit E
51
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
52
Why do we want to stay in isothenuric range in myopathy case
To avoid pigment nephropathy from myoglobin
53
Why do we need to be more careful with NSAID use in myopathies
Bceause kidneys already exposed to nephrotoxic myoglobin
54
What is atypical myopathy
Disease of muscle degeneration due to failure of energy production due to an acquired deficiency in acyl-coA dehydrogenase
55
What toxin can cause atypical myopathy
Hypoglycin A from sycamore seedlings --> COnverted to MPCA-CoA which causes irreversible inactivation of dehydrogenases
56
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
57
What muscles are affected by atypical myopathy
Type 1 muscle cells; postural muscles Cardiac muscle
58
Clinical signs of atypical myopathy
Weakness, stiffness, recumbency, trembling, sweating Pigmenturia Dysphagia Tachycardia tachypnoea/dyspnoea
59
What is the key way to differentiate atypical myopathy from colic
Pigmenturia present in atypical myopathy
60
WHat is it causing pigmenturia in atypical myopathy
Myoglobin
61
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
62
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
63
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
64
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
65
What metabolism process is compromised in atypical myopathy
Fatty acid beta-oxidation Hence why type 1 muscles affected more
66
Is CK relevant in prognosis for atypical myopathy
NO because not a linear relatioship with muscle damage
67
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

Equine (26 decks)

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