Musculoskeletal

Question 1

Which muscle fibres are initially recruited with slow exercise and how does the fibre type change as exercise speed or intensity increases?

Answer 1

During slow exercise Type 1 fibres and a small number of Type 2a fibres predominate. As the speed or duration increases more fibres will be recruited in the order of Type 1, Type 2a and Type 2x.

Question 2

What is percussion myotonia?

Answer 2

When a muscle holds its contraction for several seconds after percussion.

Question 3

Regardless of the cause of rhabdomyolysis the final pathway is cell death due to what?

Answer 3

Aberrant calcium cycling

Question 4

What are the general mechanisms by which aberrant calcium cycling/calcium accumulation occurs?

Answer 4

• Energy pathways that generate ATP for the Ca pump can be impaired
• Ca pump or channels aren’t functioning adequately
• Cell membranes becomes damaged.

Question 5

Histologically how can you differentiate neurogenic from myogenic muscle atrophy?

Answer 5

Neurogenic: involves Type 1 and Type 2 fubres, characterised by small, angular atrophied fibres.
Myogenic: fast twitch fibres predominantly, characterised by anguloid atrophy.

Question 6

List differentials for muscle fasciculations.

Answer 6

• Nerve root irritation
• Electrolyte abnormalities
• Weakness
• Fatigue
• Anxiety
• Cold
• Ion channel defects within the sarcolemma causing abnormal propagation of muscle cell depolarisation

Question 7

What is the normal time to peak concentration and half life of CK, AST and LDH in cases of muscle damage?

Answer 7

CK: Peaks within 4-6 hours, declines to normal within 48 hours unless elevation is above 100,000 iu/L in which case it may take relatively longer to return to normal. Indurance rides may cause increase between 1000-4000iu/L and prolonged recumbency without myopathy can result in increase to 3000iu/L.
AST: Peaks within 24 hours, not muscle specific, plasma half life is 7-10 days (some sources say 7-8) so can take weeks to return to normal.
LDH: Peaks within 24 hours and half life is intermediary between CK and AST - probably around 7 days. Not muscle specific.

Question 8

What is a reasonable exercise response test in a fit and an unfit horse to provoke subclinical exertional rhabdomyolysis?

Answer 8

Fit horse: walk for 3 mins then trot for 12 mins
Unfit horse: alternate between 2 mins walking, 2 mins trotting. Should see less than 3 fold increase (most healthy horses show no change at this level).

Question 9

Which electrolytes should be measured as part of examination for mod-severe rhabdomyolysis or disease with muscle fasciculations as a feature?

Answer 9

Na, K, Ca, Cl and P

Question 10

In cases of atypical myopathy/hypoglycin A toxicity, what is the expected urine pH?

Answer 10

Acidic.

Question 11

Specific muscle groups are indicated for biopsy as a diagnosis of certain diseases - which ones are these?

Answer 11

• EMND: Sacrocaudalis dorsalis medialis muscle
• Hypoglycin A: Diaphragm and deep postural muscles
• Recumbency from severe rhabdomyolysis: deep pelvic muscles such as iliopsoas
• Immune-mediated myositis (eg in QH): gluteal or lumbar biopsy or biopsy of an atrophied muscle.

Question 12

What are the normal and abnormal findings on EMG (specifically denervation, electrical conduction defects, and myopathic changes)?

Answer 12

Normal muscle: regular wave patterns suggesting adjacent motor units are being recruited.
Denervation: abnormal spontaneous electrical activity in the form of fibrillation potentials and positive sharp waves.
Electrical conduction defects: complex repetitive discharges or myotonic discharges
Myopathic changes: decreased duration and amplitude of motor unit action potentials.

Question 13

What are the typical histologic findings with repetitive overtraining?

Answer 13

Increased muscle fibre size variation and centrally displaced myonuclei in muscle biopsies.

Question 14

What are the recommended provisions of dietary electrolytes for horses exercising in hot humid conditions or sweating excessively?

Answer 14

30-50gNaCl/day
15-25g light salt containing KCl/day
Ca : P ratio of 2:1

Question 15

What treatments may be indicated for acute rhabdomyolysis?

Answer 15

• Rest (don’t transport for 24-48hrs) and increased susceptibility to re-injury for 2 weeks after an acute episode.
• IVFT and address electrolyte and acid base derangements (typically low Na, low Cl and high K and often alkalotic
• Anxiolytics such as ACP may help; also increases blood flow through vasodilation
• Analgesia with NSAIDs (caution if dehydrated due to risk of renal damage, particularly with concurrent pigmenturia), Dom/Torb may also be used as analgesics if required.
• IV or enteral DMSO may help as an antioxidant, anti-inflammatory and osmotic diuretic
• Methylprednisolone succinate once.
• Muscle relaxants such as methocarbamol may have variable results
• Dantrolene may decrease release of Ca from the SR which may help reduce further aggravation of muscle contraction and necrosis but is contraindicated in HYPP due to increases in K concentration

Question 16

List examples of chronic exertional myopathies

Answer 16

• RER
• Malignant hyperthermia
• PSSM (type 1 and type 2)
• Idiopathic exertional rhabdomyolysis
• Mitochondrial myopathy

Question 17

What is the classic signalment of horses with RER and during what kind of exercise are episodes most likely to occur?

Answer 17

• Typically nervous temperament, SB and TB over-represented, young females over-represented
• Often exercise is preceded by a day or two of rest
• Usually occurs when exercise is restricted/the horse is held back (rarely occurs in horses allowed to freely gallop, hence not associated with lactic acid)

Question 18

True or false: 2yo fillies have bigger fluctuations in their CK values than 3yos?

Answer 18

True

Question 19

True or false: Abnormal amylase resistant polysaccharide has not been identified in horses with RER but increased sub-sarcollemmal amylase sensitive glycogen has been?

Answer 19

True.

Question 20

What are the rest recommendations with horses with ER?

Answer 20

If sporadic ER, rest until CK normalises
With RER daily exercise should continue to prevent further episodes (only when CK <3000iu/L). If CK >3000iu/L then a brief period of rest may be indicated.

Question 21

What are the exercise recommendations to minimise the risk of further episodes of ER?

Answer 21

• Interval training and reduction of job miles to <15min/session will benefit SBs
• For ridden horses a relaxed warm up with intermittent long and low stretching and regular breaks to stretch.

Question 22

What are the nutritional recommendations for horses with RER?

Answer 22

• Less than 20% of the DE should be supplied by Non Struct Carbohydrates (low glycaemic diets help with a calmer demeanour and low pre-exercise HR)
• At least 20% of DE should be supplied by fat (high fat diet is less about changing the muscle metabolism and probably more about reducing anxiety and exciteability which are closely linked to RER).
• Low quality hay is less of an issue with TBs than QH due to less pronounced insulinaemic response to high NSC hay.
• As lactic acidosis is no longer thought to be associated with RER supplements that reduce lactic acidosis are not indicated.

Question 23

What additional therapeutics can be used to reduce the impact/severity of RER?

Answer 23

• ACP pre-exercise to reduce excitement
• Reserpine and fluphenazine have longer effects although fluphenazine has been associated with extra-pyramidal effects
• Dantrolene may reduce [Ca] and decrease signs of rhabdomyolysis (significantly lower CK 4 hrs post exercise in horses given dantrolene 1 hr before exercise)
• Phenytoin may help prevent rhabdomyolysis by its effects on ion channels (including Na and Ca channels). However can cause drowsiness and ataxia at high doses so therapeutic monitoring and maintenance of 8ug/mL in blood is advised. * is a monoaminoxidase activator so affects [plasma] other drugs.

Question 24

What is the affected gene and mode of inheritance of malignant hyperthermia and which breeds are affected?

Answer 24

• Exon 46 of the skeletal muscle ryanodine receptor 1 gene (RYR1)
• Autosomal dominant mutation
• QH and paints

Question 25

What does the RYR1 defect do in cases of malignant hyperthermia?

Answer 25

Lowers the activation and heightens the deactivation threshold of the ryanodine receptor which intermittently can result in a dramatic efflux of Ca from the sarcoplasmic reticulum, increasing cyotplasmic Ca and producting a contracture. Anaerobic glycogen metaboilsm is activated, lactate is produced and excessive heat is generated and massive muscle necrosis ensues.

Question 26

What are the common triggers for malignant hyperthermia and what concurrent defect may exacerbate the signs?

Answer 26

Rhabdomyolysis may be induced by exercise or anaesthesia (typically halothane anaesthesia). Exacerbated by a concurrent mutation of the GYS1 gene causing PSSM1.

Question 27

What are the clinical signs and cause of death in horses with malignant hyperthermia?

Answer 27

• Hyperthermia (if develops during anaesthesia discontinue immediately and begin active cooling)
• Hypercapnoea
• Acidosis (treat with NaHCO3 if develops)
• Haemoconcentration, increase Ca, P, glucose and creatinine
• Death from cardiopulmonary arrest

Question 28

True or false: muscle biopsy is often not that useful in diagnosis of malignant hyperthermia

Answer 28

True.

Question 29

What treatments may be useful in malignant hyperthermia, particularly if anaesthesia is necessary?

Answer 29

Dantrolene 30-60 minutes before anaesthesia (unless they concurrently have HYPP in which the increased K with dantrolene makes in contraindicated).

Question 30

What is the GYS1 gene associated with, how is it inherited and which condition is this a feature of?

Answer 30

Associated with increased amylase-resistant polysaccharide in skeletal muscle. It is an autosomal dominant misense mutation resulting in higher than normal activity of glucogen synthase both t basal states and when activated by glucose-6-phosphate. The GYS1 gene has been associated with PSSM1

Question 31

In which breeds is PSSM1 common?

Answer 31

• European drafts but less commonly Shires or
  Clydesdales
• Irish Draught, Cob and Conemarra
• QH, particularly halter horses (Type 1 accounts for 72% of QH with PSSM)
• WB (Type 1 accounts for 18%)
  Low prevalence in light breeds

Question 32

True or false: No temperament, body type or gender predilection exists for PSSM1?

Answer 32

True

Question 33

True or false: Signs of PSSM1 most commonly occur after strenuous exercise, particularly if exercise occurs every day.

Answer 33

False.
Most common at walk and trot, particularly after several days of rest.

Question 34

What are the distinctive features of PSSM1 on histology?

Answer 34

Numerous subsarcolemmal vacuoles and dense crystalline period acid-schiff (PAS) positive and amylase resistant inclusion in fast twitch fibres.

Question 35

What is the typical signalment and presenting clinical signs in horses with PSSM1?

Answer 35

• Age of onset is 1-14 yrs, average 5yrs.
• Tucked up, fasciculations on the flank, muscle stiffness, sweating, reluctance to move forward and overt firm muscle contractures
• Hindlimbs more often affected .
• Chronic signs include lack of energy under saddle, reluctance to move forward, stopping and stretching as if to urinate, sour attitude to exercise
• Chronic back pain, reluctance to round over fences and fasciculations or pain on palpation of the lumbar muscles.
• Progressive weakness and muscle loss resulting in difficulty rising may be seen in draft breeds.

Question 36

What are the defining histological features of PSSM2?

Answer 36

Not just defined by presence of amylase resistant polysaccharide but also abnormal appearance of amylase-sensitive glycogen. Muscle glycogen concentrations aren’t typically as high as those with PSSM1. Centrally located nuclei, subsarcolemmal vacuoles, muscle necrosis, macrophage infiltration of myofibres, regenerative fibres and anguloid myofibre atrophy may all be seen with PSSM2.

Question 37

True or false: Highly trained horses have increased glycogen storage as a normal response to training.

Answer 37

True

Question 38

What are the important management factors for cases of PSSM?

Answer 38

• Provide a low NSC diet, increasing fat in the diet (unless overweight, in which case fast 6 hrs before to increase blood [FFA]) to increase the amount of nonesterfied fatty acid available for muscle metabolism,
• Provide adequate time to adjust to the dietary modifications before resuming exercise
• Duration rather than intensity of exercise is often more important
• Exercise programme must be gradually increased and consistently performed
• Minimise days without worth or some form of exercise
• If an episode occurs, don’t box rest more than 48 hours, small paddock turnout (2wks) is best so they can moderate their own exercise but continue to move.

Question 39

Why is it important to reduce an insulinaemic response in horses with PSSM?

Answer 39

Insulin stimulates the already overactive glycogen synthase.

Question 40

What are the histologic features of myofibrillar myopathy and what distinguishes this condition from PPSM2.

Answer 40

• Increased aggregates of cytoplasmic glycogen
• Amylase-resistant polysaccharide in a few fibres
• Centrally located myonuclei in mature myofibres
• Distinguished from PSSM2 by presence of disrupted myofibrillar alignment and largem desmin and alpha-beta crystallin positive cytoplasmic aggregates in those with recent ER.

Question 41

In which breeds has myofibrillar myopathy been reported?

Answer 41

Arabians and Warmbloods - in WBs desmin positive aggregates were found in myofibres indicating a potentially heritable form (found in multiple affected generations). Muscle tissue is characterised by ectopic accumulation of desmin and Z disc and myofibrillar degeneration.

Question 42

Mitochondrial myopathy characterised by a deficiency of respiratory chain function was identified in a 3yo Arabian filly with profound exercise intolerance and normal CK post exercise. The condition was progressive. What was the defect identified in this condition?

Answer 42

Deficiency in complex 1 (nicotinamide adenine dinucleotide : ubiquinone reductase)

Question 43

What is the specific defect in glycogen branching enzyme deficiency?

Answer 43

Premature stop codon in exon 1 of the glycogen branching enzymes I gene (GBE1)

Question 44

List the clinical signs of glycogen branching enzyme deficiency and the histologic features

Answer 44

• Abortion in 2nd or 3rd trimester or stillbirth (3% of abortions in QH and related breeds are thought to be due to this condition)
• Hyperthermia at birth
• Mild flexural limb deformities
• Intermittent seizures
• Skeletal and respiratory muscle weakness
• Sudden death
  Histo: Muscle, heart and liver typically show absence of PAS staining for glycogen as well as PAS positive globular or crystalline intracellular inclusions. All affected foals die.

Question 45

Nutritional myodegeneration (white muscle disease) is an acute degenerative disease affecting cardiac and skeletal muscle of young foals that are rapidly growing and born to dams that consumed vitamin E and/or Se diets during gestation - Se and Vit E appear synergistic in preventing NMD but which one is thought to be most important in the disease pathogenesis?

Answer 45

Se is thought to be most important as Se deficiency seems to contribute more to oxidant damage of muscle cell membranes.

Question 46

What are the roles of vitamin E and selenium with respect to cellular function

Answer 46

Se: key component of glutathione peroxidase that acts to destroy hydrogen peroxide and lipoperoxides that are generated during normal muscle metabolism.
Vit E: acts within cell membranes as an antioxidant that scavenges free radicals that otherwise might react with unsaturated fatty acids to form lipid hydroperoxides.

Question 47

What are the typical clinical signs of foals with NMD and how does the prognosis vary with each?

Answer 47

• Cadiorespiratory syndrome characterised by dyspnoea, rapid irregular heartbeat, weakness, recumbency and death. Prognosis is poor.
• Skeletal muscle syndrome with weakness, trembling, stiffness and inability to stand for more than short periods. Tends to be more amenable to treatment.
• Dysphagia due to necrosis of the tongue, often with secondary aspiration pneumonia, may be the only sign.
  Muscles typically affected: Tongue, gastrocnemius, semitendinosus, semimembranosis, biceps femoris, lumbar, gluteal and neck musculature.

Question 48

What are the characteristic gross necropsy and histologic findings with NMD?

Answer 48

• Grossly muscles appear dry, pale and streaked
• Histologically you may see calcification and oedema in bilaterally symmetrical muscle groups, hypercontracted and fragmented fibres

Question 49

Vitamin E deficient myopathy is similar to equine motor neuron disease and may be a predecessor. What are the distinguishing features between these conditions?

Answer 49

• Vit E deficient myopathy lacks the hallmark neurogenic atrophy in the sacrocaudalis dorsalis medialis muscle that is seen with EMND, and instead shows myogenic features.
• Vit E deficient myopathy shows characteristic alterations in mitochondrial distribution that appears to be a reversible manifestation of skeletal muscle mitochondrial oxidative stress
• Vit E deficient myopathy is generally responsive to treatment with Vit E.

Question 50

What are the characteristic features of a biopsy from a horse with vitamin E deficient myopathy?

Answer 50

“Moth-eaten” staining pattern in mitochondrial stains while other muscles are normal.

Question 51

Although commonly asymptomatic, what are the clinical signs of sarcocystosis in true pathologic cases?

Answer 51

Fever, malaise, chronic muscle atrophy, stiffness and weakness, sometimes with fasciculations may be noted. Normochronic normocytic anaemia and increased CK and AST may also occur.

Question 52

What is the pathogenesis and most common isolated associated with Clostridial myositis?

Answer 52

Several Clostridia can cause it but most commonly C. perfringens.
Dormant spores of Clostridia are present in the liver and muscle (original access via GIT). IM injection of irritating drugs such as NSAIDs, prostaglandins, anthelmintics and antihistamines are often implicated as the inciting cause for onset of myonecrosis.
When local tissue is devitalised (eg after injection of irritant) and the appropriate anaerobic condition is created, spores may vegetate and begin exponential growth, releasing powerful exotoxins that act locally and systemically to create widespread organ dysfunction. Signs present within 48 hours and usually include depression, fever, toxaemia and tachypnoea. Can develop crepitus due to migration along fascial planes and can lead to MOD/DIC and death

Question 53

With clostridial myositis associated with C. perfringens, what are the common toxins, and which clostridial types have the highest mortality?

Answer 53

C. perfringens mostly alpha toxin which is a dermonecrotic toxin with phospholipase and sphingomyelinase activity. Although theta, kappa and mu toxins may also play a role.
C. septicum, C chauvoei and C. sporogenes have high fatality rates.

Question 54

What are the two proposed mechanisms for the development of Strangles-associated myopathy?

Answer 54

1. A toxic-shock-like reaction from profound non-specific T-cell stimulation by streptococcal superantigens with the release of high levels of inflammatory cytokines.
2. Bacteraemia with local multiplication and production of exotoxins or proteases within skeletal muscle.

Question 55

what are the virulence factors associated with S. equi that account for muscle necrosis?

Answer 55

• Proteases
• An unidentified cytotoxic protein
• Streptokinase
• Streptolysin

Question 56

What are the clinical signs and clinical progression of S. equi myositis?

Answer 56

Often have enlarged submandibular lymph nodes or guttural pouch empyema and develop a stiff gait that progresses to markedly firm, swollen, painful epaxial and gluteal muscles. The majority of cases become recumbent, are unable to rise and develop unrelenting pain necessitating euthanasia.

Question 57

What is the pathogenesis and commonly associated pathogens with infarctive purpura haemorrhagica?

Answer 57

• Immune complexes in the sera of horses with infarctive purpura haemorrhagica appear to be composed of IgM, IgA and Streptococcal M protein.
• Complement is deposited near the immune complexes in vessel walls and may result in cell membrane destruction, cell death and vascular occlusion. Often occurs in muscles that are compressed during recumbency and progresses to involve many organs, including the GIT and MM.
• Often a history of exposure to S. equi within 3 weeks previous, vaccination for S. equi, or a concurrent Salmonella infartum infection.

Question 58

What are the clinical signs and disease progression with infactive purpura haemorrhagica?

Answer 58

• Focal firm muscle swellings in the abdominal, pectoral, adductor and tarsocrural muscles.
• Reduced GIT borborygmi and haemorrhagic gastric reflux
• Neutrophilia with left shift and toxic changes, hypoproteinaemia, hypoalbuminaemia, and marked increase in CK and AST.
• Serum titres for M protein are usually markedly elevated.
• Petechae, oral infarctions resembling ulcers, well demarcated moderate limb oedema.
• Biopsies show diffuse acute coagulative necrosis with infarction of skeletal muscle, skin, GIT, pancreas and lungs often with S. equi equi abscessation of lymph nodes.

Question 59

What are the clinical findings and proposed mechanisms behind immune mediated myositis in QH and related breeds?

Answer 59

• Malaise, rapid onset atrophy particularly affecting epaxial and gluteal muscles and a high serum CK and AST.
• Muscle atrophy is rapid and may progress to include 40% of the horse’s muscle mass within a week.
• Lymphocytic destruction of myofibres by CD4 and to a lesser extent CD8 cells.
• Due to loss of self-tolerance of antigens expressed on muscle cells that occurs for unknown reasons after rhabdomyolysis, infection with S. equi or vaccination.
• May be due to activation of otherwise inactive autoreactive T cells by either: 1 shared epitopes with an infectious agent causing antigenic mimicry; 2 microbial superantigens; 3 high concentraiton of local cytokines, 4 expression of an abnormal protein on sarcolemmal membranes.

Question 60

What are the histologic features of IMM in QH related breeds? And what is the mainstay of treatment?

Answer 60

Infiltration of myofibres with lymphocytes, lymphocytic vasculitis, anguloid atrophy of the myofibre, fibre necrosis and multinucleated giant cells. Semi-mem/semi-ten may be useful but epaxial and gluteals are best.
Tx is steroids (anti-inflammatory rather than immune suppressive is probably sufficient)

Question 61

What are the presenting signs and signalment of affected horses with systemic calcinosis?

Answer 61

• Mild fever, malaise, stiffness and loss of muscle mass mostly over the lumbar/gluteal area - presents the same as generallised IMM but progresses to weakness, inability to remain standing, respiratory distress, laminitis or GIT inflammation and diverse organ failure and death.
• QH and QH related breeds and all <9yrs.

Question 62

What are the proposed mechanisms behind development of systemic calcinosis?

Answer 62

A Ca x P product >66 has been present in all cases - hyperphosphataemia can induce dystrophic calcification through several mechanisms:

1. Passive calcium phosphate deposition from phosphate supersaturation in the blood.
2. An active process promoting conversion of smooth muscle cells to osteogenic cell types.
3. Directly increasing parathyroid hormone secretion and transcription
4. Interference with renal production of 1,25-(OH)2D levels.

Question 63

What are the histologic features of systemic calcinosis and treatment options?

Answer 63

Resembles IMM however multinucleated giant cells are consistently present and dystrophic calcification of muscle fibres is also evident.
Tx should be directed at the underlying inflammatory cause. In humans steroids are thought to trigger this condition but in horses they are often used since it so closely resembles IMM.

Question 64

What is the pathogenesis of atypical myopathy?

Answer 64

Hypoglycin A is metabolised in the liver to methylenecyclopropylacetic acid (MCPA) and MCPA CoA irreversibly binds to multiple acyl CoA dehydrogenases which are enzymes that are essential for metabolism of short and medium chain fatty acids and branched chain amino acids. Accumulation of fat esters damages muscle cell membranes, and an energy deficiency arises from inability to metabolise fat.

Question 65

What are the clinical signs of atypical myopathy and recommended treatment options?

Answer 65

Clinical signs develop within 3-5 days of exposure

• Muscular weakness, sweating, fasciculations, stiffness, tachycardia, tachypnoea, recumbency and myoglobinuria.
• A rapid rise in RR is usually followed by collapse and death from cardiorespiratory failure
• An acidic urine should make you suspicious but definitive diagnosis requires identification of serum acylcarnitines and urine organic acids and glycine conjugates typical of deficiency of multiple acyl Co-A dehydrogenases or isolation of MCPA or hypoglycin A in blood or urine.
• Aggressive IVFT, anti-inflammatories, DMSO, vit E, vit C, NSAIDs.

Question 66

Which muscles are typically affected with atypical myopathy?

Answer 66

Deep postural and respiratory musculature and the myocardium.

Question 67

MAP below what level increases the risk for post anaesthetic myopathy?

Answer 67

70mmHg.

Question 68

Which muscles are most susceptible to focal post anaesthetic myopathy?

Answer 68

Muscles with dense fascia. These include triceps, deltoid, masseter, hindlimb extensors or if in dorsal, the hindlimb adductor and gluteal muscles.

Question 69

What treatments may be indicated with focal post anaesthetic myopathy and what preventatives are possible?

Answer 69

IVFT, NSAIDs, DMSO?. dantrolene 2-4mg/kg may be useful.
Dantrolene pre-op may reduce the risk although reduced cardiac output is associated with higher doses, as well as maintaining blood pressure >MAP80-85mmHg.

Question 70

What are the clinical findings with generalised post-anaesthetic myopathy?

Answer 70

Systemic hypotension and hypoxaemia creates local ischaemic lesions with pathologic changes becoming generalised. Horses are often unable to rise and may struggle hence exacerbating trauma.

Question 71

What risk factors increase the chances of generalised post-anaesthetic myopathy?

Answer 71

An underlying myopathy
HYPP (need to pre-med with acetazolamide or low doses of dantrolene (above 6mg/kg it causes increase [K] which is detrimental in these cases and also reduces CO)

Question 72

What is myotonia and what are the causes of it?

Answer 72

Delayed relaxation of muscle after mechanical stimulation or voluntary contraction caused by abnormal membrane exciteability.

• Congenital: defects in skeletal muscle Cl channels (myotonia congenita) or Na channels (HYPP)
• Acquired: spinous ear ticks (Otobius megnini)

Question 73

What are the typical findings with myotonia congenita?

Answer 73

Well muscled with mild-mod pelvic limb stiffness, most pronounced when exercise begins and diminishing with continuing exercise. Usually noted in first yr of life. Bilateral dimpling of thigh and rump muscles may be obvious and percussion dimpling occurs with tactile sitmulation (for up to 1min or more). Progression beyond 6-12mo doesn’t typically occur.

Question 74

What are the typical findings with myotonia dystrophica?

Answer 74

Also well muscled foals with stiff hindlimb gain but weanlings have more progressive multifocal muscle atrophy, hypertrophy and persistent stiffness that worsens with exercise. Retinal dysplasia, lenticular opacities and gonadol hypoplasia have been documented. Definitive diagnosis requires EMG (pathognomonic high frequency repetitive discharges that wax and wane creating dive bombers due to repetitive firing of affected muscles.

Question 75

What are the histologic features of myotonia congenita and myotonia dystrophica?

Answer 75

May be normal or may show variable fibre diameter up to 3x normal. Type 1 fibre hypertrophy or hypotrophy is reported. Pathology is more dramatic with myotonia dystrophica with ringed fibres centrally displaced myonuclei, sarcoplasmic masses and an increased endomysial or perimysial connective tissue. Fibre type grouping and atrophy of both Type 1 and Type 2 fibres are present.

Question 76

What is the pathogenesis of HYPP?

Answer 76

An autosomal codominant myotonia of QH and related breeds from the stallion ‘Impressive’. Due to a mutation in the gene encoding voltage dependent skeletal muscle Na channels (F1416L mutation in SCN4A gene encoding the alpha subunit of the Na channel). The result is these horses have resting sarcolemmal membrane potentials that are closer to firing. When the muscle cell begins to depolarise, a subpopulation of Na channels fail to inactivate, producing an excessive inward flux of Na and outward flux of K, resulting in persistent depolarisation of muscle cells, general muscle fasciculations and weakness.

Question 77

What are the clinical signs of HYPP?

Answer 77

Often big muscled horses.
Clinical signs develop by 2-3yo. May show muscle fasciculations and weakness. Episodes often begin with a brief period of facial myotonia and potentially prolapse of the 3rd eyelid. Sweating and fasciculations progress over the flanks, neck and shoulders. Movement may exacerbate. In mild attacks horses remain standing but with severe attacks this may evolve to severe weakness, swaying, staggering, dog sitting and recumbency. In severe case paralysis of URT muscles may necessitate a tracheotomy. Differentiated from a seizure as horses remain conscious and alert despite recumbency. Episodes last 15-60 min after which time the horse stands and appears normal.

Question 78

What could be presenting clinical signs in a foal with HYPP?

Answer 78

Dysphagia, stridor and periodic URT obstruction.

Question 79

What are the dietary factors and general triggers that can precipitate HYPP? And what dietary management is advised.

Answer 79

Diets high in K (lucerne, molasses, kelp-based supplements) should be avoided
Triggers can include dietary changes, fasting, GA, heavy sedation, transport, stress, cold, pregnancy and concurrent disease. Not usually exercise.
Dietary management: Balanced diet of 0.6-1.1% total K by weight and less than 33g K/meal. Forage analysis is advised. Pasture is good due to high water content making excessive K consumption unlikely. Oats, corn, wheat, barley and beet pulp should be fed in small meals several times/day. Soybean meal, sugar molasses or beet molasses are high in K so should be avoided.

Question 80

What clinicopathologic changes may be seen with HYPP?

Answer 80

Hyperkalaemia (6-9mEq/L)
Haemoconcentration
Hyponatraemia (mild)
Normal acid base.

Question 81

In a horse with HYPP, if an episode is thought to be just begining, what treatment/management could be implemented to prevent worsening?

Answer 81

Provision of corn syrup
Mild exercise
Adrenaline (3mL of 1:1000/500kg)
Acetazolamide (3mg/kg PO) - encourages renal K excretion and stimulates insulin secretion
or Ca gluconate (0.2-0.4mL/kg of a 23% solution)
An increase in extracellular Ca raises the muscle membrane threshold potential, which decreases membrane hyperexciteability. Can also give IV dextrose or NaHCO3 to encourage intracellular K movement.

Question 82

What are the clinical signs and pathogenesis of hypocalcaemic tetany?

Answer 82

Usually due to lactation, parturition, endurance rides or transport.

• Stiff stilted gait
• Muscle fasciculations (masseter, temporal muscle, triceps)
• Trismus
• Dysphagia
• Synchronous diaphragmatic flutter
• Convulsions, coma and death in severe cases.

Question 83

What are the Ca concentrations with which clinical signs are associated?

Answer 83

Below normal but >8mg/dL (2mmol/L) - exciteability
5-8mg/dL(1.25-2mmol/L) - tetanic spasms and incoordination
<5mg/dL (<1.25mmol/L) - recumbency, stupor.
Often also see metabolic alkalosis, hypo or hypermagnesaemia and hyper or hypophosphataemia.

Question 84

What is the treatment of hypocalcaemia?

Answer 84

IV 20% calcium borogluconate - dilute 1:4 in saline and administer at a rate of 250-500mL/500kg (pre-dilution). Dilution reduces the risk of cardiotoxicity. You will normally see an ionotropic effect but alteration in rate and rhythm warrant suspending administration. If no response to the first dose, a second dose 15-30 minutes later can be given.

Question 85

What is the pathogenesis of synchronous diaphragmatic flutter?

Answer 85

Due to fluid and electrolyte imbalances disrupting the membrane potential of the phrenic nerve. It then begins to discharge in concert with atrial depolarisations with subsequent contraction of the diaphragm.
Clinicopathologically you see low serum ionised calcium and hypochloraemic metabolic alkalosis which may alter the ratio of free to bound Ca (increases protein binding). Hypocalcaemia may be due to lactation, transport, endurance, primary hypoparathyroidism, digestive disturbances, furosemide and ingestion of blister beetles.

Question 86

What are the clinical signs of synchronous diaphragmatic flutter?

Answer 86

In addition to “thumps”, you may see inappropriate sweating, inappetence, fever or hyperthermia, depression and aperistalsis.

Question 87

What is the treatment of synchronous diaphragmatic flutter and how can it be prevented?

Answer 87

Supplement with Ca and Mg, as for Tx of hypocalcaemia.
Prevention: Provision of Cl, K and Na during prolonged exercise may help prevent metabolic alkalosis, and supplementing Ca and Mg in those prone to SDF may be helpful. Decreasing dieetary Ca a few days before endurance work helps to stimulate endocrine homeostatic mechanisms and increase osteoclastic activity. Calcium losses in sweat are therefore overcome by release of Ca from bone stores. Horses fed lucerne may be at increased risk due to the high Ca content.

Question 88

non exertional rhabdomyolisis

Answer 88

• Metabolic myopathy
  
  • a. Glycogen branching enzyme deficiency in Quarter Horses
  • b. Type 1 and type 2 polysaccharide storage myopathy
  • c. Malignant hyperthermia
• 2. Inflammatory myopathies
     * a. Immune mediated •
• Infarctive hemorrhagic purpura
• Immune-mediated myopathy
• 3. Infectious
     * a. Clostridial myositis
     * b. S.equi myositis
     * c. Anaplasma myositis
     * d. Viral myositis
     * e. Sarcocystis myositis
• 4. Nutritional myopathy
     * a. Vitamin E and selenium deficiency
• 5. Toxic myopathy
     * a. Ionophore toxicity
     * b. Pasture myopathies
     
     • Hypoglycin A myopathy
     • Rayless goldenrod/white snakeroot
     • Cassia occidentalis
• 6. Traumatic myopathy
     * a. Compressive anesthetic myopathy
     * b. Trauma