LA LMN, peripheral nerve, and neuromuscular diseases

Question 1

describe equine motor neuron disease

Answer 1

1. acquired neurodegenerative disease in horses; associated with vitamin E deficiency resulting in oxidative damage to motor neurons (spinal cord ventral horn) leading to neuron cell edeath and clinical signs
   -most commonly in NE US in winter (lack of fresh forage)

clinical signs:
1. typically slowly progressive
2. muscle weakness: short-strided gait but no ataxia
-stand with all four limbs together (like balancing on a ball; often look worse standing than walking)
-weight shifting, muscle fasciculations, excessive sweating, low head carriage, tail elevation, frequently lay down
3. muscle atrophy: generalized and symmetric
4. black dental tartar
5. retinal lipofuscin deposition
can have subclinical presentation!:
-subtle muscle weakness present as poor performance, toe dragging or stumbling, more prone to injury
-subtle muscle atrophy: lightly muscled topline, difficulty getting fit and staying fit

Question 2

describe equine motor neuron disease diagnostics (3)

Answer 2

1. muscle enzyme activity
   -increased in subacute cases
   -often normal in chronic cases
2. serum vitamin E: low in subacute/chronic cases
3. MUSCLE BIOPSY: sacrocaudalis dorsalis muscle
   -severe degeneration, muscle atrophy, and fibrotic contracture
   -90% sensitive and specific = best way to diagnose!

Question 3

describe management and prevention of equine motor neuron disease

Answer 3

management:
1. treat: vitamin E supplementation
-may halt progression, but rarely reverses signs except for possible early subclinical cases
-prognosis is guarded to poor

prevention: is best!
1. ensure quality forage in diet
2. supplement vitamin E if inside for a long time or soaking hay in metabolic issues
3. check serum vitamin E in stablemates where another horse diagnosed

Question 4

describe hypocalcemia clinical signs

Answer 4

1. clinical signs typically apparent when [tCa] < 6.5 mg/dL
2. increases neuromuscular excitability
   -hyperesthesia
   -muscle fasciculations
   -muscle cramping
   -stiff gait
   -synchronous diaphragmatic flutter (thumps) in time with heartbeat due to phrenic n. abnormality
   -decreased myocardium contractility
   -recumbency
   -respiratory muscle paralysis
   -eventually death

Question 5

what are 6 causes of hypocalcemia?

Answer 5

1. hypoalbuminemia: not usually on its own
2. decreased PTH activity
3. inadequate Ca absorption in intestine or mobilization from bone (lactation)
4. excess urinary Ca excretion
5. Ca binding with other anions
6. Ca deposition during fracture healing

Question 6

describe treatment of hypocalcemia

Answer 6

1. supplement with calcium
2. 23% calcium borogluconate typically diluted in fluids
   -can precipitate with other supplements/meds (esp bicarbonate)!!

Question 7

describe hypercalcemia

Answer 7

1. clinical signs typically apparent when [tCa] > 16 mg/dL
2. disruption of neuronal stability and decreased excitability
   -muscle weakness
   -cardiac dysrhythmias
   -abnormal mentation
   -soft tissue mineralization of chronic enough

Question 8

what are 5 causes of hypercalcemia?

Answer 8

1. increased Ca absorption in intestine or mobilization from bone
   -increased PTH or PTHrP activity
2. hypervitaminosis D
   -exogenous (rodenticide or toxic plants) or endogenous (neoplasia)
3. decreased urinary excretion of Ca (renal failure common cause, esp in horses)
4. increased protein bound Ca
5. iatrogenic infusion of Ca

Question 9

describe treatment of hypercalcemia

Answer 9

1. only when [Ca] > 15mg/dL and having dysrhythmias
2. non-calcium containing fluids to promote diuresis
3. calcium wasting diuretic (furosemide)
4. corticosteroids
5. calcitonin
6. low calcium feed
7. address underlying cause if possible; prognosis poor to guarded

Question 10

describe clinical signs and causes of hypokalemia

Answer 10

clinical signs: muscle weakness

causes:
1. metabolic alkalosis
2. inappatence/dietary deficiency
3. increased loss
4. iatrogenic:
-K wasting diuretics
-dextrose/insule
-bicarbonate

Question 11

describe treatment of hypokalemia

Answer 11

when [K] < 3mEq/L; inappetance greater than 3 days duration, or low/normal [K] with acidosis

1. supplement IV fluid therapy
   -MAX rate 0.5mEq/kg/hr
   -do NOT give faster than this rate- can lead to atrial standstill
   -typically aim for concentration of 20-40mEq/L
2. supplement orally: for non-emergent

Question 12

describe clinical signs of hyperkalemia

Answer 12

depend on severity and rate on onset; usually asymptomatic until [K] > 6.5

1. leads to decreased cell membrane excitability
   -skeletal muscle weakness- decreased excitability
   -cardiac muscle weakness- decreased excitability, increased refractory period, slowed conduction; dysrhythmias can be life threatening

Question 13

describe causes of hyperkalemia (7)

Answer 13

1. metabolic acidosis
2. intravascular hemolysis in animals with high [K] in RBCs (horses, pigs, most cattle and small ruminants)
3. massive tissue necrosis or myonecrosis
4. HYPP in horses
5. decreased renal excretion:
   -oliguric or anuric renal disease/failure
   -urethral obstruction
   -uroabdomen
6. increased intake
7. iatrogenic:
   -overdose
   -rapid K penicillin dosing

Question 14

describe treatment of hyperkalemia

Answer 14

1. indicated when [K] >6mEq/L, when there is dysrhythmia, or when animal collapses
2. use medications that drive potassium into cells
   -dextrose-containing IV fluids (or karo syrup orally)
   -insulin
   -bicarbonate-containing fluids
3. use non potassium containing fluids to dilute and promote diuresis: saline
4. supplement calcium gluconate for myocardial protective effects
5. address underlying cause if possible

Question 15

describe polyneuritis equie (2)

Answer 15

1. also called cauda equina syndrome; affects adult horses
2. potentially immune mediated granulomatous inflammation resulting in destruction of the roots of the cauda equina and sometimes cranial nerves

Question 16

describe classical presentation of polyneuritis equi

Answer 16

classical syndrome:
1. hyperesthesia progressing to anesthesia
2. loss of tail/anal tone
3. urinary +/- fecal incontinence/retention
4. +/-hindlimb weakness and muscle atrophy

alternate presentation:
1. mild lameness ad muscle atrophy
2. cranial nerve signs:
-masticatory muscle atrophy
-facial nerve paralysis

Question 17

describe polyneuritis equi diagnostics (4)

Answer 17

hard!!

1. muscle biopsy (+/- electromyography): neurogenic atrophy
2. CSF centesis:
   -increased protein +/- increased NCC
   -maybe increased P2 myelin
3. exclude other differentials
4. definitive diagnosis: postmortem histopath of cauda equina nerve roots

Question 18

describe treatment of polyneuritis equi (4)

Answer 18

1. corticosteroids, other immunosuppressive meds
2. manual rectal eval, possible help clear
3. other supportive care
4. unrewarding, prognosis guarded to poor

Question 19

describe botulism (3)

Answer 19

1. clostridium botulinum: gram positive, anaerobic, spore forming rod found in soil; all LA species susceptible
2. botulinum toxin: types A-F
   -type B is most common!
   -A or C occasionally
3. infection one of 3 ways:
   -ingestion of preformed toxin: forage poisoning, typically affects adults

-ingestion of spores, germination, toxin released and absorbed in GIT; toxicoinfectious, shaker syndrome, typically affects foals

-spores enter a wound, germination, toxin release and absorbed into vasculature; wound botulism; rare

Question 20

describe pathophysiology of botulism (2)

Answer 20

1. blocks Ach release at the NMJ
   -binds to receptor on motor endplate, endocytosis of toxin into endplate, blocks Ach release from vesicles
2. FLACCID paralysis!! IRREVERSIBLE once toxin taken into and blocks end plate, so animal must live long enough to regenerate new motor end plates to recover; take weeks

Question 21

describe clinical signs of botulism (7)

Answer 21

1. progressive flaccid paralysis
2. poor tongue tone/function: very slow consumption of food; dysphagia
3. poor tail tone, poor eyelid tone
4. low head carriage (spontaneous reflux due to poor esophageal sphincter tone)
5. weakness, muscle fasciculations
6. frequently lay down and progress to consistent recumbency
7. eventually respiratory paralysis and death

Question 22

describe diagnostics and treatment and prevention of botulism

Answer 22

diagnosis:
1. clinical signs
2. abnormal EMG (nonspecific)
3. blood work and CSF often normal
4. find toxin (serum, feed, feces)
5. exclude other differentials

treatment:
1. neutralize circulating toxin: mutivalent antitoxin or Type B ASAP!!!
2. antibiotics if toxicoinfectious wound or concerned about pneumonia
3. supportive care:
-fluids, nutrition, decrease activity/stress, manage recumbency, mechanical ventilation
4. prognosis guarded!! fair if standing, breathing, baby, and owners have money

prevention: vaccinate with type B toxoid in endemic areas!!

Question 23

describe tetanus (3)

Answer 23

1. clostridium tetani: gram positive, anaerobic, spore forming rod found in soil
2. produces tetanolysin toxin
3. all LA species susceptible

Question 24

describe pathophysiology of tetanus

Answer 24

1. spore germinate into vegetative form in the right environment: anaerobic, exudative, necrotic tissue (puncture wound)
2. produces toxins:
   -tetanolysin: promotes tissue necrosis and spread
   -tetanospasmin: diffuses into vasculature
   -travels to presynaptic motor end plate and internalized
   -transported to spinal cord ventral horn (CNS)
   -acts on interneurons (renshaw cells) to inhibit release of inhibitory neurotransmitters
   -loss of inhibition = SPASTIC PARALYSIS

Question 25

describe clinical signs of tetanus (3)

Answer 25

1. usually appear 2-4 weeks after bacterial inoculation
2. progressive spastic paresis and hypertonia
   -sawhorse stance, grimace, stiff gait
   -spasm of 3rd eyelid when stimulated or consistent prolapse of 3rd eyelid
   -difficulty prehending/chewing/swallowing food due to lockjaw
3. progresses to spastic paralysis, resulting in recumbency and eventually respiratory paralysis and death

Question 26

describe diagnosis and treatment of tetanus, give prognosis and prevention too

Answer 26

diagnosis:
1. clinical signs
2. culture of C. tetani from wound-uncommon
3. no characteristic test or findings at necropsy

treatment:
1. antitoxin to eliminate any unbound toxin
2. eliminate infection:
-drain/oxygenate wound
-antibiotics
3. muscle relaxants: not rly effective
4. supportive care: fluids, nutritional support, non-stimulating environment

prognosis:
1. guarded to poor
-fair if standing, breathing normally, and owners have money
-survival >7 days is a good prognostic indicator

prevention is key!!
-tetanus toxoid vaccine; cheap and effective

Question 27

describe stringhalt (3)

Answer 27

1. gait abnormality characterized by rapid, exaggerated flexion of hindlimbs
2. etiology:
   -plant toxin ingestion: most likely when plant is stressed by drought (false dandelions, dandelions, sweet peas, mallows)
   -idiopathic: possible trauma, possible dysfunction of golgi tendon organ (where muscle attaches to bone)
3. pathology: only reported with toxin ingestion
   -demyelination
   -loss of large myelinated fibers
   -schwann cell proliferation in muscle

Question 28

describe clinical signs of stringhalt (2)

Answer 28

1. bilateral or unilateral
2. rapid, exaggerate flexion of hindlimbs during stride; looks like kicking up at their abdomen while walking

Question 29

describe treatment of stringhalt

Answer 29

1. medical:
   -remove from source (pasture) if applicable
   -anti-inflam
   -anti-convulsants
   -muscle relaxants
   -botox injections
2. surgical:
   lateral digital extensor myotenectomy

Question 30

describe the etiology and clinical signs of individual peipheral neuropathies

Answer 30

etiology
1. trauma
2. pressure: during anesthesia, recumbency, parturition

clinical signs:
1. suprascapular nerve paresis/paralysis/Sweeney: decreased/inability to adduct the shoulder

2. radial nerve paresis/paralysis:
   -Common after external trauma or following anesthesia in lateral recumbency w/o proper cushioning
   -Unable to flex shoulder, extend limb, advance limb
3. obturator nerve paresis/paralysis:
   -Often post-parturition/dystocia&raquo_space; “calving paralysis”
   -Decreased/in-ability to adduct the hindlimbs
4. Femoral – post dystocia w/ hip lock most common; decreased/inability to flex hip and extend stifle
5. Sciatic – post dystocia also common; decreased/inability to extend hip, flex stifle, and extend lower limbs
6. Peroneal – following trauma or prolonged recovery; decreased/inability to extend fetlocks/lower limbs

Question 31

describe treatment of individual peripheral neuropathies

Answer 31

1. anti-inflammatories:
   -NSAIDs
   -corticosteroids
2. antioxidants: vitamin E
3. supportive/nursing care
4. bandages/splints/hobbles: for certain ones
5. rehab exercises