LA LMN, peripheral nerve, and neuromuscular diseases Flashcards
describe equine motor neuron disease
- 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
describe equine motor neuron disease diagnostics (3)
- muscle enzyme activity
-increased in subacute cases
-often normal in chronic cases - serum vitamin E: low in subacute/chronic cases
- MUSCLE BIOPSY: sacrocaudalis dorsalis muscle
-severe degeneration, muscle atrophy, and fibrotic contracture
-90% sensitive and specific = best way to diagnose!
describe management and prevention of equine motor neuron disease
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
describe hypocalcemia clinical signs
- clinical signs typically apparent when [tCa] < 6.5 mg/dL
- 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
what are 6 causes of hypocalcemia?
- hypoalbuminemia: not usually on its own
- decreased PTH activity
- inadequate Ca absorption in intestine or mobilization from bone (lactation)
- excess urinary Ca excretion
- Ca binding with other anions
- Ca deposition during fracture healing
describe treatment of hypocalcemia
- supplement with calcium
- 23% calcium borogluconate typically diluted in fluids
-can precipitate with other supplements/meds (esp bicarbonate)!!
describe hypercalcemia
- clinical signs typically apparent when [tCa] > 16 mg/dL
- disruption of neuronal stability and decreased excitability
-muscle weakness
-cardiac dysrhythmias
-abnormal mentation
-soft tissue mineralization of chronic enough
what are 5 causes of hypercalcemia?
- increased Ca absorption in intestine or mobilization from bone
-increased PTH or PTHrP activity - hypervitaminosis D
-exogenous (rodenticide or toxic plants) or endogenous (neoplasia) - decreased urinary excretion of Ca (renal failure common cause, esp in horses)
- increased protein bound Ca
- iatrogenic infusion of Ca
describe treatment of hypercalcemia
- only when [Ca] > 15mg/dL and having dysrhythmias
- non-calcium containing fluids to promote diuresis
- calcium wasting diuretic (furosemide)
- corticosteroids
- calcitonin
- low calcium feed
- address underlying cause if possible; prognosis poor to guarded
describe clinical signs and causes of hypokalemia
clinical signs: muscle weakness
causes:
1. metabolic alkalosis
2. inappatence/dietary deficiency
3. increased loss
4. iatrogenic:
-K wasting diuretics
-dextrose/insule
-bicarbonate
describe treatment of hypokalemia
when [K] < 3mEq/L; inappetance greater than 3 days duration, or low/normal [K] with acidosis
- 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 - supplement orally: for non-emergent
describe clinical signs of hyperkalemia
depend on severity and rate on onset; usually asymptomatic until [K] > 6.5
- 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
describe causes of hyperkalemia (7)
- metabolic acidosis
- intravascular hemolysis in animals with high [K] in RBCs (horses, pigs, most cattle and small ruminants)
- massive tissue necrosis or myonecrosis
- HYPP in horses
- decreased renal excretion:
-oliguric or anuric renal disease/failure
-urethral obstruction
-uroabdomen - increased intake
- iatrogenic:
-overdose
-rapid K penicillin dosing
describe treatment of hyperkalemia
- indicated when [K] >6mEq/L, when there is dysrhythmia, or when animal collapses
- use medications that drive potassium into cells
-dextrose-containing IV fluids (or karo syrup orally)
-insulin
-bicarbonate-containing fluids - use non potassium containing fluids to dilute and promote diuresis: saline
- supplement calcium gluconate for myocardial protective effects
- address underlying cause if possible
describe polyneuritis equie (2)
- also called cauda equina syndrome; affects adult horses
- potentially immune mediated granulomatous inflammation resulting in destruction of the roots of the cauda equina and sometimes cranial nerves
describe classical presentation of polyneuritis equi
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
describe polyneuritis equi diagnostics (4)
hard!!
- muscle biopsy (+/- electromyography): neurogenic atrophy
- CSF centesis:
-increased protein +/- increased NCC
-maybe increased P2 myelin - exclude other differentials
- definitive diagnosis: postmortem histopath of cauda equina nerve roots
describe treatment of polyneuritis equi (4)
- corticosteroids, other immunosuppressive meds
- manual rectal eval, possible help clear
- other supportive care
- unrewarding, prognosis guarded to poor
describe botulism (3)
- clostridium botulinum: gram positive, anaerobic, spore forming rod found in soil; all LA species susceptible
- botulinum toxin: types A-F
-type B is most common!
-A or C occasionally - 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
describe pathophysiology of botulism (2)
- blocks Ach release at the NMJ
-binds to receptor on motor endplate, endocytosis of toxin into endplate, blocks Ach release from vesicles - 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
describe clinical signs of botulism (7)
- progressive flaccid paralysis
- poor tongue tone/function: very slow consumption of food; dysphagia
- poor tail tone, poor eyelid tone
- low head carriage (spontaneous reflux due to poor esophageal sphincter tone)
- weakness, muscle fasciculations
- frequently lay down and progress to consistent recumbency
- eventually respiratory paralysis and death
describe diagnostics and treatment and prevention of botulism
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!!
describe tetanus (3)
- clostridium tetani: gram positive, anaerobic, spore forming rod found in soil
- produces tetanolysin toxin
- all LA species susceptible
describe pathophysiology of tetanus
- spore germinate into vegetative form in the right environment: anaerobic, exudative, necrotic tissue (puncture wound)
- 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
describe clinical signs of tetanus (3)
- usually appear 2-4 weeks after bacterial inoculation
- 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 - progresses to spastic paralysis, resulting in recumbency and eventually respiratory paralysis and death
describe diagnosis and treatment of tetanus, give prognosis and prevention too
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
describe stringhalt (3)
- gait abnormality characterized by rapid, exaggerated flexion of hindlimbs
- 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) - pathology: only reported with toxin ingestion
-demyelination
-loss of large myelinated fibers
-schwann cell proliferation in muscle
describe clinical signs of stringhalt (2)
- bilateral or unilateral
- rapid, exaggerate flexion of hindlimbs during stride; looks like kicking up at their abdomen while walking
describe treatment of stringhalt
- medical:
-remove from source (pasture) if applicable
-anti-inflam
-anti-convulsants
-muscle relaxants
-botox injections - surgical:
lateral digital extensor myotenectomy
describe the etiology and clinical signs of individual peipheral neuropathies
etiology
1. trauma
2. pressure: during anesthesia, recumbency, parturition
clinical signs:
1. suprascapular nerve paresis/paralysis/Sweeney: decreased/inability to adduct the shoulder
- 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 - obturator nerve paresis/paralysis:
-Often post-parturition/dystocia»_space; “calving paralysis”
-Decreased/in-ability to adduct the hindlimbs - Femoral – post dystocia w/ hip lock most common; decreased/inability to flex hip and extend stifle
- Sciatic – post dystocia also common; decreased/inability to extend hip, flex stifle, and extend lower limbs
- Peroneal – following trauma or prolonged recovery; decreased/inability to extend fetlocks/lower limbs
describe treatment of individual peripheral neuropathies
- anti-inflammatories:
-NSAIDs
-corticosteroids - antioxidants: vitamin E
- supportive/nursing care
- bandages/splints/hobbles: for certain ones
- rehab exercises
