Neuromuscular disease - equines

Question 1

Where do the UMN run?

Answer 1

run in the ventral funiculus of white matter of spinal cord

Question 2

Where do the LMN run?

Answer 2

synapse with the UMN in the ventral portion of the grey matter of the spinal cord

Question 3

CS - UMN weakness

Answer 3

inability to control mm, normal or increased tone, no mm atrophy

Question 4

CS - LMN weakness

Answer 4

inability to contract the mm, flaccidity, mm atrophy if chronic

Question 5

Ddx – acute onset generalised, symmetrical neuromuscular defect (junction or nerve) or primary myopathy

Answer 5

• Atypical myopathy
• Exertional rhabdomyolysis – do UA (myoglobinuria), bloods (mm enzymes – CK and AST high). Both these tests could be used for atypical myopathy and exertional rhabdomyolysis.
• Botulism ( commoner in USA, diagnosis based on CS)
• Equine motor neurone disease (=ALS)
• (MG) – never confirmed in horses
• Toxicity? Digitalis (foxgloves) –> cardiac and skeletal mm effects.

Question 6

Botulism -methods of disease acquisition

Answer 6

• FORAGE POISONING (often silage, ingestion of preformed toxin)
• TOXICOINFECTIOUS (foals): Foal: Bacteria proliferates in GIT and produces toxin here, foals better able to absorb toxin/ haven’t developed antitoxin Ab 
• WOUND (very rare) – invades and multiplies in wound

Question 7

Toxins involved in botulism pathology

Answer 7

• Toxin types B and C usually.

Question 8

Tx - botulism

Answer 8

• mostly supportive
• Nursing care
• Botulism antitoxin?
• ABs? (especially recumbent horses  risk of pneumonia because of poor drainage)
• Fluids
• NG feeding
• Ventilation?

Question 9

Prognosis - botulism

Answer 9

Mortality high in recumbent horses

Question 10

Aetiology - grass sickness

Answer 10

• Aetiology unclear (Botulism type C toxin recently incriminated, not proven)

Question 11

What does grass sickness cause pathophysiologically?

Answer 11

• Enteric or more generalised dysautonomia (acute, sub-acute, chronic)

Question 12

Which horses are affected by grass sickness?

Answer 12

• Certain regions

- Horses at pasture and certain fields

Question 13

CS - grass sickness

Answer 13

• Insidious onset often, bad disease
• Acute –> ileus (develop large volume of NG reflux)
• Sub-acute –> impaction colic
• CS
  o Colic
  o Dysphagia
  o Mm tremors
  o Patchy sweating
  o Mm atrophy
  o Rhinitis sicca (dry snotty crusts in nose)

Question 14

Dx - grass sickness

Answer 14

o Biopsy – ileum – look for reduced myenteric neurons and other markers

Question 15

Features of equine motor neuron disease

Answer 15

o	Generalised weakness
o	Wastage of postural mm
o	Shifting weight, excessive recumbency
o	Walk better than they stand
o	Lumbs tucked under body ('elephant on a drum' stance)
o	Elevated tail head
o	Lowered head carriage
o	Good appetite. 
o	Retinopathy – brown pigment deposited in non-tapetal fundus in squiggly lines (deposits of myelin that has been damaged by free radicals).

Question 16

Dx - equine motor neuron disease - 3

Answer 16

o Hx, CS and r/o other ddx (weight loss and mm weakness)
o Low serum vitamin E concentrations (also EDM)
o Biopsy of sacrocaudalis dorsalis medialis mm (alongside tail head)

Question 17

Describe tetanus bacteria

Answer 17

• Clostridial bacteria, anaerobe

Question 18

Outline tetanus infection

Answer 18

• Generally following penetrating wound 2-9 days previously, usually distal limb (reduced BF)
• Clostridial bacteria, anaerobe
• Often unvaccinated, can occur in vaccinated horses
• Survival more likely in a vaccinated horse

Question 19

CS - tetanus

Answer 19

o Hyperaesthesia
o Prolapse of TE (not seen in many other conditions)
o Opisthotonous (all mm along back are tense)
o Mm rigidity
o ‘saw horse’ stance
o Sardonic grin (mm in face gone into spasm)

Question 20

Tx - tetanus

Answer 20

o Penicillin
o Tranquilizers
o tetanus toxoid (an inactivated form of toxin treated with chemicals so won’t cause disease but will cause immune response, what is present in vaccines)
o tetanus antitoxin (preformed Ab)
o manage environment (quiet as increased mm activation –> increased CS)
o give toxoid and antitoxin at same time (tx current infection and future)
o Antitoxin given cerebrally into subarachnoid space

Question 21

Pathophysiology - tetanus

Answer 21

enter presynaptic NMJ, carried by retrograde transport to peripheral nn to ventral horn grey matter, then leaves cell body of motor nerve and enters inhibitory interneurons and it acts here. Prevents release of NT at inhibitory interneuron –> excitation (spastic paralysis). See red part on image.

Question 22

Pathophysiology - botulism

Answer 22

enter presynaptic NMJ, remains here and acts to stop release of Ach  flaccid paralysis. See blue part on image.

Question 23

What is stringhalt?
Cause?
Location?
What about the unilateral type?

Answer 23

= gait deficit, dramatic and intermittent flexion of HL, unilateral or bilateral
• Toxic plant - Hypochaeris radicata = false dandelion, implicated but horse needs to eat a lot before CS.
• Lesion thought to be related to afferent motor neuron pathway
• Australia especially but UK too
• Unilateral stringhalt – associated with dorsal/cranial trauma to hock, develop gait 2-3 weeks after, can get better but often have it for rest of life, not uncommon

Question 24

Describe Shivers

Answer 24

• Difficulty voluntarily pick HL up, TL fine
• When you try and pick up HL, tail head elevates/ shivers/trembles slightly
• Unknown if reflex arc defect or cerebellar defect or neurotransmitter defect
• Unknown aetiology
• Possibly a cerebellar defect. Other possibility too – reflex arc defect or neurotransmitter defect
• Usually slowly progressive –> gets worse as animal ages

Question 25

What is likely to cause ACUTE NEUROMUSCULAR DEFICITS IN A HERD OF HORSES?

Answer 25

tetanus

Question 26

What is lathyrism?

Answer 26

	Spastic paraparesis
	V. rare in UK
	Sweet pea plants (Lathyrus hirsutus) --> beta oxalyl-amino-L-alanine acid
	Excitatory and neurotoxic effects
	Generalised spasticity

Question 27

What is stiff horse syndrome?

Answer 27

glutamic acid (inhibitory NT) decarboxylase Abs are incriminated (i.e. decreased inhibition at SC) –> mm spasm