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Flashcards in Neuromuscular disease - equines Deck (27):
1

Where do the UMN run?

run in the ventral funiculus of white matter of spinal cord

2

Where do the LMN run?

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

3

CS - UMN weakness

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

4

CS - LMN weakness

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

5

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

- 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.

6

Botulism -methods of disease acquisition

- 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

7

Toxins involved in botulism pathology

- Toxin types B and C usually.

8

Tx - botulism

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

9

Prognosis - botulism

Mortality high in recumbent horses

10

Aetiology - grass sickness

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

11

What does grass sickness cause pathophysiologically?

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

12

Which horses are affected by grass sickness?

- Certain regions
- Horses at pasture and certain fields

13

CS - grass sickness

- 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)

14

Dx - grass sickness

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

15

Features of equine motor neuron disease

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).

16

Dx - equine motor neuron disease - 3

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)

17

Describe tetanus bacteria

- Clostridial bacteria, anaerobe

18

Outline tetanus infection

- 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

19

CS - tetanus

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)

20

Tx - tetanus

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

21

Pathophysiology - tetanus

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.

22

Pathophysiology - botulism

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

23

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

= 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

24

Describe Shivers

- 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

25

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

tetanus

26

What is lathyrism?

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

27

What is stiff horse syndrome?

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