Neuromuscular Disorders and Peripheral Neuropathies Flashcards
Botulism etiology
clostridium botulinum is a gram negative, spore forming anaerobic bacillus that normally inhabits the soil. The toxin prevent releases of acetylcholine at the NMJ causing progressive flaccid paralysis.
botulism pathophysiology
round bale hay
Horses get botulism by ingestion of the pre formed toxin in poorly made silage, contaminated feed, rotted hay/grain, poultry litter. It may also be from growth of the organism within the wound or production by the organism in the GI tract
botulism clinical signs
Foals: clinical signs usually occur around 1-2 months of age with a rapid onset causing stumbling, weak, dragging toes, recumbency, dehydrates, hypoglycemic
Adults: clinical signs often dysphagia (feed falling out of mouth), lowered head, dull appearance, weak, decreased PLR, weak tail and anal tone, ileus muscle fasiculations + weakness
botulism diagnosis
There is no pre mortem test for botulism but you can do the grain test: normal horse will eat 250 ml of sweet feed < 2 min (not specific but does happen with botulism)
botulism treatment
Botulism antitoxin can be given and will get the circulating toxin but will not take care of the toxin thats already causing clinical signs. If you’re suspicious that the toxin is from a carcass give bivalent antitoxin. Supportive care will be needed for at least 2 weeks while it recovers.
botulism prognosis
Foals: GOOD with intensive care
Adults: 60-90% mortality if the animal goes recumbent
What is Polyneuritis Equi?
progressive granulomatous polyradiculoneuritis of the cauda equina and less commonly cranial nerves
polyneuritis equi pathophysiology
Cytotoxic T cell and macrophage infiltrates from autoimmune and hypersensitivity reactions
polyneuritis equi clinical signs
cutaneous and muscular hyperesthesia around hindquarters, progressive desensitization, progressive paresis, fecal retention with urinary incontinence, weakness/ataxia, asymmetric muscle atrophy
could look like EPM local to sacrum or multifocal
polyneuritis equi diagnosis
CSF: mononuclear pleocytosis with high TP
Necropsy: thickened, discolored, edematous cauda equina, granulomatous inflammation, axonal degeneration, demyelination
polyneuritis equi treatment
Anti inflammatories (corticosteroids) and immunosuppressive drugs (gold salt/azathioprine) are palliative not curative. Bladder catheterization and manual removal of feces may be needed.
polyneuritis equi prognosis
hopeless
Peripheral Neuropathies etiology
nerve injury where various peripheral nerves may be affected
peripheral neuropathies pathophysiology
Nerve injury occurs due to trauma, stretching, compression or severance. A combination of neuropraxia, axonotmesis, neurotmesis.
facial nerve paralysis clinical signs
ear droop, ptosis, muzzle deviation away from lesion, quidding due to compression over facial crest, middle ear/guttural pouch, brainstem disease.
suprascapular nerve clinical signs
sweeney
Often occurs in horses that are pulling things causing atrophy of the supra and infraspinatus, abduction of shoulder while weight bearing, subluxation of shoulder, and difficulty advancing the limb
radial nerve paralysis clinical signs
shoulder trauma, post anesthesia that can be +/- brachial plexus injury. The elbow, knee, fetlock is flexed, dorsum of the foot is rested on the ground and elbow is dropped. Overall they bear weight poorly or not at all.
suprascapular nerve injurt treatment
chronic- scapular notch that releases the nerve as it goes over the shoulder and is maybe not the best efficacy
neuropraxia
Bruising and inflammation of the nerves that is transient and resolves within 3-6 weeks.
axonotmesis
crushing of nerve, epineurium and perineurium remain intact
neurotmesis
whole fiber severed, wallerian degeneration in distal segment
t/f: failure for a nerve injury to heal beyond 12 months has poor prognosis
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t/f: denervated muscles lose 50% of mass by 2 weeks
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