Neuro 1 Flashcards
3 ways a nerve can be injured
transect compress/crush stretch
Wallerian degeneration is? causes death of what? why does it matter? mistakes lead to?
degeneration of distal component of injured axon, causes death of DISTAL segment, important to localize where injury occured, mistakes can lead to neurofibroma (proliferation of axons without rein nervation)
3 examples of trauma to PNS
brachial plexus avulsion eg. HBC, facial nerve paralysis horses, obturator nerve paralysis cows
equine laryngeal hemiplasia also known as? which side? which breeds? cause?
roarer’s, left, tall large breeds, Wallerian degeneration of recurrent laryngeal nerve (left is longer)
4 causes of roarer’s
direct trauma, toxins, inflammation from guttural pouches, or inherited
who gets colonic agangliosis? what is it also known as
American paint horses: white foals with over markings. lethal white foal syndrome
signs of colonic agangliosis/lethal white foal syndrome
foals die within a few days of birth and the GIT is functionally obstructed
history finding of lethal white foal syndrome
lack of myenteric and submucosal ganglia
myasthenia gravis, acquired, is caused by what
immune-mediated Abs against cholinesterase receptors
acqueried myasthenia gravis is linked to what
in some cases thymic abnormalities
what type of paralysis is seen with acquired myasthenia gravis? what would be seen at necropsy?
flaccid; megaesophagus, hypothyroidism, thymoma
three clinical forms of acquired myasthenia graves
generalized, localized, fulminating
cauda equine syndrome is observed in two species, one more than other. what are general C/S and 4 specific ones
horse and then similar condition in dogs. slowly progressive signs relating to hind end: hypotonia (decreases rear end sensation), urinary bladder paresis, fecal retention and colic, rear limb weakness and atrophy
history lesion with cauda equine syndrome
nodular granulomatous inflammation, fibrosis of giant cells
what does acute polyradiculoneuritis progress to? what scary disease could that resemble?
ascending flaccid paralysis. rabies (also both CAN get from raccoons)
cause of acute polyradiculineuritis? target?
immune mediated primary demyelination which targets ventral spinal nerve roots and their peripheral nerves
vitamin A deficiency cause? effect in neonatal calves and pigs? effect in puppies?
defective remodelling of membranous bone. neonatal calves and pigs narrows optic foramina, compressing nerves, causing blindness. deafness in puppies
botulism important clinical signs (2). cause?
ascending FLACCID paralysis and loss of tongue tone. Clostridium botulinum
Gram, spore status, metabolism of Clostridium botulinum?
Gram positive spore forming anaerobic
compare botulism cause in foals vs adult horses
foals ingest and enters through gastric ulcers. adults ingest or less commonly get wound infection
pathogenesis of botulism
toxin enters blood and goes to NMJ. prevents release of ACh at presynaptic junction. causes flaccid paralysis
contrast botulism and tetanus. type of paralysis? entry? where does toxin bind? transport? effect on NTs?
botulism=ascending flaccid paralysis. enters either ingestion and gastric ulcers (foals) or ingestion/wound infection (adults). from blood to NMJ and block ACh release. tetanus=spastic paralysis. enters wound. toxin binds to NMJ or sensory nerve, retrograde axoplasmic flow to CNS to block inhibitory transmitters.
when are outbreaks of botulism seen in wild ducks
spring and summer
how do you diagnose botulism? tetanus?
clinical diagnosis for both
clinical signs tetanus? cause? species?
SPASTIC paralysis, prolapse 3rd eyelid, sawhorse stance, seizing. Clostridium tetani. horses.
Gram status, spore status, metabolism of tetanus causing agent
Clostridium botulism: Gram positive, spore forming, anaerobic
pathogenesis of tetanus
wound contaminated by C tetani (eg. we see 10-14 days after castration). toxin produced binds at NMJ or sensory nerve. retrograde axoplasmic flow, moves to CNS, blocks release of inhibitory NTs, causing uncontrolled stimulation motor nerves
where do you see histo lesions with equine grass sickness?
autonomic and enteric ganglia (think of how they are eating grass and we know this is a PNS disease, what 2 ganglia)
stringhalt affects which limb? which species and/or breed? clinical signs? which direction? which gait? can we localize the lesion?
pelvic limb neuropathy, exaggerated flexion of one or both hindlimb. visible for any gait and direction. is in horses. we don’t know the cause and can’t localize the lesion, no.
shivers affects which limb? clinical signs? which direction? which gait? which species or breed? can we localize the lesion?
like stringhalt, is a pelvic limb neuropathy, but there are more specific signalment and C/S details. this is in TALL horses. difficulty walking BACKWARDS, only visible at WALK, and is localized to cerebellum
tumor time! how can we group all the tutors of the PNS (2 names)
peripheral nerve sheath tumours or nerve sheath tumours
two big categories of PNS tumors are? which are the ones we are learning about?
we are learning about tutors of grossly discernible nerves. there are also tumors of skin and subcutis which are under umbrella of soft tissue sarcomas
common location of benign tumors of PNS in dogs?
spinal nerves
cell of origin for benign tumours of PNS? name for them?
Schwann cells. Schwannoma
common species for benign tumors of PNS? 2 of them
cattle and dogs
where do malignant peripheral nerve sheath tumours occur
close to spine to cranial nerves
infectious tumor of Schwann cell origin that we learned about in a specific Oceanic mammal
Tasmanian devil facial tumour
