Neuro 1 Flashcards
what is Wallerian degernation?
degernation in the distal component of an injured axon. Can happen in the PNS and the CNS. Results in structural and functional alterations in the cell body. Can help you identify where an injury occurred for example in Wobbler’s
what is equine laryngeal hemiplasia and what is the common name?
“roarers” is when there is paralysis of the left side of the larynx leading to roaring sounds on inspiration esp with exercise. The left side is almost always affected because the left recurrent laryngeal nerve is longer and more prone to degeneration
what causes roarers?
equine laryngeal hemiplasia is caused by direct trauma to the left recurrent laryngeal nerve, or extension of inflammation from guttural pouches (this nerve runs through the pouch), toxins, inherited
WOT🤠
equine laryngeal hemiplasia
there is a unique congenital anomaly that happens in american paint horses where white foals are born to overo parents. What is this called and what happens to the foal?
Colonic Agangliosis (lethal white foal syndrome)
the foal does not develop it’s peripheral nervous system normally due to a mutation, and the foal will show signs of colic, have a functional obstruction (no actual blockage, things just arent moving) of the GIT, and/or die within a few days of birth. grossly the foal appears normal
immediately what are you worried about? if this foal died what would you go looking for on histo?
colonic agangliosis (lethal white foal syndrome)
histo: lack of myenteric and submucosal ganglia
what are the two types of Myasthenia gravis and which is more common?
congenital and acquired. Acquired is more common esp in dogs.
explain the differences between congenital and acquired myasthenia gravis (in somewhat detail plx and thx)
congenital: defect in Ach end plate receptors, autosomal recessive disease, animals usually develop exercise intolerance/weakness at 5 weeks to 12 months
acquired: immune mediated antibodies against cholinesterase receptors leading to immune complexes at the neuromuscular junction, can be linked to thymic abnormalities specifically thymoma and may resolve if thymoma is treated/removed
There are 3 forms of Acquired myasthenia gravis. describe them
generalized form: weakness of appendicular muscles with exercise and megaesophagus
localized form: face, esophagus, pharyngeal muscles (causes megaesophagus and regurgitation)
Fulminating: rapidly developing and sustained weakness, most severe of the 3
with aquired myasthenia gravis, what kind of paralysis do you see? What might you see on necropsy?
flaccid paralysis
necropsy: megaesophagus, thymoma, or hypothyroidism
what is cauda equina syndrome? why is it considered a disease of the PNS? What are some clinical signs?
usually happens in horses, the cauda equina gets EFFED UP. It is considered PNS because it is outside the spinal cord proper. dogs can get something similar. there does not seem to be any breed, gender, or sex predisposition
C/S: slowly progressive signs related to the hind end: hypotonia, decreased sensation of the tail, anus, and perineum, urinary bladder paresis with sabulous cystitis, fecal retention and colic, rear limb weakness and atrophy chronically.
how do you diagnose myasthenia gravis?
electrodiagnostic testing, detect antibodies, treatment trials
on necropsy there are no PNS or CNS lesions
what are gross lesions of cauda equina syndrome and what are the histo lesions? what do we think causes this disease?
edema and hemorrhage and enlargement of the nerves coming off of the cauda equina
histo: nodular granulomatous inflammation with fibrosis and demyelination
cause is unknown but thought to be immune mediated after a viral infection
what is acute polyradiculoneuritis? what are the clinical signs, and what causes this disease?
also known as coonhound paralysis, it occurs in dogs 1-2 weeks after being bitten or scratched by a racoon (alsoreported in dogs not bitten or scratched by racoons), and is also seen in cats and horses.
caused by an immune mediated primary demyelination that targets the ventral spinal nerve roots and their peripheral nerves. thought to maybe be trigger by a microme like toxoplasma, but unsure
C/S: ascending flaccid paralysis, weakness, ataxia, etc
what does vitamin A deficiency do? what feeds are low in vitamin A and what foods are high in vitamin A? Clinical signs?
causes an indirect peripheral neuropathy, defective remodelling of membranous bone resulting in many CNS and PNS abnormalities
low: old hay and grain
high: corn, fresh silage, green forage
C/S: in neonatal cows and pigs it causes blindness, and deafness in puppies, squamous metaplasia in birds and other animals
what are clinical signs of botulism? what causes botulism?
ascending flaccid paralysis, loss of tongue tone
cause: clostridium botulinum, gram positive, spore forming, anaerobic bacteria that is normally found in the soil
how is botulism different in foals vs adult horses?
foals ingest it and then it gets into circulation via gastric ulcers. in adults, they can ingest it but more commonly they get it via wound infection.
explain the pathogenesis of botulism
the toxin/bacteria enters in the BLOOD and moves to the neuromuscular junction, moves to the presynaptic junction and prevents release of acetylcholine leading to flaccid paralysis
how do you diagnose botulism?
it is very difficult because there are no gross or histologic lesions. you can try to sample the feed or GI contents or swab the wound if there was one BUT a negative test does not rule it out sadly
this disease often has outbreaks in the summer and spring in wild duck populations. who am i?
botulism (clostridium botulinum)
what are clinical signs of tetanus? what is the cause? pathogenesis?
C/S: spastic paralysis, prolapse of the 3rd eyelid, sawhorse stance, seizing, seen post castration 10-14 days
cause: clostridium tetani (gram +, spore forming, anaeroic)
pathogenesis: wound contaminated by the bacteria allows proliferation and toxin production, toxin binds at local neuromucular junction to the sensory nerve, retrograde axoplasmic flow allows it to get to the CNS where it blocks release of inhibitory neurotransmitters resulting in uncontrolled stimulation of motor nerves. DOES NOT ENTER THE BLOOD
how do you diagnose tetanus? are there any gross or histo lesions to help you?
diagnosis is very difficult and there are no gross or histo lesions except for maybe a wound you could culture from, or a history of castration.
what kind of animal is resistant to tetanus?
birds
what is equine grass sickness?
when horses eat stressed pasture grass with recent rapid growth or sudden onset of cold weather. May involve clostridium botulinum type C. horses will experience dysphagia and reflux esophagitis and gut stasis.
NOT the same as grass tetany or grass staggers in cattle which is from low magnesium
What is Stringhalt? describe what a horse with Stringhalt might look like?
a neuromusular gait abnormality affectin the pelvis limbs
horses will have exaggerated rapid flexion of one or both hindlimbs best seen when walking backwards or turning BUT CAN SEE IT WHEN MOVING FORWARD and can see it at a WALK AND A TROT
dont know cause but can be associated with roarers
what is shivers and how is it different than Stringhalt?
shivers is another pelvis limb neuromuscular lameness but it is more common in tall horses, and the horses will have difficulty walking backwards. They will hyperflex and hyperabduct the limbs while moving backwards (and not seen going forwards), and it can only be seen at a walk.
the problem is in the cerebellum with shivers
tumors of the peripheral nervous system can be grouped together as ____________ or ___________
peripheral nervesheath tumors
nerve sheath tumors
what are some common locations to get tumors of the peripheral nervous system? What is the most common cell of origin and the coresponding tumor name?
- common in the spinal nerves like the brachial plexus in dogs specifically
- schwann cells/schwannoma (a peripheral nerve sheath tumor)
- most common in dogs and cattle
where do malignant peripheral nerve sheath tumors happen?
close to the spine or cranial nerves. they are more aggressive and can metastasize
what is unique about the tasmanian devil facial tumor?
it is an infectious tumor of schwann cell origin spread by biing/fiting
