PNS Flashcards
Where do afferent and efferent signals enter the spinal cord?
AFFERENT = sensory neurons from skeletal muscle enter through the dorsal nerve root
EFFERENT = ventral nerve roots give off spinal nerves
PNS degeneration:
What cells produce the myelin for PNS neurons? What is the point?
Schwann cells surround axons and supply multiple at once
increases conduction velocity —> damaged myelin/no myelin = slow conduction, gait abnormalities
Myelinated nerve fiber:
neurotubules and filament within neuron produce NT and induce their excretion + collagen fibers in endoneurium
Nerve fascicle, H&E:
- epineurium: entire neuron
- perineurium: multiple fascicles
- endoneurium: one fascicle
How are peripheral nerves prepared to maintain its structure?
myelin lipids are lost during normal processing, leaving only the neurokeratin
- osmium fixation embedded in plastic/resin preserves these sheaths
What is cranial PNS neuritis in horses commonly associated with?
guttural pouch mycosis and empyema - inflammation extends to facial and glossopharyngeal nerves
What is coonhound paralysis? What syndrome is seen in dogs that lack exposure?
acute ascending paralysis in dogs following scratches or bites from a raccoon, leading to the production of antibodies that target antigens similar to peripheral nerves
acute idiopathic polyradiculoneuritis (nerve roots) - no history of contact with raccoons, mites?
What is coonhound paralysis compared to in humans? What lesions are characteristic?
Guillain-Barre syndrome - autoimmune response following viral illness, vaccination, or disease that leads to demyelination or nerve roots and peripherals
demyelination and influx of inflammatory cells with axonal degeneration
What are the most common signs of coonhound paralysis?
- hyperesthesia, weakness, ataxia
- tetraparesis may last for weeks or months
- denervation atrophy
recovery is common, but takes a long time
Coonhound paralysis:
demyelination - splitting of myelin lamellae, myelin debris
Coonhound paralysis, demyelinated axon:
myelin debris from myelin breakdown within cytoplasmic processes of macrophages
- naked axon without myelin
Coonhound paralysis, axonal degeneration:
loss of morphologic detail in axoplasm and abundant myelin debris
- black discoloration
- secondary myelin destruction, splitting, debris in Schwann cells and macrophages
What is cauda equina neuritis in horses? What are the most common clinical signs?
tail and sphincter paralysis resulting from chronic inflammation of the extradural portions of the nerve roots of the cauda equina
- perineal paresthesia-anesthesia
- urinary incontinence
- fecal retention
- tail paralysis
- croup muscle atrophy (between lumbosacral joint and base of tail)
- hindlimb ataxia and weakness
What lesions are characteristic of cauda equina neuritis? What is thought to be the etiology?
thickened nerve roots due to moderate to severe inflammatory cell infiltration (lymphocytes, plasma cells, macrophages, multinucleated giant cells) leading to granulomatous inflammation, demyelination, and axonal degeneration
immune-mediated response similar to Guillain-Barre