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Nutritional Causes: Toxic/Metabolic Disease: Neuropathology - Coggle…
Nutritional Causes: Toxic/Metabolic Disease: Neuropathology
general concepts
affects animals at all ages
frequently affects multiple animals in herd
rapid disease progression
lesions
bilateral
malacia/necrosis +/- hemorrhage
selective nuerons, axonal, or myelin loss
status spongiosus
selective neuronal necrosis
due to high metablic rate
minimal or no gross cahnges
pan-necrosis
general insults affecting all tissue elements
"selective regional vulnerability"
copper deficiency
swayback
neuro signs at nirth
ataxia
spastic paralysis
lesions
bilteral symmetrical gelatinous transformation in the cerebral periventricular white matter
histo
Wallerian degenration in dorsolateral and ventromedial tracts through SC
chromoatolysis
w/n several brain nuclei
spinal motor neurons
enzoonotic ataxia or lambs and goats
"delayed swayback"
neuro signs in older kids/lambs
essential mineral element
co-factor of many enzyme systems
cytochrome oxidase
superoxide dismutase
thiamine (b1) deficiency
polioencephalomalacia
ruminants
suggested mechanisms
decreased ruminal production by ruminal microflora
feeder cattle
timainases consumption
amprolium(coccidostaticum)
plants
horsetail
bracken fern
decreased thiamine absorption
excessive sulfide intake
most cases occur in feedlot cattle 15-30d after intro to high sulfur diet
lesions
edema of neuropil
prominent small vessels
neuronal necrosis
cerebal swelling +/- herniation
flattening of gyri
pallor/yellow hue
petechiae
malacia/"cortical laminar necrosis"
gitter cell accumulation
deep lamina involvement
thin line following sulci and gyri
autofluroresence
Chastek's paralysis
dogs
mink
lack of dietary thiamine for carnivores
initial histo change
edema
vascular dilation
2-4w after deficiency
vascular changes predominate
lesions
hemorrhage
neuronal degredation
necrosis
malacia
cofactor in oxidative e pathways
changes
degenerative
necrotic
CNS tissue most suspectible due to high E needs
vascular damage
neuronal necrosis
malacia
decreased CNS tissue
decreased thiamine-dependent serum enzymes
pyruvate kinase
positive response to treatment with thiamine
vitamine E deficiency
equine degenerative myeloencephalopathy
clinical signs
chronic weakness
trembling
fasculations
muscle atrophy
pigmentary retinopathy
lesions
chronic weakness
spinal cord motor neuron chromatolysis/necrosis
secondary demyelination
Wallerian degenration
denervation atrophy of postural mm.
spheroids
