Lecture 34: Nervous 3 Flashcards
What are the clinical signs of hepatic encephalopathy
seizures
ataxia
head pressing
can also see icterus/ascites from liver disease
What are the gross signs of hepatic encephalopathy
bilateral symmetrical spongy change on histo
What causes hepatic encephalopathy?
acute or chronic liver failure
or
vascular shunts
it causes reduced hepatic function and increased ammonia in the blood
What are the main features of neurodegenerative diseases?
inherited/familial and breed related
What are degenerative leukomyopathies
a heterogenous group of diseases affecting the white matter of the spinal cord
What are 2 classes of degenerative diseases and what animals do they each affect?
familial
- labs
- jack russel
- holstein freisians
- brown swiss cow
acquired
- tripe fed to hunting dogs
What are the clinical signs of degenerative leukomyopathies
ataxia
dysmetria
paresis
What are the lesions associated with degenerative leukomyopathies
symmetrical axonal degeneration in the white matter
the axons befome spheroid on histo
with secondary demyelination
What causes epileptic seizure brain damage
secondary to CNS malformation and/or tumors that cause prolonged convulsive seizures
What are the gross lesions associated with epileptic seizure brain damage
secondary cerebral edema
- flat and wide gyri and narrow sulci
neuronal necrosis
What is the pathogenesis of epileptic seizure brain damage
unknown
maybe…
- increased metabolic demand
- accumulation of neurotoxic neurotransmitters
What animals are most affected by salt toxicity
pigs
poultry
What is the pathogenesis of salt toxicity
hypernatremia
- increased in diet
- dehydration
reduced water in the brain = ostomic dysregulation
brain makes organic osmolytes (amino acids) to fix the osmotic imbalance
Then = free access water
- drink lots
hypernatremia shifts to a hyponatermia
osmotic imbalance because ions are removed from the brain but the organic osmolytes cannot be
= brain edema
What are the clinical signs of salt toxicity
dehydration
anorexia
head pressing/blindness/circling/convulsions
acute death
What are the gross lesions associated with salt toxicity
cerebral/meningeal congestion and edema
cortical laminar necrosis
neuronal necrosis
pigs can have lots of eosinophils in the meninges and perivascular space
Where is Clostridium tetani found?
in the soil
it can contaminate wounds
What is the pathogenesis of C. tetani
It forms a neurotoxin that inhibits the inhibitory neurotransmitters
This reduced modulation of excitatory impulses
excessive excitation and generalized muscle spasms
What species is C. tetani toxicity common in
horse and sheep
What animals are most affected by lead toxicity
can affect any
mainly cattle
What does lead toxicity cause
it crosses the BBB via the ion transport system and induces apoptosis in neurons mainly (also astrocytes and endothelium
What are the clinical signs of lead toxicity
depression
anorexia
d+
bruxism
circling
head pressing
ataxia
blindness
What are the gross lesions of lead toxicity
hemorrhage and edema
cortical laminar necrosis
polioencephalomalacia
if chronic = cortical atrophy and reduced white matter
What are the histologic lesions of lead toxicity
neuronal and laminar necrosis
macrophages can accumulate if it is chronic
What are the 4 main causes of polioencephalomalacia
thiamine (B1) deficiency
sulfur toxicity
lead toxicity
salt toxicity
also cobalt toxicity and molassas/urea based diets
List 3 common sources of sulfur?
diet
water
plant
(sulfur/sulfate/sulfide)
List 4 ways thiamine deficiency occurs?
disruption to normal rumen flora (usually make thiamine)
ingestion of thiaminase rich plant (bracken fern) or animal (fish diet)
young ruminants cant produce it
It is destroyed if the diet is treated with excess heat or SO2
What are the gross lesions associated with polioencephalomalacia
cerebral edema
- falt/wide gyri and narrow sulci
hemorrhage
normal white matter with soft/jelly/red grey matter
- multifocal distribution
it autofluoresces under UV light
