neuropathology 3 Flashcards
CNS noninflammatory disease - 2 main causes
- ammonia
- ischemic-hypoxic-toxic-metabolic
CNS: Noninflammatory disease (-opathies)
- terminology
> malacia?
> opathy?
Malacia = Death
◼ polioencephalomalacia (PEM)
◼ cerebrocortical necrosis (CCN)
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Degenerative (-opathy) diseases
◼ equine degenerative myeloencephalopathy (EDM)
◼ equine herpesviral encephalomyelopathy (EHV)
◼ degenerative myelopathy of German Shepherds
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Malacia = softening, Polio = gray
non-inflammatory CNS disease due to NH3, types
- signs referable to what?
Uremic, Hepatic, Colitis
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◼ Hepatic encephalopathy
◼ Uremia associated encephalopathy
◼ Colitis associated encephalopathy
◼ Signs referable to cortical disease
Hepatic encephalopathy
- associated with what in young and adult?
- pathogenesis?
◼ Young with portosystemic shunts
◼ Adults with acquired liver disease
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Pathogenesis -
◼ hyperammonemia
◼ cytotoxic edema
◼ cortical dysfunction
Hypoxic - Ischemic - Toxic - Metabolic
CNS: Noninflammatory disease
- types:
Localised: Focal malacia/infarct
Generalised: Polioencephalomalacia
Hypoxic-ischemic injury
◼ Hierarchy of injury, from most to least sensitive:
◼ neurons
◼ oligodendrocytes
◼ astrocytes
◼ microglia
◼ fibrovascular tissue
Hypoxic-ischemic injury
- ragions affected? localized vs generalized, causes.
Localised
◼ Infarcts
◼ Focal malacia
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Generalised
◼ Laminar cerebrocortical necrosis (malacia)
◼ Hypoxic, hypoglycemic, toxic
Hypoxic - ischemic encephalopathy
– common clinical syndromes
◼ Equine Hypoxic Ischemic encephalopathy (Neonatal
maladjustment)
◼ Anesthetic deaths
◼ Feline ischemic encephalopathy
◼ Cerebrovascular accident
◼ Seizure activity
◼ Intracarotid injections
◼ Fibrocartilagenous emboli
Generalised
Polioencephalomalacia
- occurs in what situation?
◼ thiamine deficiency
◼ sulphur induced toxicosis
◼ acute lead toxicosis
◼ hypoxia
◼ salt toxicosis
◼ edema disease of pigs
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Energy / thiamine
Acute Lead toxicosis
Salt toxicosis
Edema disease
toxic, metabolic:
Polioencephalomalacia (PEM)
> what is this? when do we see it?
◼ Syndrome named on one important histological lesion!
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◼ Lesion seen in:
◼ thiamine deficiency
◼ sulphur induced toxicosis
◼ acute lead toxicosis
◼ hypoxia
◼ salt toxicosis
◼ edema disease of pigs
Polioencephalomalacia – the syndrome
- gross lesions, progression
- histo
Gross lesions
◼ gyri flattened
◼ tentorial herniation
◼ coning of cerebellum
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After several days:
◼ cerebrum is yellow tan and more friable
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◼ Cerebrocortical laminar malacia
◼ Autofluorescence
◼ Sulphur related PEM lesion:
necrotic tissue in the basal ganglia
> the necrotic area develops hemorrhage and turns black
Polioencephalomalacia -Thiamine responsive
- what happens???
◼ Dynamic balance - thiamine vs thiaminase production
in rumen
◼ Ruminants are borderline thiamine deficient???
◼ High dietary carbohydrate > shifts flora to produce thiaminase
◼ Thiamine dependent energy production pathways -
tricarboxylic acid pathway
Polioencephalomalacia - sulphur related, causes
◼ sulphur, sulphates, sulphites, H2S
◼ drinking water
◼ molasses and urea
Polioencephalomalacia - Salt toxicosis
- what happens, lesions
◼ Balance - salt and drinking water
◼ Usually indirect
◼ Cerebral edema or cerebrotoxic effect
> laminar cortical necrosis - energy deprivation type
> eosinophilia of perivascular space
