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VMS 2007 > Neuropathology: Degenerative, Metabolic, Toxic > Flashcards

Neuropathology: Degenerative, Metabolic, Toxic Flashcards

1
Q

What causes Polioencephalomalacia?

also known as softening of the grey matter

A

Thiamine deficiency

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1
Q

Name 5 things that may cause a thiamine deficiency

A
  1. Alteration of ruminal microflora
  2. Destruction of thiamine within the GIT
  3. Inactivation of thiamine by excess dietary sulphate
  4. Production of inactive thiamine analogues by bacteria
  5. Decreased absorption or increased faecal excretion of thiamine
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2
Q

In what animals is PEM most commonly seen?

A

young cattle 6-18 months old, sheep 2-7 months old

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3
Q

What are the clinical signs of PEM in ruminants?

A

Anorexia, dullness, head pressing, central blindness, teeth grinding, salivation, seizures, coma and death

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4
Q

How could you cure PEM in ruminants?

A

Early administration of thiamine
survivors with advanced lesions may be partially blind/ mentally incompetent

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5
Q

When are sheep most likely to get polioencephalomacia?

A
  • Peaks in summer and autumn
  • Peaks at 4 and 7 months of age
  • Contributing factors such as parasitism, nutritional pressures and altered rumen flora
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6
Q

What does PEM look like grossly?

A
  • Acute diffuse cerebral oedema -> brain enlargement, yellow discolouration of the grey matter
  • Severe cases cause bilaterally symmetrical malacia of cerebrocortical grey matter
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7
Q

What does polioencephalomalacia look like histologically?

A

laminar necrosis of the cerebral cortex
neuronal necrosis
oedema
vacuolation of the neuropil

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8
Q

What may cause a thiamine deficiency in carnivores?

A
  • thiaminase that is naturally present in many fish species
  • excessive cooking/ heating of meat
  • preservation of meet with sulphur dioxide
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9
Q

What causes equine nigropallidal encephalomania?

A

Prolonged ingestion of yellow star thistle

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10
Q

What does equine nigropallidal encephalomania look like grossly?

A

brain lesions are uni or bilateral, sharply demarcated, caviting foci of malacia in the globus pallidus and substantia nigra

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11
Q

What is the pathogenesis of equine nigropallidal encephalomania?

A

repin causes glutathione depletion -> cell membrane injury from reactive oxygen species

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12
Q

What causes indirect salt poisoning of pigs?

A

hyperosmolarity of the brain -> subsequent water intake -> water then follows the osmotic gradient

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13
Q

What causes Equine Leukocephalomacia?

A

Horses eat mouldy feed contaminated with fungus, Fusarium Monoliliforme

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14
Q

What is the main mycotoxin that promotes lipid peroxidation of cell membranes?

A

fumonisin B

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15
Q

In what animals is focal symmetrical encephalomalacia most common?

A

Young unvaccinated sheep

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16
Q

Why is focal symmetrical encephalomalacia also called overeating disease?

A

high carb diets create optimal conditions for intestinal overgrowth of Clostridium Perfringens

17
Q

What is oedema disease also known as?

A

enterotoxaemic colibacillosis

18
Q

What is neuronopathy?

A

degenerative changes and loss of neurons in specific neuroanatomic structures or in functionally related neuronal populations in different areas of the CNS

19
Q

What are the two patterns of axonopathy?

A
  • Fragmentation of the axon and secondary demyelination (wallerian-like degeneration)
  • Formation of axonal swellings (spheroids) in the white matter
20
Q

What is wallerian degeneration?

A

degeneration of the distal component of an injured axon

21
Q

What does wallerian degeneration lead to?

A

functional and structural alterations in the cell body and proximal internode segment of the axon and in secondary demyelination

22
Q

What causes enzootic ataxia?

A

Copper deficiency

23
Q

What animal species are most affected by copper deficiency?

A

Sheep and Goats

24
Q

When are the Neurological signs from copper deficiency most present?

A
  • at birth
  • delayed up to 6 months (enzootic ataxia) in lambs or kids
25
Q

What do enzootic ataxia lesions look like in the brain?

A

microscopic lesions in the grey/white matter of the brainstem and the ventral spinal cord

26
Q

What is the pathogenesis of Enzootic ataxia?

A

altered function of the cytochrome oxidase -> energy failure -> neuronal and axonal degredation

27
Q

What are the contributing factors of polioencephalomalacia in ruminants?

A
  • Parasitism
  • Nutritional pressures
  • Altered ruminal flora
28
Q

What is thought to be the primary injury in Equine Leukoencephalomalacia

A

lesions follow the course of blood vessels so vascular damage is
thought to be the primary injury

29
Q

What colonises the intestine of pigs in oedema disease?

A

Young pigs with intestinal colonisation by strains of Escherichia coli producing Shigalike toxin type IIe

30
Q

What is a neurodegenerative disease?

A

non-inflammatory disease in which there is selective neuronal degeneration either involving the axons or neurons in their entirety

31
Q

What are the two major morpholgical patterns of an Axonopathy?

A
  1. Fragmentation of the axon and secondary demyelination
  2. Formation of axonal swellings in the white matter or in the grey matter when the dystrophic procceses occur at the pre-terminal portion of the axon
32
Q

What neurological signs are present during enzootic ataxia (copper deficiency)

A
  • swayback in lambs, rarely in kids
  • delayed up until 6 months of age
33
Q

What is hepatic encephalopathy?

A
  • Liver fails to detoxify ammonia which is then metabolised to glutamine which is neurotoxic
34
Q

What is the function of thiamine?

A
  • Critical cofactor for various enzymes in carbohydrate metabolism
35
Q

What causes a thiamine deficiency?

A

CNS depletion of high energy phosphates e.g ATP and a decrease in glucose utilisation

36
Q

When do the clinical signs of chasteks paralysis develop?

A

Carnivores have an absolute dietary requirement for thiamine and therefore clinical signs may appear within 2-4 weeks of being fed a deficient diet

37
Q

What is the pathogenesis of oedema disease in pigs?

A
  • Toxin absorption from the intestines into the circulation
  • Toxin then binds to endothelial receptors
  • This causes vascular injury in multiple body systems
38
Q

What is hypomyelinogenesis?

A

Absence or reduction in myelination

39
Q

What is leukodystrophic myelinolytic disease?

A

Loss of myelin that had initially been formed

40
Q

What is spongy myelinopathies?

A
  • Vacuolation of the myelin sheath
  • Idiopathic, genetic, toxic/ metabolic

VMS 2007 (28 decks)

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