CNS, Pt. 2 Flashcards

1
Q

What are the 3 results of traumatic injuries to the brain? Are these types of injuries common in veterinary medicine?

A
  1. concussion - temporary loss of consciousness
  2. contusion - bleeding/bruising
  3. laceration - rupture of parenchyma

no - animals with 4 legs and smaller brains are less susceptible

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2
Q

What 3 motions cause traumatic brain injuries?

A
  1. axial - front to back
  2. angular - side to side
  3. rotational
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3
Q

What are coup and countercoup lesions?

A
  • initial impact (coup - forward), causes a countercoup (backward) when brain strikes inside of the skull
  • shaking disrupts the brain’s normal chemical balance, causing loss of consciousness
  • brain swells, and in severe cases, puts pressure on the brainstem, which controls breathing and other basic life functions
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4
Q

What is a common brain lesion in boxers?

A

chronic repeated head trauma causes chronic traumatic encephalopathy, boxer’s encephalopathy, or dementia pugilistica —> neurofibrillary tangles

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5
Q

What is a common lesion in horses that have fallen backward?

A

basilar bone fracture —> head hits floor, resulting in ataxia and collapse

(requires a sagittal section of head to observe)

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6
Q

Injury to what artery results in cranial hemorrhage?

A

meningeal artery

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7
Q

What are 3 common causes of intrinsic spinal cord injuries?

A
  1. intervertebral disk disease
  2. vertebral abscesses
  3. cervical stenotic myelopathy (Wobbler disease) - Great Danes, Rottweilers, young horses
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8
Q

What is the most common etiology of polioencephalomalacia? What are 3 other causes?

A

(degeneration of gray matter in the brain)

thiamine deficiency

  • sulfur toxicity: high sulfate in water, ingestion of sulfate-accumulating plants
  • lead toxicity
  • salt poisoning/water deprivation
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9
Q

Why does thiamine deficiency cause polioencephalomalacia? In what animals is this most common? What is the most common presentation?

A

vitamin B1 is necessary for brain health —> produced by bacteria in the rumen and dysbiosis may result in the proliferation of thiaminase-producing bacteria

young lambs and cattle

opisthotonus - marked dorsal extension of the head and neck in an arching position accompanied by rigid extension of the limbs (“stargazing”)

  • dorsal medial strabismus and blindness is also common
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10
Q

How does polioencephalomalacia present grossly?

A

subtle pallor/yellowish discoloration (malacia) of the surface —> gray matter becomes harder to tell apart from white matter

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11
Q

Polioencephalomalacia, calf:

A

yellowish discoloration of cortical gray matter - degenerative necrosis

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12
Q

What is a common way to view polioencephalomalacia? In what situations does this occur?

A

autofluorescence under UV lights (Wood’s lamp)

only associated with thiamine deficiency (special pigment produced?) —> not all necrosis fluoresces

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13
Q

Chronic polioencephalomalacia, cattle:

A

cerebral cortical gray matter atrophy

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14
Q

What is the most common cause of polioencephalomalacia in pigs and poultry?

A

salt poisonin/water deprivation common due to salty feed and winter freezing of pipes

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15
Q

Polioencephalomalacia, pigs:

A
  • most common cause is salt poisoning/water deprivation
  • pink, necrotic, shrunken neurons with pyknotic nuclei
  • spongiform change
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16
Q

Other than polioencephalomalacia, what can also be observed with salt poisoning/water deprivation in pigs and poultry?

A

perivascular and meningeal eosinophilic infiltration

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17
Q

What are 2 common causes of thiamine deficiencies in cats, dogs, and farmed mink/foxes? What is this called?

A
  1. diets containing fish as the primary ingredient, which contain high levels of thiaminase
  2. diets based entirely in cooked meat, since warming of the food can destroy thiamine

Chastek paralysis (foxes and mink**)

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18
Q

What is the distribution of lesion of polioencephalomalacia (Chastek’s paralysis) in cats, dogs, and wild carnivores?

A

brainstem —> malacia, necrosis, hemorrhage around ventricles

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19
Q

Chastek’s paralysis, histology, fox:

A

brainstem and hippocampus —> shrunken, eosinophilic neurons with spongiform change

20
Q

What lesion on the brainstem is especially prominent in carnivores with thiamine deficiency?

A

necrosis of caudal colliculi with cavitation (prominent in carnivores)

(cats will commonly roll around with ventral flexion of head)

21
Q

How is the CNS affected by severe liver disease?

A

neurological signs (worst after feeding) and polymicrocavitations/spongiform change of white matter (ballooning of myelin) caused by liver damage allowing accumulation of toxins like ammonia, short-chain fatty acids, and mercaptans in systemic circulation

(hepatic encephalopathy)

22
Q

What causes focal symmetric encephalopathy? In what animals is this most common?

A

Clostridium perfringens type D epsilon toxin damages blood vessels in the brain near the basal nuclei/ganglia (floor of lateral ventricles)

sheep/lambs

23
Q

Multifocal bilaterally symmetric encephalomalacia, lamb:

A

Clostridium perfringens type D - epsilon toxin (FSE)

(symmetric = toxin, not infection)

24
Q

What causes moldy corn toxicity? In what animals is this most common?

A

ingestion of moldy feed, especially corn and corn byproducts contaminated by Fusarium verticillioides or proliferatum toxin, fumonisin B1

horses

25
Q

How does moldy corn toxicity present grossly?

A

equine (mycotoxic) leukoencephalomalacia with cavitation confined to the white matter

26
Q

What is Chewing Disease of horses? What causes this?

A

nigropallidal encephalomalacia causing dysfunction of muscles of prehension, mastication, and deglutition innervated by motor fiber of CN V, VII, and XII

repin from Centaurea solstitialis (N/S CA, OR) or repens (CO, UT) causes glutathione depletion, resulting in oxidative damage, mitochondrial dysfunction, and neuronal cell death

27
Q

What is the classic lesion of nigropallidal encephalomalacia?

A

chewing disease in horses —> bilaterally symmetric foci of liquefactive necrosis within the substantia nigra within the mesencephalon

28
Q

What are the clinical signs of nigropallidal encephalomalacia?

A
  • idle drowsiness
  • inability to grasp food or drink water
  • purposeless chewing motions
  • death due to starvation, dehydration, or aspiration pneumonia
29
Q

Nigropallidal encephalomalacia, horse:

A

chewing disease —> bilaterally symmetric lesion located in globus pallidus (basal nuclei)

30
Q

What are 3 routes of infection that can cause CNS inflammation?

A
  1. hematogenous - bacteremia, viremia, emoblic
  2. direct extension - sinusitis, otitis media
  3. neurogenic - rabies and tetanus via axonal transport, listeria via trigeminal nerve
31
Q

Suppurative meningitis, foal:

A
  • cloudy fluid in sulci rich in neutrophils
  • wider, flat gyra
  • hyperemia of meningeal arteries
  • swollen/edema —> increased intracranial pressure
32
Q

Why is it important to check all of the brain for evidence of inflammation?

A

gravity may cause exudate to pool on the ventral side of the brain, so entire brain must be checked, especially if neonatal bacteremia and meningitis is suspected

33
Q

Suppurative meningoencephalitis, dog:

A
  • inflammation within the meningeal surface and parenchyma
  • marked hyperemia
  • suppurative exudate
34
Q

What are 2 common causes of suppurative meningitis in pigs?

A
  1. Streptococcus suis
  2. E. coli
35
Q

Why are pigs especially susceptible to abscessation leading to ependymitis and ventriculitis? What does this lead to?

A

respiratory anatomy leaves pigs likely to develop upper respiratory disease, leading to eustachitis and middle ear infections that can travel to the brain

E. coli infection leads to abscessation, which causes the lateral ventricles to dilate and lose their symmetry, leading to acquired hydrocephalus due to the increased inflammatory cells and necrotic debris

36
Q

What is a common bacteria that affects feedlot cattle? What does it cause?

A

Histophilus somni

thrombotic meningoencephalitis (TME) - bacteria damages endothelium, causing vasculitis and ischemic necrosis, which commonly leads to fibrinosuppurative, hemorrhagis, and necrotizing lesions

37
Q

Other than cows, what other species is commonly affected by Histophilus somni?

A

sheep —> also develop thrombotic meningoencephalitis

38
Q

Thrombotic meningoencephalitis (TME), 9 m/o Angus steer:

A
  • Histophilus somni
  • necrosis and hemorrhage
39
Q

How does thrombotic meningoencephalitis (TME) present histologically?

A
  • parenchymal necrosis
  • hypercellularity
  • fibrinonecrotizing vasculitis and thrombosis
40
Q

Thrombotic meningoencephalitis (TME), histology:

A
  • thrombus containing necrotic debris
  • fibrinonecrotizing vasculitis and thrombosis
  • Histophilus somni
41
Q

In what species is listeriosis most common? What is the causative agent? What causes it?

A

sporadic in adult sheep and cattle

Listeria monocytogenes

periodontitis, tooth eruption, silage, etc. allows for infection and retrograde travel of the bacteria to the brain via the trigeminal nerve

42
Q

What are the most common clinical signs associated with listeriosis? How is it diagnosed?

A
  • circling
  • head tilting
  • facial paralysis (VII)
  • drooling saliva (V)
  • abortion, septicemia, conjunctivitis
  • death within a few days

histopathology, IHC, culture

43
Q

What is the classical gross lesion associated with listeriosis in the CNS?

A

medullary abscess —> where the trigeminal nerve connects to the brain

44
Q

Listeriosis, sheep, histology:

A

microabscess in the medulla oblongata with a focal increase in neutrophils

45
Q

What is the best way to diagnose listeriosis?

A

Gram stain —> stains positive (blue/purple) within microabscess