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Pathology I > Lecture 4: Neuropathology: inherited, congenital, and degenerative diseases > Flashcards

Lecture 4: Neuropathology: inherited, congenital, and degenerative diseases Flashcards

1
Q

What are some potential causes of congenital malformations

A
  1. Viruses
  2. Toxins
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2
Q

What are some viruses that cause congenital malformations

A
  1. Orthobunya viruses
  2. Orbiviruses- bluetongue
  3. Pestiviruses- BVD, border disease
  4. Parvoviruses
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3
Q

Parvoviruses cause ___malformations

A

Cerebellar

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4
Q

What is anencephaly

A

Brain largely absent at birth

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5
Q

What happens to fetus of sheep infected with blue tongue at 50 days

A

Severe hydrancephaly

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6
Q

What happens to fetus of sheep infected with blue tongue at 75 days

A

Scattered proencephalic cysts

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7
Q

What happens to fetus of sheep infected with bluetongue at 100 days

A

No gross lesions

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8
Q

What this and potential cause

A

hydrancephaly
Cause: blue tongue virus

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9
Q

What happens in hydrancephaly

A

Cerebrum and cerebellum are replaced by thin-walled, fluid filled cysts

Only brainstem preserved

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10
Q

What causes this

A

Ingestion of Veratrum californium by pregnant eyes during 14th day of gestation

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11
Q

What is the most common mechanism of hydrocephalus

A

Obstructive- fluid accumulates in front of obstruction or resorbed back into venous circulation

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12
Q

What is the most common site of obstructive hydrocephalus and due to what

A

Stenosis or inflammation leading to obstructive hydrocephalus at mesencephalic aqueduct

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13
Q

What wrong

A

Left: bilateral hydrocephalus
Right: asymmetrical hydrocephalus

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14
Q

Who is affected with congenital hydrocephalus

A

Toy breed dogs (chihuahuas)

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15
Q

What causes the congenital hydrocephalus

A

Fusion of rostral colliculi resulting in obstruction of aqueduct

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16
Q

What are the consequences of hydrocephalus

A

Dilation of ventricles from increased CSF pressure and gradually causes compression atrophy off surrounding neural parenchyma

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17
Q

Describe these lesions and what caused them

A

Ventricular dilation before skull bones ossify leading to enlargement of cranium with open fontanelles

Cause: hydrocephalus

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18
Q

What is porencephaly

A

Fluid filled cystic spaces that may or may not communicate with the ventricular system

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19
Q

Identify which one is hydrocephalus vs porencephaly

A

Left: hydrocephalus
Right: porencephaly

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20
Q

What is a meningocele

A

Defect in calvarium that allows outpocuhing of meninges
Brain unaffected

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21
Q

What is a meningoencephalocele

A

Ddefect in calvarium that allows out poaching of both brain and meninges

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22
Q

What this

A

meningocele

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23
Q

What is lissencephaly

A

Failure of gyro and Sulli to develop resulting in smooth cerebral surface

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24
Q

What causes lissencephaly

A

Arrest of normal migration of neurons during development

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25
Q

What species is lissencephaly normal in

A

Rodents, birds, reptiles and some primates

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26
Q

What this

A

lissencephaly

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27
Q

What are some clinical signs of cerebellar malformations

A

Base-wide stance, spastic hypermetric gait, loss of balance/ataxia

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28
Q

What is the timing for cerebellar malformations

A

Most active period of proliferation of external germinal layer of the cerebellum is shortly after birth through 2 weeks postnatal

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29
Q

What is the most common cause of cerebellar malformations

A

Viral induced necrosis of external granular cell layer—> cells do not migrate to internal granular cell layer- cerebellar hypoplasia

30
Q

What viral families are typically involved in cerebellar malformations

A
  1. Parvoviruses- canine parvovirus and feline panluekopenia virus
  2. Pestiviruses- border virus and BVD
31
Q

What wrong

A

cerebellar hypoplasia

32
Q

What is neuronal abiotrophy

A

Premature accelerated degeneration of fully formed neurons

33
Q

What is the best described neuronal abiotrophy

A

Cerebellar cortical abiotropgy

34
Q

What are some clinical signs of cerebellar cortical abiotrophy

A

Cerebellar ataxia, head tremor, symmetric hypermetria, spasticity, broad-based stance, loss of balance

35
Q

What is the age of onset of cerebellar cortical abiotrophy

A

Normal at birth, clinical signs show up around 4-16 weeks

36
Q

What are the microscopic lesions associated with cerebellar abiotrophy

A

Marked Purkinje cell necrosis, dengeration and loss

37
Q

Which normal vs abnormal and what is wrong

A

Left: Normal
Right: cerebellar abiotrophy- loss of Purkinje cells

38
Q

What horse breed is predisposed to cerebellar abiotrophy

A

Arabians

39
Q

What is dysraphism

A

Developmental anomaly involving failure of fusion of the neural tube

40
Q

What is the most common form of dysraphism

A

Spina bifida

41
Q

What is spina bifida

A

Fusion defect limited to the spine, most commonly lumbo-sacral region

42
Q

What is the mild form of spina bifida

A

Small opening in the vertebral column—spina bifida occulta

43
Q

What is the intermediate form of spina bifida

A

Meninges go out opening—meningocele

44
Q

What is the severe form of spina bifida

A

Meninges and spinal cord go out- myelomenigocele

45
Q

What wrong

A

spina bifida

46
Q

What cat breed has high incidence of spina bifida

A

Manx cats

47
Q

What is syringomyelia

A

Results in development of fluid containing cavities within the parenchyma of spinal cord as a consequence of abnormal CSF movement through foramen magnum

48
Q

What does this show

A

syringomyelia

49
Q

What wrong

A

syringomyelia

50
Q

The pathogenesis of syringomyelia involves ___

A

Occipital dysplasia

51
Q

What is occipital dysplasia also called

A

Chiari-like malformation

52
Q

How does occipital dysplasia cause syringomyelia

A

Cerebellum at foramen magnum results in crowding and creates turbulent flow in CSF which can result in accumulation of free fluid within the spinal cord

53
Q

What’s wrong and what is the result

A

chiari-like malformation/ occipital dysplasia
Can cause syringomyelia

54
Q

What breed is poster child for syringomyelia

A

KCCS

55
Q

___% of KCCS have chiari-like malformation and ___% of ___as a result

A

95-99%, 70% have syringomyelia

56
Q

What are some clinical signs of syringomyelia

A

Phantom scratching, cervical pain, rubbing face, neck and ears

57
Q

What is demyelination

A

Loss of normal myelin around axons

58
Q

What is dysmyelination

A

Formation of abnormal myelin during development

59
Q

What is hypomyelination

A

Partial or complete lack of myelin development

60
Q

Dysmyelination and hypomyelination are known as ___

A

Leukodystrophies

61
Q

What are the microscopic lesions associated with degenerative myelopathy

A

White matter degeneration in caudal thoracic and lumbar spinal cord- demyelination

62
Q

What breeds commonly get degenerative myelopathy

A

GSD and corgis

63
Q

What are some clinical signs of degenerative myelopathy

A

Progressive ataxia and paresis and ultimately paralysis of pelvic limbs

64
Q

What this and what caused

A

Meningeal fibrosis- opacity most apparent over Sulci
Age related lesion

65
Q

What is dural osseous metaplasia

A

Islands of mature bone within the meninges of spinal cord and sometimes bone marrow

66
Q

What breeds likely get dural osseous metplasia

A

Large breeds- GSD

67
Q

T or F: dural osseous metaplasia is an incidental finding that typically doesn’t;’t cause clinical signs

A

True

68
Q

What wrong and what caused

A

dural osseous metaplasia
Age related lesion

69
Q

What is equine choroid plexus cholesterol granuloma and where is it

A

aggregates of cholesterol typically found in ventricles and meninges

70
Q

Horse: What this and what cause

A

Equine choroid plexus cholesterol granuloma
Age related lesion

71
Q

T or F: equine choroid plexus cholesterol granuloma is a neoplasm

A

False

72
Q

Equine choroid plexus cholesterol granuloma are typically incidental but when large can cause ___

A

Depression due to compression/ atrophy

Pathology I (23 decks)

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