Nervous system pathology 4 Flashcards

1
Q

Define hernitation

A

When something comes out of the area where it is normally placed and crushes against the spinal cord, brain or nerves

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2
Q

Name and describe the two types of intervertebral disc herniation

A

Hansen type 1: Extrusion of degenerated disc material

Hansen type 2: Protrusion without rupture of the annulus fibrosus

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3
Q

What is meant by coup and contre-coup?

A
  • Coup: traumatic lesion just beneath the site of impact

- Contre-coup: on the opposite side

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4
Q

Describe impact on the skull/brain and the effect this has on the site of impact and on the opposite side

A

If there is impact the brain will follow, even if the skull stops, the brain will continue to more (inertia) because it is unable to stop itself, the only way to stop it is by pulling on the vessels attached to the brain which causes haemorrhage in the exact opposite place to where the trauma occurred (e.g. to the skull)

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5
Q

Describe the effect of acceleration-deceleration injuries, or injuries by fall, at the site of impact and on the opposite side

A
  • Caused by the sudden stop (deceleration or negative acceleration) of the head
  • At the site of impact (impact site), cutaneous and cortical haemorrhages can be seen but are minimal
  • At the diametrically opposite site (controlateral haemorrhage site), intensity of lesions is much more pronounced with consistent cortical haemorrhages
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6
Q

Describe the effects of deformation or injury by blow on the site of impact and on the contralateral side

A
  • Caused by a kinetic energy delivered with higher velocity at the impact point
  • Kinetic energy transforms into deformation of the skull or fracture
  • Large contusion and lacerations extending deeply into the neuroparenchyma at the impact site
  • Contralateral haemorrhages are mild or not present
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7
Q

Accumulation of fluid in the ventricles is termed?

A

Hydrocephalus

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8
Q

On a PM what would be an indicator of immediate death following an impact lesions?

A

Any impact on the midline injuries would lead to death immediately
Any impact to the brainstem

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9
Q

Describe the features of acute spinal cord contusion due to a vertebral fracture

A

Haemorrhage, axonal damage and gliotic and inflammatory reaction

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10
Q

What are some general features of abnormal development in the CNS?

A
  • Congenital malformations are structural abnormalities of prenatal origin present at birth
  • Long period of development, starting early during embryogenesis
  • Higher severity when acting early (first third) during gestation
  • Environmental factors (viruses, toxic compounds, vitamin deficiencies, etc..) act often together with genetic mutations
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11
Q

Name two conditions caused by neural tube closure defects

A

Cranium bifida

Spina bifida

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12
Q

Malformation of the caudal fossa leads to which conditions?

A
  • Cerebellar agenesis

- Cerebellar hyperplasia and dysplasia

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13
Q

Name 3 conditions cause by abnormalities of the CSF

A
  • Hydrocephalus
  • Hydromyelia
  • Syringomyelia
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14
Q

What causes spina bifida?

A

Failure of development of the vertebral arch of the spine (lumbar)

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15
Q

What is anecephaly?

A

Lack of brain development

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16
Q

What is holoprosencephaly?

A

Lack of development of the cerebral hemisphere

17
Q

Define hydrocephalus

A

Increase in volume of CSF (water in the brain)

18
Q

What is communicating hydrocephalus

A

Bilateral and symmetrical dilation without detectable lesions (toy breed)

19
Q

Define syringomyelia

A

Fluid-filled (CSF) cavity within the spinal cord following rupture of the ependymal covering

20
Q

Define syringobulbia

A

Similar to syringomyelia but also involves the brainstem

21
Q

Define hydromyelia

A

Fluid-filled (CSF) cavity within the spinal cord, lined by a continuous layer of ependyma

22
Q

Define Encephalomalacia

A

The softening or loss of brain tissue after cerebral infarction, cerebral ischemia, infection, craniocerebral trauma, or other injury.

23
Q

Describe the lesion distribution pattern in metabolic/toxic CNS lesions

A

Symmetrically affecting specific areas

24
Q

Describe the histopathological presentations of metabolic/toxic CNS lesions

A
  • Malacia (polio- or leuko-)
  • Specific cell necrosis
  • Spongy change
25
Q

What is the clinical hallmark of metabolic/toxic CNS lesions

A

Acute to subacute onset of progressively worsening neurological dysfunctions

26
Q

How are acute corticocerebral necrosis lesions characterised?

A

Oedema (spongy state) and red hypoxic neurons affecting specific laminae of the cerebral cortex (laminar necrosis) -> swollen brain

27
Q

How are chronic corticocerebral necrosis lesions characterised?

A

Cavitation of the affected cortex, gitter cell proliferation, glial scar formation

28
Q

What are two suspected causative agents of corticocerebral necrosis?

A

Sulphur intoxication and thiamine deficiency

29
Q

Focal symmetrical encephalomalacia affects which spp?

A

Sheep
Cattle
Pigs

30
Q

Describe the pathogenesis of Focal symmetrical encephalomalacia

A

Alterations in intestinal environment due to sudden diet changes (e.g. sudden feeding of large amounts of grain) -> inadequate ruminal flora for digestion of starch -> undigested starch passes into intestine and acts as a substrate for bacteria, promoting C. perfringens type D growth and proliferation
Glucose in environment is low due to poor digestion of feed -> decreased glucose stimulates Epsilon exotoxin production -> facilitates its own absorption through the intestinal mucosa -> endothelial damage and increased vascular permeability (especially in lungs and brain) -> vasogenic brain oedema -> hypoxic-ischemic necrosis

31
Q

What is the cause of swayback?

A

Congenital copper deficiency in lambs

32
Q

What is the progression of sway back disease?

A

Animal are blind and ataxic -> severe incoordination -> immobility -> death

33
Q

How does swayback appear grossly?

A

Ventricular distension due to bilateral symmetrical rarefaction of the periventricular grey matter

34
Q

Describe the pathogenesis of hepatic encephalopathy

A

The detoxifying role of astrocytes (ammonia removal) is overwhelmed by increased haematic concentration -> metabolized to glutamine -> cytotoxic oedema (astrocyte cell swelling)

35
Q

What is the main histological finding for hepatic encephalopathy?

A

Severe spongy state of the white matter