CNS 4, 5 and Practical Flashcards

1
Q

What parts of the CNS are mainly affected by corticocerebral necrosis?

How are acute and chronic lesions characterised?

What are the suspected causative agents?

A

Mainly affects the cerebral cortex

Acute lesions are characterized by oedema and red hypoxic neurons affecting specific laminae of the cerebral cortex- swollen brain

Chronic lesions are characterized by cavitation of the affected cortex, gitter cell proliferation, glial scar formation

Sulfur intoxication and thiamine deficiency are suspected, causative agents

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2
Q

What agent causes focal symmetrical encephalomalacia in ruminants?

Describe the pathogenesis

What happened in chronic lesions?

A

Clostridium type D in ruminants- e toxin

Pathogenesis-
Alterations in the intestinal environment cause inadequate flora and undigested starch passes into the intestine and promotes C. perfringens growth low glucose stimulates epsilon exotoxin production
passes through intestinal mucosa causes endothelial damage and increased vascular permeability
causes vasogenic brain oedema and hypoxic-ischaemic necrosis

Chronic lesions- severe symmetrical encepholomalacia

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3
Q

What causes swayback?

What causes it?

What are the symptoms?

How does is grossly appear in the CNS?

A

Congenital copper deficiency in lambs

Copper-deficient or molybdenum-rich diets during gestation

Neurological symptoms at birth-
animals are blind and ataxic, immobility, death

Grossly- ventricular distension due to bilateral symmetrical rarefaction of the periventricular grey matter

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4
Q

What can moderate/chronic porto-systemic shunts or severe or acute hepatic dysfunctions provoke?

Describe the pathogenesis?

A

Can provoke toxic encephalopathy

Pathogenesis- the detoxifying role of astrocytes is overwhelmed by increased haematic concentration which is metabolised to glutamine leading to cytotoxic oedema

Severe spongy state of the white matter and Alzheimer’s type II cells

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5
Q

What are the different developmental abnormalities of the CNS?

A
  • Neural tube closure defects
  • Defects of forebrain induction
  • Neuronal migration disorders and sulcation defects
  • Encephaloclastic defects
  • Malformation of the caudal fossa
  • Abnormality of the CSF
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6
Q

What is spina bifidia (SP)?

What are the different forms?

A

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

SP occulta- skin covering is incomplete

SP aperta- spinal defect is visible through open skin

Meningocele- fluid-filled hernial sac composed of arachnoid dura mater

Meningomyelocele- fluid-filled hernial sac composed of trophies neroparenchyma

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7
Q

What does hydrocephalus mean?

What is communicating hydrocephalus?

What can cause it?

A

Hydrocephalus- increase in volume of CSF

Communicating hydrocephalus- bilateral and symmetrical dilation without detectable lesions

Acquired, congenital or obstructive (parasites, viruses)

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8
Q

What do the following terms mean?:

Hydromyelia

Syringomyelia

Syringobulbua

A

Hydromyelia- fluid-filled cavity within the spinal cord, lined by a continuous layer of ependyma

Syringomyelia- fluid-filled cavity within the spinal cord following rupture of the ependymal covering

Syringobulbia- similar lesion involving the brain stem

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9
Q

What kind of tumour is this?

Where do they commonly arise?

How does the cut surface commonly appear?

What increases the chance of malignancy?

A

Astrocytoma- tumour of astrocytes

Generally arie supratentorially (cerebral hemispheres, white matter)

On cut surface appear firmer than normal parenchyma, whitish and poorly un-demarcated

Increasing malignancy- cell atypia, infiltrative -> neogenesis to necrosis

Graded I to IV

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10
Q

What is an oligodenroglioma?

What species does is affect?

Where is it frequently located?

What tendencies does it have?

How does it grossly and histologically appear?

A

Oligodendrocytes tumour- produced myelin

Occurs in dogs, cattle, cat and horse

Frequently in frontal, temporal and parietal cortex

Strong tendency to induce a pronounced neoagniogenesis and intratumoural haemorrhages

Grossly- well circumscribed, sharply demarcated, gelatinous
Areas of necrosis, haemorrhage, cystic degeneration and are associated with increased malignancy

Histo- honeycomb appearance, small nuclei surrounded by empty halo

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11
Q

What does an meningoma arrise from?

Where is it more commonly located?

How does it grossly appear?

How can it present in cats?

A

Very common in dogs and cats

Arising from the meninged covering the CNS

Preferentially located in the anterior fossa, more commonly over the cerebral convexities

Grossly- lobulated, often granular, white to tan with a broad based attachment to the meninged

In cats- can be multiple and expand causing compression of the CNS

Most commonly transitional

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12
Q

Where are choroid plexus carcinomas/pappilomas likely to arrise?

How do they appear grossly?

Where does an ependymoma arise from?

What condition are they commonly associated with?

How do they appear grossly and histologically?

A

Airise from epithelium of choroid plexus, mainly in 4th ventricle

Grossly- large, granular and rough texture
In carcinomas- haemorrhage, necrosis, infiltration

Ependymoma- arising from ependyma lining the ventricles

Frequently associated with obstructive hydrocephalus

Grossly- large, well demarcated, tan solid intraventricular mass

Histo- pseudorosettes and GFAP variably positive
metastsis can occur by CSF

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13
Q

What is the difference between these two neoplasms?

A

Top right- haemangiosarcoma (right ventricle, spleen)

Bottom left- melanoma

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14
Q

What is axonal degeneration?

How does it appear histologically?

What does the description wallerian like mean and what does it lead to?

A

Segmental degeneration of axons and myelin caudally to the site of an insult

Histo-

  • Formation of multiple spherical enlargments containing swollen axons
  • Leads to disintegration of myelin leading to necrosis leading to macrophages
  • Leads to proliferation of schwann cells in repair attempt- axonal sprouting

Wallerian like- degeneration that is not due to focal trauma

Consequent lack of conduction- deneravation atrophy of the effector organ, anterograde and retrograde transynaptic neuronal degeneration

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15
Q

What causes vascular disease of the PNS - ileo-aortic thromboembolism

What is it associated with?

How does it clincally appear?

A

Thrombosis of distal abdominal aorta and the junction with internal and external iliac arteries leads to acute ishemic infarction of the peroneal and tibial nerves and muscles

Associated with vulvular endocarditis and asymmetrical cyanonosis of plantar surface

Clinical- sudden paraparesis or paraplegia with painful hard muscle and lacking of femoral pulse- common in cats

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16
Q

What is ganglionitis?

What is ganglineuritis?

A

Ganglionitis- spinal ganglia

Ganglinueritis- spinal ganglia and related nerves

17
Q

What are the different effects of trauma on nerves of the PNS?

A

Neuropraxia- pins and needles
Nerve structurally intact, machanically contused trauma impaired the transmissino of impulses, full recovery

Axonotmesis-
Axon is structurally damaged and interupted, basal lamina intact- regenerates in on months or years depedning on distance with effector organ

Neurotmesis-
Entire nerve is truncated and regeneration will not be effective

Compression of the caudal equine-
associated with stenosis of lumbosacral spinal canal- chronic axonal degeneration will follow

18
Q

What is dysautonomias?

What is the more common name for equine dysutonomia?
What are the three histological forms?

A

Neuronal degeneration followed by reactive gliosis/satellitosis

Equine dysautonomia- grass sickness
can be acute or chronic
Clinical symtpom immobility of the intestines

Histological forms-
Acute- plexues contain an elevated number of neurons in association with mild to moderate prolifertation on non-neuronal elements
Sub-acute- plexuses contain a reduced number of neurons in association with mild to moderate proliferaiton on non-neuronal elements
Chronic- plexues difficult to detect, cellularity is severly decreased, marked proliferation of non-neuronal elements

19
Q

This image shows the histology from a brainstem lesion in a 3yo freisian cow with progressive dysfunction in motility of the tongue

What are the following letters?:

M

H

N

B

What is the MD?

A

M- necrotic neuron

H- Microabscesses

N- Odedma of the myelin axon

B- spongiosis

MD- bovine brainstem- focal, severe and subacute supprative and lymphoplasmacytic encephalitis with spongiosis and neuronal necrosis

20
Q

GSD with rapid progression of neurological signs, where is the lesion?

A
21
Q

What is the lesion highlighted on this image mainly affecting?

A

Optic tract

22
Q

What type of matter is affected in this image?

What is E, B and G?

A

E- perivascular cuff

B- spongiosis

G- Engorged blood vessel- hyperaemia

23
Q

What are the letters showing?

H

M

J

A

H- oedema wuthin the myelin axonal fragmentation

M- perivascular cuff

J- geminstocytic astrocyte

24
Q

What is

E

B

I

A

E- perivascular cuff

B- Severe spongiosis

I- Meningeal hyperaemia

25
Q

What are the arrows pointing to in this image?

A

Intranuclear inclusion bodies

26
Q

Wheres it the lesion located?

What kind of mass is it?

How is it characterised?

A

Brain stem

Focal mass

Caviation- intense rarefraction of the parenchyma (reduction in density)

27
Q

What are the boxes showing?

E

I

F

A

E- parencymal cavitation

F- perivascular cuff

I- Gliosis

Glia- are the non-neuronal cells in the CNS (oligodendrocytes, astrocytes, ependymal cells, microglial cells)

28
Q

What does this image show and what is it?

A

Gitter cells-

enlaerged phagocytic cell of microglial cell origins having the cytoplasm distended with lipid granules

29
Q

What does the box show?

A

Gemistocytic astrocyte