Nervous System

Question 1

Grey matter

Answer 1

neurons – horns of the spinal cord, cerebellar/cerebral cortex

Question 2

White matter

Answer 2

myelinated axons – medullary center of brain, outer cortex of spinal cord

Question 3

What is the function of oligodendrocytes?

Answer 3

Form myelin the wraps around axons (CNS)~ similar to Schwann cells in PNS

Question 4

What is the function of Astrocytes?

Answer 4

cell processes form BBB and repair CNS after injury

Question 5

What is the function of Microglia?

Answer 5

Phagocytic cells “fixed macrophages of CNS”

Question 6

What is central chromatolysis?

Answer 6

Response of nervous system to injury involving degenerative change & swelling with dispersal of Nissl substances

Question 7

What is neuronophagia?

Answer 7

Occurs when microglia surround degenerate or necrotic neurons and phagocytose it to remove debris

Question 8

What are the histologic characteristics of axonal (Wallerian) degeneration?

Answer 8

i. Axon degeneration (spheroid appearance~ swollen/eosinophilic)
ii. Gitter cells remove axon & myelin debris (microglia with foamy cytoplasm)
iii. Empty dilated axon sheaths  cant regenerate in CNS

Question 9

What is a spheroid?

Answer 9

Focal axonal swellings filled with degenerate organelles

Question 10

What is astrocytosis?

Answer 10

increase size & number of astrocytes in response to injury

Question 11

What are gemistocytic astrocytes?

Answer 11

Plump reactive astrocytes with eosinophilic cytoplasm~ look like necrotic neurons but have healthy nucleus

Question 12

What is the appearance of Alzheimer’s type II astrocytes, and what disease process are these cells typically seen in?

Answer 12

appear “reactive” found around neurons, enlarged with vesicular nuclei. Found with hepatic encephalopathy

Question 13

What are the different types of hydrocephalus?

In which breeds of dog is hydrocephalus most common?

Answer 13

Internal (fluid in ventricles- most common), External (fluid in arachnoid space) & communicating (fluid in ventricles & arachnoid space)

• Brachycephalic dogs

Question 14

Hydranencephaly

Answer 14

near complete/ complete absence of cerebral hemispheres~ have CSF fluid filled sacs formed by meninges. Often associated with arbovirus or pestivirus

Question 15

Porencephaly

Answer 15

cystic cavitation of brain (involves white mater)~ occur later in development

Question 16

Lissencephaly

Answer 16

brain lacking normal gyri & sulci, this is not normal for domestic mammals (everything that is non-mammal normally lissencephalic)

Question 17

Prosencephalic hypoplasia

Answer 17

cerebral aplasia; absence of cerebral hemispheres with preservation of some portion of the brainstem

Question 18

Cranium bifidum/spina bifida

Answer 18

defect which brain/ spinal cord & meninges can protrude~ almost always dorsal midline

Question 19

What is the underlying cause of storage diseases?

Answer 19

Defective catabolism (often result of a defect in lysosomal enzyme)

Question 20

How are storage diseases named

Answer 20

Named according to the substance that has defective degradation

Question 21

How are storage diseases inherited, and when do they typically present with neurologic signs?

Answer 21

Usually autosomal recessive condition & present with neurologic signs early in life.

Question 22

Which cells in the CNS are most sensitive to ischemia?

Answer 22

Neurons & oligodendroglia; grey matter is more sensitive than white d/t to its higher O2 dependence.

Question 23

polioencephalomalacia causes

Answer 23

Necrosis of grey matter, causes often unknown~ however thiamine deficiency / disturbance high sulfur intake & water deprivation may be implicated

Question 24

Distribution: Asymmetric vs symmetric lesions

Answer 24

Asymmetric: infectious
Symmetric: think systemic- toxin, nutritional or metabolic

Question 25

What causes leukoencephalomalacia?

Answer 25

moldy corn consumption (fumonisin toxin)

Question 26

What causes indirect salt poisoning? What are the associated lesions?

Answer 26

Ingestion of high salt diet + restricted water intake | - Cerebral edema, laminar cortical necrosis, nonsuppurative and eosinophilic meningoencephalitis.

Question 27

What are the ways in which bacterial infections commonly get to the CNS?

Answer 27

Septicemia (young animal), septic emboli (endocarditis) & abscess (hematogenous spread or direct invasion via cribriform plate/ middle ear)

Question 28

In what species do we most often see listeriosis or "circling disease"? a. What is the causative agent of listeriosis? b. What are the characteristic lesions, and where are the lesions typically located?

Answer 28

ruminants Listeria monocytogenes Microabscesses, sometimes within foci of microgliosis. Typically located in brainstem

Question 29

What is the causative agent of thrombotic meningoencephalitis (ITME)?

Answer 29

Histophilus somni

Question 30

What is ITME pathogenesis in development of CNS lesions, and what are the lesions?

Answer 30

Septicemia then cerebral vasculitis with hemorrhage, necrosis and thrombosis. You’ll see vasculitis, thrombosis, infarction, neutrophilic meningoencephalitis and it can form abscesses

Question 31

What are the general histologic features of viral infections?

Answer 31

Non-suppurative meningoencephalitis, perivascular cuffing, gliosis +/- viral inclusions & neuronal degeneration

Question 32

What are the principal reservoirs for rabies in the US?

Answer 32

Skunks, foxes, bats & raccoons

Question 33

What is the pathogenesis of rabies viral infection from inoculation to spread to the CNS?

Answer 33

Virus inoculated in wound (bite)-->virus replicates in muscle cells (near inoculation site) & spreads to sensory ganglia, then travels along peripheral nerves to CNS

Question 34

Pseudorabies clinical signs

Answer 34

i. Spp other than pigs: pruritis, high mortality, fever & neurologic fatal ii. Pig: mild fever, no pruritis, but may see convulsion and high mortality rate in piglets. Soes- abortion, stillborn & mummified fetus

Question 35

What are the clinical signs of caprine arthritis-encephalitis virus and visna-maedi virus?

Answer 35

Hind limb ataxia, paresis, paralysis, death (CAE causes arthrtitis in adults; VM causes pneumonia)

Question 36

In what age animals is neurologic disease typically observed in CAE & VM?

Answer 36

i. CAE: kids 2-4 mo. | ii. Visna-maedi: sheep > 2 yo

Question 37

What are the lesions associated with CAE & VM?

Answer 37

i. CAE: non-suppurative leukoencephalomyelitis, demyelination ii. Visna-maedi: nonsupprative meningoencephalitis (affect white matter) & demyelination

Question 38

Cryptococcus neoformans species, how it gets in brain & histologic lesions?

Answer 38

- spp: cat, horse & dog - Starts as nasal or sinus infection-->enters brain (direct extension through cribriform plate); can also spread to brain hematogenous from pulmonary infection - Non-staining mucopolysaccharide capsule (soap bubble appearance).

Question 39

Cause of equine protozoal myelitis?

Answer 39

Sarcocystis neurona

Question 40

What are the lesions of TSEs?

Answer 40

Intracytoplasmic neuronal vacuolation & astrocytosis