Neuropathology: Normal

Question 1

encephalo

Answer 1

brain

Question 2

myelo

Answer 2

spinal cord

Question 3

polio

Answer 3

grey matter

Question 4

leuko

Answer 4

white matter

Question 5

osis

Answer 5

degeneration

Question 6

malacia

Answer 6

gross softening of the brain (necrosis)

Question 7

what is chromatolysis?

Answer 7

• degenerative change in cell body associated with axonal injury
• swelling of nerve cell body (perikaryon) and displacement of the nucleus
  ex: lamb with copper deficiency

Question 8

what is acute neuronal necrosis?

Answer 8

ischemic cell change
- irreversible

Question 9

what causes ischemic cell change>

Answer 9

• various insults: ischemia, hypoxia, hypoglycemia, nutritional deficiency, etc
• excitatory toxicity: most common: excessive sustained release or reduced clearance of NTs

Question 10

how does ischemic cell change appear histologically?

Answer 10

shrunken and angular cell bodies with hypereosinophilic cytoplasm and pyknotic nuclei

Question 11

lysosomal storage disease

Answer 11

• inherited enzyme deficiencies
• swelling of the neuronal cell body with finely vacuolated cytoplasm
  ex: locoweed intoxication

Question 12

neuronal vacuolization in prion diseases

Answer 12

• large discrete cytoplasmic vacuoles
• ex: transmissible spongiform encephalopathy

Question 13

aging changes in neurons

Answer 13

• accumulation of orange-brown granular pigment “wear and tear” in aging neurons: lipofuscin
• normal animals have no harmful effects of this

Question 14

what are the classic causes of seeing inclusion bodies?

Answer 14

viral diseases: RV (Negri bodies), herpes (pseudorabies), canine distemper virus etc

Question 15

response of axons to injury

Answer 15

• depend on neuronal cell body for delivery of nutrients and essential materials (ex neurofilaments) and removal of debris by active transport
• injury to cell body can lead to axonal changes
• primary axonal injury: trauma, nutritional deficiencies, toxicoses, inherited defects (accumulation of different things, rare)

Question 16

what is the classic stage of neuronal degeneration?

Answer 16

swelling (spheroid) –> fragmentation –> removal by microglial cells (Gitter cells)

Question 17

Wallerian degeneration

Answer 17

degeneration of the axon and its myelin sheath DISTAL to the site of focal axonal injury (ie away from its cell body)

Question 18

in the spinal cord, where will Wallerian degeneration occur?

Answer 18

1. ascending tracts (tracts heading cranially towards brain): cranial to the site of focal axon injury
2. descending tracts (tracts heading further caudally toward the axon synapse): caudal to the site of axon injury

Question 19

axonal regeneration?

Answer 19

• if the neuronal cell body survives following axonal injury:
• regeneration from proximal stump can occur
• budding axon sprouts “neurites” can grown but is much slower in CNS
  requires intact endoneurium and schwann cells in PNS or oligodendrocytes in CNS

Question 20

hyperplasia

Answer 20

astrocytosis

Question 21

hypertrophy

Answer 21

astrogliosis
increased #, size and complexity of processes

Question 22

cell swelling (degeneration) astrocyte response to injury

Answer 22

Alzheimer type 2 astrocytes
- swollen, degenerating cells with clear cytoplasm and pale staining nuclei
most often seen with renal or hepatic encephalopathy

Question 23

when are Alzheimer type 2 astrocytes most commonly seen?

Answer 23

hepatic or renal encephalopathy

Question 24

what are the 2 types of oligodendrocytes?

Answer 24

1. interfascicular (white matter): formation and maintenance of myelin in CNS
2. perineuronal “satellite” cells - gray matter: neuronal metabolism

Question 25

what do schwann cells do?

Answer 25

myelinating cell of PNS

Question 26

2 types of demyelination

Answer 26

1. primary: degeneration/degradation of myelin sheath with sparing of axon 2. secondary: secondary to primary axonal injury: ex Wallerian degeneration

Question 27

causes of primary demyelination

Answer 27

direct damage to myelin sheath or damage to myelin producing cells (ie schwann cels and oligodendrocytes) - toxic: ex bromethalin - metabolic: ex hepatic encephalopathy - inherited enzyme defect in myelin metabolism - inflammatory/immune mediated: DAPP, caprine arthritis encephalomyelitis virus

Question 28

what are the 2 types of inadequate myelination/

Answer 28

1. hypomyelinogenesis: hypomyelination: insufficient or absent myelin production (ex in utero pestivirus) 2. dysmyelination: formation of abnormal or unstable myelin: premature demyelination: ex inhertied leukodystrophies

Question 29

what are microglial cells?

Answer 29

resident mononuclear phagocytes: resident macrophages of the CNS - disruption of BBB allows monocytes from peripheral circulation to enter the CNS - response to injury: hypertrophy, hyperplasia, phagocytosis of debris and dead neurons

Question 30

phagocytosis of lipid/myelin debris by microglial cells

Answer 30

gitter cells

Question 31

phagocytosis of dead neurons by microglial cells

Answer 31

neuronophagia

Question 32

status spongiosis

Answer 32

spongy appearance of parenchyma (non specific change) that can result from - postmortem artifact - intra myelinic edema - loss of axons/myelin anything that causes vacuolization of neuronal cells/glial cells

Question 33

repair in the CNS

Answer 33

- healing in the CNS differs from other tissue - if the lesion is SMALL: is achieved by proliferation of astrocytes/processes - healing from astrocyte proliferation cannot occur with LARGER LESIONS: get CAVITATION OR CYSTIC SPACES

Question 34

oligodendrocyte hyperplasia

Answer 34

satellitosis: response to neurons in distress

Question 35

cell swelling/degeneration of oligodendrocytes

Answer 35

if injury becomes irreversible = primary demyelination

Question 36

remyelination of oligodendrocytes

Answer 36

limited capacity compared to Schwann cells in PNS

Question 37

what is primary demyelination?

Answer 37

degeneration/degradation of myelin sheath, with sparing of axon direct damage to myelin sheath or damage to myelin-producing cells (ie schwann cells and oligodendrocytes)

Question 38

what are examples of primary demyelination?

Answer 38

toxic (Bromethalin) metabolic (hepatic encephalopathy) inherited enzyme defect inflammatory/immune mediated: canine distemper, caprine arthritis-encephalomyelitis virus, coonhound paralysis

Question 39

what is secondary demyelination?

Answer 39

secondary to primary axonal injury: ex Wallerian degeneration myelin depends on integrity of axon

Question 40

what are disorders of inadequate myelination/

Answer 40

1. hypomyelinogenesis (hypomyelination): insufficient or absent myelin production (ex: in utero pestivirus infx) 2. dysmyelination: formation of abnormal or unstable myelin: leads to premature demyelination. inherited "leukodystrophies"

Question 41

microglial cells

Answer 41

- resident mononuclear phagocytes (resident macrophages of the CNS0 - disruption of BB allows monocytes from peripheral circulation to enter the CNS - responses to injury: hypertrophy, hyperplasia - phagocytosis of lipid and myelin debris = gitter cells, dead neurons = neuronophagia

Question 42

what are gitter cells?

Answer 42

microglial cells that phaogocytize lipid/myelin debris

Question 43

what is neuronophagia

Answer 43

microglial cells that eat up dead neurons

Question 44

what are rod cells

Answer 44

activated macrophages with prominent cytoplasm that respond to hypertrophy

Question 45

what is status spongiosis?

Answer 45

spongy appearance of parenchyma (non specific change) postmortem artifact, intra myelinic edema, loss of axons, vacuolation of neurons, glial cells, or processes

Question 46

how does repair happen in the CNS?

Answer 46

- if lesion small, proliferation of astrocytes and processes can heal - healing from astrocyte proliferation cannot occur with larger lesions: cavitation or cystic spaces