CNS2 Flashcards

1
Q

Neuronal injuries affecting axons (axonopathies) - list three

A

Wallerian degeneration; proximal axenopathy; distal axonopathy

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2
Q

Neuronal injuries affecting the cell body of the neuron - list three

A

Central chomatolysis; inclusions; neuronal necrosis and its resolution (differs from pannecrosis)

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3
Q

Some conditions affecting the neuron can affect only the axon, and are at least theoretically reversible. True or False.

A

True - If you have axonal injury you have some hope for regeneration - neurons will try to regenerate their processes

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4
Q

Wallerian Degeneration is the most common axonopathy in vet med. True or False.

A

True

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5
Q

Wallerian degeneration follows ____ or ____ axonal transection/separation) in PNS or CNS.

A

Physical or functional

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6
Q

Wallerian Degeneration –> ___ and ____ degeneration together.

A

Axon and myelin

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7
Q

What is the first step (can occur within minutes) in Wallerian Degeneration? (following trauma vs. ischemia secondary to compression)

A

Cytoskeletal degeneration in the axon; microfilaments fall apart; in trauma = dephosphorylation of neurofilament arms; in ischemia secondary to compression = ATP reduction –> leads to a transport blockade

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8
Q

In Wallerian Degeneration, cytoskeletal degeneration in the axon leads to ______ of axon ____.

A

Denaturation of axon proteins

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9
Q

Wallerian degeneration (PNS) - in 24 hours, what is the finding?

A

Tissue collapse

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10
Q

Wallerian degeneration (PNS) - in 2-10 days, what is the finding?

A

Phagocytosis of debris; muscle atrophy; attempted regeneration (neuron shifts from making synaptic vesicles to structural parts of the axon - and sends it down to the ends of the axon and starts proliferating axonal processes - axonal sheath is a good thing because you can’t get lost)

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11
Q

Wallerian degeneration (PNS) - in 2-3 weeks, what is the finding?

A

Remyelination with altered length between nodes if successful; Bungner’s bands and chronic atrophy if unsuccessful

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12
Q

Motor neurons start to make what growth factor that serves as a stimulus for axonal growth in motor neurons?

A

NGF - neuronal growth factor

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13
Q

If regeneration is successful, we get ____ atrophy.

A

Reversed

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14
Q

If regeneration is unsuccessful, we get ____ atrophy of distal nerve and muscle and _____ formation.

A

permanent; neuroma

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15
Q

What factors determine whether WD is repaired successfully?

A

Depends on success of axon regeneration - how well the proximal and distal ends of nerves are aligned; whether PNS vs CNS is involved; how close the transection is to the cell body

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16
Q

Where is regeneration more likely to occur, PNS or CNS and why?

A

PNS because PNS has a basement membrane - no BM in CNS

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17
Q

Brachial plexus avulsion (trauma-driven Wallerian degeneration in PNS)

A

Trauma drives the limb caudally along the body, pulls the spinal nerves away from the cord at vertebral foramina, first ventrally, then dorsally

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18
Q

Bunger’s bands are indication of successful resolution of WD and return of function. True or False.

A

False

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19
Q

A short time after brachial plexus avulsion (days) you could detect microscopic degeneration or loss of axons and myelin, and muscle atrophy. True of False.

A

True

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20
Q

Lesions associated with spinal cord compression: WD caused by ischemia –> most WD affects ____ funiculi most severely.

A

Ventral

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21
Q

Lesions associated with spinal cord compression: WD caused by ischemia: describe lesions listed in increasing severeity

A

With moderate ventral compression, ventral white tracts degenerate; Wallerian degeneration of lateral then dorsal funiculi as compression is more severe; Malacia of gray matter

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22
Q

Not all injuries will involve all funiculi at the site of compression. True or False.

A

True

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23
Q

When WD affects the spinal cord after a compressive insult, it is primarily a result of which process? Thrombosis, severed nerve roots, ischemia, inflammation?

A

Ischemia

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24
Q

What area of the cord would be affected first if compression occurred on the dorsal surface instead of ventrally?

A

Sensory

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25
Q

In “watershed lesions” of severe Wallerian Degeneration; posterior tot he site of greatest injury, what degenerates?

A

Ventral white tracts

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26
Q

In “watershed lesions” of severe Wallerian degeneration; cephalic to the site of injury, what degenerates?

A

Dorsal white tracts degenerate

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27
Q

Both posterior to the site of greatest injury and cepahlic to the site of injury in watershed lesions of severe Wallerian degeneration; cause axons distal to the cell body to degenerate, starting at the point of injury. True or False.

A

True

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28
Q

If a relatively mild ventral spinal cord compression causes WD limited to the ventral cord at TL, what lesion would be present in the dorsal white matter?

A

WD would not be present in dorsal white matter.

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29
Q

Type I intervetebral disk diseases causing WD

A

Occurs in old dogs; cervical; annulus fibrosis degenerates, protrusion

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30
Q

Type II intervertebral disk disease causing Wd

A

Occurs in chondrodystrophic dogs; T-L junction; nucleus pulposis degenerates; extrusion; multiple discs affected in 25% of affected Dachshunds

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31
Q

What is more severe, type I or type II intervetebral disk disease?

A

Type II

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32
Q

Equine cervical instability:

A

recurrent transietn deformation with vertebral over-riding

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33
Q

Equine vertebral affects young, growing male horses. specifically these breeds:

A

TB, TW, WB

Throwback, tenessee walker, warm blood

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34
Q

Equine vertebral instability affects which cervical vertebra?

A

C3-4, 5-6, 6-7

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35
Q

Equine vertebral instability –> _____ joint pathology

A

intervertebral

36
Q

Canine Vertebral malformation –> instability has breed predispositions, true or false?

A

True

37
Q

Dobermans have ___ compression of the cord in canine vertebral malformation.

A

Dorsal

38
Q

Static stenosis does not occur in canine vertebral malformation. True or False.

A

False –> static stenosis can occur but is less common, and it can also affect horses

39
Q

Diskspondylosis, epidural abscess, vertebral malformation, neopasltic metastases, and fracture/luxation all can cause _____ in the spinal cord.

A

Wallerian degeneration

40
Q

Wallerian degeneration –> failure of ___ transport.

A

fast ortho-grade transport

41
Q

Proximal axonopathy –> failure of ___

A

slow ortho-grade transport

42
Q

Distal axonopathy –> failure of

A

retrograde (anterograde) transport

43
Q

Equine degenerative myeloencephalopathy proximal axonopathy: natural disease

A

Proximal axonoapthy; altered proprioception; lots of species affected; inherited/acquired vitamin E deficiency/aging

44
Q

Equine Laryngeal Hemiplegia - A distal axonopathy –> lesions

A

Distal axonoapthy; distal axonal degeneration from the ends of longest nerves: left recurrent laryngeal nerve and others; herediatry tendency

45
Q

What distinguishes Wallerian degeneration from other axonopathies?

A

Morphologic answer: Simultaneous degeneration of axon and myelin

46
Q

Injuries to the cell body: central chromatolysis

A

nonspecific reaction to injury to a living cell body reflects change; such cells frequently lose synaptic contact with neighbors; loss of Nissl substance is visible 2d - 6 wks after injury

47
Q

List different types of neuronal inclusions:

A

Secondary lysosomes in storage diseases; viral inclusions (not every one - DNA viruses - nuclear; RNA viruses - cytoplasmia); Insoluble products of proteosomal degradation - unfolded protein response and cell death (some are specific to certain diseases like AD, PD, prions); Other cell types can ALSO have inclusions

48
Q

RNA viruses usually have inclusions at what location in the cell?

A

Cytoplasm (exception - canine distemper has intranuclear viral inclusions)

49
Q

Acute, neuronal necrosis

A

Red is dead, pyknosis; can be selective and/or localized (depends on cause); followed by neuronophogia

50
Q

Neuronal necrosis by itself results in _______ microscopically, and results grossly in brain ____.

A

neuronal loss; brain atrophy

51
Q

In temporal sequence, what is the correct order of microscopic events following neuronal necrosis?

A

neuronal necrosis –> Neuronophagia –> neuronal loss –> brain atrophy

52
Q

Why do neurons die after ischemia?

A

Increased glutamate release from ischemic excitatory neurons –> astrocyte detox (glu –> gln) is disabled; Glutamate binding to susceptible dendrites –> dysfunctional ion pumps –> cytosoloic flodding by Ca2+ –> lactic acidosis, cell swelling; location varies with insult

53
Q

In slow, incremental neuronal degeneration and loss, do we see any acute changes?

A

NO

54
Q

Motor neuron disease - how is it determined?

A

genetically or idiopathically –> results in loss of previously “normal” neurons (denegeration of spinal motor neurons) - and may occur over a long period

55
Q

Cerebellar abiotrophy

A

primary degeneration/loss of purkinje cells, and sometimes neurons in other areas (multisystem atrophy). Very orderly in a given group of patients, very different between them

56
Q

The time course of purkinje cell loss is similar in all cerebellar abiotrophies. True or False.

A

False

57
Q

Spinal Muscular atrophy is a motor neuron disease that is caused by what?

A

Genetically determined or idiopathic degeneration of spinal motor neurons

58
Q

In spinal muscular atrophy, what enzyme is dysfunctional? what is deficient?

A

Superoxide dismutase dysfunction; cytoskeletal deficiency, vitamin E deficiency

59
Q

How can you treat spinal muscular atrophy in horses?

A

You can treat with vitamin E, which will stop it from progressing, but won’t fix it

60
Q

Oligodendrocyte/Schwann cell injury results in…

A

demyelinination - primary destruction of the myelin sheath

61
Q

demyelination from oligodendrocyte/schwann cell injury is due to ______

A

attack on myelin heath and death of parent cell

62
Q

Demyelination can be a random event. True or False.

A

True

63
Q

Demyelination affects _____ (longest or shortest) fibers most severely because ____

A

longest - because they have the most affected segments

64
Q

Demyelination can be focal and severe. True or False.

A

True

65
Q

Describe gross lesions of demyelination

A

Gross lesions are discoloration of the white matter and may not be grossly vissible.

66
Q

Microscopic appearance of demyelination

A

there is a special stain for myelin, and loss of this stain shows areas of demyelination

67
Q

Three mechanisms of demyelination

A

(1) Oligodendrocyte lysis/death - due to viral, chemical or nutritional causes
(2) Inflammatory attack on myelin sheat - due to viral, or autoallergic
(3) Chemical damage to myelin sheath - due to chemical or metabolic causes

68
Q

Central Pontine Myelinolysis is demyelination due to what?

A

demyelination due to oligodendrocyte death

69
Q

Coonhound paralysis is inflammatory demyelination of ….

A

ventral roots, affecting peripheral and cranial nerves

70
Q

Coonhound paralysis is caused by?

A

coonhounds eating raccoons

71
Q

Experimental allergic encephalitis, experimental allergic neuritis, and multiple sclerosis are all examples of ______ demyelination.

A

autoimmune

72
Q

Repair of myelin sheath injury (remyelination) is more effective in PNS or CNS? why?

A

PNS - schwann cells divide rapidly and there is a 1:1 relationship with axon; in the CNS oligodendrocytes can proliferate but there is only one oligodendrocyte per several axons, and no basement membrane for guidance; and seondary axonal loss makes damage permanent

73
Q

What makes demyelination permanent in the CNS?

A

secondary axonal loss

74
Q

Two astrocytic reactions to injury:

A

hypertrophy and hyperplasia

75
Q

Two types of astrocyte hypertrophy are?

A

fibrillary and gemistocytic

76
Q

Describe fibrillary astrocyte hypertrophy

A

increase in cell processes with more GFAP +/- vimentin; enlarged nuclei with HE

77
Q

Describe gemistocytic astrocyte hypertrophy

A

swollen, reactive astrocytes

78
Q

What is astrogliosis

A

diffuse increase in number of processes and number of cells present mixed with surivivng normal cells

79
Q

Astroglial scars are partly derived from stem cells and consito f what?

A

nothing but astrocytes - occurs at edge of severe injury - resident astrocytes normally remain at the periphery of an astroglial scar and new astrocytes that have migrated as precursors from near the ventricles form the center of the scar

80
Q

Why are microglial cells called rod cells?

A

they have elongated nuclei

81
Q

Brain macrophages have readily visible cytoplasm. True or False.

A

True.

82
Q

Microglia develop activated phenotype and with cell death become ____

A

macrophages

83
Q

Perivsacluar cuffs

A

cytokine-stimulated influx of microglia after injury

84
Q

gitter cells

A

active phagocytosis of microglial cells in tissue

85
Q

In meninges and PNS, external _____ influx occurs after injury.

A

Macrophage

86
Q

Can you see perivascular brain macrophgaes and microglia in the brain?

A

Yes