Sys Path > Neuropath > Flashcards

Neuropath Flashcards

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1
Q

what is the term for spinal diseases

A

myelopathy or myelitis

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2
Q

what is the term for brain diseases

A

encephalitis or encephalopathy

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3
Q

what are the terms used for diseases of the PNS

A
  • axonopathy
  • myelinopathy
  • neuronopathy
  • neuritis
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4
Q

what types of disorders (broad categories) affect the nervous system

A
  • pigment/minerals
  • degeneration/cell death
  • growth disturbances
  • circulatory disturbances
  • inflammation
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5
Q

what is the difference between -itis and -opathy

A

itis = inflammation
opathy = degenerative process

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6
Q

what two cells produce myelin

which cell is in the CNS and which is in the PNS

A

neurolemmocyte (PNS) and oligodendrocyte (CNS)

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7
Q

what cells produce CSF and what cells help move it

A

CSF produced by choroid plexus; moved by ependymal cells

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8
Q

what is the difference between the grey matter and white matter in the CNS

A

grey: cell bodies + neuropil + glial processes
white: myelinated axons + oligodendroglia + astrocytes

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9
Q

what does the term neuropil refer to

A

unmyelinated axons, dendritic processes, ECM

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10
Q

what space contains the CSF

A

subarachnoid

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11
Q

how does the composition of the grey and white matter differ between the brain and spinal cord

A

brain: white internally, grey externally
spinal cord: white externally, grey internally

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12
Q

what is the role of microglia and macrophages in the CNS

A

immunosurveillance and phagocytosis

myelin macrophages indicate damage when present

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13
Q

what are the roles of astrocytes

A
  • support
  • regulate extracellular environment
  • repair
  • barrier
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14
Q

what are the two types of stem cells in the CNS

A
  • neuroblasts
  • aldynoglia
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15
Q

T/F the choroid epithelial cells and ependymal cells help contribute to the BBB

A

T

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16
Q

what is the general response of neuronal cell bodies to injury

A
  • central chromatolysis (vacuolated, peripherally displaced nucleus)
  • necrosis (red dead)
  • microgliosis (clustering)
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17
Q

what is the general response of axons to injury

A
  • degeneration of distal axon
  • demyelination
  • focal swelling
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18
Q

what is a consequence of edema in the CNS

A

herniation and increased intracranial pressure

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19
Q

what are the 4 categories of CNS malformation

A
  • hereditary
  • spontaneous
  • toxic
  • post-infectious
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20
Q

what are the top 3 malformations of the CNS?

A
  • hydrocephalus
  • hydranencephaly
  • cerebellar hypoplasia
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21
Q

what is the most common congenital malformation of the CNS in domestic animals

A

hydrocephalus

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22
Q

what are common causes of hydrocephalus

A
  • in utero viral infection (that targets ependymal cells/neuroblasts)
  • developmental abnormalities in the ependyma/ventricular system
  • infection/blockage of the ventricular system
  • periventricular parenchyma loss
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23
Q

is internal or external hydrocephalus more common

A

internal (aka within the ventricular system)

(external is within the subarachnoid space btw)

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24
Q

what is the hallmark gross lesion of hydrocephalus

A

dilated ventricles

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25
what is the flow of CSF through the ventricular system
produced at choroid plexus -> lateral ventricle -> interventricular foramen -> third ventricle -> cerebral aqueduct -> forth ventricle -> lateral aperture of fourth ventricle -> central canal
26
what would happen if the following locations were blocked: 1) blockage of the interventricular foramen 2) blockage of both interventricular foramina
1) unilateral dilation of the lateral ventricle 2) bilateral dilation of the lateral ventricle
27
what would happen if the mesencephalic duct (cerebral aqueduct) was blocked
bilateral dilation of the lateral ventricles and the third ventricle and dilation of the mesencephalic duct proximal to the blockage
28
what would happen if the lateral aperture of the fourth ventricle was blocked
bilateral dilation of the lateral ventricles, third ventricle, mesencephalic duct and fourth ventricle
29
what would happen if reabsorption was blocked
dilation of the entire ventricular system and subarachnoid space
30
what are causes of acquired hydrocephalus
- compression by a cerebral abscess/neoplasm - blockage by infection/inflammatory exudate - cholesteatoma (horse)
31
how could you tell apart congenital vs acquired hydrocephalus
if the bone of the calvaria is normal, it is acquired
32
what is hydranencephaly and what should you think of when you see it
no development of the cerebrum; think of in utero infection
33
what is the term for a mild, focal hydranencephaly
porencephaly
34
what is the target site of cerebellar hypoplasia
external granular layer of the cerebellum +/- immature Purkinje cell layer
35
T/F cerebellar hypoplasia occurs secondary to infection in early gestation
F; late gestation
36
what are common causes of cerebellar hypoplasia
- feline panleukopenia virus - BVDV - classical swine fever (hog cholera) - border disease Note: BVDV, border disease and CSF are all pestiviruses
37
what viruses commonly cause hydranencephaly
Orthobunyavirus: - Akbane virus - Cache Valley virus - Schmallenburg virus
38
what are the 5 types of infectious categories of encephalitis
- neutrophilic (bacteria) - lymphocytic (viral) - granulomatous (fungal, protozoal) - eosinophilic (parasitic) - necrotic/myelinopathy/malacic
39
parasitic encephalitis can manifest in what ways
- granulomatous (classically) - neutrophilic - lymphocytic
40
what is the general pathogenesis of agents that cause meningitis/encephalitis/myelitis
exposure -> primary replication outside CNS -> blood -> CNS
41
what are the routes of CNS infectio
- hematogenous - direct extension - along nerves - CSF - leukocyte trafficking
42
what influences the success of hematogenous agents entering the brain
- regional blood flow - BBB intergrity
43
what are common outcomes of hematogenous infections in the CNS
- meningitis - multifocal microinfarcts/hemorrhage (vascular injury) - diffuse encephalopathy (toxins/metabolic) - septic embolic +/- vasculitis/thrombosis
44
from what structures can infection extend directly into the brain
- nasal cavity/sinuses - middle/inner ear - orbit - teeth - skull wounds/trauma
45
what are common outcomes of direct extension of infection into the brain
- localized meningitis/abscessation - may have bone involvement (osteomyelitis)
46
what are examples of agents that can enter peripheral nerves and travel retrograde into the CNS
- rabies - herpes - listeria
47
_________/_____________ can seed adjacent parenchyma
ependymitis/ventriculitis
48
most neutrophilic inflammation involves what type of pathogen and what type of spread to the brain
bacteria; hematogenous
49
what bacterial agents can cause meningitis
- E. coli - Streptococcus
50
abscesses in the brain secondary to a bacterial infection usually arise in grey/white matter and at what specific location
grey; grey-white junction (cortex-subcortical white matter juncton)
51
what are examples of bacterial agents that commonly cause abscesses in the brain
- Streptococcus - Staphylococcus - Corynebacterium - E. coli - Klebsiella - Pseudomonas
52
what agent commonly causes pituitary abscesses secondary to dehorning
T. pyogenes
53
what is the typical pathogenesis of listeria monocytogenes infection
trauma to oral mucosa -> trigeminal nerve sensory and motor branches -> retrograde transport to ganglia -> brainstem sets up microabscesses in the pons and medulla
54
what unique pathogenesis and gross lesions are formed by H. somni infection in the brain
endothelial injury -> necrosis of small vessels, neutrophils -> thrombosis -> microinfarcts -> malacia
55
what histologic lesion is characteristic of viral encephalitis
lymphoplasmacytic perivascular cuffing
56
besides perivascular cuffing, what are other signs of lymphocytic (viral) encephalitis
- focal and diffuse gliosis (clustering of micro/macroglia) - necrosis - satellitosis - neuronophagia (phagocytosis)
57
what area of the brain does rabies infect
hippocampus and cerebellum
58
what is the characteristic lesion associated with rabies virus
Negri bodies
59
what is the pathogenesis of rabies
bite -> replication in mm or peripheral nerve -> retrograde axonal transport -> dorsal root ganglion -> spinal cord -> ascends to the brain via ascending and descending nerve tracts -> infects brain -> salivary glands/eye
60
what virus is the exception to the lymphoplasmacytic rule (presents differently)
FIP - granulomatous and suppurative
61
what are some protozoal causes of granulomatous encephalitis
- Sarcocystis neurona (horse) - Toxoplasma gondii (cats) - Neospora caninum
62
what are 2 fungal causes of granulomatous encephalitis
Cryptococcus (dogs, cats, horses) and Blastomyces
63
what is an examples of inflammatory disease with malacia/demyelination in cattle
Thrombotic Meningoencephalitis (H. somni)
64
what is an examples of inflammatory disease with malacia/demyelination in horses
EHV-1 - causes vasculopathy, Type III Arthus reaction, immune vasculitis
65
what is an example of inflammatory disease with malacia/demyelination in dogs
CDV - causes demyelination
66
non-infectious inflammation in the brain is considered
immune-mediated
67
granulomatous meningoencephalitis occurs in what age group and species
young to middle aged small-breed dogs
68
what part of the nervous system is affected by granulomatous meningoencephalitis
white matter of cerebrum, brain stem, spinal cord and meninges
69
what are histological features of granulomatous meningoencephalitis
- perivascular cuffing of lymphocytes and macrophages +/- plasma cells, neutrophils, collagen, reticulin
70
what breed does necrotizing leukocencephalitis occur in
yorkies
71
what is the gross apperance of necrotizing leukoencephalitis
bilateral cavaitation and necrosis of the cerebral hemisphere white matter (midbrain, pons, cerebellum)
72
what is seen on histo in dogs with necrotizing leukoencephalitis
lymphocytes, macrophages, gliosis, cavitation, edema, gitter cells
73
what breed gets necrotizing meningoencephalitis
pugs, shih tzu, maltese
74
what is the appearance of necrotizing meningoencephalitis
bilateral foci of malacia in cerebral hemispheres, gray matter or grey-white matter interface (brainstem, cerebellum)
75
what is the histo appearance of NME
non-suppurative (lymphocytes and macrophages) with gliosis
76
what are some different types of malacia
polioecephalomalacia; cerebrocortical necrosis; focal symmetrical encephalomalacia (C. perfringens Type D); edema disease (shiga-like toxin)
77
what are the 3 types of ammonia diseases of the CNS
- colitis - uremic - hepatic
78
uremic, hepatic and colitis-associated encephalopathy has signs referable to disease in what area of the brain
cortex
79
what are causes of hepatic encephalopathy
- acute or chronic liver failure - severe hepatic atrophy - PSS
80
what are the neurotoxic effects of ammonia
- alters neuronal membrane transport and neurotransmission - increased BBB permeability - cytotoxic and vasogenic edema
81
what is the primary target cell of hepatic encephalopathy? how is it altered?
astrocytes (normally converts ammonia to glutamine via glutamine synthetase) becomes overwhelmed by excess glutamine -> swelling results in status spongiosus (myelin vacuolation) and Alzheimers Type II astrocytes
82
what are the effects of uremia associated encephalopathy
disruption of the BBB -> astrocyte swelling -> cerebral edema
83
what causes colitis associated encephalopathy
systemic absorption of LPS and ammonia from the intestines -> cerebral edema
84
what is the term for generalized hypoxic-ischemic-toxic-metabolic disease in the CNS
polioencephalomalacia
85
what is the hierarchy of injury (first thing affected to last) in the CNS
neurons -> oligodendrocytes -> astrocytes -> microglia -> fibrovascular tissue
86
localized regions of hypoxic/ischemic injury in the CNS are typically
infarcts or focal malacia
87
generalized hypoxic/ischemic injury in the CNS is usually
laminar cerebrocortical necrosis (malacia)
88
you can usually break down generalized hypoxic/ischemic injury in the CNS into what 3 categories
hypoxic, hypoglycemic, toxic
89
what is the cause of equine hypoxic ischemic encephalopathy (dummy foal)
impaired umbilical blood flow during parturition (red bag delivery, dystocia, endophyte fescue toxicity)
90
what lesions are associated with dummy foals: - early - if they survive several days
early: widespread hemorrhage and cerebral edema after a few days: laminar cortical necrosis
91
feline ischemic encephalopathy is caused by
abberant migration of cuterebrae larvae
92
what is the likely mechanism underlying feline ischemic encephalopathy? what is the associated lesion
vasospasm of the middle cerebral artery focal/unilateral cerebral ischemia and infarction
93
what are the causes of polioencephalomalacia
- energy/thiamine deficiency - lead - salt - edema disease - sulphur - hypoxia
94
T/F laminar cortical necrosis, polioencephalomalacia and cerebrocortical necrosis are all the same thing
T
95
what are gross lesions of polioencephalomalaca
- flattened gyri - tentorial herniation - coning of cerebellum - yellow-tan, friable cerebrum
96
how does carbohydrate overload in ruminants lead to polioencephalomalacia
high carbohydrates -> ruminal acidosis -> disrupted microflora -> increased thiaminase-producing bacteria -> thiamine destruction -> thiamine deficiency -> PEM
97
how does thiamine deficiency lead to PEM
impaired thiamine-dependent enzymes -> impaired aerobic glucose metabolism -> selective cortical neuronal necrosis
98
why are neurons highly susceptible to thiamine deficiency
they have a high metabolic demand and rely entirely on aerobic glucose metabolism
99
what is a gross sign of PEM
autoflourescence under Woods lamp
100
sulphur-related PEM tends to be ___________ and affects
hemorrhagic; basal ganglia
101
why does excessive sulphur cause PEM
interferes with cytochrome oxidase -> disrupted respiratory chain
102
what species are most susceptible to salt toxicosis
pigs and poultry
103
explain how salt toxicosis causes PEM
1st stage: hypernatremic - osmotic loss of water from brain -> cerebral shrinkage -> influx of K, Na, Cl and eventually organic osmolytes 2nd stage: rehydration - water flows into hypernatremic cerebral cells -> cerebral edema
104
what is pathognomonic for salt toxicosis in pigs
eosinophils surrounding the perivascular space and PEM
105
what are the 3 presentations of lead toxicosis
acute subacute chronic (more common in dogs)
106
describe the following presentations of lead toxicosis: - acute - subacute - chronic
acute: blindness and seizures subacute: depression, head pressing, cortical blindness, diarrhea (in cows) chronic: behavioural changes, peripheral neuropathy, myelin degeneration
107
how does lead spread and be stored in the body following ingestion
accumulates in soft tissue (kidney, liver, brain) and stored in bone
108
how does lead toxicosis cause PEM
binds sulfhydryl groups on enzymes and disrupts mitochondrial function -> interferes with Ca homeostasis -> neuron dysfunction
109
what are characteristic findings of lead toxicosis on histology
- perivascular edema - PEM - endothelial injury - astrocyte swelling - intranuclear inclusion bodies
110
what area of the brain is affected by focal symmetrical encephalomalacia and what is the cause?
basal nuclei ; C. perfringens Type D (epsilon toxin)
111
what is the pathogenesis of FSE
high carbohydrate intake -> C. perfringens Type D overgrowth -> epsilon toxin production -> endothelial injury -> edema/ischemia
112
what area of the brain is targeted by edema disease (shiga-toxin producing E. coli)
brainstem
113
what is the pathogenesis of edema disease
weaning stress -> intestinal colonization by STEC -> shiga toxin production -> vascular endothelial injury -> increased vascular permeability -> edema
114
describe Equine Degenerative Myeloencephalopacy
- unknown mechanism but suspected to be related to genetics and low vitamin E - bilateral axonal and myelin degeneration in the dorsal funiculi of the spinal cord - causes symmetrical ataxia in young horses
115
what is the pathogenesis of equine herpesviral encephalomyelopathy
viremia -> vascular endothelium of CNS -> vasculitis -> ischemia -> lumbosacral spinal cord/brainstem necrosis/hemorrhage
116
what are clinical signs of equine herpesviral encephalomyelopathy
acute onset ataxia, hindlimb weakness, urinary retention, tain tone loss
117
what is the pathogenesis of degenerative myelopathy in german shepherds
defect in superoxide dismutase -> oxidative stress -> axonal and myelin degeneration in dorsal and lateral funiculi of spinal cord
118
how much to axons regrow per day
1mm
119
neurolemmocytes produce _______ and are S100(+/-); neural fibroblasts produce ______ are are S100(+/-)
myelin; positive; fibrous tissue; negative
120
what are the different compartments/levels of the peripheral nerve
endoneurium, perineurium, epineurium
121
what contributes to the blood-nerve barrier
tight junctions in endoneural capillaries; perineural cells
122
what are the effects of the following degrees of nerve injury and what is the consequence on healing - mild - intermediate - severe
mild: blocks conduction (axon intact) - can fully recover intermediate: leaves connective tissue intact - potential to regenerate severe: transects nerve and supporting framework - heals by fibrosis
123
what is the response of a peripheral neuron to injury
- axonal swelling and fragmentation - myelin sheath swelling - digestion chamber (myelin macrophages)
124
what are causes of neuronopathy (targeting the neuron cell body)
- cisplatin - doxorubricin - mercury - vitamin B6 deficiency OR toxicosis
125
what neurons in particular are targeted by: - doxorubricin - mercury - vitamin B6 deficiency - vitamin B6 toxicosis
doxorubricin: dorsal root ganglion and autonomic cell bodies mercury: dorsal root ganglion (sensory) vitamin B6 deficiency: sensory vitamin B6 toxicosis: sensory and motor
126
what are 3 causes of primary axonopathy
- diabetes - laryngeal hemiplegia - organophosphate toxicosis
127
what are causes of primary demyelination (myelinopathy)
- chronic lead toxicosis - acute polyradiculoneuritis (Coonhound paralysis) - hypothyroidism - hypercorticism - copper deficiency - immune mediated
128
what are the types of nerve sheath tumors
- neurofibroma - neurolemmocyte tumor - perineuroma - neurofibromatosis
129
what is a ganglioneuroma
tumor of the nerve cell body and axon
130
what is the etiology of equine motor neuron disease
chronic vitamin E deficiency -> oxidative injury -> degeneration of LMN
131
what is the primary target of equine motor neuron disease
LMN in ventral horns of spinal cord and motor nuclei of the brainstem
132
what are secondary effects of equine motor neuron disesase
- secondary degeneration of ventral nerve roots and peripheral roots - denervation atrophy
133
equine grass sickness is characterised by selective degeneration of ____________ neurons, resulting in
autonomic neurons; ileus and dysautonomia
134
what is the suspected etiology of equine grass sickness
C. botulinum Type C
135
what parts of the nervous system are mainly affected by equine grass sickness
- enteric ganglia - autonomic ganglia - dorsal root ganglia - brainstem autonomic nuclei
136
what is the cause of Coonhound paralysis (acute idiopathic polyneuritis)
immune-mediated; often triggered by exposure to raccoon saliva, vaccination and infection
137
what is the target of Coonhound paralysis
LMN peripheral nerve roots and peripheral nerves
138
if rabies spreads back into the PNS, what are the neuroanatomic targets
- peripheral nerves - cranial nerve ganglia - spinal ganglia - autonomic ganglia
139
what are the neuroanatomic targets of herpes viruses
- cranial nerves - spinal nerves - autonomic ganglia
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