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Systemic Pathology > Neuro Pathology > Flashcards

Neuro Pathology Flashcards

1
Q

What is Nissl substance?

A

cytoplasmic basophilic granular material found in rough ER and polysomes

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2
Q

What substance do you use to stain myelin?

A

Luxol fast blue stain

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3
Q

What do ependymal cells do?

A

they line ventricles

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4
Q

What is the function of astrocytes?

A

star-shaped cells w/ elaborate cell processes that form the blood-brain barrier

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5
Q

What are microglia?

A

phagocytic cells of the CNS w/ small nuclei and relatively little cytoplasm

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6
Q

Oligodendrocytes form myelin which wraps around axons in the ____, which Schwann cells form myelin for the ___

A

CNS; PNS

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7
Q

Name the various cells and enzymes that make up the blood-brain barrier

A

Active barrier

  • efflux transporters
  • influx transporters
  • metabolizing enzymes

Passive barrier

  • astrocytes
  • tight junctions
  • endothelial cells
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8
Q

Rod-shaped microglia are what?

A

activated

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9
Q

What are gitter cells?

A

microglia ingesting myelin debris with foamy cytoplasm

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10
Q

Define chromatolysis

A

degenerative change, dispersal of Nissl substance

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11
Q

Define neuronophagia

A

microglia surround a necrotic neuron and phagocytose it to remove the debris

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12
Q

What are spheroids?

A

focal axonal swellings filled w/ degenerate organelles

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13
Q

What is Wallerian degeneration?

A

focal damage to a myelinated axon resulting in degeneration of the axon segment distal to the site of damage

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14
Q

Describe the process of Wallerian degeneration

A
  1. Axon degenerates (spheroid)
  2. Gitter cells remove axon and myelin debris
  3. Empty dilated axon sheath
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15
Q

True or False: Following Wallerian degeneration, regeneration can occur in both the PNS and the CNS

A

False; regeneration can only occur in the PNS, not the CNS

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16
Q

What are some features of the CNS that inhibit regeneration following Wallerian degeneration?

A
  • no basement membrane
  • oligodendrocytes poorly regenerative
  • CNS astrocytes secrete substances inhibitory to axon growth
  • astrocyte proliferation can create a “glial scar” - physical barrier
  • myelin breakdown products are inhibitory to axon growth
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17
Q

What are some features of the PNS that allow regeneration following Wallerian degeneration?

A
  • Schwann cells have a basement membrane
  • after injury, Schwann cells proliferate–> form a scaffold to direct sprouting axons
  • Schwann cells then remyelinate new axon
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18
Q

Describe the process of astrocytosis (astrogliosis)

A
  • incr in size and number of astrocytes in response to injury
  • repair after CNS injury is largely the job of astrocytes
    • swell and divide and cell processes proliferate
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19
Q

Define a gemistocytic astrocyte

A

a plump, reactive astrocyte with eosinophilic cytoplasm

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20
Q

What are the characteristics of Alzheimer’s type II astrocytes?

A
  • enlarged, vesicular nuclei
    • these are typical of hepatic encephalopathy
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21
Q

What might you see microglial nodules in conjunction with?

A

viral infections

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22
Q

What are some types of CNS malformations?

A
  1. Failure or abnormality of structural development
  2. Slowing of normal development
  3. Premature degradation of normally formed tissue (abiotrophy)
  4. Primary functional disturbances
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23
Q

What are some causes of CNS malformations?

A
  • inheritied genetic mutations
  • in utero infections
  • in utero exposure to teratogens
  • in utero exposure to physical agens (e.g. hyperthermia)

cause in a single individual animal = rarely determined

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24
Q

What are the 3 types of hydrocephalus?

A
  1. Internal: fluid in ventricles
  2. External: fluid in arachnoid space
  3. Communicating: fluid in ventricles and arachnoid space
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25
Q

In what breeds is hydrocephalus most common?

A

brachycephalic and some toy breeds

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26
Q

What is another name for an abnormally small brain?

A

microencephaly

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27
Q

What is lissencephaly?

A

brain lacks normal gyri and sulci

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28
Q

In what species is lissencephaly normal?

A
  • certain mammals
    • indian flying fox
    • mouse
    • rabbit
    • Florida manatee
    • common marmoset
  • any non-mammals
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29
Q

What is dysraphia and what are two examples of this?

A

neural tube closure defects

  • Anencephaly - absence of the brain
  • Prosencephalic hypoplasia (aka cerebral aplasia) - absence of cerebral hemispheres w/ preservation of at least some portion of the brainstem
  • Cranium bifidum/spina bifida - defect through which the brain/spinal cord and meninges protrude; almost always on dorsal midline
    • meningocele
    • meningoencephalocele
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30
Q

What is the difference between a meningocele and a meningoencephalocele?

A
  • Meningocele: herniation of meninges
  • Meningocephalocele/meningomyelocele: herniation of meninges and brain/spinal cord
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31
Q

What is hydraencephaly?

A
  • near complete or complete absence of the cerebral hemispheres, leaving CSF-filled sacs formed by the meninges
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32
Q

What is porencephaly?

A
  • cystic cavitation of the brain, usually involving cerebral white matter
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33
Q

What happens in cerebellar hypoplasia, and what disease processes do you see this with?

A
  1. destroy the external granular layer​
    • Border dz
    • feline panleukopenia
    • BVD d. 100-170 of gestation
  2. inhibits cells division/maturation
    • classical swine fever
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34
Q

What might you see cyclopia with?

A

Veratum californicum ingestion (particularly in sheep)

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35
Q

Describe storage diseases

A
  • accumulation of substances in cells
  • usually d/t defective catabolism, particularly lysosomal enzymes
  • the most active tissues in turning over substrate are most affected
  • typically autosomal recessive conditions, present w/ neuro signs early on in life
  • progressive and fatal
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36
Q

What are the various types of storage diseases?

A
  • Sphingolipidoses
  • Glycoproteinosis
  • Mucopolysaccharidoses
  • Glycogenoses
  • Ceroid lipofuscinoses

*named according to the substrate that has defective degradation

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37
Q

Describe what the neuronal cells of an animal with a storage disease might look like

A
  • distended cells containing vacuoles w/ excess stored material
    • neurons which accumulate substance often don’t die
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38
Q

What is lipofuscin?

A
  • “wear and tear” pigment, accumulates w/ advanced age
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39
Q

What is the pathogenesis of ceroid lipofuscinosis?

A
  • likely a heterogenous dz
  • maybe a mitochondiral defect
  • presumptively inherited
  • accumulation of pale brown to colorless, autoflorescent granular material; neuronal necrosis/loss common
40
Q

Describe the various types of cerebral edema

A
  • localized edema = trauma, neoplasia, inflammation
  • generalized edema = systemic & localized conditions
  • cytotoxic edema = d/t direct injury to cells, cell swelling
  • vasogenic edema = extracellular fluid accumulation, d/t injury to endothelial cells
41
Q

What are the gross and histologic lesions seen with cerebral edema?

A
  • Gross: maybe nothing or can see flattening of gyri/sulci, cerebellar herniation
  • Histo: vacuolation, incr clear space around vessels; white matter typically more affected than grey matter
42
Q

What cell types are most susceptible to ischemic lesions? What about brain matter?

A
  • neurons
    • cerebral cortical neurons
    • hippocampal neurons
    • Purkinje cells
  • oligodendroglia
  • grey matter
43
Q

When might you see a global ischemic lesions?

A
  • cardiac arrest
  • prolonged severe hypotension/hypoxia
44
Q

Histologic lesions of neuronal necrosis typically take a minimum of how long to develop?

A

3-6 months

45
Q

Describe fibrocartilaginous embolisms

A
  • typically asymmetric SC signs, non-progressive after 1st 24-48 hrs
  • material thought to arise from nucleus pulposus of IVD
  • usually have mult. occluded vessels
46
Q

Describe neonatal maladjustment syndrome of foals

A
  • “dummy foals”
  • presumed to be d/t ischemia and reperfusion
  • lesions: laminar neuronal necrosis, multifocal small hemorrhages
47
Q

Describe malacic diseases

A

i.e. softening - usually means necrosis in the CNS

48
Q

What is polioencephalomalacia?

A
  • necrosis of the grey matter of the brain
  • affects sheep, goats and cattle
  • laminar cortical necrosis
  • C/S: blindness, dullness, head pressing, anorexia, mm tremors, opisthotonos, recumbency, bruxism, ptyalism, nystagmus, coma, death
49
Q

Describe the pathogenesis of polioencephalomalacia

A
  • cause often unknown
  • a deficiency in thiamine or disturbance in thiamine metabolism implicated
  • maybe d/t a high sulfur intake
  • water deprivation
50
Q

What are the clinical signs of thiamine deficiency, and what species does it affect?

A
  • C/S: ataxia, neck ventroflexion, incoordination, mydriasis, convulsions
  • Lesions: hemorrhage, necrosis and neutrophil vacuolation predominantly in periventricular grey matter
  • seen in foxes, cats and mink consuming fish/horses consuming plants containing thiaminase
51
Q

Describe the pathogenesis of direct salt poisoning

A
  • ingestion of excessive salt, usually d/t high salinity in drinking water
  • mainly affects cattle
  • C/S: V/D, paresis, blindness, abd pain
  • Lesions: congestion of abomasal mucosa, dark watery intestinal contents, no CNS lesions
52
Q

Describe the pathogenesis of indirect salt poisoning

A
  • ingestion of a high salt diet in conjunction with restricted water intake for several days
  • C/S: blindness, deafness, head pressing, convulsions
  • Lesions: cerebral edema, laminar cortical necrosis, nonsuppurative and eosinophilic meningoencephalitis
53
Q

What is Nigropallidal encephalomalacia?

A
  • happens in horses d/t ingestion of yellow star thistle and Russian knapweed
  • putative neurotoxin is repin - seems to cause glutathione depletion
  • C/S: somnolence, incoordination of lips and tongue that leads to difficulty prehending food, persistent chewing motions, death often from starvation/dehydration
    • Malacia in the globus pallidus and substantia nigra
54
Q

Describe leukoencephalomalacia in horses

A
  • caused by moldy corn consumption for > 1 month
    • toxin is fumonisin produced by Fusarium
  • C/S: circling, somnolence, visual impairment, weakness, pharyngeal paralysis; usually die 2-3d after the onset of C/S
  • Lesion: necrosis of the cerebral white matter
55
Q

What lesions do you see with lead poisoning in cattle?

A
  • C/S -staggering, mm tremors, convulsions, head pressing, blindness, hypersalivation, ruminal atony, recumbency, hyperesthesia, death
  • lesions - only seen if dz course is at least several days –> laminar cerebral cortical necrosis
56
Q

What lesions do you see with lead poisoning in dogs?

A
  • white matter edema in brain/SC, demyelination, vascular damage, hemorrhage, neuronal necrosis/loss in caudate nucleus, subthalamus, deep cortical layers
57
Q

What determines the neurotropism of an infectious agent?

A

their ability to breach the BBB and BCSFB

58
Q

Bacterial infections are most commonly secondary to what in young animals?

A

septicemia

59
Q

What are the other causes of neuronal bacterial infections?

A
  • septic emboli with endocarditis
  • abscesses
    • hematogenous spread
    • direct invasion
      • usually thru cribriform plate or from middle ear
60
Q

What are the most common agents involved in forming abscesses from septic embolism?

A
  • Pigs: Erysipelothrix rhusiopathiae
  • Cattle: Trueperella pyogenes
  • All species: Streptococccus spp.
61
Q

What are the most common locations of septic emboli formation?

A

hypothalamus and junction of cerebral gray and white matter

62
Q

Describe listeriosis

A
  • “circling disease” - caused by Listeria monocytogenes that most commonly affects ruminants
  • outbreaks usually assoc. w/ silage feeding
  • C/S: head tilt, circling, confusion, depression, head pressing, unilateral facial n. paralysis, masticatory mm paralysis, purulent endophthalmitis
63
Q

Describe the lesions and pathogenesis of listeriosis

A
  • Lesions most common in brainstem
  • usually no gross lesions
  • Histologic lesions: microabscesses, sometimes within foci of microgliosis
  • Pathogenesis: bacteria invade oral mucosa, spread up the branches of CN V
64
Q

Describe infectious thrombotic meningoencephalitis (ITME)

A
  • cause by Histophilus somni
  • affects cattle (young in feedlots) and sheep
  • organism normally in genital tract & nasal cavity
  • Causes septicemia –> cerebral vasculitis w/ hemorrhage, necrosis and thrombosis
65
Q

What are the lesions of ITME?

A
  • Gross lesions: multifocal hemorrhage, necrosis
  • Histo lesions: vasculitis, thrombosis, infarction, neutrophilic meningoencephalitis, may form abscesses
66
Q

What are the general features of viral infections of the nervous system?s

A
  1. non-suppurative meningoencephalitis (+/- myelitis)
  2. perivascular cuffing
  3. gliosis
  4. +/- viral inclusions
  5. +/- neuronal degeneration/necrosis
67
Q

What are the principal reservoirs of rabies and what structures does it exhibit a tropism for?

A
  • Reservoirs: skunks, foxes, raccoons, bats
  • Tropism for CNS and salivary gland
68
Q

What is the pathogenesis of the rabies virus?

A

virus inoculated into wound, usually thru a bite –> virus r_eplicates in muscle cells_ near inoculation site –> spreads to sensory paravertebral ganglia –> virus travels along peripheral nerves to the CNS

69
Q

What are the lesions seen with rabies?

A
  • nonsuppurative encephalomyelitis, ganglioneuritis, and parotid adenitis
  • Negri bodies (cytoplasmic inclusions) in hippocampus in carnivores and Purkinje cells in herbivores
70
Q

Describe pseudorabies

A
  • caused by suid herpesvirus-1
  • can affect all of the common domestic species
  • spread b/t pigs d/t contact of virus-infected secretions with abraded skin or nasal mucosa
  • highly contagious
  • carnivores - infected via consuption of infected pig meat
71
Q

What is the pathogenesis of pseudorabies?

A
  • local reaction at site of inoculation –> spreads up related nerve to SC –> spread within CNS and out into other periph nn.
72
Q

What are the clinical signs of pseudorabies in pigs? What about all the other species?

A
  • Pigs
    • Most: mild fever, no pruritus
    • Young: prostration, convulsions, mm tremors/twitching, high mortality rate
    • Sows: abortion, stillbirth and mummified fetuses
  • Other spp:
    • intense pruritus, high mortality rate, fever, neuro signs, always fatal
73
Q

What are the lesions you see with pseudorabies?

A
  • Gross lesions: no specific lesions, no CNS lesions, may have dermatitis at site of inoculation and lesions of self-trauma
  • Histo: nonsuppurative encephalitis, gliosis, neuronal degeneration, intranuclear inclusion bodies in neurons and astrocytes
74
Q

What are three arboviruses?

A
  • Eastern, Western and Venezuelan equine encephalomyelitis viruses
75
Q

How are EEE and WEE transmitted and what are the lesions of these viruses?

A
  • Transmission: mosquito-borne
  • Lesions:
    • lymphohistiocytic and neutrophilic polioencephalomyelitis
    • neutrophils may also infiltrate the grey matter
    • gliosis, neuronal degeneration/necrosis, vasculitis, meningitis, and thrombosis
76
Q

How is West Nile transmitted (Flavivirus) transmitted and what are the lesions of these?

A
  • Transmitted: Mosquito-borne
  • Lesions: nonsuppurative encephalomyelitis, gliosis, occasional neuronal generation/necrosis
77
Q

Describe caprine arthritis encephalitis virus

A
  • a lentivirus
  • nervous system signs seen in kids 2-4 mo. old
  • C/S: hind limb ataxia, paresis, paralysis, often death
  • Lesions: non-suppurative leukoencephalomyelitis, demyelination
  • Adults can get arthritis, mastitis, pneumonia
78
Q

Describe visna-maedi virus

A
  • lentivirus
  • neuro dz usually occurs in sheep > 2 y.o.
  • C/S: hindlimb ataxia, trembling of lips, progressing to hindlimb paralysis; death is d/t secondary infection or starvation
  • lesions: nonsuppurative meningoencephalitis most severely affecting the white matter demyelination
  • virus also causes pneumonia, mastitis and arthritis
79
Q

Describe canine distemper virus

A
  • Morbillivirus
  • C/S: usually start w/ fever and conjunctivitis, progresses to resp and GI signs; can get neuro signs 1-4 wks later, or neurologic dz may be the primary manifestation
    • can get secondary infections d/t immune suppression
80
Q

What are the lesions of CDV?

A
  • Gross: none in CNS
  • Histo: nonsuppurative encephalitis, gliosis, neuronal necrosis, intranuclear and intracytoplasmic inclusions primarily in astrocytes, white matter demyelination
81
Q

Describe equine herpesviral myelencephalopathy

A
  • caused mainly by EHV1 and 4
  • spread: inhalation of nasal aerosols, contact w/ infected fetus/placenta, direct contact
  • virus replicates in endothelial cells, causes necrotizing vasculitis w/ thrombosis
  • C/S: ataxia, paresis, paralysis
  • vaccination does not necessarily protect against neuro dz
  • virus infects endothelial cells in CNS
82
Q

What are the lesions seen with EHV myeloencephalopathy?

A
  • gross lesions: none or random foci of hemorrhage in brain, very severe cases may have small foci of hemorrhage/malacia
  • histo: non-suppurative necrotizing vasculitis and thrombosis
83
Q

What fungus is the only one with a predilection for the CNS?

A

Cryptococcus neoformans

84
Q

What is the pathogenesis of Cryptococcus neoformans?

A
  • usually starts as a nasal or sinus infection and enters brain via direct extension thru cribriform plate; may also spread to brain hematogenously from pulm infection
  • affects cats, dogs and horses
85
Q

What are the lesions seen with a Cryptococcus neoformans infection?

A
  • Gross lesions: grey, gelatinous foci in brain and meninges
  • Histo lesions: from no inflammation to granulomatous inflammation; thick non-staining mucopolysaccharide capsule which imparts a ‘soap-bubble’ appearance in tissue sections
86
Q

Describe equine protozoal encephalomyelitis

A
  • primarily Sarcocystic neurona
  • C/S: ataxia, lameness, weakness of limb(s), mm atrophy
  • Pathogenesis? - think sporocysts are ingested, multiply in viscera and are transported to the CNS
87
Q

What are the lesions seen with equine protozoal encephalomyelitis?

A
  • Gross lesions: typically none, may see random foci of hemorrhage and necrosis
  • Histo lesions: hemorrhage, necrosis, perivascular cuffs of lymphocytes, macrophages, neutrophils and eosinophils; astrocytosis
88
Q

Why are the organisms that cause equine protozoal encephalomyelitis not seen in most cases?

A
  • b/c it is easily diagnosed, and frequently treated, but typically the horse does not survive
    • so by the time the horse is necropsied, the organisms will all be gone
89
Q

Describe toxoplasmosis

A
  • Toxoplasma gondii
  • primates especially susceptible
  • Gross lesions: hemorrhage and necrosis
  • Histo lesions: necrosis, hemorrhage, perivascular histiocytic and lymphoplasmacytic cuffs, tachyzoites and cysts containing bradyzoites
90
Q

Describe Neosporosis

A
  • Neospora caninum
  • Cattle: abortion – hepatitis, myocarditis, placentitis and myositis in fetus; small foci of necrosis in brain +/- SC
  • Dogs: generalized or localized infections, mixed inflamm (granulomatous and lymphoplasmacytic, occasionally w/ eosinophils) meningoencephalomyelitis, gliosis
91
Q

Describe necrotizing meningoencephalitis (NME) and necrotizing leukoencephalitis (NLE)

A
  • NME = “pug dog encephalitis,” in pugs, Shih tzus, Chi chis, Maltese
  • NLE = Bostons, Chi chis, Yorkies
  • Causes bilateral, asymmetrical lesions, mostly in cerebral cortex
  • lymphoplasmacytic and histiocytic meningitis with cells extending into and destroying underlying cerebral cortex
92
Q

Describe granulomatous meningoencephalitis (GME)

A
  • affects mostly small breeds, young to middle aged
  • unknown cause – infectious or autoimmune?
  • Histo lesions: perivascular lymphoplasmacytic and histiocytic infiltrates w/ nodular aggregates of macrophages; predominantly affects white matter
93
Q

Describe spongiform diseases

A
  • Transmissable spongiform encephalopathies are caused by prions - abnormal isoforms (PrPSc) of a normal cellular protein - the prion protein (PrPc)
    • ​PrPSc acts as a template for re-folding PrPc
  • primarily transmitted horizontally via consumption of infected feed material
  • lesions: intracytoplasmic neuronal vacuolation, astrocytosis
94
Q

What are some examples of spongiform diseases?

A
  • Bovine spongiform encephalopathy
  • Scrapie
  • Chronic wasting disease
  • Feline spongiform encephalopathy
  • Transmissable mink encepalopathy
95
Q

Describe meningiomas

A
  • seen in cats, dogs, horses, cattle and sheep
  • tumors located on the meningeal surface of the CNS
  • well-demarcated, encapsulated, expansile masses that are grey-white to red-brown
96
Q

Describe astocytomas

A
  • _​_reported in dogs (esp. brachycephalic breeds), cats and cattle
  • poorly demarcated, firm, grey-white masses in white matter and grey matter, well-differentiated neoplasms may be difficult to differentiate from surrounding brain matter
  • most commonly affected sites: pyriform and temporal lobes
97
Q

Describe oligodendroglioma

A
  • reported in dogs (esp. brachcephalic breed), cats and cattle
  • grey to pink-red, soft to gelatinous mass in white matter or grey matter of cerebrum and brainstem

Systemic Pathology (8 decks)

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