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Neuropath > Inflammatory, Ischemic, Toxic > Flashcards

Inflammatory, Ischemic, Toxic Flashcards

1
Q

what are the 4 types of classical/charcot MS?

A
  1. relapsing remitting
  2. secondary progressive
  3. primary progressive
  4. relapsing progressive
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2
Q

what are the 2 rare rapidly progressive forms of MS?

A
  1. Acute/Marburg type
  2. concentric sclerosis (Balo’s dz)
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3
Q

MS plaques can have CD4 predom or CD8 predom lesions. When do those each happen?

A

CD4 predom: active plaques
CD8 predom: less active

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4
Q

Do normal CNS cells express MHC II ags?

A

nope
but it can happen in several inflammatory disorders, including MS

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5
Q

what are shadow plaques?

A

they have reduced but not absent myelin staining (usually demyelinated and remyelinated)

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6
Q

what is solochrome cyanin?

A

stains myelin

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7
Q

Inactive plaques are hypocellular; when you DO see cells, what are they?

A

astrocytes
they lose oligos

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8
Q

What is the characteristic histo feature of Balo’s?

A

plaques comprised of alternating concentric rings of demyelinated and myelinated white matter

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9
Q

T/F: you only see the Balo finding in Balo’s

A

false; you can see plaques with bands or islands of preserved myelin in classic MS

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10
Q

4 grades of subependymal/germinal matrix hge

A
  1. germinal matrix only
  2. extend into lateral ventricle
  3. expand lateral ventricle
  4. extend into adjacent brain parenchyma
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11
Q

Most (60%) of supendymal/germinal matrix hge happens when?

A

within 48h of birth
(anywhere from 6h to 8d postpartum)

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12
Q

what population of neonates get cerebellar hemorrhages?

A

low birth weight preemies

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13
Q

5 micro findings of telencephalic leukoencephalopathy

A
  1. hypocellular WM
  2. no myelination glia
  3. diffuse gliosis
  4. karyorrhectic glial nuclei
  5. amphophilic globules
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14
Q

what is unique about purkinje cells and hypoxic injury in babies before 37w gestation?

A

they are LESS vulnerable to hypoxic injury than the internal granular layer cells

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15
Q

what ischemic spinal cord damage happens in preemies?

A

infarction in central lumbosacral cord segments

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16
Q

what ischemic spinal cord damage happens in term neonates?

A

diffuse necrosis affecting ventromedial neurons

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17
Q

what is a pattern of “selective vulnerability to hypoxia in neonates” in the cerebellum?

A

necrosis of DEEP cerebellar cortex with sparing of the superficial parts of the folia

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18
Q

what happens after a small germinal matrix bleed happens? like how does it resolve/manifest

A

periventricular cysts
aka
subependymal matrix cysts

they have tiny little projections into the cyst, which are residua of matrix tissue

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19
Q

what are the 2 manifestations of post-white matter necrosis d/t birth injury?

A
  1. sclerotic atrophy (centrum semiovale)
  2. cysts traversed by gliomesodermal bands (corners of LVs)
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20
Q

what are the post-grey matter necrosis findings?

A
  1. ulegyria (mushroom)
  2. cortical marbling (irregular myelination/etat fibromyelinique)
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21
Q

what is status marmoratus?

A

after pre or postnatal hypoxia but before myelination (so before 6mo)

gliotic/cystic BG/thalamus lesions (chronic) with hypermyelination + gliosis

marbled parenchyma, corrugated surface

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22
Q

gross findings of crossed cerebellar atrophy

A

unilateral cerebral hemisphere injury (chronic)
ipsilateral atrophy of basis pontis
contralateral atrophy of cerebellum

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23
Q

what kind of bilirubin do you have in kernicterus?

A

unconjugated

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24
Q

what are the characteristically affected structures in kernicterus?

A
  1. subthalamic nucleus
  2. globus pallidus
  3. lateral thalamus

(less common: CA2, LGN, colliculi, SN, pars reticularis, brainstem reticular formation, cranial nerve nuclei, Purkinjes, dentate & olivary nuclei)

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25
Q

2 characteristic things of neuromyelitis optica

A
  1. optic neuritis
  2. acute transverse myelitis
    (within weeks of each other)
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26
Q

what are the 3 supportive criteria for neuromyelitis optica that you need 2 of?

A
  1. contiguous spinal cord MRI lesion over 3+ vertebral segments
  2. brain MRI NOT dx of MS
  3. NMO-Ig seropositive (serum has aquaporin 4 antibodies)
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27
Q

what are 2 AQP4-rich regions in the brain?

A

hypothalamus
periaqueductal region
(you can see demyelinating lesions here [or elsewhere])

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28
Q

what inflammatory cells dominate in neuromyelitis optica?

A

neutrophils
eosinophils

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29
Q

in neuromyelitis optica, what do you lose WITH AQP4?

A

EAAT2 (Na+ dependent excitatory amino acid transporter 2)

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30
Q

what does the spinal cord look like in resolved neuromyelitis optica?

A

brown discoloration

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31
Q

what usually precedes ADEM?

A

systemic viral infxn or vaccination

or nothing!

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32
Q

most common preceding etiologies of ADEM

A

infxn: (tbh, think of vaccines, even tho it’s not) MMR, VZV, flu, and mono/EBV

vax: smallpox, rabies

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33
Q

characteristic ADEM micro

A

periVENULAR inflammation (NOT around arteries) with a (tight!) zone of demyelination

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34
Q

difference in clinical prognosis between ADEM and AHL

A

ADEM is usually recoverable

AHL is usually fatal within days

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35
Q

gross appearance of brain in ADEM

A

congested WM BVs surr by ill-defined gray discoloration (that’ll be the demyelination zone)

Mottled CC

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36
Q

AHL gross appearance

A

perivascular WM hge (petechial and some coalescent) and associated gray-brown d/c

involvement of brainstem & cerebellum

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37
Q

micro findings of AHL

A

Ring- and ball-shaped perivascular hges

BVs > fibrinoid necrosis > zone of necrotic tissue w/ debris > larger zone of hge

(they also get perivascular demyelination like in ADEM)

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38
Q

what are most cases of trigeminal neuralgia caused by?

A

compression of trigeminal nerve root by an aberrant loop of artery or vein + de/remyelination

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39
Q

what is specifically implicated in the psychosis of Wernicke-Korsakoff?

A

medial dorsal (or medial thalamic) nuclei

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40
Q

besides the mammillary bodies, where ELSE can you see wernicke’s?

A

hypothalamus
medial thalamic nuclei
floor of 3rd ventricle
periaqueductal region
colliculi
pontomedullary tegmental nuclei (esp dorsal motor nucleus of vagus)
inferior olives
cerebral cortex (oh good)

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41
Q

how does a wernicke lesion typically look microscopically?

A

edema
PRESERVED neurons
loss of intervening tissue
loss of myelinated fibers

(makes the capillaries seem really prominent)

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42
Q

what causes pellagra?

A

nicotinic acid deficiency
OR
tryptophan deficiency

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43
Q

micro finding in pellagra

A

striking chromatolysis of Betz cells and pontine/cerebellar dentate neurons

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44
Q

what is the clinical triad of pellagra?

A
  1. dermatitis
  2. diarrhea
  3. dementia
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45
Q

what setting is most likely to be the culprit in vitamin B6 deficiency?

A

pts receiving isoniazid (or other pyridoxine antagonists)

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46
Q

what is the other name for vitamin B6?

A

pyridoxine

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47
Q

why do pyridoxine deficiency and pellagra have some syndrome overlap?

A

pyridoxine deficiency impairs the synthesis of niacin from tryptophan

pellagra is tryptophan deficiency

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48
Q

how does pyridoxine deficiency cause seizures?

A

Vitamin B6 is involved in GABA synthesis
no B6 = no GABA = seizures

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49
Q

what does the spinal cord look like in severe vitamin B12 deficiency?

A

mildly shrunken
discolored posterior & lateral columns (esp in lower cervical & thoracic regions)

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50
Q

what’s the other name for vitamin B12

A

cobalamin

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51
Q

What does vitamin B12 deficiency look like microscopically?

A

symmetric spongy vacuolation & myelin degen

THORACIC cord

first in post columns, then corticospinal/spinocerebellar tracts in lateral columns

52
Q

what causes subacute combined degeneration?

A

vitamin B12/cobalamin deficiency

53
Q

what is the usual cause of vitamin B12 deficiency?

A

autoimmune atrophic gastritis

54
Q

what is the earliest histologic abnormality in subacute combined degeneration?

A

vacuolation within myelin sheaths in posterior columns

55
Q

what’s the other name for vitamin E?

A

alpha-tocopherol

56
Q

why does alpha-tocopherol absorption require biliary, pancreatic, and small intestine function?

A

because it’s fat-soluble

57
Q

what vitamin deficiency causes acanthocytosis?

A

vitamin E/alpha-tocopherol

58
Q

micro finding of vitamin E deficiency

A

axonal swellings, esp distal parts of longer axons
most prominent in gracile & cuneate fasciculi
neuronal loss of DRG

59
Q

what are the most susceptible neurons to hypoglycemia?

A

cortex (layers 3, 5, & 6)
caudate
putamen
CA1
Dentate nucleus in INFANTS

60
Q

What is the MAJOR difference in histo btwn hypoxic-ischemic and hypoglycemic injury?

A

PURKINJES ARE SPARED in hypoglycemia!!!

61
Q

gross findings of long-term survivors of hypoglycemia

A

granular & atrophic neocortex
hippo & tail of caudate atrophy
irregular shrinkage of caudate, causing bumpy ventricular surfaces

62
Q

what 2 structures are usually SPARED in long-term survivors of hypoglycemia?

A

cerebellar cortex (incl Purkinjes)
&
globus pallidus

63
Q

what are the general micro features of long-term survivors of hypoglycemia?

A
  1. cortical laminar neuronal loss (layers 3, 5, 6)
  2. gliosis & capillary proliferation, esp in hippo/subic/dentate
  3. WM rarefaction & gliosis
64
Q

what does hyperthermia look like on microscopy?

A

just like acute hypoxic-ischemic injury, including affecting Purkinjes

65
Q

what is osmotic demyelination syndrome?

A

central pontine myelinolysis
which can also manifest as extrapontine demyelination fwiw

66
Q

gross appearance of central pontine myelinolysis

A

basis pontis has soft, granular fusiform gray discoloration which can be v asymmetric

67
Q

where is central pontine myelinolysis most noticeable usually (lesion has the largest area)?

A

upper pons

68
Q

central pontine myelinolysis usually spares what?

A

myelin in a narrow rim of subpial tissue (of basis pontis)

69
Q

what are the extrapontine areas that can get osmotic demyelination syndrome?

A

cerebellum
LGN
capsula externa or extrema
subcortical WM
BG
Thalamus
internal capsule

70
Q

how can you tell (nonpontine) osmotic demyelination syndrome from an active MS plaque?

A

distribution
age of lesions (they’ll all be the same age in ODS)
ODS will have less lymphocytes

71
Q

what are the other 2 names for Fahr’s disease?

A

Familial idiopathic calcifications of the BG
&
striopallidodentate calcinosis

72
Q

what’s the difference between Fahr’s disease & calcs in primary hypoparathyroidism?

A

calcs are usually more diffuse in hypoparathyroidism

73
Q

T/F: the mineralized vessels in Fahr’s disease are made up of only calcium

A

FALSE
Ca AND
iron, magnesium, aluminum, & glycoproteins

74
Q

what’s the underlying issue in posterior reversible encephalopathy syndrome (PRES)?

A

hypercalcemia

75
Q

what is affected in PRES?

A

predominantly posterior white matter, subcortical (& overlying cortical) lesions (edema)

SYMMETRIC

76
Q

PRES is usually a/w what very common issue in adults?

A

hypertension

77
Q

what are the micro findings of hypertension &/or PRES?

A

microvascular necrosis
perivascular exudates
microhemorrhages
edema

78
Q

when do you see Alzheimer type II astrocytes?

A

acquired hepatic encephalopathy
OR!
uremia (non-hepatic metabolic encephalopathies)
OR!
Wilson’s disease!

79
Q

what is the technical description of alz type II astrocytes?

A

enlarged vesicular nucleus with marginated chromatin
scanty cytoplasm
little or no GFAP

80
Q

where are the alz type II astrocytes weirdly lobulated?

A

pallidum
subthalamus
dentate nucleus
brainstem

81
Q

what 3 sequelae are found in chronic/recurrent hepatic encephalopathy?

A
  1. patchy pseudolaminar necrosis/microcavitation @ depths of sulci @ G-W jxn
  2. dorsal pole of putamen neuronal loss/gliosis/microcavitation
  3. degeneration of corticospinal tract fibers (chronic hepatic myelopathy)
82
Q

what are Opalski cells?

A

altered astrocytes with small hyperchromatic nucleus & finely granular deeply eosinophilic cytoplasm
(central nucleus does not seem to be reliable)

83
Q

what disease are Opalski cells a/w?

A

WILSON’S DZ (esp in GP)
and
hepatic encephalopathy

84
Q

gross lesions of Wilson’s disease

A

brown, shrunken caudate and putamen
especially middle third of putamen
centrally cavitated putamen

85
Q

what does the micro of the putamen look like in Wilson’s disease?

A

neuron loss
lipid & pigment laden macs
fibrillary astrocytes
Alz type II astrocytes

86
Q

most common neuro abnormality in celiac disease

A

cerebellar atrophy
> loss of Purkinjes
> variable loss of granule cells
> Bergmann gliosis

87
Q

what’s the underlying cause of dialysis dementia?

A

aluminum toxicity

88
Q

what’s the underlying cause of dialysis dysequilibrium syndrome?

A

cerebral water intoxication d/t hypo-osmolality

89
Q

is dialysis dysequilibrium syndrome more frequently due hemo or peritoneal dialysis?

A

hemodialysis

90
Q

what happens to axons in multifocal necrotizing leukoencephalopathy?

A

Swollen axons in areas of necrosis
then the swollen axons calcify (hematoxyphilic)

91
Q

what is the toxic element in dialysis encephalopathy syndrome?

A

aluminum

92
Q

what is the histo finding in dialysis encephalopathy syndrome?

A

argyrophilic material (containing aluminum) in choroid plexus & brainstem nuclei

93
Q

what does chronic arsenic intoxication cause and how?

A

peripheral axonal neuropathy

mechanism: binds sulfhydryl groups > inhibit cellular respiration

94
Q

what pathology do you see in chronic arsenic intoxication?

A

chromatolysis + loss of anterior horn cells
THAT’S WHAT YOU SEE IN POLIO!!!!!

95
Q

what is the treatment for trypanosomiasis and what can it cause accidentally

A

Melarsoprol

can cause AHL

96
Q

what kind of clinical syndrome does Bismuth xs cause?

A

CJD-like
anxiety, depression, insomnia, myoclonus, gait issues

97
Q

what can lead poisoning look like in the CNS?

A
  1. edema/hydrocephalus
  2. endothelial swelling, petechial hge, capillary necrosis, thrombosis
  3. perivascular PAS+ globules
98
Q

how does manganese toxicity work? (mechanism)

A

astrocytic mitochondria take it up, then they can’t undergo oxidative phosphorylation

99
Q

what is the pathology of manganese toxicity?

A

gliosis & neuron loss in BG
but NOT substantia nigra

100
Q

the clinical presentation of manganese looks like WHAT? and how can you tell them apart?

A

looks like parkinson’s
manganese will have preserved SN

101
Q

what does in-utero mercury exposure affect most severely?

A

cerebellum degen
(and cortical spongiform degen)

102
Q

what 2 structures does thallium affect?

A

motor neurons (chromatolysis)
and
posterior columns

103
Q

how does triethyl tin manifest clinically and histo?

A

Clin: increased ICP and flaccid paraparesis

Histo: WM edema 2/2 vacuoles in myelin

104
Q

How does triMethyl tin manifest clinically and histo?

A

clin: confusion, confab, amnesia

histo: CA3 neurons apoptosis, BG, amygdala

105
Q

acrylamide causes a distal degen of long axons in the CNS. what do the axonal swellings contain?

A

neurofilaments

106
Q

which toxin results in increased atherosclerosis?

A

carbon disulfide
(cellophane, rayon, viscose, adhesives)

107
Q

what are the crystals in ethylene glycol poisoning?

A

calcium oxalate

108
Q

what are the toxins a/w pain/varnish/glue solvents?

A

hexacarbons (distal axonopathy)
N-hexane and
Methyl N-butyl ketone

and
toluene (cerebellar atrophy)

109
Q

why is Methanol toxic?

A

formaldehyde/formic acid formation in the liver

110
Q

how does methanol cause blindness?

A

degeneration of retinal ganglion cells > optic nerve atrophy + gliosis

111
Q

besides vision, what else does methanol affect?

A

PUTAMEN
symmetric petechial hges/hgic infarcts in putamina!

112
Q

toxic oil syndrome & eosinophilia/myalgia syndrome are prob 2 manifestations of ingestion of what?

A

aniline derivatives

113
Q

what is the clinical for toxic oil syndrome/eosinophilia-myalgia syndrome

A

BIPHASIC
1. acute: systemic hypereosinophilia + HA, rash

  1. 3-6w: paresthesias, myalgias, weight loss, memory/cognition
114
Q

pathology of toxic oil syndrome/eosinophilia-myalgia syndrome

A

inflammatory vasculitis in PNS and skeletal muscle

also distal axonopathy with neurofilament accumulation

115
Q

toxin that results in cranial nerve AND peripheral nerve neuropathies

A

trichlorethylene (dry cleaning)

116
Q

5 toxic causes of bilateral BG necrosis

A
  1. CO
  2. cyanide
  3. methanol
  4. marchiafava-bignami (chronic alcohol)
  5. heroin (or other global cerebral hypoxia)
117
Q

3 metabolic causes of bilateral BG necrosis

A
  1. Leigh’s disease
  2. Infantile holotopisstic/bilateral striatal necrosis (duh)
  3. Wilson’s disease
118
Q

mechanism of CHRONIC nitrous oxide exposure

A

inactivates cobalamin > inhibits methionine synthase > SACD 2/2 cobalamin deficiency

119
Q

2 things to a/w amphotericin B tox

A
  1. parkinsonism
  2. multifocal necrotizing leukoencephalopathy
120
Q

what syndrome does clioquinol result in?

A

subacute myelo-optic neuropathy

121
Q

what is the overlap between clioquinol tox and rabies?

A

nodules of Nageotte (degen of DRG cells, proliferation of satellite cells which make little clusters)

122
Q

complication of L-asparaginase treatment

A

small cortical hgic infarcts 2/2 superior sagittal thrombosis

123
Q

histo of chasing the dragon

A

leukoencephalopathy with sparing of U-fibers

124
Q

how does botox work

A

inhibits ACh release at NMJ

125
Q

how does tetanus work

A

toxin (C. tetani) enters at NMJ then travels up axon (retrograde) and blocks release of GABA and glycine from spinal inhibitory interneurons

(no inhib = spasms/rigidity)

126
Q
A

Neuropath (6 decks)

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