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Neuro > Intro to Neuro > Flashcards

Intro to Neuro Flashcards

1
Q

Match: round and oval, oligodendrocytes and astrocytes (subset of glial cells)

A

astrocytes–>oval

oligodendrocytes–>round

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2
Q

What stain picks up astrocytes?

A

GFAP

gliofibrillary acidic protein

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3
Q

Describe selective vulnerability in astrocytes

A

set of neurons sharing 1+ properties responding to an insult (not necessarily located together)

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4
Q

What is the term for neurons that undergo acute neuronal response to injury?

A

RED neurons, less than 24 hours

earliest morphologic indicator of acute injury

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5
Q

Describe neurons in acute neuronal response to injury

A

pyknosis (cell body shrinks)

loss of nucleolus and nissl substance–> get fuzzy

intense eosinophilia in cytoplasm

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6
Q

What are some injuries that cause acute neuronal response to injury?

A

hypoxia
hypoglycemia
trauma

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7
Q

Describe subacute and chronic neuronal response to injury

A

DEGENERATION, progressive

best indicator of neuronal injury

cell loss and reactive gliosis

apoptosis

can have abnormal protein accumulation–> ALS, Alzheimers

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8
Q

When do you find gliosis?

A

chronic CNS injury, looks like scar tissue but not

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9
Q

What is the axonal reaction?

A

increased protein synthesis associated with axonal sprouting

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10
Q

What do neurons look like in an axonal reaction to injury?

A

enlarged, round cell body

peripheral displacement of nucleus

enlarged nucleolus

central chromatolysis: nissl removed from center of cell to periphery

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11
Q

When do you see central chromatolysis?

A

axonal reaction to CNS injury

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12
Q

What are neuronal inclusions?

A

accumulation of substances in neurons d/t injury or infection

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13
Q

What are examples of intranuclear neuronal inclusions?

A

Herpes–> Cowdry body

CMV–> Owl’s eye (both intranuclear and cytoplasmic)

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14
Q

What are examples of intracytoplasmic neuronal inclusions?

A

lipofuscin, proteins, carb

Rabies–> Negri body

Alzheimers–> neurofibrillary tangles

Parkinson–> Lewy body

CJD–> vacuolization of perikaryon and neuronal processes

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15
Q

Are chromatolysis and neuronal inclusions normal?

A

YES, normal process when injured

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16
Q

What is the most important histopathologic indicator of CNS injury?

A

gliosis

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17
Q

What is gliosis

A

hypertrophy and hyperplasia of astrocytes in response to CNS injury

also can cause gemistocyte formation

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18
Q

What act as metabolic buffers and detoxifiers in the brain, with foot processes contributing to the BBB?

A

astrocytes

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19
Q

What are bright pink astrocytes with enlarged, vesicular, dislocated nucleus and prominent nucleoli?

A

gemistocyte

what astrocytes can turn into during gliosis

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20
Q

When do you see Alzheimers 2 astrocytes?

A

hyperammonemia states (chronic liver disease)

wilson disease

hereditary metabolic urea cycle disorder

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21
Q

Describe Alzheimers 2 astrocytes

A

in gray matter

very large nucleus and nucleolus with pale staining

intranuclear glycogen droplet

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22
Q

What are 2 examples of reactive astrocytes?

A

gemistocytes

Alzheimers 2 astrocytes

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23
Q

Gliosis is a common reaction to what common supratentorial tumor of childhood?

A

craniopharyngioma

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24
Q

Describe craniopharyngioma

A

benign, slow growing supratentorial tumor

derived from remnants of Rathke’s pouch (ectoderm)

Calcification (can have teeth)

cholesterol crystals found in motor-oil fluid within tumor

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25
Q

Describe Rosenthal fibers

A

thick, elongated, pink (eosin), corkscrew/sausage structures in astrocytic processes

B crystalline and HSP27 with ubiquitin

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26
Q

Where are Rosenthal fibers found?

A

slow growing, benign process

areas of longstanding gliosis

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27
Q

What is a common tumor that you can find Rosenthal fibers in?

A

pilocytic astrocytoma

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28
Q

What is a disease that you can find Rosenthal fibers in?

A

Alexander disease

–> leukodystrophy; perivascular, periventricular, subpial rosenthal fibers

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29
Q

What polyglucosan bodies are found in normal aging?

A

corpora amylacea

increase with increased age

represent degenerative change

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30
Q

Describe corpora amylacea

A

PAS +

round, onion skin adjacent to end process of astrocyte

subpial and perivascular

glycosaminoglycan polymers with HSP and ubiquitin

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31
Q

What are the macrophages of the CNS and what markers are on their surface?

A

microglia

CR3 and CD68 (same as peripheral macrophages)

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32
Q

What are microglia responses to injury?

A

Proliferation

Elongated “rod cell” nuclei–> seen in neurosyphillis

Microglial nodules

Neuronophagia

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33
Q

When would you see elongated nuclei in microglia?

A

neurosyphillis

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34
Q

What are microglial nodules?

A

microglia aggregate around small foci of necrosis

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35
Q

What is neuronophagia?

A

microglia congregate around cell bodies of dying neurons

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36
Q

What are ciliated columnar cells that line ventricles?

A

ependymal cell

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37
Q

What are ependymal granulations?

A

small irregularities on ventricular surface (blebs off ependymal lining)

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38
Q

What damages ependymal cells and creates viral inclusions?

A

CMV

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39
Q

What is oligodendrocyte response to injury?

A

demyelinating disorder

leukodystrophies
–> progressive multifocal leukoencephalopathy (intranuclear inclusions)

–> multiple system atrophy with glial cytoplasmic inclusions of alpha-synuclein

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40
Q

Define cerebral edema

A

accumulation of fluid in brain parenchyma

can be vasogenic or cytotoxic

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41
Q

Describe vasogenic cerebral edema

A

increased extracellular fluid (d/t BBB disruption–> increased vascular permeability) causes shift from intravascular to intercellular spaces

NO LYMPH to resorb excess fluid

can be localized or generalized

often follow ISCHEMIC INJURY (d/t damaged vessel walls)

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42
Q

Describe cytotoxic edema

A

increased intracellular fluid secondary to neuronal, glial or endothelial CELL MEMBRANE INJURY
–> via generalized hypoxic/ischemic insult or metabolic derangement

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43
Q

What will you see structurally in cerebral edema

A

flattened gyri and narrow sulci (smooth surface)

ventricles compressed d/t fluid

can lead to HERNIATION

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44
Q

In clinical practice, you will see what types of cerebral edema?

A

both vasogenic and cytotoxic

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45
Q

What can cause herniation?

A

cerebral edema

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46
Q

Describe hydrocephalus ex vacuo

A

excess fluid as brain compensates for decreased brain mass (degenerative disease)

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47
Q

Describe the pathogenesis of hydrocephalus

A

increased production of CSF from choroid plexus papilloma (rare)

obstruction (exudate, tumor, blood clot, congenital stenosis/atresia, INFECTIONS)

decreased absorption d/t outflow obstruction (CSF doesn’t reach the point of absorption d/t block before it)

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48
Q

What are responses to increased CSF/hydrocephalus?

A

PAPILLEDEMA (increased ICP)

enlargement of third ventricle downward

stretching/perf of septum pellucidum that separates horns of ventricles

thinning of cerebral mantle

elevation of corpus callosum

dilation of frontal and temporal horns of ventricles

absorption in transventricular and nerve root sleeves

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49
Q

Craniopharyngioma can compress the optic chiasm leading to ________

A

bilateral hemianopsia

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50
Q

Pyogenic meningitis causes supprative exudate that covers the brainstem and cerebellum, thickens the leptomeninges and leads to ________

A

obstructive hydrocephalus

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51
Q

What are congenital causes of hydrocephalus?

A 
TORCH infections (preg)
agenesis/atresia/stenosis
AV malformation
Arnold Chiari malformations
Dandy Walker syndrome
cranial defects
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52
Q

What are acquired causes of hydrocephalus?

A

Infections–> meningitis, meningoencephalitis, cysticercosis

Mass lesions–> medulloblastoma, astrocytomas

Inflammation–> brain abscess

Post Hemorrhage–> IVH, SAH, injury

choroid plexus papilloma

hypervitaminosis A

idiopathic

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53
Q

What type of hydrocephalus occurs when CSF is not absorbed at dural sinus level and leads to symmetric dilated ventricles?

A

communicating

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54
Q

What hydrocephalus has normal CSF pressure?

A

hydrocephalus ex-vacuo

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55
Q

Why does the brain shrink in hydrocephalus ex vaco?

A

frontal atrophy with increased age

stroke or other injury

chronic neurodegenerative disease (alz, park, huntington)

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56
Q

What is the mnemonic for normal pressure hydrocephalus?

A

wet, wacky, wobbly

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57
Q

Describe normal pressure hydrocephalus

A

symmetric, blockage occurs slowly over time

over 60 years, mimics dementia of Alz and gait of Park

idiopathic (main) or secondary to hemorrhage, trauma, tumor, infection

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58
Q

Is normal pressure hydrocephalus reversible?

A

yes

59
Q

Symptoms of normal pressure hydrocephalus

A

gait disturbance–> magnetic gait, broad based

dementia (much less impaired recognition vs Alz but misdiagnosed anyway)

urinary incontinence

60
Q

How does increased ICP cause ischemia to the brain?

A

after brain can’t compensate anymore, venous sinuses have minimal blood to reduce pressure

cerebral swelling–> herniation that (depending on which kind) causes torsion of brainstem and reduced local blood flow to brain–> no perfusion to the brain–> death

61
Q

What can cause increased ICP?

A

generalized brain edema

expanding mass lesion (tumor, abscess, hemorrhage)

increased CSF volume

62
Q

What are the 3 types of herniations that can occur with increased ICP/CSF?

A

subfalcine (cingulate?

transtentorial (central vs uncal)

tonsillar

63
Q

What herniation can cause cardiac and respiratory depression?

A

tonsillar

cerebellar tonsils through foramen magnum–>compress brainstem

64
Q

What herniation compresses temporal lobe against tentorium?

A

uncal/transtentorial

65
Q

What herniation causes dilated pupil and impaired eye movement?

A

uncal type of transtentorial

compresses oculomotor nerve (CN 3)

66
Q

What herniation causes displacement of cingulate gyrus under falx and anterior cerebral artery compression?

A

subfalcine/cingulate

falx separates hemispheres

67
Q

What is a consequence of central vs uncal transtentorial herniation?

A

central–> Duret hemorrhage (fatal)

uncal–> Kernohan phenomenon

68
Q

Describe Duret hemorrhage

A

transtentorial herniation central/ downward so displaces brainstem caudally

ruture of paramedian basilar artery brances–> hemorrhagic lesions in midbrain and pons

often fatal

69
Q

Describe Kernohan phenomenon

A

compression of cerebellar peduncle d/t uncal transtentorial herniation–> makes notch in peduncle called Kernohan notch

ipsilateral hemiparesis or hemiplegia (on side of herniation)

70
Q

Why is the Kernhoan phenomenon unique

A

false localizing sign (injury on opposite side of brain to notch) and also ipsilateral sx

Right herniation–> causes notch in left peduncle–> right sided motor impairment

71
Q

Compare early vs late uncal herniation

A

early: ipsilateral blown pupil with contralateral heimparesis (d/t crossing fibers in peduncle)
late: Kernohan (contralateral blown pupil, ipsilateral hemiparesis)

If R herniation–> L Kernohan notch (compresses L side of peduncle which sends info to R brain)—> R hemiparesis

72
Q

What’s the effect of injury to cerebellum and cerebellar peduncles (generally)?

A

cerebellum affects ipsilateral side

cerebellar peduncle crosses fibers to cerebellum (attaches both) so contralateral

73
Q

Low partial pressure of oxygen

A

hypoxia

74
Q

Impairment of blood’s oxygen carrying capacity or inhibition of oxygen use

A

ischemia

75
Q

area of necrosis resulting from sudden insufficiency of arterial or venous blood supply

A

infarct

76
Q

what can cause cessation of blood flow

A

decreased perfusion pressure (hypotension)

small or large vessel obstruction

both

77
Q

Describe purkinje and pyramidal cell response to hypoxia

A

shrunken, eosinophilic, pyknotic (red neurons)

pyramidal cells of sommer’s sector (CA1 and CA2) have decreased number of cells

78
Q

What type of necrosis is found in the CNS (also abscesses)?

A

liquefactive

liquid viscous mass of dead tissue, no architectural remains

79
Q

What causes CNS liquefactive necrosis?

A

CNS infarct (all other organs have coagulative necrosis with intact architecture remains)

80
Q

What can you see histologically in cerebral infarction?

A

No myelin or decreased

dead red neurons

PMNs (neut, bas, eos)

macrophages (microglia)

gliosis

missing, pale neuropil (decreased cells)

81
Q

Define hygroma

A

separation of arachnoid from dura d/t contraction of underlying brain parenchyma s/p infarct

82
Q

Old vs new infarct

A

old: hygroma (may have shifted structures in brain) or cavitation
new: liquefactive necrosis

83
Q

Examples of posterior fossa anomalies

A

Arnold-Chiari (type 1 and 2)

Dandy-Walker

Joubert syndrome

Syringomyelia (syrix)

84
Q

What malformation creates a small posterior fossa

A

Chiari

85
Q

Which Chiari is more severe with a misshapen midline cerebellum with downward extension of vermis through foramen magnum?

A

type 2

usually has non-comm hydrocephalus (d/t aqueductal stenosis from entry into foramen magnum) and myelomeningocele

86
Q

Which Chiari is silent but d/t low lying cerebellar tonsil extension into vertebral canal?

A

type 1

87
Q

What malformation has an enlarged posterior fossa and expanded roofless fourth ventricle>

A

Dandy-Walker

88
Q

Is the cerebellar vermis present in Dandy-Walker?

A

no- absent or rudimentary

replaced by a cystic enlargement of 4th ventricle

89
Q

What syndrome has hypoplasia of vermis, elongation of cerebellar peduncles (molar tooth sign) and deepened interpeduncular fossa?

A

Joubert syndrome

90
Q

What can occur with Dandy Walker malformation?

A

non-comm hydrocephalus

spina bifida

91
Q

Describe syringomyelia/syrinx

A

fluid-filled, cleft-like cavity (cystic cavity) in the inner portion of the cord

–> loss of pain and temp in BL UE

92
Q

What fibers are damaged in syringomyelia?

A

spinothalamic tract (pain and temp) that cross the anterior white commissure

CAPE-LIKE distribution

93
Q

What is syringomyelia associated with?

A

Chiari type 1

94
Q

What forebrain anomaly has decreased number of gyri with a sooth, cobblestone surface?

A

lissencephaly

95
Q

What is microcephaly associated with?

A

fetal alcohol syndrome
HIV acquired in utero
Zika virus

96
Q

What has entrapment of meningeal tissue d/t irregularly formed, numerous gyri?

A

polymicrogyria

97
Q

What cause forebrain anomalies?

A

abnormal generation or migration of neurons

98
Q

What are neuronal heterotopias associated with?

A

epilepsy

neurons in inappropriate places

x chromosome

99
Q

What is cyclopia and arrhinenceophaly (absence of olfactory CN) associated with?

A

holoprosencephaly

incomplete separation of cerebral hemispheres midline (prosencephalon wk 5-6)

100
Q

What is holoprosencephaly associated with?

A

trisomy 13 and FAS

sonic hedgehog signaling pathway

101
Q

What does moderate holoprosencephaly have?

A

cleft lip/palate

102
Q

What is associated with bat-wing lateral ventricles?

A

agenesis of corpus callosum

MR or normal mentation

103
Q

What is the most common CNS malformation, when does it occur, and what is it due to?

A

Neural tube defects
–> normal close by day 28

folate deficiency

104
Q

What are examples of neural tube defects?

A 
spina bifida
meningocele
myelomeningocele
myeloschisis
anencephaly
105
Q

Define spina bifida/occulta

A

asymptomatic

failure of caudal neuropore to close (bones don’t fuse), no herniation of spinal cord

dura intact, tuft of hair common

106
Q

Define meningocele

A

only meninges (no neural tissue) protrude from opening in bone

107
Q

Define meningomyelocele

A

CNS tissue goes through opening in bone along with meninges

motor and sensory deficits of LE, bower and bladder implications, superimposed infections d/t exposed cord

108
Q

Define encephalocele

A

brain tissue extends through defect in cranium in posterior fossa (ball at back of head)

nasal glioma–> extension through the cribriform plate (ball between eyes)

109
Q

Define anencephaly

A

absence of most of brain and calvarium

d/t disruption of forebrain around 28 days

110
Q

Define myeloschisis

A

exposed, unfused neural tissue without skin/meningeal covering

111
Q

What is a non-progressive neuro motor defect a/w insult occurring during the prenatal and perinatal period?

A

cerebral palsy

112
Q

What perinatal brain injury causes spasticity, dystonia, ataxia/athetosis and paresis?

A

cerebral palsy

113
Q

What perinatal brain injury is seen in the germinal matrix of premature infants between the thalamus and caudate nucleus?

A

intraparenchymal hemorrhage

d/t fragile matrix in babies

114
Q

Describe intraparenchymal hemorrhage

A

germinal matrix of premies

goes into ventricles b/t thalamus and caudate nucleus, can progress to subarachnoid hemorrhage

115
Q

What perinatal brain injury is infarcts in supratentorial white matter of premies? What do the infarcts look like?

A

periventricular leukomalacia

chalky yellow plaques represent necrosis and calcification

116
Q

What is perinatal brain injury with extensive ischemic damage of white AND gray matter–> large destructive cystic lesions?

A

multicystic encephalopathy

cystic spaces with widespread ischemia

117
Q

What is a perinatal brain injury with perinatal ischemic lesions in the depths of sulci that lead to thinned-out gliotic gyri?

A

ulegyria

118
Q

Describe awake vs LOC skull fractures?

A

awake–>fall backward, so occipital fx

LOC–> pass out and fall forward, frontal fx

119
Q

What is a diastatic fracture?

A

fracture that crosses a suture

120
Q

How can you tell if a fracture is new or old?

A

newer fracture lines DON’T extend across previous fracture lines

121
Q

Describe a displaced or depressed skull fracture

A

Bone displaced into cranial cavity BY A DISTANCE weighs more than the thickness of a bone

122
Q

What is a good indication that you have a basal skull fx?

A

CSF drainage from ear or nose (oto/rhinorrhea)

raccoon eyes (orbital/mastoid hematomas)

hemotympanum

battle sign behind ears

123
Q

Are head injury and TBI synonymous?

A

NO

TBI is altered LOC w/ or w/o altered brain fxn d/t external mechanical trauma

124
Q

What causes chronic traumatic encephalopathy?

A

repeated head blows or concussive injuries

must be dx after death

125
Q

What is the pathology behind chronic traumatic encephalopathy?

A

tau build-up in brain w/ neurofibrillary tangles

depigmentation of substantia nigra

126
Q

What is a direct parenchymal injury?

A

hit to head–> crests of gyri most susceptible

contusion to brain (wedge-shaped, broad base at point of impact)

127
Q

What are the different types of contusions?

A

coup (contusion at point of impact)

contrecoup (opposite side of coup, seen in sudden deceleration)

plaque jaune ( old yellow-brown trauma lesions of countercoup in inferior frontal cortex, temporal and occipital lobes)

128
Q

Define diffuse axonal injury (DAI)

A

direct action of mechanical forces–> axonal swelling w/ or w/o focal hemorrhagic lesions

appear within hours and persist

increased microglia and degeneration of involved tracts (later on)

129
Q

What picks up DAI?

A

silver stain, APP (amyloid) or alpha-synuclein

130
Q

What can produce DAI even in absence of impact?

A

angular acceleration

–> why babies so easily get this when shaken, decreased myelin–> no structure or protection

131
Q

50% of people that have coma, even without cerebral contusions, have what?

A

DAI/ diffuse axonal injury

132
Q

Where can you see axonal spheroids?

A

DAI

133
Q

Shaken baby overview

A

shaking violently stops crying d/t brain damage

most don’t die but live with brain damage

several occasions–> second concussion syndrome (die hours after d/t DAI and brain swelling)

134
Q

How to recognize shaken baby syndrome

A

DAI/cerebral edema

subdural hematomas

retinal hemorrhages

subgaleal hemorrhages (extracranial)

microscopic iron (detect old bleed)

NEVER normal after shaking

135
Q

What type of hematoma is a/w skull fracture in adults, ARTERIAL, with rapidly evolving neuro sx (immediate intervention)?

A

epidural hematoma

middle meningeal artery rupture often

136
Q

What type of hematoma is a/w mild trauma, VENOUS, slowly evolving neuro sx with delay from time of injury?

A

subdural hematoma

137
Q

What type of hematoma is a/w SUDDEN ONSET of severe headache, rapid neuro degeneration and often secondary injury d/t vasospasm/reperfusion?

A

subarachnoid (trauma, AV malformation, aneurysm)

often on crests of gyri w/ contusions

138
Q

What is a common presentation for epidural hematoma?

A

transient LOC–> recovery/ lucid interval–> rapid deterioration d/t expansion

139
Q

Where can you see transtentorial herniation and CN III palsy?

A

epidural hematoma

expansion of blood against brain pushes it to side–> herniation

140
Q

What hematoma is seen in shaken babies?

A

subdural hematoma

141
Q

Crescent shaped vs Biconvex (almost circular) hemorrhages

A

subdural–> crescent

epidural–> convex

142
Q

Which hematoma crosses suture lines?

A

subdural

143
Q

What hemorrhage is most commonly caused by systemic HTN?

A

intraparenchymal hemorrhage

Neuro (18 decks)

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