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17. Central Nervous System Pathology Flashcards

1
Q

Neural crest cells develop into what system?

A

PNS

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2
Q

Wall of the neural tube develops into what system?

A

CNS

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3
Q

Lumen of the neural tube develops into what?

A

ventricles, spinal cord canal

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4
Q

Neural tube defects associated with what (nutritional deficit)?

A

inadequate folate intake by mom prior to conception.

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5
Q

how can you detect a neural tube defect prior to birth?

A

elevated AFP (alpha-fetoprotein) in amniotic fluid and maternal blood.

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6
Q

anencephaly can result in what in the mother?

A

maternal polyhydramnios: since fetus is lacking CNS-controlled swallowing center, doesn’t swallow/resorb amniotic fluid: leads to polyhydramnios.

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7
Q

spinal bifida is failure of what to close?

A

posterior vertebral arch (caudal end of neural tube)

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8
Q

spinal bifida occulta is what?

A

almost-closed neural tube: leaves little tuft of hair or dimple

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9
Q

spinal bifida is what? what are the 2 types?

A

neural tube didn’t close; meningiocele (protrusion of meninges alone) or meningiomyelocele (meninges + spinal cord)

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10
Q

what is cerebral aqueduct stenosis?

A

congenital stenosis of the cerebral aqueduct

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11
Q

what does the cerebral aqueduct do?

A

drains fluid from the 3rd to 4th ventricles

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12
Q

what results from cerebral aqueduct stenosis?

A

accumulation of CSF -> hydrocephalus, large head circumference.

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13
Q

what is dandy-walker formation?

A

cerebellar vermis does not develop

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14
Q

how does a dandy-walker formation present?

A

very small cerebellum, massively dilated 4th ventricle, often hydrocephalus

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15
Q

what is an arnold-chiari malformation

A

congenital extension of the cerebellar tonsils through the foramen magnum

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16
Q

Type 1 vs Type 2 Arnold-chiari malformation?

A

Type 1: no sx

Type 2: obstruction of CSF flow -> hydrocephalus

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17
Q

in addition to hydrocephalus, what 2 other things can be associated with an arnold-chiari malformation?

A

meningiomyelocele, syringomyelia

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18
Q

what are the leptomeninges?

A

the Pia and the arachnoid layers. these are more fragile/light than the dura, which is DURAble!

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19
Q

from the brain to the skull, what is the order of the layers?

A

acronym = PAD: pia, arachnoid, dura

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20
Q

meningitis is inflammation of which layers?

A

the leptomeminges: pia and arachnoid.

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21
Q

in neonates, what are the 3 most common agents of meningitis?

A

Group B Strep, E Coli, Listeria monocytogenes. (BEL: babies come from BELlies!)

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22
Q

how do neonates get meningitis?

A

during birth/vag canal, from mom

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23
Q

how do we try to prevent neonatal meningitis?

A

by treating mom with abx if she has Group B strep.

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24
Q

most common cause of meningitis in children/teens? how does it get to the meninges?

A

Neisseria meningiditis. (also Strep pneumo) gets in via nasopharynx, gets into bloodstream, from there gets to meninges.

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25
Q

most common cause of meningitis in adults/elderly?

A

strep pneumo, N meningiditis

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26
Q

most common cause of meningitis in unvaccinated infants?

A

H flu

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27
Q

most common VIRAL cause of meningitis?

A

coxsackie virus via fecal-oral transmission

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28
Q

cause of meningitis in immunocompromised?

A

fungi

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29
Q

presentation of pts with meningitis?

A

classic triad: headache, neck stiffness, fever. may also see photophobia (esp with virus), vomiting, altered mental status

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30
Q

lumbar puncture: between what vertebrae? why?

A

L4-L5. spinal cord stops at L2, but subarachnoid space continues til S2

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31
Q

when doing LP, what layers will you cross?

A

skin, ligament, epidural space, dura, subdural space, arachnoid. NOT pia.

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32
Q

LP sample containing neutrophils with low glucose suggests what cause of meningitis?

A

bacterial: immune reaction, and they will eat the glucose

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33
Q

LP sample containing lymphocytes with normal CSF glucose suggests what cause of meningitis?

A

viral.

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34
Q

LP sample containing lymphocytes with normal glucose suggests what cause of meningitis?

A

fungal

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35
Q

how does the normal CSF glucose level relate to the normal serum glucose level?

A

CSF should be 2/3 serum glucose level.

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36
Q

complications of meningitis classically seen with what type of cause? why?

A

bacterial. because pus, inflammation will put pressure on the brain, causes herniation

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37
Q

what can brain herniation cause?

A

death

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38
Q

symptoms associated with healing from bacterial meningitis?

A

from healing, have massive fibrosis. this can cause:

  • hearing loss (nerve damage)
  • hydrocephalus (normal CSF path is blocked)
  • seizure (scarring to brain surface)
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39
Q

what are a few forms of dementia/degen disorders?

A

Alzheimers, Vascular dementia, Pick disease, Parkinson’s, Huntington’s, Normal Pressure Hydrocephalus, Spongiform Encephalopathy

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40
Q

basics of degenerative disorders: characteristic is loss of what? often this is due to what?

A

characteristic loss of neurons within the grey matter. often this is due to accumulation of proteins, which damages neurons

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41
Q

degen of the cortex leads to what, in general?

A

dementia (this is grey matter loss)

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42
Q

degen of the brainstem/basal ganglia leads to what, in general?

A

movement disorders (also grey matter loss, but not cortical grey matter)

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43
Q

Alz: onset is generally around what age? what happens to risk with age?

A

onset around 60. risk doubles every 5 yrs thereafter.

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44
Q

Alz: degen disease of what part of brain?

A

cortex

(mainly temporal lobes and hippocampus according to Swenson & other sources)

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45
Q

what is the most common degen disease?

A

Alz

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46
Q

Alz: clinical features

A
  • slow-onset memory loss, progressive disorientation
  • loss of learned motor skills, language
  • changes in behavior and personality
  • mute and bedridden; infection commonly causes death
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47
Q

Alz: focal neuro defecits?

A

not generally seen. no focal tremor, no ataxia, no chorea

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48
Q

what are the two basic types of Alz?

A

sporadic (seen in elderly) and early-onset

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49
Q

most cases of Alz are sporadic or early onset?

A

95% sporadic

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50
Q

sporadic Alz: what allele is associated with incr risk? decr risk?

A

ApoE4 - incr risk

ApoE2 - decr risk (remember 4>2 therefore greater risk)

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51
Q

risk factors for sporadic form of Alz?

A

age, ApoE4

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52
Q

risk factors for early-onset Alz?

A

mutations in presenilin 1 and 2 genes, Down’s syndrome

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53
Q

what is the connection between Down’s and Alz?

A

Downs: 3 copies of chromo 21.

Amyloid Precursor Protein is on that chromo

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54
Q

how does the Amyloid Precursor Protein lead to Alz?

A

APP is a receptor on neurons. it is broken down by either alpha-amyloid or beta-amyloid. if person has ApoE4 allele, APP will be broken down by beta-amyloid, and resulting protein cannot be broken down –> Alz.

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55
Q

Alz: appearance of gross brain?

A

diffuse cerebral atrophy with narrowing of gyri, widened sulci, dilated ventricles

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56
Q

Alz: what are the plaques made of? what is their appearance?

A

neuritic plaques: made of beta-amyloid and trapped neuritic processes. look like blobby/diffuse Lewy bodies?

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57
Q

Alz: how can amyloid deposits incr hemorrhage?

A

they may also deposit around vessels

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58
Q

Aside from neuritic plaque, what is a path feature of Alz?

A

neurofibrillary tangles: intracellular aggregates of fibers made of Tau.

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59
Q

why would Tau protein get tangled in Alz? what do these tangles look like?

A

in Alz, it is hyperphosphorylated, and cannot organize cellular microtubules in that state. flame-like tangles

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60
Q

Alz: what loss occurs in the nucleus basalis of Meynert?

A

loss of cholinergic neurons

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61
Q

Alz: how is diagnosis reached?

A

clinical dx, dx of exclusion until confirmation at autopsy

62
Q

what is the 2nd most common cause of dementia?

A

vascular dementia

63
Q

what is vascular dementia?

A

multifocal infarction and injury due to HTN, atherosclerosis, or vasculitis (all causing decr bloodflow to brain)

64
Q

why does vascular dementia cause memory loss?

A

decr blood flow to brain/hippocampus

65
Q

vascular dementia: selective damage to what areas?

A

areas of selective vulnerability, esp cortical layers 3, 5 and 6. Pyramidal neurons (grey matter)

66
Q

Beta-amyloid: intra or extracellular?

A

extracellular deposit

67
Q

Pick disease - what portions of the brain does it affect?

A

degenerative disease of the frontal and temporal cortex.

spares the parietal and occipital lobes

“Picks” the front

68
Q

pathologically, what is characteristic of Pick’s disease?

A

round aggregates of tau protein (Pick bodies)

69
Q

clinically, what does Pick dz look like?

A

behavioral and language symptoms, eventual progression to dementia

70
Q

Parkinsons: loss of neurons where? what type?

A

dopaminergic neurons in pars compacta/substantia nigra of basal ganglia

71
Q

what is dopamine used for? what pathway?

A

nigrostriatal pathway of basal ganglia uses dopa to initiate movement

72
Q

Etiology of Parkinson’s?

A

unknown. Some rare cases seen with illicit drug synthesis (MPTP exposure)

73
Q

Parkinson’s: clinical features?

A

TRAP: Tremor, Rigidity, Akinesia, Postural instability

74
Q

Describe the Parkinson’s tremor?

A

pill-rolling tremor at rest, disappears with movement. typical starts as unilateral and progresses to the contra side

75
Q

describe rigidity in Park?

A

cogwheel rigidity in the extremities

76
Q

describe the akinesia/bradykinesia in Park?

A

slowed voluntary movement, expressionless face

77
Q

describe the postural instability in Park?

A

shuffling gait, arms held close to sides, multi-step turns

78
Q

Park: characteristic pathology?

A

loss of pigmented neurons in SN, round, pink inclusions of alpha-synuclein in neurons (Lewy bodies)

79
Q

Park: feature of late disease?

A

dementia

80
Q

Early-onset dementia with parkinsonian features suggests what?

A

Lewy body dementia. characterized by dementia, hallucinations, parkinsonian features. histology reveals cortical (rather than basal ganglia)Lewy bodies.

81
Q

describe the normal initiation of movement

A

cortex sends signal to basal ganglia (striatum) which then either stimulates or inhibits the signal and sends it back to cortex. Basal ganglia also receives input from Substantia Nigra (dopamine).

82
Q

what is the typical effect of the substantia nigra/dopamine on movement?

A

typically acts between basal ganglia and cortex: increases stimulation, decreases inhibition. overall increases movement signal to cortex

83
Q

Park: how does the disease state decr movement?

A

decr dopamine in substantia nigra: not able to intervene as much to incr signal between basal ganglia and cortex for movement.

84
Q

typical age of onset for Huntington?

A

30-50

85
Q

Huntington: what is degenerating?

A

GABA neurons in caudate nucleus of the basal ganglia. results in larger ventricles (hydrocephalus ex vacuo)

86
Q

hunt: genetic cause?

A

expansion of trinucleotide repeats (CAG) in huntingtin gene

87
Q

Hunt: what is anticipation?

A

genetic phenomenon where an expansion of trinucleotide repeats yields disease state earlier for subsequent generations

88
Q

Hunt: common presentation?

A

chorea, progresses to dementia and depression

89
Q

Hunt: common cause of death?

A

suicide

90
Q

how does Hunt cause chorea?

A

loss of GABA (inhibitory) neurons at the caudate means a loss of movement inhibition. yields chorea

91
Q

what is the normal role of the caudate in movement?

A

normally the caudate and putamen inhibit movement via GABA neurons to the cortex

92
Q

what is Normal Pressure Hydrocephalus? etiology?

A

increased CSF leading to dilated ventricles, due to stretch and damage to paraventricular neurons. idiopathic

93
Q

what does normal pressure hydrocephalus cause?

A

dementia in adults.

94
Q

Normal Pressure Hydrocephalus: presentation?

A

Wet, Wobbly and Wacky: incontinence, gait instability, dementia

95
Q

Normal Pressure Hydrocephalus: treatment?

A

lumbar puncture can improve sx, or ventriculoperitoneal shunting

96
Q

how does Normal Pressure Hydrocephalus occur?

A

normally CSF is resorbed in the venous sinus via granulation. less resorbtion stretches the corona radiata nerves

97
Q

what is the most common spongiform encephalopathy?

A

Creutzfield Jacob disease

98
Q

what is spongiform encephalopathy?

A

degenerative disease due to prion protein. protein is normally in alpha-helical formation, but in disease states it converts to beta-pleated. not degradable.

99
Q

spongiform encephalopathy: general types of disease?

A

sporadic, familial, transmitted

100
Q

spongiform encephalopathy: pathology appearance?

A

intracellular vacuoles, spongy degeneration. damage to neurons and glial cells

101
Q

CJD: presentation?

A

rapidly progressive dementia associated with ataxia and startle myoclonus

102
Q

what is startle myoclonus?

A

involuntary contractions with minimal input

103
Q

CJD: what is seen on EEG?

A

periodic sharp waves

104
Q

CJD: prognosis?

A

death usually less than 1 yr

105
Q

what is Variant CJD?

A

due to exposure to bovine spongiform encephalopathy (mad cow)

106
Q

what is familial fatal insomnia?

A

inherited form of prion disease: severe insomnia, exaggerated startle response

107
Q

Foramen of Monroe: CSF goes through this from where to where?

A

Lateral ventricles into 3rd ventricle.

108
Q

CSF flows from 4th ventricle to subarachnoid space via what foramina?

A

Magendie and Luschka

109
Q

What is syringomyelia? What is it associated with/what can cause it?

A

Cystic degeneration of the spinal cord. Can be caused by trauma or associated with Arnold-Chiari malformation

110
Q

Syringomyelia: occurs in what portion of the spinal cord?

A

C8-T1

111
Q

What is the presentation of syringomyelia? Why does this presentation occur?

A

Presents in upper extremities. Sensory loss of pain and temp; sparing of position and fine touch. “Cape-Like”

Because of destruction of the anterior white commissure of the Spinothalamic Tract - Pain and touch from both sides ascends through this.

112
Q

In syringomyelia, if the cystic degeneration expands beyond the Anterior White Commissure, what structures can be damaged? What are the resulting symptoms?

A

Can damage lower motor neurons of the anterior horns. –> muscle atrophy and weakness, decr muscle tone, impaired reflexes

113
Q

in syringomyelia, if the degeneration expands to the lateral horn of the hypothalamospinal tract , what can result? what symptoms?

A

Can cause Horner syndrome: ptosis, miosis, anhidrosis of the face.

–> due to disruption of the lateral horn of the hypothalamospinal tract (sympathetic input to the face)

114
Q

what is poliomyelitis? what causes it/what sx?

A

Damage to the anterior motor horn due to poliovirus infection

Sx: lower motor neuron signs: flacid paralysis, muscle atrophy, fasciculations, weakness with decr muscle tone, impaired reflexes, negative Babinski.

115
Q

what is Werndig-Hoffman Disease? what causes it/what sx?

A

similar to poliomyelitis - but congenital

Inherited degradation of anterior motor horn

Presents as “floppy baby”. Death a few years after birth.

116
Q

Amyotrophic Lateral Sclerosis (ALS): what is the bottom line?

A

Upper and Lower motor neuron signs

Degenerative disorder of upper and lower motor neurons of the corticospinal tract.

117
Q

AMS: what causes the lower motor neuron signs? what are those signs?

A

Caused by anterior motor horn degeneration.

Signs are flaccid paralysis with muscle atrophy, fasciculations, weakness with decr muscle tone, impaired reflexes, negative Babinski.

118
Q

AMS: what causes the upper motor neuron signs? what are those signs?

A

Lateral corticospinal tract degeneration

Spastic paralysis, hyperreflexia, incr muscle tone, positive Babinski

119
Q

ALS: what is an early sign?

A

atrophy and weakness of hands

120
Q

ALS: what distinguishes it from syringomyelia?

A

ALS: no sensory impairment

Syringomyelia: loss of pain and temp due to degradation of the anterior white commissure (BIL pain/temp of spinothalamic tract). intact dorsal column-medial lemniscus.

121
Q

ALS: what causes the familial type?

A

mutation of SOD1 (zinc-copper superoxide dismutase). Causes decreased 02- –> H2O2, resulting in free radical damage to neurons

122
Q

Friedreich Ataxia: what is a basic description?

A

Ataxia + multiple spinal cord tract issues.

123
Q

Friedreich ataxia: what causes the ataxia?

A

degeneration of the cerebellum

124
Q

Friedrich ataxia: what is the ultimate cause of all the issues?

A

auto recessive: due to expansion of unstable trinucleotide repeat (GAA) in the frataxin gene. Frataxin is important for iron regulation in mitochondria: loss –> iron buildup and Free Rad damage.

125
Q

Friedreich ataxia: when does it present? what is it associated with?

A

Presents in early childhood

patients are wheelchair bound within a few years

associated with hypertrophic cardiomyopathy

126
Q

Friedreich ataxia: what tracts are involved? what sx?

A

multiple spinal cord tracts: loss of vibratory sense and proprioception, muscle weakness in lower ext; loss of deep tendon reflexes

127
Q

Spinothalamic tract: what does it do?

A

Pain and temp sensation from body

128
Q

Spinothalamic tract: First order neuron? where is cell body?

A

Peripheral nerves to posterior horn. Cell body is in dorsal root ganglion

129
Q

Spinothalamic tract: where is second order neuron?

A

from posterior horn, crosses over in anterior white commissure, ascends via spinothalamic tract to the thalamus

130
Q

Spinothalamic tract: third order neuron?

A

From thalamus to cortex

131
Q

DC-ML: what does it do?

A

Pressure, touch, vibration, proprioception

132
Q

DC-ML: first order neuron? cell body?

A

peripheral nerves to medulla via dorsal column.

Cell body is in dorsal root ganglion

133
Q

DC-ML: second order neuron?

A

arises from medulla, crosses, ascends via the medial lemniscus to thalamus

134
Q

DC-ML: third order neuron?

A

thalamus to cortex

135
Q

Lateral corticospinal tract: first order neuron?

A

Pyramidal neurons in cortex descend, cross over in medullary pyramids, and synapse on the anterior motor horn of the cord (upper motor neuron)

136
Q

Lateral corticospinal tract: what does it do?

A

voluntary movement

137
Q

Lateral corticospinal tract: second order neuron?

A

arises from anterior motor horn; synapses on muscle (lower motor neuron)

138
Q

Lateral corticospinal tract: third order neuron?

A

none!

139
Q

hypothalamospinal tract: what does it do?

A

sympathetic input of the face

140
Q

hypothalamospinal tract: first order neuron?

A

arises from hypothalamus, synapses on the lateral horn at T1

141
Q

hypothalamospinal tract: second order neuron?

A

arises from lateral horn at T1; synapses on the superior cervical ganglion (sympathetic)

142
Q

hypothalamospinal tract: third order neuron?

A

superior cervical ganglion to eyepids, pupil, skin of face

143
Q

Epidural hematoma: blood collects where? what shape? what structure has ruptured?

A

Blood collects between skull and dura

Convex/double clamshell shape due to attachment points

Ruptured artery (high pressure flow required to separate dura from brain); often Middle Meningeal due to temporal fracture

144
Q

Epidural hematoma: what is presentation?

A

lucid interval may precede neuro signs

Herniation is a lethal complication (bust through one of the attachment points)

145
Q

subdural hematoma: location? what has ruptured? shape?

A

Between dura and arachnoid (subdural)

rupture of bridging veins (this is a potential space, so even the low pressure veins can cause hematoma)

crescent shaped - can be diffuse

146
Q

subdural hematoma: presentation?

A

progresive neuro signs

herniation is a lethal complication

147
Q

subdural hematoma: incrased occurrence in what population?

A

Elderly: due to cerebral atrophy and stretching of bridging veins.

148
Q

Herniation: definition?

A

displacement of brain tissue due to mass effect (hematoma, tumor) or increased ICP

149
Q

tonsillar herniation: structures involved? causes what sx?

A

cerebellar tonsils into foramen magnum.

compression of the brain stem -> cardiopulm arrest!

150
Q

subfalcine herniation: structures involved? causes what sx?

A

cingulate gyrus moves under the falx cerebri

causes compression of the Anterior Cerebral artery: infarction

151
Q

uncal herniation: structures involved? causes what sx?

(three things are compressed)

A

displacement of temporal lobe uncus under the tentorum cerebri

  1. CN III compressed: eye moves down and out, pupil dilates due to loss of parasympathetics
  2. PCA compressed: leads to infarctin of occipital lobe -> contralateral homonymous hemianopsia
  3. paramedian artery rupture (brainstem) -> brainstem hemorrhage

x Pathoma (19 decks)

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