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USMLE: step 1 > CNS > Flashcards

CNS Flashcards

1
Q

Cause of neural tube defects?

A

Low folate prior to conception

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2
Q

What is elevated AFP seen in ?

A

Neural tube defects

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3
Q

What does failure of posterior vertebral arch cause?

A

Spina bifida

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4
Q

Foramen of monro?

A

CSF from lateral to third ventricle

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5
Q

Cerebral aqueduct?

A

Drains 3rd - 4th ventricle

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6
Q

Presentation of aqueduct stenosis?

A

Enlarging head circumference in infant

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7
Q

Dandy walker?

A
  • Failed cerebellar vermis
  • Dilated 4th
  • Absent cerebellum
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8
Q

Arnold chiari?

A

Cerebellar tonsils through foramen magnum
Type 1: asymptomatic
Type 2: obstructed CSF flow

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9
Q

Cause of syringomyelia?

A

Cystic degeneration of spinal cord from:

  1. Trauma
  2. Arnold chiari
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10
Q

Where does syringomyelia usually occur?

A

C8 - T1

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11
Q

Presentation of syringomyelia?

A
  1. Loss of pain and temp
  2. Intact proprioception
  3. LMN signs in expands to lower motor horn
  4. Horner’s if lateral horn knocked out
    * **STT knocked out as this crosses in center where syrinx is DCP is preserved as syrinx is not hitting dorsal spinal cord
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12
Q

What occurs is syrinx knocks out lateral horn?

A

Horner’s

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13
Q

Polio?

A

Anterior motor horn damage = LMN signs

  1. Atrophy
  2. Weakness
  3. Flaccid paralysis
  4. Imparied reflexes
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14
Q

What is werdnig hoffman?

A

“Floppy baby syndrome”

Inherited degeneration of anterior motor horn: presents just like polio buy in baby

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15
Q

What is ALS?

A
  • ## Degenerative UMN and LMN (think ALS is hitting “all the motor horns”)
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16
Q

Destruction of what causes UMN and LMN signs?

A

LMN: anterior motor horn
UMN: lateral corticospinal tract

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17
Q

What is atrophy / weakness of hands early sign of?

A

ALS

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18
Q

How to tell ALS form syringomyelia?

A

In ALS, there is not loss of pain and temperature sensation

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19
Q

Cause of familial ALS?

A

Zinc-copper superoxide dismutase mutation

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20
Q

What is SOD?

A

“Superoxide dismutase”

  • Converts Oxide to hydrogen peroxide to prevent free radical damage
  • Loss of enzyme implicated in familial cases of ALS
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21
Q

What is friedreich ataxia?

A
  • Degeneration of spinal cord and cerebellum:
    1. Ataxia: cerebellar
    2. Vibratory / proprioceptive loss
    3. Lower extremity weakness
    4. Absent DTRs
    5. HOCM
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22
Q

Cause of freidrichs?

A

AR: GAA repeat in frataxin gene

- Responsible for iron regulation if out of order leads to ROS via fenton rxn

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23
Q

What are the leptomeninges?

A

“Light meninges”

- Pia and arachnoid that surround brain - what is inflamed in meningitis

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24
Q

Meningitis in non vaccinated infant?

A

H flu

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25
Q

Viral meningitis?

A

Coxsackie

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26
Q

Meningitis presentation?

A
  1. Headache
  2. Neck stiffness
  3. Fever
  4. Vomit
  5. Photophobia
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27
Q

Where is lumbar puncture?

A

L4-5: iliac crest

  • Cord ends at L2 and we dont want to hit this
  • Trying to hit subarachnoid that continues lower
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28
Q

What does LP go through?

A 
Skin 
Ligaments
Epidural 
Dura
Arachnoid
***DO NOT pierce pia
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29
Q

LP fluid diagnosis?

A

Bact: Neuts, low glucose
Viral: Lymph, normal glucose
Fungal: Lymphocytes, low glucose

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30
Q

CV ischemia or hemorrhage more common?

A

Ischemia

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31
Q

Mild global ischemia?

A

Transient confusion with complete recovery: seen in insulinoma dropping brain sugar

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32
Q

Severe global ischemia?

A
  • Brain necrosis from ischemia - death or coma
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33
Q

What does moderate global ischemia cause?

A

Watershed infarct

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34
Q

What are pyramidal neurons?

A
  • Layers 3/5/6 of cortex

- Highly vulnerable to ischemia “cortical laminar necrosis”

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35
Q

Areas vulnerable to moderate global?

A
  1. Pyramid 3/5/6 “cortical laminar necrosis”
  2. Pyramid of hippocampus
  3. Cerebellar purkinjes
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36
Q

Difference in transient ischemic attack and stroke?

A

TIA:

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37
Q

Cuase of pale and hemorrhagic infarct in stroke?

A

Pale: thrombosis
Hemorrhagic: embolism

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38
Q

Most common source of embolic stroke?

A

Afib LA: to MCA

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39
Q

What is lacunar stroke?

A
  • Hyaline arteriolosclerosis in small vessels of brain

- Most often in lenticulostriate vesicles feeding deep structures of brain

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40
Q

Microscopic progress of ischemic stroke?

A

Liquefactive necrosis in following steps:

  1. Red neurons: 12 -24 hours
  2. Neuts / microglia / granulation tissue (week)
  3. Fluid cyst surrounded by gliosis (Month)
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41
Q

What is gliosis?

A

Reactive astrocytes lining cystic space

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42
Q

What are microglials?

A

Macs in brain

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43
Q

Common cause of intracerebral hemorrhage?

A
  • Rupter of charcot bouchard microaneurysm from HTN
  • Usually impact basal ganglia
  • Also are occurring in lenticulate from atherosclerosis weakening walls
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44
Q

Most common area impacted by charcot bouchard microaneurysm?

A

Basal ganglia

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45
Q

Worst headache with xanthochromia on LP?

A

Subarachnoid

- Usually from berry in anterior willis at branch of anterior communicating artery

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46
Q

What does Berry lack?

A

Medial layer

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47
Q

2 berry aneurysm associations?

A
  1. Marfan’s

2. ADPKD

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48
Q

What is epidural hematoma?

A
  • Collection of blood on top of dura
  • From temporal bone fracture and rupture of MMA
  • High pressure surface so bleeds fast
  • Lense shaped lesion
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49
Q

What is talk and die syndrome?

A

Epidural hematoma

- Herniation of the hematoma causing this as the artery a is a high pressure circuit

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50
Q

Tonsillar herniation?

A
  • Cerebellar tonsils through magnum compressing brain stem

* Cardiopulmonary arrest

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51
Q

Subfalcine herniation?

A

Cingulate gyrus herniates under falx cerebri (butt crack of brain) compressing ACA

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52
Q

Uncal herniation?

A

Uncus of temporal lobe between cerebellum and brainstem causing:

  1. CN 3 compression: down and out with dilated pupil
  2. PCA compression: occipital infarct
  3. Pull on marmedian a.: brainstem hemorrhage
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53
Q

What happens if CN3 compressed?

A

Down and out dilated pupil

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54
Q

What myelinates axons?

A

CNS: oligodendrocytes
PNS: Schwann

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55
Q

What happens in demyelinating disorders?

A
  • Preserved axons with destruction of oligos or myelin

- Conduction velocity is greatly impaired

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56
Q

What is leukodystrophy?

A
  • Impairment of enzymes necessary to make myelin
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57
Q

What is metachromatic leukodystrophy?

A
  • Arylsulfatase deficiency: cannot degrade myelin so it accumulates in lysosomes
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58
Q

What is following:

Arylsulfatase deficiency: cannot degrade myelin so it accumulates in lysosomes

A

Metachromatic leukodystrophy

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59
Q

Krabbe disease?

A

Galactocerebrosidase B-galactosidase deficiency

- Galactocerebroside accumulates in macs

60
Q

What is following:
Galactocerebrosidase B-galactosidase deficiency
- Galactocerebroside accumulates in macs

61
Q

What is adrenoleukodystrophy?

A
  • Impaired CoA addition to long fatty acids

- Accumulation in adrenals and white matter

62
Q

What is following:

  • Impaired CoA addition to long fatty acids
  • Accumulation in adrenals and white matter
A

Adrenoleukodystrophy

63
Q

What is MS?

A

AI destruction of myelin AND oligodendrocytes

- HLA DR2 association

64
Q

MS presentation?

A
  1. Blurry vision in 1 eye
  2. Vertigo and scanning speech (brainstem)
  3. INO (MLF)
  4. Hemiparesis
  5. Bowel bladder sexual dysfunction
65
Q

What is MLF?

A

Connects CN III to VI
- When want to look left, CNVI fires pulling left Lateral rectus then shoots message to MLF telling CNIII to pull medial rectus of right eye in same direction

66
Q

How does MLF damage present?

A

“INO”

Left eye can look left, but bright eye cannot as VI can no longer communicate with III

67
Q

How to diagnose MS?

A 
MRI: multiple plaques
CSF: 
1. Oligoclonal bands 
2. Increased Ig
3. Lymphocytes
4. Myelin basic protein
68
Q

When are grey areas seen in white matter?

A

MS - this is AI destruction of myelin which is the white matter

69
Q

MS Rx?

A

Corticosteroids or acute and interferon B slows progress

70
Q

What causes subacute sclerosing panencephalitis?

A

Measles

- Viral inclusion bodies in grey matter (neurons) and white matter (oligodendrocytes)

71
Q

What is PML?

A

“Progressive multifocal leukoencephalopathy”

  • JV infx of oligodendrocytes
  • Usually from immunosuppression reactivating latent infx
  • Rapid neuro signs = death
72
Q

Central pontine myelinolysis presentation?

A

Locked in syndrom

73
Q

What does degeneration of cortical grey cause?

74
Q

What does degeneration of basal ganglia (deep grey) cause?

A

Movement disorder

75
Q

What is APP? Problem?

A

“Amyloid precursor protein”

  • Protein that receptor on neurons is derived from
  • Alpha break down is normal
  • Beta breakdown = deposition of A-beta-amyloid
76
Q

What is dementia?

A

Memory loss + cognitive dysfunction - loss of consciousness

77
Q

What type of neurologic deficits seen in alzheimer’s?

78
Q

What increases risk of sporadic alzheimer’s? Decreases?

A

Increases: Epsilon4 allele of APOE (Think, 4 is more so higher risk)
- Increases conversion of APP to beta form
Decreases: Epsilon2 allele of APOE

79
Q

Genetics of early alzheimer’s?

A
  1. Presenilin 1 mutation

1. Down syndrome: APP gene found on chromosome 21 so increased risk

80
Q

What is presenilin 1 mutation put you at risk for?

A

Early onset alzheimer’s

81
Q

What is diffuse cerebral atrophy with wide sulci / narrow giri?

A

Alzheimers

82
Q

What is hydrocephalus ex vacuo?

A
  • Apparent dilation of ventricles due to decreased brain mass
  • Seen in alzheimer’s
83
Q

What are neuritic plaques and what are they composed of?

A

Seen in alzheimer’s:

  1. A-beta amyloid from APP
  2. Entrapped neuritic processes
84
Q

What is cerebral amyloid angiopathy?

A
  • Deposition of AB amyloid in vessels of brain: weakens walls increasing risk of hemorrhage
85
Q

What are neurofibrillary tangles?

A

Composed of hyperphosphorylated TAU “microtubule associated proteins”

86
Q

Histo of alzheimers?

A
  1. Neurofibrillary tangles: hyperphosphorylated tau

2. Neuritic plaques: AP amyloid / Entrapped neuritic processes

87
Q

What is vascular dementia?

A
  • Decreased blood flow to brain = many micro infarcts and injury causing dementia
  • By product of moderate global ischemia: pyramidal neurons in 3/5/6
88
Q

What is Picks?

A
  • Frontal (behavioral issues) and temporal (language issues) degeneration sparing occipital and parietal
89
Q

What is dementia with early behavior and language problems seen in?

90
Q

2 presentations of tau and diseases?

A

Picks: round tau aggregates

Alzheimer’s: Neurofibrillary tangles: hyperphosphorylated tau

91
Q

What is parkinson’s?

A

Dopaminergic neuron loss in substantia nigra pars compacta (SNPC) of basal ganglia

92
Q

What is following:

Dopaminergic neuron loss in substantia nigra pars compacta of basal ganglia

A

Parkinson’s

93
Q

What is striatum?

A
  • Portion of basal ganglia sending +/- signals to cortex

- Receives input from cortex and SNPC

94
Q

What does dopamine from SNPC do to striatum?

A

D1 binding on striatum: increased cortical stimulation

D2: decreases cortical inhibition (increased stimulation)

95
Q

What can cause parkinson’s?

A

Usually idiopathic but can be caused by MPTP in illicit drugs

96
Q

Parkinson’s presentation?

A
  1. Pill rolling tremor at rest
  2. Cogwheel rigidity
  3. Expressionless face: can’t move muscles
  4. Brady / akinesia
  5. Shuffling gait / postural instability
97
Q

What are lewy bodies?

A

Inclusions seen in parkinson’s compose alpha synuclein

98
Q

Histo marker of parkinson’s?

A

Lewy bodies composed of alpha synuclein

99
Q

Is dementia seen in parkinson’s?

A
  • Can be a late sign

- If seen in first year diagnosis is lewy body dementia

100
Q

What is lewy body dementia?

A
  1. Parkinsonisms
  2. Hallucinations
  3. Dementia
    * **Cortical Lewy bodies: normally in SNPC in parkinsons
101
Q

When are cortical lewy bodies seen?

A

Lewy body dementia

102
Q

What is huntington’s?

A

Knocking out of GABAergic (inhibitory) neurons in caudate of basal ganglia
- Loss of inhibitory gaba = random firing on cortex = random movements (chorea)

103
Q

What is following:

Knocking out of GABAergic (inhibitory) neurons in caudate of basal ganglia

A

Hungtingons

104
Q

What is striatum composed of?

A

Caudate + Putamen

105
Q

What abuts the lateral ventricles?

A

Cauded nucleus with putamen cust under it: together they make the striatum

106
Q

Cuase of Huntington’s?

A

AD trinucleotide repeats of CAG

  • Anticipation seen: earlier in subsequent generations
  • Expansion is occurring during spermatogenesis
107
Q

Huntington’s presentation?

A
  1. Chorea
  2. Depression: suicide most common cause of death
  3. Demention
  4. Athetosis: slow, snake like movement of fingers
108
Q

What is normal pressure hydrocephalus?

A 
Increased CSF dilates ventricles strechting corona radiata causing:
1. Urinary incontinence
2. Dementia
3. Gait instability 
"Wet, wacky, wobbly"
109
Q

What is following:

  1. Urinary incontinence
  2. Dementia
  3. Gait instability
A

“Wet, wacky, wobbly”

- Normal pressure hydrocephalus

110
Q

Normal pressure hydrocephalus treatment?

A
  1. Lumbar puncture

2. Peritoneal ventricular shunt

111
Q

What are arachnoid granulations?

A

Outpouchings of arachnoid through dura to venous sinus allowing draining of CSF
- Decreased absorption here results in normal pressure hydrocephalus

112
Q

What is spongiform encephalopathy?

A
  • Degenerative disease from prions
113
Q

What is PrPC?

A
  • Alpha conformation of prions normally found in human brains
  • Conversion to beta pleated PRPSC = prions and spongiform encephalopathy
114
Q

Pathology of spongiform?

A
  1. Beta pleated PRPSC converts normal alpha PRPC into beta
  2. Beta sheets accumulate in cytoplasm
  3. Creates intracellular vacules
115
Q

When are intracellular vacuoles seen?

A

Spongiform encephalopathy

116
Q

What is CJD?

A
  • Sporadic form of spongiform encephalopathy

- Can arise from exposure to infected human tissue

117
Q

CJD presentation?

A
  1. Rapid dementia
  2. Ataxia
  3. Startle myoclonus
  4. Death in 1 year
  5. Spike wave complex on EEG
118
Q

What is startle myoclonus?

A

Involuntary contraction of muscle with minimal stimulus

119
Q

What is following:

  1. Rapid dementia
  2. Ataxia
  3. Startle myoclonus
  4. Death in 1 year
  5. Spike wave complex on EEG
120
Q

Which are the glial cells?

A
  1. Microglials
  2. Ependymal
  3. Oligodendrocytes
121
Q

Astrocyte tumor in kids and adults?

A

Kids: Pilocytic astrocytoma
Adults: Glioblastoma multiforme

122
Q

What is tentorium and what is significance relative to tumors?

A

Line in brain just above cerebellum:

  • Adult tumors occur above
  • Kids below
123
Q

What is GBM?

A

“Butterfly glioma”

  • GFAP
  • Astrocytic tumor in adults
  • Cerebral hemispheres crossing midline (corpus callosum)
  • Central necrosis with pseudopalisading and endothelial proliferation
124
Q

What is following:

- Central necrosis with pseudopalisading and endothelial proliferation

125
Q

When in GFAP seen?

A

GBM: glial marker

126
Q

What is meningioma?

A
  • Benign tumor of arachnoid cells
  • Seen in women: ER +
  • Round mass attached to dura: seizures
  • Whorled appearance and psammoma bodies
127
Q

What is following:

- Round mass attached to dura: seizures

A

Meningioma

128
Q
  • Whorled appearance and psammoma bodies
A

Meningioma

129
Q

Schwannoma?

A
  • Bening schwann cell tumor
  • CN VIII at cerebellopontine angle
  • S100 positive
  • NF2 bilaterally
130
Q

Tumor seen in NF2?

A

Schwannoma

131
Q

S100 +?

A

Schwannoma

132
Q

Oligodendroglioma?

A
  • Calcified in white matter of frontal lobes
  • Seizures
  • Makes sense in white matter as oligodendrocytes myelinate white matter
    “Fried egg appearance” Ol “EGG” odendroglioma
133
Q

Calcified in white matter of frontal lobes?

A

Oligodendroglioma

134
Q

Fried egg on histo?

A

Oligodendroglioma

135
Q

Cerebellar tumor in kids?

A

Pilocysticastrocytoma

136
Q

Pilocytic Astrocytoma?

A
  • Cerebellar in kids
  • Cystic lesion with nodule growing on it
  • Rosenthal fibers
  • GFAP +
137
Q

Rosenthal fibers?

A

Pilocytic Astrocytoma

138
Q

Medulloblastoma?

A
  • From granular cells of cerebellum
  • Small round blue cells: “Bluestoma”
  • Homer wright rosettes
  • Neuroectoderm in nature
  • Drop metastasis to spinal cord
139
Q
  • Small round blue cells

- Homer wright rosettes

A

Medulloblastoma

140
Q
  • Drop metastasis to spinal cord?
A

Medulloblastoma

141
Q

Ependymoma?

A
  • 4th ventricle in kids
  • Presents with hydrocephalus
  • Perivascular pseudo rosettes
142
Q
  • 4th ventricle in kids

- Presents with hydrocephalus

A

Ependymoma

143
Q
  • Perivascular pseudo rosettes?
A

Ependymoma

144
Q

Craniopharyngioma?

A
  • From epithelial remnants of rathke’s pouch
  • Optic chiasm compression = bitemporal hemianopsia
  • Often calcified
145
Q

What does upward protrusion of mouth become?

A
  • Protrusion is known as rathke’s pouch

A. pituitary

146
Q

What does downward protrusion of base of brain become?

USMLE: step 1 (15 decks)

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