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Neurology > Week 1 > Flashcards

Week 1 Flashcards

1
Q

ST contains which CN?

A

1 and 2

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2
Q

PF contains which CN?

A

3-12

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3
Q

Headache lesion at which level?

A

ST, PF or both

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4
Q

Nuchal rigidity level?

A

Spinal

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5
Q

Personality change level?

A

ST

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6
Q

ST lesion face? body?

A

face and body: both contralateral

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7
Q

seizures usually due to lesion at which level?

A

ST

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8
Q

PF lesion face? body?

A

face: ipsilateral
body: contralateral

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9
Q

bladder bowel disturbance due to what kind of lesion?

A

spinal, midline

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10
Q

glove and stocking distribution is what kind of lesion?

A

peripheral

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11
Q

cerebellar lesion leads to deficit on which side?

A

same side

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12
Q

Does the cell body reside in white or gray matter?

A

gray

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13
Q

Where can we find Nissl bodies?

A

Neurons, and maybe dendrites. NOT in axons

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14
Q

MAP2 found where?

A

dendrites

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15
Q

What kind of protein is found in axons?

A

Tau

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16
Q

What kind of substance can go through the BBB?

A

lipid soluble

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17
Q

What is reactive gliosis?

A

scar formation and repair in the brain in response to injury by astrocytes

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18
Q

What are ependymal cells responsible for?

A

They line the ventricular surface of the brain and are ciliated to enhance the movement of CSF along the ventricular space

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19
Q

What are the main immune cells in the CNS?

A

microglia. Think of them as CNS phagocytes

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20
Q

What happens to microglia in HIV patients?

A

They fuse to form multinucleated giant cells in the CNS

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21
Q

Microglia embryology origin?

A

from mesoderm

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22
Q

Guillain-Barre syndrome destroys what kind of cells?

A

Schwann

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23
Q

Name the layers of the nervous system (hint…starts with epineurium)

A 
Epineurium
Nerve
Perineurium (this is the layer that needs to be reattached in microsurgery)
Fascicle 
Endoneurium
Nerve fibers
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24
Q

BBB is formed by which 3 substances?

A

Tight junctions between capillary endothelial cells
basement membrane
astrocyte foot processes

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25
Q

NEural crest eventually forms

A

PNS neurons and Schwann

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26
Q

CNS neurons, ependymal cells, astrocytes, oligodendrocytes derived from what?

A

neuroectoderm

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27
Q

Mesoderm forms?

A

microglial, meninges, blood vessels

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28
Q

central chromatolysis is neuronal cell body reaction to what kind of damage?

A

axon

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29
Q

what are some distinct pathologic findings in central chromatolysis?

A

cell body swells “ballooned” neuron, nissl and nucleus are displaced

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30
Q

Axonal spheroid id also another marker of axonal damage. How does it occur?

A

axon is damaged, the flow system that shuttles molecules up and down the axon becomes impaired and shuts down. This leads to accumulation of material that results in a swollen profile

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31
Q

Amyloid precursor protein in response to axonal damage?

A

it becomes upregulated and accumulates

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32
Q

Distal/wallerian degeneration is due to what kind of damage?

A

descending tract degeneration secondary to damage upstream

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33
Q

“red, dead” neurons seen in which kind of damage?

A

acute ischemic cell change, which occurs due to ischemia/hypoxia to brain

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34
Q

Negri bodies in hippocampus seen in which type of infection?

A

rabies

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35
Q

intranuclear inclussions and reactive astrocytes seen in which disease process

A

SSPE (measles)

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36
Q

Ectoderm layers results in which two structures?

A

neural tube and neural crest

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37
Q

Mesoderm results in which two structures?

A

notocord and somites

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38
Q

Neural tube eventual derivative is…

A

brain and spinal cord

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39
Q

neural crest eventual derivative is…

A 
dorsal root ganglia
autonomic ganglia
melanocytes
adrenal medulla cells
craniofacial bone and cartilage
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40
Q

Somite eventual derivative is…

A 
skeletal muscle
catilage
tendons
dermis
endothelium
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41
Q

Notocord eventual derivative is…

A

Nucleus pulposus

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42
Q

End results of dorsal induction?

A

neural tube closes

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43
Q

Telencephalon includes

A

cerebrum and lateral ventricle

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44
Q

diencephalon includes

A

thalamus and 3rd ventricle

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45
Q

Metacephalon includes

A

pons, cerebellum, upper part of 4th ventricle

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46
Q

mesencephalon includes

A

midbrain and AS

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47
Q

Myelencephalon includes

A

Medulla and lower portion of 4th ventricle

48
Q

Alar plate vs basal plate gives rise to

A

Alar: dorsal, sensory
Basal: ventral, motor

49
Q

Migration occurs at weeks 12-20. In what direction do they migrate and what assists them in doing so?

A

Migrates from ventricles to cortex. Assisted by radial glial cells

50
Q

Tongue development 1st branchial arch forms what?

A

anterior 2/3 of tongue (sensation via CN V3, taste via CN VII)

51
Q

tongue development 3rd and 4th arches form?

A

posterior 1/3 (sensation and taste via CN IX)

52
Q

Taste CN?

A

7, 9 10

53
Q

Pain CN in tongue?

A

V3, 9, 10

54
Q

Motor in tongue CN?

A

12

55
Q

What is used as confirmatory test in neural tube defect?

A

elevated AChE in amniotic fluid (fetal AChE in CSF crosses defect into amniotic fluid)

56
Q

difference between meningocele and myelomeningfocele?

A

both have protruding meninges but myelomeningocele also has protruding spinal cord/nerve

57
Q

What is chiari malformation?

A

cerebellum and brainstem tissue into foramen magnum, usually with myelomeningocele

58
Q

Which type of Chiari is more severe and what are the symptoms?

A

II. more herniation of cerebellar tonsillar through foramen magnum with aqueduct stenosis and hydrocephalus. Paralysis below defect is often present

59
Q

Tethered cord syndrome is what? What are the symptoms?

A

congenital attachment of spinal tip, limits movement of cord. This becomes a problem as the child grows

Symptoms include bowel/bladder problems, lower extremity weakness

60
Q

Syringomyelia symptoms?

A

Cystic enlargement of central canal of spinal cord. spinothalamic tract most often affected due to crossing. Results in cape like bilateral loss of pain/temp sensation in upper extremities.

Associated mostly with Chiari I malformation

61
Q

Ancephaly due to?

A

malformation of anterior neural tube, no forebrain. brain elements damaged due to exposure to amniotic fluid. associated with DM type I mothers

62
Q

Encephalocele is what?

A

defect in skull allows herniation of blood tissue

63
Q

What is holoprosencephaly?

A

brain fails to cleave into two hemispheres. Occurs around week 5-6. No cleavage of prosencephalon during ventral induction

64
Q

Microcephaly due to?

A

failure of neuronal and glial proliferation. Associated with developmental delays

65
Q

Heterotropic gray matter is due to defect in?

A

migration. nodules of gray matter where it shouldn’t be, such as lining ventricular surface. Common cause of seizures. X linked disorder in girls (males are non-viable)

66
Q

What is lissencephaly

A

failure of migration of cells to surface, resulting in smooth brain surface without any gyri.

67
Q

Germinal matrix hemorrhage is bad because?

A

occurs in close proximity o ventricles. Most common cause of 2nd trimester abortions

68
Q

Periventricular leukomalacia is….

A

intrauterine hypoxia due to white matter infarct

69
Q

Cortical dysplasia is what

A

cortical neurons are arranged in abnormal way. can cause epilepsy

70
Q

Down syndrome neurons?

A

same number of neurons but less dendritic complexity

71
Q

Why are some skin problems associated with neuro problems?

A

skin and nervous system both develop from ectoderm

72
Q

Neurofibromatosis type I vs II?

A

I: nerve tumors, optic gliomas, pheochromocytomas, skin abnormalities, lisch nodules (pigmented iris). Mutated NF1 gene on chromosome 17

II:bilateral acoustic neuromas (schwannomas)

73
Q

Sturge-weber syndroms if what?

A

port wine stain typically in V1 distribution of face

abnormal blood vessels, loss of nerve cells and calification of cerebral cortex of brain on same side as birthmark

May cause seizures, mental retardation

74
Q

how to treat trigeminal neuralgia?

A

carbamazepine

75
Q

caused by blood vessel loop pushing on nerve?

A

trigeminal neuralgia

76
Q

Referred pain is mediated by what?

A

dorsal horn neuron

77
Q

Treatment for migraine?

A

Sumatriptan (5-HT agonist)

DHE (also a 5-HT agonist)

78
Q

How to triptans work to inhibit migraines?

A

release of CGRP at trigeminovascular junction is inhibited

79
Q

cluster headache symptoms

A

severe orbital pain with unilateral autonomic symptoms

80
Q

Whats the difference between cluster headahces and paroxysmal hemicrania?

A

paroxysmal hemicrania are shorter, maybe more frequent, no cycle pattern, INDOMETHACIN works

81
Q

Trigeminal neuralgia treatment?

A

Carbamazepine: epileptic drug, sodium channel blocker

82
Q

How to check and treat for temporal arteritis?

A
  1. Check ESR
  2. treat with steroids (prednisone)
  3. Confirm with temporal artery biopsy
83
Q

Describe transduction of pain

A

Step 1. Upregulation of voltage gated Na channels results in increased activity of Vanilloid receptor (TRPV1)–>calcium influx

84
Q

What’s step 2 of pain?

A

Transmission.
Calcium influx in presynaptic terminal of DRG neuron causes release of glutamate into synaptic cleft.
Glutamate binds AMPA receptors on postsynaptic dorsal horn neurons which triggers opening of Na channels and depolarization

85
Q

What contributes to vasodilation and increased vascular permeability of pain?

A

retrograde release of substance P and other NTs (such as CGRP) at site of injury

86
Q

What is the gate control theory?

A

Non-nocicpetive inputs (pressing on temples when you have a HA) blocks transmission of painful inputs, likely activating inhibitory interneurons

87
Q

What is the wind up phenomenon

A

repetitive firing of peripheral nociceptive fibers leads to increased activity of dorsal horn neurons

88
Q

What does substance P bind and what does that result in?

A

NK1 receptors. Results in inhibition of K efflux, which increases neuronal exitability

89
Q

Mechanism of opiods?

A

inhibit presynaptic calcium channels, activate post synaptic K channels

90
Q

Na/K ATPase pumps what in and what out?

A

3 Na out, 2 K in

91
Q

RMP becomes more positive if you open __ or ___channelas

A

Ca, Na

92
Q

RMP becomes more negative if you open ___or ____channels

A

K, Cl

93
Q

Increased extracellular (serum) K results in hyper or depolarization?

A

depolarization

94
Q

NT in synaptic cleft eliminated in what 3 ways?

A
  1. metabolism/degradation
  2. reuptake by astrocytes in CNS
  3. reuptake into nerve terminal via endocytosis or transporter
95
Q

L glutamate inhibitory or excitatory?

A

excitatory

96
Q

L glutamate binds what kind of receptor?

A

AMPA, NMDA

97
Q

What is te most important inhibitor?

A

GABA

98
Q

what does NMDA look like at resting state?

A

calcium channel that is blocked by Mg

99
Q

NMDA receptors need what to happen for activation to occur?

A

Glutamate binds AND
Glyine binds allosteric site AND
membrane depolarization to relieve Mg blockade

100
Q

Energy failure (hypoxia ex) leads to what?

A

ATP depletion results in failure of Na/K ATPase. RMP moves more positive and eventually Na channels inactivate so cells cannot initiate action potential. Depolarization also kick Mg out of NMDA receptor so that becomes activates. Loss of Na gradient leads to impaired reuptake of NTs by astrocytes. Glutamate still in synapse, binds NMDA receptor, Ca influx, cells accumulate Ca, results in cell death because Ca activates degrading enzymes

101
Q

Carbamazepine mech?

A

Na channel blocker

102
Q

LIdocaine mechanism

A

Na channel blocker

103
Q

Benzodiazepine mech

A

GABA agonist

104
Q

How do K channel blockers work?

A

slow/prolong repolarization, increase refractory period

105
Q

3,4 DAP mech

A

K channel blocker

106
Q

What is CSF made of

A

ependymal cells of choroid plexus

107
Q

What is papilledema?

A

increased intracranial pressure through ventricular system results in optic disc becoming enlarged

108
Q

When do you see papilledema?

A

sign of hydrocephalus

109
Q

What is normal pressure hydrocephalus?

A

increased subarachnoid space volume but no increase in CSF pressure

110
Q

Classic triad seen in normal pressure hydrocephlus?

A 
gait change (CSF stretches legs in motor cortex)
dementia
urinary incontinence (bladder regulation fibers affected)
111
Q

Hydrocephalus ex vacuo is what?

A

increased CSF in atrophy (think alzheimer’s)

112
Q

How does hydrocephalus ex cavuo differ from normal pressure hydrocephalus?

A

intracranial pressure is normal, triad not seen in hydro ex vacuo

113
Q

NEVER do a LP in what?

A

non communicating hydrocephalus or suspected intracranial mass

114
Q

Ventriculoperitoneal shunt may correct what kind of hydrocephalus?

A

communicating and non communicating. Dratin CSF via tube from ventricule to peritoneum of abdomen

115
Q

Third ventriculostomy shunt corrects what kind of hydrocephalus?

A

Non comunicating downstream from 3rd ventricles. Typically in cerebral aqueduct. Poke hole in floor of 3rd ventricle to drain CSF

116
Q

Layers that LP passes through?

A 
skin
superficial fascia
paraspinal mucle
ligamentum flavum
dura mater
arachnoid mater

Neurology (3 decks)

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