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Neuro2 > pathophys > Flashcards

pathophys Flashcards

1
Q

primary HA

A

migraine, cluster, tension, misc - usually subacute presentation

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2
Q

phys of all HAs

A

inflamm or physical traction of pain sens nerve fibers

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3
Q

pain sens structures of the head

A

dura and meninges at base of brain, large arteries at base, meningeal arteries, venous sinuses, scalp muscles, upper cerv muscles, periosteum of skull, facial and head structures (eyes, skin, teeth, sinuses, muscles)

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4
Q

brain parenchyma is ___ to pain

A

insensitive

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5
Q

CNV1 innervates pain sens structures of

A

ant/middle cranial fossa and scalp

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6
Q

CNIX, X and C2/3 innervate

A

posterior fossa and cervical muscles, post scalp

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7
Q

pain sens fibers synapse

A

in trigem nucleus caudalis and dorsal horn of upper cervical cord

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8
Q

central pain fibers synapse

A

in VPL and VPM of thalamus and then head to sensory cortex

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9
Q

migraine

A

frequently unilateral, pulsating, mod/severe, 4-72hr, nausea and possible vomiting, photo and phonophobia, prodromal phase, may have aura (20%), specific triggers, family history

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10
Q

migraine prodrome experienced by ___

A

40%

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11
Q

migraine prevalence

A

15-25%. More common in women, usually begins before age 20. decreased occurrence after age 55

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12
Q

familial hemiplegic migraine

A

dominant gene

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13
Q

vascular changes associated with migraine mediated by

A

aff/eff trigem nucleus caudalis and superior salivatory nucleus

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14
Q

migraine aura phys

A

scintillations - excitation of calcarine cortex with cortical spreading depression following. Hyperemia followed by oligemia.

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15
Q

important NT in pathogen migraine

A

CGRP and SP (vasodilatory properties)

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16
Q

5HT1D R

A

peripheral neuron (trigem)

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17
Q

5HT1B/D/F R

A

central neuron (trigem)

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18
Q

5HT1B R

A

vascular terminals

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19
Q

actions of CGRP

A

dural artery, on mast cells, NT at a central trigem synapse

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20
Q

gepants

A

CGRP antagonists - decrease blood flow in cerebral vessels, block neurogenic inflammation, inhibit pain transmission

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21
Q

cluster HAs

A

unilateral pain, frontal, retro-orbital, unilat conj injection and rhinorrhea, unilat Horners and lacrimation, constant severe, non pulsating, duration ~ 3 mins, daily attacks for weeks then remission for yrs

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22
Q

epidem cluster HAs

A

M>W 4:1, onset ~ 25y/o, alc and tobacco are triggers, rare family hx

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23
Q

cluster HA tx

A

nasal oxygen, subcut sumatriptan. Prophylax with calc chan blockers, lithium, valproic acid, prednisone

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24
Q

Tension HA

A

bilateral/band dist, no aura, no N/V, no photophobia or phonophobia, duration minutes-3 hours. daily attacks <15days/month - episodic. More - chronic

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25
Q

Tx of tension HA

A

if chronic - refer to neurologist or HA expert. Episodic - usually OTC

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26
Q

Pseudotumor Cerebri - idiopathic intracranial hypertension

A

HA variable, papilledema, transient visual obscurations, diplopia secondary to CN VI paresis, tinnitus, visual field defects

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27
Q

Epi of Pseudotum cerebri

A

W>M 9:1 age 20-45. overweight individuals

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28
Q

pathogenesis of pseudotumor

A

primary idiopathic - inc CSF prod, dec reabsorption
primary symptomatic - hypervitaminosis A, antibiotics (tetracycline), steroid withdrawal
secondary - venous sinus thrombosis, chronic meningitis, chiari malformation

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29
Q

dx pseudotumor

A

MRI, LP - opening pressure >250 mm H2O, measure visual fields.

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30
Q

tx pseudotumor

A

weight loss! most effective but difficult, acetazolamide or furosemide to decrease CSF production, repeat LPs, optic nerve fenestrations, shunts, monthly f/u for visual system analysis.

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31
Q

Giant cell arteritis

A

autoimmune, systemic vasculitis causing granulomatous infiltration and occlusion of med/small elastic arteries. Associated with polymyalgia rheumatica

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32
Q

Giant cell arteritis sx

A

HA- unilateral, point scalp tenderness, visual sx

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33
Q

Giant cell arteritis dx

A

increased ESR, CRP elev, biopsy (inflamm and multinuc giant cells in elastic lamina)

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34
Q

Giant cell arteritis tx

A

start corticosteroids right away - emergency! perform bx ASAP

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35
Q

CNS tumor cure rate

A

65%

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36
Q

NF1 gene

A

chrom 17

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37
Q

NF2 gene

A

chrom 22

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38
Q

tuberous sclerosis gene

A

9q/16p

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39
Q

VHL gen

A

chrom3

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40
Q

Turcot

A

germline mut in APC

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41
Q

tumor in turcot

A

medulloblast, GBM

42
Q

tumor in VHL

A

hemangioblast

43
Q

tumor in tuberous scle

A

subependymal giant cell

44
Q

tumor in NF1

A

optic glioma, meningioma, ependymoma

45
Q

tumor in NF2

A

bilateral vestibular schwanomma

46
Q

cowden gene

A

PTEN, leading to hyperactive mTOR path

47
Q

tumor cowden

A

dysplastic gangliocytoma of the cerebellum

48
Q

tumor li fraumeni

A

astrocytoma and medulloblast

49
Q

li fraumeni gene

A

p53 mut

50
Q

nevoid basal cell carcinoma AKA gorlin syndrome gene

A

PTCH mut on chrom 9

51
Q

tumor in gorlin

A

medulloblastoma

52
Q

increased ICP triad

A

AM vomiting, HA, lethargy

53
Q

MC childhood brain tumor

A

low grade astrocytoma

54
Q

malignant astrocytoma

A

glioblastoma multiforme

55
Q

juvenile pilocytic astrocytoma histology

A

eosinophilic rosenthal fibers and hyalination of blood vessels

56
Q

juv pilo ast genetics

A

activating MAPK pathway, KRAS act, BRAF act etc.

57
Q

mut location for juv pilo ast

A

BRAF fusion - cerebellar; BRAF V600E - extracerebellar; NF1 loss in optic pathway

58
Q

medulloblast age peak

A

3-4 yrs

59
Q

medulloblast more common in

A

males

60
Q

if in cerebrum medulloblast is called

A

PNET

61
Q

medullo blast are 40% of

A

post fossa tumors

62
Q

medulloblast tend to spread

A

through CSF, also hard to get full resection, adjuvant therapy beneficial

63
Q

medulloblast hist

A

densely cellular, round, oval or angulated, low vascular, homer wright rosette

64
Q

pathways in medulloblast

A

SHH and Wnt, B cat can travel to nuc and is a trans activator. Wnt tumors have good prognosis, SHH tumors involving PTCH mut good prog in infants and intermediate if older. Myc amplification is very poor prognosis.

65
Q

brainstem glioma is

A

uniformly fatal in 18-24 months

66
Q

tx brainstem glioma

A

sx is contraind. radiation provides temp improvement, supportive care

67
Q

diffuse intrinsic pontine glioma prognosis

A

dismal, median age is 7

68
Q

sx of DIPG

A

long tract signs, ataxia, CN6,7,8 defecits

69
Q

dx of DIPG

A

MRI - engulfs basilar artery diffuse extension into pons

70
Q

tx DIPG

A

sx not possible, radiation prolongs life

71
Q

bx DIPG

A

No!

72
Q

ependymoma sites

A

60% post fossa, SC 10%

73
Q

highest incidence of ependymoma

A

first 7 yrs of life

74
Q

ependymoma hist

A

perivasc pseudorosettes of glial tumor cells radially arranged around blood vessels and true rosettes with tumors forming a lumen

75
Q

M:F ependymoma

A

1:1

76
Q

staging of ependymoma includes

A

CSF examination and spinal MRI

77
Q

absence seizure can be induced by

A

hypervent

78
Q

gen 3 Hz spike and wave discharges

A

absence seizure

79
Q

mc childhood seizure

A

febrile - 2-5% of kids in US

80
Q

peak febrile seziures

A

18 months age

81
Q

dx for first simple febrile seizure

A

LP, EEG, blood studies maybe. Don’t neuroimage

82
Q

febrile Status Epilepticus at increased risk

A

acute hippocampal injury

83
Q

febrile SE associated with

A

HHV-6B infection, HHV7 less often

84
Q

1st afebrile seizure

A

get EEG, bloodwork/tox maybe, LP if meningeal signs,

85
Q

epilepsy

A

occurrence of multiple unprovoked seizures separated by more than 24 hrs

86
Q

hypsarrhythmia

A

infantile spasms - high voltage chaotic activity between seizures. may have diffuse voltage dep during seizure

87
Q

West Syndrome

A

triad of infantile spasm, hypsarrhythmia, developmental arrest or regression

88
Q

what to give if infantile spasm is due to tuberous sclerosis?

A

vigabatrin (inhibits catab of GABA)

89
Q

Tx infantile spasm

A

ACTH, vigaba, topiramate, zonisamide, valproic, bnzs, ketogenic diet

90
Q

Lennox-Gastaut

A

onset 1-8 yrs, some pts have infantile spasms, triad of at least 2 seizure types (atypical), slowing of mental devel, slow spike and wave EEG

91
Q

EEG of Lennox-Gastaut

A

slow background, burst of diffuse slow spike and wave 1.5-2.5 Hz

92
Q

Lennox-Gastaut tx

A

valpro, lamo, topir, zoni, felb, bnzs, ketogenic diet, corpus callosotomy, vagus n stimulator

93
Q

childhood onset absence

A

3 Hz spike and wave, normal EEG background, occur mult times a day, onset 4-8yrs,

94
Q

absence tx

A

ethosux preferred, maybe valproic acid or lamo

95
Q

juvenile myoclonic epilepsy

A

adolescent onset, can be tonic clonic, myoclonic, or absence. myoclonic jerks worse in the morning. Lots of stim including photo, sleep dep, stress. req lifelong tx

96
Q

juvenile myoclonic epilepsy tx

A

valpro, topir, levetiracetam, lamo, zoni

97
Q

juvenile myoclonic epilepsy gen

A

thought to be au dom - chrom 6

98
Q

Benign rolandic epilepsy

A

mc form of benign partial ep in childhood, discharges from lower rolandic area. onset 4-12 yrs peaks at 9.

99
Q

Benign rolandic epilepsy presentation

A

nocturnal gen tonic clonic seizures

100
Q

Benign rolandic epilepsy respond to

A

carbamezepine or valproate, remit by 14-16 yrs old

101
Q

Benign rolandic epilepsy EEG

A

central temporal spikes

Neuro2 (6 decks)

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