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Neuro 2 > Trivia > Flashcards

Trivia Flashcards

1
Q

What is a stroke?

A

An injury to the brain from interrupted blood flow or bleeding. Produces abrupt onset of focal neurological deficits and inc. risk of permanent disability/death

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2
Q

What is a TIA?

A
  • abrupt focal neurologic deficits that resolve within 1 hour
  • warning sign of future stroke
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3
Q

What is a silent stroke?

A
  • abrupt onset of focal neurological deficits that resolve in more than 1 hour
  • structural change
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4
Q

What does the MCA supply?

A

primary sensory/motor - arm/face
FEF
Broca/Wernicke
Visual Radiation

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5
Q

What do the Lenticulostriate branches of the MCA supply?

A

internal capsule

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6
Q

What does the ACA supply?

A

mid-sagittal region - lower extremities

parietal lobe

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7
Q

What does the PCA supply?

A

mediate occipital lobe (visual radiations)

Deep - thalamus, hippo, corpus callosum

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8
Q

“Go to sleep” switch

A

VLPO: inc. in GABA that inhibits the other 6 arousal nuclei. Induces NREM

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9
Q

“REM-On” switch

A

PPT and LDT nuclei (ACh)

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10
Q

“REM-Off” switch

A

Locus Ceruleus (NE)

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11
Q

Somnogens

A

Adenosine
Cytokines (IL-1b, TNFa)
Melatonin

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12
Q

Presentation of a supratentorial tumor in kids

A

localized findings - seizures, hemiparesis

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13
Q

Presentation of midline tumors in kids

A

endocrinopathies + hydrocephalus (early AM HA, N/V, Lethargy)
** signs of hydrocephalus in kids: sundown eyes, CN6 palsy, bulging fontanelle

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14
Q

Dx of brain tumors

A

MRI > CT > Bone Scan (for mets)
MRI is good for distinguishing tumor,
CT is good for seeing calcification

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15
Q

MC pediatric tumors (frequency)

A

astrocytoma > PNET > glioma > ependymoma

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16
Q

What is the RAS and what composes it?

A
  • areas of the reticular formation that produces coma when damaged
  • known to receive collaterals from sensory afferents
  • intralaminar thalamic nuclei, midbrain, upper 1/3 of pons
  • close to the uncus and tentorium cerebelli
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17
Q

Lesion to the upper 1/3 of pons

A

causes coma with intact diencephalon

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18
Q

Pontine hemorrhage

A
  • causes coma if upper 1/3 of pons (intact vertical gaze but not horizontal gaze, flaccid quadriplegia, pinpoint pupils)
  • quadriplegia if lower 1/3 of pons
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19
Q

Arousal nuclei (ascending arousal system)

A
  1. Cholinergic: project to thalamus, inh thalamic firing to promote wakefulness. This is why anticholinergics make you sleepy.
  2. Monaminergic: project to cortex, inc signal from thalamus. Failure results in delirium.
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20
Q

VLPO

A

Sleep promoting center.
Uses GABA and galanin to inhibit the ascending arousal system
- where EtOH and Benzos work
- lesion causes insomnia

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21
Q

Narcolepsy

A
  • selective loss of orexin neurons in the posteriolateral hypothalamus
  • sleep attacks and cataplexy
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22
Q

Sleeping sickness

A
  • lesion to the region between PAG and VLPO
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23
Q

Feedback to the ascending arousal system

A
  • from thalamus, limbic system, frontal cortex
  • emotional memories
  • lesion causes apathy/indifference to stimuli (abulia/akinetic mutism)
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24
Q

Transtentorial/uncal Herniation

A
  • can be caused by epidural hematoma
  • Compresses:
    1. CN3 - ptosis/paresis
    2. Midbrain - lethargy, stupor, coma
    3. Descending motor pathways - contralateral/ipsilateral hemiparesis
    4. PCA - Contralateral hemianopia
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25
Q

Central herniation

A
  • bilateral subdural hematoma, hepatic encephalopathy
  • Causes:
    1. Lethargy - P on reticular gray in thalamus
    2. small reactive pupils - P on hypothalamus dec. SNS
    3. loss of pupil tone - P on EW nucleus in midbrain
    4. Cheyne Stokes respiration - apneic w. hyperventilation (call a code)
    5. decorticate (flexor) –> decerebrate (extensor)
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26
Q

Falcine herniation

A
  • unilateral mass effect pushing brain under falx cerebra

- compresses ACA –> parasagittal ischemic stroke

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27
Q

Major difference between structural and metabolic coma

A

Structural will cause early loss of pupillary reflex. Will happen much later in metabolic coma.

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28
Q

Signs/sx of metabolic encephalopathy

A
  • pupils remain reactive to light until end (except atropine, botulism, glutethemide)
  • asterix
  • multifocal myoclonus
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29
Q

What indicates a poor prognosis for coma?

A

non traumatic coma: absent pupillary light/corneal reflex by day 3
hypoxic coma: absent motor movements by day 3

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30
Q

Presentation/Labs of LMN Dz

A 
weakness
atrophy (denervation on EMG)
fasciculations
dec. reflexes
normal sensation
normal nerve conduction velocity
atrophic fibers on biopsy
dec. # motor units
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31
Q

Progressive bulbar palsy

A
  • similar to ALS presentation
  • tongue/palate weakness (muscles innervated by medulla neurons)
  • swalowing, phonation problems dominate
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32
Q

Progressive Lateral Sclerosis

A
  • similar to ALS presentation but more benign

- but mainly an UMN Dz

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33
Q

Spinal Muscular Atrophy

A
  • anterior horn dz
  • AR mutation on Chr 5 in the Survival Motor Neuron Gene (inc. copies = less severe)
    1. Infantantile: Werdnig Hoffman (AR, frog leg posture)
    2. Juvenile: Wohlfart-Kugelberg Welander (AR, pectoralis and thigh atrophy, arm hyperpronation)
    3. Adult Onset SMA (sporadic)
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34
Q

How can you differentiate a LMN dz from a myopathy? (esp for Wolfart Kugelberg Welander dz)

A
  • normal CPK means it’s not a myopathy

- EMG shows denervation changes in a LMN Dz

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35
Q

Etiology of ALS

A
  • most cases are idiopathic (inc. Glutamate activity)
  • MCC of genetic form is Chr 9 C90RF72 Expansion
  • familial: AD SOD mutation on Chr 21
  • juvenile: Ch 9, 2q33, 15q15, 8q21
  • with FTD: Chr 17
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36
Q

Pathology of ALS

A

gross: lack of myelin in CST and loss of anterior horn neurons
microscopic: Bunina bodies, eosinophilic inclusion bodies in anterior horn neurons, and inc. in ubiquitin

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37
Q

Presentation of ALS

A

LMN signs: weakness of distal muscles first, tongue atrophy
UMN signs: weakness, inc. reflexes, etc
Sensation is normal

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38
Q

Differential for ALS

A 
Rule out spondylosis via MRI
MSA
Hereditary Cerebellar Dz ( + ataxia)
Craniocervical tumors
Cervical canal dz
Post-Polio syndrome 
Polyglucosan body Dz (biopsy)
Tay Sach ( + ataxia)
Kennedy Dz (gynecomastia, bulbar muscular atrophy)
HyperPTH (look for inc. Ca)
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39
Q

Basic Rules of phototransduction

A
  1. Cells release NT when depolarized
  2. Light hyper polarizes photoreceptors
  3. Photoreceptors depolarize horizontal cells
  4. Horizontal cells hyper polarize photoreceptors
40
Q

Path of transduction via rods

A

rods –> alpha ganglion cells –> magnocellular of LGN (layers 1/2) –> 4Calpha of cortex via M Pathway

  • *space info to cortex**
    • rods are located peripherally
41
Q

Path of transduction of cones

A

cones –> beta ganglion cells –> parvocellular of LGN (layers 3-6) –> 4Cbeta of cortex via P pathway

  • *form info to cortex**
    • cones are located centrally
42
Q

Diabetic retinopathy

A
  • MCC blindness in working age adults
  • lose ALL vision (vs. MD)
  • high glucose changes vasculature and neurons (dec. photoreceptors and ganglion cells)
  • will see light spots (dec. blood flow), inferior optic disc (damaged blood vessels, edema)
  • dec. pericytes, BM thickening, inc. permeability
43
Q

Macular degeneration

A
  • MCC blindness in elderly
  • Age is the greatest risk factor
  • lose central vision from macular damage
  • damage to choroidal vasculature, breaks through RPE, gets to macula and distorts vision
  • dry form: Drusen, little vision loss often in one eye
  • dry can progress to wet: commonly both eyes
44
Q

What is the difference between trophia and phoria?

A

Trophia is a devision of visual axes that is always present. Phoria is present only when disrupting fusion (covering one eye).

45
Q

What is the difference between paralytic strabismus and non-paralytic strabismus?

A

Paralytic: adult, has diplopia but no amblyopia

Non-paralytic (comitant): early childhood type, has amblyopia but no diplopia (b/c brain suppresses one of the images)

46
Q

What eye muscles are intorters?

A

SR and SO

47
Q

What eye muscles are extorters?

A

IR and IO

48
Q

Diplopia

A
  • doubling of vision d/t misalignment of visual axes
  • CN paresis, dec. muscle response
  • deviation is greatest in the direction of action of weak muscle
  • relieved by closing one eye; monocular diplopia goes away with affected eye closed; usually cataracts
49
Q

Complete CN 3 palsy

A
  • no PaNS: non reactive pupil
  • eye is down and out w. ptosis (no levator palpebri)
  • vertical diplopia
  • paresis + HA = PCOMM aneurysm unless proven otherwise
50
Q

Microvascular CN 3 palsy

A
  • PaNS function is intact
  • motor paresis is the first sign
  • DM and HTN
51
Q

CN 6 Palsy

A
  • eye is in eso position from unopposed MR
  • horizontal diplopia
  • gaze toward weak side
52
Q

CN 4 Palsy

A
  • vertical/oblique diplopia w. spontaneous head tilt to opposite side
53
Q

First thing to do in ocular history

A

check visual acuity

54
Q

if change in vision is near/far distance

A

refractive error

55
Q

transient change in vision in 1 eye

A

papilledema (seconds)
TIA (5-10 min)
Amourosis Fugax

56
Q

transient change in vision in both eyes

A

basilar artery insufficiency

57
Q

recurrent scintillating scotoma

A

migraine

58
Q

vision loss + pain

A

optic neuritis
acute narrow angle glaucoma
uveitis
endopthalmitis

59
Q

vision loss - pain

A

cataracts
CRA/CRV occlusion
retinal detachment

60
Q

gradual progressive loss of vision

A

brain tumor

61
Q

sudden loss of vision in 1 eye

A

adult - vascular

young - optic neuritis

62
Q

visual loss but normal pupillary reflex

A

lesion posterior to LGN

63
Q

abnormal RAPD

A

lesion to optic nerve, optic chiasm, optic tract anterior to LGN

64
Q

lesion posterior to optic chiasm

A

homonymous hemianiopsia - field defect in contralateral side of both eyes
Congruous HH: occipital cortex lesion
Incongruous HH: more anterior

65
Q

optic neuritis

A
  • optic nerve dz in young/middle aged pts
  • presenting sign of MS
  • pt can’t see object directly but has to look to the side slightly
  • normal or swollen optic disk
  • abnormal RAPD in that eye
  • types: retrobulbar, papillitis (swollen OD)
  • improves in 3 weeks. tx steroids
66
Q

optic disk exam

A 
color
contour
circumference
cup size
spontaneous venous pulsations (can be physiologic)
retinal vessels
67
Q

pale optic disk and altitude hemianopsia

A

ischemic optic neuropathy (usually one eye)

68
Q

cherry red macula spot

A

(ischemic infarct in retina)

= central retinal artery occlusion

69
Q

large optic cups and glaucoma

A

optic atrophy

70
Q

Rx that can inc. ICP

A

tetracyclines

lithium (psych)

71
Q

chronic open ended glaucoma

A
  • inc. intraocular pressure, damage of optic nerve
  • enlarged optic cup, atrophy
  • early scomata
  • subtle visual field defects
72
Q

Where is high frequency sound localized in the inner ear?

A

on basilar membrane, near the base of the cochlea

73
Q

Where is low frequency sound localized in the inner ear?

A

on basilar membrane, near apex of cochlea (helicotrema)

74
Q

Meniere’s Dz

A
  • dec. resorption of endolymphatic fluid –> builds up and ruptures membrane –> endolymph and perilymph mix –> change in electrical firing
  • Sx: vertigo, sensorineural hearing loss, tinnitus
  • audiogram: inc. threshold for low frequencies first
  • Tx: low salt diet, diuretics
75
Q

Tympanic membrane rupture

A
  • conductive hearing loss commonly caused by infx or trauma
  • size of rupture determines hearing loss
  • audiogram: inc. threshold for esp 4000Hz
76
Q

Otosclerosis

A
  • inc. in abnormal bond growth around otic capsule can cause stapes fixation
  • conductive hearing loss that can b/c sensorineural
  • audiogram: inc. threshold for low frequencies
  • Tx: hearing aid or stapedectomy can help
77
Q

Vestibular Schwannoma

A
  • cerebellopontine angle compression that caused hearing loss with corrected vertigo
  • CN 8 compression is slow and CNS corrects it
  • inc. risk of CN 5 and 7 compression, hydrocephalus, damaged pyramidal tract (crus)
78
Q

Sensorineural vs. conductive hearing loss

A
  • conductive is structural blockage: Weber will lateralize to affected ear and Rinne will show BC > AC
  • sensorineural is damage to cochlea or auditory N: Weber lateralizes to normal ear and Rinne is normal BC > AC
79
Q

What can tympanometry be useful for?

A

diagnosis of otitis media and effusion

80
Q

Can sensorineural hearing loss be d/t damage to brain parenchyma?

A

not likely b/c redundancy (crossover) of afferents

81
Q

Peripheral vertigo

A
  • More common than central vertigo
  • Inner ear etiology (semicircular canal debris, vestibular nerve infx, Meniere)
  • positional testing: delayed horizontal nystagmus
82
Q

Central vertigo

A
  • Less common than peripheral vertigo
  • Brain stem or cerebellar lesion (stroke affecting vestibular nuclei or posterior fossa tumor)
  • directional change of nystagmus, skew deviation, diplopia, dysmetria.
  • Positional testing: immediate nystagmus in any direction. May change directions. Focal neuro findings
83
Q

Area supplied by ASA

A 
medial lemniscus
lateral CST
caudal medulla (hypoglossal n.)
PPRF/MLF
pontine nuclei
84
Q

Area supplied by PICA

A 
**lateral medulla**
vestibular nuclei
sympathetics
lateral spinothalamic tract
nucleus ambigus
spinal trigeminal 
inferior cerebellar peduncle
85
Q

Area supplied by AICA

A 
**lateral pons**
vestibular nuclei
sympathetics
spinal trigeminal 
cranial nerve nuclei
facial nuclei
cochlear nuclei
middle/inferior cerebellar peduncles
86
Q

Infantile spasms

A
  • general onset ped seizure
  • pyridoxine dependent, PKU, MSUD, Glutx def, tuberous sclerosis
  • 3-7mo
  • West syndrome: infantile spasm + hypsarrythmia + developmental arrest/regression
  • Flexor spasm + stomach crunch + Lightning attack
  • EEG: hypsarrythmia, inc amplitude delta waves, multifocal spikes
  • Tx: ACTH, Vigabatrin (Tuberous Sclerosis)
87
Q

Lennox Gastaut

A
  • general onset ped seizure
  • 1-8yo
  • atypical absence seizure + slow spike and wave (1.5-2.5Hz) EEG + developmental delay
  • Tx: Rufinamide, difficult to control, lifelong
88
Q

Childhood Absence Epilepsy (CAE)

A
  • general onset ped seizure
  • 4-8yo
  • Absence seizures with spike and wave 3Hz pattern
  • triggered by hyperventilation
  • normal neuro status
  • Tx: Ethosuximide, Benign outcome
89
Q

Juvenile Myoclonic Epilepsy

A
  • general onset ped seizure
  • adolescents
  • Ch 6 hereditary
  • precipitated by sleep deprivation, EtOH, stress, photic stimuli
  • absence (7-13yo), myoclonic (12-18yo, in AM), tonic clonic (13-20yo)
  • consciousness intact
90
Q

Benign Rolandic Epilepsy

A
  • MC benign partial epilepsy in kids
  • 4-12 yo w/peak 8-9yo
  • nocturnal general tonic-clonic seizures
  • facial motor ticks
  • EEG: central temporal spikes
  • Tx: carbamezapine, valproate, lacosamide
91
Q

Febrile Seizure

A
  • MC childhood seizure 18mo
  • absence of intracranial infx, metabolic change, or history of afebrile seizures
  • usually simple
  • 32% recurrence
  • first febrile: don’t do EEG, blood studies, imaging, or anticonvulsant therapy
  • LP doesn’t show CSF pleocytosis
92
Q

Work up of first non febrile seizure

A

determine if true or psychogenic

  • EEG recommended (focal slowing inc. recurrence)
  • LP, blood studies, imaging optional
  • Tx of first unprovoked dec. risk of 2nd seizure BUT NOT long term remission
93
Q

REM sleep

A

eye movements, muscle paralysis, inc. HR/BP/RR/T/BMR, vivid dreams, erection

inc. brain activity: amygdala, parahippo gyrus, anterior cingulate cortex
dec. brain activity: frontal cortex, posterior cingulate cortex

94
Q

Arousal pathways/nuclei

A

ACh - PPT + LDT - arousal beta waves (awake and REM)
NE - Locus ceruleus - wake, some in NREM, not in REM
DA - SN - wakefulness
5HT - Raphe Nuclei - wake, some in NREM, not in REM
H - tubulomammary nuc - wake, some in NREM, not in REM
O/H - lateral hypothalamus - inc. wakefulness

95
Q

Activation of VLPO

A

inc GABA neurons that inhibit the other 6 arousal nuclei, induce NONREM SLEEP

96
Q

Inhibition of VLPO

A

unbalanced wakefulness = INSOMNIA

97
Q

REM Sleep Behavior Disorder

A
  • loss of paralysis/atonia in REM sleep
  • MC men > 50
  • primary: alpha synucleopathy (like PD, PSP, MSA)
  • secondary to alc withdrawal, or inc. TCA/SSRI
  • Tx: clonazepam

Neuro 2 (6 decks)

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