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Peds neuro boards, V2 > Cranial nerves > Flashcards

Cranial nerves Flashcards

1
Q
A
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2
Q

Only Cranial nerve that does NOT synapse with thalamus

A

Olfactory

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3
Q

Olfactory nerve pathway: fill in the blank

A
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4
Q

Foster-Kennedy Syndrome

  1. What causes it?
    1. Buzzword
  2. Key features
A
  1. Cause
    1. Typically frontal lobe lesion (classically optic groove meningioma; buzzword = SMO mutation)
  2. Features
    1. Ipsilateral optic nerve atrophy
    2. contralateral papilledema
    3. Ipsilateral anosmia
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5
Q

Pseudo Foster Kennedy syndrome

  1. What Causes it?
  2. What are the features of the disease?
A
  1. Cause
    1. Pre-existing optic nerve atrophy (i.e. from MS)
    2. Subsequent development of increased ICP
  2. Features
    1. Ipsilateral optic nerve atrophy = Yes
    2. Contralateral papilledema = Yes
    3. Anosmia = NO
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6
Q

Hemianopsia breakdown:

  1. Bitemporal hemianopsia, think ____
  2. Unilateral blindness, think_\_(3)___\_
  3. Altitudinal vison loss, think _____
  4. Central scotoma, ____
A
  1. Something pressing down on optic chiasm
    1. I.e. Pituitary tumors
  2. Unilateral blindness, think either opthalmologic, vascular (i.e. ischemic optic neuropathy), or autoimmune (i.e. optic neuritis)
  3. Altitudinal visual loss, think vascular (i.e. ischemic optic neuropathy)
  4. Central scotoma, think autoimmune (i.e. optic neuritis)
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7
Q

Visual Pathways of Brain (show left vs right)

A
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8
Q

Where are rods versus cones located in the eye?

What is the Foeva?

A

Rods (black and white, low-light) = Periphery

Cones (RGB) = in macula

Foeva = central part of macula with most cones

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9
Q

Blood supply to the eye

A
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10
Q

Types of Optic Neuropathy:

Presentation and exam findings

  1. AION (5)
  2. PION (2)
  3. Optic Neuritis (7)
  4. Leber’s optic Neuropathy (5)
A
  1. Anterior Ischemic optic neuropathy
    • Acute
    • painless or minimally painful
    • altitudinal visual loss
    • minimal recovery
    • Optic disc swelling on exam
  2. Posterior Ischemic optic neuropathy
    • Similar in presentation on exam to AION, but NO swelling on ophtho exam
    • less common than AION
  3. optic neuritis
    • subacute (hours - days)
    • often not complete blindness (recovery 2-4 weeks and continues to 12 months, 2/3 pts can improve to 20/20
    • centrocecal scotoma (Blind spot in center of vision)
    • red desaturation (90%)
    • APD
    • MRI may have enhancement (rarely seen in AION/PION)
    • Prolonged P100 on VEP
  4. Leber’s optic neuropathy
    • acute - subacute (weeks-months)
    • sequential in 3/4 pts (simulatneous in remaining 1/4)
    • painless
    • M>F (3:1-8:1)
    • onset in adolescence
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11
Q

Types of Optic Neuropathy

Associated conditions

  1. AION
  2. PION
  3. Optic Neuritis
  4. Leber’s hereditary optic neuropathy (2)
A
  1. AION
    1. Vascular risk factors
    2. temporal arteritis
  2. PION
    1. vascular risk factors
  3. Optic Neuritis
    1. Most commonly associated with MS and NMO
  4. Leber’s hereditary optic neuopathy
    1. Mitochonidrial disease
    2. associated withWold-Parkinson-white
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12
Q

Types of Optic neuritis (4)

A
  1. Retrobulbar: optic nerve
  2. Papillitis: optic disc
  3. Perineuritis: optic nerve sheath (no nerve involvement)
    1. More common in syphilis or sarcoid
  4. Neruonitis: swelling of optic nerve and macula
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13
Q

Function of Cranial Nerve III

A
  1. Extraocular movements
  2. Lifts Eyelids
  3. Constricts pupil
  4. Accomodates
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14
Q

Path of CN III

A
  1. Emerges betwen posterior cerebral artery (PCA) and superior cerebellar artery (SCA)
  2. Runs adjacent to posterior communicating artery (Pcomm) just below tentorium
  3. Runs through lateral wall of cavernous sinus
  4. Exits through superior orbital fissure
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15
Q

Pathway for Afferent pupillary defect

A

Due to damage to CN III, light does not constrict pupil when shown in affected eye. However, will dilate when light is shown in opposite eye due to concentual response through cilidary ganglion still intact

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16
Q

Blood supply for CN III

A
  1. Intracranial supply
    1. perforating branches of PCA
    2. Posterior communicating artery
    3. superior cerebellar
    4. basilar artery
  2. Extra cranial (after passing through Superior orbital fissure)
    1. opthalmic artery
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17
Q

sympathetic pathway for pupillary response

A

Note: NOT from CN III

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18
Q

Extra CNS causes for Myadriasis (3)

A
  1. Tumor at apex of lung (i.e. pancoast tumor)
  2. Impinging at carotid bifurcation
  3. Carotid sinus obstruction (w/ V1)
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19
Q

Required feature in CN III lesion to consider compressive lesion

A

Pupillary defect (CN III w/o pupillary defecect is NOT consistent with compressive lesion)

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20
Q

Head tilt in CN IV palsy

A

Head tilts away from side of palsy

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21
Q

Pathway of CN IV (3) and other factoid (1)

A
  1. Originates dorsally, then decussates
  2. Runs under tentorium, to the lateral wall of cavernous sinus
  3. Exits through SoF
  4. Note: longest CN course with the least # of axons
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22
Q

Symptoms of CN IV palsy (4)

A
  1. Vertical dypolpia worse with down gaze and adduction
  2. head tilt (away from Palsy)
  3. bielschowsky test
    1. symptoms Incrase with head tilt toward the lesion
  4. Diminished downgase
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23
Q

Causes of CN IV injury (3)

A

NOTE: lesions are CL to affected eye

  1. Congential
    1. most common cause of chronic
    2. typically CN IV dysgenesis
  2. Trauma
    1. MC acquired
  3. Compressive
    1. Infectious
    2. autoimmune
    3. neoplastic
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24
Q

Syndromes associated with CN VI palsy

  1. A (5)
  2. B (4)
  3. C (6)
  4. D (6)
  5. E (1)
A
  1. Mobius Syndrome
    1. Bilateral CN VI injury
    2. inability to smile, frown, grimace, or blink (CN VII)
    3. micrognathia / microstomia
    4. +/- chest wall, limb, corneal abnormalities
    5. autism (1/3)
  2. Millard-Gubler
    1. Pontine lesion
    2. IL CN VI palsy
    3. IL facial weakness
    4. CL hemiparesis
  3. Foville syndrome
    1. Result of AICA infarct (most commonly)
    2. IL CN VI
    3. IL facial weakness
    4. CL hemiparesis
    5. CL sensory loss
    6. INO
  4. Wallenberg syndrome
    1. injury of lateral medulla
      1. IL CN V
      2. vertigo
      3. hoarseness / dysphagia
      4. horner syndrome
      5. Hemiparesis
      6. Balance issues
  5. Sturge Weber
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25
Q

Exits of CN V and which go through cavernous sinus?

A

SRO

  1. V1 (opthalmic) - Supieror orbital Fissure
  2. V2 (maxillary) Foramen Rotundum
  3. V3 (mandibular) foramen Ovale
    1. Joined by motor root

V1 and V2 go through cavernous sinus, but V3 does not

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26
Q

Motor innervations of CN V

A
  1. Masseter (bilateral)
  2. temporalis (bilateral)
  3. tensor tympani (unilateral)
  4. Medial / lateral pterygoid
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27
Q

Innervations of CN VII
Motor (2)
autonomic (3)
Sensory (2)

A
  1. Motor movements
    1. IL face
    2. Stapedeus = decreases loud sounds
  2. Parasympathetic
    1. lacrimal
    2. submandibular
    3. sublingual
  3. Taste
    1. anterior 2/3 of tongue (tractus solitarius)
  4. Sensation
    1. Posterior surface of external ear and canal
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28
Q

What non-bony, non-vascular structure does CN VII pass through?

A

Parotid gland

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29
Q

Ramsay-Hunt syndrome

  1. What causes it?
  2. What other CN can be involved?
  3. Treatment (2)
A
  1. Zoster infection of geniculate ganlion / auditory canal vesicles
  2. may also cause vertigo / hearing loss (VNII run close together here
  3. Antivirals +/- Steroids
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30
Q

Blepharospasm versus hemiphacial spasm

Blepharospasm

  1. What is it?
  2. Causes (3)

Hemifacial spasm

  1. What causes it?
  2. symptoms
A

Blepharospasm

  1. Repeated involuntary contractures of obicularis oculi muscles
  2. Common causes
    1. Idiopatchic = meige syndrome
      1. Blepharospasm + orobmandibular dystonia
        1. sustained grimacing around mouth
        2. Platysma contracture
        3. sustained nec flexion
    2. MS
    3. MSA

Hemifacial spasm

  1. lesion near CP angle (MC)
  2. symptoms
    1. insidious onset of unilateral painless, arrhythmic, tonic or clonic spasms
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31
Q

Anti-hypertension medication known to cause hearing loss

A

Loop diuretics such as furosemide

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32
Q

Rinne / Weber Tests

A
  1. Rinne
    1. Tuning fork on mastoid, then ear
      1. Bone conduction > air = conductive
      2. Bone conduction < air = sensorineural
  2. Weber
    1. Tuning fork in middle of calvarium
      1. Sound better in impaired ear = conductive
      2. sound better in normal ear = sensorineural
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33
Q

Brainstem auditory evoked potentials

A
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34
Q

Abnormalities in BAER and associated diseases

A
  1. Brain Death
    1. Wave I may still be present
  2. CP angle Tumor
    1. (-) wave 1
    2. or (+) wave I, but prolonged latency I-III or I-V
  3. MS
    1. Prolonged latency of I-III or III-V
35
Q

Central (6) Versus Peripheral (4) Vertigo

A

Central

  1. nystagmus in any direction
  2. lack of symptom resolution with eye fixation
  3. persistent balance problems
  4. focal neurologic symptoms
  5. less severe
  6. longer duration

Peripheral

  1. More severe
  2. shorter duration
  3. more likely to have nausea and vomiting
  4. unidirectional nystagmus
36
Q

List of ototoxic medications (4)

A
  1. Loop diuretics (i.e. furosemide)
  2. Cisplatin
  3. High-dose Aspirin
  4. Aminoglycosides (gentamicin)
37
Q

Exits through skull of:

Vagus

Glossopharyngeal

Accessory

Hypoglossal

A
  1. Glossopharyngeal (IX) - jugular foramen
  2. Vagus (X) - jugular foramen
  3. Accessory (XI) - jugular foramen
  4. Hypoglossal (XII) - Hypoglossal canal
38
Q

Functions of Glossopharyngeal nerve (3) and how to test it

A
  1. Sensory
    1. posterior 1/3 of togue
    2. pharynx
    3. middle ear
    4. carotid sinus
  2. parasympathetic
    1. parotid
  3. Motor
    1. stylopharyngeus (involved in swallowing)
  4. Test by - + gag reflex
    1. also inovles IX b/c it’s invovled in Afferent function
39
Q

Functions of Spinal Accessory Nerve

A
  1. Motor
    1. Sternocleidomastoid
      1. (turns head away from nerve)
    2. Trapezius
      1. shoulder shrug
      2. Lesion = lowered at rest on affected side
40
Q

Functions of Vagus Nerve

  1. Parasympathetic (3)
  2. Motor (3)
  3. Sensory (4)
A
  1. Parasympathetic
    1. Decreases HR
    2. Decreases BP
    3. Bronchoconstriction
  2. Motor
    1. Pharynx
    2. Larynx
    3. Uvula (will result in CL uvular deviation)
  3. Sensory
    1. pharynx
    2. larynx
    3. external ear / canal
    4. posterior fossa meninges
41
Q

Important localization note regarding inability to turn head a certain direction

A
  1. Lesion of peripheral CN XI > right SCM doesn’t function > head can’t turn left
  2. Left frontal (supranuclear) lesion could cause similar deficit.
42
Q

Components traveling inside the cavernous sinus (5)

A
  1. CN III (with parasympathetic fibers)
  2. CN IV
  3. V1, V2, but not V3
  4. CN VI
  5. ICA (with sympathetic fibers)

CN II travels adjacent but not IN the sinus

43
Q

Common CP angle tumors

(7)

A

Think of the troll “SMMELCH” who lives tucked in the CP angle

  1. Schwannoma
  2. Meningioma
  3. Mets
  4. Epidermoid (primary cholesteatoma)
  5. Lipoma
  6. Choroid plexus papilloma
  7. Hemangioma (if present, think VHL)
44
Q

Parasympathetic Innervation of the Eye

  1. Nucleus A
  2. Nucleus B
A

​CN III > Edinger Westphal Nucleus > Ciliary body

  1. Afferent

CN VII > superior salivatory nucleus (lacrimal nucleus > Pterygopalatine ganglion

  1. Efferent
45
Q

Structures exiting throught he Superior Orbital Fissure

A

Live Frankly To See Absolutely No Insult

  1. Lacrimal branch of V1
  2. Frontal Branch of V1
  3. Trochlear
  4. Superior division of occulomotor
  5. Abducens
  6. Nasocilliary branch of V1
  7. Inferior division of occulomotor
46
Q

Common origin of trigeminal Nerve

A

Semilunar ganglion

47
Q

Nerves passing through the Cavernous Sinus

A
  1. Oculomotor (CN III)
  2. Trochlear (CN IV)
  3. V1
  4. V2
  5. Abducens (CN VI)
48
Q

Nucleus Ambiguus

  1. Location
  2. contains cell bodies of ____
A
  1. medullary reticular formation
  2. Contains motor fibers from
    1. Vagus nerve (branchial)
    2. glossopharyngeal nerve
    3. spinal accessory nerve
49
Q

Gottfredson’s syndrome

  1. Cause (2)
  2. Symptoms (2)
A
  1. Malignancy
    1. MC = metastatic tumor of clivus
    2. Second MC = infiltrating nasopharyngeal carcinoma
  2. IL abducens palsy (can’t abduct eyes)
  3. IL glossopharyngeal palsy (IL tongue deviation)
50
Q

Vernet’s Syndrome

  1. AKA
A
  1. AKA “jugular foramen syndrome”
  2. Symptoms
    1. Pharyngeal paralysis (IX, X, XI)
    2. Laryngeal paralysis (X, XI)
    3. SCM / Trapezius dysfunction (XI)
51
Q

Cranial nerves passing through jugular foramen

52
Q

Components of Gag reflex

Motor:

Sensory:

A
  1. Motor = vagus nerve
  2. Sensory: Glossopharyngal
53
Q

Adie’s tonic pupil

  1. Mechanism behind injury
  2. Symptoms (4)
A
  1. denervation of parasympathetic ganglion
  2. Symptoms
    1. dilated pupil > sluggishly reactive pupil + increased accomodation
    2. hypersensitivity to constrictive agents
    3. veriform movements at pupillary border
    4. Segmental iris constriction
54
Q

Nucleus Tractus Solitarius

  1. Components to Caudal(2) versus rostral (3) portion
A
  1. Glossopharyngeal
    1. Caudal portion
      1. visceral sensory fibers through glossopharyngeal nerves from carotid sinus baroreceptros
      2. internueurons then travel to dorsal motor nucleus of vagus
    2. Rostral portion
      1. viseral sensory fibers through chorda tympani (from facial nerve (anterior 2/3 of tongue)
      2. glossopharyngeal nerve posterior 1/3 of tongue
      3. vagus nerves (from epiglottis)
55
Q

Patient with diplopia worst when looking down likely has _____

A

Trochlear nerve palsy

head tilt, affected eye is elevated in primary gaze

Worse when tilting head toward side of involved eye

56
Q

Mnemonic for trochlear nerve

A

four D’s of cranial nerve IV

  • *D**ouble vision worse when looking Down
  • *D**orsal brainstem exit point
  • *D**ecussates in medulla
57
Q

How to worsen a patient’s diplopia if it is mainly in lateral gaze

A

Abducens palsy

exacerbated by looking toward the lesion

58
Q

A patient unable to make tears in right eye has pupillary dilation when you pinch his neck.

what does this exclude?

A

Horner’s syndrome (Afferencts in C2 and C3)

59
Q

Non-standard facial nerve lesions,
where is the lesion if:

Tearing is still present
hearing is normal
NO facial weakness but no taste or salivation
only loss of taste to anterior 2/3 of tongue

A

Tearing still present = after geniculate ganglion

hearing normal = after nerve to stapedius

NO facial weakness but no taste / salivation = after splits to chordae tympanae

ONLY loss of taste = after submandibular ganglion

60
Q

Relationship between Parotid gland and Two different cranial nerves

A

Innervated by Glosopharyngeal nerve

but facial nerve passes through it

61
Q

Uvula deviation to the left

What cranial nerve lesion and what side?

A

Right (contralateral) Vagus nerve

62
Q

Label the following

63
Q

Nerves exiting through superior orbital fissure

A

“Live Frankly To See Absolutely No Insult”

L-Lacrimal branch of V1

F - Frontal branch of V1

T - Trochlear nerve

S- Superior division of oculomotor nerve

A - abducens

N - nacosiliarry branch of V1

I - Inferior division of oculomotor nerve

64
Q

Components of Gag reflex (brain + Afferent + Efferent)

A

Brain region: nucleus ambiguus

Afferent: glossopharyngeal

Efferent: Vagus

65
Q

Gag reflex results and damaged cranial nerves

  1. Unilateral rise, no response on other
  2. soft palate rises when either side is touched, but only to one side
  3. No response on either side when one side is touched, but symmetric rise when other side is touched
A
  1. Unilateral rise, no response on other
    1. both glossopharyngeal and vagus nerve damaged on paralyzed side
  2. soft palate rises when either side is touched, but only to one side
    1. vagus nerve affected (pulls toward NON-affected side)
  3. No response on either side when one side is touched, but symmetric rise when other side is touched
    1. Glossopharyngeal nerve is damaged on side that DOESN’T respond to touch
66
Q

Cranial nerve most likely injured in:

head trauma

increased ICP

Ischemia:

A

Head trauma: CN IV (exits posteriorly, longest course of all extraocular moves)

Increased ICP: CN VI

Ischemia: VI (less commonly CN III, but important boards question due to pupil changes)

67
Q

cranial nerve anatomy: cross

68
Q

Patient presents with Left-sided CN III palsy and Right-sided contralateral hemitremor

What was injured?
What is this called?
What artery was injured

A

Injured: Red nucleus and CNIII fascicle
It’s called Benedikt’s syndrome

69
Q

Patient presents with Left CN III palsy and contralateral hemiparesis?

What was injured?
what is it called?

A

Injured: Fascicle and pyramidal tract of CN III
Called Weber syndrome

70
Q

Patient presents with Left-sided CN III Palsy and Cerebellar ataxia
What was injured?
What is it called?

A

Injured: fasicle and superior cerebellar Peduncle

Called Nothnagel’s syndrome

71
Q

Named syndromes: Cranial IL CN III palsy and…

CL hemitremor
CL Hemiparesis
Cerebellar ataxia
Both hemitremor AND cerebellar ataxia

A

CL tremor = benedikt’s syndrome

CL hemiparesis: weber’s syndrome

Cerebellar ataxia: Nothnagel’s syndrome

Both tremor and ataxia: Claude’s syndrome

72
Q

Syndromes:
Patient presents with CN VI palsy and:

CN VII palsy and CL hemiparesis:

CN V palsy + CN VII palsy + CL horners

A

CN VI palsy + CN VII palsy + CL Hemiparesis: Millard-Gubler

CN VI palso + CN V palsy + CN VII palsy + CL horners: Fovile’s syndrome
(Lesion of V, VI, and VII sympathetics)

(VI and VII fascicles + pyramidal tract)

73
Q

Patient presents with vertical gaze palsy and convergence restraction nystagmus:

What two additional finding would you expect to confirm diagnosis?

A

Vertical gaze palsy + convergence retraction nystagmus +

  • *lid retraction + pupillary light/near dissociation with BIG pupils** =
  • *parinaud’s syndrome (aka Dorsal midbrain syndrome:**
74
Q

Light-near dissocation with _____ pupils =

BIG pupils

Small pupils

tonic pupil

A

Big pupils = Parinauds syndrome
(convergence retraction nystagmus + vertical gaze palsy + Convergence retraction nystagmus + lid retraction

Small pupils = argile robinson pupil
(accomodates but does not react)

tonic-pupil: adies tonic pupil

75
Q

Patient looks like this when asked to look to the right but positive doll’s eye maneuver

what is it?

A

frontal lobe stroke

76
Q

Patient presents with vertical gaze palsy but intact doll’s eye maneuver looking down

What disease do you suspect?

A

Supranuclear palsy = steel-richardson disease

Parkinsonism / PSP

77
Q

what is this?

A

Intranuclear opthalmoplegia (limitation of adduction)

Damage of median longitudinal fasciculus (MLF)

78
Q

what is damaged?
What side?

what is it called?

A

Damage to parapontine reticular formation (PPRF) + VI nucleus

NOTE: side damaged is the side that has total palsy (i.e. eye that cannot adduct)

(one-and-a-half syndrome)

79
Q

Patient presents with: right-sided headache, right horners, right vision loss, diplopia, and contralateral hemiparesis

What is damaged?

What typically causes this?

What is a common hobby for these people?

A

Carotid artery dissection

typically in setting of trauma

Commonly seen in Long distance bike-riding

(always rule out when you have a painful horners)

80
Q

Child presents with horners.

What is one way to differentiate between acquired and congenital disease?

Why is it important?

A

hypomelanation = congential

acquired = rule out neuroblastoma

81
Q

Test for tonic pupil and what is the result?

A

Dilute pilocarpine: will constrict if affected

82
Q

“pie in the scky” homonymous field defect =

A

Temporal lobe lesion

83
Q

Key feature differentiating horners from carotid dissection compared to other causes (spinal cord syrinx, lung cancer, etc.)

A

if sweat function is not impaired, think carotid artery.

(also often painful, but above is anatomically the “true” statement)

84
Q

what non-opthalmic feature could you see if patient present with this field defect?

A

Olfactory / gustatory hallucinations

(“pie in the sky” field cut in temporal lobe lesion)

in this case; right

Peds neuro boards, V2 (29 decks)

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