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PT 680 Clinical Medicine > Vestibular Anatomy, Pathology, and Test > Flashcards

Vestibular Anatomy, Pathology, and Test Flashcards

1
Q

what detects movement of endolymph

A

cupula

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2
Q

tilted slightly upward from horizontal and primarily detects forward and backward movement (walking)

A

utricle

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3
Q

tilted slightly off vertical and detects up and down movement primarily (sitting –> standing)

A

saccule

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4
Q

calcium carbonate crystals aka

A

otoconia

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5
Q

does the fast phase of nystagmus go toward active or inhibited side

A

active

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6
Q

where are cell bodies of the vestibular branch of CN 8 found

A

scarpa’s ganglion

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7
Q

what does the superior vestibular N communicate with

A

anterior and lateral SCC
utricle

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8
Q

what does the inferior vestibular N communicate with

A

posterior SCC
saccule

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9
Q

where does CN 8 exit and enter

A

exit: internal auditory canal with CN 7 and labyrinthine A
enter: brainstem at pontomedullary junction

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10
Q

what do the 4 vestibular nuclei in the brainstem have connections to

A

cerebellum
reticular activating system
CN 3, 4, 6

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11
Q

the vestibular nuclei on the two sides of the brainstem are connected to each other via _____ resulting in one combined message to CNS

A

commissural fibers

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12
Q

where does lateral vestibular nucleus receive information from and where does it project it to

A
  • from: maculae of utricle
  • to: lateral vestibulospinal tract
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13
Q

indirectly influences LMN that innervate antigravity extensors through vestibulospinal reflex (VSR)

A

lateral vestibular nucleus

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14
Q

where does the medial vestibular nucleus receive information from and where does it project it to

A
  • from: cristae ampullaris
  • to: medial vestibulospinal tract
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15
Q

indirectly influences LMN that stabilize the head through the vestibulocolic reflex (VCR)

A

medial vestibular nucleus

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16
Q

name for the cupulla and hair cells

A

cristae ampullaris

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17
Q

where does the superior vestibular nucleus receive information from and where does it project it to

A
  • from: cristae ampullaris
  • to: MLF
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18
Q

coordinates movement of eyes and head through vestibulo-ocular reflex (VOR)

A

superior vestibular nucleus

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19
Q

where does the inferior vestibular nucleus receive info from and where does it project to

A
  • from: cristae ampullaris and maculae in utricle
  • to: cerebellum
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20
Q

influences balance and postural awareness through the medial and lateral vestibulospinal tracts

A

inferior vestibular nucleus

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21
Q

what is a major recipient of information in and out of vestibular complex; primarily involved in adjust and maintaining calibration of VOR and static and dynamic posture via VSR

A

cerebellum

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22
Q

information from the vestibular complex is relayed where on cerebellum

A

cerebellar vermis aka flocculonodular region

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23
Q

lesions to cerebellum cause what

A

produce gait and truncal ataxia and nystagmus (central vestibular dysfunction)

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24
Q

allows SCC input (head velocity) to be used for orientation after head movement stops; after cupula stops being deflected, signals are still being interpreted as movement in vestibulocerebellum and vestibular nucleus

A

velocity storage –> could be why when you stop spinning and cupula returns to normal that you still see nystagmus and feel spinning

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25
Q

list the final destination areas of vestibular input

A
  • brainstem complex (for reflex responses)
  • thalamus –> partietal lobe and insular cortex
  • 2 descending extra-pyramidal tracts (medial and lateral vestibulospinal tracts)
  • hippocampus (for spatial mapping)
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26
Q

what arteries supply the vestibular system

A

All major A - vertebral, basilar, PICA, AICA, labyrinthine, anterior vestibular, posterior vestibular A

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27
Q

what does the anterior vestibular A supply

A

anterior and lateral SCC
utricle

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28
Q

what does the posterior vestibular A supply

A

posterior SCC
saccule

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29
Q

what artery supplies the peripheral vestibular system

A

anterior inferior cerebral artery (AICA)

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30
Q

what reflex allows us to visually fixate

A

vestibulo-ocular (VOR)

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31
Q

maintains image stationary on retina (high speeds) during head movements

A

VOR

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32
Q

what is the only reflex that works at high speeds

A

VOR

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33
Q

without the VOR, images would blur –> what is another name for blurred vision

A

oscillopsia

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34
Q

what is vestibular gain of VOR

A

1:1
eye movement : head velocity

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35
Q

equal but opposite head and eye relationship

A

vestibular phase VOR

36
Q

what is the bundle of axons that carry information to CN 3, 4, and 6

A

medial longitudinal fasciculus (MLF)

37
Q

what vestibular nucleus controls VOR

A

superior vestibular nucleus

38
Q

occurs when visual, somatosensory, and vestibular systems work appropriately and seamlessly, normal postural control engages and balance occurs subconsciously; somatosensory and visual cues are compared with vestibular cues to produce compensatory oculomotor and postural responses

A

sensorimotor integration

39
Q

is the process of the CNS continuously determining/adjusting the percentage of input needed from each of the 3 sensory system (visual, somatosensory, vestibular) to remain upright

A

sensory reweighting

40
Q

neurologic conditions that occur with vestibular system

A

neuritis/labyrinthitis/vestibulopathy (peripheral vestibular deficit)
central vestibular dysfunction (TBI, stroke, MS, PD)

41
Q

mechanical condition with vestibular system

A

Benign paroxysmal positional vertigo

42
Q

structural conditions with vestibular system

A
  • superior canal dehiscence
  • perilymphatic fistula
43
Q

space occupying lesion with vestibular system

A

vestibular schwannoma/acustic neuroma

44
Q

occurs due to damage directly to CN 8

A

peripheral vestibular lesion

45
Q

peripheral vestibular lesion s/s

A

hearing loss, tinnitus, imbalance, episodic sx with movement

46
Q

describe the nystagmus associated with peripheral lesion to vestibular system

A
  • nystagmus does not change direction
  • nystagmus amplitude increases when looking toward fast phase (alexander’s law)
  • nystagmus decreases with visual fixation
47
Q

amplitude of nystagmus increases when looking toward fast phase

A

Alexander’s law –> peripheral lesion sx

48
Q

UVL

A

unilateral vestibular lesion complete/incomplete

49
Q

what are the causes of peripheral vestibular lesions

A

viral
herpes simplex virus, EBV, mumps, rubella

50
Q

what nerve is affected with labyrinthitis and state presentation

A

vestibulocohlear N
hearing affected

51
Q

what nerve is affected with neuronitis/neuritis and presentation

A

superior vestibular N
hearing NOT affected

52
Q

neuronitis or labyrinthitis

A

vestibulopathy

53
Q

what can we dx peripheral vestibular lesions as as a PT

A

hypofunction

54
Q

UVL clinical manifestion

A
  • URI/gastritis 2 weeks before sx develop
  • sudden onset vertigo, spontaneous horizontal nystagmus, nausea, vomiting –> can last several days
  • after acute sx, c/o disequilibrium, dizziness lasting with quick head movements
  • causes vestibular hypofunction on affected side - brain readjusts firing rate in 2 weeks and sx resolve
55
Q

what can be used and is very effective is sx do not resolve by brain with UVL

A

vestibular rehabilitation therapy (VRT)

56
Q

BVL

A

bilateral vestibular lesion complete/incomplete

57
Q

most common cause of BVL

A

ototoxicity - caused by medications

58
Q

what is the most common medication that causes BVL and why

A

gentamicin
damages vestibular hair cells, spares hearing

59
Q

clinical manifestation of BVL

A
  • severe disequilibrium
  • c/o visual blurring with head movement (oscillopsia)
  • NO vertigo (dizziness)
  • may be complete (both vestibular N not working, will not get dizzy bc no imbalance in firing rate) or incomplete (both sides not working but imbalance in firing rate)
  • if incomplete, will learn to substitute with use of visual and somatosensory input
60
Q

what would spontaneous nystagmus indicate for pathology

A

acute U/L vestibular loss or brainstem/cerebellum abnormality

61
Q

what would no spontaneous nystagmus, but loss of VOR indicate for pathology

A

chronic vestibular hypofunction

62
Q

what would impaired visual tracking indicate for pathology

A

brainstem abnormality

63
Q

what would nystagmus and vertigo only elicited during movement indicate for pathology

A

BPPV
peripheral hypofunction
rarely central positional vertigo or nystagmus
PLF
hypermobile stapes
Meniere’s

64
Q

what would skew eye deviation indicate for pathology

A

disruption of central and peripheral utricle pathways (otolith organs)

65
Q

what would imbalance while standing and walking indicate for pathology

A

anything vestibular related

66
Q

differentiate between central vs peripheral vertigo based on the effect of fixation

A
  • peripheral: nystagmus decreases
  • central: nystagmus either does not change or may increase
67
Q

differentiate between central vs peripheral vertigo based on effect of gaze

A
  • peripheral: nystagmus increases toward side of fast phase (alexander’s law)
  • central: nystagmus may not change or reverse direction
68
Q

mechanisms of recovery for vestibular system

A

spontaneous
adaptation
habituation
substitution

69
Q

episodic positional vertigo caused by calcium carbonate crystals (otoconia) deflecting cupula

A

benign paraxysmal positional vertigo

70
Q

main sx of BPPV

A

room spinning sensation that lasts 5-90s

71
Q

what is the most common peripheral vertigo

A

BPPV

72
Q

1/3 of pt spontaneously have sx resolution after _____ and _____% recur

A

3 weeks
40%

73
Q

what type of problem is BPPV

A

MECHANICAL

74
Q

otoconia breaks loose from utricle and falls into SCC

A

BPPV

75
Q

most to least affected SCC with BPPV

A

posterior
horizontal
anterior

76
Q

what does BPPV typically occur secondary to

A

head trauma or neuronitis
- migraine-induced ischemia, dehydration, more common as you age

77
Q

list some causes for BPPV

A
  • 50% idiopathic (age)
  • head trauma (whiplash, TBI)
  • viral neuronitis (superior vestibular N)
  • VBI
78
Q

describe canalithiasis BPPV

A
  • free floating crystals deflect cupula
  • can have latency
  • sx typically 5-60s
79
Q

describe cupulolithiasis

A
  • crystals adhere to cupula
  • turns SCC into gravity sensor
  • sx can be immediate
  • sx typically last 60-90s (longer)
80
Q

what time of day are sx worse for BPPV

A

most symptomatic in AM

81
Q

pts to screen for BPPV for

A
  • if pt does not lay flat at night
  • anyone over 65 y/o who have balance problems
  • many people will avoid positions causing dizziness
  • BELIEVE NO ONE
82
Q

what direction nystagmus does posterior BPPV cause

A

upward/torsional

83
Q

what direction nystagmus does horizontal BPPV cause

A

lateral

84
Q

what direction nystagmus does anterior BPPV cause

A

downward/torsional nystagmus

85
Q

how to describe nystagmus associated with horizontal canal

A
  • geotropic: toward ground (canalithiasis)
  • ageotropic: toward the ceiling (cupulolithiasis

PT 680 Clinical Medicine (18 decks)

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