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Adv Neuro: Vestibular > Week 2 Highlights > Flashcards

Week 2 Highlights Flashcards

1
Q

what is the pathophys of meniere’s dz

A

inc hydraulic pressure w/i inner ear endolymphatic system

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2
Q

what are 7 sx experienced during a Meniere’s attack

A

fullness of ear
reduction in hearing
tinnitus
vertigo
postural imbalance
nystagmus
followed by n/v

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3
Q

what is the duration of meniere’s attack

A

> 20min to <24hrs

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4
Q

what is the symptomology s/p a meniere’s attack

A

gradual abatement of sx
s/p severe attack - exhaustion, sleep for hours
generally ambulatory w/i 72hrs
may have some postural unsteadiness for days-weeks then will return to normal

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5
Q

how can hearing be impacted after a meniere’s attack and long term

A

hearing can return to baseline or may have residual permanent sensorineural hearing loss (SNHL) w/ lower frequencies

long term decline inhearing is expected

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6
Q

what is our main focus when treating someone w meniere’s

A

education

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7
Q

what role does vestibular play in treating meniere’s dz

A

not the primary treatment

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8
Q

when could vestib rehab be useful in treating meniere’s (3)

A

s/p vestib ablation procedure
hypofunction present
impaired postural control

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9
Q

what is vestibular “prehab”, when is it implemented in meniere’s and why

A

vestibular rehab 2wks prior to planned vestibular ablation (ITG)

induce compensation pre-op
enhance post op recovery

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10
Q

what are 3 other disorders associated w vestib migraines

A

motion sensitivity
meniere’s
idiopathic BPPV

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11
Q

per IHS criteria, what is a migraine w/o aura

A

lasts 4-72hrs if not treated

must have 2:
* U/L location
* pulsatile quality
* * mod to severe intensity*
* * aggravated by exertion/stair negotiation*

must have 1:
* n/v
* photophobia
* phonophobia

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12
Q

what is the HINTS exam

A

stroke suspected if any of the following exist:
* normal head thrust
* direction changing nystagmus in eccentric gaze
* skew deviation (vertical ocular misalignment)

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13
Q

what are the vestibular connections to oculomotor nuclei

A

3 neuron arc from SCC:
* vestibular nuclei
* ascending tracts (b/l via MLF)
* oculomotor nuclei in brainstem (CN III, IV, IV)

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14
Q

what function do several vestibular connections have and where are the majority located

A

autonomic functions

in midbrain, pons, and medulla

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15
Q

what oculomotor deficit is commonly seen in advanced PD

A

slow hypometric saccades

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16
Q

what are some examples of vestibular interventions appropriate for a pt w advanced PD

A

work on saccades
occular function
incorporate visual exercises into training (ie during balance training)

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17
Q

what is the relationship b/w slow saccades and fall risk in PD

A

turning performance is impaired in PD and may be influenced by saccade dysfunction
* association b/w saccade function and turning performance may be indicative of the key role saccades plays in initiating proper turning kinematics

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18
Q

what is the pathophys of cerebellopontine angle lesions

A

compression of brainstem and CNVIII

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19
Q

what is are the 2 most prevalent etiologies of cerebellopontine angle lesions

A

acoustic neuroma
meningioma

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20
Q

how are cerebellopontine angle lesions dx (5)

A

hearing loss
ringing in ear

sometimes: dizziness, fullness, imbalance

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21
Q

what imaging would show cerebellopontine angle lesions

A

MRI w contrast

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22
Q

what is subjective visual vertical

A

ability to detect subjective tilt

23
Q

subjective visual vertical

impairments can be secondary to:

A

injury to otoliths or nerve connections

24
Q

what are 2 impairments that result from subjective visual vertical

A

causes sensory conflict
can’t be used to assess utricular function U/L

25
Q

normal vs abnormal subjective visual vertical

A

normal: adjust illuminated rod to vertical w mean error of <2.5deg

abnormal: >2.5 deg error noted in pts w central and peripheral path

26
Q

what are 5 disorders that present with pathological subjective visual vertical

A
  1. acute peripheral neuritis
  2. wallenberg syndrome
  3. internuclear opthalmoplegia
  4. midbrain lesion
  5. vestib neuronitis
27
Q

how is abnormal subjective visual vertical defined in children

A

> 2.13deg of deviation is significant (compared to >2deg using conventional testing)

28
Q

what is internuclear opthalmoplegia and what are the 2 sx it is characterized by

A

specific gaze abnormality

  1. impaired horizontal eye mvmts w weak ADD in affected eye
  2. ABD nystagmus of contra eye
29
Q

what is the pathophys of internuclear opthalmoplegia

A

localizing brainstem syndrome resulting from lesion in the MLF in dorsomedial brainstem tegmentum of either pons or midbrain

30
Q

what is the most common etiology for B/L internuclear opthalmoplegia in a young adult

A

MS

31
Q

what is the most common etiology for U/L internuclear opthalmoplegia in middle aged and elderly adults

A

brainstem infarction

32
Q

what is PPPD

A

persistent sensations of rocking/swayign and/or non-vertigo type dizziness on most days for >3 months

33
Q

what 3 primary complaints in PPPD

A

hypersensitivity to visual flow (ie grocery stores, windshield wipers, busy flooring, computer images/scrolling)

head fullness

perception of veering

34
Q

what is the frequency of sx in PPPD

A

min of 15days for every 30
majority daily sx
doesn’t need to be continuous

35
Q

what are aggravating factors for PPPD (3)

A
  1. upright posture
  2. busy environments (complexity and/or motion)
  3. head or body mvmt (active or passive body motion w/o reguard to direction or position)
36
Q

what are 2 nullifiers for PPPD

A
  1. avoidance of provoking environments/triggers
  2. lying down
37
Q

how consistent is the severity of PPPD

A

fluctuates

38
Q

what are 4 precipitating factors for PPPD

A
  1. medical, psychosocial, or environmental event causing acute vestib sx or imbalance
  2. coexisting vestib disorders
  3. h/o vertigo
  4. pre-existing anxiety disorder
39
Q

what are psych or behavioral predisposing or coinciding factors for PPPD

A
  • anxiety & depression
  • other psychiatric disorders
  • pre-existing anxiety
  • heightened anxiety w vestib problem
  • anxiety, cautiousness, neg expectation for recovery have greater chance of developing
40
Q

how is PPPD dx

A

based on sx presentation:
* tempo
* aggravators
* triggering events

no specific test
tests tend to be normal, may be (+) for other conditions
no present neuro-otologic dysfunction
no ongoing med etiology
not a psychiatric condition

41
Q

what improves the prognosis for PPPD

A

when migraine medically managed and psych care to address anxiety

42
Q

psych probs and pt w dizziness

what is the challenge with getting a definitive dx

A

dizziness can lead to neg psych impact
psych disorders can result in profound dizziness

43
Q

how does the incidence of psych disorders as primary cause of dizziness change

A

declines w inc age

44
Q

what are general associations seen b/w psych problems and pt w dizziness

A
  • psych probs often coexist w balance disorders
  • common for anxiety to accompany vestib disorder
  • depression more common in those w migraines/HAs than those w/o
  • high prevalence of mood disorders and psych probs in pts w dizziness
45
Q

what are general management strategies for psych problems and pts w dizziness

A
  • recognize presence of disorder
  • discuss w pt the disorder when appropriate and depending on dx
  • provide reassurance
  • relate emotions/stress can cause same sx as vestib disorder
  • destigmatize by telling prevalence of disorder
  • refer pt for med mgmt, CBT, etc.
  • individualize HEP
  • assure continued PT involvement
  • wean inappropriate ADs
46
Q

psych probs and pt w dizziness

at what point to you discuss the presence of one of the following disorders in the pt’s POC:
* anxiety
* depression
* CSD
* PPPD
* somatoform
* factitious

A

anxiet/depression/CSD/PPPD = early
somatoform - avoid in 1st visit
factitious - defer unless deemed clinically appropriate
* they don’t want to get better

47
Q

what is MdDS

A

central vestib (neuro) disorder

*not a peripheral vestib (inner ear) disorder/dz

48
Q

what are non-motion triggered MdDS (aka “rockers” or “spontaneous MdDS”)

A

individuals w similar sx w/o preceding motiono exposure

49
Q

what is a challenge w treating non-motion triggered MdDS

A

possibly more difficult to treat w habituation but still able to cure >50%

50
Q

what is the pathogenesis of MdDS

A

pathogenesis and lesion site unknown
no particular injury

most agree it is a variant of motion sickness

51
Q

what are possible etiologies of MdDS

A
  • otolith dysfunction
  • d/t or exacerbated by anxiety/somatoform disorder
  • variant of migraine
  • processing error - inappropriate high weighting of somatosensory input for balance
52
Q

what is a PT strategy for treating MdDS

A

work on pushing somatosensory reference back b/w vestib mechanism and somatosensory system

53
Q

what is the Dai Protocol for in MdDS

A

established to address theory of Maladaption of VOR

Adv Neuro: Vestibular (6 decks)

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