Vestibular Lecture Flashcards
Flowchart of Vestibular Function
Sensory input (vestibular, somatosensation, vision) –> Cerebellum and vestibular nuclei –> motor output (reflexes, postural, eye movement)
Peripheral Components
- Membranous Labyrinth, sits in…
- Bony Labyrinth, supported by…
- Perilymph
What is perilymph?
Similar to CSF with an increased Na:K ratio
Peripheral (Sensory) components
- 3 Semicircular Canals (SCC): Anterior, Posterior and Horizontal canals
- 2 Otolith Organs: Utricle and Saccule located within the Vestibule
- Other important landmarks: 8th Cranial Nerve, Endolymphatic Sac, Round & Oval Windows
Semi Circular Canals
- Oriented in 3 canal planes
- Each canal is paired with a canal on the opposite side
- Anterior canal with opposite Posterior canal
- Two Horizontal canals
Ampullofugal Stimulation
- displacement of cupola away from utricle
- excitation
Ampullopetal Stimulation
- Displacement of cupola towards utricle
- inhibition
what is the taller hair cell called?
Kinocillium
what is entering the hair cell that causes the channel to open?
glutamate and aspartate
Does excitatory stimuli or inhibitory stimuli cause a greater response?
- excitatory
- If you turn your head very quickly, your inhibiting ear may not be inhibiting enough –> fast motions become a problem
Nystagmus at rest: non-pathologic
L: 90 spikes/sec
R: 90 spikes/sec
Nystagmus at rest: pathologic
L: 40 spikes/sec
R: 90 spikes/sec
**will feel like you are turning to the right
What are the 2 Otoliths
Utricle and Saccule
Oriented in 2 different planes
What do the utricle and saccule detect?
linear acceleration and tilt
Is the vestibular nerve considered part of the periphery or central?
periphery
Where do afferent signals of the vestibular nerve project?
- From scarpa’s ganglion through the internal auditory canal with cochlear and facial nerve (sensory branch) and labyrinthine artery
Where does superior vestibular nerve go?
anterior and horizontal canals
utricle
where does the inferior vestibular nerve go?
posterior canal and saccule
Where does the vestibular nerve enter the brainstem?
at the ponto-medullary junction
“root entry zone”
what does PICA supply
inferior portion of the cerebellar hemispheres
dorsolateral medulla
what does the basilar artery supply?
pons
what does the AICA supply?
peripheral vestibular system via labyrinthine artery
an ICA stoke is likely to cause what?
vestibular issues
From where do nuclei receive input?
peripheral vestibular system, vision, and somatosensory afferents
How do the vestibular nuclei process and relay information?
- eye movement control for gaze stability during movement
- ANS control: BP, arousal
- Postural Control and Movement: brainstem
- Cortex for spatial orientation
What does the cerebellum do
modulates vestibular reflexes
what does the flocculus do?
adjusts/maintains gain of VOR
what does the nodulus do?
adjusts duration of VOR and processes otolith information
What is the anterior-superior vermis involved with?
vestibule-spinal reflex
VOR
stable vision during head motion
Vestibulo-spinal reflex
stable body during head motion
Vestibulo-Collic Reflex
Stable neck during head motion
What is required in order to prevent retinal slip in VOR?
- velocities of eye movements need to match the velocity of head movement
What is VOR gain equation and what should it be equal to?
Eye velocity/head velocity
1
What occurs to the VOR gain when excitation and inhibition isnt working properly?
gain is no longer 1
result = retinal slip
Non pathologic push-pull phenomenon for R head turn
L: 20
R: 160
Pathologic push-pull phenomenon for R head turn
L: 20
R: 90
What is nystagmus?
- distorted vestibular input from one side causing an imbalance in the firing rates which produces a rhythmic oscillatory movement of the eyes
- usually occurs in pathologic vestibular system
What is vertigo
abnormal sensation of illusion of motion
what is alexanders law
you really have to know this
vestibular nystagmus increases if the person looks with their eyes toward the past phase of the nystagmus and decreases if eyes are toward the slow phase
Say it again for the people in the back…
What strictures are part of the peripheral vestibular system?
- vestibular end organs (2 semicircular canals and utricle and saccule)
- vestibular portion of CNVIII
What structures are part of the central vestibular system
- vestibular nuclei
- vestibulocerebellum
- vestibuloocular pathway
- vestibulospinal pathways
- vestibular areas in the cortex
- vestibulo-autonomic pathways
Vestibulospinal Reflex
- Medial vestibulospinal tract: MLF to cervical cord –> head movements and integrating head and eye movements
- Lateral Vestibulospinal tract: To thoracic spinal cord –> head and body position in space for walking
Central Vestibular Function
- Discrimination between self movement vs. that of the environment
- spatial awareness and perceived vertical
- “personal space”
- Visuo-vestibular integration
- self-motion perception
- multisensory spatial coding (proprioceptive, auditory, visual, tactile)
Vestibular Connections to autonomic nervous system
– Locus coeruleus (stress and panic)
– Nucleus of the solitary tract (Vagus nerve: nausea)
– Area postrema (vomiting)
– Central nucleus of amygdala (emotional memory)
– Parabrachial nucleus (arousal)
– Infralimbic cortex (fear, emotional regulation)
– Hypothalamus (memory, BP, circadian rhythm)
Most common diagnoses in vestibular practice
– BPPV
– Vestibular Migraine
– Vestibular Neuritis
– PPPD/Anxiety-related Dizziness
– Meniere’s Disease
Peripheral Diagnoses
- Benign Paroxysmal Positional Vertigo (BPPV)
- Labyrinthitis/Neuritis
- Meniere’s Disease (endolymphatic hydrops)
- S/P Acoustic Schwannoma (Neuroma)
- Bilateral vestibular loss
Central Diagnoses
- Traumatic Brain Injury/concussion
- Vestibular Migraine
- Persistent Postural-Perceptual dizziness (PPPD)
- Cerebellar disorders
- Multiple Sclerosis
- Stroke- brainstem and cerebellar
Non-Vestibular Diagnoses
- Balance disorder
– orthopedic or neurologic etiology - Cervicogenic Dizziness
- Multisensory Dysequilibrium
Other things that can cause dizziness:
– Medications
– Cardiac
– Postural hypotension
– Diabetes mellitus
– Thyroid condition
– Renal failure
– Visual changes
– Anxiety
what is oscillopsia?
a perception of the world bouncing
Vestibular Labrynthitis
- Viral>Bacterial infection of the vestibular nerve and labyrinth, sometimes cochlea
- Typically results in gradual onset spinning, nausea & vomiting, peaking in 24 hours
- Worst symptoms 5-7 days, following pattern of typical viral infection
- Often must be in bed first few days as symptoms are severe
- Hearing loss and vestibular symptoms
- Residual symptoms may take weeks to resolve
Vestibular Neuritis
- Same as Labyrinthitis but primarily affects the vestibular nerve and labyrinth but not cochlea
- No hearing loss
- Both neuritis and labyrinthitis often diagnosed by symptoms only, used lavishly
- Both have no recovery from the impaired side, but CNS compensates for the loss
What is Meniere’s disease?
- Disorder caused in theory by too much
endolymph in the system causing
membranous distention - Endolymphatic sac may be producing too much endolypmh or endolymph not being reabsorbed enough within the labyrinth
- Affects females>males, mid-life (30-50 at onset)
Clinical Presentation of Meniere’s Disease
- Episodic in nature
- Symptoms come on suddenly, lasts from several minutes to a few hours, leaves suddenly
- During an episode, will have vestibular testing similar to a unilateral vestibular loss
- Between spells, testing will be normal
- Fluctuating hearing w/progressive low frequency hearing loss on audiogram
Symptoms of Meniere’s disease
a. Mild to severe spinning (Nausea & vomiting, Imbalance & falls)
b. Aural fullness, fluctuating hearing
c. Tinnitus
Progression of Meniere’s Disease
– Early: Symptom free in-between episodes
– Late: Permanent hearing loss and vestibular impairment
When is PT indicated for Meniere’s Disease
If patient is experiencing imbalance or dizziness in between episodes
Treatment for Meniere’s Disease
– Low sodium diet/diuretics to attempt to manage fluid imbalance
– Transtympanic gentamycin or steroid injections
– Surgery for endolymphatic shunt, labyrinthectomy
What is an Acoustic Schwannoma?
- Nerve sheath tumor occurs on 8th cranial nerve, usually originates from vestibular nerve
- Benign and usually slow growing
- Third most common intracranial tumor
Where are Acoustic Schwannomas located?
internal auditory canal at
cerebellopontine angle
Symptoms of Acoustic Schwannomma
– Progressive, unilateral hearing loss
– Tinnitus
– Mild dysequilibrium
– Vertigo
**diagnosis confirmed with MRI
Treatment for Acoustic Schwannoma
– Watchful waiting
– Removal via stereotactic radiosurgery or micro-surgical excision
– Vestibular rehab before and/or following surgery
Possible causes of bilateral vestibular loss?
- Ototoxicity
- Bilateral acoustic neuroma
(neurofibromatosis) - Autoimmune disease
- Otosclerosis/degeneration
Presentation of Bilateral Vestibular Loss
– Potential hearing loss
– Significant oscillopsia
– Dysequilibrium in low light, complex visual environment, uneven surfaces
– No significant complaints of dizziness if loss is complete
What types of functional impairments are seen with bilateral vestibular loss?
– Gait slow, little visual scanning
– Usually requires an assistive device for safety
– High risk for falls due to lack of stability, esp. changes in sensory environments
What can cause Central Vestibulopathy?
- Traumatic Brain Injury/concussion
- Vestibular Migraine
- Persistent Postural-perceptual Dizziness (PPPD)
- Cerebellar disorders
- Multiple Sclerosis
- Stroke
Diagnostic criteria for vestibular migraine
– No documented vestibular pathology
– Migraine diagnosis according to International
Headache Society (IHS) criteria- new in 2018
– Can use the Migraine Assessment Tool to help
determine Migraine
– Intermittent vertigo or dysequilibrium- at least
2 episodes
– Accompanied by photo or phonophobia, visual aura, not necessarily headache
Vestibular Migraine Overview
- Females > males
- Can have migraines for years without dizziness, then develop dizziness
- Prevalence 23.4% of people with dizziness
- Comorbidity with BPPV and Meniere’s disease
What shows the best improvements in balance and vestibular migraine symptoms?
Medical management and vestibular rehabilitation
Pts with vestibular migraine have difficulty in what types of environments
wide open spaces, busy visual environments
What is found to be equally effective as meds or relaxation for vestibular migraine
exercise
intervention strategy for vestibular migraine
- Education!
- Collaboration with physician to decrease frequency of migraines
- Intervene with vestibular rehab for signs/symptoms that persist in between migraines
- No intervention for dizziness that occurs
during migraine
Mild TBI/Concussion
- Impairment may be either peripheral, central, or
neither - Large comorbidity with migraine and anxiety (Concussion causes post-traumatic headache)
- Autonomic dysfunction can lead to exercise
intolerance - Management involves accurate identification of
impairment and then appropriate interventions
Mild TBI/Concussion Acute Stage management
(24-48 hours) involves rest, but then pt.
should be progressed as tolerated
Persistent Postural Perceptual Dizziness (PPPD) Presenting Symptoms
Anxiety leads to:
- heightened ANS reactivity (constant fight or flight stage)
- decreased tolerance for postural disturbance
- increased sensitivity to visual stimuli
- less flexibility in postural control strategies
- altered integration of sensory information (decreased use of vestibular cues, visual dependence) –> overusing visual for balance
= conundrum and chaos
In what positions is there a sensation of imbalance and disequilibrium with PPPD?
- when upright
- relieved when sitting or lying down
symptom of PPPD
- more than 3 months of near daily symptoms
- balance that feels worse than it is
- hypersensitivity to motion
What is PPPD exacerbated by?
- complex visual environments
- wide open spaces with shiny floors
- scrolling
- reading
- close visual work
What to look for in assessment for PPPD:
- postural stability: pt reported perception of motion/instability
- greater caution in volitional movements and greater use of cognition
- no other vestibular or central disorders that can account for symptoms
- perceived threat: pt feels unsafe during typical functional tasks
- less flexibility to postural control strategies
- sensory organization impairment
What is the primary symptom of Multisensory Disequilibrium? (AKA Disequilibrium of Aging)
imbalance during functional mobility
what does Multisensory Disequilibrium result from?
degradation of two or more sensory systems responsible for balance
– Bilateral vestibular degeneration
– Peripheral neuropathy
– Visual deficits
What is cervicogenic dizziness and how is it diagnosed?
- dizziness and disequilibrium that is associated with neck pain
what is the current theory of cervicogenic dizziness?
cervical dysfunction causes abnormal input into the vestibular nuclei from the proprioceptors of the upper cervical region
Diagnosing Cervicogenesis Dizziness
- Diagnosis of exclusion - no vestibular pathology
- Close temporal relationship between neck pain and dizziness
- Previous neck injury or pathology
- Elimination of other causes of dizziness
- Cervical Relocation Test can give
information about cervical proprioceptive deficits
Cervicogenic Dizziness Intervention
- manual therapy to address upper cervical trigger points and hypomobility
- work on cervical strength and proprioception
Subjective clinical impression of COVID 19 causing dizziness
– Migraine- exacerbated, progression to vestibular
migraine
– Autonomic dysfunction- POTS
– PPPD with medical etiology
what is the most common cause of vertigo in pt’s with peripheral vestibular dysfunction
BPPV
what population is BPPV seen in?
- adults of all ages
- more common with advanced age
- rarely seen in children
BPPV Pathology
– Otoconia from the otolithic organs become dislodged and make their way into one of the semicircular canals
– Biomechanical problem in which one or more of
the semicircular canals is inappropriately excited
* Otoconia sloughs off just like skin
* New otoconia is formed, old sloughs off and absorbed by the endolymph
* Aging- lose the ability to absorb the otoconia before it gets into the canals
Common characteristics of BPPV
– Vertigo when the head is moved into various positions or head changes occur
– Rolling over in bed, bending over, looking up, lying flat or turning the head
– Sensation of true spinning after position changes that last for seconds to minutes
– Complaints of imbalance or gait problems, especially with head turns
In pts with BPPV, when do symptoms and nystagmus fatigue?
with repeated stimulation
Is BPPV episodic or constant?
episodic
lasts < 60 seconds
- usually a “spinning” sensation
Etiology of BPPV
- Post-traumatic
- Post-acute vestibulopathy
- Idiopathic
- Meniere’s Disease
- Migraine
- Diabetes
What causes nystagmus in BPPV?
- Otoconia are dislodged and float into semicircular canal (usually posterior)
- with head movement, the otoconia move within the canal resulting in abnormal, unilateral stimulation of the particular canal
Canalithiasis
- Free-floating debris in the canal
- Results in transient, brief nystagmus
Cupulothisasis
- debris adhered to the cupula and not free-floating
- Results in sustained nystagmus
Hallmark sign of BPPV
- Rotational Nystagmus
2 components of BPPV nystagmus
- Torsional: either right or left side
- Vertical: either up or down in canal
- direction of nystagmus indicates canal involved
EXCEPT for horizontal canal involvement
What type of nystagmus occurs with horizontal canal involvement?
horizontal nystagus
geotropic
- beating toward the ground
- canalithiasis = free floating debris
Apogeotrophic/ageotrophic:
- beating away from the ground
- cupulothiasis: adhered to the cupula
what test should you use to assess anterior and posterior canals?
dix-hallpike
what test should you use to assess horizontal canals
roll test
Assessment and Interventions Considerations for BPPV
- MUST explain procedure to patient
- Nausea can occur with episodes –> Cervical cold pack can be helpful in managing nausea
- Clear the cervical spine –> ROM, pain, neuro changes
- Name the nystagmus to ensure appropriate
treatment - Complete all tests prior to treatment
How to perform right Dix-Hallpike Test
- Patient’s head is moved 45º to right
- Patient moves to supine and head extended to 30º
- Look for nystagmus
- Maintain position for 30-60 seconds
- Keep head in position & assist patient to sitting, monitor nystagmus
Right Posterior Canal Identification
- R Dix-Hallpike: upbeat and R torsional
- Return to sitting: downbeat and L torsional
Right Anterior Canal Identification
- R Dix- Hallpike: Downbeat and R torsional
- return to sitting: upbeat and L torsional
Left Posterior Canal Identification
- R Dix-Hallpike: Upbeat and L torsional
- Return to sitting: Downbeat and R torsional
Roll Test
- Patient is supine with neck flexed to 20-30º
- Quickly turn head to left, look for nystagmus, hold for 30-60 seconds
- Come back to center
- Quickly turn head to right, look for nystagmus, hold for 30-60 seconds
- Canal involved will be the side which the
nystagmus is most vigorous, symptoms most
intense
Intervention options for BPPV
- wait and see
- Brandt- Daroff Exercises (lying down and sitting up in both directions)
- Canalith Repositioning Maneuver
- Liberatory Maneuver
What intervention technique do you use for Anterior and posterior canal BPPV?
CRM
what intervention technique do you use for horizontal canal BPPV?
Lempert/BBQ Roll
CRM - Right Posterior Canal
- Patient goes into right Dix-Hallpike position and holds for 30-60 sec
- In at least 30 degrees of extension slowly rotate head to left and hold for 30-60 sec
- Patient rolls to left sidelying and head is turned to 45º so that head is looking down toward floor, hold for 30- 60 sec and slowly sit up from sidelying
- Make sure to hold onto the patient once in
sitting
Horizontal Canal Repositioning
- Patient starts sitting with head flexed 30º
- Lie patient down to supine, turn head to affected side, hold 30-60 seconds
- Turn head away from affected side to middle, 30-60 seconds
- Turn head quarter turn to unaffected side, 30-60 seconds
- Maintain head in this position while patient rolls to sidelying
- Patient then rolls into supine on elbows, head down
- At this time, maneuver is complete
- Recommended way to complete maneuver is to continue to roll in the same direction until sidelying, then sit up slowly
Post-maneuver instructions
– Do not look up or down for a few hours
– You may feel off balance after the repositioning
BPPV Management
- most effective if perform multiple repositioning maneuvers in one session (1-3 maneuvers, waiting 5-10 mins every day)
- do not treat more than every other day unless in acute hospital
- do not treat multiple canals in one session
- may need to repeat maneuvers
- may treat subjective symptoms if they correlate with typical pattern (latency duration)
how to decrease nausea/vomiting during BPPV management
use cervical cold pack to decrease symptoms
Central positional nystagmus is similar in presentation to BPPV except:
- no latency
- does not fatigue
- long duration
- may be apogeotropic (horizontal)
Central positional nystagmus vs. BPPV
- Vertical nystagmus may also be present
- +Nausea/vomiting, even with single maneuver
- Co-existing cerebellar or central oculomotor signs
- Lesion of vestibulo-cerebellum-flocculonodular lobe