Vestibular Flashcards
Hair cells (aka ___) are located within the __ of the __. The hair cells are embedded within a membrane (aka ___) which sits in ___, which is the fluid that fills the SCCs. The ampulla is the [narrow / wide] end of each canal and articulates directly with the [utricle / saccule].
Hair cells (aka CILIA) are located within the AMPULA of lthe SEMICIRCULAR CANAL. The hair cells (cilia) are embedded within a membrane (aka CUPULA ) which sits in ENDOLYMPH, which is the fluid that fills the SCCs. Cupula weighs the same as the endolymph around it (unless things are stuck to it - if it's too heavy, it'll "sink down" when in a dependent position, which triggers the hair cells! Vs alcohol, which is lighter than endolymph. It diffuses into the cupula faster than the endolymph, which renders the cupula lighter than the surrounding endolymph -> cupula "floats up," which triggers hair cells -> feels like your head is rotating when you lie down! Thus rendering your cupula sensitive to gravity)! Cupula is attached at both ends, so it billows when it is displaced, doesn't blow in the wind. So with that in mind, SCCs do NOT typically detect gravitational forces, only ROTATIONAL forces (angular accelerations and decelerations of your head, but NOT constant movement!). The ampulla is the WIDE (~5x larger than the canal itself!) end of each SCC (so there are 6 total, 1 at each end of each SCC) and articulates directly with the UTRICLE.
Semicircular canals work in functional pairs, e.g. right anterior canal is paired with the [R / L] [anterior / posterior / horizontal ] canal. When one canal in the pair is excited, its paired canal is [excited as well / inhibited }. When dysfunctional, chief complaint tends to be [vertigo and spinning / imbalance]
Semicircular canals work in functional pairs, e.g. right anterior canal is paired with the LEFT POSTERIOR canal. When one canal in the pair is excited, its paired canal is INHIBITED. When dysfunctional, chief complaint tends to be VERTIGO/SPINNING.
*Posterior canal runs roughly parallel with posterior canal!
Orientation of the kinocilia:
Ant SCC: kinocilium sits [closet to / far from] from utricle
Post SCC: kinocilium sits [closet to / far from] utricle
Horiz SCC: kinocilium sits [closet to / far from] the utricle
When the hair cells are deflected TOWARD the utricle, we term this ___ displacement - identify if this excitatory or inhibitory in each canal.
Orientation of the kinocilia:
Ant SCC: kinocilium sits FAR from utricle
Post SCC: kinocilium sits FAR from utricle
Horiz SCC: kinocilium sits CLOSET TO the utricle
When the hair cells are deflected TOWARD the utricle, we term this UTRICULOPETAL displacement, which is INHIBITORY for the ant and posterior canals, but EXCITATORY for the horizontal canal, and vice versa.
Hair cell deflection AWAY from the utricle = UTRICULOFUGAL (fugal, think fugative, running away from the utricle!) which is excitatory for the ant and post canals, inhibitory for horizontal canal.
Utricle sits in [horizontal / vertical ] plane, vs saccule sits in [horizontal / vertical ] plane. The utricles and saculues together are termed ___. These [are / are not] sensitive to gravity, and help us sense linear acceleration and tilt of head in space. Chief complaint tends to be [vertigo and spinning / imbalance]
Utricle sits in HORIZONTAL plane (with hair cells w/otoconia attached on the floor of it), vs saccule sits in VERTICAL plane (with hair cells w/otoconia attached on medial wall of saccule). The utricles and saculues together are termed OTOLITHS. These ARE sensitive to GRAVITY, and help us sense linear acceleration (saccule = vertical linear acc, utrical = horizontal linear acc) and tilt of head in space. The weight of the otoconia displacing the hair cells help us detect linear acceleration , e.g. gravity. Chief complaint tends to be imbalance.
Age related changes in otoconia include…
Increased variability in size Hypertrophy Fragmentation Fissured Pitted Weakening of linking filaments
Particles fall out of utricle into SCCs (typically into Post SCC or Horiz SCC) -> BPPV
___ cells are involved with the maintenance of homeostasis within the endolymph, including potassium transport and calcium homeostasis. They are located in the canal side of the __ of the ___, as well as the [ant/post] wall of the __. They might be responsible for the degradation of loose ___. We see a reduced density of these cells in __ disease, resulting in highly recurrent BPPV.
DARK CELLS are involved with the maintenance of homeostasis within the endolymph, including potassium transport and calcium homeostasis. They are located in the canal side of the AMPULA OF THE SCC and POSTERIOR WALL OF UTRICLE. They might be responsible for the degradation of loose OTOCONIA. We see a reduced density of these cells in MENIERE’s disease or Labrynthitis resulting in highly recurrent BPPV
The ___ reflex operates with the shortest latency of any reflex in the human body. This reflex allows for…
The VESTIBULO OCULAR reflex operates with the shortest latency of any reflex in the human body (~10ms). This reflex allows for GAZE STABILIZATION ON A TARGET OF INTEREST DURING DYNAMIC HEAD MOVEMENTS
Given a normal VOR…
Head turn R stimulates what canal?
Head turn R stimulates what canal?
Given a normal VOR…
R head turn = R horizontal canal excitation
L head turn = L horizontal canal excitation
Given a normal VOR…
Stimulation of R posterior canal (tipping head back to R) drives your eyes [up/down] [r/L] torsion?
Stimulation of L posterior canal (tipping head back to L) drives your eyes [up/down] [r/L] torsion?
Stimulation of R anterior canal (tipping head forward to R) drives your eyes [up/down] [r/L] torsion?
Stimulation of L anterior canal (tipping head forward to L) drives your eyes [up/down] [r/L] torsion?
Given a normal VOR…
Stimulation of R posterior canal (tipping head back to R) drives your eyes DOWN and with L TORSION
Stimulation of L posterior canal (tipping head back to L) drives your eyes DOWN and with RIGHT TORSION
Stimulation of R anterior canal (tipping head forward to R) drives your eyes UP with LEFT torsion?
Stimulation of L anterior canal (tipping head forward to L) drives your eyes UP with RIGHT torsion?
[Vestibular / somatosensory] cues are strongly utilized to regulate proximal postural control strategies, e.g. to stabilize the head, neck, trunk, and hip mm activation/ strategies. With deficiency here, the [intensity / timing] of evoked responses to perturbations is disrupted most, where as [intensity / timing] is less affected.
[Vestibular / somatosensory] cues are more responsible for activation of distal mm and [intensity / timing ] of balance reactions. With this kind of loss, a hip strategy is adopted in situations where an ankle strategy would have been more efficient.
VESTIBULAR cues are strongly utilized to regulate proximal postural control strategies, e.g. to stabilize the head, neck, trunk, and hip mm activation (including hip strategies with balance). With deficiency here, the INTENSITY of evoked responses to perturbations is disrupted most, where as TIMING is less affected.
SOMATOSENSORY cues are more responsible for activation of distal mm and [intensity / timing ] of balance reactions. With this kind of loss, a hip strategy is adopted in situations where an ankle strategy would have been more efficient.
In what context (acuity, subtype etc) are sedatives and/or antiemetics most reasonable for use in vestibular dysfunction?
What meds do we commonly see used?
Best for use with ACUTE ONGOING vertigo and nausea/ emesis (not great for brief attacks of vertigo or BPPV). May be helpful in the acute phase of unilateral vestibular loss (first few days), but NOT typically helpful or indicated for BPPV-related dizziness. Ideally, these should be discontinued before bedside vestibular exam or initiating vestibular exercises
Acutely: benzodiazepines (diazepam/Valium or Lorazepam/Ativan) for acute or severe vertigo. Peak concentration ~1 hr, Valium half life 24-48h, vs Ativan half life 10-20 h.
Chronic vertigo may benefit from ANTIHISTAMINES (e.g. Meclizine - half life 6h, Diazepam (half life ~24h) + Meclizine which might help w/acute vestibular syndrome). Diazepam IS a benzo and can be habit-forming.
Antiemetic: Zofran - pretty safe, but $$
With unilateral vestibular loss, symptoms are made worse by ___. Nystagmus beats toward __ side, and spontaneous nystagmus with fixation should resolve after ~ [how much time?]. People tend to fall/ lose balance toward the [affected/intact] side.
With unilateral vestibular loss, symptoms are made worse by HEAD MOVEMENT. Nystagmus beats toward INTACT side, and spontaneous nystagmus with fixation should resolve after ~1 WEEK. People tend to fall/ lose balance toward the AFFECTED side (side with decreased activity)
How to treat unilateral vestibular loss?
- Meds?
- PT?
- Prognosis?
- Factors which might indicate not as great prognosis?
How to treat unilateral vestibular loss?
- Meds? Vestibular suppressants for several days can help, but using them much longer than this can prolong recovery (and they induce sleepiness, pts can’t drive on them, etc)
- PT? Vestibular adaptation exercises appear to speed along recovery!
- Prognosis? EXCELLENT prognosis for vestibular compensation
- Factors which might indicate not as great prognosis? Anxiety, if other systems affected (e.g. visual or somatosensory loss too)
Vestibular neuritis is likely caused by __. May be preceded by __ or __ infection (in ~50% cases). Recurrence is [common/ uncommon]. Typically involves the __ nerve only. Typically is reasonable to trial ___ for medical management of this.
Vestibular neuritis is likely caused by HSV-1. May be preceded by RESPIRATORY or GASROINTESTINAL infection (in ~50% cases). Recurrence is UNCOMMON (~5% cases). Typically involves the SUPERIOR VESTIBULAR NERVE only (because it goes through a tight bony tunnel so it can be easily compressed; inferior vestib nerve less so). Typically is reasonable to trial STEROID (prednisone) TAPER for medical management of this. (Neuritis is typically viral, so does not warrant antibiotics)
Superior vestibular nerve innervates [what parts of vestibular apparatus?] vs inferior vestibular nerve innervates …
Vestibulocochlear nerve has 3 big divisions: superior and inf vestib nerve, and cochlear n.
Superior vestibular nerve: (most affected in vestibular neuritis!)
- Anterior SCC
- Horizontal SCC
- Utricle (horizontal mvmt)
Inferior vestibular nerve
- Posterior SCC
- Saccule (vertical mvmt)
*Cochlear innervation is from the cochlear division of the vestibulocochlear n!
Potential VASCULAR cause of unilateral vestibular dysfunction?
- Risk factors for this?
- Diagnosis by…
Potential VASCULAR cause of unilateral vestibular dysfunction: ANTERIOR VESTIBULAR ARTERY ISCHEMIA via occlusion
- Risk factors for this? HTN, AFib, carotid artery stenosis, smoking, diabetes, hyperlipidemia, hypercoaguable states, obesity, prior TIA/CVA
- Diagnosis by exclusion, imaging (including MRA) typically is not sensitive
Management:
- Medically manage cardiac risk factors (especially AFib and HTN)
- Good candidates for vestibular rehab/training
Blood supply to vestibular system?
(Hint: if pt had no infectious precursor, has acute vestibular syndrome, and cardiac risk factors, think it might be vascular!)
Largely stems from POSTERIOR circulation from the basilar artery - consider vertebral basilar insufficency!
Basilar -> AICA -> Labrynthine artery -> anterior vestibular artery -> anterior and horizontal SCC, and utricle
Basilar -> AICA -> Labrynthine artery -> common cochlear artery -> posterior vestibular artery -> POSTERIOR SCC and Saccule
Labyrinthitis is an infection, typically [viral / bacterial] to the labyrinth. Acutely, it is associated with __ and __, as well as acute vestibular symptoms. Medically, treat with ___
Labyrinthitis is an infection, typically VIRAL to the labyrinth. Acutely, it is associated with TINNITUS and HEARING LOS, as well as acute vestibular symptoms. Medically, treat with STEROIDS (PO prednisone or via TRANSTYMPANIC INJECTION)
Hearing changes with age
High frequency hair cells are the first to decline, common to see more normal hearing at low frequency/pitch sounds, but impaired at higher frequency. Typically should be symmetrical loss. Tinnitus tends to match your hearing loss (e.g. high pitch non-pulsatile tinnitus).
Causes of unilateral vestibular loss
- Infection - vestibular neuritis or labrynthitis (associated hearing loss/tinnitus!), both viral typically, both treat w/steroid course and vestibular exercises
- -> also Ramsay Hunt Syndrome (varicella-zoster virus, HHV-3 reactivation): acute onset painful vesicles in external ear, ipsilateral hearing and vestibular loss and facial weakness
- Vascular - anterior vestibular artery ischemia (affects horizontal and ant canal, and utricle), manage cardiac risk factors, treat w/vestib exercises
- Trauma: temporal bone fracture (Vestibular hypofxn more common with otic capsule involving fx or transverse/oblique temporal bone fx)
- S/p surgery: eg. post vestibular schwannoma resection, post ablative procedure (labyrinthectomy, transtympanic gentamicin injection) for Meniere’s
OR idiopathic!
Diagnostic criteria for Meniere’s Dz (per AAO-HNS 8/2015) :
- Recurrent attacks (2 or more episodes) of spontaneous vertigo that last 20 mins - 12 hrs
- No clear provocative factors
- Audiometrically- documented LOW to MEDIUM frequency sensorineural hearing loss - bummer because this is right in the range of speech! (different from age-related hearing loss which is higher freq; need to do the formal testing when their hearing is down, but it can fluctuate)
- Fluctuating aural symptoms (tinnitus/ fullness, LOW pitched, usually unilateral)
- EXCLUSION of other causes (including NORMAL MRI, BPPV w/u negative)
- Head impulse test is typically NEGATIVE
- See a UNIDIRECTIONAL nystagmus during attacks , as well as w/mastoid vibration bilaterally and caloric weakness
Cause of Meniere’s dz?
Demographics?
Cause?
- Unknown, ?malabsorption of endolmph in the endolymphatic duct and sac?
- Viral?
- Loose otoconia obstructing endolymphatic duct
- Genetic predisposition
- Autoimmune
- If you have Meniere’s dz, you likely have hydrops = distention in membranous labyrinth, typically in utricle and saccule. BUT presence of hydrops doesn’t mean you have Meniere’s necessarily.
M=W, adults
Bilateral in ~19%
Typically has symptoms ~7 years if untreated
0.2% (2/1000) of US population has Meniere’s
May note progressive hearing loss, tinnitus, and imbalance as dz progresses
What is an otolithic crisis event of Tumarkin and how on earth does it relate to Meniere’s Dz?
What is an otolithic crisis event of Tumarkin and how on earth does it relate to Meniere’s Dz?
- Conscious drop attack
- NO warning
- Violent
- Brief (a few seconds)
- Typically occur in late stages of Meniere’s dz
- No vertigo/ spinning, pt feels like they were pushed
Not super common, limited literature but anecdotally ~15% of pts with Meniere’s get this
Medical management of Meniere’s dz?
Role of PT?
Conservative:
- Vestibular suppressants during acute attacks ONLY (ativan is more appropriate than valium given duration of their attacks - ativan half life 10-20 hrs, vs valium is 24-48; most patients do best just lying still instead of meds)
- Limit Na+ intake (~1200mg/day)
- Dyazide (diuretic)
- Steroids? Oral vs transtympanic
Surgical/ Ablative management:
- Required in ~1/3 of cases to control episodic vertigo and/or drop attacks
- Low-dose transtympanic gentamicin injections (it’s vestibular toxic - knocks out vestibular hair cells, some risk of damage to cochlear hearing cells too so it’s a better option for those who might already have lots of hearing loss and don’t have anything to lose!)
Alternate ablative treatments:
- Vestibular nerve section (but higher risk as it’s an intracranial surgery)
- Labyrinthectomy (loses hearing and vestibular fxn)
- Semicircular canal plugging
PT? Not indicated in pts with spontaneous vertigo attacks.
- Fair potential for pt with nonfluctuating imbalance without frequent acute attacks of spontaneous vertigo
- Seconary BPPV is common! (38% of those w/Menieres!) Can treat this w/maneurvers!
- Good potential for improvement w/PT following gentamicin injection /surgical intervention because now they have STABLE unilateral vestibular loss!
Acoustic Neuromas (Vestibular Schwannomas, to be precise) are a tumor occurring on the __ nerve, typically more the [inferior / superior] __ nerve. Accounts for ~85% of tumors of the cerobellopontine angle, incidence of 1/1000. Gadolinium-enhanced MRI of the internal auditory canal is the gold standard for identification, CT is insensitive.
Acoustic Neuromas (Vestibular Schwannomas, to be precise) are a tumor occurring on the VESTIBULOCOCHLEAR CRANIAL NERVE (CN VIII), typically more the INFERIOR VESTIBULAR NERVE. Accounts for ~85% of tumors of the cerobellopontine angle, incidence of 1/1000. Gadolinium-enhanced MRI of the internal auditory canal is the gold standard for identification, CT is insensitive.
Vestibular schwannoma causes symptoms including:
- Progressive sensorineural ___, ___, and imbalance.
- Spontaneous vertiginous attacks are [ common / not common] - why?
Vestibular schwannoma causes symptoms including:
- Progressive sensorineural HEARING LOSS ( 51.5%), TINNITUS (unilateral tinnitus 11.2%), and IMBALANCE (dizziness in 17%).
- -> Incidental finding on imaging in 10.2%!
- Spontaneous vertiginous / spinning attacks are NOT COMMON as vestibular loss is typically gradual as the schwannoma grows!
**Keep in mind, CN VIII is close to CN VII - as schwannoma gets larger OR if CN VII is nicked when the schwannoma is resected, you can see unilateral (ipsilateral) LMN facial weakness!
Medical Management of Vestibular Schwannomas
- Watchful waiting; serial MRI/audiograms / vestibular studies to monitor mass (many grow then plateau!)
- Surgical removal (if mass is >2.5 cm) via crani. Able to preserve facial nerve in ~90%. Hearing is largely preserved, but vestibular not as likely - but if vestib was pretty impaired pre-op, they might feel better right away post! Vs many feel more dizzy initially, but then they have a non-flucutuating hypofunction which PT can treat. Inferior vestibular nerve preserved in ~28%, whereas in ~75% of cases, superior vestibular n can be preserved.
- Radiosurgery (if size of mass <2.5cm)
Superior canal dehiscence can best be detected on ___ [imaging] as it is a bony defect - specifically, it is an opening in the bone overlying the [upper/ lower ] portion of the superior canal. It results in abnormal communication between the labyrinth and the brain.
Superior canal dehiscence can best be detected on CT SCAN (temporal bone CT) as it is a bony defect - specifically, it is an opening in the bone overlying the UPPER portion of the superior canal. It results in abnormal communication (“third window”) between the labyrinth and the brain. (because some of that energy goes out to stimulate auditory function instead!)
Superior canal dehiscence history/ symptoms…
- Pressure sensitivity (Sneezing, coughing, valsalva, lifting, bowel mvmt)
- Imbalance (may be constant; is accentuated with head movement and in dark environments)
- Sound sensitivity
- -> Internal (e.g. hearing heel strike with gait, eye movement, heartbeat, own voice)
- -> External (e.g. phone ring, music)
- Hearing loss / pulsatile tinnitus / aural fullness
Superior canal dehiscence epidemiology:
- Male __ Female
- Etiology?
- Correlation with __ and ___, suggesting possible relationship with increased intracranial pressure
- ___ predisposition likely
- Impact of aging?
Superior canal dehiscence epidemiology:
- Male = Female
- Etiology? ?Trauma - 59% of patients with SCD can report an inciting factor
- Correlation with OBESITY and OBSTRUCTIVE SLEEP APNEA, suggesting possible relationship with increased intracranial pressure
- GENETIC predisposition likely
- More common w/age, d/t thinning of bone
- RARE In kids
- Bilateral in ~25% of cases
- Presence of dehissicence does NOT always equate to symptoms
Superior canal dehiscence exam findings…
Auditory testing?
Vestibular testing?
Imaging: + high res CT
Superior canal dehiscence exam findings…
Auditory testing?
- Low frequency air-bone gap noted with audiometry, present stapes reflex
- Bon econduction thresholds may be <0 dB
- Weber test may lateralize to affected ear
- Vibration fork placed to distal bony landmark (lateral malleolus) may localize to affected ear
Vestibular testing?
- Hennebert sign: nystagmus induced by sealed pressure (tragal pressure/ Bruening otoscope) applied to external auditory canal
- Valsalva -> nystagmu
- Tullio phenomenon: nystagmus evoked in response to particular tones/sounds
- Vestibular evoked myogenic potential (VEMP) testing: responses at <75 dB
Medical management of superior canal dehiscence?
Role of PT?
Conservative:
- Avoid offending stimuli (e.g. exertion, use earplug to avoid noises)
Surgery
- Canal plugging and /or resurfacing
PT IS NOT HELPFUL
Most common cause of a bilateral vestibular disorder is use of ___. This vestibular loss is usually [ temporary / permanent ]. Common impairments include…
Also see impaired ___ learning likely related to atrophy of [specific area of brain matter] following vestibular loss
Most common cause of a bilateral vestibular disorder is use of IV ANTIBIOTICS (aminoglycosides; used for heavy duty infection like osteomyelitis, endocarditis), results in loss of vestibular hair cell…and they don’t regenerate well. This vestibular loss is usually PERMANENT. Common impairments include…
- Oscillopsia (d/t loss of VOR)
- Imbalance
- Possibly hearing loss
- You DO NOT commonly see attacks of vertigo/ spinning!
Also see impaired SPATIAL LEARNING (e.g. difficulty wayfinding, getting lost more often than usual) learning likely related to atrophy of HIPPOCAMPAL GRAY MATTER following vestibular loss
Antibiotics linked to vestibulopathy and bilateral vestibular dysfunction?
Class of abx = aminoglycosides (end with -Y/ICIN)
Strong:
- Gentamicin
- Streptomycin
- Tobramycin
Weak:
- Neomycin
- Amikacin
- Netilmicin
- Vancomycin
** You might see individuals with CF on some of these!
Other (non abx) etiologies of vestibulopathy and bilateral vestibular dysfunction?
- MOST CASES ARE IDOPATHIC (even more so than abx cause!)
But also…
- Amiodarone (antiarrhythmic)
- CANVAS disorder (Cerebellar Ataxia, Neuropathy, Vestibular Areflexia Syndrome)
- -> 25% of pts with bilateral vestibular loss appear to have Cb syndrome
- ~33% of these patients also have polyneuropathy
- Thiamine (B1) deficiency (Wernicke encephalopathy)
- Cis-platinum (chemo)
- Neurofibramatosis Type 2 (NF2)
- Syphilis
- Lyme dz
- Autoimmune disorders
- Meningitis
- Aging
Exam findings with vestibulopathy and bilateral vestibular dysfunction?
+ Head impulse test B
Abnormal caloric testing, VEMP, dynamic visual acuity test, and Romberg
MRI/CT (focused on internal auditory canal) (could be abnormal w/meningitis, B vestibular schwannomas i/s/o NF2)
W/u for atypical causes: Lyme titer, syphilis (FTA-ABS), autoimmune markers
How to treat vestibulopathy and bilateral vestibular dysfunction?
Meds?
PT?
Surgery?
Medications?
- Vestibular suppressants are NOT helpful (they’re already suppressed!), typically worsen symptoms
PT? Vestibular compensation exercises are HIGHLY recommended?
No surgical intervention available to restore function (yet), but ongoing research re: vestibular implants (but implant can damage hearing!) and vestibular hair cell regeneration
What is persistent postural-perceptual dizziness?
Described as…
Typically follows a ___
High [visual / sensory/ vestib] dependency for balance is common
Common comorbidities?
Biomarkers ?
PPPD has been described as visual vertigo, phobic postural vertigo, and chronic subjective dizziness.
Typically arises following a vestibular insult (e.g. neuritis) or other condition that impacts balance
High VISUAL dependency (overdependence) for balance is common - they don’t learn to trust somatosensory or vestibular cueing following an insult. BUT this is harder when there is visual motion (e.g. busy lobby) or any visual-vestibular mismatch.
Anxiety/panic/depression is common but no a prerequesite
No biomarkers
Diagnostic criteria for Persistent Postural Perceptual Dizziness?
- Primary dizziness-type symptom (non-vertiginous dizziness, commonly reports feeling they’re rocking/swaying) present >50% of time for >3 MONTHS
- Onset following an event that involved acute vestibular symptoms (e.g. neuritis) or impaired postural control
- Symptoms exacerbated by UPRIGHT posture, motion, visual stimuli, or complex visual patterns (can use Visual Vertigo Analog Scale to quantify visual motion intolerance!)
- Symptoms cause significant distress, functional impairment (e.g. missing work)
- Symptoms not better explained by another disorder
Mangement of PPPD
- Do not overestimate abnormal test findings if they seem irrelevant based on pt’s hx
- Stress lack of sinister findings
- Reassure pt that their symptoms are no less real, even though no organic cause is identifiable
- Discourage use of assistive devices
- Consider trial of antianxiety agents with primary care provider if indicated
- Recommend counseling / psychotherapy
- Suggest participation in tai chi/ relaxation / controlled deep breathing
- Use graded and very gradual exposures to provocative environments (desensitization). Avoid extreme stimulation.
- Make exercises as task specific as possible; need graded exposure to the stimulus that is bothering them
- Consider balance stance drills that decrease reliance on visual cues. Focus on PROPRIOCEPTIVE cues.
- Use progressive store walking (habituation to visual motions that bother them! Build duration, crowdedness, reduction of support device e.g cart)
- Sensory reweighting: increase their sense of somatosensation, postural control, and balance confidence. They tend to overuse visual info and don’t use vestib inputs well, so the above things help to give them a better sense of where they are in space in busy visual environments, and THEN gradually build up how much they rely on vestibular inputs)
We expect a good outcome!
Name the reflex in charge of teach of the following:
(1) ___= Stable vision during head motion
(2) ___ = Stable body during head motion
(3) ___ = Stable neck during head motion
Name the reflex in charge of teach of the following:
(1) VESTIBULO-OCULAR REFLEX (VOR) = Stable vision during head motion
(2) VESTIBULO-SPINAL REFLEX (VSR) = Stable body during head motion
(3) VESTIBULO-COLIC REFLEX (VCR) = Stable neck during head motion
Role of Vestibulo-ocular reflex?
Keeps VISION stable while head is moving
Role of Vestibulo-Spinal reflex?
Keeps BODY stable while head is moving.
Important for postural control.
Role of Vestibulo-Colic reflex?
Keeps NECK stable while head is moving
There are 4 vestibular sub-nuclei. They all receive input from the periphearl vestibular system, vision, and somatosensory afferents. Primary functions of these include… (4)
Vestibular nuclei act as RELAY stations to assit with:
(1) Eye movement control for gaze stability during movement; input from the semicircular canals to the superior vestibular nucleus (more so than the inferior one) = VOR
(2) Autonomic nervous system control of BP, arousal (largely from inferior nucleus)
(3) Postural control and movement: brain stem (largely to the medial and lateral nuclei)
(4) Cortex for spatial orientation
In depth…
Lateral (Dieter’s) nucleus: gives outputs to the Cb (feedback) and to the lateral vestibulospinal tract to facilitate extensors (postures, mm of arms and legs)
Medial nucleus: provides descending output to mm of head and neck via medial longitudinal faciculus (MLF; head position)
Superior nucleus: provides ascending output (via the MLF) to the vision-related nuclei (CN III, IV, and VI) - primary function is the VOR
Inferior nucleus: outputs to the Cb (feedback), the reticular formation (arousal and ANS), and to vision nuclei (CN III, IV, and VI; VOR)
VOR is a [#] neuron arc that [ has / has no] cortical involvement and allows for __ stabilization while the head is moving. It’s [fast / slow] .
VOR is a 3-NEURON arc that HAS NO CORTICAL INVOLVEMENT and allows for IMAGE stabilization while the head is moving. It’s FAST! It can be moderated by the Cerebellum but has NO direct cortical involvement.
Labyrinths -> input to vestib nuclei -> ascending tracks, cross at MLF, go to CN III/IV/VI -> excitatory projections to one eye mm and inhib to other eyes -> equal and opp head movmeent!
