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!
Vestibulospinal reflex gives [ ascending / descending ] outputs which to the ____ via the __ tract. Describe the medial vs lateral portions and their role.
VSR gives descending outputs which travel to C-spine via vestibulospinal tract. Has a medial and lateral portion:
Medial portion of vestibulospinal tract: travels BILATERALLY through MLF to cervical spinal cord, involved with integrating head and eye movements. Keeps head/eye where it needs to be in space!
Lateral vestibulospinal tract : travels ONLY IPSILATERALLY to the THORACIC spinal cord. Responsible for head and body position in space, important for righting and equilibrium reactions, postural control w/gait.
Functionally, if you tilt head to one side = stimulates SCCs and otoliths on the SAME side -> INCREASED output through vestibular nerve to the vestibular nuclei (still that same side) -> sends impulses through the lateral and medial vestibulospinal tracts to the spinal cord -> increased EXTENSION IPSILATERAL to the head tilt and FLEXION on the opposite side
Vestibulocerebellum roles
It’s largely inhibitory to override the reflexes!
- Responsible for postural and gaze stabilization: modulates VOR, VOR cancellation, and inhibitory drive of VOR
- Fluid, controlled motion which requires stabilization and controlled mobility –> both the VSR and VOR must be “cancelled” in order to produce movement at times! This is mediated by Cb and Basal Ganglia
Vestibular loss results in postural and oculomotor hypermetria
Ascending vestibular tracts relay in the [area?] of the ___. It has connections with the vestibular cortex and reticular formation for __ and ___ awareness of the body. Helps to discriminate from self-movement vs that of the environment, spatial awareness and perceived vertical, and “personal space”
Ascending vestibular tracts relay in the POSTEROLATERAL THALAMUS. It has connections with the vestibular cortex and reticular formation for AROUSAL and CONSCIOUS awareness of the body. Helps to discriminate from self-movement vs that of the environment, spatial awareness and perceived vertical, and “personal space”
The vestibular cortex describes the areas of the brain that are involved in processing vestibular info. These include…
- Parieto-insular Vestibular Cortex (PIVC) - junction of parietal and insular lobe; target for afferents from Cb and vestibular nuclei
- Medial Superior Temporal Region : visuo-vestibular integration, perception fo self- motion
- Ventral intraparietal region: multisensory spatial coding (proprioceptive, auditory, visual , and tactile inputs) and weight these inputs for movement.
- Projects also to many other areas including occipital cortex (vision posterior parietal cortex, and premotor cortex)
Role in vestibular connections to ANS?
- Vestibular nuclear projections to:
- 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 rhythms)
Role of HINTS in evaluating for acute vestibular syndrome?
HINTS: applicable ONLY with a patient with spontaneous nystagmus
IF (-) impulse test (rules out peripheral system) PLUS
- Direction changing nystagmus with eccentric gaze
OR
-Skew deviation (vertical ocular malalignment; via cover uncover test you see an upward OR downward movement of the uncovered eye; might also see ocular tilt)
What is Horner’s syndrome?
Think “PAM” Horner!
P: Ptosis
A: Anhydrosis (decreased sweating on affected side of face)
M: Miosis (constriction of pupil)
Wallenberg’s Syndrome = [alternate name?]
- Areas impaired?
- Vasculature driving this?
- Clinical findings?
Wallenberg’s syndrome = LATERAL MEDULLARY SYNDROME
Wallenberg’s syndrome = LATERAL MEDULLARY SYNDROME
Clinically: we see dramatic shift in midline orientation = ipsiversive lateropulsion (impaired subjective visual vertical. Visual cues don’t help. Pt leaning toward side of lesion: L lesion = decreased L side vestibular input = pt feels like they’re leaning to the right d/t increased R vs L firing rate -> increased extension/pushing on R -> left {toward lesion} lean )
NO change in strength
+Oculomotor signs (torsional toward that side of lesion; skew with lesioned side lower; impaired ocular tilt rxn; tilt of perceived visual vertical; torsional spontaneous nystagmus or impaired head impulse)
Abnormal Vestibulospinal reflex
Areas affected/findings:
- Inferior Cb peduncle = IPSILATERAL limb ataxia, dysmetria
- Vestibular Nuclei = vertigo, nystagmus, imbalance (d/t vestibular spinal tract invovlement)
- Trigeminal nucleus and tract = IPSILATERAL facial hemianesthesia (decreased facial pain and temp sensation)
- Lateral spinothalamic tract: Contralateral pain and temp from body
- Descending sympathetic fibers = ipsilateral Horner’s syndrome
- Nucleus ambiguus (CN 9 and 10) -> hoarseness (vocal cord paralysis), dysphagia, decreased gag reflex, palatal weakness
- Nucleus solitarius (taste from CN 7, 9, 10) -> decreased taste IPSILATERALLY )
Deiterich Lateropulsion Grades:
Used with ___
Grade I:
Grade II:
Grade III:
Grade IV:
Deiterich (1992) Lateropulsion Grades:
Used with LATERAL MEDULLARY/ WALLENBERG SYNDROME
All have head and body tilt…
Grade I: … without imbalance
Grade II: …with considerable imbalance, but no falls
Grade III: … falls only with eyes closed
Grade IV: …falls only with eyes open
Lateropulsion DOES tend to recover with time! ~2.5 months.
Thalamic lesions will present with impaired ___ but intact ___
Thalamic lesions will present with impaired VESTIBULAR FUNCTION, PERCEPTUAL AND POSTURAL DEFICITS but intact OCULOMOTOR FUNCTION (because oculomotor centers are just in brainstem!)
Similarities and differences between “Pusher” syndrome vs Wallenberg Syndrome?
Both with impaired orientation to vertical
- Pusher: altered perception fo POSTURAL vertical stemming from THALAMIC lesion, pushes toward IMPAIRED side of body. Resists passive correction. Give tactile and visual feedback re: visual vertical which helps, ask pt to lean toward midline - active movement toward goal gives them a better sense of the error and they tend to fight passive movement anyway!
- -> Brain can compensate for this, but it takes 63% longer than pt’s who don’t push to reach same fxn’l level. Pushing rarely evident >6 months post CVA, at which point fxn’l deficits and hemiplegia are more pronounced.
- Wallenberg/Lat medullary: altered VISUAL vertical, leaning toward side of lesion d/t imbalance in vestibular input. Visual feedback less helpful here (vs pusher’s syndrome) d/t visual vertical being so impaired.
PICA stroke
HOARSENESS is unique to PICA strokes! (“You have to pike to get up on the horse!”) (Also get saccadic lateropulsion, skew deviation, and vocal cord paralysis)
Affects dorsolateral medulla (aka Wallenberg syndrome) and inferior portion of cerebellum
BOTH PICA and AICA strokes see:
- Vestib nystagmus/vertigo
- Decreased facial sensations IPSILATERALLY
- Dissociated sensory loss to pain and temp CONTRALATERALLY
- Horner’s syndrome (PAM: Ptosis, Anhydrosis ipsilaterlaly, and Miosis)
- Ipsilateral limb ataxia
- Gait ataxia
AICA stroke
TINNITUS, HEARING LOSS are unique to AICA strokes d/t Impact on peripheral vestib system (labyrinthine artery). Also see dizziness, facial weakness, gaze palsy.
Impacts lower 2/3 of pons and ventrolateral Cb
BOTH PICA and AICA strokes see:
- Vestib nystagmus/vertigo
- Decreased facial sensations IPSILATERALLY
- Dissociated sensory loss to pain and temp CONTRALATERALLY
- Horner’s syndrome (PAM: Ptosis, Anhydrosis ipsilaterlaly, and Miosis)
- Ipsilateral limb ataxia
- Gait ataxia
How do you differentiate central positional nystagmus (CPN) vs BPPV?
CPN has:
- NO latency
- Does NOT fatigue
- Long duration
- May be vertical nystagmus +/- apogeotropic
- May have severe nausea/vomiting even with a single maneuver (normally w/BPPV, it’s the repeat testing/maneuvers that makes them feel yucky)
- Coexisting Cb or central oculomotor signs
- Lesion of vestibulo-Cb - Flocculonodular lobes
Chiari Malformation classification
Type I-IV - what is most severe?
Describe each type
Type I least severe -> Type 4 MOST severe
Type I: Caudal herniation of Cb tonsils <=5mm below foramen magnum (not usually accompanied by descent of brainstem or 4th Ventricle, not associated w/presence of hydrocephalus)
Type II: Caudal herniation of Cb vermis, brainstem, and 4th ventricle through foramen magnum
Type III: Occipital encephalocoele, with some of the intracranial defects associated with Chiari II malformation
Type IV: Cereellar aplasia or hypoplasia, associated iwth aplasia of the tentorium cerebelli
Symptoms of chiari malformation
- Suboccipital HA
- Neck pain (non-radicular, constant/burning, WORSE with Valsalva)
- Vestibular symptoms: positional or movement related dizziness
- Oculomotor abnormalities: diplopia, photophobia, downbeat nystagmus
Management of Chiari Malformation?
Surgical: decompress posterior fossa (but you can’t actually translate/shift the Cb back to where it was supposed to be!)
Rehab: PT to address cervical impairment, postural control
Pain management: HA, chornic neck pain
Downbeat nystagmus may be seen with…
- Bilateral CEREBELLAR lesion of the flocculus or paraflocculus, or a lesion at the bottom of the 4th ventricle
- Craniocervical junction anomalies, Chiari malformation, Cb degeneration, drug-induced dysfunction, or congenital!
Impact of downbeat nysgamus on function
Beats downward in primary gaze position and increases with eccentric gaze (e.g. look a little to R or L)
Pts tend to fall BACKWARD!
The petrous bone is part of the ___ bone located near the internal auditory meatus. Common findings if you fracture your petrous bone include…
- Hemodympanum
- CSF otorrhea
- Facial paralysis
- Ossicular dislocation (hearing)
- Dizziness in ~50%
- Positional nystgamus (most common related vestib impairment)
- UVH can also occur
With temporal bone fractures, we tend to see what symptoms?
With a longitudinal temporal bone fx (force vector traveling laterally, like its going in your right ear and toward midline):
- Conductive hearing loss (50-65%) but damage to vestibular or cochlear nerves is infrequent
- CSF and hemorrhagic otorrhea
- Facial nerved involved 10-20% of the time, usually in labyrinthine segment or genticulate ganglion
With transferse temporal bone fx (force vector coming in your forehead traveling posteriorly, results in diagonal fx of temporal bone)
- Hearing and vestibular loss in 80-95% of pts! Lacerates labyrinth or vestib/cochlear nerve
- Facial nerve in 50-65%
- CSF often fills middle ear, drains into Eustachian tube -. Pts feel salty taste/fluid down throat (which is the CSF!)
- Tympanic membrane usually intact but hemotympanum frequent
Migraine - what is it?
Neurochemical event in the CNS that…
- Activates the trigeminovascular pain system
- Migraine generator is in the brainstem
- Serotonin and NE released
- More than 1 initiating process
We see a wave of neurogenic/ vascular changes in brain, with cortical-spreading depression (hyperpolarization then depolarization in the brain)
Results in vasodilation and protein extravasation (inflammatory response)
Sensitization that lowers the response threshold of mechano receptors (causes pain and other sensory sensitivity)
Symptoms depend on location of all of the above in the brain (e.g. light, movement or pain sensitivity)
Accumulating evidence that there is a strong genetic component
Migraine criteria
- Headache attacks lasting 4-72 hours if untreated
- At least 2 of the following:
Unilateral location
Pulsating quality
Moderate to severe pain intensity
Aggrivation by routine physical activity
During HA, need at last 1 of the following:
Nausea and/or vomiting
Photophobia and phonophobia
Could also he migraine w/aura! Includes the above as well as one or more completely reversible aura symptoms that indicate focal cerebral cortical and brain dysfunction:
- Visual scotoma (area of diminished visual feield)
- Visual hallucination (zig zag or wavy line, colored lights or balls, shimmering pattern)
- Hemibody weakness or numbness
Testing: low amplitude positional nystagmus, mild impairment in DVA, no evidence of UVH with head impulse testing, symptoms of visual motion intolerance and motion sickness, and a recent increase in frequency and intensity of migraines would point to vestib migraine
Vestibular migraine criteria
(1) Diagnosis of migraine
(2) 2 episodes of intermittent vertigo or disequilibrium (+ phono or photo phobia, visual changes) that is associated w/migraine
Migraine interventions?
Exercise (20 mins 4x/week ) is EQUALLY effective as meds (topomax) or relaxation at preventing/decreasing HA frequency!
Efficacy of PT for central vestibular disorders?
Pts with central vestib disorders DO improve dizziness and imbalance after PT…but cerebellar dz improves the least.
Pts with the most severe disability (highest DHI = dizziness handicap inventory) has the greatest improvement after PT!
BUT central vestibular disorders have generally worse outcomes than JUST central (without vestib involvement) or JUST Peripheral vestib disorder.
Slower progression, duration of intervention tends to be longer
Central vestib disorders tend to do better than mixed central and peripheral impairment!
Spontaneous nystagmus
Central features?
Peripheral features?
Central: vertical, torsional, or pure horizontal; more likely to be present on a chronic basis; fixation removal may increase or decrease intensity of nystagmus
Peripheral: mixed horizontal/torsional; present with fixation on a short-term basis (<1 week until CNS compensates); enhanced or exclusively present with fixation removed (w/Frenzels or light in eye)
What is “Alexander’s Law” as it applies to nystagmus?
Peripheral vestibular-origin nystagmus INCREASES in intensity with gaze toward fast phase (toward intact side) and decreases toward slow phase (affected side)
Head impulse test needs to be ___ deg/sec velocity within the plane of the canal to be tested.
Head impulse test needs to be 180 deg/sec velocity within the plane of the canal to be tested. Any slower, they can use smooth pursuit to stay with you!
Rapidly moving nose toward the side that you are testing
If you look at head impulse for the anterior (start in upright, move quickly in plane of anterior canal down to R = testing R anterior canal) or horizontal canal (the usual side to side in 30 deg flex) or in the plane of the utricle (horizontal shift) bias the SUPERIOR vestibular nerve
Plane of posterior canal (start in flexion and move diagonally back toward upright!) looks at INFERIOR vestibular nerve function
Sn and Sp vary based on severity of the unilateral loss, but if you pool all pts together:
Sensitivity 76% (can get false negatives in some scenarios)
Specificity 94%
Role of hyperventilation in vestibular testing?
Useful to assess exertionally induced dizziness; can act as a strong irritant to vestibular dysfunction and induce hyperactivity on affected side (and in this weird situation, fast phase toward affected side!) Can be c/f demyelination (schwannoma vs MS on 8th nerve, vs a lighter response may suggest neuritis, hypofxn etc)
1 breath/sec for 40 seconds, use frenzels!
Symptoms within 20 sec without nystagmus MAY suggest anxiety
Nystagmus induced by hyperventilationonly may imply unilateral vestibular hypofunction or Cb pontine angle tumor.
Pt tends to fall/LOB AWAY from fast phase
More common to be abnormal in Cb pontine angle tumors/schwannoma that tends to beat TOWARD SIDE OF INVOLVEMENT
Role of Mastoid Vibration in vestibular testing?
Uses 100Hz vibrator to each mastoid process
Normal: = nystagmus bets TOWARD side being vibrated
Abnormal = nystagmus beats in the SAME direction no matter which side the vibration is applied to.
98% of the time, nystagmus is directed toward the INTACT (contralesional) side
Sensitivity:
98% with complete unilateral vestib loss vs 75% with partial unilateral vestib loss
During vestibular testing, use Frenzel lenses to block fixation during [which tests?]?
- Spontaneous nystagmus and gaze holding (assess w/fixation and again w/goggles!)
- Head shake nystagmus
- Hyperventilation
- Mastoid vibration
CTSIB
Which condition biases vestibular input?
Condition 4 (foam, EC) - tells you pt is not using vestibular cues well to maintain balance!
FYI: it was demonstrated for assessment, NOT to monitor change over time!
Timed Up and Go
Cutoffs for fall risk in…
>___ sec in community-dwelling adults
>___ sec in bilateral vestibular disorders
>___ sec in variety of vestib disorders
Cutoff for probable ADL impairment?
Timed Up and Go Cutoffs for fall risk in... >13 sec in community-dwelling adults >13.5 sec in bilateral vestibular disorders >11.1 sec in variety of vestib disorders
Cutoff for probable ADL impairment is >30 sec
Correlates with 5x Sit to Stand
Performance may decline w/loss of saccular fxn, but not loss of horizontal/utricle canal fxn!
Four Square Step Test
Fall risk predicted by cutoff score of __ sec in community-dwelling older adults
> __ sec suggests increased fall risk in pts w/vestibular disorders
Four Square Step Test
Fall risk predicted by cutoff score of 15 sec in community-dwelling older adults
> 12 sec suggests increased fall risk in pts w/vestibular disorders
Good test retest reliability
5 Times Sit to Stand Test
Cutoff: >___ sec identifies high fall risk
Cutoff: >15 sec identifies high fall risk in vestibular; >12 sec CVA; >16 sec PD
MCID >2.3 sec
Norms by age:
50s: 7.1 sec
60s: 8.1 sec
70s: 10 sec
80s: 10.6 sec
43cm high chair w/backrest but no armrests, arms across chest
Excellent test retest reliability
DGI
<=___ correlated with high fall risk
MCD = __
8 tasks scored 0-3, max score (best) 24
<=19 correlated with high fall risk
MCD =2.9
Excellent test retest reliability!
Better than Berg at identifying fall risk in those w/vestib disorders! BUT might have a ceiling effect for pts w/vestib disorders - FGA might circumvent that problem
Fall risk cutoff scores on the…
DGI =
Four-Square Step test =
5 time sit to stand =
TUG =
Fall risk cutoffs:
DGI = <19 / 24
Four-Square Step test = >12 sec vestib (>9.68 PD, >15 CVA,
5 time sit to stand = >15 sec
TUG = >13.5 community dwellers, >14 CVA, >7.95 vs >11.5 PD, >11 vestib (and >30 sec is probable ADL impairment)
Which of the following will resolve with time without vestibular rehab?
Which of the following have enhanced recovery with vestibular rehab?
- Decreased responsiveness of VOR to angular accelerations
- Gaze-evoked nystagmus
- Lateropulsion
- Decreased responsiveness of the VOR to translations
- Spontaneous nystagmus
- Dynamic postural imbalance
STATIC deficits; resolve with time (if otherwise normal nervous system) vestibular rehab won’t help much:
- Spontaneous Nystagmus
- Gaze-evoked nystagmus
- Lateropulsion
DYNAMIC deficits (occur with head movement)for which recovery is enhanced with vestibular rehab:
- Decreased responsiveness of VOR to ANGULAR accelerations or TRANSLATIONS (need to generate error signal with ACTIVITY to stimulate adaptation!)
- Dynamic postural imbalance
What strategies do patients learn to use to enhance gaze stabilization following vestibular loss and compensate for oscillopsia?
- Preprogrammed saccades (embedded in head movements; this is the primary one)
- Blink with head movement
- Utility of smooth pursuit to maintain gaze stabilization may be enhanced by ~10%
- Reweighting of sensory cue utilizaiton (a function of the Cb)
- Cervico-ocular reflex enhancement? (limited to low frequency movements)
With Gaze Stabilization exercises, what drives compensation?
Slippage = error signal!
Try to get them to move a little quicker so they can induce the impairment and drive compensation!
Progress from handheld (has some kinesthetic input) targets to those in environment
Vary target distance, axis of rotation/plane (all SCCs, utricle and saccule!)
Mix in balance exercises, varied surrounds!
Remember, just smooth pursuit or saccades (without head movement) do nothing because that’s training the CNS not peripheral system! So move the head!!
What drives balance compensations in vestibular disorders
(1) Enhance use fo proprioception
- Reduced Cb inhibition of proprioceptively triggered postural responses -> sensory reweighting!
- Synaptogenesis at the level of the vestibular nuclei that represents increased somatosensory inputs!
(2) Using residual vestibular function in a more meaningful way
(3) Using sensory substitution (light touch - e.g. furniture, cane, and vision)
(4) Sensory addition?
- Vibratory or auditory prosthetic to augment sense of where you are in space
Any role for biofeedback/vibration in balance retraining in vestibular dysfunction?
- Provides vibratory feedback/cues through the trunk in response to a M/L tilt
- In individuals with unilateral vestibulopathy, device seems to improve both STATIC and DYNAMIC postural control!
In community dwelling older adults at risk for falls, this decreases M/L sway with gait and improves DGI score!
BPPV Hx: Possible provocative factors or activities which bring it on?
Bed mobility (rolling, supine to sit)
Rising from couch/chair
Reaching for objects on floor, under cupboard, top shelf
Grooming (washing hair,e ye drops, dressing)
working under car, carpetry, painting
Dental chair (might also be a time you acquire BPPV given position + vibration may loosen/mobilize otoconia!)
Diagnositc procedures w/head dependent (CT, MRI, surgery)
If pt gets dizzy rolling over in bed and it lasts >15 seconds, highly predictive of BPPV!
BPPV demographics
F>M (~66% female)
Increasingly common as we age due to deterioration of otoconia integrity, might be more common w/osteoporosis too (hence the F>M)
Sometimes incited by head trauma
By canal, MOST (~80%) are posterior canalithiasis, followed by horizontal canalithiasis (7%) or multicanal involvement. Anterior canal is pretty rare!
BPPV - describe cupulolithiasis vs canalithiasis
CUPULOLITHIASIS
- Otoconia adherent to cupula of the involved semicircular canal, which is then displaced by gravitational forces.
- Immediate onset vertigo and nystagmus (no latency)
- > 60 sec duration, gradually decays
- Nystagmus intensity is typically less than that seen w/canalithiasis
CANALITHIASIS:
- Free-froating debris entrapped within the SCC
- Debris is likely a cluster of cross-linked utricular otoconia with underlying otolithic membrane
- Variable latency (0-30 sec, on average ~4.25 sec; so HOLD POSITION for a full 30 sec! But not longer) followed by…
- Nystagmus with symptoms which lasts ~14 sec
- You see REVERSAL of the nystagmus in ~75% of trials with return to sitting after Dix-Hallpike testing!
When you’re supine, how do otoconia get into your SCCs and why are some more likely than others?
When supine, otoconia can get into canals via common crus (which if you continue traveling toward the bed pops you into the posterior canal) or into the horizontal canal!
The anterior canal comes off of the common crus too BUT it is really horizontal (parallel to the bed) there, mechanically would be really hard in supine (without flipping back onto your head) to get otoconia there
What explains the latency of BPPV/nystagmus onset?
Latency explained by the movement of detached otoconia through the ampulla.
We see no nystagmus initially while because pressure caused by the moving otoconia is negligible while moving through (falling down in) the wide ampulla… until it enters the narrow duct of the semicircular canal, at which point we see onset of symptoms and nystagmus!
Otoconia move SLOWLY - ~0.2mm/s, ~1% of the circumference of the canal each second.
Interaction between the particle and the wall of the ampula vs SCC accounts for a considerable amount of variation in duration and latency of BPPV.
Dispersion of a clump of otoconia creates MORE (not less) pressure therefore MORE nystagmus, so it does not explain fatiguability.
Cupulolithiasis likely produces a far WEAKER nystagmus than canalithiasis.
The inertial effects of treatment maneuvers cause negligible movement of otoconia - BPPV depends on GRAVITY not you slamming the patient into the table
Predisposing / risk factors for BPPV
- Age: Older more likely (~10% of adults >65yo have it) <3% are under 40yo
- 2:1 F>M
- Genetic: Chromosome #15?
- Inner ear disease (“secondary BPPV”)
- —> Meniere’s
- —> BIlateral incomplete ototoxicity
- —-> Condition after stapedectomy
- Osteopenia / osteoporosis
- Serum vitamin D levels
- Head trauma / sudden acceleration or deceleration of the head (not uncommon for these types to be bilateral, multicanal, and harder to treat after trauma)
- Sleeping position/prolonged immobility (more common in the “down ear” if you’re a side sleeper)
- Right BPPV > Left BPPV (1.4: 1 ratio) (largely because people seem to sleep with dominant side down)
Horixontal canal - how to know which side it is?
Geotropic - feel worse and bigger nysgamus with INVOLVED ear down
Ageotrophic -feel worse and bigger nystagmus with UNINVOLVED ear down because creates excitatory signal from opposite side!
What is subjective BPPV?
Subjective BPPV: history consistent with BPPV, but nystagmus apparent with symptom provocation during positioning tests
- Repeat testing advisable, along with very close inspection for nystagmus
- Reasonable to trial canalith repositioning maneuvers on a limited basis based on history
- Evidence of significant improvement in DHI scores in subjects treated with maneuvers
What is secondary BPPV?
Secondary BPPV = BPPV along with additional evidence of labyrinthine dysfunction:
- presence of caloric weakness associated with greater number of canalith repositioning maneuvers to control BPPV
- Mean # of treatments required, higher recurrence rate
- -> Idiopathic BPPV: ~1.34 treatment sessions
- –> Secondary BPPV: ~4.28 treatment sessions
- Multicanal involvement more common
Describe findings for:
- Posterior canal BPPV canalithiasis
Posterior canal BPPV canalithiasis =
UPBEAT + torsional (toward down ear) nystagmus, lasts seconds
Describe findings for:
- Posterior canal BPPV cupulolithiasis
Posterior canal BPPV cupulolithiasis =
UPBEAT + torsional (toward down ear) nystagmus, lasts >1 minute
Describe findings for:
- Horizontal canal (posterior arm) BPPV canalithiasis
Horizontal canal (posterior arm) BPPV canalithiasis GEOTROPIC nystagmus, lasts seconds, more intense with AFFECTED EAR DOWN
Describe findings for:
- Horizontal canal (anterior arm) BPPV cupulolithiasis
Horizontal canal (anterior arm) BPPV cupulolithiasis AGEOTROPIC nystagmus, lasts >1 min, more intense with UNAFFECTED EAR DOWN
Describe findings for:
- Horizontal canal (posterior arm) BPPV cupulolithiasis
Horizontal canal (posterior arm) BPPV cupulolithiasis Persistent apogeotropic nystagmus, more intense with UNAFFECTED ear dependent
Describe findings for:
- Anterior canal BPPV canalithiasis
Anterior canal BPPV canalithiasis (rare)
- Torsion to the AFFECTED side and DOWNBEAT nystagmus lasting seconds
Other causes of positional dizziness / nystagmus
Migrainous positional vertigo (for example, if you do a roll test, see geotropic nystagmus >1 minute, there is no peripheral explanation for this [ since cupulolithiasis would result in AGEOtropic nystagmus!], so it stems from some central cause, e.g. migraine even without active HA!)
Cerebellar degeneration (Pure downbeat nystag w/ Dix-Hallpike c/f Cb involvement)
Chiari malformation
Anxiety/phobia
Malingering
Blood product in endolymph
Orthostatic HoTN
Peripheral vestib hypofxn (tends to be worse with involved ear down)
Intoxication (alters weight of the cupula)
MS lesions
CPA mass or stroke
How to test for posterior canal calithiasis?
DIX HALLPIKE (loaded dix hallpike = false negative <5% = better sensitivity but pts can be more symptomatic) - 45 deg rotation (loaded dix = flex forward 30 deg first and hold there 30 sec to load otoconia toward cupula) THEN flatten and tip head back ~20 deg, watch eyeballs. Hold at least 30 sec. Watch if nystagmus is > or < 1 min. Then sit back up and keep head rotated. Guard closely to make sure pt doesn't fall backward once they're up!
SIDELYING TEST (alternative to Dix Hallpike, good for pts with LBP or limited spinal mobility / lots of kyphosis, and maybe those with CHF that can't tolerate supine) - Head rotated 45 deg CONTRALATERAL to the posterior canal being tested, then descend to the side that is ipsilateral to the canal being tested (i.e. test R PC = rotate head L, then tip down quick onto R shoulder in sidelying) once down, chin should be ~30 deg higher than forehead, watch nystagmus!
How to test with posterior canal cupulolithiasis?
“Half Dix-Hallpike”
- Cupula sits at roughly a 30 deg angle to the post SCC itself, so to really bias the cupula and put it perpendicular to gravity, need to modify head position in the dix hallpike so that pt is about 30 deg FLEXED (in supine) instead of being supine and 20-30 deg extended.
- Sustained UPBEAT nystagmus with TORSION toward the affected/down ear suggests post SCC cupulolithiasis. Should be more intense here compared with formal Dix-Hallpike testing. Should NOT reverse when returned to upright sitting. Does NOT benefit from any “loading” (pre-dix hallpike flexion of neck) as the crystals are already on the cupula.
How to test with horizontal canal canalithiasis?
SUPINE ROLL TEST
- Supine, with head flexed to 30 deg. Then rotate head ~60 deg to 1 side, watch for nystagmus. Most of the time, come back to midline and pause (though may evoke stronger nystagmus without the pause), then retest to other side. Do several cycles to compare L to R to discern if nystagmus is stronger to one side or the other. Can also do w/ a logroll to one side or the other if cervical rotation is limited.
BOW AND LEAN TEST
(bow is the coming forward, and “lean back” )
Lean forward with goal to tip head down ~120 deg (video goggles are really helpful!), then once nystagmus stops, then sit up and tip head BACK 60 deg! No rotation R/L throughout.
This helps to LOCALIZE to the involved ear (particularly if you can’t sort it out with roll test).
Canalithiasis: nystgamus will beat to INVOLVED Side with bow (fwd; bow is excitatory for horiz canal!) and to the UNINVOLVED SIDE with lean (backward)
Cupulolithiasis: : nystgamus will beat to INVOLVED Side with lean (back) and to the UNINVOLVED SIDE with bow (fwd)
BPPV testing guidelines…
- Thoughts on repeat examination?
- Thoughts on premedication?
- Thoughts on guarding/safety?
- Thoughts on vomit?
BPPV testing guidelines…
- Thoughts on repeat examination?
- –> Repeat exam may be necessary to confirm BPPV!
- Thoughts on premedication?
- —> Vestibular setatives (especially valium d/t short acting!) may be helpful especially if pt very anxious. Sublingual Zofran can help w/nausea/emesis. In RARE cases, anesthesia (propofol) can be used.
- Thoughts on guarding/safety?
- –> GUARD SO closely especially when you bring them back up!
- Thoughts on vomit?
- –> Let pt’s know they may become ill/dizzy - “this may provoke your symptoms, you could get nauseous or produce emesis, but it should go away after a matter of second”
Any role for surgical management in BPPV?
Can do canal plugging - reasonable to consider in patients with recurrent BPPV if maneuvers fail to provide relief for a substantial period of time, often in individuals that have an occupation where they can’t avoid aggravating positions
RISKS:
- Total hearing loss in ~1%
- Total loss of vestibular function in ~13%
(it’s an intracranial sugery)
How to treat posterior canal canalithiasis?
Modified Epley maneuver
OR Semont/Liberatory Maneuver
STRONGER evidence for Modified Epley, but in theory, Semont should work (though is more prone to operator error in novice clinicians). Could consider adding vibration during Semont maneuver in both the initial positon and when you flip them if you’re treating CUPULOlithiasis
Might fix it in 1 maneuver, but recheck and do a 2nd…maybe a 3rd if you still see nystagmus.
Modified Epley:
1) Start w/Dix hallpike position, hold initial position ~30 sec past resolution of nystagmus.
2) Keep neck extended, rotate head to 45 deg rotation to other side
3) Bend knee and roll onto sidelying in the direction head is facing and KEEP HEAD rotated - this spot tends to be dizzy too
4) Once in sidelying, tuck chin into the bottom shoulder - nose should be at 45 deg angle to the ground. Wait for nystag resolution + 30 sec (or longer, just needs to be long enough)
5) Now have pt grab your forearms, drop feet off of bed, and assist to sit up KEEPING CHIN TO CHEST!
Successful maneuver = nystagmus does NOT reverse once upright
Semont/Liberatory Maneuver:
1) Start in sitting, rotate head away from posterior SCC to be treated. Quickly lie down into ipsilateral sidelying (treating R post SCC -> rotate L -> lie down on R side) just like the sidelying test. Chin ~20 deg above forehead. Hold for nystagmus duration + 30 sec.
2) QUICKLY (<1.33 sec) bring patient back up through sitting and over onto the opposite shoulder, now nose should be toward the bed/floor (40 deg angle toward floor) and tuck chin to the bottom shoulder. Hold for duration of nystagmus + 30 sec. Nystagmus here should be the SAME as in the first position (if treating R post SCC, should be upbeating and torsion to R)
3) Sit back up, keep chin to chest, and guard pt.
Common complication of treating (e.g. right) posterior canal BPPV?
- Conversion to ipsilateral horizontal canal BPPV, as noted by short (<60 sec) duration geotrophic nystagmus during repeat Dix Hallpike testing. Then, you want to go treat that with a RIGHT Gufoni maneuver!
- Reversal in nystagmus (in reassessment via Dix Hallpike) so you might see a downbeating left torsional nystagmus, suggesting debris REENTERED the canal from the utricle
- Consistent upbeating R torsional nystgamus, suggesting debris is still trapped in the posterior canal - continue with the Modified Epley!
How to treat horizontal canal canalithiasis?
Gufoni’s Maneuver
- Advisable to repeat maneuver, minimal risk fo debris re-entry into horizontal or posterior canal
- Doesn’t work after several trials? Consider treating the opposite side! You might have misdentified affected side with roll testing.
- Nausea/vomiting is more common when testing/treating horizontal BPPV
- Maneuver is supported by meta-analyses
[Can ‘pre-load’ for this: Tip head ~60 deg back obliquely toward SIDE YOU ARE TREATING to load debris in the back arm/posterior aspect of the horizontal canal]
(1) Keep head tipped back and toward affected side, then quickly assist pt to lie down toward their UNINVOLVED side, now with head in neutral rotation and parallel to ground, facing you. Hold for duration of nystagmus + 30 sec.
(2) Body stays still, rotate head down to look at the bed, hold for duration of nystagmus + 30 sec.
(3) Assist pt back to upright sitting, guard closely
How to treat horizontal canal cupulolithiasis?
Best bet is Kim Maneuver (but needs further studies to support efficacy here)
E.g. to treat L side horiz canal cupulolithiasis
(1) Start in L sidelying.
(2) Rotate head to left (nose toward table) and use a vibrator to L mastoid process in this position x1-2 mins, then wait here another 1-2 mins.
(3) Stay in L sidelying, but bring head back to neutral rotation and hold until nystagmus abates.
(4) roll to supine, keep head/neck ~20-30 deg flexed. In this position, if you get a strong burst of R-beating nystagmus (opposite to side you’re testing), that’s a strong indication the debris is loose! That’s good! If you’re supine and see light L-beating nystagmus (toward side you’re testing), the debris is likely still adhered to cupula.
(5) Roll into R sidelying (affected ear up), keeping head parallel to ground and in neutral rotation. If pt has persistent ageotropic nystagmus in this position, vibrate again! Clearly particles are still stuck. Goal is to loosen them. IF you get a burst of GEOtropic nystagmus that lasts seconds then stops, thats good! That means debris is loose. So need to watch closely here.
(6) Body stays, turn nose down to ground, hold here for nystagmus duration + 30 sec
(7) Assist pt to sit up keeping head/neck neutral
GOAL IS TO CONVERT TO GEOTROPIC NYSTAGMUS (then you can treat that w/Gufoni’s maneuver).
If still ageotropic, nystagmus is still adherent!
Vibration is applied x30 seconds in the positions noted above. Vibration is an effective stimulus to detach otoconia from cupula!
Any precautions for patient after BPPV treatment maneuvers?
- Avoid affected ear dependency x1-2 days
- –>Sleep in recliner
- –> Sleep with HOB slightly elevated (wedge, extra pillow); sleep on unaffected side to reduce recurrence
Efficacy rate for 1 treatment session with maneuvers is 80-90% - so ~1/10 will need f/u treatment session to be effective BUT recommend a f/u treatment session regardless to do repeat roll & Dix-Hallpike testing to make sure it’s totally cleared.
Not every therapist does this FYI
Recurrence in BPPV
Recurrence rate at 1 year =
Recurrence rate at 5 yrs
What does or doesn’t help recurrence?
Recurrence in BPPV?
Recurrence rate at 1 year = ~25% (higher short term recurrence in individuals w/head trauma in the 1st yr, though they recur less longer term!)
Recurrence rate at 5 yrs = ~50%
What does or doesn’t help recurrence?
- Instruct in self-diagnosis and treatment if indicated!
- Use of daily Brandt-Daroff exercises does NOT appear to reduce recurrence rate
- Daily performance maneuvers does NOT appear to reduce the recurrence rate!
