peripheral vestibular disorders Flashcards
red flags
- lightheadedness
- disequilibrium without dizziness
- sudden onset of hearing loss
- drop attacks
- severe neck pain and instability
- facial numbness
- unexplained neurological signs
membranous labyrinth
- structured suspended within the bony labyrinth by fluid and is supported by connective tissue
- contains the membranous portion of the three SCC, utricle, saccule
- filled with endolymph
cupula
- located within the ampullae, bulbous gelatinous mass that surrounds the hair cells
ampullae
-widened portion of the SCC near the urticle which contain the sensory hair cells
semicircular canals
- measures angular acceleration
- inertial forces on the endolymph fluid withinthe canal that cause relative fluid flow around the canal in the opposite direction if the direction of the acceleration. this deflects the cupula and bends the hair cells proportional to the accleration
push-pull orientation
- each canal has a mate on the other side that lies on the same plane
- each pair works in a push-pull manner where one canal of the pair is excited and the other is inhibited during head rotations
- reciprocating connections between the MVN
scarpa’s ganglion
- portion of the VIII, vestibular nerve innervates the labyrinth
- the nerve contains two fascicles: superior- utricle andt. and horizontal SCC
- inferior- saccule and post SCC
-cell bodies of each axon lie on the VIII nerve lie within Scarpas’s ganglion located in the internal auditory canal
otoliths
- strutures within the inner ear that sense linear acceleration and sustained head tilt relative to gravity
- contain a region of hair cells. the hair cells protrude into a gelatinous matrix called the macula
- maculae is covered by a surface of calcium carbonate crystals called otoconia
Bending away or towards the kinocilia
- bends towards kinocilia the result is incr neural firing
- bends away from the kinocilia the result is decr neural firing
Vestibulo-ocular Refelx VOR
- vestibular afferents to the vestibular nuclei
- vestibular nuclei output to oculomotor components resulting in:
- -coordinated head and eye movment
- gaze stabilization with eyes moving equal to but in the opposite direction of head movement
angular VOR
- mediated by the SCC
- moves the eyes in the opposite direction and synchronously with the angular motion of the head to keep the eyes stable
VOR cancellation –pos
- central involvement.
- override reflex
linear VOR
- linear VOR mediated by the ptoliths and moves the eyes horizontally in the opposite direction
ocular tilt
mediated by the utricle and rights the head towards vertical, torts the eys opposite to thebody tilt and elevated the dependent eye
Peripheral vestibular disorders primary S/S
- dizziness or vertigo
- imbalance
- nausea
- disequilibrium, general motion intolerance
- disrupted vision
Peripheral vestibular disorders secondary S/S
- falls and secondary injury
- anxiety, depression
- fatigue
- deconditioning
- poor memory, concentration
- loss of confidence, reduced independence
- neckpain and stiffness
duration of dizziness
- acute dizziness (cont < 3days)
- chronic dizziness (persistent >3 days)
- spells
- -lasts sec- BPPV, perilymphatic fistula, orthostatic hypotension
- -lasts minute- TIA, migraine,panic attack
- -hours or days- Meniere’s and hydrops
BPPV
- most common peripheral vestibular disorder
- brief episodes of vertigo generated with positional change
- most common cause of dizziness encountered in the clinic
pathophysiology of BPPV
-canalithiasis
-otoconia are freely mobile in one of the SCC, usually the posterior canal and fall to the lowest portion of the canal. movement of the otoconia induces flow of the endolymph and deflection of the cupula
pathophysiology of BPPV
- cupulolithiasis
otocnia have adhered to the cupula increasing the density of the cupula so the canal becomes sensitive to grvaity
classic symptoms of BPPV
- brief episodes of vertigo associated with changes in head position relative to gravity
- lying down or rising froma horizontal position
- rolling over in bed
- bending over
- looking up
- accompanied by nystagmus
- motion sensitivity
- nausea
nystagmus
- direction usually up-beating and torsional
duration generally <2minutes - fatigues in canalisthiasis
- doe snot fatigue in cupulolithiasis
direction of nystagmus for what canals
- posterior canal: up beat and torsional
- anterior canal: down beat and torsional
- horizontal canal- ageotrophic
only upbeating: central issue
labyrinthitis
- inflammation of the inner ear including the cochlea
- viral and bacterial causes
- hearing impaired
- plateaus in 24 hours
- peak symptoms continue for 2-4 days
chronic complaints of labyrinthitis
- some hearing loss persists
- head motion intolerance
- decr balance in the dark or busy visual environments
labyrinthiatis treatment/recovery
- antivert, valium during acute stages
- viral steroids, antibotics
- vestibular rehabilitation emphasizing habituation to motion intolerance, gaze stabilization, balance re-training
vestibular neuritis
- second most common cause of vertigo
- ages 30-60 most commonly affected
- usually secondary toa viral infection
- gradual but rapid onset
- peak at 24 hrs and cont for 3-4 days
residual sx of vestibular neuritis
head movement intolerance
- postural imbalance
- generalized motion sensitivity
clinical findings of vestibular neuritis
- nystagmus
- saccadic VOR with head rotation to the affected side
- imbalance
- rigid trunk and head with gait “ en-bloc”
- head shake induced nystagmus
- impaired dynamic visual acuity
- ataxic gait
- no hearing loss
tx and recovery for vestibular neuritis
- antivert, valium
- antihistamine
- vestibular rehab: habituation for motion intolerance, gaze stabilization, balance re-trainning
Meniere’s disease and hydrops
- plumbing problem
- decr reabsorption of the endolypmh in the endilymphatic sac
- increased endolymph volume leads to membranous labyrinth distension. ruptures of membranes, K+ imbalances, receptor activity inhibition
meniers and hydrop Symptoms
- aural fullness
- fluctuating hearing loss
- tinnitus
- vertigo which peaks in munutes of onset and can take hours to subside
- postural intability
- generally progressive
clinical findings in meniers and hydrops
- asymptomatic between episodes
- progresses to inter-episode symptoms gradually worsening
- fluctuating hearing with progressive low Hz loss
tx menier’s and hydrops
- diest/salt restrictions
- diuretics
- surgical: endolymphatic shunt, vestibular nerve section, labyrinthectomy, gentamicin
- vestibular rehab
perilymphatic fistula
- rupture between the middle and inner ear. perilymph leaks into middle ear
- precipitating event: head trauma, barotrauma, tympanic penetration
- patient will often report a “pop” at onset
patients symptoms in perilymphatic fistula
- vertigo
- tinnitus and hearing loss (conductive)
- imbalance
- gaze stability
- symptoms can be elicited by auditory stimuli
- symptoms can be eased with res/quiet
clinical findings of perilymphatic fistula
- vertigo
- nystagmus or skew deviation
- symptoms increased with valsalva
tx of perilymphatic fistula
- bed rest with head elevated for up to 3 weeks
- no Valsalva stool softners
- avoid cogh sneeze
- surgical patch if hole seen in round or oval window
- vestibular ex if indicated
acoustic neuroma
-nerve sheath tumors occurring in the internal auditory canal at the cerebellopontine angle
acoustic neuroma symptoms
- progressive, unilateral sensorineural hearing loss
- tinnitus and mild imbalance
- vertigo present n less than 20% of cases
clinical findings of acoustic neuromas
- may see positive head thrust towards the involved side
- positive head shake (nystagmus)
- smooth pursuit and saccadic deficits if the cerebellum or brainstem involved
tx of acoustic neuroma
0- wait
- radiosurgery
- surgical resection
- vestibular rehab after surgery
- “full” function return one year after surgery
bilateral vestibular loss
- meningitis
-ostosclerosis
-polyneuropathy
bilateral tumor
-congenital malformation
ototoxicity
- irreversible
- vestibular loss occurs before hearing loss
- aminoglucosides have ototoxic effects
clinical findings of otoxicity
- decr VOR
- postitive VOR
- positive sharpended Romberg
- pos dynamic visual acuity test
- imbalance
treatment of ototoxicity
- avoid vestibular suppressants/otitoxins
- vestibular rehabilitation
- 6-18 months of optimal recovery