Hearing & Balance/Vestibular therapy Flashcards
(112 cards)
1
Q
Vestibular system made up of 3 components:
A
- peripheral sensory apparatus
- central processor
- mechanism for motor output
2
Q
What nerves innervate the vestibular system?
two branches?
A
CN VIII (vestibulocochlear nerve)
- Superior division: utricle and anterior and horizontal semicircular canal
- Inferior division: saccule and posterior semicircular canal
3
Q
Describe vascular supply to vestibular system:
A
Basilar artery –> AICA –> Labyrinthine artery –> DIVIDES:
- Anterior vestibular artery: Anterior SCC, Horizontal SCC, Utricle, vestibular nerve
- Common Cochlear Artery –> posterior vestibular artery: posterior SCC, sacule
4
Q
Canals are responsible for: ______.
three parts:
A
angular acceleration of the head:
Anterior semicircular canal
Posterior semicircular canal
Horizontal semicircular canal
5
Q
What are the otolith organs?
Responsible for?
A
Utricle and Saccule
Linear acceleration of head
6
Q
What are the motion sensors of the VS?
A
hair cells
7
Q
- Semicircular canals are arranged _____ to each other
2. ___#__ semicircular canals become __#__ coplanar pairs
A
perpendicular to each other. 6 semicircular canals become 3 coplanar pairs. - right and left horizontal - left anterior and right posterior - right anterior and left posterior
8
Q
What are the 3 axes of semicircular canals?
A
Roll, Pitch, Yaw
9
Q
Describe the push pull arrangement of coplanar pairing:
A
when angular head motion occurs within their shared plane, the endolymph of the coplanar pair is displaced in opposite directions with respect to their ampullae and neural firing increases in one vestibular nerve and decreases on the other side.
10
Q
Sensory redundancy is an advantage of the push-pull system. If damage occurs to the semicirucular canal’s imput from one member of the pair (Ie vestibular neuritis or BPPV), then:
A
CNS will still receive vestibular information about head velocity within that plan from the contralateral member of the coplanar pair.
11
Q
____ is a reflex eye movement that stabilizesimages on the retina during head movement. Produces eye movement in the direction opposite to head movment
A
VOR: vestibulo-ocular reflex
- EOM are arranged in pairs, which are oriented in planes close to those of the canals.
- This arrangement allows a single pair of canals to be connected predominantly to a single pair of extraocular muscles
- this results in conjugate eye movements in the same plane as head motion
12
Q
The vestibular nerve is unique among the cranial nerves in that:
A
neurons are constantly firing at 100spikes/sec even with the head still.
13
Q
With sudden loss of vestibular nerve function on one side, there is:
A
strong bias into the brainstem from the intact side (a relative excessive excitation), resulting in nystagmus that is present even without head movement.
14
Q
Name 6 common vestibular disorders
A
- BPPV - benign paroxysmal positional vertigo
- unilateral hypofunction
- bilateral hypofunction
- Meniere’s disease/migraine
- Central vertigo
- Perilymphatic fistula
- superior canal dehiscence
15
Q
Typical presentation of vestibular disorders: 6)
A
- dizziness induced by motion of head/body
- complaints of movement in the environment
- impairment in balance
- nausea/sweating/emesis
- ringing in ears
- decreased concentration/mild memory deficits/decreased focus/anxiety
16
Q
What is the most important component in correctly diagnosing a patient with complaints of dizziness?
A
taking a proper history
17
Q
Name the 8 common medications to treat dizziness
A
- meclizine (antivert, bonine) - antihistamine
- Lorazepam (ativan)
- Clonazepam (Klonopin)
- Dimenhydrinate (Dramamine) - antihistamine
- Promethazine (Phenergan) - 1st gen antihist - neuroleptic
- Amitriptyline (elavil) - TCA
- Scopolamine (patch) muscarinic antagonist
- diazepam (valium)
18
Q
4 classes of medications to consider during assessment and treatment:
A
- ototoxic meds (any history of bad infection requiring strong abx?)
- Amiodarone (cardiac med that can be very toxic)
- Chemotherapy meds (any history of cancer?)
- anticonvulsants
19
Q
4 most common vestibular function testing
A
- VNG/ENG (video or electronystagmography)
- VEMP (Vestibular-Evoked Myogenic Potential)
- Rotary chair testing
- CDP (computerized dynamic posturography)
20
Q
VNG/ENG testing is comprised of (5)
A
- calibration testing - saccades
- spontaneous nystagmus test
- pursuit testing
- postitional tests (Hallpike)
- Caloric tests
21
Q
1. What is the purpose of VEMP testing? (Vestibular evoked myogenic potential) 2. electrodes attached to: 3. How performed? 4. When considered abnormal?
A
- to determine if the saccule and the inferior portion fo the vestibular nerve and central connections are intact and working normally
- SCM bilaterally
- Head is lifted when loud clicks are introduced. The response evoked in the neck EMG is recorded for each side.
- abnormal when they are asymmetrical, low in amplitude, or absent.
22
Q
Purpose of the rotary chair test:
3 parts:
A
to determine whether or not dizziness is due to a disorder of the brain or inner ear.
(assesses lateral canal)
- chair test
- optokinetic test
- fixation test
23
Q
Indications for rotary chair test: (5)
A
- Gold standard test for bilateral vestibular loss
- good for testing special populations (peds, handicapped)
- inconclusive ENG results
- eval of vestibular compensation
- ototoxicity management
24
Q
_____ test has been validated by controlled research studies to isolate the functional contributions of vestibular inputs, visual inputs, somatosensory inputs, central integrating mechanisms, and neuromuscular system outputs for postural and balance control.
A
Computerized dynamic posturography (CDP)
25
Computerized dynamic posturography (CDP) test protocols include (3)
1. sensory organization test (SOT)
2. Motor control test (MCT)
3. Adaptation test (ADT)
26
____ is the mechanical disorder of the inner ear caused by abnormal stimulation of 1 or more of the 3 semicircular canals within the ear.
Benign paroxysmal positional vertigo
27
BPPV is the most common cause of _____
vertigo
28
Benign paroxysmal positional vertigo is characterized by (2)
1. vertigo/dizziness (typically 50% of patients)
29
BPPV onset is usually ____. In the elderly it may mimic _____.
Spontaneous
| neuritis crisis
30
Predisposing factors to BPPV: 8
1. head trauma
2. labyrinthitis
3. ischemia in anterior vestibular artery
4. advanced age
5. female gender
6. meniere's disease
7. migraine
8. Osteoporosis, osteopenia
31
Conditions that require caution with positional testing: 9
1. limited cervical ROM
2. severe rheumatoid arthritis
3. down syndrome
4. cervical radiculopathies
5. paget's disease
6. low back dysfunction
7. spinal cord injuries
8. torn/detached retina
9. glaucoma
32
For nausea medications given prior to vertigo examination, _____ does not suppress ocular nystagmus while ____ and ____ do.
Zofran
| Diazepam (valium) and meclizine
33
BPPV mechanism:
caused by movement of calcium carbonate crystals from utricle to semicircular canal -- known as otoconia
34
in BPPV: in canal involvement, treatment is always based on ____
direction of nystagmus
35
in BPPV, with canal involvement, treatment is always based on direction of nystagmus:
1. upbeating nystagmus
2. downbeating nystagmus
3. right torsion
4. left torsion
1. posterior canal
2. anterior canal
3. right side involvement
4. left side involvement
36
______ is performed with the patient sitting[3] upright on the examination table with the legs extended. The patient's head is then rotated to one side by approximately 45 degrees. The clinician helps the patient to lie down backwards quickly with the head held in approximately 20 degrees of extension. This extension may either be achieved by having the clinician supporting the head as it hangs off the table or by placing a pillow under their upper back. The patient's eyes are then observed for about 45 seconds as there is a characteristic 5–10 second period of latency prior to the onset of nystagmus. If rotational nystagmus occurs then the test is considered positive for benign positional vertigo. During a positive test, the fast phase of the rotatory nystagmus is toward the affected ear, which is the ear closest to the ground. The direction of the fast phase is defined by the rotation of the top of the eye, either clockwise or counter-clockwise. Home devices are available to assist in the performance of the Dix–Hallpike Maneuver for patients with a diagnosis of BPPV
Dix-Hallpike
37
Which test:
The patient begins seated at side of an examination table. The head is turned 45 degrees away from side being tested to align the posterior semicircular canals with the plane of movement; patient is quickly laid onto the table onto the side being tested. The clinician observes the patient’s eyes for one minute.
Sidelying test
Benign paroxysmal positional vertigo of the posterior canal is diagnosed if an upbeating and rotational nystagmus (fast phase towards the ear being tested) is observed with the patient in this test position. The nystagmus should begin after a brief latency (5-10 seconds), last less than one minute, and should correlate with symptoms of vertigo
38
Practically lateral canal BPPV can almost always be seen on the Dix Hallpike test, especially if the examiner does not attain a substantial head-hanging posture but instead tests the patient supine. Nevertheless, the best position to see the direction changing horizontal nystagmus of lateral canal BPPV is not the Dix-Hallpike maneuver. Rather one starts with the body supine, head inclined forward 30 degrees, and then turns the head to either side. This is called the
"supine roll test)
39
_____ nystagmus might be a signal that there is lateral canal cupulolithiasis
apogeotropic nystagmus
40
Treatment of BPPV depends on ____
correctly identifying involved canal and mechanism
41
describe canalith repositioning maneuver (or epley maneurver)
The following sequence of positions describes the Epley maneuver:
The patient begins in an upright sitting posture, with the legs fully extended and the head rotated 45 degrees towards the affected side.
The patient is then quickly and passively forced down backwards by the clinician performing the treatment into a supine position with the head held approximately in a 30 degree neck extension (Dix-Hallpike position) where the affected ear faces the ground.
The clinician observes the patient's eyes for “primary stage” nystagmus.
The patient remains in this position for approximately 1–2 minutes.
The patient's head is then turned 90 degrees to the opposite direction so that the unaffected ear faces the ground, all while maintaining the 30 degree neck extension.
The patient remains in this position for approximately 1–2 minutes.
Keeping the head and neck in a fixed position relative to the body, the individual rolls onto their shoulder, rotating the head another 90 degrees in the direction that they are facing. The patient is now looking downwards at a 45 degree angle.
The eyes should be immediately observed by the clinician for “secondary stage” nystagmus and this secondary stage nystagmus should beat in the same direction as the primary stage nystagmus. The patient remains in this position for approximately 1–2 minutes.
Finally, the patient is slowly brought up to an upright sitting posture, while maintaining the 45 degree rotation of the head.
The patient holds sitting position for up to 30 seconds.
The entire procedure may be repeated two more times, for a total of three times.
During every step of this procedure the patient may experience some dizziness
42
epley maneuvers are intended for what branches of BPPV?
anterior or posterior canalithiasis
43
describe the liberatory maneuver (semont)
Step 1: Start with the patient sitting on a table or flat surface with head turned away from the affected side. Step 2: Quickly put the patient into the side-lying position, toward the affected side with the head turned up. Nystagmus will occur shortly after arriving at the side-lying position. Keep the patient here until at least 20 seconds after all nystagmus has ceased. Step 3: Quickly move the patient back up and through the sitting position so that he or she is in the opposite side-lying position with head facing down (head did not turn during the position change). Keep the patient in this position for ~30 seconds (some recommend up to 10 minutes). Step 4: At a normal or slow rate, bring the patient back up to the sitting position.
treats anterior and posterior canal cupulolithiasis
44
Describe the canalith repositioning maneuvery for horizontal canal BPPV (BBQ roll, log roll, also called Lampert maneuver)
Step 1: Seat the patient on a table positioned so they may be taken back to the head hanging position with the neck in slight extension. Stabilize the head with your hands and move the head 45 degrees toward the side you will test. Move the head, neck and shoulders together to avoid neck strain or forced hyperextension. Step 2: Observe for nystagmus and hold the position for ~10 seconds after it stops. Step 3: Keeping the head tilted back in slight hyperextension, turn the head ~90 degrees toward the opposite side and wait 20 seconds. Step 4: Roll the patient all the way on to his or her side and wait 10 to 15 seconds. Step 5: From this side-lying position, turn the head to face the ground and hold it there 10 to15 seconds. Step 6: Keeping the head somewhat in the same position, have them sit up then straighten the head. Hold on to the patient for a moment because some patients feel a sudden but very brief tilt when sitting up. REPEAT: After waiting 30 seconds or so, repeat the whole maneuver. If there is not paroxysmal nystagmus or symptoms during Dix-Hallpike positioning (Steps 1, 2) then there is a high likelihood of success.
45
top three ways to treat horizontal canal cupulolithiasis?
This is apogeotropic nystagmus with roll testing:
1. Forced prolonged positioning (lie down on back, roll to involved side. sleep on involved side)
2. modified brandt-Daroff for horizontal canal cupulolithiasis
3. cupulolith repositioning followed by log roll (idea here is to convert to canalithiasis, then treat)
46
Post-treatment instructions for BPPV: 4
1. wear soft collar for 24h
2. during that time, avoid head movements
3. sleep with head elevated 45 degrees for one night only
4. do not roll onto affected side for 5 days
controversial in literature.
47
Efficacy of cupulolith repositioning therapy (CRT/CRP/CRM)
____% with single treatment
____% with repeated treatments
____% recover without treatment or with sham treatment by one month
75%
>95%
38%
48
```
Recurrence rate of BPPV:
____ % in first year after treatment.
____% recur during first 5 years
____% overall recurrence rate
Females ___ males
higher in ___ decade of life
```
```
80
94
50
females > males
Lower in 7th versus 6th decade of life.
```
49
Describe the oculomotor exam tests: 8
1. spontaneous nystagmus
2. smooth pursuit
3. gaze holding nystagmus
4. saccadic eye movements
5. VOR fast and slow
6. VOR cancellation
7. static and dynamic visual acuity
8. optokinetic nystagmus
50
____ is involuntary oscillation of the eyes. typically has fast and slow phase and is named by direction of the fast component
nystagmus.
Normal physiologic nystagmus is observed during
1. rotational chair
2. calorics
3. optokinetics
4. end-point
51
What are the three types of pathological nystagmus
1. spontaneous - sitting quietly with eyes straight ahead with no external stimulus
2. Gaze-evoked - induced by changes in gaze position stimulus
3. positional - not present in sitting with the head in neutral but is present in some other head or body position
52
Three visual systems work together to maintain gaze stability:
1. Saccade system - brings an object into focus as quickly as possible when there has been an error in the direction of gaze
2. Smooth Pursuit system - maintain gaze on a moving target
3. optokinetic system - primitive form of smooth pursuit that uses corrective saccades to relocate gaze on new targets in the visual field.
53
Guidelines for oculomotor exam:
1. make sure object is ____ away from clients nose
2. instruct the client prior to
3. use clinical judgement in cases of _____ or ____
4. If client wears glasses, perform with glasses ____
18-24inches
instruct the client regarding the intended movement before moving.
Use clinical judgment in cases of cervical pain or limited ROM
glasses on
54
Explain the test for spontaneous nystagmus:
client sitting quietly, instruct them to look at your nose done with and without fixation.
Observation: observe the client's eyes for any spontaneous nystagmus. If nystagmus is present, this is an abnormal sign. Note the direction of the nystagmus.
55
explain the test of smooth pursuit
client sitting quietly, instruct them to follow your index finger as you slowly move it from side to side then up and down.
Observation: note the quality of eye movement. It should be smooth during movement and when changing directions. It is abnormal when the movement is saccadic and not smooth in nature.
56
Describe test for gaze-holding nystagmus
Test: with client sitting quietly, ask them to look 30 degrees to the left and hold, 30 degrees to the right and hold, up and hold, down and hold. perform with fixation blocked as well.
Observation: observe the clients eyes for nystagmus at hte holding points. If nystagmus is present, this is abnormal. Note the direction of the nystagmus. Make sure the client is not at the end of their visual field; end-range gaze holding nystagmus is normal.
57
describe the test for saccadic eye movement
test: client sitting quietly, instruct them to look back and forth between the therapists nose and index finger which is located to the right or left of their nose (about 30 degrees of eye movement). Test horizontally and vertically.
Observation: movement of the eyes should be quick and accurate. Note any corrective saccades to reach the target (overshoot or undershoot) more than 1-2 corrective saccades is abnormal.
58
Describe VOR to slow head movements test
Test: client is to look at your nose. HOld the clients head firmly between your hands, flex the head forward 30 degrees. Slowly move the clients head back and forth approximately 30 degrees from midline.
Observation: normal is the ability to maintain visual fixation. Abnormal response would be the presence of saccades.
59
Describe VOR fast head movements (head thrust)
test: instruct client to keep their eyes on your nose as you move their head bakc and forth and then quickly move head from midline to one side. repeat to opposite side.
Observation: normal response is the ability to maintain visual fixation. Abnormal response is a corrective saccade to refixate. Not the dirrection of the head movement that caused the corrective saccade.
- a positive head thrust to the right indicates a hypofunction on the right. a corrective saccade to the left would be observed as the client attempted to keep their eyes on the target
- a unilateral hypofunction disrupts the balance of information being sent to the brainstem by the canals (push/pull mech). A loss of one side will cause the brain to make rapid corrective eye movements toward the unaffected side.
60
Describe optokinetic nystagmus test
test: use a striped piece of fabric and have the client count the stripes as the go by.
Observation: normal response is optokinetic nystagmus. Note if the client does not produce slow phase movements int he direction of the rotation of the striped fabric.
61
describe VOR cancellation test:
test: have client lace fingers together and place on thumb on top of the other. Hold arms out straight in front of the eyes. Move arms and head side to side keeping the nose, thumbs, and eyes all in line with each other.
Observation: normal response is the ability to maintain visual fixation. abnormal response would be the presence of saccades.
62
Describe static and dynamic visual acuity test
test: using an eye chart, determine the lowest line the client can correctly read. Standing behind the client with both hands firmly on the sides of their heads, flex their head forward 30 degrees. Rotate the head back and forth 2 cycles/second and have the client read the lowest line they can correctly identify all characters in.
Observation: a change of 3 or more lines in visual acuity is indicative of impairment with the VOR
63
Describe the head shake testing:
Test: holding the clients head firmly between your hands, flex the head 30 degrees. instruct the client that they may close their eyes while you quickly move their head back and forth 20 times. When the movement stops, have the client open their eyes and look straight forward.
Observation: observe for nystagmus. If nystagmus is present, this is an abnormal response. Note the direction of the fast phases.
64
____ typically occurs secondary to viral infection that affects the superior portion of the vestibular nerve. Onset is sometimes preceded by viral infection of the URI or UGIT
vestibular neuritis
65
Vestibular neuritis:
Vestibular function test results:
1. ENG:
2. Rotary chair:
3. Posturography:
4. Audiometric testing:
1. ENG: caloric weakness (partial or complete) on affected sie
2. Rotary chair: acutely, decreased gain at low and high velocities. Chronically, normal gain at low velocities and decreased gain at higher velocities with rotation toward the involved side
3. sub-acutely will demonstrate increased difficulty with conditions 5 and 6. Chronically, may be normal or isolated difficulty depending on degree of compensation.
4. hearing intact
66
Acutely in vestibular neuritis, occulomotor findings include:
horizontal nystagmus toward the unaffected ear.
67
In vestibular neuritis, regarding postural stability, romberg is generally ____. with eyes closed is _____. Ambulates with little head or trunk rotation. When asked to move head while ambulating _____
normal
abnormal
gait becomes ataxic
68
Vestibular neuritis treatment:
Medical:
Rehab:
Med: acutely treated with vestibular suppressants, corticostaroids, medication for n/v. Should be avoided long-term since they impede central compensation. Chronically, surgical intervention (eg: labyrinthectomy, vestibular nerve section) may be used if central compensation does not occur.
Rehab: vestibular adaptation exercises, habituation, balance exercises depending on clients impairments
69
Vestibular neuritis outcomes
1. positive:
2. Negative:
1. symptoms are usualy self-limiting for approximately 6 weeks. expect full recovery within 6 months.
2. prolonged use of vestibular suppressants will increase amount of time for central compensation to occur. Lack of compliance with the exercise program, an unstable lesion, CNS pathology, advanced age or other sensory system involvement will also impact the patient's ability to recover.
70
_____ is an infection in the membranous labyrinth caused by a virus or bacteria. It initially affects the otic capsule, the perilymphatic space, and finally the membranous labyrinth
labyrinthitis
71
Labyrinthitis:
1. acute complaints (3)
2. Chronically? 3
1. hearing loss,
2. vertigo
3. n/v peaking wihtin 24h and lasting 3-4 days.
chronically client is left with residual hearing loss, sensitivity to head movements, and imbalance (especially in dark or busy visual environments)
72
```
Labyrinthitis
Vestibular function test results:
1. ENG:
2. Rotary Chair
3. Posturography
4. Audiometric testing
```
1. ENG - unilateral vestibular loss (partial or complete) in the affected ear
2. Rotary chair - acutely, decreased gain at low and high velocities. Chronically normal gain at low velocieites and decreased gain at higher velocities with rotation toward the affected side.
3. Posturography - subacutely will demonstrate increased difficulty with conditions 5 and 6. chronically may be normal with isolated difficulty.
4. profound sensorineural hearing loss on affected side.
73
Labyrinthitis clinical findings
1. oculomotor exam;
2. postural stability
1. Acute - horizontal nystagmus toward unaffected side. Chronic - may be normal, or may see positive head thrust test toward the affected ear.
2. Romberg normal. Sharpened romberg may be positive with eyes open, typically positive with eyes closed. Ambulates with little head movement, when asked to move head while ambulating, gait becomes more ataxic.
74
Labyrinthitis treatment:
1. Medical:
2. Rehab:
1. Acutely, vestibular suppressants, meds for n/v, and if caused by a viral infection, may be on oral steroids. if suspected to be bacterial, may be on abx. Chronically, surgical intervention (ex: labyrinthectomy, vestibular nerve section) may be used if central compensation does not occur.
2. vestibular adaptation exercises, habituation exercises, balance techniques depending on needs of individual patient
75
Labyrinthitis outcomes
1. positive
2. negative
1. self-limiting at 6 weeks. expect full recovery within 6 months
2. hearing loss may be permanent. prolonged use of vestibular suppressants will increase time for central compensation to occur.Lack of compliance with exercise program, unstable lesion, CNS pathology, advanced age, or other sensory involvement will also impact the clients ability to recover.
76
_____ is loss of peripheral neuroepithelium, most commonly the result of ototoxicity from aminoglycosides (gentamicin, tobramycin, and streptomycin) or cisplatinum (chemo).
bilateral vestibular loss
77
Bilateral vestibular loss causes:
1. three aminoglycosides
2. Chemo drug
3. Other causes 3
1. gentamicin, tobramycin, streptomycin
2. cisplatinum
3. autoimmune inner ear disease, syphilis, sequential unilateral loss of vestibular function
78
Bilateral vestibular loss
| Patient complaints 2
1. dysequilibrium when standing or walking
2. visual blurring that occurs during head movements (oscillopsia)
3. dizziness is not typically a problem
79
What is oscillopsia?
visual blurring that occurs during head movements
80
```
bilateral Vestibular loss
function testing:
1. ENG:
2. Rotary chair
3. Posturography
4. Audiometric tests
```
1. variable testing results: some function may remain or can be completely gone
2. rotary chair - variable testing results, some function may remain or can be completely gone
3. increased sway on conditions 2 and 3 and loss of balance on conditions 5 and 6.
4. variable
81
Bilateral vestibular loss
clinical findings
1. oculomotor exam:
2. postural stability:
1. impaired VOR to slow and rapid head thrusts, decrease in dynamic visual acuity (greater than 3 line change)
2. romberg acutely abnormal; sharpened romberg with eyes closed unable to complete; can not perform tandem walking; demonstrates a wide based gait and ataxia that increases with head movement.
82
Bilateral vestibular loss: Treatment
1. MEdical
2. rehab
1. prevention is best
2. substitution strategies such as increasing reliance on the visual and somatosensory information (using an assistive device, keeping lights on when walking), use of corrective saccades. Postural control activities, including static and dynamic exercises.
83
Bilateral vestibular loss
| outcome:
typically return to many functional activities but continue to have difficulty when visual and somatosensory cueing is diminished or absent.
84
Recovery of bilateral vestibular loss is ____ than unilateral loss. Can occur over a ____ period. Recovery can be impeded by other medical problems, especially those that _____.
____ is essential to recovery.
slower.
2 year period
impact sensory system (ie peripheral neuropathy, vision impairments)
Compliance - a person with bilateral loss may need to always continue vestibular exercises.
85
_____ is believed to be due to an increase in the volume of endolymph associated with the distension of the entire endolymphatic system and subsequent rupture of the membranous labyrinth.
Manieres disease
86
Manieres disease is characterized by (3)
fluctuating hearing loss
tinnitus
vertigo
87
Patient's complaints: recurrent attacks characterized by initial sensation of ear fullness, decreased hearing, and tinnitus, follwoed by vertigo.
menieres disease
complaints also include imbalance, movement of visual environment, and n/v.
88
Meniere's disease attacks may last ____
minutes to hours with some residual dizziness and unsteadiness remaining for a few days. Generally asymptomatic between attacks.
89
Menieres disease
Oculomotor exam:
postural stability:
1. between spells may be normal. depending on progression, may show signs of unilateral vestibular loss.
2. between spells may have normal balance
90
Meniere's disease: Treatment:
Medical
1. Acute
2. remission
limits: 5
Final option?
Initially: vestibular suppressants and diuretics.
Remission: dietary restrictions - low salt diet (1.5-2grams/day)
Limits: salt, caffeine, nicotine, alcohol, sugar
Surgery or other destructive procedures to the vestibular system are considered a final option
91
Menieres disease
| rehab treatment
vestibular dysfunction with meniere's is episodic and between spells the system usually returns to normal
therefore, vestibular exercises are not appropriate unless there is permanent loss of function.
Vestibular rehab will not assist in preventing attacks. IF attacks or intervention has caused hypofunction, then vestibular rehab can be helpful.
92
Menieres disease outcomes:
1. Positive
2. negative
1. post-surgery expect a full recovery within 6 months to a year
2. hearing loss may become permanent as disase progresses. A chance exists that the menieres disease could develop bilaterally. Surgery couldbe unsuccessful
93
____ is an abnormal connection between the air filled middle ear and the perilymphatic space of the inner ear.
Perilymphatic fistula
94
perilymph fistulas can occur through what 3 areas
bony labyrinth
oval window
round window
95
Perilymphatic fistulas are typically brought on by 4
head trauma
barotrauma
mastoid or stapes surgery
penetrating injury to the tympanic membrane
96
Patient presents acutely with complaintsof an audible "pop" in the nner ear, followed by hearing loss, vertigo, and tinnitus. Chronically may complain of nonspecific imbalance. sneezing, straining, or nose blowing can elicit symptoms after the initial event
perilymphatic fistula
97
perilymphatic fistula
ENG:
Rotary chair
posturography
normal or unilateral weakness in the affected ear
variable
variable
all clinical findings variable
98
Perilymphatic fistula treatment:
1. medical
2. rehab
1. Acute - absolute bed rest with head elevated for 1-3 weeks. Avoidance of straining, sneezing, coughing, or head hanging.
Chronically - clients undergo surgery ot pack the oval and window ear areas in order to stabilize hearing loss and relieve symptoms
2. used sometimes as a diagnostic tool. If client does not improve with vestibular rehab, may need surgery
99
perilymphatic fistula outcomes
1. positive
2. negative
1. most heal spontaneously
| 2. surgery improves vestibular function but is less effective for improving hearing
100
Acoustic Neuromas arise from
AKA vestibular schwannoma
relatively benign tumors that arise from schwann cells that line the axons of the vestibular portion of CV VIII.
101
Acoustic neuromas/vestibular schwannomas typically are located _____ or ____.
internal auditory canal or cerebellar pontine angle
pressure the tumor places on surrounding structures produces the symptoms
102
Patient presents complaining of slow progressive hearing loss, may have ipsilateral facial weakness, tinnitus, and dysequilibrium. very infrequently will have vertigo. Post, op patients can have vertigo, imbalance, and gaze instability
acoustic neuroma/vestibular schwannoma
103
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Acoustic neuroma/vestibular schwannoma
testing:
1. ENG
2. Rotary chair:
3. Audiometric tests:
4. imaging:
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1. ENG - unilateral loss in affected ear
2. unilateral vestibular loss with high frequency rotations
3. unilateral high-frequency sensorineural hearing loss
4. MRI with gadolinium is gold standard for diagnosis
5. posturography - variable
104
Acoustic neuroma/vestibular schwannoma
Clinical findings
1. oculomotor exam
2. postural stability
1. variable. depends on size of tumor. May see positive head thrust, head shaking nystagmus, smooth pursuit and saccade abnormalities with cerebellar and brainstem involvements
2. variable, depends on size of tumor and if cerebellum is involved
105
Acoustic neuroma/vestibular schwannoma treatment
1. medical
2. rehab
1. observation, surgical resection, gamma/cyber knife surgery to remove tumor
2. post-op for unilateral vestibular loss (adaptation, habituation, balance activities) and possibly for facial nerve injury. May also see for therapy while MDs are "watching"
106
Acoustic neuroma/vestibular schwannoma
outcome:
1. positive
2. negative
1. full recovery after surgery within one year
2. clients remain sensitive to rapid movemetns, prolonged recovery if cerebellar or brainstem involvement. If client is of advanced age, or wiht prolonged use of vestibular suppressants.
107
Vestibular disorders post head trauma
| 3
1. BPPV
2. Unilateral hypofunction (labyrinthine concussion, skull fracture - temporal bone, perilymphatic fistula)
3. central vertigo
108
Labyrinthine concussion
1. define
2. disruption from
3. Pt will present like
4. compain of 3
1. bleeding within the labyrinthine capsule
2. mechanical membrane disruption from acceleration/deceleration
3. person will present like an acute unilateral peripheral hypofunction
4. ataxia, sensorineural hearing loss, imbalance
109
Perilymphatic fistula in head injury
1. may produce:
2. symptoms worsened by
3. treatment
1. rupture of membranes
2. vertigo and tinnitus exacerbated by straining or valsalva maneuver
3. surgical grafting
110
_____ describes injuries outside of the vestibular system
central vertigo
in cerebellum - noted nystagmus, denied rotational or spinning vertigo. complaints of dizziness with standing or walking. may have mixed central and peripheral component
111
what are balance retraining exercises?
Exercises designed to improve coordination of muscle responses as well as the organization of sensory information from eyes, ears and tactile/muscle receptors for balance control (measured by a computerized forceplate).
112
What are habituation vestibular exercises?
Specific movements or positions that provoke the patient's dizziness are provided and the patient is asked to repeat these movements until the brain habituates the response or adapts to the conflicting information. This process resolves the conflict between the brain and the ear.
