Vestibular Flashcards
1
Q
Roles of vestibular system
A
- Orientate to vertical
- Control center of mass
- Stabilise head
- Sense and perceive self motion
2
Q
Bony Labyrinth Anatomy
A
Sits within the temporal bone
Forms the structure and chambers of the peripheral vestibular system
Has 3 semicircular canals, vestibule (central chamber) and the cochlear
Filled with perilympatic fluid - high Na:K ratio
3
Q
Membranous Labyrinth Anatomy
A
Sits suspended within the bony labyrinth and perilympahtic fluid (5% of space within bony)
Contains the 5 sensory organs (3 semicircular canals and 2 otolith organs)
Filled with endolymphatic fluid high K:Na ratio meaning it has a higher viscosity
4
Q
Layers of the vestibular organ
A
Bony labyrinth → perilymph → membranous labyrinth → endolymph
Endolymph has higher viscosity due to high K:Na ratio
5
Q
SCC structures and functions
Ampulla, Cupula and Hair cells
A
- Ampulla
- Bulb like expansion at the base of each of the canals
- Contains the cupula as well as the crista ampullaris (tuft of blood vessels, nerve fibers and supporting structures)
- Cupula
- Bridges the width of the ampulla which seals off the canal so endolymph cannot go from one side to the other
- Hair cells
- Housed within cupula
- 50-70 small stereocilia and one long kinocilium (these are arranged from smallest to longest)
6
Q
Stimulation of hair cells within the SCC
A
- Each afferent neuron has a basal firing rate (base activity level), approx. 1.1.5 Hz
- Deflection of air cells with either excite of inhibit this firing rate based on the direction, this defection is caused by movement of endolymph fluid
- Excitation - stereocilia deflected towards kinocilium
- Inhibition - stereocilia deflected away from kinocilium
7
Q
Structure of the otolith organs and the two types
A
Sensory maculae are hair cells covered in a gelatinous membrane
Otoconia refers to the calcium carbonate crystal imbedded into this membrane which provide increases mass making the membrane heavy.
This mass causes them to be sensitive to gravity and accelerations
Utricles - sensitive to horizontal motion
Saccule - sensitive to vertical
8
Q
Vestibular nerve pathway and portions
A
- Primarily afferent fibers wit only 5-8% efferent
- Travels through the internal auditory canal to enter the brainstem at the pontomedullary junction
- Has 2 portions (pathologies may only effect one portion)
- Superior - supplies the anterior canal, lateral canal and utricle
- Inferior - supplies the posterior canal and saccule
9
Q
Blood supply to the vestibular system
A
Supplied by the labyrinthine artery which originates from the anterior inferior cerebella artery (AICA) and basilar artery
There is no collateral blood supply meaning ischemic event or stroke will cause immediate damage
Also supplies cochlear meaning occlusion causes hearing loss with vestibular symptoms
The PICA supplies cerebellum so an occlusion hear will cause vestibular dysfunction within interruption to hearing
10
Q
4 major vestibular nuclei in the brainstem
A
- Superior and medial - mostly input from SCC
- Lateral and inferior - mostly input from otolith organs
11
Q
SCC function
A
- Provide information about velocity and direction, particularly CHANGES in these
- Enable VOR reflex, generates eye movement that match head velocity
- They are in a perpendicular arrangement, meaning each canal is perpendicular to the other two which allows for sensing of movement in all planes (yaw, pitch and roll)
12
Q
What is Co-planar pairing of SCC
A
- 6 SCC form 3 pairs
- Laterals/horizontal pair
- LARP (left ant and right post)
- RALP (right ant and left post)
These are aligned with the optimal pull of the ocular muscle causing quick and effective VOR
It creates a push-pull rhythm meaning the endolymph within the pair is displaced in the opposite directions causing increased neural firing rate in one and decreased in the other.
13
Q
Advantages of co planar pairing of SCC
A
- Creates a sensory redundancy when there is a unilateral loss meaning the brain will still receive information from the opposite side
- The brain can ignore changes in the neural firing rate that occur on both sides simultaneous. Such as when there is increased body or environment temp causing the endolymph to swell and increase viscosity
- Assists in compensation of sensory overload
14
Q
Which direction does excitation occur
A
A canal is excited by head motion towards that canal in the appropriate plane e.g. L horizontal excited by L turns. Will cause excitation in one canal and inhibition in its pair.
However, the neural firing rate cannot go below 0 causing the sensory redundancy feature of the pair to not be accurate at high speeds (>180 deg/s) as the excitatory side is still increasing while the inhibitory side can no longer decrease.
15
Q
Ampullopetal and Ampullofugal flow
A
Ampullopetal flow = toward the ampulla
Ampullofugal flow = away from ampulla
16
Q
Ewald’s Laws
A
These laws are only appropriate for peripheral disorders!
1st
- Eye and head movement always occur in the same plane as the canal being stimulated
- Axis of nystagmus should match axis of SCC that generated it
2nd
- In horizontal SCCs ampullopetal flow cause greater stimulation than ampullofugal
3rd
- In vertical SCC ampullofugal flow causes greater stimulation than ampullopetal
17
Q
Functions of the otolith organs
A
Sense linear acceleration of the head in all 3 planes in an upright position and the orientation of the head with respect to gravity
Utricle = horizontal
Saccule = vertical
They are very curved and the hair cells are fanned out meaning that can detect effects of gravity in all 3 planes (bean shaped)
18
Q
What are the 3 main vestibular reflexes
A
Vestivulo ocular reflex
Vestibulospinal Reflex
VestibuloCollic Reflex
19
Q
VOR - Vestivulo ocular reflex main function
A
- Maintains stable and clear vision during quick or non constant head movements. Maintains the image on the fovea f the retina during movements
- Head must be moving at variable velocity, visual target can be stationary or in motion
20
Q
VOR Gain
A
Output (eye movement) : input (head movement)
- Gain of 1 - output = input
- Gain of 2 output is twice that of input
- Gain of 0.5 output is half that of input
Vestibular loss causes the gain to reduce → difficulty keeping eyes on target during fast head movements (retinal slip which will cause corrective saccade)
21
Q
VSR - Vestibulospinal Reflex function and pathways
A
- Stabilises the head on the body and maintains upright posture
- Uses more input from otolith than SCC
- 3 major connections:
- Lateral vestibulospinal tract - anti grav postural motor activity
- Medial vestibulospinal tract - Ongoing postural changes and head position in response to SCC
- Reticulospinal tract - most balance reflexes
22
Q
VCR - VestibuloCollic Reflex
A
- Acts on neck muscles to stabilise the head
- Reflex movement counters movement sensed by vestibular sensory organs
23
Q
Outline of Vestibular Neuritis
A
- 2nd most common cause of vertigo
- Caused by acute inflammation of the Vestibular nerve CN 8
- Normally preceded (sometimes) by viral infection such as herpes, GI or upper resp infection
- Can be partial or full depending of which portions of the nerve are affected
- Superior VN= ant SCC, horizontal SCC and utricle (more common)
- Inferior VN = Posterior SCC and Saccule
24
Q
Symptoms of Vestibular Neuritis
A
Symptoms:
- Acute onset of prolonged vertigo (1-4 days) this is referred to as Acute Vestibular Syndrome
- Nausea/vomiting
- Imbalance - sudden loss of one nerve will change basal firing rate
- NO hearing loss or other hearing symptoms as cochlea nerve remains intact
Sub acute symptoms:
- Movement induced giddiness
- Imbalance
- Nausea
- Fatigue
- Blurred or jumpy vision with head movement
25
Labyrinthitis outline and symptoms
Inflammation of the labyrinth within inner ear
Presents identical to neuritis (1-4 day, nausea, imbalance ect) but will also have hearing loss (normally unilateral)
Needs to differentiated from more central vestibular disorders such as AICA stroke (AICA also supplied cochlear)
Therefore, medical emergency with patients with unilateral hearing loss
26
Meniere's Disease outline and symptoms
Accumulation of endolymph in the cochlear and vestibular organs either from increased production or decreased absorption, episodic due to fluid flucutation
- Two or more spontaneous episodes of vertigo each last 20 mins to 12 hrs
- Low to medium frequency hearing loss in one ear + low frequency tinnitus
- Lower frequencies are detected in the middle of the cochlear and due to pressure accumulation the center of the spiral or more susceptible
- Fluctuating aural symptoms
27
Phases of Meniere's Disease
Acute:
- Acute onset vertigo, 20 mins -12 hrs (<1day)
- Unilateral auditory symptoms on effected side
- Imbalance +/- directional propulsion (feel like being pushed)
- Nausea/vomiting
- Horizontal nystagmus TOWARDS affected ear (if its cute go towards)
Sub Acute:
- Giddiness worsens with movement
- Symtpoms may fully resolve
- Pressure damage to the hair cells may cause residual HL/tinnitus
- Vertigo lessens with disease progression, dead ear stage no hearing no vertigo
- Horizontal nystagmus away from affected ear (causes damage to hair cells and function over time)
28
Acoustic Neuroma cause and symptoms
Non malignant tumor of the vestibular portion of CN 8
Vestibular schwannoma is the abnormal growth of Schwann cells
Third most common intercranial tumor in adults
Symptoms:
- Unilateral HL +/- tinnitus (first sign)
- Imbalance and directional propulsion (feel like being pushed)
- Headaches
- Giddiness/rocking sensation
- Facial weakness and numbness as tumor grows and invades facial nerve
- Rarely causes vertigo, due to slow growth of the tumor the body has time to adapt
29
Third Window 2 common causes
2 most common third window syndromes are Peri lymphatic Fistula and Superior Canal Dehiscence
- Perilymphatic Fistula
- Occurs at oval or round window
- Often due to head trauma, surgery or straining
- Superior Canal Dehiscence
- Occurs at superior semicircular canal
- Thinning and loss of bone at roof of SCC due to age or postnatal development
30
Third window symptoms
- Brief episodes of dizziness that are often aggravated by pressure or sound
- Associated imbalance
- Nausea
- Auditory symptoms of hearing loss and autophony (heading body movements such as pulse or eyes moving)
31
Vestibular Migraine Diagnosis
Varied presentation meaning it can mimic other vestibular conditions particularly MD, diagnosis of exclusion.
Typical onset between 30-60 yrs and more common in women around menopause
Diagnosis:
- Current or past Hx of migrain +/- aura (sparkles in vision)
- 5 episodes that have mod-sever vestibular symptoms (5 mins to 72 hrs) or 50% of dizzy episodes are associated with headache/visual aura/ photophobia
32
5 D's
- Dizziness
- Diplopia (double vision or visual field loss)
- Dysarthria/dysphasia (difficulty with speech or finding words)
- Dysphagia (difficulty swallowing of horse voice)
- Drop Attacks (sudden collapse without loss of consciousness)
33
3 N's
- Nystagmus
- Nausea/vomiting
- Numbness or paraesthesia
34
Acute management of Neuritis and Labyrinthitis
- Vestibular suppressants for symptom relief
- Labyrinthitis refer to ENT
- Corticosteroids often used to assist inflammation particularly for labyrinthitis
- Gentle head movements and mobility encouraged
35
Sub Acute management of Neuritis and Labyrinthitis
- Vestibular and balance rehab
- Wean off vestibular suppressants
- Possible hyperbaric oxygen therapy for hearing loss
36
3 Main consideration of history of presenting condition
Symptoms experienced - vestibular, auditory, neuro, N/V, vision
Temporal
Circumstance of onset
37
What is the TiTraTe diagnostic approach
Classifies vestibular condition into 4 dizziness syndrome based on Timing (acute vs episodic) Triggers and Targeted exam
Acute and Episodic have both spontaneous and triggered sub categories (4)
38
AVS from TiTraTe
- Timing = Sudden vertigo lasting from seconds >24 hrs. Also associated N/V, imbalance, nystagmus and head motion intolerance
- Spontaneous = No obvious or specific trigger
- Neuritis, labyrinthitis, stroke, MD or VM
- Triggered - trauma or toxin
- TBI, concussion, third window, intoxication
39
EVS from TiTraTe
- Timing - Recurrent episodes of vertigo 30 mins <24hrs. Also associated N/V, imbalance, nystagmus and head motion intolerance
- Spontaneous - No obvious or specific trigger
- Meniere’s Disease, Vestibular migraine, Vasovagal, Panic
- Triggered - Specific head motion or body positions
- BBPV, central positional vertigo, orthostatic hypotension
40
4 components of objective assessment
Oculomotor
VOR testing
Positional testing
Balance and functional
41
Components of the oculomotor exam (7)
- Cervical ROM and VBI
- Spontaneous nystagmus
- Gaze evoked Nystagmus
- Ocular ROM
- Smooth pursuit
- Saccades
- Test of Scew
42
3 VOR tests
- Head impulse test
- Dynamic Visual acuity
- Head shake nystagmus
43
What is a Nystagmus
Involuntary rhythmic oscillation of the eyes defined by a slow drift phase (pathological) and fast phase correction (central). Brain detects slow drift and corrects
Named in the direction of the fast phase
44
What is Ewald's law for peripheral nystagmus
Axis of nystagmus matches axis of the semicircular canal that generated it
- Horizontal canal = horizontal nystagmus
- Ant/post canal = vertical and torsional nystagmus
45
What are alexanders law's for peripheral nystagmus
- Nystagmus will increase with gaze in direction of nystagmus and decrease with gaze away
- Nystagmus does not change direction
- 1st degree = same side, second = same and mid, third = same, mid and opposite
- Peripheral nystagmus will decrease with fixation present and increase when it is removed (google and IR camera) =, takes away cerebella inhibition. If no change then the nystagmus is central in origin.
46
What is the HINTS exam (and HINTS+)
HINTS = rules out vertebra-basilar stoke in AVS (acute vestibular syndrome)
Used within first 48 hrs (must be in acute stage with symptoms)
Head Impulse (right and left) Nystagmus type (spontaneous or gaze evoked) Test of Skew
Same as above + sudden unilateral hearing loss, same side as the positive HIT indicates vascular lesion
47
How is the HINTS exam interpreted
Impulse Normal, Fast-phase Alternating (direction change with gaze not EOR), Refixation on Cover Test
This is used to interpret the HINTS exam
Impulse test should not be normal, if they have acute vestibular symptoms then either right or left will be altered
48
Key components of occulomotor exam indicating central condition
Changing direction of nystagmus
Abnormalities with smooth pursuit
Saccades testing, dysmetric is bad accuracy:
Hypometric (small is normal in elderly) is midbrain or pons
Hyper is always abnormal and indicates cerebellar issue
Refixation on cover test
49
Head impulse test
Turn patients head within 30 degree quickly and see if they can keep eyes on your nose
Refixation is sign of hypofunction
50
Dynamic Visual aquity
Tests VOR function
Make sure distance from letters is same between tests
Twist head to one side at 60 bpm or 120 bpm across both
Abnormal is 3 lines gap and indicates VOR deficit
51
Head shake Nystagmus
Best done without fixation
Shake at 2 hz, 20 cycle per second for 20 cycles and observe nystagmus
Indicates vestibular hypofunction
Nystagmus towards side with more neural input i.e. right nystagmus is left hypofunction
If nystagmus is not horizontal then it is a central finding
52
Designing the right treatment program with deficits in mind
- Do they have BPPV = repositioning maneuvers
- VOR deficit or poor DVA = adaption exercises (gaze stability)
- Motion sensitivity = Habituation exercises (desensitising)
- Reduce static or dynamic balance = balance and mobility retraining
- Substitute for poor vestibular input (not responding) = Substitution exercises and education on falls prevention
53
3 BPPV assessment test and what canals do they relate to
HPD and side lying HPD do ant and post (canal vs cupulo dependant on symptoms duration ect)
Head roll for horizontal
54
Head roll interpretation
Up is CUP is LEAST
Ageotropic means cupulo - worse to unaffected
Geotrophic means canal - worse to effected
55
Causes of BPPV
Most are idiopathic but head trauma, vestibular neuritis or osteoporosis can all contribute
56
Diagnostic criteria for BPPV
- Recurrent attacks of positional verite or position dizziness provoked by lying down or turning over in supine position
- <1 mins duration
- Not attributed to another disease
- The nystagmus direction is specific to each canal
- Post - torsional verticle
- Horizontal - horinzontal
57
How to perform HPD + diagnosis
Turn patient head towards testing side (45)
Move back quickly extending to 30 and holding for at least 1 min or double duration of symptoms
Maintain rotation and return patient to sitting, make sure to observe as symptoms may reverse.
```
PCS = ipsilateral rot with upbeat
ACS = ipsilateral rot with downbeat
```
Canal vs cupulo dependent on symptoms
58
How to perform sideling HPD
Patient towards head away from testing side (45)
| Move patient down so they looking at ceiling
59
How to perform a head roll test + interpretation
Patient on pillow (20 yaw for plane optimisation)
Turn head quickly to one side (90)
Observe nystagmus and ask for patient intensity rating
Go back to neutral and wait for symptoms to subside
Repeat on the other side
Latency and duration are still the same for canal vs cupolu
But remember UP is CUP is LEAST
60
How to perform modified Epley repositioning manoeuvre
Sit upright in long sitting, rotate head towards affected side (45)
Lie back supine with 30 neck extension
Turn head 90 to unaffected side
Roll onto unaffected side maintaining head angle
Bring legs to the floor and sit up (nose to armpit)
61
How to perform a BBQ roll
Supine with head in pillow
Turn head to affected (hold 2x symptoms)
Rotate to centre (hold 2x symptoms)
Turn to unaffected side (2x symptoms)
Roll body and turn head to face the plinth (2x symptoms)
Continue
62
What canal is the sermont liberating manoeuvre for and how to perform it
PSC
Patient sits on the edge of the bed turning head 45 toward unaffected side
Patient quickly onto affected side maintaining head position, hold for 2 mins
Move rapidly onto unaffected side
63
What canal is the modified sermont liberating manoeuvre for and how to perform it
ASC
Patient sits on the edge of the bed turning head 45 toward affected side
Patient quickly onto affected side maintaining head position, hold for 2 mins
Move rapidly onto unaffected side
64
What canal is the Gufoni for Ageo for and how to perform it
Horizontal
AAA = ageo, affected side down, turn head away from ground
```
Patient sits on edge of bed
Lie onto affected side (onto pillow)
Hold for 2 mins
Look away from ground and hold for 2 mins
Slowly sit up
```
65
Differences between canal and cup
- Canalithiasis - otoconia floating in canal (Crescendo effect - latency, quick build up and eases 30-60 secs)
- Cupulolithisis- otoconia attached to Capula (stimulate as long as head in position - doesn't relay on endo movement, otoconia will pull on cupula based on position). Will start immediately
