2. Vertigo
What is vertigo?
A sensation of rotation or
movement of one’s self or of
one’s surrounding
The Environment is ‘Spinning’
ex: rotational, linear, or tilting movement
3. Vertigo vs Dizziness
Dizziness: Imprecise term
: To describe a variety of symptoms
It could mean
-Vertigo
-Dysequilibrium
-Lightheadedness/Presyncope
-Rocking or swaying as if on a ship
-Motion sickness
-Nausea & Vomiting
-Oscillopsia(visual disturbance in which objects in the visual field
appear to oscillate)
https://www.youtube.com/watch?v=5Jj1NjFspaM
-Floating,swimming,spinning inside of head
4. Types of Dizziness Patients
Experience
Mechanism
Vertigo Illusion of movement of
patients or Surroundings
Disturbance of peripheral or CNS
pathways of vestibular system
Dysequilibrium Imbalance or unsteadiness
while standing or walking
Vestibulospinal, propioceptive,
visual or motor dysfunction, joint
pain or instability , psychological
factors
Syncope or Presyncope Impending loss of
consciousness
Momentary reduce in blood flow to
brain eg.) cardiac obstructive
problem
Mal de débarquement Sense of rocking or swaying
as if on a ship
Vestibular adaptive process to the
continuous, passive motion,and
must re-adapt once environment is
stable
Motion sickness Episodic
dizziness,tiredness,pallor,
diaphoresis, salivation, nausea
& vomiting
Visual-vestibular mismatch
Eg.) riding in a car or viewing
action sequence in large screen
theater
Nausea & Vomiting Stimulation of vagus centers in
medulla
5. Types of Dizziness Patients Experience Mechanism
Oscillopsia Subjective illusion
of visual motion
Spontaneous :
acquired nystagmus
Head induced :
severe,bilateral loss
of the VOR
Floating,swimming,
spinning inside of
head
Frequently
psychological
symptoms of
anxiety,somatoform
disorders, and
depression
7. Vestibular System
Contributor to our balance system
Maintain spatial orientation & stabilize vision
Provides information related to movement and head
position
8. Vestibular System
Detects angular and linear acceleration via these
end organs :
1. Saccule
2. Utricle
3. Semicircular canals : Angular acceleration
Otolith : Linear accelerations
9.
10. Semicircular Canal
They respond to angular acceleration and deceleration.
Contain sensory hair cells that are activated by
movement of inner ear fluid (endolymph). As the head
moves, hair cells in the semicircular canals send nerve
impulses to the brain by way of the acoustic nerve.
Vestibular System
11. Utricle & Saccule
Utricle and saccule is stimulated by linear acceleration
and deceleration or gravitational pull during the head
tilts.
The utricle is sensitive to change in horizontal
movement. The saccule is sensitive to the change in
vertical acceleration (such as going up in an elevator).
Vestibular System
13. Vertigo and Dizziness
Normally there is balanced input from both vestibular
systems
Vertigo develops from asymmetrical vestibular activity
Abnormal bilateral vestibular activation results in truncal
ataxia
14. Vertigo and Dizziness
Nystagmus
Rhythmic slow and fast eye movement
Direction named by fast component
Slow component due to vestibular or brainstem activity
Slow component usually ipsilateral to diseased structure
Fast component due to cortical correction
Physiologic Vertigo
“motion sickness”
A mismatch between visual, proprioceptive and
vestibular inputs
Not a diseased cochleovestibular system or CNS
16. Vertigo-History
Is it true vertigo?
Autonomic symptoms?
Pattern of onset and duration
Auditory disturbances?
Neurologic disturbances?
Was there syncope?
Unusual eye movements?
Any past head or neck trauma?
Past medical history?
Previous symptoms?
Prescribed and OTC medications?
Drug and alcohol intake?
17. Vertigo-Physical Exam
Cerumen/FB in EAC
Otitis media
Pneumatic otoscopy
Tympanosclerosis or TM
perforation
Nystagmus
Fundoscopic exam
Pupillary abnormalities
Extraocular muscles
Cranial nerves
Internuclear ophthalmoplegia
Auscultate for carotid bruits
Orthostatic vital signs
BP and pulse in both arms
Dix-Hallpike maneuver
Gross hearing
Weber-Rinne test
External auditory canal vesicles
Muscle strength
Gait and Cerebellar function
18. Classification of Vertigo
Disorder of vestibular system
Peripheral
Which involve vestibular end organs and their first order
neurons (i.e. the vestibular nerve). The cause lies in the
internal ear or the Vlllth nerve. They are responsible for
85% of all cases of vertigo.
Central
Which involve central nervous system after the entrance
of vestibular nerve in the brainstem and involve vestibulo-
ocular, vestibulo-spinal and other central nervous system
pathways.
24. Benign Paroxysmal Positional Vertigo (BPPV)
Acute attacks of transient vertigo lasting
seconds to minutes initiated by certain
head position accompanied by torsional
(rotatory) nystagmus.
Most common cause of vertigo
Not associated with auditory or
neurological symptoms
Epidermiology: women (64%), 40 – 50 y/o
Aetiology: head trauma, viral infection,
degenerative disease, idiopathic.
25. How it occurs?
• As a result of otoliths, tiny crystal of calcium
carbonate (normal part of inner ear) detach
from otolithic membrane in the utricle and
collected in one of the semicircular canals.
• Head still -> gravity cause otoliths clump and
settle
• Head moves -> otoliths shift -> stimulates
cupula to send false signal to brain -> vertigo
and nystagmus occur
26.
27. Clinical presentation
Symptoms: VERTIGO onset: 5-10s after
changing head position (getting out of
bed, looking upward, rolling position last
for seconds to min.
Often rotatory vertigo,Dizziness
(lightheadedness), imbalance, difficulty
concentrating, N+V, visual disturbance
(nystagmus)
Signs: Hallpike maneuver: rotatory
nystagmus. The top pole of the eyes
rotates toward the undermost (affected)
ear.
28. Dix-Hallpike maneuver
Rapidly moving the patient from a sitting position to the supine position
with the head hanging over the end of the table, turned 45° to one
side.
Hold for 15-20s to elicit nystagmus.
Onset of vertigo and rotary nystagmus indicate positive test for the
dependent side
29. Dix-Hallpike Maneuver
Figure 1. Dix-Hallpike maneuver (used to diagnose benign paroxysmal
positional vertigo). This test consists of a series of two maneuvers: With
the patient sitting on the examination table, facing forward, eyes open,
the physician turns the patient's head 45 degrees to the right (A). The
physician supports the patient's head as the patient lies back quickly from
a sitting to supine position, ending with the head hanging 20 degrees off
the end of the examination table. The patient remains in this position for
30 seconds (B). Then the patient returns to the upright position and is
observed for 30 seconds. Next, the maneuver is repeated with the
patient's head turned to the left. A positive test is indicated if any of
these maneuvers provide vertigo with or without nystagmus.
31. Treatment
Reassure patient that process resolves
spontaneously
Particle repositioning maneuvers
Main Aim: Reposition the otoliths back to utricle
- Epley maneuver (performed by MD)
- Brandt-Daroff exercise (performed by patient)
Surgery for refractory cases
Anti-emetics for nausea and vomiting
36. Labyrinthitis
Labyrinth is the structure of the inner ear :
Consist of :
1. Semicircular canals
2. Vestibule
2. Cochlea
Balance &
equilibrium
Hearing
37. Labyrinthitis - (inflammation of the labyrinth)
occurs when an infection affects the whole
structure of inner ear (labyrinth). Affect both
the vestibular apparatus and cochlea
Resulting in hearing changes as well as
dizziness or vertigo.
38. Different from..
Vestibular neuritis- ‘Neuritis’ (inflammation
of the nerve) affects the branch associated with
balance, resulting in dizziness or vertigo but no
change in hearing.
39. Etiology
Occurs as a complication of acute and
chronic otitis media, bacterial meningitis,
cholesteatoma, and temporal bone fractures
Bacterial : S. pneumonia, H. Influenza, P.
aeruginosa, P. mirabilis
Viral : rubella, CMV, measles, mumps,
varicella zoster
Inner ear infections that cause vestibular
neuritis or labyrinthitis are usually viral
rather than bacterial
40. Clinical presentation
Sudden onset of vertigo, nausea, vomiting,
tinnitus, and unilateral hearing loss, with no
associated fever or pain
Age: Middle aged adults (30-40) peak around
41 years old
No male or female predominance
Usually unilateral, sometimes can be
bilateral
It usually preceded with URTI infection
It can last for some days, or even weeks
Meningitis is a serious complication
41.
42. Investigation
No specific test. The diagnosis can usually be made clinically.
Lab test:
FBC: To see elevated TWC (infection)
Lumbar puncture, CSF culture & gram stain: if suspect Meningitis
Other:
MRI- MRI with gadolinium to exclude a retrocochlear cause
of hearing loss (such as acoustic neuroma)
CT Head
Pure Tone Audiogram- to document the extent of hearing
loss and to confirm the affected ear
Electronystagmography (ENG)- Records eye movements and
responses to ocular and vestibular stimuli
45. Meniere’s Disease- an idiopathic peripheral
vestibular disorder attributed to excess
endolymphatic fluid pressure, causing episodic
inner ear dysfunction.
Distension of endolymphatic system due to
increased volume of endolymph
49. Clinical presentation
Early stage: Sudden, episodic vertigo (>20 min,<24hr) nausea and vomiting,
nystagmus and aural fullness.
Intermediate stage: attacks of vertigo+tinnitus + fluctuating sensorineural
hearing loss.
Late stage: hearing loss + balance difficulties + tinnitus.
50. Diagnosis criteria:
by American Academy of otolaryngology, head & neck surgery
2 or > definitive spontaneous episodes of vertigo lasting
20 min/>
Audiometrically documented hearing loss >1 occasion
Tinnitus /aural fullness in affected ear
All other causes excluded.
51. Investigations
No definitive test, depends on history
Dix-Hallpike positional test: +ve indicates coexisting benign paroxysmal
positional vertigo (BPPV)
Romberg test: instability while eye closed
Tuning fork test: sensorineural hearing loss (Rinne: +ve, Weber lateralised to
unaffected ear)
Caloric test
MRI: vestibular schwannoma or superior canal dehiscence
Audiometry, electrocochleography ( may indicate increased inner ear fluid
pressure in some cases of Ménière’s disease) & electronystagmography( to
evaluate balance function)
52. Management
Acute Management
Reassurance and psychological support
Bed rest
Vestibular sedatives to relieve vertigo – dimenhydrinate
(Dramamine), promethazine theoclate (Avomine)
Long term
Medical:
-Low salt diet, diuretics (e.g. hydrochlorothiazide, amiloride),
intratympanic gentamicin therapy (control vetrtigo up to 80% of
the patient)
Surgical:
- Decompression of endolymphatic sac
- Transtympanic labyrinthetomy
54. Acoustic neuroma(vestibular
scwannoma)
Definition
Scwannoma of the vestibular portion of CN VIII
Acoustic neuroma is the most common intracranial tumor causing
SNHL and the most common cerebellopontine angle tumour.
SNHL* Sensoryneural hearing loss
Pathogenesis
Starts in the internal auditory canal and expends into cerebellopontine
angle (CPA), compressing cerebellum and brainstem
When associated with type 2 neurofibromatosis (NF2) : bilateral
acoustic neuromas, café-au-lait lesions, and multiple intracranial
lesions.
55. Clinical features
Usually presents with unilateral SNHL or tinnitus
Dizziness and unsteadiness may be present, but true vertigo is
rare as tumour growth occurs slowly and thus compensation
occurs
Facial nerve palsy and trigeminal (V1) sensory deficit(corneal
reflex) are late complications
Acoustic neuroma(vestibular
scwannoma)
56. Diagnosis
MRI with gadolinium(gold standard)
Audiogram
Poor speech discrimination relative to the hearing loss
Stapedial reflex absent or significant reflex decay
ABR- increase in latency of the 5th wave
Vestibular test : normal or asymmetric caloric weakness(an
early sign)
Treatment
Surgical excision
Other: gamma knife, radiation
Acoustic neuroma(vestibular
scwannoma)
