Chronic Vertigo

A young lady complains of 3 months of dizziness.

She had a road traffic accident then and sustained a
mild head injury. She has otherwise recovered fully.
Causes of Vertigo
Central Vertebrobasilar
Insufficiency

Multiple Sclerosis

Peripheral Acoustic Neuroma

Common Structural Infections

Acute
Vestibular Cholesteatoma
Neuronitis Serous OM
Perilymphatic fistula
BPPV RH Syndrome
Temporal Bone Fracture
Meniere’s Labyrinthitis
Disease Labyrinthine Concussion
History
When it began
Confirm vertigo
Time course
Aggravating factors
- Head movement
- Coughing, sneezing, exertion, loud noises
History
Associated symptoms
- Nausea and vomitting
- Postural instability
- Deafness, tinnitus
- Headache, photophobia
- Neurological dysfunction
- Drop attacks
- Loss in spatial orientation
Past medical history and drug
history
Trauma: site, nature
Viral illnesses
Past history of vertigo
Family history
Drug history
Physical Examination
 Vital signs
 - presence of fever
 - rapid/irregular pulse
 - supine and standing BP:
 any drop in BP on standing up? (orthostatic
hypotension)
 standing provokes symptoms?

 If standing does provoke symptoms, postural symptoms should be

distinguished from those triggered by head movement by returning
the patient supine until symptoms dissipate and then rotating the
head.
Physical Examination
 Checking for Nystagmus
 - With the patient supine, the eyes are checked for presence,
direction, and duration of spontaneous nystagmus

 - Direction and duration of nystagmus and development of

vertigo are noted.
What is Nystagmus?
 - Rhythmic movement of the eyes

 - Vestibular disorders can cause nystagmus because the vestibular

system and the oculomotor nuclei are interconnected.

 - Presence of vestibular nystagmus helps identify vestibular disorders

and sometimes distinguishes central from peripheral vertigo.

 - The direction of the nystagmus is defined by the direction of the

quick component

 - Nystagmus may be rotary, vertical, or horizontal and may occur

spontaneously, with gaze, or with head motion.
How to check for Nystagmus?
 - Initial inspection for nystagmus is done with the patient lying
supine with unfocused gaze

 - Patient is slowly rotated to a left and then to a right lateral

position.

 - Direction and duration of nystagmus are noted.

 - If nystagmus is not detected, then the Dix-Hallpike maneuver is

performed.
    Peripheral Central
Nystagmus
Direction Unidirectional, fast Sometimes reverses
phase toward the direction when patient
normal ear; never looks in the direction
reverses direction of slow phase
Type Horizontal with a Can be any direction
torsional component,
never purely torsional
or vertical
Effect of visual fixation Suppressed Not suppressed

Other neurologic Absent Often present

signs
Postural instability Unidirectional Severe instability,
instability, walking patient often falls
preserved when walking
Deafness or tinnitus May be present Absent
Difference between nystagmus secondary to
peripheral nervous system and CNS cause

 - Nystagmus secondary to peripheral nervous system disorders

has a latency period of 3 to 10 sec and fatigues rapidly

 - Nystagmus secondary to CNS causes has no latency period

and does not fatigue.

 - During induced nystagmus, the patient is instructed to focus

on an object. Nystagmus from peripheral disorders is inhibited
by visual fixation.
Inducing Nystagmus
 - Caloric stimulation of the ear canal induces nystagmus in a person with an intact
vestibular system.

 - Failure to induce nystagmus or > 20% difference in duration between sides

suggests a lesion on the side of the decreased response

 - Quantification of caloric response is best done with formal (computerized)

electronystagmography.

 - Care should be taken not to irrigate an ear with a known tympanic membrane
perforation or chronic infection.

 - With the patient supine and the head elevated 30°, each ear is irrigated
sequentially with 3 mL of ice water. Alternatively, 240 mL of warm water (40 to
44°C) may be used

 - Cold water produces nystagmus to the opposite side; warm water produces
nystagmus to the same side. A mnemonic device is COWS (Cold to the Opposite
and Warm to the Same).
BPPV

Provoking a BPPV attack – Dix-Hallpike manoeuvre

With the patient sitting, the neck is extended and turned to

one side. The patient is then placed supine rapidly, so that
the head hangs over the edge of the bed. The patient is
kept in this position and observed for nystagmus.
Nystagmus usually appears with a latency of a few
seconds and lasts less than 30 seconds. It has a typical
trajectory, beating upward and torsionally, with the upper
poles of the eyes beating toward the ground. After it stops
and the patient sits up, the nystagmus will recur but in the
opposite direction.

If nystagmus is not provoked, the maneuver is repeated

with the head turned to the other side. If nystagmus is
provoked, the patient should have the maneuver repeated
to the same (provoked) side; with each repetition, the
intensity and duration of nystagmus will diminish.
Other examination
 - Complete head and neck examination
 - Ear Canal and hearing:
 Weber test and Rinne test are used to document sensorineural or conductive
hearing losses
 Ear canal is inspected for discharge and foreign body, and the tympanic
membrane is checked for signs of infection or perforation using a otoscope.

 - Neurological examination:
 Cerebellar function is tested by assessing gait and doing a finger-nose test and
Romberg's test.
 Test the rest of the cranial nerves

 - Nasopharyngoscopy and indirect laryngoscopy

 - Fistula test
Fistula Test

• Entails making a sensitive recording of

eye movements while pressurizing each
ear canal with a pneumatic otoscope

• A positive test is good grounds for surgical

exploration.
Investigations
Imaging- Xray, CT, MRI, MRA
Electronystagmography (ENG) and
video-nystagmography (VNG)
Vestibular evoked myogenic potentials
(VEMP)- tests otoliths of vestibular
system
Audiometry – low frequency hearing loss
can confirm Meniere’s disease, or reflect
traumatic sensorineural loss
ENG
Oculomotor evaluation
Positioning/positional testing
Caloric stimulation of the vestibular
system (COWS). If poor reflex, means
vestibular weakness of horizontal
semicircular canal of the side being
stimulated.
Can help to discriminate between central
and peripheral etiologies
Labyrinthine concussion
Can occur in the absence of fracture
Pressure waves in skull base may damage
the membranous labyrinth, VIII nerve or
even the brainstem due to shearing forces
a/w high-frequency hearing loss
+/- tinnitus
May recover or not
“Whiplash”- Cervical vertigo
vertigo or dizziness that is provoked by a
particular neck posture no matter what the
orientation of the head is to gravity
estimated that 20-58% of patients who
sustain closed-head injuries or whiplash
experience late onset symptoms of dizziness,
vertigo and dysequilibrium
no hearing symptoms (other than tinnitus) or
hearing loss but there may be ear pain
(otalgia)
Cervical vertigo - Cont.
Possible causes:
◦ Vascular compression (central vertigo)
◦ Abnormal sensory input from neck
propioceptors
◦ Cervical cord compression (most common)
◦ Etc.
 Temporal Bone Fracture
Bones in the temporal Associated with
region are usually the basilar fracture
thinnest and therefore at ◦ Battle’s sign
the greatest risk of ◦ Racoon eyes
fracture ◦ CSF rhinorrhoea
Types ◦ Cranial nerve palsy
◦ Longitudinal (most ◦ Bleeding from eyes and
common) nose
◦ Transverse ◦ Hemotympanum
◦ Oblique ◦ Ocular nerve entrapment
Longitudinal fracture Oblique fracture
Perilymphatic Fistula

Infrequent complication of head injury

Fistula develops at otic capsule (most commonly at round or
oval window)

Allow communication of fluid-filled inner and air-filled
middle ear

Permits transfer of pressure changes to macular and
cupular receptors

Patients c/o episodic vertigo, tinnitus and/or hearing loss
provoked by sneezing, lifting, straining, coughing and loud
sounds
Investigations for perilymph fistula
History is more sensitive than imaging
MRI with intrathecal gadolinium
enhancement can detect inner and middle ear
communication
Hennebert sign- apply positive and negative
pressure to the intact eardrum using a
pneumatic otoscope. Positive results include
the elicitation of nystagmus or onset of
dysequilibrium with the sensation of motion
or nausea. May be used with ENG
 BPPV

Benign paroxysmal positional vertigo

Symptoms:

Patients c/o recurrent episodes of vertigo, lasting one
minute or less

Lasts for weeks to months (median duration 2 weeks)

Vertigo provoked by specific head movements (e.g.
Looking up while standing, getting up from bed, rolling
over in bed)

Associated with nausea and vomiting
 BPPV

Mostly due to calcium debris (otoconia – loose calcium
carbonate crystals)

Usually deposit in posterior semicircular canal –
canalithiasis

less commonly, can also be anterior canal or horizontal
canal

Semicircular canals normally detect head accelerations

Debris in the canal causes inappropriate sensation of
spinning when head moves with respect to gravity
 BPPV

In the setting of trauma:

Prior head trauma present in approximately 15% of BPPV

Head injury can cause displacement of otoconia, which can
then settle into one of the semi-circular canals

May be a delay of weeks or even months between injury
and onset of BPPV
BPPV

Important to differentiate from central positional
nystagmus, as central lesions often require intervention

Dix-Hallpike manoeuvre helps to confirm BPPV, and
establish it as peripheral

Typical features suggest peripheral lesion:

Peripheral Central
Latent period before 2 to 20 seconds None
onset
Duration of nystagmus < 1 min > 1 min
Fatiguability Fatiguing with Non-fatiguing
repetition
Direction Only one type; May change direction
horizontal/rotatory with given head
position
Intensity of vertigo Severe Less severe
Benign paroxysmal positional
vertigo

1. Particle repositioning maneuver

2. Vestibular rehabilitation
3. Surgical options?
Particle repositioning maneuver
Epley maneuver
Modified Epley maneuver
Modified Semont maneuver
 In patients with benign paroxysmal positional vertigo due to
canalithiasis, the particle repositioning maneuver encourages the
calcium carbonate debris to migrate toward the common crus of the
anterior and posterior canals and exit into the utricular cavity. Step 1 is
the standard Dix-Hallpike positioning test.
 This maneuver should be carried out three times a day. Repeat this daily until you
are free from positional vertigo for 24 hours.

Reproduced from Http://www.charite.de/ch/neuro/englishL.htm

Modified semont maneuver
VIDEO ON EPLEY’S MANEUVER

http://www.youtube.com/watch
?v=NQr7MKJBAJY&NR=1
Brandt-Daroff exercise
http://www.tchain.com/otoneurology/disorders/bppv/
brandt/first.html
Vestibular rehabilitation
activities should involve using the eyes while the head
and body are in motion.
Surgical options?
POSTERIOR CANAL PLUGGING
MENIERE’S DISEASE
Non-Interventional:
• Lifestyle modifications
• Medication
• Rehabilitation

Interventional
Lifestyle adjustments
Salt
restriction
Limiting caffeine
Medication
Acute episodes: vestibular suppressants
and antiemetics
Diuretics and betahistine
Interventional
Destructive : intratympanic
gentamicin injection, surgical
labyrinthectomy, and vestibular nerve
section.
Non-destructive:
◦ Surgical: endolymphatic sac procedures
(enhancement or shunting or both) and
sacculotomy.
◦ Intratympanic glucocorticoids 
◦ Positive pressure pulse generator (Meniett) 
Brainstem concussion - Vestibular
rehabilitation

 Labyrinthine concussion – Vestibular

suppressants and vestibular rehabilitation,
Labyrinthectomy or vestibular nerve
section are options.
Perilymphatic fistula – Bed rest for at
least 5 days and the avoidance of the
Valsalva maneuver. Middle ear
exploration and tympanotomy and
placement of soft tissue graft over the
fistula are options.

Cervical vertigo - Vestibular

rehabilitation and anti-inflammatory
medications
Meniere’s Disease

Definition: Disorder of the inner ear characterized by episodic vertigo, fluctuating

sensorineural hearing loss, tinnitus, and aural fullness with progressive sensorineural
hearing loss.

Epidemiology
•Incidence: 0.5–7.5 per 1000 persons annually, often other causes of peripheral
vertigo are misdiagnosed as this disorder.
•Onset most frequently in the fifth decade of life, may also occur in young adults or
the elderly
•Sex : Affects males and females equally

Etiology
•Etiology is unknown.
•Pathophysiology: Accumulation of fluid within the endolymphatic system of the
inner ear (endolymphatic hydrops) leading to degeneration of vestibular and
cochlear hair cells
•Most cases are idiopathic (the term Ménière’s disease should be applied strictly to
these patients). Secondary causes of this pathology include: Infection, Trauma ,
Autoimmune disease, Inflammatory causes, Tumor.
Signs and symptoms:
•Episodic vertigo
•Often occurs with nausea and vomiting
•Usually not positional
•Aural fullness or pressure in the ear often accompanies these vertiginous episodes.
•Fluctuating sensorineural hearing loss
•Any pattern of hearing loss can be observed.
•Low-frequency, unilateral sensorineural hearing impairment is typical.
•Gradual progression of hearing deficit is common.
•Tinnitus
•Usually low pitch
•May be absent during the initial attacks of vertigo
•Invariably appears as the disease progresses
•Increases in severity during an acute attack
•Often associated with distortion of auditory perception

Ddx: Damage to hair cells/Damage to central auditory pathways

Diagnosis
 There is no definitive test for Ménière’s disease.
 Careful history and physical examination of the patient with episodic vertigo
◦ Vertigo
◦ Hearing loss
 Audiometry should be used to document sensorineural hearing loss in the affected ear
at least once during the course of the disease and can be used to follow progression
and response to treatment.
◦ Tinnitus
◦ Aural fullness
 Appropriate testing to exclude other etiologies
 Electrocochleography can be useful.

Lab tests: to exclude other suspected diseases.

Imaging: MRI
 Best imaging study for sensorineural hearing loss
 May obtain to exclude retrocochlear pathology
◦ Vestibular schwannoma
◦ Meningioma
◦ Other lesions/tumors of cerebellopontine angle
◦ Demyelinating lesions/disorders of the brainstem (which only rarely mimic
this condition)
 Superior to CT for imaging retrocochlear pathology
Diagnostic Procedures
 Audiometry
 Brainstem auditory evoked potentials
 Electronystagmography
 Otoscopy
 Caloric test/electronystagmography (ENG)
 Electrocochleography
◦ Measures the earliest evoked potentials generated in the cochlea and the
auditory nerve
◦ An elevation of the ratio of summating potential to action potential is seen
in Ménière’s disease.
Treatment Approach
 There is no cure for Ménière’s disease.
 Control of vertigo is the focus of treatment.
 There is no effective treatment for the other manifestations of the disease.
◦ Hearing loss
◦ Tinnitus
◦ Aural fullness
Specific Treatments
Therapy for vertigo
 Low-salt diet
◦ Mainstay of control of rotatory vertigo
◦ Many clinicians also recommend discontinuation of caffeine and tobacco products.
 Vestibular therapy
◦ Can be provided by special vertigo clinics and rehabilitation centers
◦ Only a minority of patients experience significant improvement.
 Medications
◦ Meclizine: 25–50 mg PO q6h prn
◦ Scopolamine: 1.5-mg transdermal patch behind the ear q3d prn
◦ Diazepam: 5–10 mg PO q 6 h prn
◦ Prochlorperazine: 5–10 mg PO q6h prn; 25 mg PR q12h prn
◦ Promethazine: 25–50 mg PO/PR q6h prn
◦ Diuretics
◦ Short course of glucocorticoids for acute attacks
◦ Intratympanic gentamicin
◦ Many patients will end up taking a combination of 2 or more of these medications.
 Surgical therapy: reserved for unresponsive cases
◦ Endolymphatic sac decompression
◦ Labyrinthectomy (resolves rotatory vertigo in >90% of the cases)
◦ Vestibular nerve section (resolves rotatory vertigo in >90% of the cases)
Therapy for tinnitus
 Hearing aids
 Tinnitus maskers
 Antidepressants
 Monitoring
 Monitor response to treatment.
 Periodically monitor hearing status through audiometry.

Complications
 Hearing loss/deafness
 Injury due to falls
 Inability to work
 Anxiety regarding symptoms

Prognosis
 Course is variable.
◦ It is not fatal.
◦ There are usually alternating periods of attacks and remissions.
◦ Over time, tinnitus and hearing loss usually progress.