Document 6888

Dizziness and Vertigo
Dr. Anirban Biswas
Neurotologist,
Vertigo and Deafness Clinic, Kolkata
Introduction
Good balance is an imperative skill for sustenance of daily life that
requires the complex integration of sensory information regarding
the position of the body relative to the surroundings and the ability
to generate appropriate motor responses to control body movement
and stabilize posture and gaze.
Gaze stabilization is as important as stabilization of posture. If there
is a defect in gaze stabilization, the surroundings appear to be
moving with the subject and feels like vertigo. If there is a defect in
postural stability, subject gets the feeling of imbalance or instability.
Balance calls upon contributions from vision, vestibular sense (i.e.,
the sensation from the balance organ in the ears), proprioception,
musculoskeletal coordination, and even cognitive skills.
Like all the body reflexes, the reflex system that controls balance
has a sensory organ (the eyes/vestibular labyrinth in the ears/
proprioceptors in the soles of the feet, back and buttocks) that senses
the stability of the ground and the surroundings. An afferent pathway
carries the sensation to the centre of the reflex in the vestibular
3
nuclei of the brainstem. An afferent motor pathway are neural
pathways or nerves that carry the motor output in the form of
neural impulses to the effector motor organs, which are the muscles
of the limbs/trunk for stabilization of posture and to the muscles of the
eyes for stabilization of gaze.
With advancing age, there is a progressive loss of functioning of all
these systems, which can contribute to balance deficits. Balance
disorders represent a growing public health concern due to the
association with falls and fall-related injuries, particularly in regions
of the world in which high proportions of the population are elderly.
The major functional objectives
of the balance system aret
a)Maintenance of clear and very distinct image of the surrounding
visual field with the head in motion, the surrounding objects in
motion, or both the head and the surrounding objects in relative
motion. Objects in the surroundings should not appear to be
rotating or spinning if they are not actually spinning/rotating.
Stable objects should appear fixed and stable in the visual
environment.
b) Perceptions of orientation relative to gravity like going up or
down in a lift, perceiving the direction and speed of movement,
and when a change in the speed or direction of movement takes
place.
c) The ability to maintain static and dynamic upright stance, and to
perform volitional movements ranging from routine ambulation
to complicated balance tasks involved in activities like playing
4
tennis, badminton, cycling, skiing, dancing, tight rope
walking, walking on a fence, etc.
Classification of balance disorder1:
• Sensory factors affecting balance:
⊲Vision
⊲ Vestibular sense
⊲ Proprioception
⊲ Sensory integration
• Motor system factors affecting balance:
⊲Strength
⊲ Reaction time i.e., the time taken for the reflex contraction of
the muscles of the body/eyes after the sense organs have
perceived a movement
Dizziness
Dizziness is a general term used for a sense of disorientation.
Diagnosing the cause of dizziness can be difficult because symptoms
are often non-specific and the differential diagnosis is broad. However,
a few simple questions and physical examination tests can narrow the
possible diagnosis. It is estimated that primary care physicians treat
more than 50% of all patients who present with dizziness. Dizziness
is the chief presenting symptom in about 3% of primary care visits
5
for patients aged 25 years and older, and in nearly 3% of all
emergency department visits.
Dizziness can be classified into four main types viz., vertigo,
disequilibrium, pre-syncope and lightheadedness (Table 1).2
Category
Description
Percentage of
patients with
dizziness
Vertigo
False sense of motion, possibly
spinning sensation
45–54
Disequilibrium
Off-balance or wobbly or instability
Up to 16
Pre-syncope
Feeling of losing consciousness or
blacking out or a sinking sensation
Up to 14
Lightheadedness
Vague symptoms, possibly feeling
disconnected with the environment/disorientation
Approx. 10
Table 1: Main categories of dizziness2
Causes of dizziness2
Dizziness may be attributed by a wide variety of causes. Some of
the causes are of sinister significance and can be life threatening,
and therefore require immediate medical attention. Some causes are
trivial self-limiting disorders that need to be managed just by providing
symptomatic relief for a few days. The problem is that, the presentation
is the same irrespective of whether it is a life-threatening condition
or any self-limiting benign disorder. Selected causes, category and
diagnostic criteria are listed in Table 2.
6
Causes
Category of
dizziness
Diagnostic criteria
from history
Benign
paroxysmal
positional
vertigo
Vertigo
Positive findings with
Dix–Hallpike test;
episodic vertigo for
a few seconds only
on change of head
position, without
hearing loss
Hyperventilation
syndrome
Lightheadedness
Symptoms
reproduced
with voluntary
hyperventilation
Ménière’s
disease
Vertigo
Episodic vertigo with
hearing loss/aural
fullness/tinnitus
Migrainous
vertigo
(vestibular
migraine)
Vertigo
Episodic vertigo with
signs of migraine,
plus photophobia,
phonophobia, or aura
during at least two
episodes of vertigo;
some will have history
of typical migraine
headache, not all
7
Orthostatic
hypotension
Pre-syncope
Decrease of
systolic blood
pressure by 20
mm Hg; decrease
of diastolic blood
pressure by 10 mm
Hg; or increase of
pulse by 30 bpm on
sudden standing
Parkinson’s
disease
Disequilibrium
Shuffling gait
with reduced arm
swing and possible
hesitation; typical
dull emotionless
face
Peripheral
neuropathy
Disequilibrium
Decreased
sensation in
lower extremities,
particularly the feet
Table 2: Selected causes of dizziness
8
Patients presents with dizziness
Ask about medication regimen; caffeine, nicotine, and alcohol intake; and
history of head trauma or whiplash
What sensation on dose the patient describe?
False sense of motion or
spinning sensation
Vertigo
Ask about migraine
symptoms
Migrainous vertigo is
diagnosed with history
of episodic vertigo with
a current migraine or
history of migraine and
one of the following
symptoms during at
least two episodes
of vertigo: migraine
headache, photophobia,
phonophobia, aura
Off-balance or
wobbly
Dysequilibrium
Pre-syncope
Consider possible
underlying conditions, Ask about history
of arrhythmias
such as peripheral
and myocardial
neuropathy and
infarction
Parkinson’s disease
Lightheadedness
Ask about history
of anxiety or
depression
Re-check medication Re-check medication
Perform
regimen, especially in regimen, especially hyperventilation
older patients
in older patients provocation test
Examine gait and vision,
Measure
perform Romberg’s test, orthostatic blood
screen for neuropathy
pressures
Consider cardiac
testing in patients
with relevant history
Hearing loss?
No
Yes
Episodic vertigo?
Yes
Feeling of losing Vague symptoms,
consciousness or possibly feeling
blacking out disconnected with the
environment
No
Episodic vertigo?
Yes
Ménière’s Labyrinthitis Benign paroxysmal
disease
positional vertigo
No
Vestibular
neuritis
Perform Dix–Hallpike maneuver
Table 3: Algorithm for the initial evaluation of a patient with dizziness2
9
Vertigo
Vertigo is a sub-type of dizziness, which results from a disparity in the
electrical discharge in between the left and right vestibular labyrinths.
Vertigo is a spinning sensation, and in medical parlance is defined as
an illusion of rotational motion.
Physiology of vertigo3
Most vertigo is caused by dysfunction of the vestibular labyrinth(s)
of the inner ear, which houses the rotational velocity sensors. In the
normal situation, individuals continuously process three types of
sensory inputs: vestibular (inner ear), visual and somatosensory/
proprioceptive. These three streams of information from the sides of
the body as well as from the front and back are combined or integrated
in the central vestibular apparatus in the brain to assess the stability
of the ground and the surroundings, and thereby form an estimate
of orientation and motion of the head and body. Asymmetrical
or defective input into the central vestibular apparatus (that is the
central nervous system) or asymmetrical central processing leads to
physiological and pathological vertigo. In disorders of the vestibular
labyrinth, which will be resulted by various causes like inflammatory,
degenerative, neoplastic, vascular or infective, the input from one
or both vestibular labyrinths in the central nervous system is either
symmetrical or sub-normal.
Neurochemistry of vertigo
There are at least six neurotransmitters of the vestibular system
involved in the three-neuron arc between the vestibular hair cells and
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oculomotor nuclei that drive the vestibulo–ocular reflex (see
Table 4). There are also a host of other neurotransmitters that
modulate function or involved in a more minor way.
Neurotransmitter
Peripheral role
Central role
Glutamate
Excitatory
Excitatory
Acetylcholine
Excitatory for
efferent synapse
Excitatory
GABA
Unclear
Inhibitory
Dopamine
Excitatory
Noradrenaline
(norepinephrine)
Modulator
Histamine
Unclear
Table 4: Neurotransmitters of the vestibular system
A lot of current medication in the management of vertigo consists of
modulating the excitatory or inhibitory effects of the neurotransmitters.
11
Classification of vertigo
Based on
Based on site
Prolonged vertigo usually a
Otomastoiditis
Central vertigo
Peripheral vertigo
Vestibular neuronitis
Labyrinthine concussion
Lateral medullary infarction
Cerebellar infarction
Recurrent episodes of vertigo
Ménière’s syndrome
Auto-immune inner-ear disease
Perilymph fistula
Migraine-related vertigo
Benign positional paroxysmal vertigo
Vertebrobasilar insufficiency
12
Etiology of vertigo4
Vertigo related to the inner ear (vestibular labyrinth – semicircular
canals/otolith organs viz., uticle and saccule) may be caused by:
• Benign paroxysmal positional vertigo
• Drugs such as aminoglycoside antibiotics, cisplatin, diuretics, or
salicylates
• Injury (such as head injury)
Infections
Epilepsy
Diseases of blood vessels
Multiple sclerosis
Trauma
Middle ear:
otitis media
Tumors
Labyrinthitis,
Ménière’s disease
Medicines
Fig. 1: Possible causes of vertigo
Adapted from Netter.
13
•Labyrinthitis
•Ménière’s disease
• Perilymph fistula
Vertigo related to disorders of vestibular nerve may be caused by:
• Inflammation (neuronitis)
• Pressure on the vestibular nerve (most often due to a non-cancerous
tumor such as a meningioma or schwannoma, commonly called
as acoustic neuroma)
• Effect of some drugs like oral contraceptives
• Trauma to the nerve as in transverse fracture of the temporal bone
usually after traffic accidents
Vertigo related to the brainstem may be caused by:
• Blood vessel disease
• Drugs (anti-convulsants, aspirin, alcohol)
• Migraine
• Multiple sclerosis
• Seizures (rarely)
Central vs peripheral vertigo
• Peripheral vertigo occurs if there is a problem with the part of the
inner ear that controls balance (vestibular labyrinth) or with the
vestibular nerve, which connects the inner ear to the brainstem.
14
• Central vertigo occurs if there is a problem in the brain,
particularly in the brainstem or the cerebellum.
Central vertigo
Intermediate vertigo
Peripheral vertigo
Fig. 2: Sites of vertigo
15
Clinical
history (in
addition
to vertigo,
nausea, and
vomiting)
Otomastoiditis Previous ear
infections,
otorrhea, ear
pain, hearing
loss
Examination
(in addition to
nystagmus and
imbalance)
Management
(in addition to
treatment of
symptoms)
Otitis media,
tympanosclerosis,
cholesteatoma,
granuloma
Vestibular
neuritis
No other clinical
findings other
than nystagmus,
positive findings in
some of the clinical
neurotological steps
like stepping test
Antibiotics,
surgical
removal of
infected tissue/
cholesteatoma,
vestibular
rehabilitation
Brief course
of high-dose
steroids,
vestibular
rehabilitation
Labyrinthine
concussion
16
Previous
influenza-like
symptoms,
acute onset of
severe vertigo
persisting for
1–3 days, no
hearing loss
Onset after
blow to head,
hearing loss
and tinnitus,
symptoms
of brain
concussion
Hearing loss,
possible blood or
CSF in ear canal
Vestibular
rehabilitation
Lateral
medullary
infarction
Vascular
Ipsilateral Horner’s
Control of
risk factors,
syndrome, facial
vascular risk
sudden
numbness, lack
factors
onset, facial
of coordination,
numbness
decreased gag
and
reflex, contralateral
weakness,
numbness in limbs
diplopia,
dysphagia,
lateropulsion
Cerebellar
Cardiac
Truncal ataxia, limb Control
infarction
disease,
ataxia, or both
of source
vascular
of emboli,
risk factors,
other risk
sudden onset,
factors, gait
profound
and balance
imbalance,
training
possible
lack of limb
coordination
Table 5: Common causes of prolonged non-episodic vertigo3
17
Clinical history
(in addition to
vertigo, nausea,
and vomiting)
Ménière’s
Fluctuating
syndrome
hearing loss, ear
fullness, roaring
tinnitus, rarely
sudden falls
(otolithic crises)
Autoimmune Fluctuating
inner-ear
or slowly
disease
progressive
hearing loss,
possible systemic
symptoms of
autoimmune
disease
Perilymph
“Popping” sound,
fistula
hearing loss,
or tinnitus after
head trauma,
barotrauma,
cough, sneeze,
straining
18
Examination
(between
attacks)
Lowfrequency
hearing loss
(unilateral in
most cases)
Management
(in addition to
treatment of
symptoms)
Low-salt diet,
diuretics,
surgery only for
intractable but
confirmed cases
Hearing loss
(bilateral in
many cases),
interstitial
keratitis,
arthritis, rash
High-dose
steroids
Possible
positive
fistula sign
(nystagmus
induced by
pressure
change in
external ear
canal)
Bed rest,
avoidance
of straining,
exploratory
tympanotomy
for fistula if
symptoms
persist
Migraine
Headache,
visual aura,
unilateral
numbness,
motion
sensitivity
dysphagia,
lateropulsion
Normal in
most cases
Vertebrobasilar
insufficiency
Visual loss,
diplopia,
ataxia,
dysarthria,
numbness,
weakness
Normal in
most cases
β-blockers,
calcium-channel
blockers,
tricyclic antidepressants
Anti-platelet
drugs (aspirin
75–330 mg
daily, ticlopidine
500 mg daily),
anti-coagulation
for severe
progressive
symptoms
Table 6: Common causes of recurrent attacks of vertigo3
19
Vestibular neuritis (vestibular neuronitis)
Vestibular neuronitis/neuritis is the second common cause of vertigo
seen in peripheral labyrinthine disorders. It occurs due to viral/
bacterial inflammation of the vestibular nerve, and usually follows an
upper respiratory tract infection.
The onset of vertigo, usually with nausea, and vomiting but without
any ear-related symptoms like deafness/tinnitus/aural fullness in
vestibular neuritis is typically acute, over minutes to hours. Symptoms
usually peak within 1–6 h and resolve slowly over 2–3 days, but may
sometimes continue for about a week. During the first day, the patient
has severe truncal unsteadiness and imbalance, and has difficulty in
focusing the eyes because of spontaneous nystagmus. The course
is usually benign, with complete recovery in 4–6 weeks. Recovery
of the presenting symptoms of vertigo with nausea and vomiting
occurs spontaneously in most cases even when the unilateral loss of
vestibular function is permanent because the brain compensates for
the vestibular loss. There are exceptions, particularly in older patients
and the ill patients who will be taking the symptom relieving and the
vertigo drugs for a prolonged period, in which compensation may be
slow or incomplete.
Vestibular neuritis is thought to have a viral origin, but proof in an
individual case is difficult. MRI with contrast enhancement occasionally
reveals an inflammation of the 8th cranial nerve, but these findings are
non-specific and have little diagnostic value. Serological studies may
show a viral infection but cannot prove that a virus has caused the
inner ear damage. Vestibular neuritis is different from Ramsay Hunt
syndrome, which is also a viral inflammation of the vestibulo–cochlear
20
nerve that is caused by varicella zoster virus. In this disease, visible
eruptions are quite often seen in the external auditory meatus along
with facial paralysis and hearing loss, none of which are present
in vestibular neuritis. In Ramsay Hunt syndrome, patients typically
have a deep burning pain in the ear, which is never seen in vestibular
neuritis.
Ménière’s syndrome3
In 1861, Prosper Ménière first described the triad of fluctuating
hearing loss, tinnitus, and episodic vertigo. This is the hallmark of
Ménière’s syndrome even today, and the diagnosis of Ménière’s
disease is based on this typical presentation, where the patient will
have recurrent episodes of vertigo, which will last for anything between
21
half an hour and 12 h, and rarely a little more but definitely less
than a day, along with ear-related symptoms like deafness,
tinnitus, and a fullness of one ear. In between two attacks of vertigo,
the patient does not have any significant imbalance or any vertiginous
sensation, but some ear-related problems like deafness and tinnitus
are usually persistent. The ear-related symptoms of an aggregate is
observed just prior to or during the episode of vertigo. Patients with
Ménière’s syndrome have different symptoms, in different stages
Endolymphatic sac
Endolymphatic duct
Utricle
Saccule
Stapes
Fig. 3: Engorged endolymphatic compartment of the
inner ear in Ménière’s disease
Adapted from Hain and Uddin.
22
of the disease. Diagnosis is difficult, particularly in the early
stages and remains uncertain in the first one or two attacks
of vertigo as the ear-related symptoms may not be apparent in the
very early stages. By definition, Ménière’s disease can be diagnosed
without the combination of fluctuating hearing loss and vertigo.
Simply recurrent attacks of vertigo even if episodic cannot be labeled
as Ménière’s disease, if there is no ear-related symptoms. Delayed
Ménière’s syndrome can develop in an ear that has been damaged
years before, usually by a viral or bacterial infection. Patients with
this type of Ménière’s syndrome report a long history of hearing
loss sometimes since early childhood, followed many years later by
episodes of vertigo.
In such cases hearing loss is generally profound, and the vertigo
is not accompanied by fluctuating hearing loss and tinnitus. Though
the disease is primarily diagnosed from its typical presentation as
described above, yet for confirmation certain investigations need
to be done namely video-nystagmography, pure tone audiometry
with glycerol test and other localizing tests, brainstem-evoked
response audiometry, and electrocochleography. Imaging studies
like an MRI of the brain or inner ear does not help even though it is
not unwise to have an imaging study done to rule out an acoustic
neuroma, which can also be present with vertigo and deafness
with tinnitus. However, in an acoustic neuroma, there is practically
never an episodic vertigo as is present in Ménière’s disease. The
main pathological finding in patients with Ménière’s syndrome is an
increase in the volume of endolymph, associated with distension
of the entire endolymphatic system (endolymphatic hydrops). The
episodes of hearing loss and vertigo may be caused by ruptures in
the membranes separating endolymph from perilymph, which lead to
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a sudden increase in potassium concentration in the perilymph.
Another possible explanation for the fluctuating symptoms is
mechanical deformation of the end organ, which is reversible as the
endolymphatic pressure decreases. The incidence of sudden falling
are probably due to sudden distension and deformation of one of the
otolith organs.
Healthy inner ear:
Balance
canal
Endolymphatic sac
Hearing and
balance nerve
Hearing canal
Ménière’s disease:
Backed-up fluid
leads to swelling
and pressure
Swelling
distorts
balance
information
Swelling distorts
sound information
24
Distorted
information
travels to brain
Benign paroxysmal positional vertigo4
Patients with benign paroxysmal positional vertigo (BPPV) develop
brief episodes of vertigo with position change, typically when turning
over in bed, getting in and out of bed, or extending the head back to
look upwards or even downwards. Typically, the spinning sensation
occurs just for a few seconds to less than a minute. The diagnosis is
easily made from the typical history, and confirmed by identification
Posterior
semicircular
canal
Utricle
Vestibule
Cupulolithiasis, debris
attached to cupula
Canalithiasis, debris
in posterior canal
Fig. 4: Canalolithiasis mechanism of benign paroxysmal
positional vertigo
(Adapted from Hain and Uddin.)
25
of the characteristic torsional nystagmus after the patient is
moved from the sitting to the sideward – head hanging position
(the Dix–Hallpike test). This type of vertigo can occur in otherwise
perfectly normal ears with normal vestibular function be it a sequelae
of head trauma or vestibular neuritis. Migrainous patients are very
susceptible to BPPV, and the incidence of this disorder is quite high
in patients with migraine.
The BPPV can involve any of the three semi-circular canals. Most
often, posterior semi-circular canal is involved, followed by lateral
semi-circular canal and rarely the superior semi-circular canal. The
pathology of BPPV is attributed to the sequestrated otoconia moving
into the cupula or the canal, called cupulolithiasis or the canalolithiasis.
Psychogenic vertigo5
Balance disorders and psychological disorders are believed to be
comorbid conditions and there is enough of published research
work to support this. About 64% of vertigo patients had psychiatric
symptoms, and 45% of vertigo patients had panic symptoms. Vertigo/
imbalance and psychiatric disorders coexist as a result of neurological
links between vestibular and autonomic systems – neuroanatomic
connections between the two systems have now been established.
The uncertainty of the timing and severity of the attacks of vertigo, the
loss of confidence that occurs due to imbalance, the frustration that
occurs due to inefficiency of diagnosis/treatment leads to anxiety,
helplessness, panic disorders, agoraphobia, somatization, and
depression psychopathology in patients. In between the attacks of
vertigo there is quite often instability, lassitude, and a constant fear of
recurrence of vertigo leading to a markedly severe negative effect on
26
the quality of life. Primary psychogenic vertigo can be suspected
if vertigo is precipitated by social/psychological stimuli, or if the
patient expresses extreme anxiety/fear (inappropriately more than
clinical features), and if the patient complains of severe rotational
vertigo but no clinical evidence of nystagmus, and other signs of actual
vertigo/instability is found in the clinical tests and investigations.
Psychogenic vertigo is caused by an independently diagnosable
psychiatric problem such as anxiety, depression, somatization or
malingering. Psychiatric-associated vertigo is the coexistence of
an organic vertigo with an independently diagnosable psychiatric
condition, such as anxiety, which might be comorbid or reactive.
27
Migraine-associated vertigo and basilar migraine
The manifestations of migraine-associated vertigo are quite
varied and may include episodic true vertigo, positional vertigo,
constant imbalance, movement-associated disequilibrium, and/
or lightheadedness.6,7 Symptoms can occur before the onset of
headache, during a headache, or most commonly, during a headachefree interval. As such, many patients who experience migraines have
vertigo or dizziness as the main symptom rather than headache.
For this reason, this article is devoted to the description of migraineassociated vertigo.
28
Basilar migraine, also known as Bickerstaff syndrome,8 is an
important variant of migraine with aura. Bickerstaff syndrome
consists of two or more symptoms (i.e., vertigo, tinnitus, decreased
hearing, ataxia, dysarthria, visual symptoms in both hemifields of
eyes, diplopia, bilateral paresthesias, or paresis, decreased level of
consciousness) followed by a throbbing headache.
Vascular ischemia
The sudden onset of vertigo in a patient with additional neurologic
symptoms (e.g., diplopia, dysarthria, dysphagia, ataxia, weakness)
suggests the presence of vascular ischemia.
Treatment of transient ischemic attack (TIA) and stroke includes
preventing future events through blood pressure control, cholesterollevel lowering, smoking cessation, inhibition of platelet function
(e.g., aspirin, clopidogrel, aspirin–dipyridamole) and possibly anticoagulation by warfarin.
Acute vertigo caused by a cerebellar or brainstem stroke is treated
with vestibular suppressant medication and minimal head movement
for the first day. As soon as tolerated, medication should be tapered,
and vestibular rehabilitation exercises should be initiated.
Placement of vertebrobasilar stents may be considered in a patient
with symptomatic critical vertebral artery stenosis that is refractory
to medical management. Rarely, infarction or hemorrhage in the
cerebellum or brainstem may present with acute vertigo as the only
neurologic symptom. Given the risk of brainstem compression with
a large cerebellar stroke, neurosurgical decompression may be
indicated.
29
Lateral medullary syndrome
The PICA syndrome is also known as “lateral medullary syndrome”,
or “Wallenberg’s syndrome”, after Wallenberg’s description in 1895.
This is the most common brainstem stroke. It is typified by vertigo,
ipsilateral hemiataxia, dysarthria, ptosis, and miosis. Most patients
with this stroke recover very well and often resume their previous
activities.9 Patients often have a Horner’s syndrome (unilateral ptosis,
miosis, and facial anhidrosis). Also there may be saccadic dysmetria
(overshoot), and/or saccadic pulsion (pulling of the eye during vertical
saccades toward the side of lesion). Prognosis is generally quite
good with full or near-full recovery expected at 6 months. Diagnosis is
generally via MRI. CT-angiography with 3D reconstruction has gotten
good enough in recent years to be helpful too.
Auditory brainstem response (ABR) testing is often abnormal in
persons with central Horner’s syndrome10; however, as the lesion
in Wallenberg syndrome is usually below the auditory connections,
Horners due to Wallenbergs are not generally associated with
abnormal ABR.
The PICA syndrome may arise from the vertebral artery (the usual
case), or as a separate branch of the basilar artery. Due to far more
common origin from the vertebral artery, most PICA syndrome
strokes actually are due to vertebral artery occlusion. Cardiac
embolism causes only 5% of these strokes, while dissection causes
15%.11 PICA is the most common site of occlusion from propagating
thrombus or embolism caused by injury to the third section of the
vertebral artery, and Wallenberg’s syndrome is the most common
stroke caused by chiropractic manipulation.12
30
Perilymph fistula
A perilymph fistula (perilymphatic fistula [PLF], labyrinthine fistula)
is a pathologic communication between the fluid-filled space of the
inner ear and the air-filled space of the middle ear, most commonly
occurring at either the round or oval window.
The symptoms of PLF may include dizziness, vertigo, imbalance,
nausea, and vomiting. However, patients usually report an
unsteadiness, which increases with activity that is relieved by rest.
Some people experience ringing or fullness in the ears, and many
notice a hearing loss. Some people with fistulas find that their
symptoms get worse with coughing, sneezing, or blowing their noses,
as well as with exertion and activity. This sort of symptom goes under
the general rubric of “valsalva-induced dizziness”, and it can also be
associated with other medical conditions.13
Fistula
31
Acoustic neuromas
Acoustic neuromas, also known as vestibular schwannomas, are
non-malignant tumors of the 8th cranial nerve. Most commonly they
arise from the covering cells (Schwann cells) of the inferior vestibular
nerve. They can also arise within the labyrinth. Acoustics comprise
about 6% of all intracranial tumors, about 30% of brainstem tumors,
and about 85% of tumors in the region of the cerebellopontine angle
– another 10% are meningiomas.
Hearing loss is the most frequent symptom of acoustic neuroma.
Tinnitus is very common in acoustic neuroma, which is usually
unilateral and confined to the affected ear. Vertigo is more common
with smaller tumors. Unsteadiness is much more prevalent than
vertigo, and approximately 70% of patients with large tumors have
this symptom.
Acoustic neuroma
Facial nerve
Cochlea
32
Examination and investigations in
vertigo patients
A physical examination may reveal:
• Eye movement
(nystagmus)
problems
or
involuntary
eye
movements
• Lack of coordination and balance
• Difficulty in walking
• Hearing loss
• Weakness of the limbs/trunk
Spontaneous nystagmus
Eyes open
No nystagmus
Nystagmus
Eyes closed
Eyes closed
No nystagmus
Nystagmus No nystagmus
Peripheral
disorder
Central
disorder
Nystagmus
Peripheral
or central
disorder
33
In all patients with vertigo or imbalance, there has to be at least
a brief examination of the neurological system consisting of
deep tendon reflexes, planter flexor/extensor, to look for any motor
or sensory loss, the cerebellar tests, and of course a thorough
examination of the balance system that consists of the vestibulospinal
tests and the vestibulo-ocular tests. The vestibulospinal tests
consist of the stepping test, the standing test that is the Romberg’s
test, and the gait test. The vestibulo-ocular tests consist of tests
for spontaneous nystagmus or any abnormal spontaneous eye
movement like opsoclonus, ocular bobbing, etc., and some tests for
provoked nystagmus include tests like the Dix–Hallpike test, test for
gaze nystagmus, and the oculomotor tests.
Sign/symptom
Severity
Associated symptoms
Imbalance
Positional
Compensation
Pre-morbid
Spontaneous
nystagmus
• Nystagmus direction
• Nystagmus fixation
34
Peripheral vertigo
Severe with
vomiting
Mild
Mild
Often triggered
Rapid, subsides
in 48 h
Hearing loss, ear
infection
Mixed
Horizontal and
torsional
Suppression with
fixation
Central vertigo
Moderate
Severe
Severe
May be worsened
Slow, persistent
Hypertension,
cardiovascular
disease
Pure nystagmus
vectors
Pure horizontal and
pure vertical
No suppression with
fixation
VOR – Head thrust test
Smooth pursuit
Direction of associated
nystagmus
Purely horizontal
nystagmus
Vertical or purely
nystagmus
Visual fixation
Impaired
Intact pursuit
Uni-directional,
fast phase
opposite lesion*
Always
Never present
Intact
Broken pursuit
Bi- or uni-directional
May be vertical,
torsional or horizontal
May be present
Inhibits
No inhibition of the
nystagmus
nystagmus
14
Table 7: Peripheral vertigo vs central vertigo
*In Ménière’s disease, the direction of fast phase is variable.
Investigations
• Caloric test without electronystagmography (ENG) or video
nystagmography (VNG) recording is now obsolete and not
advocated.
• ENG/VNG should include all the oculomotor tests, test for
spontaneous nystagmus, test for positional and positioning
nystagmus, and of course the caloric tests. The rotational tests are
helpful if available, but are not essential in each and every patient.
While recording nystagmus by ENG or VNG, the eye movements
in both horizontal as well as vertical directions should be recorded.
Other tests that should also be done are the vestibular-evoked
myogenic potentials (VEMP), posturography, craniocorpography, and
35
the basic audiological tests like pure tone audiometry, brainstemevoked response audiometry and electrocochleography as
and when required. Imaging studies are not required in each and
every patient of vertigo, but if the clinical tests or other investigations
suggest possibility of some neoplastic, degenerative or vascular
problem in the brain, then of course an imaging study specifically an
MRI of the brain preferably with contrast is necessary.
Pharmacotherapy5
Vertigo or imbalance is just a manifestation of some underlying
disorder and not a disease in itself. Vertigo is just like fever in malaria
or typhoid. The fever in such diseases is symptomatic and must be
managed by treating the underlying cause by anti-malarial or antityphoid drugs. Similarly, for the management of vertigo, the clinician
should first try to diagnose the cause of the vertigo or imbalance and
then treat the underlying cause, and not merely try to suppress the
symptoms. Prolonged symptomatic treatment of vertigo or imbalance
by the so-called anti-vertigo drugs does more harm to the patient
than good. It is similar to treating the fever in malaria or typhoid
with paracetamol for months together. Unfortunately this is what
is commonly practiced, which is not only unjust and unethical but
also deplorable and condemnable. The symptom-relieving vestibular
sedatives or anti-vertigo drugs like prochlorperazine, meclizine,
dimenhydrinate, cinnarizine or betahistine are best when used for a
very short duration of 3–7 days only, and should be discontinued as
soon as the acute symptoms of vertigo subside. If a proper history
is taken and clinical tests and investigations are properly performed,
the underlying cause of the vertigo/instability can be treated ethically
36
and logically. There are specific treatment protocols for all
the causes of vertigo: Ménière’s disease, vestibular neuritis,
labyrinthitis, BPPV, PLF, migraine-related vertigo, psychogenic
vertigo, cerebellar stroke, etc.
Vertigo
suppression drugs
Drugs modifying
underlying pathology
Vestibular suppressants
Cerebro-active drugs
Anti-cholinergics
Vasodilators
Anti-histamines
Diuretics
Benzodiazepines
Corticosteroids
Calcium-channel
antagonists
Anti-bacterial
drugs
Anti-emetics
37
Treatment
Treatment of vertigo can be divided into three main categories:
specific, symptomatic, and rehabilitative.
• Specific treatment for Ménière’s syndrome involves restriction
of salt intake (1–2 g daily), diuretics (hydrochlorothiazide,
acetazolamide), and rarely surgery for intractable cases.
Vertebrobasilar insufficiency can be treated with anti-platelet
drugs (aspirin 75–330 mg daily or ticlopidine 500 mg daily) and
with anti-coagulants if the symptoms are severe and progressive.
Migraine-related vertigo is treated by propranolol, imipramine and
drugs like flunarizine or divalproic sodium. The specific treatment
protocols for a few of the common causes of vertigo have been
enumerated above.
• Symptomatic therapy is used to control the troublesome symptoms
of vertigo, nausea, and vomiting, whatever the cause. Commonly
used vestibular suppressants include prochlorperazine meclizine,
dimenhydrinate, promethazine, betahistine, cinnarizine, and
diazepam.
When nausea and vomiting persist, an anti-emetic drug such as
domperidone or ondansetron can be combined with the vestibular
suppressant drug. Though prochlorperazine is labeled as antiemetic drugs in pharmacology textbooks, it has very good antivertigo effect and is primarily used to control symptoms of acute
vertigo. Of all the drugs available for symptomatic relief, the most
effective is prochlorperazine. It not only manages vertigo but also
the accompanying nausea and vomiting owing to the anti-muscarinic
38
(controls the vertigo) as well as anti-dopaminergic (controls
the nausea and vomiting) properties associated with the drug.
In case of acute vertigo, the dose regime commonly followed for
prochlorperazine is 1 tablet (5 mg) thrice daily for 3–5 days. In chronic
vertigo management, betahistine has been the trusted therapy since
1968. Betahistine is a histamine analog with an agonistic action. It is
a H1 receptor agonist and antagonizes the H3 receptors. It increases
cochlear and cerebral blood flow and regulates firing activity of the
vestibular nuclei. Betahistine dose is advised as 24–48 mg/day. The
biggest advantage of betahistine is that it is the only non-sedating
anti-vertigo drug. All the other anti-vertigo drugs have some sedative
effect, and therefore depress the central nervous system, which is
detrimental to the central vestibular compensatory mechanism. This
central vestibular compensatory mechanism is a faculty of the brain
that restores normal balance function after a vestibular assault
(vestibular labyrinth has been damaged). This is a natural mechanism
which normalizes the patient’s balance system after it has been
damaged by disease. Betahistine being a non-anti-histaminic
and a non-sedative anti-vertigo drug can be used for somewhat
longer periods unlike the anti-histaminic anti-vertigo drugs like
prochlorperazine, cinnarizine, meclizine, and dimenhydrinate.
• Vestibular rehabilitation helps the patient compensate for
permanent vestibular damage.8 Vestibular exercise should begin
as soon as the acute stage of nausea and vomiting has ended,
and when the underlying disease process is subsiding. Many of
the exercises result in dizziness. This sensation is a necessary
stimulus for compensation; vestibular suppressants should be
avoided during this period to ensure the maximum beneficial
effect. Different types of exercises are available, the most popular
39
one being the age-old Cawthrone–Cooksey exercises.
However, much better options are available now and some of
the Yogic asanas and Tichi exercises have been found to be very
effective in enhancing and expediting the vestibular compensatory
mechanism.
Vestibular Rehabilitation15–17
• Adaptation – A phenomenon which helps a patient with
persisting peripheral dysfunctional state to regain normal
balance.
• Habituation – Repeated exposure of the body to
“mismatched” sensory input.
• Compensation – A goal-directed process induced by some
recognized errors, directed towards its elimination.
Exercise in bed: Eye movements
Looking up and
then down
40
Looking alternately
left and right
Convergence
exercises
Bending alternately
forward and
backward
Turning
alternatively to the
left and then right
Exercise in sitting position
Bending forward and
picking up objects
from the floor
Turning head and
trunk alternately to
the left and then right
41
Exercise in standing position
42
Changing from
sitting to standing,
initially with eyes
open and then with
the eyes closed
Throwing a ping
pong ball in an arc
from hand to hand
and following it with
the eyes
Throwing a small
ball from hand to
hand under the
knee
Throwing and
catching the ball
while walking
Walking around in
the room with eyes
open and closed
Walking up and
down a flight of
stairs
Patient Questionnaire
1. Do you feel unsteady?
2. Do you feel as if the room is spinning around you?
3. Do you feel as if you are moving when you know you
are sitting or standing still?
4. Do you lose balance and fall?
5. Do you feel as if you are falling?
6. Do you feel “lightheaded” or as if you might faint?
7. Do you have blurred vision?
8. Do you ever feel disoriented, such as losing your sense
of time or where you are?
43
Patient fill-up form
How can I help my doctor make a diagnosis?
You can help your doctor make a diagnosis and determine
a treatment plan by answering the questions below.
Be prepared to discuss this information during your
appointment.
1.The best way I can describe my dizziness or
balance problem is:
2. How often do I feel dizzy or have trouble keeping my
balance?
3. Have I ever fallen?
If yes,
A. When did I fall?
44
B. Where did I fall?
C. Under what conditions did I fall?
D. How often have I fallen?
4. The medicines I take:
(Include prescription medications and over-the-counter
medicines, such as aspirin, antihistamines, or sleep aids.)
A. Name of medicine:
B. How much (mg) and how often (times) per day:
C. The condition I took this medicine is for:
At your appointment, take a minute to write down any
instructions your doctor has given you. Be sure to ask any
questions you have before you leave the clinic/hospital.
45
References
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elderly. Neurophysiol Clin. 2008;38(6):467–478.
2. Post RE, Dickerson LM. Dizziness: a diagnostic approach. Am
Fam Physician. 2010;82(4):361–369.
3. Baloh RW. Vertigo. Lancet. 1998;352(9143):1841–1846.
4. Bauer CA, Jenkins HA. Otologic symptoms and syndromes.
In: Flint PW, Haughey BH, Lund VJ, et al. editors. Cummings
Otolaryngology: Head & Neck Surgery. 5th edition. Philadelphia,
PA: Mosby Elsevier; 2010. Chapter 126.
5. Hain TC, Uddin M. Pharmacological treatment of vertigo. CNS
Drugs. 2003;17(2):85–100.
6. Harker LA. Migraine-associated vertigo. In: Baloh RW, editor.
Disorders of the Vestibular System. Oxford, England: Oxford
University Press Inc.; 1996: pp. 407–417.
7. Buchholz DW, Reich SG. The menagerie of migraine. Semin
Neurol. 1996;16(1):83–93.
8. Bickerstaff ER. Basilar artery migraine. Lancet. 1961;1:15.
9. Nelles G, Contois KA, Valente SL, et al. Recovery following lateral
medullary infarction. Neurology. 1998;50:1418–1422.
10.Faught E, Oh SJ. Brainstem auditory responses in brainstem
infarction. Stroke. 1985;16:701–705.
46
11.Kim JS. Pure lateral medullary infarction: clinical–
radiological correlation of 130 acute, consecutive patients.
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12. Caplan LR. Vertebrobasilar disease. In: Barnet HJM, et al. editors.
Stroke: Pathophysiology, Diagnosis and Management. New York:
Chrchill-Livingstone; 1986:549–619.
13. Swartz R, Longwell P. Treatment of vertigo. Am Fam Physician.
2005;71(6):1115–1122.
14. Daroff RB. Faintness syncope, dizziness and vertigo. In: Harrisons
Principles of Internal Medicine. 14th edition, p. 105.
15.Kirtane MV. Role of adaptation exercises in clinical practice.
Indian J Otolaryngol. 1999;51(2):27–36.
16.Biswas A. Clinical Audio-Vestibulometry for Otologista and
Neurologists. 4th edition. Mumbai: Bhalani Medical Book House;
2010.
17. Biswas A. An Introduction to Neurotology. 2nd edition. Mumbai:
Bhalani Medical Book House; 2005.
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Notes
48
Notes
49
Notes
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