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(February 8, 2013)

General Data
K.S. 50/F, office employee
Chief Complaint
Persistent dizziness
History of Present Illness
Since ten months PTC, the patient has noted a persistent dizziness which was initially mild and described as,
parang umiikot na hindi naman. The patient visited an optometrist who prescribed eyeglasses. She recalls her
grade to be, 100. This seemed to slightly give some relief from the dizziness but persistent mild dizziness
Six months PTC, the patient noted dizziness to be more persistent despite taking medications suggested by a friend
(Serc) and compliant use of refractive lenses. The patient also noted that she seemed more unsteady whenever
wearing high heels, often falling to one side. The first episode of this resulted in a bad sprain of the L foot, for
which she was brought to an emergency room. She was assessed to have lax ligaments in the L foot, and was
advised to not wear high heels.
Five months PTC, the patient noted difficulty in typing, often hitting the wrong keys whenever she was typing at
her regular rapid speed. She also noted that her handwriting seemed to be getting worse. This has impacted her
work, causing increased work stress. She has noted regular recurrence of a headache that seems to go around
her temples to the sides of her head.
Review of Systems
(-) fever
(-) chills
(+) occasional L forehead pain
(-) nausea
(-) vomiting


chest pain
abdominal pain

Past Medical History

Patient has no known allergies to drugs or foods. There are no known chronic medical conditions and the patient is not
taking any medications other than what has been given in the history.
Family Medical History
Personal and Social History
Claims occasional alcoholic beverage drinking (1-2 beers/session), non-smoker
Married to an office employee, with 2 children.
Physical Examination

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HR: 90 RR: 28 BP: 100/60 T: 36.5

Patient conscious, alerted, oriented to person, place and time
Pink conjunctiva, anicteric sclera, normal looking oral mucosa, no neck masses
Equal chest expansion, clear breath sounds
Adynamic precordium, normocardic, regular rhythm, distinct S1 and S2, no murmurs
Abdomen flat, no lesions, soft, (-) tenderness, (-) palpable masses
Pulses full, pink nailbeds, (-) edema, (-) lesions

Vestibular System:
What is the vestibular system and what does it do for you?
The vestibular system is made up of:

Vestibule (sensory organ)

Cranial Nerve VIII
Brainstem vestibular nuclei
Cerebellar pathways
Vestibule-ocular reflexes (VOR)
Vestibulocollic reflexes (VCR)
Vestibulospinal reflexes (VSR)

* Provides information about head motion and orientation in respect to gravity.

* Generates eye movements to promote gaze stabilization and postural righting responses involving the head
and trunk.
Here are some anatomy basics:
1. Semicircular canals
3 bony canals in each ear Superior/Anterior, Posterior, & Horizontal
The canals are positioned at a 90 angle from one another, with the horizontal canal tipped

backwards 20-30 degrees

The parts of the canals include:

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Endolymph fluid that fills the canals

Ampulla - dilated space at the end of each canal

Cupula - gel-like bud, embedded with sensory hair cells, that sits within the ampullated
(dilated) portion of each canal

The semicircular canals detect angular accelerations of the head through displacement
of the cupula

2. Otolith Organs (Utricle and Saccule)

These organs make up the medial portion of the vestibule
The semicircular canals originate from the utricle
Sensory hair cells are embedded within the membrane (macula) of each organ
Calcium carbonate crystals called otoconia are attached to both the medial wall of the saccule and
floor of the utricle
Otoconia enable the otoliths to detect tilts and translations of the head, because they respond
primarily to linear acceleration forces like gravity

The Brain
1. Brainstem Vestibular Nuclei
Primary input comes from the vestibular portion of CN VIII (vestibular-cochlear)
There are 4 Vestibular Nuclei:

Lateral/Deiters Nucleus

Help the body maintain a desired posture

(ie. vestibulospinal reflexes)


Coordinates eye, head, and neck



Integrate information from the cerebellum

and other sensory systems

2. Cerebellum
Midline (vermal) regions regulate balance and eye movements
Lateral regions control muscles of the extremities.
The cerebellum plays a central role in modulating ocular motor reflexes with the goal of maximizing

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visual performance

The Blood Supply and Innervation

1. Vascular Supply

2. Nerve Supply
CN VIII is divided into 2 parts:

Superior portion innervates anterior and horizontal canals and utricle

Inferior portion innervates posterior canal and saccule


The hair cells of the cristae

ampullares detect rotational or
angular movement of the head

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The hair cell of maculae of the

saccules and utricles respond to
linear acceleration, gravity and tilt of
the head.

Perilymphatic space: Intervenes between the

osseous labyrinth and the membranous labyrinth.
Traversed by fibrous trabeculae. Contains the fluid,
Osseous tissue: Compact bone forming the osseous
labyrinth. The surface facing the perilymph has a
periosteum covered by mesenchymal tissue.
Endolymphatic space: The stimulation of the
vestibular receptors (the crista ampullaris and the two
maculae) depends upon the movement of endolymph,
the fluid contained within the endolymphatic space in
the semicircular canals, saccule, and utricle. Note the
mesothelial lining enclosing the endolymphatic space.


1. The vestibular ganglion occupies the distal end of

the internal auditory canal. Hence, the primary
vestibular neurons, like the primary cochlear
neurons, sit very close to their place of duty (Fig. 97). So does the sensory ganglion for CrN I.
2. The primary vestibular neurons synapse on the
vestibular nuclei at the medullopontine region of the
3. The vestibular nuclei contain the
neurons in
the vestibular pathway.


4. The central pathways for the signs of vestibular

a. Pathways from the vestibular nuclei run to
the nuclei of CrNs III, IV, and VI.
The pathway linking the vestibular system with
CrN III, IV, and VI is the medial longitudinal
b. These pathways mediate the counter-rolling
effect of the vestibular system on eye
movement and also mediate nystagmus of
vestibular origin.
c. Extensive connections between the vestibular
system and the dorsal motor nucleus of the
formation mediate the autonomic signs of
vestibular dysfunction.

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d. The vestibular nuclei send strong descending

pathways to the spinal cord via the MLF and
vestibulospinal tracts (Zilstorff-Pederson and
reticulospinal pathways coordinate postural
reflexes involving the eyes, head, trunk, and

5. The pathways for the symptoms of vestibular stimulation:

a. The vestibular nuclei connect to the thalamus by two pathways:
i. A ventral pathway, ventral to the medial lemniscus, passes lateral to the red nucleus and dorsal
to the subthalamic nucleus, terminating in the nucleus ventralis posterolateralis, pars oralis (nucleus
ventralis intermedius).
ii. A dorsal pathway runs through the lateral lemniscus and brachium of the inferior colliculus to the
medial geniculate body, thus paralleling the auditory pathway.
b. The vestibular cortex consists of adjacent areas in the inferior parietal lobe, insula, and superior temporal
region. The vestibular cortex is not confined to a discrete strip of striate cortex like other somatic senses. The
vestibular cortical regions integrate auditory, visual somatosensory, and vestibular proprioceptive impulses
that provide a sense of verticality, balance, and orientation of the body in space
6. Summary: Vestibular impulses that arrive at the vestibular nuclei can box the compass and disperse to every major
subdivision of the CNS: the cerebrum, diencephalon, brainstem, cerebellum, and spinal cord.
a. If they go caudally to the spinal cord, they descend via the MLF and the vestibulospinal tracts.
b. If they go dorsally to the flocculonodular lobe of the cerebellum, they travel via the caudal (inferior)
cerebellar peduncle.
c. If they go rostrally to nuclei for the ocular muscles, they travel via the MLF and in parallel with the auditory
d. If they go into the reticular formation, the impulses travel through many short circuits of bewildering
e. If they go to the cortex, they follow a dual pathway to the thalamus and then to areas near the posterior
end of the Sylvian fissure, close to the striate cortex of the auditory area.

History alone reveals the diagnosis in roughly three out of four patients complaining of dizziness, although the
proportion in patients specifically complaining of vertigo is unknown.10 When collecting a patients history, the
physician first must determine whether the patient truly has vertigo versus another type of dizziness. This can be
done by asking, When you have dizzy spells, do you feel light-headed or do you see the world spin around you? An
affirmative answer to the latter part of this question has been shown to accurately detect patients with true vertigo.11
The next task is to determine whether the patient has a peripheral or central cause of vertigo. Key information from
the history that can be used to make this distinction includes the timing and duration of the vertigo; what provokes or
aggravates it; and whether any associated symptoms exist, especially neurologic symptoms and hearing loss.
Characteristics distinguishing peripheral and central causes of vertigo are listed in Table 6.14,15 Rotatory illusions are
highly associated with peripheral vestibular disorders, especially when nausea or vomiting accompanies the
vertigo.1 Nystagmus in peripheral vertigo usually is horizontal and rotational, lessens or disappears when the patient
focuses the gaze, and usually is triggered by some provoking factor. In central vertigo, nystagmus is purely
horizontal, vertical, or rotational; does not lessen when the patient focuses the gaze; and persists for a longer
period.14 The duration of each episode also has significant diagnostic value; generally, the longer symptoms last, the
greater the likelihood that there is a central cause of vertigo.3 In one study,16 the presence of vertigo upon awakening
in the morning was suggestive of peripheral vestibular disorders. Peripheral vertigo generally has a more sudden
onset than vertigo of central nervous system origin, except for acute cerebrovascular events.3
Localization of Lesions Causing Vertigo: [from:
Physiologic and clinical vertigo syndromes are commonly characterized by a combination of phenomena involving
perceptual, ocular motor, postural, and vegetative manifestations: vertigo, nystagmus, ataxia, and nausea.

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Vertigo is an illusion of movement resulting from misinformation of corticospatial orientation. Nystagmus arises from a
direction-specific imbalance in the vestibulo-ocular reflex. Ataxia (or postural imbalance) results from inappropriate or
abnormal activation of vestibulospinal pathways. Nausea and vomiting develop from chemical activation of the
medullary vomiting centers.

Localizing lesions causing vertigo may be approached by considering three general categories: peripheral causes
(vestibular labyrinthine disease), central causes (dysfunction of the vestibular connections), and systemic causes
(e.g., endocrine, hemopoietic, metabolic diseases).
Peripheral Causes of Vertigo
Lesions of the semicircular canals induce rotatory sensations, whereas disease of the otolith system (utricle
and saccule) produces linear sensations of tilt or levitation. In acute vertigo due to labyrinthine disease, the diseased
side may be the more active of the two (irritative phase) for some hours or even days, but it soon becomes less active
(paretic phase). When the eyes are closed, patients feel a rotational sensation toward the side opposite to the paretic
labyrinth. By contrast, in the paretic phase the eyes tend to deviate slowly toward the side of the lesion, and to that
side, patients tend to past-point and fall when standing with eyes closed. Patients with severe vertigo feel most
comfortable lying on one side, usually with the affected ear uppermost, perhaps to use otolith inputs in order to
decrease the imbalance between the semicircular canals. In patients with labyrinthine disease, acoustic stimuli may
induce paroxysms of vertigo, oscillopsia, postural imbalance, the ocular tilt reaction, and nystagmus (Tullio's
phenomenon), perhaps through utricular stimulation.
Peripheral vestibular syndromes are usually of short duration and characterized by severe, often paroxysmal vertigo
accompanied by auditory dysfunction (tinnitus and hearing loss). Nystagmus is often present and is characteristically
unidirectional (fast phase away from the side of the lesion), horizontal rotatory (never vertical or exclusively
rotatory), and inhibited by visual fixation. The subjective environmental twirl, past-pointing, deviation of the
outstretched hands, and fall associated with the Romberg's maneuver are toward the slow phase of the nystagmus
(toward the side of the lesion). The peripheral vestibular syndrome is therefore complete (has all of the clinical
elements of vestibular dysfunction, e.g., vertigo, nystagmus, deviation of the outstretched hands, Romberg's sign,
and so on) and congruent (all the slow deviations are toward the same side, i.e., ipsilateral to the responsible
Unilateral total loss of horizontal semicircular canal function (i.e., canal paresis) may be detected by having the
patient fixate on a stationary target while the examiner turns the head from side to side [47]. In normal individuals,
no saccades (quick eye movements) are noted, indicating that the subject's gaze remained fixed on target. In patients
with total unilateral canal paresis, one large or several small oppositely directed, compensatory, refixation saccades
occur when the head is rotated toward the lesioned side.
Acquired vestibular areflexia, especially when bilateral, may also result in head movementdependent oscillopsia,
which is an illusory movement of the visual world that occurs only during head movement.
Central Causes of Vertigo
In contrast to the peripheral vestibular syndrome, the central vestibular syndrome is often prolonged
(permanent or chronic) rather than of short duration.
Dysfunction of neighboring structures, including brainstem and cerebellar structures, are usually present,
whereas auditory symptoms are less frequent. Vertigo is less severe than in the peripheral syndromes and tends to be
ill-defined and continuous in nature. The associated nystagmus is bidirectional or unidirectional, may be exclusively
horizontal, rotatory, or vertical, and is not altered by visual fixation. The directions of subjective environmental
rotation, past-pointing, deviation of the outstretched hands, and Rombergism are variable and barely altered by
changes in head position. The central vestibular syndrome is therefore incomplete or partial (does not always consist
of all elements of vestibular dysfunction), and incongruent (the nystagmus and tonic deviations are variable in
Brandt [17] classified central vestibular syndromes of the brainstem tegmentum into the following three categories:
Disorders of the vestibulo-ocular reflexVestibuloocular Reflex (VOR) in the horizontal (yaw) plane (e.g.,
horizontal nystagmus and pseudovestibular neuritis due to partial anterior inferior cerebellar artery or
posterior inferior cerebellar artery infarction or a multiple sclerosis plaque)
Disorders of the VOR in the sagittal (pitch) plane (e.g., downbeat nystagmus and vertigo or upbeat
nystagmus and vertigo)
Disorders of the VOR in the frontal (roll) plane (e.g., the ocular tilt reaction)
Systemic Causes of Dizziness and Vertigo
Systemic conditions affecting peripheral or central vestibular structures capable of producing dizziness or vertigo
include the following:
Cardiovascular disorders. Cardiac arrhythmias, aortic stenosis or other valvular lesions, congestive heart
failure, cardiomyopathies, and carotid sinus hypersensitivity may be associated with dizziness and syncope.
Vasculitides. Vertigo is a common manifestation of Cogan's syndrome, an autoimmune disorder characterized
by episodic vertigo, tinnitus, hearing loss, and nonsyphilitic interstitial keratitis [27].
Hematologic disorders. Anemia, polycythemia rubra vera, Waldenstrm's macroglobulinemia, and other
hyperviscosity syndromes may cause dizziness and hearing loss.

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Hypoglycemia. Dizziness or faintness occurring a few minutes after a meal may be secondary to reactive
hypoglycemia. Patients may also display adrenergic symptomatology.

Hypothyroidism. Symptoms of nervous system dysfunction are often prominent with hypothyroidism.
Hypothyroidism may be associated with episodic vertigo, sensorineural hearing loss, tinnitus, and signs of
cerebellar dysfunction.

Hyperventilation syndrome. Hyperventilation may account for episodes of lightheadedness often associated
with circumoral and digital paresthesias. Rapid lowering of Pco2 reduces cerebral blood flow and may cause
dizziness, confusion, and rarely seizures, even in the absence of hypoxemia.

Multiple sensory deficits. Dizziness in older patients may result from a combination of sensory deficits,
including visual impairment, proprioceptive loss due to a polyneuropathy, vestibular dysfunction, and cervical
spondylosis. Dizziness is especially prominent during ambulation, particularly when turning corners.

Drugs. Vestibular toxicity may be transient or permanent, and may be associated with symptoms of cochlear
toxicity. Dizziness is a common side effect of many drugs, including analgesics, antiarrhythmics, cytotoxic
drugs, anti-inflammatory drugs, aminoglycoside antibiotics (especially gentamycin), loop diuretics, aspirin,
sedatives, and anticonvulsants. Overdoses of phenytoin may cause dizziness and nystagmus.

Ocular disorders. Vertigo and dizziness may occur in association with glaucoma, extraocular muscle paresis,
use of strong corrective lenses, and refractive abnormalities.

Mal de debarquement (mal de mer). This condition refers to sensations of motion, rocking and swaying, that
are commonly experienced with sea travel and persist in some individuals on return to land for weeks,
months, or even years [23, 81]. Mal de debarquement may also occur after air and car travel. Patients with
mal de debarquement syndrome lack vertigo, nausea, or vomiting.
Psychiatric disorders (psychogenic dizziness). Subjective dizziness or giddiness may occur with anxiety, panic
attacks, mood, somatoform, and dissociative disorders, claustrophobia, agoraphobia, and other psychiatric
disturbances, including schizophrenia. A special form of psychogenic vertigo, thought to be unrelated to panic
attacks, is phobic postural vertigo primarily described among patients with obsessive-compulsive personality
[16, 19]. Phobic postural vertigo has six characteristic features [16].
o Dizziness and a subjective disturbance of balance occur while standing or walking despite normal
clinical balance tests (e.g., tandem walking, balancing on one foot).
o Fluctuating unsteadiness in episodes lasting seconds to minutes or momentary perception of illusory
body perturbations is noticed.
o Although the attacks can occur spontaneously, there is usually a perceptual stimulus (e.g., bridge,
staircase, empty room) or social situation (e.g., department store, restaurant, crowd) from which
patients have difficulty withdrawing and which they recognize as a provoking factor.
o Anxiety and distressing vegetative symptoms occur during or after the vertigo.
o Obsessive-compulsive type personality, labile affect, and/or mild depression are noticed.
o Onset of the condition frequently follows a period of particular emotional stress, after a serious
illness, or following an organic vestibular disorder.


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The initial description of dizziness can be difficult to obtain because patient responses are not always consistent.6
Therefore, the history should first focus on what type of sensation the patient is feeling.Table 1 includes descriptors
for the main categories of dizziness.4,5,7,8 It is important to note that some causes of dizziness can be associated with
more than one set of descriptors.

A medication history should be obtained because dizziness (especially from orthostatic hypotension) is a well-known
adverse effect of many drugs). Patients should also be asked about caffeine, nicotine, and alcohol intake.9 Head
trauma and whiplash injuries can cause a variety of dizziness symptoms, from vertigo to lightheadedness. The
incidence of dizziness with a head injury or vertigo initially after whiplash have been reported as high as 78 to 80

Otologic or vestibular causes of vertigo are the most common causes of dizziness, 21,22 and include benign paroxysmal
positional vertigo (BPPV), vestibular neuritis (viral infection of the vestibular nerve), labyrinthitis (infection of the
labyrinthine organs), and Meniere disease (increased endolymphatic fluid in the inner ear).7,13 An estimated 35
percent of adults 40 years and older have vestibular dysfunction.14
Hearing loss and duration of symptoms help narrow the differential diagnosis further in patients with vertigo. Vertigo
with hearing loss is usually caused by Meniere disease or labyrinthitis, whereas vertigo without hearing loss is more
likely caused by BPPV or vestibular neuritis.8 Unilateral auditory symptoms help localize the cause to an anatomic
abnormality, particularly in patients with peripheral disease.9Episodic vertigo tends to be caused by BPPV or Meniere
disease, whereas persistent vertigo can be caused by vestibular neuritis or labyrinthitis.8
Migrainous vertigo, or vestibular migraine, is another underlying cause of vertigo that affects about 3 percent of the
general population and about 10 percent of persons with migraine.15 This diagnosis should be considered after other
causes of vertigo have been ruled out. Diagnosis of migrainous vertigo is established in patients with a 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, or aura.15

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Cardiovascular causes of dizziness include arrhythmias, myocardial infarction, carotid artery stenosis, and ortho-static
hypotension.21 Of patients with supraventricular tachycardia, 75 percent experience dizziness and about 30 percent

experience syncope.23 Symptoms brought on by postural changes suggest a diagnosis of orthostatic hypotension.9 A
variety of cardiovascular medications increase the risk of orthostatic hypotension in older persons, including reserpine
(at doses greater than 0.25 mg), doxazosin (Cardura), and clonidine (Catapres).24
There are many underlying conditions that may cause a sense of imbalance. Stroke is an important and lifethreatening cause of dizziness that needs to be ruled out when the dizziness is associated with other symptoms of
stroke. However, other neurologic findings are generally present. In a population-based study of more than 1,600
patients, 3.2 percent of those presenting to an emergency department with dizziness were diagnosed with a stroke or
transient ischemic attack (TIA), but only 0.7 percent presenting with isolated dizziness were diagnosed with stroke or
Poor vision commonly accompanies a feeling of imbalance,16 leading to falls. The physician should inquire about a
history of other problems that may cause imbalance, such as Parkinson disease, peripheral neuropathy, and any
musculoskeletal disorders that may affect gait.17 Use of benzodiazepines and tricyclic antidepressants increase the risk
of ataxia and falls in older persons.24
Psychiatric causes of lightheadedness are common, particularly anxiety; therefore, questions about anxiety and
depression should be included in the patient history. In one study, about 28 percent of patients with dizziness
reported symptoms of at least one anxiety disorder.26 In another study, one in four patients with dizziness met criteria
for panic disorder.27 A study of patients with chronic dizziness showed that those with panic disorder were more likely
to have neurotologic findings than those without panic disorder.28 Up to 60 percent of patients with chronic subjective
dizziness have been reported to have an anxiety disorder.29 Depression and alcohol intoxication have also been found
to overlap with dizziness.21,30

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Hyperventilation syndrome is an important cause of lightheadedness. Although the condition can be associated with
anxiety disorders, many patients without anxiety experience hyperventilation. Hyperventilation is defined as breathing
in excess of metabolic requirements, causing a respiratory alkalosis and lightheadedness. Patients may sigh
repeatedly and may have associated symptoms, such as chest pain, paraesthesias, bloating, and epigastric pain.



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Knowing the severity of vertigo over time also is helpful. For example, in acute vestibular neuronitis, initial symptoms
typically are severe but lessen over the next few days. In Mnires disease, attacks of vertigo initially increase in
severity, then lessen in severity later on. Patients complaining of constant vertigo lasting for weeks may have a
psychological cause for their symptoms.
Provoking factors and circumstances around the onset of vertigo may prove useful in narrowing the differential
diagnosis to a peripheral vestibular condition. If symptoms occur only with positional changes, such as turning over in
bed,17 bending over at the waist and then straightening up, or hyperextending the neck, BPPV is the most likely
cause.1 A recent viral upper respiratory infection may precede acute vestibular neuronitis or acute labyrinthitis.
Factors that provoke migraine headaches can cause vertigo if the patient experiences this as a symptom associated
with migraine.
Vertigo can be caused by perilymphatic fistula (i.e., breach between the inner ear and middle ear).18Perilymphatic
fistula may be caused by trauma from a direct blow, or from activities such as scuba diving (from barotrauma) and
heavy weight bearing or excessive straining with bowel movements.3,12 Sneezing or movements that place the
affected ear downward also can provoke vertigo in patients with perilymphatic fistulas.19
The presence of Tullios phenomenon (i.e., nystagmus and vertigo caused by loud noises or sounds at a particular
frequency) suggests a peripheral cause for vertigo.12
Significant psychosocial stress can cause patients to complain of vertigo. Asking about psychological stressors or
psychiatric history may be important, especially in patients whose history does not necessarily fit the usual
presentation of physical causes of vertigo. For example, a history of anxiety or panic attacks associated with vertigo
may point to hyperventilation as a cause.12
Hearing loss, pain, nausea, vomiting, or neurologic symptoms can help differentiate the cause of vertigo. Most causes
of vertigo with hearing loss are peripheral, the main exception being a cerebrovascular event involving the internal
auditory artery or anterior inferior cerebellar artery. Pain accompanying vertigo may occur with acute middle ear
disease, invasive disease of the temporal bone, or meningeal irritation.12Vertigo often is associated with nausea or
vomiting in acute vestibular neuronitis and in severe episodes of Mnires disease and BPPV.1,20 In central causes of
vertigo, nausea and vomiting tend to be less severe.14 Neurologic symptoms such as weakness, dysarthria, vision or
hearing changes, paresthesia, altered level of consciousness, ataxia, or other changes in sensory and motor function
favor the presence of a central cause of vertigo such as cerebrovascular disease, neoplasm, or multiple sclerosis.
Patients with migrainous vertigo may experience other symptoms related to the migraine, including a typical headache
(often throbbing, unilateral, sometimes preceded by an aura), nausea, vomiting, photophobia, and phonophobia.
Twenty-one to 35 percent of patients with migraine suffer vertigo.
Central Vertigo



Central vertigo is vertigo due to a

disease originating from the
central nervous system (CNS). In
clinical practice, it often includes
lesions of cranial nerve VIII as
well. Individuals with vertigo
experience hallucinations of
motion of their surroundings.

sensation of movement or rotation

of the patient or his or her

Depressed consciousness

Age (50/F)

Cranial nerve deficits


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Central vertigo may be caused by

hemorrhagic or ischemic insults to
the cerebellum, the vestibular
nuclei, and their connections
within the brain stem. Other
causes include CNS tumors,
infection, trauma, and multiple

Arterial Occlusion and Ischemic Infarction
Arterial occlusion and ischemic infarction can result from cardioembolism, embolism of plaque from
a vertebral artery, or local arterial thrombosis. One or both vertebral arteries, the basilar artery, or any of
the smaller branches may be occluded. Even complete occlusion of a large artery may not result in death
because of anastomotic retrograde flow via the circle of Willis and posterior communicating arteries.
Temporary vertebrobasilar ischemia may present as migraine syndrome or transient ischemic attacks (TIAs).
While less common than cerebellar infarction, spontaneous cerebellar hemorrhage is an important lifethreatening cause of vertigo associated with hypertensive vascular disease and anticoagulation.

Chronic Subjective Dizziness



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Persistent dizziness or
Persistent dizziness >3mos.
Hx of previous psychiatric disorder
lightheadedness, heavy
Age (50)
headedness, swimming
Hypersensitivity to motion
stimuli (SMD)
Ones own movements
Movement of objects in the
Provocation with visual
Complex visual environments
Precision visual tasks
Normal physical exam and head
Exam may provoke symptoms,
but not signs of vestibular
e.g., dizziness, not nystagmus
Non-specific vestibular test
Isolated peripheral
abnormalities are common
Clinical correlation is required
Peripheral deficits constant
The age range of patients diagnosed with CSD spans from adolescence to late adulthood, but
patients are typically between 40 and 50 years of age. Most of the patients
(65% to 70%) are women.
Most patients with CSD (93%) have a psychiatric disorder that contributes significantly
to their symptoms. Based on current classifications in the fourth edition of the
Diagnostic and Statistical Manual of Mental Disorders, anxiety disorders are by far
the most common psychiatric pathology identified, including generalized anxiety disorder, panic or phobic
disorders, or minor anxiety.

persistent dizziness
parang umiikot na hindi naman.
dizziness more persistent despite taking
more unsteady whenever wearing high
heels, often falling to one side
difficulty in typing, often hitting the wrong
keys whenever she was typing at her
regular rapid speed
handwriting seemed to be getting worse
regular recurrence of a headache that seems
to go around her temples to the sides of her

Basilar artery TIAs (Transient Ischemic


feeling of swimming, swaying,

unsteadiness or light-headedness




facial or circumoral numbness

hemisensory symptoms

short-lived (5-30min) and repetitive

cerebellar ataxia
under nia to:
*lateral superior pontine syndrome (syndrome
of superior cerebellar artery)
on the side of the lesion:

ataxia of limbs and gait

falling to side of lesion



Horizontal nystagmus

Horners syndrome

Basilar artery supply the base of the pons and superior cerebellum.
3 groups:
1. Paramedian
7-10 in number
Supply a wedge of pons on either side of the midline
2. Short circumferential
5-7 in number
Supply lateral 2/3 of pons and middle and superior cerebellar peduncles
3. Bilateral long circumferential
Superior cerebellar and anterior inferior cerebellar arteries
Course around the pons to supply the cerebellar hemispheres

(due to non CSF analysis/imaging modalities performed)

Rule In

Hematogenous spread
Direct extension (sinusitis, mastoiditis, brain abcess)
(most impt. Factor)
Cerebral edema maybe present
Cornerstone Dx is CSF analysis (only if the px has no HA
and Vomiting)
Late complications may involve CNs

(+) occasional L forehead pain (maybe due to sinusitis)

RR: 28 (cerebral edema, herniation and impingement of
the medulla)
Rule OUT


Rule IN

Onset is insidious
Duration is weeks to months
Seen in px with
TB (tuberculoma maybe present)
Syphilis (afebrile syphilis)
Fungal diseases

Since afebrile it maybe latent syphilitic meningitis
CN8 involvement if there is TUBERCULOMA impinging
that area

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(-) fever
(-) chills
(-) nausea
(-) vomiting

Headache that seems to go around her temples to the
sides of her head

Rule IN

Local extensions from adjacent foci like sinuses and

mastoids is commonly involve in the pathogenesis

Headache ( maybe due to inc. ICP)

Cranial nerve number 8 involvement (maybe due
to abcess
Occupying space and impinging CNs)
(sinusitis may invole frobtal lobe, mastoiditis may
involve temporal lobe)
Rule OUT

Fibrillary (diffuse) Astrocytoma

Rule IN

Most common primary CNS tumor

Focal neurologic deficits related to anatomic site of
involvement (eg. CN 8)
Cerebral hemisphere is the common site in adults

Vertigo maybe dute to

Focal neurologic deficits related to anatomic site of
involvement (eg. CN 8)
Maybe due to Inc. ICP
Rule OUT
Peak of tumor onset is 35yrs

After the history is complete, the clinician performs the routine full
head and neck examination. This is important for two reasons:
(1) dizzy patients frequently have other ear, nose, and throat
pathology and
(2) structural problems of the ear, nose, and throat at times cause
dizziness or indicate a more widespread process.
Then, perform special examination.

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Inspection of hair, scalp, skull, face and skin. Note for
Visual acuity (Snellen chart)
Visual Fields: Confrontation Testing
Extraocular movements: H-test
Conjunctiva & Sclera: Ask the patient to look up as you
depress both lower lids with your thumbs, exposing the
sclera and conjunctiva. Inspect the sclera and palpebral
conjunctiva for color, and note the vascular pattern
against the white scleral background. Look for any
nodules or swelling.
Pupillary Reaction: Light Reflex. Check for direct and
consensual reaction.
Inspection of the auricle and external ear
Otoscopy: To see the ear canal and drum, use an
otoscope with the largest ear speculum that the canal
will accommodate. Position the patient's head so that
you can see comfortably through the instrument. To straighten the ear canal, grasp the auricle firmly but
gently and pull it upward, backward, and slightly away from the head.




Ear canal. Check for discharge, foreign bodies, cerument, redness, or swelling.
Eardrum: Color and contour, malleus
Auditory acuity: To estimate hearing, test one ear at a time. Ask the patient to occlude one ear with a
finger, or better still, occlude it yourself. When auditory acuity on the two sides is different, move your
finger rapidly, but gently, in the occluded canal. This noise helps prevent the occluded ear from doing the
work of the ear you wish to test. Then, standing 1 or 2 feet away, exhale fully (so as to minimize the
intensity of your voice) and whisper softly toward the unoccluded ear. Choose numbers or other words
with two equally accented syllables, such as nine-four, or baseball. If necessary, increase the intensity
of your voice to a medium whisper, a loud whisper, and then a soft, medium, and loud voice. To make
sure the patient does not read your lips, cover your mouth or obstruct the patient's vision.
Air and Bone Conduction: Weber Test for Lateralization & Rinne Test for comparison of air and bone

Test for nasal obstruction
Inspect the inside of the nose with an otoscope and the largest ear speculum available. Tilt the patient's
head back a bit and insert the speculum gently into the vestibule of each nostril, avoiding contact with
the sensitive nasal septum. Hold the otoscope handle to one side to avoid the patient's chin and improve
your mobility. By directing the speculum posteriorly, then upward in small steps, try to see the inferior
and middle turbinates, the nasal septum, and the narrow nasal passage between them. Some asymmetry
of the two sides is normal.
Mouth and Pharynx
Lips for color (cyanosis), moisture, lumps, ulcers, cracking, scaliness
Oral mucosa
Tongue and floor of the mouth. Inspect for symmetry (CrN12).
Pharynx. Ahhh. Note for rise of soft palate (CrN10)
Inspect the neck. Symmetry, masses, scars etc
Palpate for lymph nodes.
Inspect the trachea for any deviation.
Inspect and palpate for the thyroid gland.

I. Spontaneous Nystagmus
Action. Ask the patient to fixate on a stationary target in neutral gaze position with best corrected vision (glasses or
contact lenses in place). Observe for nystagmus or rhythmic refixation eye movements. Repeat under Fresnel lenses
to observe effect of target fixation.
Interpretation. If nystagmus is observed, particular attention is paid to the amplitude, direction, and effect of target
Lesions of the labyrinth and nerve VIII
intense, direction-fixed horizontal-rotary nystagmus that is enhanced under Fresnel lenses
intensifies when gazing in the direction of the fast phase (Alexander's law). This pattern can be seen in both
irritative (beating toward the affected ear) and destructive (beating toward the unaffected ear) lesions of the
labyrinth, nerve VIII, or (rarely) the vestibular nuclei
Lesions of the brain stem, cerebellum, and cerebrum
less intense, direction-changing horizontal, vertical, torsional, or pendular nystagmus that is diminished under
Fresnel lenses
Examples: periodic alternating nystagmus (PAN), congenital nystagmus, and lesions of the midline
II. Gaze Nystagmus
Action. Ask the patient to gaze at a target placed 20 to 30 degrees to the left and right of center for 20 seconds.
Observe for gaze-evoked nystagmus or change in direction, form, or intensity in spontaneous nystagmus.
Interpretation. The ability to maintain eccentric gaze is under control of the brain stem and midline cerebellum,
particularly the vestibulocerebellum (especially the flocculonodular lobes).
When these mechanisms fail to hold the eye in the eccentric position, the eye drifts toward the midline
(exponentially decreasing velocity), followed by refixation saccades toward the target.

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Gaze-evoked nystagmus
central in origin and always beats in the direction of intended gaze.


Causes: drug effect (sedatives, antiepileptics), alcohol, CNS tumors, and cerebellar degenerative syndromes.
Smooth Pursuit

Action. Ask the patient to follow your finger as you slowly move it left and right, up and down. Make sure the patient
can see the target clearly and you do not exceed 60 degrees in total arc or 40 degrees per second.
Interpretation. Normal eye tracking of a slowly moving discrete object generates a smooth eye movement that the
examiner can easily see.
Cerebellar or brain stem disease
cause saccadic eye tracking in which the patient repeatedly loses the target and then catches up with a small
IV. Saccades
Action. Ask the patient to look back and forth between two outstretched fingers held about 12 inches apart in the
horizontal and vertical plane. Observe for latency of onset, speed, accuracy, and conjugate movement.
Interpretation. Saccadic eye movements are refixation movements that involve the frontal lobes (voluntary
saccades), brain stem reticular formation (voluntary and involuntary saccades), and oculomotor nuclei III, IV, and VI.
Delayed saccades: cortical and brain stem lesions
Slow saccades: brain stem disease
Inaccurate saccades (especially overshoots): lesions of the cerebellar vermis and fastigial nuclei
Disconjugate eye movements with slowing of the adducting eye and overshoots of the abducting: medial
longitudinal fasciculus pathology frequently associated with multiple sclerosis.
V. Fixation Suppression Test
Action. Ask the patient to fixate on his or her own index finger held out in front at arm's length. Unlock the
examination chair and rotate the patient up to 2 Hz while the patient stares at the finger moving with them. The
examiner observes for a decrease in the visual-vestibular nystagmus that is evoked during rotation without ocular
Interpretation. Failure of fixation suppression in the presence of adequate visual acuity implies floccular

Head Thrust Test / Head Impulse Test

Action. Ask the patient to fixate on a target on the wall in front of the patient while the examiner moves the patient's
head rapidly (>2000 deg/sec2) to each side. The examiner looks for any movement of the pupil during the head
thrust and a refixation saccade back to the target. Either direct observation of pupillary movement or the use of an
ophthalmoscope is employed to document eye movement.
Interpretation. impulse test was described as a reliable sign of reduced vestibular function in the plane of rotation
for the ear ipsilateral to the head thrust. The observation of eye movement during the maneuver is a sign of
decreased neural input from the ipsilateral ear to the vestibulo-ocular reflex (VOR) because the contralateral ear is in
inhibitory "saturation" and cannot supply enough neural activity to stabilize gaze. In such instances, the eye travels
with the head during the high-velocity movement, and a refixation saccade is necessary to refoveate the target.
Bilateral refixation movements are seen frequently in cases of ototoxicity.
VII. Postheadshake Nystagmus
Action. Tilt the head of the patient forward 30 degrees and shake the head in the horizontal plane at 2 Hz for 20
seconds. Observe for postheadshake nystagmus and note direction and any reversal. Fresnel lenses are preferred to
avoid fixation The maneuver may be repeated in the vertical direction.
Interpretation. Postheadshake nystagmus is considered a pathologic sign of imbalance in the vestibular inputs in the
plane of rotation. In most instances, a peripheral cause is identified with the nystagmus directed toward the stronger
ear. A small reversal phase is sometimes observed. Signs of central etiology include prolonged nystagmus, vertical
nystagmus following horizontal headshake ("cross coupling"), and disconjugate nystagmus.
VIII. Dix-Hallpike Maneuver

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Action. With the examination chair unfolded like a bed, turn the patient's head 45 degrees to one side while seated
and rapidly but carefully have the patient recline. Observe the eyes for nystagmus and, if present, note the following
five characteristics: latency, direction, fatigue (decrease on repeated maneuvers), habituation (duration), and reversal
upon sitting up.

They include:
1- Nystagmus
2- Provocative head position
3- Brief latency to symptoms after change
in position
4- Short duration of attack
5- Fatigability of nystagmus on repeat
6-Reverse of nystagmus on returning to
upright position.
Interpretation. Positive maneuver:
diagnostic for benign position vertigo,
which is thought to be due to otoconial
debris either floating (canalithiasis) or fixed
(cupulolithiasis) within the posterior
semicircular canal of the undermost ear.
IX. Positional Tests
Action. Ask the patient to lie still in three positions -- supine, left lateral, and right lateral -- for 30 seconds and
observe for nystagmus.
Interpretation. The presence of a static positional nystagmus is nonlocalizing by itself and must be interpreted in the
light of other physical findings. In general, however, vertical positional nystagmus is central in origin, implying cranialcervical or fourth ventricle origin.
X. Limb Coordination Test
Action. Ask the patient to perform a series of coordination tasks such as finger-nose-finger, heel-shin, rapid
alternating motion, and fine finger motion (counting on all digits). Observe for dysmetria or dysrhythmia.
Interpretation. The presence of limb dysmetria or dysdiadochokinesia is a useful indicator of cerebellar cortical
disease, which may or may not accompany midline or vestibulocerebellar oculomotor dysfunction.
XI. Romberg Test
Action. Have the patient stand with feet close together and arms at the side with eyes open and then eyes closed.
Observe for the relative amount of sway with vision present versus absent.
Interpretation. Patient has a tendency to lean on one side. Vestibular disorder patients drift off to the affected
XII. Unterberger's Test
Positive test: Turning by >45 degrees suggestive of a vestibular disorder

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Gait Observation
Action. Ask the patient to walk 50 feet in the hall, turn rapidly, and walk back without touching the walls. Observe for
initiation of movement, stride length, arm swing, missteps and veering, and signs of muscle weakness or skeletal
abnormality (kyphoscoliosis, limb asymmetry, limp).
Interpretation. There is no such thing as a "vestibular gait."
Acute unilateral loss of otolithic function: the patient will tend to veer toward the side of the lesion.
Extrapyramidal disease: Difficulties with gait initiation and turns and decreased arm swing
Gait ataxia: implies cerebellar dysfunction and is distinctly different from gait deviation associated with
uncompensated peripheral vestibular disease.
Functional gait disorder: exaggerated hip sway, rhythmic deviations, and an excessive reliance on touching
the wall during walking

The inner ears vestibular organs and the associated nerves and brain centers form a complex system that serves
many functions and can be affected by a number of outside systems. A thorough evaluation of the inner ear may
therefore require several different kinds of tests.
Doctors use information from a persons medical history and findings from a physical examination as a basis for
ordering diagnostic tests to assess the vestibular system function and to rule out alternative causes of symptoms.
Most people tolerate these tests well. However, sometimes the tests are fatiguing and can result in temporary
Specific tests of vestibular dysfunction
Good balance and clear vision rely on a close linkage between the vestibular organs and the eyes. Head movement or
other stimulation of the inner ear sends signals to the muscles of the eyes via the nervous system; this is called the
vestibulo-ocular reflex, or VOR. The VOR normally generates eye movements that maintain clear vision with head
Diagnosis via Caloric Testing
In the clinic, VOR function also can be assessed by caloric tests. For caloric testing the patient is put into a reclining
position with a pillow propping the head up at a 30o angle. That brings the horizontal semicircular canals into a
vertical plane aligned with the pull of gravity.
Then either cold or warm water is infused into one ear to induce convection that causes movement of the fluid that is
within that ear's horizontal semicircular canal. Convectional flow effectively simulates the relative fluid movements
that are normally induced by head rotation.
By causing convectional fluid movements in one ear, caloric testing produces an imbalance between the two ears in
regard to the amount of neural impulses that propogate from each ear to the brain.
Normal patients will exhibit vestibular nystagmus during a caloric test. The normal fastphase direction of eye
movements can be remembered using the mnemonic C.O.W.S.
Fast phase direction of the nystagmus = C.O.W.S. = Cold-Opposite, Warm-Same

The fast phase of

patients who are
that reason, panels
3 and panel 4 of the
book figure below
show only the slow
phase deviations for

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VOR is remarkably
plastic. The gain of
the reflex changes
in response to
changes in the
visual system, such
as changes in the
magnifying power of

ENG is a battery (group) of eye-movement tests that look for signs of vestibular dysfunction or neurological problems
by measuring nystagmus (a type of involuntary eye movements) and other eye movements. ENG tests are the most
common ones administered to people with dizziness, vertigo, and/ or balance disorders, although the test battery and
some testing methods vary widely.
During ENG, eye movements are recorded and analyzed via small electrodes placed on the skin around the eyes. The
electrodes attach to the skin with an adhesive, much like a small bandage. Alternatively, eye movements may be
recorded by videonystagmography (VNG) using an infrared video camera mounted inside goggles that the patient
wears instead of sticky-patch electrodes.
One ENG/VNG test evaluates the movement of the eyes as they follow a moving target. Another observes eye
movements as the head is positioned in different directions. During the caloric test (sometimes called bi-thermal
caloric or mono-thermal caloric), warm or cold water or air is circulated in the ear canal to test the nystagmus
response stimulated by the temperature change.
Rotation tests are another way of evaluating how well the eyes and inner ear work together. For every head
movement in one direction, there is eye movement in the opposite direction.
With rotation tests (which employ the same type of sticky-patch electrodes or goggles used for ENG/VNG), the
examiner can record eye movements while the head is moving at various speeds. This provides additional information,
beyond the ENG/VNG, about how well the balance organs are functioning, along with their connections to the eye
muscles. Not all people in the diagnosis phase will need rotation tests.
There are two kinds of computerized rotation tests: auto head rotation and rotary chair. In auto head rotation tests,
the person being tested is asked to look at a fixed target and move his/her head back and forth or up and down for
short periods of time. During rotary-chair tests, the computerized chair moves for the person being tested. For safety,
a harness is worn and the head is restrained against a headrest.
Rotary-chair testing usually takes place in a darkened room. A microphone and speaker in the testing room allow
voice contact with the examiner, who is seated at a computer console just outside the door. As in ENG/VNG testing,
while the eye movements are recorded, the person being tested will be asked a series of simple questions that are
meant to keep the mind busy and alert during the tests.
Not all rotation testing is computerized. In some cases a swivel chair is used, or the doctor or other examiner simply
moves the persons head with his or her hands while observing the eye movements.
VEMP testing is used to evaluate whether the saccule and the inferior vestibular nerve are intact and functioning
normally. During VEMP testing, headphones are placed over the ears and small electrodes are attached with an
adhesive to the skin over the neck muscles. When sound is transmitted through the headphones, the electrodes
record the response of the muscle to the vestibular stimuli.
CDP tests postural stability. While ENG/VNG and rotation tests assess visual-vestibular interactions, CDP provides
information about motor control or balance function under varying environmental conditions. This is important
because the ability to maintain balance depends not only on sensory information from the vision and the vestibular
systems, but also on sensory information that the brain receives from the muscles and joints. These somatosensory
signals provide clues such as the direction of head turn and the texture and slope of the walking surface. CDP tests
the relationships among these three sensory inputs and records the balance and posture adjustments made by a
person in response to variations in reliable information provided by the vision and somatosensory systems.

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The test involves standing on a platform, typically with some form of visual target to watch. The platform and/or the
visual target move while pressure gauges under the platform record shifts in body weight (body sway) as the person
being tested maintains balance. A safety harness is worn to prevent falling during the test.

Posturography gives information about how well balance is maintained during challenging situations. It can help
doctors plan other vestibular testing, as well as assist in treatment design.
Audiometry measures hearing function. Hearing evaluations are an important part of vestibular diagnostics, because
of the close relationship between the inner ear hearing and balance organs. Several different audiometry tests,
performed by an audiologist, may be required. These tests are carried out in a sound-treated room with a set of
headphones which also allow voice contact with the audiologist through a microphone.
A person with a vestibular disorder sometimes has his/her hearing monitored at intervals over time, especially when
there is evidence of hearing loss, a sensation of fullness in the ears, or tinnitus (ringing or noise in the ears).
Pure tone audiometry
In pure tone audiometry testing, a response is requested when sounds are heard of different pitches through the
Speech audiometry tests
Speech audiometry tests can include speech reception threshold and word recognition (sometimes referred to as
speech discrimination), where the repetition or recognition of words is requested as they are presented at different
Tympanometry helps detect the presence of fluid in the middle ear, among other problems, by examining the function
of the middle ear and Eustachian tube, including the stiffness of the eardrum, when air-pressure changes are imposed
through a soft probe that is inserted into the external ear canal.
Acoustic-reflex testing
Acoustic-reflex testing measures the reflex of the stapes (one of the tiny bones of the middle ear) caused by the
response of the stapedius muscle when the ear is subjected to a loud sound.
Electrocochleography (ECoG)
ECoG measures how sound signals move from the ear along the beginning of the hearing nerve.
Otoacoustic emissions (OAE)
OAE testing provides information about how the hair cells of the cochlea are working by measuring the responsiveness
of these hair cells to a series of clicks produced by a tiny speaker inserted into the ear canal.
Auditory brainstem response test (ABR; or BER, BSER, or BAER)
The ABR measures how hearing signals travel from the ear to the brain and then within parts of the brain. Under
certain circumstances, this test can indicate the presence of an acoustic neuroma (a rare, benign tumor of the
vestibulo-cochlear nerve). It may also help identify conditions such as multiple sclerosis if they have affected the
auditory pathway to the brain.
Magnetic resonance imaging (MRI)

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MRI uses a magnetic field and radio waves to produce cross-sectional images of the parts of the body being scanned.
An MRI of the brain can reveal the presence of tumors, stroke damage, and other soft-tissue abnormalities that might
cause dizziness or vertigo. MRIs of structures in and around the inner ear may show problems such as an acoustic

Computerized axial tomography (CAT, or CT)

A CT scan is an X-ray technique that is best for studying bony structures. CTs of the temporal bone (within which the
inner ear resides) are often used to look for abnormalities such as fractures.
Depending on your circumstances, other tests are possible, such as blood work or allergy tests, in order to rule out
causes of symptoms that are unrelated to the vestibular system.
Other Source:

What is Vestibular Testing?

Vestibular testing consists of a number of tests that help determine if there is something wrong with the vestibular
(balance) portion of the inner ear. These tests can help isolate dizziness symptoms to a specific cause that can often
be treated.
Why Get Vestibular Tests?
If dizziness is not caused by the inner ear, it might be caused by the brain, by medical disorders such as low blood
pressure, or by psychological problems such as anxiety. Recent studies have documented that vestibular tests are
more accurate than clinical examination in identifying inner ear disorders (Gordon et al, 1996). Hearing pathway tests
(audiometry, auditory brainstem response, electrocorticography) can also be used for the same purpose, and are
frequently combined with vestibular tests.
Vestibular tests can help determine if more expensive tests, such as magnetic resonance imaging (MRI), are needed.
Studies (Levy and Arts, 1996) have shown that vestibular testing is much more accurate than clinical symptoms in
predicting whether neuroimaging tests will be abnormal . [See also Korres et al. (2009) for a comparison of caloric
and MRI testing]. Vestibular tests can also document objectively vestibular conditions such as benign paroxysmal
positional vertigo (BPPV), and perilymph fistula, which commonly occur after head injury; and bilateral vestibular
ototoxicity, which commonly is a side effect of medication.

Electronystagmography (ENG) testing (Image courtesy of ICS Medical,
2001). A computer is used to monitor eye movement induced by visual and
vestibular stimulation.

Electronystagmography (ENG) Test

The ENG test is used to determine whether or not dizziness may be due to inner ear disease. It consists of carefully
measuring involuntary eye movement (nystagmus) while the subjects balance system is stimulated in different ways.
There are four main parts to the ENG: the calibration test, the tracking test, the positional test, and the caloric test.
The calibration test evaluates rapid eye movements. The tracking test evaluates movement of the eyes as they follow
visual target. The positional test measures dizziness associated with positions of the head. The caloric test measures
responses to warm and cold water circulated through a small, soft tube in the ear canal.

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The present best method to measure eye movements is an infrared/video system (see Figure 2). Other methods
include electrooculography (EOG), and infrared reflectance. Video systems are usually more accurate than the older
EOG method because they are less sensitive to lid artifact and are not affected by electrical noise generated by
muscle. Infrared reflectance is little used in recent times because of nonlinearity.

The ENG test is the gold standard for diagnosis of ear disorders affecting one ear at a time. For example, the ENG is
excellent for diagnosis of acoustic neuroma as well as vestibular neuritis. The ENG is also useful in diagnosis of BPPV
and bilateral vestibular loss, although the rotational chair test is better at the diagnosis of bilateral vestibular disorders
than is the ENG. The calibration and tracking tests are intended to diagnose central nervous system disorders. These
tests are generally insensitive compared to an examination by a neurologist or a magnetic resonance imaging (MRI)
scan. ENG, however, is much less expensive than an MRI in most institutions.
Electrocochleography (ECOG)
ECOG is a variant of brainstem audio evoked response (BAER). It is not a vestibular test at all but rather a test of
hearing. It is intended to diagnose Menieres disease, and, in particular, hydrops. In this test, a recording electrode
(gold sponge) is inserted into the subjects ear canal, a wire or spring is placed on the ear canal, or a needle that
transfixes the ear drum is inserted into the ear. The subject receives a series of audible clicks.
The objective is to record wave-1 (there are 5 waves), with greater accuracy and to detect the summating potential,
which is a shoulder on wave 1. Needle type ECOGs have fallen out of favor because they are generally judged to be
unreasonably invasive.
Noise can be a major problem with ECOG. Because of this, it is not an easy test to perform. Generally, the results are
reported as a ratio of the summating potential to the action potential (the SP/AP ratio), for which generally a ratio of
0.5 or greater is considered abnormal. It is important when interpreting ECOG to consider the noise level, which is
generally assessed by obtaining multiple trials. If they are all similar, then the standard error is small and the result is
likely to be correct. If they vary widely, the reliability of the average SP/AP ratio may be questionable. Subjects with
poor high-frequency hearing are likely to have higher noise levels, and therefore the limit of normal for their ECOG
should be set higher.
Gamble and others (1999) reported that salt-loaded ECOG may be useful in subjects who have normal ECOGs but a
history suggestive of Menieres disease. Similarly it has been suggested that ECOG may be useful in detecting allergic
Menieres disease. ECOG is performed before and after challenge with an allergen (Noell et al, 2001).

Figure 2: A typical example of the apparatus used for rotatory chair

testing (Image courtesy of ICS Medical, 2001). A person is rotated
within a darkened room. Eye movements are recorded and used to
determine how well the inner ear responds to motion.

Rotational Chair Test

The purpose of rotational chair testing is to determine whether or not dizziness may be due to a disorder of inner ear
or brain. There are three parts to the test: the chair test, the optokinetic test, and the fixation test. The rotational
chair tests actually test for dizziness by recording eye movement (nystagmus) while the chair is moved in various
ways and the subject looks a different lights.

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The chair test measures dizziness while the subject is being turned slowly in a motorized chair (see Figure 2).
Subjects with inner ear disease become less dizzy than do normal persons. The optokinetic test measures dizziness
caused by viewing of moving stripes. Optokinetic testing is sometimes useful in diagnosis of bilateral vestibular loss
and central conditions. The fixation test measures dizziness while the subject is being rotated, and while they are

looking at a dot of light that is rotating with them. Fixation suppression is impaired by central nervous system
conditions and improved by bilateral vestibular loss.
Rotatory chair tests are the gold standard for diagnosis of bilateral vestibular loss. ENG tests by themselves may be
falsely positive (they are rarely falsely negative) as, for example, when wax blocks one ear canal. Rotatory chair
testing is not affected by mechanical obstructions of the ear. Rotatory chair testing is thus a valuable adjunct to ENG
testing by confirming an abnormality.

Figure 3: VORTEQ (Tm) device used for active head rotation testing (courtesy of
Micromedical technology, 2002)

There are several other alternative procedures involving rotation that provide a subset of rotational chair testing. Two
tests use active head movement brand names for these devices are VAT and VORTEQ. Both of these tests provide a
part of the the rotational chair test information (the high-frequencies), and measure something a little different: the
contribution of both the inner ear and neck inputs to nystagmus rather than the contribution of the inner ear alone. If
you have a rotational chair test, there is no need to get a VAT or VORTEQ test since the information supplied is largely
redundant. However, if a rotational chair test is not available, these test may have some value.

Figure 4: Moving platform posturography device (Micromedical Technology, 2001).

Moving platform posturography (MVP), or posturography for short, is a method of quantifying balance (although the
definition of balance can be tricky). It is most applicable in situations where balance needs to be followed
quantitatively, to determine whether a disorder is getting better or worse, or the response to treatment.
Posturography is insensitive to vestibular disorders, and normal posturography should not be considered indicative of
normal vestibular function (Jasper et al, 2008). It may add sensitivity to a vestibular battery, when combined with
other tests of vestibular function (Zhang, et al., 2009). Stewart et al (1999) suggested that audiometry combined with
posturography was a cost-effective method of documenting a vestibular disorder.
Posturography is also very useful in medical legal situations where malingering is a possibility. Click here to see an
example of a posturography output screen (courtesy of Neurocom, Inc). The main vendor of posturography equipment
used in clinical context is Neurocom incorporated. Other vendors include Micromedical Technology, and several
makers of research balance equipment (e.g. AMTI).

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Figure 5. A fistula test being performed using a Bruns otoscope and infrared
oculography. Image (c) Timothy C. Hain, 2002.

Fistula Test
The purpose of this test is to detect perilymph fistula. Pressure is applied to each ear in turn, and eye movements are
recorded with a sensitive infrared recording device. For this reason, fistula testing is about 10 times more sensitive
than conventional electrooculography (EOG) based recordings.
Fistula testing can also be done at the bedside. Pressure is applied to the ear through one of the devices seen in
Figure 4, while eye movement is either directly observed or measured with an EOG , infrared (IR), examining
microscope, or posturography.
Dizziness Questionnaires
Most practices that evaluate substantial numbers of dizzy patients use questionnaires to quantify symptoms. The
following table provides a list of some questionnaires:
Questionnaire used to quantify balance


Activities specific Balance Confidence Scale (ABC)

Powell and Meyers, 1995; Whitney et al, 1999

Modified falls efficacy scale (MFES)

Hill , Schwartz and others, 1996

Medical outcomes study short form 36 (SF-36)

Enloe and Sheilds, 1997

Dizziness Handicap Inventory

Jacobson and Newman, 1990

Vestibular Activities of Daily Living

Cohen et al, 2000

The Dizziness Handicap Inventory (DHI) is the most commonly used questionaire at this writing (2002).
New and Emerging Tests
As there are 5 individual motion sensors in each ear, and most of the testing described above is relevant only to one
of them (the lateral semicircular canal), there clearly is plenty of room for new tests. In theory, 4/5ths of your inner
ear could be destroyed yet conventional vestibular testing might not even detect it. The table below provides an
outline of the present status of vestibular testing.

Lateral (horizontal) semicircular canal

Caloric test, Rotatory chair test

Superior semicircular canal

No test exists that isolates one canal. New approaches are needed.

Anterior semicircular canal

No test exists that isolates one canal. New approaches are needed.


Ocular counter roll, Subjective vertical. Neither test isolates a single utricle.


Vestibular evoked myogenic potential. This test does assess a single saccule.

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Part of the labyrinth

positional vertigo



Meclizine (Antivert), 25 to 50 mg orally

every four to six hours

Commonly used to reduce symptoms of acute

episodes of vertigo, although there are no RCTs to
support its use; use of vestibular suppressants can
lead to brainstem compensation and prolong
vertiginous symptoms
Main benign paroxysmal positional vertigo treatment;
safe and effective compared with placebo
Series of head and neck exercises that can be
performed daily at home
Evidence for balance therapy (e.g., tai chi, Wii Fit) is
No large-scale RCTs to support these therapies

Epley maneuver (canalith repositioning)

Vestibular rehabilitation

Salt restriction (less than 1 to 2 g of

sodium per day) and/or diuretics (most
commonly, hydrochlorothiazide/triamterene
Intratympanic dexamethasone or
Referral to an otolaryngologist required; in one small
study, dexamethasone resolved symptoms in 82
percent of patients; in a larger study, gentamicin
resolved symptoms in 80.7 percent of patients
Endolymphatic sac surgery
Referral to an otolaryngologist required
Vestibular neuritis Methylprednisolone (Depo-Medrol), initially In an RCT, methylprednisolone was more effective in
100 mg orally daily then tapered to 10 mg improving peripheral vestibular function than
orally daily over three weeks
valacyclovir (Valtrex) in patients with vestibular
Migrainous vertigo Migraine prophylaxis with serotonin 5Treatment based on expert opinion, not RCTs
HT1 receptor agonists (triptans)
Review medication regimen
This is the first step, especially in older patients;
rehydration (even increased water intake) can
improve symptoms, especially in those with
autonomic failure
Midodrine (Proamatine) titrated up to 10
Alpha-1 agonist metabolite; to avoid supine
mg orally three times daily
hypertension, the third dose should be given by 6
p.m.; should be used only in severely impaired
patients; in placebo-controlled trials, midodrine was
associated with increased standing blood pressures
and fewer orthostatic symptoms compared with
Fludrocortisone, initially 0.1 mg orally daily, Mineralocorticoids, such as fludrocortisone, are used
titrated up weekly until peripheral edema
to increase sodium and water retention; monitor
develops or to a maximal dosage
blood pressure, potassium level, and for symptoms of
heart failure
Fludrocortisone and midodrine can be used in
combination if either agent alone fails to control
Pseudoephedrine, 30 to 60 mg orally
These drugs are options when midodrine and
dailyParoxetine (Paxil), 20 mg orally daily
fludrocortisone are ineffective
Desmopressin (DDAVP), 5 to 40 mcg
Nondrug therapy includes replacement of fluids,
intranasally daily
rising slowly from lying or sitting positions, sleeping
with the head of the bed elevated, increasing salt
intake, and regular exercise
Treatment of underlying cause (e.g.,
Because disequilibrium is generally a symptom of an
peripheral neuropathy, Parkinson disease)
underlying condition, treatment of the condition
improves symptoms of disequilibrium
Breathing control exercises, rebreathing
Reverses hypocapnia-related symptoms
into a small paper bag
Beta blockers
Treats associated symptoms, such as palpitations
and sweating; not for use in patients with asthma
Antianxiety agents (e.g., selective serotonin For use in patients with underlying anxiety
reuptake inhibitors) or short-term use of

Pharma Pipz and Pooks w/ Men



Meniere disease



Pharma Pipz and Pooks w/ Men