Def. Vertigo, is defined as an illusion of either oneself or the environment rotating.

It indicates involvement
of the angular motion sensing system.
Patients refer to Dizziness as
Light headedness, Sense of strangeness, Faintness, Giddy, imbalanced or out-of-it.

It’s the clinician job to determine whether the patient has actual true vertigo or any of the above
symptoms .
Pre-syncope:
Transient sensation that a faint event is about to occur. May present as nausea ,weakness, SOB
or change in vision.

Dysequilibrium
• A sensation of imbalance when standing or walking. There is No sense of illusion and
No sense of faintness.

Vague lightheadedness:
Holds the reminder of symptoms of dizziness (which can’t fit to the other categories)which
includes Psychiatric disorders, Hyperventilation syndrome and Encephalopathies.

Whenever a patient with complaints of vertigo presents in a clinic the most important aspect of
his management includes eliciting appropriate and relevant history . a good history diagnoses the
disease in 80% of the cases .

Evaluation of a patient of vertigo

History
Taking the history of a patient with a complaint related to dizziness must begin in an open-
ended fashion, allowing the patient to describe the symptoms with minimal direction from the
clinician.
Does the patient have true vertigo or something similar but not quite that ? In vertigo The
patient can feel as if the motion is internal or that objects in the surroundings are moving or
tilting. The sense of motion can be rotatory, linear, or a change in orientation relative to the
vertical. Lightheadedness, as opposed to vertigo, may indicate presyncope. Although often
related to neural factors, such as vasovagal syncope, it also can reflect cardiac disease, especially
in older patients. Generalized imbalance may reflect more central processes, including migraine.
 Some conditions, such as migraine, can manifest with nonspecific imbalance symptoms in
addition to acute vertigo.
What happened the first time the imbalance occurred?
Are the symptoms episodic or continuous, and if episodic, how long do they last?
What brings on the problem? The diagnosis of certain vestibulopathies is strongly suggested
from events or movements that trigger symptoms.
What other signs and symptoms are associated with the dizziness or vertigo?
Have there been auditory symptoms
Any recent or remote head or neck injury?
Is there a family history of imbalance or headache?
Are there other, psychogenic disorders that may be responsible for the patient's symptoms?
Are there underlying medical problems that may cause or exacerbate the patient's symptoms?

Type and Mechanism of Dizziness Associated with Commonly Used Drugs

Drug(s) Type(s) of Dizziness Mechanism(s)

Aminoglycosides,
Vertigo, dysequilibrium Damage to vestibular hair cells
cisplatin
Tranquilizers Intoxication Central nervous system depression
Antiepileptics Dysequilibrium Cerebellar toxicity
Antihypertensives, Postural hypotension, reduced cerebral
Near-syncope
diuretics blood flow
Dysequilibrium and
Amiodarone Unknown
oscillopsia
Intoxication, Central nervous system depression,
Alcohol dysequilibrium, cerebellar toxicity, change in cupular and
positional vertigo endolymphatic specific gravity
Methotrexate Dysequilibrium Brainstem and cerebellar toxicity
Anticoagulants Vertigo Hemorrhage into inner ear or brain

Physical examination

The physical examination should be goal-directed at testing hypotheses made from the history.
However basic otologic examination(including dix hall pike ) as well as tests for nystagmus ,balance and
cerebellar functions should form a part of any examination for any patient of vertigo .
Figure 1.
Dix-Hallpike maneuver (used to diagnose benign paroxysmal positional vertigo). This test consists of a
series of two maneuvers: With the patient sitting on the examination table, facing forward, eyes open, the
physician turns the patient’s head 45 degrees to the right (A). The physician supports the patient’s head as
the patient lies back quickly from a sitting to supine position, ending with the head hanging 20 degrees off
the end of the examination table. The patient remains in this position for 30 seconds (B). Then the patient
returns to the upright position and is observed for 30 seconds. Next, the maneuver is repeated with the
patient’s head turned to the left. A positive test is indicated if any of these maneuvers provide vertigo with or
without nystagmus.

Clues to Distinguish Between Peripheral and Central Vertigo

Clues Peripheral vertigo Central vertigo

Findings on Dix-Hallpike maneuver

Latency of symptoms and 2 to 40 seconds None

nystagmus

Severity of vertigo Severe Mild

Duration of nystagmus Usually less than 1 minute Usually more than 1 minute

Fatigability* Yes No

Habituation† Yes No

Other findings

Postural instability Able to walk; unidirectional Falls while walking; severe

instability instability

Hearing loss or tinnitus Can be present Usually absent

Other neurologic symptoms Absent Usually present

*—Response remits spontaneously as position is maintained.
† —Attenuation of response as position repeatedly is assumed.
INVESTIGATIONS :
No laboratory testing is absolutely indicated in the work-up of patients with vertigo. If hearing loss
is suspected, complete audiometric testing can help distinguish vestibular pathology from retrocochlear
pathology (e.g., acoustic neuroma).
Brain imaging is warranted if a tumor or stroke is suspected. A magnetic resonance imaging with contrast
medium when a patient presents with acute vertigo and sensorineural hearing loss is warranted .
Magnetic resonance angiography can be used to evaluate the vertebrobasilar circulation.

Differential Diagnosis of Vertigo

This includes the following conditions :

Duration of Auditory Peripheral or

Disorder episodes symptoms Prevalence central vertigo

Benign paroxysmal positional Seconds No Common Peripheral

vertigo

Perilymphatic fistula (head Seconds Yes Uncommon Peripheral

trauma, barotrauma)

Vascular ischemia: transient Seconds to Usually not Uncommon Central or

ischemic attack hours peripheral*

Ménière’s disease Hours Yes Common Peripheral

Syphilis Hours Yes Uncommon Peripheral

Vertiginous migraine Hours No Common Central

Labyrinthine concussion Days Yes Uncommon Peripheral

Labyrinthitis Days Yes Common Peripheral

Vascular ischemia: stroke Days Usually not Uncommon Central or

peripheral*

Vestibular neuronitis Days No Common Peripheral

Anxiety disorder Variable Usually not Common Unspecified

Acoustic neuroma Months Yes Uncommon Peripheral

Cerebellar degeneration Months No Uncommon Central

Cerebellar tumor Months No Uncommon Central

Multiple sclerosis Months No Uncommon Central

Vestibular ototoxicity Months Yes Uncommon Peripheral

*—Vertigo can be caused by vascular ischemia in the central vertebrobasilar circulation or the peripheral
circulation to the vestibular nerve and labyrinth.

TREATMENT:
Medications are most useful for treating acute vertigo that lasts a few hours to several
days .They have limited benefit in patients with benign paroxysmal positional vertigo,
because the vertiginous episodes usually last less than one minute. Vertigo lasting more
than a few days is suggestive of permanent vestibular injury (e.g., stroke), and
medications should be stopped to allow the brain to adapt to new vestibular input.
Medications Commonly Used In Patients with Acute Vertigo and
Associated Nausea and Emesis

Pregnancy
Medication Dosage Sedation Antiemesis category

Meclizine* (Antivert) 12.5 to 50 mg orally every 4 ++ + B

to 8 hours

Dimenhydrinate* 25 to 100 mg orally, IM, or IV + ++ B

(Dramamine) every 4 to 8 hours

Diazepam (Valium) 2 to 10 mg orally or IV every 4 ++ + D

to 8 hours

Lorazepam (Ativan) 0.5 to 2 mg orally, IM, or IV ++ + D

every 4 to 8 hours

Metoclopramide 5 to 10 mg orally every 6 + +++ B

(Reglan) hours

5 to 10 mg by slow IV every 6
hours

Prochlorperazine 5 to 10 mg orally or IM every + +++ C

(Compazine) 6 to 8 hours

25 mg rectally every 12 hours

5 to 10 mg by slow IV over 2
minutes

Promethazine 12.5 to 25 mg orally, IM, or +++ ++ C

(Phenergan) rectally every

4 to 12 hours
+ = mild; ++ = moderate; +++ = prominent; IM = intramuscular; IV = intravenous.

VESTIBULAR REHABILITATION EXERCISES

Vestibular rehabilitation exercises commonly are included in the treatment of vertigo.
These exercises train the brain to use alternative visual and proprioceptive cues to
maintain balance and gait. It is necessary for a patient to re experience vertigo so that the
brain can adapt to a new baseline of vestibular function. After acute stabilization of the
patient with vertigo, use of vestibular suppressant medications should be minimized to
facilitate the brain’s adaptation to new vestibular input.
ENIGN PAROXYSMAL POSITIONAL VERTIGO
Benign paroxysmal positional vertigo is caused by calcium debris in the semicircular
canals (canalithiasis), usually the posterior canal. Medications generally are not
recommended for the treatment of this condition.
The vertigo improves with head rotation maneuvers that displace free-moving calcium
deposits back to the vestibule. Maneuvers include the canalith repositioning procedure or
Epley maneuver and the modified Epley maneuver (Figure 2). The modified Epley
maneuver can be performed at home.

Figure 2.
Epley maneuver. The patient sits on the examination table, with eyes open and head turned 45 degrees to
the right (A). The physician supports the patient’s head as the patient lies back quickly from a sitting to
supine position, ending with the head hanging 20 degrees off the end of the examination table (B). The
physician turns the patient’s head 90 degrees to the left side. The patient remains in this position for 30
seconds (C). The physician turns the patient’s head an additional 90 degrees to the left while the patient
rotates his or her body 90 degrees in the same direction. The patient remains in this position for 30 seconds
(D). The patient sits up on the left side of the examination table. (E) The procedure may be repeated on
either side until the patient experiences relief of symptoms.

Patients may need to remain upright for 24 hours after canalith repositioning to prevent
calcium deposits from returning to the semicircular canals, although this measure is not
universally recommended. Contraindications to canalith repositioning procedures include
severe carotid stenosis, unstable heart disease, and severe neck disease, such as cervical
spondylosis with myelopathy or advanced rheumatoid arthritis.
VESTIBULAR NEURONITIS

Acute inflammation of the vestibular nerve is a common cause of acute, prolonged

vertigo. The vertigo usually lasts a few days and resolves within several weeks.
Vestibular neuritis is not associated with subjective change in hearing or with any focal
neurologic complaints. Many cases of vestibular neuronitis are attributed to self-limited
viral infections, although specific proof of a viral etiology is rarely identified.

Treatment should focus on symptom relief using vestibular suppressant medications,

followed by vestibular exercises. Vestibular compensation occurs more rapidly and more
completely if the patient begins twice-daily vestibular rehabilitation exercises as soon as
tolerated after the acute vertigo has been alleviated with medications.

When sudden sensorineural hearing loss accompanies vertigo with a vestibular neuritis–
like pattern, classification as a sudden sensorineural hearing loss should be considered. In
such cases, treatment appropriate for sudden sensorineural hearing loss should be
instituted and the evaluation should include evaluation for a retrocochlear lesion, such as
acoustic neuroma

MENIERE’S DISEASE

Meniere's disease (idiopathic endolymphatic hydrops) is a disorder of the inner ear

associated with a symptoms consisting of spontaneous, episodic attacks of vertigo;
sensorineural hearing loss which usually fluctuates; tinnitus; and often a sensation of
aural fullness. Meniere's disease is characterized by recurring attacks of vertigo,
sensorineural hearing loss, tinnitus, and, in some affected persons, a fluctuating sense of
fullness in the ear. Acute attacks are superimposed on a gradual deterioration in
sensorineural hearing in the involved ear, typically in the low frequencies initially. Over
time, a reduction in responsiveness of the involved peripheral vestibular system occurs

AAO-HNS Criteria for Meniere's Disease Diagnosis

Major Symptoms
Vertigo
• Recurrent, well-defined episodes of spinning or rotation
• Duration from 20 minutes to 24 hours.
• Nystagmus associated with attacks
• Nausea and vomiting during vertigo spells common
• No neurologic symptoms with vertigo
Deafness
• Hearing deficits fluctuate
• Sensorineural hearing loss
• Hearing loss progressive, usually unilateral
Tinnitus
• Variable, often low-pitched and louder during attacks
• Usually unilateral
• Subjective
 Diagnosis
Possible Meniere's disease
• Episodic vertigo without hearing loss or
• Sensorineural hearing loss, fluctuating or fixed, with dysequilibrium, but without
definite episodes
• Other causes excluded
Probable Meniere's disease
• One definitive episode of vertigo
• Hearing loss documented by audiogram at least once
• Tinnitus or sense of aural fullness in the presumed affected ear
• Other causes excluded
Definite Meniere's disease
• Two or more definitive spontaneous episodes of vertigo lasting at least 20 minutes
• Audiometrically documented hearing loss on at least one occasion
• Tinnitus or sense of aural fullness in the presumed affected ear
• Other causes excluded
Certain Meniere's disease
• Definite Meniere's disease, plus histopathologic confirmation
Treatment of Meniere's disease should be aimed at the reduction of its associated
symptoms. The optimal curative treatment should stop vertigo, abolish tinnitus, and
reverse hearing loss.

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 and stroke includes preventing future events through blood pressure
control, cholesterol-level lowering, smoking cessation, inhibition of platelet function (e.g., aspirin,
clopidogrel , aspirin-dipyridamole and, possibly, anticoagulation (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.

MIGRAINE HEADACHES
Epidemiologic evidence has shown a strong association between vertigo and migraine. Diagnostic
criteria have been proposed to provide a more specific definition of vertiginous migraine. Diagnostic
accuracy is important because vertiginous migraine may respond better to migraine treatments than to
other interventions.
PSYCHIATRIC DISORDERS
Vertigo commonly is associated with anxiety disorders (e.g., panic disorder, generalized
anxiety disorder) and, less frequently, depression.Hyperventilation usually occurs and can
result in hypocapnia with reversible cerebral vasoconstriction. Hyperventilation and
hypocapnia may be accompanied by dyspnea, chest pain, palpitations, or paresthesias.
Subclinical vestibular dysfunction may occur in patients with anxiety disorders or
depression, most commonly panic disorder with moderate to severe agoraphobia. On the
other hand classic vertigo resulting from more ostensible vestibular pathology usually
induces severe anxiety symptoms and thus can be hard to distinguish from a primary
anxiety disorder.

Vestibular suppressants and benzodiazepines most frequently are used to treat dizziness
that is associated with anxiety disorder, but these medications provide only transient or
inadequate relief.34 SSRIs such as citalopram (Celexa), fluoxetine (Prozac), paroxetine
(Paxil), and sertraline (Zoloft) may provide better relief.

VERTIGINOUS EMERGENCIES :
In situations where a patient presents with an attack of acute severe vertigo certain
guidelines can help in effective management .
Firstly take appropriate history and look for signs of any associated neurological defeciet
or central cause. Once these are ruled out the otological causes are relatively benign .
Reassure the patient and gently reaffirm him that his condition will be treated
Keep him in a position that minimizes his vertigo
Give him iv vestibular suppressants like diazepam 2mg iv stat
Meanwhile replace any fluids lost due to vomiting
Look for nystagmus and if central cause of vertigo is suspected begin management and
investigations on that lines .
DISPOSAL OFFICERS AND ORs.