Vertigo is a symptom of illusory movement and not a diagnosis .It is due to asymmetry of vestibular system due to damage or dysfunction of the Labyrinth and vestibular nerve, or Central vestibular structures in the brainstem

1. Vertigo –The Dizzy Patient:-
An Evidence-Based Diagnosis and Treatment strategy
Dr. Sachin Verma MD, FICM, FCCS, ICFC
Fellowship in Intensive Care Medicine
Infection Control Fellows Course
Consultant Internal Medicine and Critical Care
Ivy Hospital Sector 71 Mohali
Web:- http://www.medicinedoctorinchandigarh.com
Mob:- +91-7508677495

2. Table of Contents:
1. What is vertigo?
2. Anatomical aspects.
3. Pathophysiology.
4. Causes of vertigo.
5. General Examination
6. Neurological examination
7. Lab investigations.
8. Management.

3. 1.What is vertigo?
Vertigo is a symptom of illusory movement and not a
diagnosis .It is due to asymmetry of vestibular system due
to damage or dysfunction of the
 Labyrinth and vestibular nerve, or
 Central vestibular structures in the brainstem.
It is subjective and objective illusion of movement

4. Differential Diagnosis Is it vertigo ?
Vertigo can be easily differentiated from other causes of dizziness by a
“sensation of motion”. The sensation can be
1. subjective (patient is moving)
2. or objective (environment is moving).
1. Lightheadedness: - which includes nonspecific
symptoms related to multiple sensory disturbances,
side effect of medications that alter the sensorium
or certain psychiatric disturbances.
2. Disequilibrium: - caused by motor dysfunction that
impairs balance and gait. ( “Dizziness of feet”)
3. Presyncope: - a sense of impending loss of
consciousness due to hypoperfusion of brain or
metabolic causes such as hypoglycaemia.
4. Vertigo: - a sensation of movement due to disorder
of labyrinth or its central connection.
Usually benign
Rule out PSEUDOVERTIGO

5. 2. Anatomical aspects
Ear has auditory system and vestibular
system
Auditory system –Cochlea
Vestibular system – It has a set of
 -Three-dimensional angular
velocity transducers, the
semicircular canals,
First, each canal within each labyrinth is
perpendicular to the other canals,
which is analogous to the spatial
relationship between two walls and
the floor of a rectangular room.
Second, the planes of the semicircular
canals, between the labyrinths, are
close to each other.
 -A set of three-dimensional linear
acceleration transducers, the
otoliths (saccule and utricle ).

6. 2. Anatomical aspects -cont
SCC - mainly for Angular
motion- do not have otoliths
Otoliths (saccule and utricle ).
In an upright person, the saccule is
vertical (parasagittal), whereas the
utricle is horizontally oriented (near
the plane of the lateral semicircular
canals ( SCC )
 The otoliths are also arranged in
such a way that they can respond
to motion in all three linear
dimensions.
 The otolithic membranes contain
calcium carbonate crystals called
otoconia

7. 3.Pathophysiology. WHY DOES VERTIGO DEVOLOP?
The three stabilizing systems
(mentioned earlier) overlap
sufficiently to compensate
(partially or completely) for
each other's deficiencies.
Vertigo may represent either
physiologic stimulation or
pathological dysfunction in
any of the three sensory
systems.
When Otoconia come in SCC ,
then cause BPPV.

8. 4.Common causes of vertigo:-
Peripheral and Central causes
A.Peripheral etiology
a. Acute labyrinthitis and Vestibular neuronitis
b. Meniere’s disease
c. Benign Peroxysmal positional vertigo (BPPV)
d. Toxins - alcohol. Aminoglycosides, Quinine
(Tinnitus ,Hearing loss vomiting and vertigo)

9. B.Central etiology
a. Vertebrobasilar insufficiency (TIA )
b. Brainstem Stroke - Ischemia or Haemorrhage
c. Demyelinating disorder eg Multiple
Sclerosis(MS).
d. Space occupying lesion in brain stem (rare)-
CP angle SOL –
-CP angle Tumor of the Schwann cells around the 8th cranial
nerve.
-Vertigo with hearing loss and tinnitus
-With tumor enlargement, it encroaches on the
cerebellopontine angle causing neurological signs.
-Mostly in women during 3rd and 6th decades

10. A.Peripheral etiology
(i) Labrynthitis and Vestibular Neuronitis
 Common term for an acute unilateral loss of
peripheral vestibular function associated with
nausea, vomiting,
vertigo
spontaneous nystagmus, and
disequilibrium.
 It is generally peaking during the first day,
then gradually improving over the next few
days
 Generally due to a viral infections.

11. Vestibular Neuronitis
• It is also termed as acute vestibular failure.
• Sudden onset acute severe vertigo but there is no auditory
symptom.
• The single episode of severe vertigo -for one or two days but
patients may remain symptomatic for months.
• Etiology -viral infection in young patients causing injury to
the vestibular apparatus, but in older patients, vascular
causes are more likely.
Post-traumatic Vestibular syndromes
A rare cause of peripheral vertigo is perilymphatic fistula .
Post-traumatic lesion involves an abnormal connection between the middle and inner ear.
It can be caused by
i. a direct blow to the ear,
ii. a forceful Valsalva maneuver,
iii. acute external pressure changes
( as in scuba diving or descent in an airplane)

12. (ii) Ménièr’s Disease
 Triad of –
a) Tinnitus ,
b) Vertigo and
c) Fluctuating Sensory neural deafness.
 May occur in clusters and have long episode-free
remissions
 Usually low pitched tinnitus
 Symptoms subside quickly after attack
 No CNS symptoms
 No positional vertigo is present
 Often patients have eaten a salty meal prior to attacks

13. (iii)BPPV- Benign Peroxysmal positional vertigo
 Extremely common – 40 % of all vertigo patients BPPV
 Otoconia displacement.and drag endolymph.
 No hearing loss or tinnitus
 Short-lived episodes brought up by rapid changes in
head position
 Usually there may be a single position that elicits vertigo
 Top shelf vertigo
 Horizontal rotatory nystagmus after a short latency
period
 Less pronounced with repeated stimuli
 Typically can be reproduced at bedside with positioning
maneuvers

14. (iv) Toxins
(i)Streptomycin and gentamycin –
 These cause injury to peripheral end organ, since they are
concentrated in the endolymph and perilymph.
 Patients usually report progressive unsteadiness, particularly
when visual input is diminished, as happens at night or in a
darkened room.
 Extreme caution should be used in patients with even mild
renal disease because most of these agents are primarily
removed by the kidney.
(ii) Anticonvulsant toxicity, phenytoin or carbamazepine,
may cause CNS depression, nystagmus, and ataxia
(iii) Benzodiazepines, barbiturates,
(iv) Alcohol, and other CNS depressants may present as
nonspecific dizziness

15. What differentiates labyrinthitis or vestibular neuritis (VN)? from BPPV
 Labyrinthitis/VN BPPV
a) No head movement a. Requires head movement
needed
b) Duration of hours/days b. Duration of seconds
c) Any age c. Usually in elderly
d) Viral syndrome usually d. No relation to viral
syndrome
precedes e. Responds to Epley
a) Epley maneuver is maneuver
ineffective

16. Central vertigo –features
Causes include disorders with significant potential morbidity .
a) Vertebrobasilar Insufficiency
b) Stroke - Cerebellar Hemorrhage
c) Multiple Sclerosis
d) Tumors
Symptoms associated with brainstem ischemia
include
a. Diplopia,
b. Dysarthria
c. Ataxia
d. facial weakness or sensory symptoms
Unlike their peripheral counterparts, they have little nausea
or any auditory symptoms.

17. Vertigo :Peripheral v/s Central
PERIPHERAL CENTRAL
i. Onset Sudden Slow, gradual
i. Intensity Severe ILL defined
i. Duration Paroxysmal Constant
i. Nausea Frequent Infrequent
i. CNS signs Absent Usually present
i. Tinnitus/heari Can be present Absent
ng loss
i. Nystagmus Torsional /horizontal Vertical
Fatigable Non-fatigable
i. Course Limited usually Non specific

18. Step 5.General Examination of a patient.
1. General examination
Orthostatic vital signs
BP and pulse in both arm
2.Eye and Cranial nerves examination
3.Ear examination
4.Neurological examination
Gait and Cerebellar function

19. 2.Eye examinaton –Eye movements and Nystagmus
 In peripheral vertigo –  In central disorders,
Spontaneous nystagmus Spontaneous nystagmus may
continues in only one change its direction whenever
direction even when the there is a change in the
direction of gaze changes. direction of gaze (gaze-evoked
nystagmus)
Nystagmus is typically Vertical nystagmus is due to a
horizontal-rotary with a central neurological cause until
slow and fast component proved otherwise.

20. How to elicit nystagmus
Patient is seated in front of the examiner or lies supine in the bed.
The examiner keeps his finger about 30 cm from the patient’s
eye in the central position and moves it to the right or left,
up or down, but not moving at any time, more than 30° from
the central position to avoid gaze nystagmus. Presence of
spontaneous nystagmus always indicates an organic lesion.
Vestibular nystagmus has a slow and a fast component and, by
convention, the direction of nystagmus is indicated by the
direction of the fast component. Intensity of nystagmus is
indicated by its degree.
i. 1st degree It is weak nystagmus and is present when
patient looks in the direction of fast
component.
i. 2° degree It is stronger than degree nystagmus and is
present when patient looks straight ahead.
i. 3rd degree It is stronger than 2nd degree nystagmus
and is present even when partial looks in the
direction of slow component.
Nyst video

21. Eye examination

23. 3.Ear examination
a. Examine the tympanic membranes and
external auditory canals (EAC) for the
presence of infection, tympanic membrane
rupture, or foreign body
b. Ipsilateral facial nerve palsy with presence of
vesicles within the EAC suggest herpes zoster
infection (Ramsay hunt’s syndrome)
c. The presence of recent unilateral hearing loss
in the setting of vestibular symptoms suggests
Meniere’s disease
d. Acoustic neuromas, due to their slow growth,
typically present with gradual decline in
hearing and are rarely accompanied by
symptoms of vestibulopathy.

24. Dix-Hallpike Test method-
1.Patient sits on a couch. Examiners
holds the patient’s head ,turns it
45° to the right
2.Then places the patient in a supine
position so that his head hangs
30* below the horizontal.
3.Patient is asked to look to opposite
side and eyes are observed for
nystagmus.
4.If patient is made to sit with head
rotated , there is change in the
direction of nyatagmus .
The test is repeated with head turned
to left and then again in straight
head-hanging position.
Four parameters of nystagmus are
observed :
i. latency,
ii. duration,
iii. direction and
iv. fatigability
Dix video

26. Interpretations of Nystagmus in Hallpike
Finding Peripheral Central ( ?King )
Latency Yes 3-10 sec. No
Fatigability Yes No
Nystagmus direction Fixed, typically mixed Changing, variable and pure
rotational vertical or pure horizontal
Suppression by Yes No
visual fixation
Severity Marked severe Mild to moderate
But patient can not walk
easily
Consistency Less consistent More consistent
Past pointing In direction of slow In direction of fast phase
phase

27. 6.Neurological examination
 One should begin with a thorough cranial nerve exam,
including evaluation of cranial nerves and cerebellar
function using finger to nose and rapid alternating
movement tests
 Involvement of other cranial nerves in addition to the
vestibulocochlear nerve strongly suggests central
disease
Patient with peripheral vertigo are typically able to
walk without assistance, although they tend to veer
to one side.
Video – Cerebellar and Rhomerg;s

30. 7.Lab investigations.
1. Routine lab test include complete blood count,
electrolytes, glucose and creatinine levels
2. Cardiac – Holtor monitoring and EKG-
When evaluating the dizzy patient who complains
of near syncope, the EKG is very important.
Look for
Rapid or slow rates
Prolongation of QT interval.
A wide QRS complex with slurred upstroke- in
association with a short PR interval may indicate Wolff-
Parkinson-White (WPW) syndrome.
3. Caloric test
4. Electronystagmography (ENG )
5. Optokinetic test
6. Imaging (CT and MRI)

31. Neuroimaging
1. Patients with severe headache and with hard
neurological findings - ( include motor deficits,
particularly crossed hemiplegia; dysarthria or
dysphagia; inability to walk; bidirectional or vertical
nystagmus; and sings of cerebellar dysfunction )
2. Patient with prolonged vertigo symptoms with no other
neurological deficits They may have evidence of
vertebrobasilar insufficiency by MR angiography, with
the greatest incidence in elderly patient
CT is more sensitive for hemorrhage, but MRI is more
likely to detect subtle brainstem or cerebellar infarction

32. CT / MRI findings

33. 8.Treatment
1. General treatment
symptomatic treatment -is useful to lessen the abnormal
sensations and to alleviate vegetative symptoms .
It includes -
antibiotics for infections ,
bed rest,
low salt diet,
adaptation exercises ,
diuretics for meniere’s
and surgical repair for fistulas.
Symptomatic treatment of nausea, vomiting and dizziness is done.
2. Specific drug treatment
3. Exercise
4. Surgery

34. Treatment of specific conditions -
(i)Labyrinthitis –
Bed rest and hydration .
Severe nausea and vomiting-benefit from IV fluid
Cinnarizine -25-75 mg TDS
Short course of steroid i.e.methylprednisolone may help.
Antivirals like acyclovir, famciclovir may help in hastening
the recovery in viral causes.
(ii)Vestibular neuronitis –
(a) Vestibular suppressants –
Meclizine, promethazine or prochlorperazine -
may be given for short period to tackle severe
vertigo and vomiting if present.
Cinnarizine -25-75 mg TDS
(b) methyl prednisolone
3 week course tapered from 100 mg down to 10 mg
daily may reduce long term loss of vestibular function.

35. Tr Treatment of specific conditions -
cont
(iii)Meniers disease -
Needs Low salt diet
Vestibular suppressant
Vasodilators and
Diuretics .
(iv)BPPV –
The treatment of choice for BPPV is
-CRP (Canalith repositioning procedure).
It is also known as the Epley maneuver.
-Brandt- Duroff exercises

36. Drug treatment -Labyrinthine suppressants - mainly used in acute attack
(i). Antihistamines
 Dimenhydrinate -50 mg thrice daily.SE – Drowsiness .Useful in
acute attacks
 Promethazine Hcl -10-20 mg TDS. SE- Sedation or
extrapyramidal synd. Useful in acute attacks,
Used with caution in prostatic hypertrophy, glaucoma and CVS
pathology.
 Cinnarizine -25-75 mg TDS . SE -drowsiness.
(ii) Phenothiazines
• Prochorperazine Orally/I V/IM 5-25 mg SOS/TDS.
SE- Hypotension
Useful in acute attacks; acts on vomiting centre.
• Trifulpromazine 10mg SOS/TDS - SE-Hypotension .
Useful in acute attacks; acts on vomiting center.

37. Drug treatment -Labyrinthine suppressants - mainly used in acute attack
iii) Anticholinergics
• Meclizine 12 5mgTDS. SE- Drowsiness . in acute attacks; acts on
vomiting center
• Scopolamines 0.6mg BD ,TDS Use with caution in glaucoma .
(iv) Newer vasodilator - Histamine Agonist/H2 antagonist
• Betahistine dihydrochioride 8-16mgTDS SE-GI upset .
• Betahistine Mesylate, Chemical name: 2-(2-methylamino ethyl)
pyridine dimethane sulfonte ,
C/I in bronchial asthma and phaeochromocytoma .
Maximum efficacy of betahistine is obtained with long periods of
treatment of 3-8 weeks and with daily doses of 32 to 36 mg

38. 3. Exercises (i)Epley’s maneuver (CRP)- first identify the side of lesion
by neck extension
The operator stands behind the patient with the
assistant on the side One repositioning cycle
has five positions.
PositionA:The patient sits on the table so that
when lying, the head is positioned beyond the
edge of table.
 Position B: The head is placed over the edge of
the table, 45 degrees to one side.
 Position C While the head is tilted down it is
rotated 45 degrees to the opposite side.
 Position D: The head and body are rotated until
they face downwards 135 degrees from the
supine position. Face should face the ground –
This step is ignored by clinicians.
 Position E: With the head still tilted, the
patient is made to sit. The head is turned
forward and chin down by 20 degrees.
There should be pause at each position until
there is no nystagmus or there is slowing of
the nystagmus before changing to the next
position.
This ejects crystals from the Utricle .
The patient is instructed to wear a neck brace for 24 hours and to not bend down or lay flat
for 24 hours after the procedure. One week after the CRP, the Dix-Hallpike test is repeated.
If the patient does experience vertigo and nystagmus, then the CRP is repeated with a
vibrator placed on the skull in order to better dislodge the otoconia.

39. ii)Brandt- Duroff exercises
One sits in the positions as described .
Patient needs to spend 30 seconds in each of the positions .
It is repeated 5-6 times twice a day.

40. (iv) Surgery
Three surgical procedures have been used to control vertigo.
 (i)Singular neurectomy: The singular nerve supplies the
ampulla and can be approached through the middle ear. The
nerve lies close to the round window membrane at a depth
of 1- 2 mm.
 (ii)Posterior canal occlusion: The posterior canal is exposed
through a transmastoid approach. Drilling is done to reach
the perilymphatic space and then plugged with fascia and
bone dust. Again, sensorineural hearing loss can occur in
about 5 of cases. It is an effective procedure to control
vertigo and has been recommended as the procedure of
choice.
 (iii)Vestibular nerve section: Vestibular nerve is sectioned
through the middle cranial fossa. Although this procedure
controls vertigo, it entails an intracranial operation with its
attendant risks.

41. B For central vertigo -
Vertebrobasilar insufficiency(TIA)
 BP control, lipid and blood sugars control,
smoking caesation.
 Aspirin, anticoagulation as per requirement.
 Vestibular suppressant medications plus initiation
of rehabilitation procedures.
 Cerebral activators –
 (i)Piracetam –
2.4 to 3.6 gm daily in 3 divided doses .
Side effects -Insomnia, Hyperkinesia, GI upset
Contra indicated in recent MI, pregnancy, renal
and hepatic diseases.
 (ii)Priabedil - 50 mg once daily.

42. Take home message
1. First decide between true vertigo and pseudovertigo.
2. Then differentiate between peripheral and central vertigo.
3. Peripheral causes are common .Cervical spondylitis is not
usually a cause of Vertigo.
4. Vertical nystagmus is due to a central neurological cause until
proved otherwise. Central causes are not too many but need
urgent recognition as they have different treatment and
prognosis.
5. Cinnarizine can be prescribed in both central and peripheral
causes of vertigo.
6. Betahistine is prescribed mainly in meniere’s disease and also
in other peripheral vertigo cases. Both the vestibular
suppressants should be prescribed for minimum possible
interval of time and not for long .
7. BPPV occurs in 40 % cases of peripheral vertigo. It is treated
by Epley’s method.
8. Adaptation exercise should be highlighted in clinical practice.
Reality is merely an illusion, albeit a very persistent one- Albert Einstein