This document discusses vertigo, including its causes and management. It defines vertigo as a subjective sense of imbalance or spinning. The vestibular system, which includes the inner ear and brainstem regions, provides input about movement and spatial orientation. Disruptions in the vestibular system or its central connections can cause vertigo. Common causes include benign paroxysmal positional vertigo (BPPV), Ménière's disease, vestibular neuronitis, and acoustic neuromas. Treatment depends on the cause but may include repositioning maneuvers, medications, or surgery. A thorough history and physical exam are important for diagnosis.

1. VERTIGO: CAUSES &
MANAGEMENT
Dr Harjitpal Singh
Assistant Professor(ENT),
Dr RKGMC, Hamirpur.

2. DEFINITION
SUBJECTIVE SENSE OF IMBALANCE
“Sensation as if the external world is
revolving around the patient or as if he
himself is revolving in space”

3. VESTIBULAR SYSTEM
 Peripheral vestibular system:-include the vestibular apparatus( 3 SCC ,
Utricle & Saccule) and vestibular nerve
 Five Vestibular Receptor organs are present in the Vestibular Labyrinth.
o Two Maculae in utricle and saccule (otolith organs) --- Linear
Acceleration.
o Three Cristae Ampullares of SSC --- Angular Accleration.
 Central vestibular system(within CNS):starts from vestibular nuclei in the
Pons and its central connection(including cerebellum)

4. PATHOPHYSIOLOGY
Balance requires –
 Normal functioning vestibular system
 Input from visual system (vestibulo-ocular)
 Input from proprioceptive system (vestibulo-spinal)
Central causes compromise central circuits that
mediate vestibular influences on posture, gaze control,
autonomic function
Disruption of balance between inputs results in vertigo
Goal of treatment: restore balance between different
inputs

5. PATHOPHYSIOLOGY(cont)
Vestibular system influences autonomic system
Intimate linkage in brainstem pathways between
vestibular and visceral inputs
Alteration of vestibular inputs results in:
Nausea, vomiting
Pallor
Respiratory/circulatory changes

6. Causes of peripheral vestibular system
Like any organ in the body, the vestibular system can be affect by:-
A) Congenital malformation:-but it is a symptomatic as central compensation occur early
in infancy
B) Acquired:-
1.Infections:- bacterial or viral ;acute or chronic e.g labrynthitis, vestibular neuritis,
syphilis
2.Tumour:-like acoustic neuroma(vestibular schwannoma)
3.Trauma:-temporal bone fracture, perilymph fistula
4.Autoimmune:- autoimmune inner ear diseases
5.Vascular:- labyrinthine apoplexy
6.Degenerative:- Dysequilibrium of ageing (presbyastasis )
7.Miscillaneous:- Meniere's disease, benign paroxysmal positional vertigo(BPPV)

7. CLASSIFICATION
• ANATOMICAL
• DURATION OF VERTIGO
• NATURE OF VERTIGO

8. ANATOMICAL
A) PERIPHERAL VESTIBULAR DISORDERS
 BPPV
 Meneir’s disease
 Vestibular neuronitis
 Labyrinthitis
 Vestibulotoxic drugs
 Head trauma
 Perilymph fistula
 Syphilis
 Acoustic neuroma

9. ANATOMICAL(cont)
B) CENTRAL VESTIBULAR DISORDERS
Vertebrobasilar insufficiency
Posterior inferior cerebellar artery syndrome
Basilar migraine
Cerebellar disease
Multiple sclerosis
Tumors of brainstem
Epilepsy

10. DURATION OF VERTIGO

11. NATURE OF VERTIGO
ROTATIONAL
UNSTEADINESS

12. ROTATIONAL
BPPV
Labyrinth fistula
Vertebrobasilar insufficincey
Meniere’s disease
Vestibular neuronitis
Trauma
Labyrinthitis
Metastatic deposits in CP angle

13. UNSTEADINESS
Drugs
Travel sickness
Perilymph fistula
Hyperventillation
Vestibular insufficiency
CNS lesions

14. BENIGN PAROXYSMAL POSITIONAL
VERTIGO (BPPV)
 Most common cause
 Dysfunction of posterior SCC
 Cupulolithiasis vs. Canalithiasis
 Cupulolithiasis
 Calcium deposits embedded on cupula
 PSCC becomes dependent on gravity
 Canalithiasis
 Calcium debris (otoconia) displaced into PSCC
 Does not adhere to cupula

15. BPPV(cont)
 Head movements
 Looking up
 Lying down
 Rolling onto affected ear
 Result in displacement of “sludge” / otoconia
 Vertigo lasting a few seconds
 Treatment approaches
 Laboratory maneuvers
 Particle repositioning
 Habituation exercises

16. MENIERE’S DISEASE
Is an inner ear disease characterized by :-
• Episodic vertigo ,hearing loss ,tinnitus and
ear fullness lasting for minutes –days.
• The disease affect cochlea and SCC and
vestibule(whole membranous labyrinth)
which reflect its symptoms

17. MENIERE’S DISEASE (cont)
Pathogenesis
Distension of the membranous labyrinth or
endolymphatic hydrops is postulated as a
cause of this condition either due to excessive
production or impair absorption of endolymph
The attack occurs due to small ruptures in
Reissner membrane leading to mixing of the
endolymph and perilymph.

18. MENIERE’S DISEASE (cont)
Clinical features
 The duration of the vertigo last usually for 30 minutes
to 4 hours
 The vertigo is often disabling and very acute in onset
 Associated with nausea and vomiting
 The patient feels tired for the next few days after the
attack.

19. MENIERE’S DISEASE (cont)
 Hearing loss is sensorineural in type and in early stage of the disease affects the
lower frequencies and return to normal after the attack (fluctuating hearing loss )
 Tinnitus and a feeling of fullness or pressure in the affected ear may precedes the
attack
 Over the course of the disease hearing loss and tinnitus become permanent
 The disease is usually unilateral initially but can become bilateral
 Sign:- spontaneous rotatory nystagmus
 Investigations:- P.T.A. , brain MRI may be needed to role out central causes

20. ACOUSTIC NEUROMA
Vestibular symptoms are variable and tinnitus
is common.
Diagnosis is made on the basis of radiological
investigations.
 Treatment depends upon size of tumour.
 Various modalities are surgery, steriotactic surgery.

21. VESTIBULAR NEURITIS
Etiology
 Most likely due to viral infection supported by polymerase chain reaction to detect viral DNA
 In postmortem study mostly Herpes simplex virus type one
Symptoms
 Acute spontaneous vertigo associated with nausea and vomiting lasting from days –weeks,
 No cochlear & CNS involvement, no
 The symptoms subside over the following days but many patients have residual imbalance that
last for months .
 Hearing is normal
Sign
 Acute attack there is nystagmus (horizontal towards the unaffected side )
 After acute stage passed, nystagmus disappear but patient characteristically rotate towards the
affected side when attempt to march on a spot with their eyes closed positive Unterberger test
 PTA ,brain MRI may be needed if central vertigo cannot be excluded easily

22. TRAUMATIC INNER EAR DISEASE
 Non-Operative: Labyrinthine concussion or fracture of temporal bone.
 Post-Operative: A perilymph fistula may occur after ear surgery esp.
`stapedectomy
Temporal bone fractures
 Longitudinal fractures 80 -90 % , Usually spare the labyrinth and facial
nerve
 Transverse fractures 10- 20% , Transverse fracture usually involve the
labyrinth and thus lead to sensorineural hearing loss with profound
vertigo. This vertigo will settle with time as central compensation occurs .

23. TRAUMATIC INNER EAR DISEASE(cont)
Management
 For fracture itself--conservative plus broad spectrum antibiotic
 Vertigo---vestibular sedative
 Haemotympanum----conservative treatment usually resolves within 3-4 weeks
 Tympanic membrane perforation----usually heals within 3 months if persists then myringoplasty
 Facial nerve paralysis:
a. Immediate paralysis treated by surgical exploration with attempt to repair the nerve.
b. Delayed paralysis : usually treated conservatively
 CSF leak :
 Medical treatment : bed rest ,head elevation, stool softener , lumbar drain and antibiotics to
prevent meningitis
 Surgical closure of the defect if medical treatment fail

24. LABYRINTHITIS
Inflammation of labyrinth due to any cause.
May be viral or bacterial.
Viral may occur during course of an
exanthematous disease like mumps/measles
or influenza type illness.
Bacterial labyrinthitis may be circumscribed,
serous or suppurative in a case of otorrhoea.
It may also occur during course of meningitis.

25. SUPERIOR SEMICIRCULAR CANAL
DEHISCENCE SYNDROME
Syndrome of vertigo and oscillopsia induced by
loud noises or by stimuli that change middle
ear or intracranial pressure
 Tullio phenomenon - eye movement - loud noise
Hennebert's sign
 “Third mobile window

26. MIGRAINE
Concomitant vertigo and disequilibrium
Headache control improves vertigo
Diagnostic criteria
Personal/family history
Motion intolerance
Vestibular symptoms - do not fit other causes
Theories - vascular origin, abnormal neural
activity (brainstem), abnormal voltage-gated
calcium channel genes.

27. VERTEBROBASILAR INSUFFICIENCY
Vertigo, diplopia, dysarthria, gait ataxia and
bilateral sensory & motor disturbance
Transient ischemia - low stroke risk
Antiplatelet therapy - aspirin 325mg qD
Ticlid
Platelet aggregate inhibitor
Risk of life-threatening neutropenia
Only in patients unable to tolerate aspirin

28. CNS NEOPLASM
Tumors involving brainstem, cerebellum or
midbrain
Other signs of intracranial disease are found
On ENG nystagmus is found to be irregular
and enhanced on eye opening.

29. POSTERIOR INFERIOR CEREBELLAR ARTERY
THROMBOSIS (LATERAL MEDULLARY SYNDROME
Onset is with severe vertigo with contralateral
hemianalgesia.

30. Management

31. HISTORY
DESCRIPTION
 Ask the patient to describe the problem
 True rotatory vertigo or dizziness.
 Severity
 Number of attacks
 Temporal pattern (continuous vs. episodic / short vs. prolonged)
 If associated with turning the head, lying supine, or sitting upright.
 Vestibular & cochlear symptoms (hearing loss either fluctuating or progressive, tinnitus, ear
pressure, nausea and vomiting)
 Degree of impairment during the attack
 Syncope:Transient loss of consciousness with loss of postural tone
 Presyncope: Lightheadedness-an impending loss of consciousness
 Psychiatric dizziness: Dizziness not related to vestibular dysfunction
 Disequilibrium: Feeling of unsteadiness, imbalance or sensation of “floating” while walking

32. SECONDARY SYMPTOMS
Tinnitis
Hearing impairment
Headache or visual symptoms.
Neurological abnormalities
• Brainstem symptoms (diplopoia, dysarthria,
facial paraesthesia, extremity numbness or
weakness.)

33. PREVIOUS HISTORY
 Injuries:
 Head trauma in the past (post traumatic hydrops)
 History Of prior ear surgery (labyrinthine fistula,
perilymphatic fistula.)
 Drugs : Aminoglycosides, cisplatin, miocycline
 Stress situations
 Family illness
 Systemic Diseases:
 History of DM (causes visual, proprioceptive, vascular
problems) HTN, cardiovascular and cerebrovascular
diseases

34. GPE
 Cardiovascular, BP (including orthostatic) in both
arms, pulse
 Neurologic
ENT HEAD AND NECK EXAMINATION
 Detailed ENT Examination
 Tympanic membrane for retraction, perforation,
Infection, cholesteatoma,valsalva
 Assess hearing on both sides
 Cranial nerves
 Bruits in the neck

35. SPECIFIC VESTIBULAR SYSTEM EXAMINATION
(Balance tests need not be performed in acute vertigo)
 Nystagmus
 Corneal test
 Fistula test
 Romberg test
 Gait
 Past-pointing and falling
 Hallpike-manoeuvre (positional test)
 Caloric tests
 Electronystagmography
 Test of cerebellar dysfunction

36. Nystagmus
 Defined as involuntary, rhythmical, oscillatory
movement of eyes
 It is an important sign in evaluation of vestibular
system
 It can be either horizontal /vertical/rotatory nystagmus
 It has 2 components : SLOW & FAST
 The direction of fast component indicates the direction
of the nystagmus
 Slow component usually ipsilateral to diseased
structure
 Fast component due to cortical correction

37.  Intensity of nystagmus is indicated by its degree.
 AS PER ALEXANDER’S LAW
 1st DEGREE
It is weak nystagmus and is present when patient looks in the direction of fast
component
 2nd DEGREE
It is stronger than 1st degree and is present when patient looks straight ahead
 3rd DEGREE
It is stronger than the 2nd degree and is present when the patient looks in the direction
of the slow component
 This law may not hold true in case of nystagmus of central region

38.  PRESENCE of spontaneous nystagmus is indicative of ORGANIC LESIONS - Tone
of imbalance of vestibulo-ocular reflux
 Peripheral nystagmus – is suppressed by optic fixation
 Enhanced by darkness and use of FRENZEL GLASS
 Central nystagmus is not supressed by optic fixation
 TORSIONAL NYSTAGMUS – Indicates lesion of brainstem/vestibular nuclei e.g.
SYRINGOMYELIA
 VERTICAL DOWNBEAT NYSTAGMUS – Lesion is at cranio-cervical region e.g.
Arnold-chiari malformation/degenerative lesion of cerebellum
 VERTICAL UPBEAT NYSTAGMUS – Lesion at the junction of pons and
medulla/pons and midbrain
 PENDULAR NYSTAGMUS – congenital/acquired e.g. Multiple sclerosis
 May also be disconjugate Via., vertical in one eye and horizontal in other.

39. Central Peripheral
Spontaneous nystagmus that cannot be Suppressed by fixation suppressed by fixation.
Changes direction with gaze Doesn’t change direction
with gaze.
Purely vertical, Horizontal, rotatory,
horizontal, or torsional Never vertical
Paroxysmal but Not fatigable Paroxysmal but fatigable in
in Dix-hallpike test, Dix-hallpike test, has latency,
no latency, Lasting lasts less than a minute,
longer than 60 sec. and doesn't change direction with
often vertical, may different head positions.
change direction with
different head positions.

40. CORNEAL TEST
Loss of corneal reflex -- Cerrebelopontine
Angle Lesion

41. FISTULA TEST
Apply intermittent pressure on tragus OR By using Siegel's speculum
 IN NORMAL PERSON: NEGATIVE
 Because pressure changes in external auditory canal can’t be transmitted to
labyrinth
 ABNORMALITY: POSITIVE
 Erosion of horizontal semi-circular canal- cholesteatoma
 Surgically created window in horizontal canal- fenestration operation
 Abnormal opening in oval window- post stapedectomy fistula
 Abnormal opening in round window- rupture of round window membrane
 ALSO INDICATES THAT LABYRINTH IS STILL FUNCTIONAL

42.  FALSE NEGATIVE FISTULA TEST :
 IN CHOLESTEATOMA: it covers the site of fistula and it
doesn’t allow pressure changes to be transmitted to the
labyrinth
 IN LABYRINTH DEAD
 FALSE POSITIVE FISTULA TEST :
 Means +ve test without presence of fistula
 It is seen in two conditions : 1.congenital syphilis
2.Meniere’s disease.
 Congenital syphilis: stapes footplate is hypermobile
 Meniere’s disease: due to fibrous bands connecting
utricular macula to the stapes footplate.

43. ROMBERG TEST
 Patient is asked to stand with feet together and arms by side with
eyes first open and then closed.
 With eyes open : patient can still compensates the balance
 With eyes closed : patient cant compensate –Here vestibular system
is at more disadvantage
 Central: instability
 Peripheral: Patient sways to side of lesion
 If patient perform this test without sway then SHARPENED
ROMBERG TEST is performed.
• Patient is asked to stand with one heel in front of toes and arms
folded across the chest.
• Inability to perform this test indicates vestibular impairment

44. GAIT
Patient walks along a straight line to a fixed
point first with eyes opened and then closed.
In the case of uncompensated lesion of
peripheral vestibular system, with eyes closed
Patient deviates to affected side

45. HALLPIKE MANOEUVRE (POSITIONAL
TEST)
USES
 When patient complains of vertigo in head position
 Helps to differentiate a peripheral from a central lesion.
METHOD
 Patient sits in the couch
 Examiner holds the patient’s head, turns it 45˚ to the right and then places the
patient in a supine position so that his head hangs 30˚ below the horizontal.
 Patient’s eyes are observed for nystagmus
 The test is repeated with head turned to left and then again in straight head-
hanging position .
 Four parameters are observed:
1. Latency
2. Duration
3. Direction
4. Fatiguability

46. Dix-Hallpike manoeuvre

48. In benign paroxysmal positional vertigo
Nystagmus appears after latency : 2-20s
Duration : less than 1 min
Direction : towards the ear that is under most
• On repetition : Nystagmus may be elicited but
lasts for a shorter period.
• On subsequent repetition : Nystagmus
disappears altogether
• NYSTAGMUS IS FATIGUABLE

49.  IN CENTRAL LESIONS
 Tumours of 4th ventricle
 Cerebellum
 Temporal lobe
 Multiple sclerosis
 Vertibrobasilar insufficiency
 Raised intracranial tension
 Nystagmus is produced immediately as soon as the head is in critical
position
 No latency
 Duration: lasts as long as head is in that critical position
 Direction: changes
 Fatiguability: nonfatiguable

50. TEST OF CEREBELLAR
DYSFUNCTION For cerebellar diseases – all cases of giddiness should be tested.
 CEREBELLAR HEMISPHERE CAUSES:
1. Asynergia(abn finger-nose test)
2. Dysmetria(inability to control range of motion)
3. Adiadochokinesia (inability to perform rapid alternating movements)
4. Rebound phenomenon (inability to control movement of extremity when
opposing forceful restraint is suddenly released)
 MIDLINE DISEASE OF CEREBELLUM CAUSES:
1. Wide base gait
2. Falling in any direction
3. Inability to make sudden turns while walking
4. Truncal ataxia

51. Nystagmus observed in cerebellar diseases
either in hemisphere or midline diseases
include
GAZE
EVOKED NYSTAGMUS
REBOUND NYSTAGMUS
ABNORMAL OPTOKINETIC NYSTAGMUS

52. Caloric test
Patient 45 degrees on couch
Water 33degrees or 45 degrees
Normal nystagmus
COLD: OPPOSITE
WARM: SAME

53. 1.CANAL PARESIS:
Decreased duration of nystagmus
Both hot and cold
2.DEAD LABYRINTH:
No nystagmoid response
3.DIRECTION PREPONDERANCE:
BY Both Hot and Cold
CENTRAL/PERIPHERAL lesion

54. Electronystagmography
Now a routine investigation in Vertigo
ADVANTAGES:
Closed eyes nystagmus recorded
Small amplitude Nystagmus

55. Treatment

56. Medical Treatment
Symptomatic
Specific therapy
Vestibular rehabilitation

57. Symptomatic Pharmacotherapy
 Predominant targeted vestibular neurotransmitters:
• Cholinergic
• Histaminergic
• GABA neurotransmitters - negative inhibition
 Vomiting center transmitters:
• Dopaminergic (D2)
• Histaminergic (H1)
• Seratonergic
 Multiple classes of drugs effective

58. Antihistaminergic – dimenhydrinate
Anticholinergics - scopolamine, meclizine
Anti-dopaminergic - droperidol
Gamma-aminobutyric acid enhancing (GABA-
ergic) agents - lorazepam, valium

59. Some drugs of the antihistamine class are
useful for symptomatic control of vertigo
Have anti-motion sickness properties in large
part due to inhibition of vestibular system H1
histaminergic neurotransmitters
Examples include dimenhydrinate
(Dramamine) and promethazine (Phenergan)
Also suppress the vomiting center

60. Common drugs used for vertigo

61. Specific Pharmacotherapy
Vestibular Neuritis
Meniere’s Disease
Benign Paroxysmal Positional Vertigo
Otosyphilis
Vertebrobasilar Insufficiency
Migraine (with vertigo)

62. Vestibular Neuritis
Acute stage
• Bed rest , vestibular sedative, steroids can be used to
shorten the course of the disease
• Antiviral??
Resolution stage
After vertigo subsides (vestibular rehabilitation
exercise) will enhance central compensation(as it is a
paretic pathology)

63. Meniere's ‘s disease
In acute phase :- treatment consists of
vestibular sedative(stugerone, anti-emetics),
Betahistine(betaserc) ,diuretics
In long term :-avoidance of caffeine and salt
and reassurance can reduce the number of the
attacks and increase the patient ability to cope
with the attacks

64. Surgical Treatment:- rarely needed
A. Endolymphatic sac surgery: By transmastoid
approachch the endolymaphatic sac either
decompressed or a shunt is placed in the sac
that communicates with the subarachnoid
space or mastoid cavity
B. Vestibular nerve section:- in patients with
serviceable hearing
C. Labyrinthectomy : - in patients with
unilateral Meniere’s disease and poor
hearing

65. Ablation therapy
• Gentamycin is given through the tympanic
membrane will be absorbed through the round
window and selectively damage the vestibular
cells relative to the cochlear cells

66. BPPV
Treatment approaches
Liberatory maneuvers
Particle repositioning
Habituation exercises

67. The Epley and Semont Maneuvers
 Are both intended to move debris out of the sensitive
part of the ear (posterior canal) to a less sensitive
location. Each maneuver takes about 15 minutes to
complete.
 Semont maneuver: It involves a procedure whereby the
patient is rapidly moved from lying on one side to lying
on the other.
 Epley Maneuver: It involves sequential movement of
the head into four positions, staying in each position for
roughly 30 seconds

68. Modified Epley Maneuver

69. Semont maneuver

70. Home Treatment Of BPPV:
Brandt-Daroff Exercises
 The Brandt-Daroff Exercises is a method of treating BPPV, usually used
when the office treatment fails. They succeed in 95% of cases.

71. Selective posterior canal plugging offers a
reasonable surgical approach to intractable
symptoms.
Singular neurectomy, an older procedure, is
less popular because it produces hearing loss
in 7 to 17% of patients and fails in 8 to 12%.

72. Otosyphilis
Penicillin established treatment
IM and IV routes acceptable
IM - 2.4 million units benzathine PCN weekly
x 3 consecutive weeks is minimal treatment
(some advocate up to 1 year)
IV - 10 million units PCN G qD in divided
doses x 10 days, followed by 2.4 million units
benzathine PCN x 2 weeks

73. Vertebrobasilar insufficiency
 Vertigo, diplopia, dysarthria, gait ataxia and bilateral sensory &
motor disturbance
 Transient ischemia - low stroke risk
 Antiplatelet therapy - aspirin
 Ticlid
 Platelet aggregate inhibitor
 Risk of life-threatening neutropenia
 Only in patients unable to tolerate aspirin

74. Migraine
Treatment
 Modifying risk factors
 Exercise and diet
 Avoid nicotine, caffeine, red wine and chocolate
 Abortive medical therapy
 Ergots
 Sumatriptin
 Midrin
 Prophylactic medical therapy
 B blockers, Ca channel blockers, NSAIDs, amitryptiline, and lithium

75. Vestibular Rehabilitation
• Promoting vestibular compensation
• Habituation
• Enhancing adaptation of VOR & VSR
• May have initial exacerbation

76. Cawthorne Cooksey Exercises:
Sitting
 Eye movements and head movements
 Shoulder shrugging and circling
 Bending forward and picking up objects from the ground
Standing
 Eye, head and shoulder movements as before
 Changing form sitting to standing position with eyes open and shut
 Throwing a small ball from hand to hand (above eye level)
 Throwing a ball from hand to hand under knee
 Changing from sitting to standing and turning around in between
Moving about (in class)
 Circle around center person who will throw a large ball and to whom it will be
returned
 Walk across room with eyes open and then closed

77. Habituation of pathologic responses
Postural control exercises
Visual-vestibular interaction
Conditioning activities
B.I.D., most improve after 4-6 weeks
VRT - Elderly
Multifactorial causes of balance difficulty
Need 2 of 3 systems functional : vestibular, visual,
proprioceptive

78. Conclusions
Vestibular complaints common to ENT
Thorough evaluation and understanding
Dx and treat acute symptoms
Wean vestibular suppressants
Specific pharmacotherapy instituted
Chronic, uncompensated disease benefits from
early VRT

79. THANKS