As the world Turns

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Presented by Dr. Johar Iqbal
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VERTIGO

• BY DR. JOHAR IQBAL
• TMO, FCPS II,
• ENT, HMC.

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CONTENTS

• Difference between dizziness and vertigo.
• Diagnostic approach to True vertigo.
• Characteristics of Peripheral vertigo.
• Characteristics of Central vertigo.
• Treatment Considerations.

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Patients refer to Dizziness as

• Light headedness
• Sense of strangeness
• Faintness
• Giddy
• Imbalanced

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Most dizzy patients can be placed in to one of
four categories

• 1-True Vertigo (50)
• 2-Pre-syncope
• 3-Dysequilibrium
• 4-Vague lightheadedness

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Most dizzy patients can be placed in to one of
four categories

• 1-True Vertigo (50)
• 2-Pre-syncope
• Transient sensation that a faint is about to
  occur.
• May present as nausea ,weakness, SOB or change
  in vision.

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Most dizzy patients can be placed in to one of
four categories

• 3-Dysequilibrium
• A sensation of imbalance when standing or
  walking.
• No illusion.
• No sense of faintness.
• 4-Vague lightheadedness
• Psychiatric disorders,
• Hyperventilation syndrome
• Encephalopathies

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What is Vertigo?
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True vertigo

• Defined as an illusion or hallucination of
  movement.
• Both vertigo and dysequilibrium imply a loss of
  balance,
• but vertigo involves a sense of motion.

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How do we maintain equilibrium?
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Visual input
EQUILIBRIUM
Proprioceptiual input
Vestibular input labyrinths.
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Anatomy Semicircular canals

• Semicircular Canals (SCC)
• Horizontal
• Anterior
• Posterior
• Cupula
• End organ receptors
• Endolymph

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Anatomy Utricle

• Utricle
• Connected to SCC
• Contains endolymph
• Otoliths (otoconia)
• Calcium carbonate
• Attached to hair cells
• Maculae (end organ)

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Sensory hair cells of the vestibular organs.
TypeI (left) and Type II (right).
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VESTIBULAR SYSTEM

• Tells brain which way the head moves without
  looking
• SCC Angular acceleration
• Utricle Saccule Static Linear acceleration

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Scarpas ganglion
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CENTRAL VESTIBULAR CONNECTION

• The fibres of vestibular nerve end in vestibular
  nuclei and some go to the cerebellum directly.
• Vestibular nuclei are four in number,
• Superior,
• Medial,
• Lateral and
• Descending.
• Afferents to these nuclei come from
• (i) Peripheral vestibular receptors (semicircular
  canals,utricle and saccule)
• (ii) Cerebellum
• (iii) Reticular formation
• (iv) Spinal cord
• (v ) Contralateral vestibular nuclei.

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CENTRAL VESTIBULAR CONNECTION

• Efferents from vestibular nuclei go to
• (i) Nuclei of CN Ill,IV,VI via medial
  longitudinal bundle.
• It is the pathway for vestibulo-ocular reflexes
  and this explains the genesis of nystagmus.
• (ii) Motor part of spinal cord (vestibulospinal
  fibres).
• This coordinates the movements of head, neck and
  body in the maintenance of balance.

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CENTRAL VESTIBULAR CONNECTION

• (iii) Cerebellum (vestibulocerebellar fibres).
• It helps to coordinate input information to
  maintain the body balance.
• (iv) Autonomic nervous system.
• This explains nausea,vomiting,palpitation,sweating
  and pallor seen in vestibular disorders
  (e.g.Meniere's disease).
• (v) Vestibular nuclei of the opposite side.
• (vi) Cerebral cortex (temporal lobe).
• This is responsible for subjective awareness of
  motion.

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How can we clinically evaluate the patient with
vertigo?
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CN VIII (Vestibular portion)
Labyrinth
Vertigo
Cerebellum
Brainstem
Vestibular nuclei
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Vertigo
Central (5)
Peripheral (95)
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CAUSES OF VERTIGO

• PERIPHERAL
• BPPV
• Meniers disease
• Acute labyrinthitis
• Vestibular neuronitis
• Vestibulotoxic drugs
• Head trauma
• Perilymphatic fistula
• Syphilis

• CENTRAL
• Vertebrobasillar insufficiency
• Cerebellopontine angle tumor
• Cerebrovascular disease
• Basilar Migraine
• Multiple sclerosis
• Posterior inferior cerebellar artery syndrome
• Cervical vertigo

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VARIETY OF DISORDERS THAT GIVE RISE TO VESTIBULAR
DYSFUNCTION

• Ocular pathology LABYRINTHINE pathology
  CNS Disease
• CVS disorders Psychiatric morbidity
• Renal disease
• Genetic disorders Haematological disorders
  Endocrine disorders
• Orthopedic/ Rheumatological Autoimmune disease

VESTIBULAR DYSFUNCTION
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NONVESTIBULAR CAUSES OF DIZZINESS

• Endocrine HypogIycemia
• 
  Adrenal failure
• 
  Pheochromocytoma
• Cardiovascular Vasovagal syncope
• 
  Orthostatic hypotension
• 
  Embolic disease
• 
  Cardiac dysrrhythmias
• Hematological Hyperviscosity syndromes
• 
  Anaemias
• Psychological Anxiety
• 
  Phobias
• 
  Panic attacks

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• Both dr. and patient get depressed.
• WHY?
• Because they are not at same wave length.
• So a good Hx is of paramount importance.
• In 80 of cases if no Dx is made at the end of
  Hx. Then no Dx can be made at the end of
  examination and investigations.

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HISTORY

• Details of first and recent attacks.
• Duration.
• Body posture
• Episodic or prolonged
• If rotatry Hx and Dx is easy
• If unsteady Hx and Dx is difficult.
• History of systemic disease
• Drug history

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• Associated symptoms such as
• Chronic ear discharge
• Deafness
• Tinnitus
• Nausea
• Vomiting
• Diplopia
• Blurring of vision
• Headache
• Anaesthesia of face.
• Sudden attack of fall and unconsciousness

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SHORT LIVED EPISODIC VERTIGO

• Benign Paroxysmal positional vertigo.
• Labyrinthine fistula.
• Vertebrobasilar insufficiency.

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Vertigo Lasting from few minutes hours

• Menieres disease.
• Syphilitic hydrops.
• Following middle ear surgery.
• Perilymph fistula
• Hyperventilation
• Travel sickness
• Drug induced
• Functional

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Vertigo lasting from days weeks

• Vestibular neuronitis
• Labyrinthitis
• Labyrinthectomy vestibular neuronectomy
• Acoustic neuroma (bilateral)

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EXAMINATION

• Otological Examination (otoscopy,hearing test,
  fistula test) .
• Eye examination (Nystagmus)
• Positional test (Dix- halpike)
• Rapid assessment of cranial nerve.
• Full Neurological examination.
• Cerebellum and balance tests (Romberg test, gait
  test, past pointing falling).
• Peripheral and central pulses, B.P.

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INVESTIGATIONS

• Pure tone audiogram (PTA)
• Caloric tests.
• Electronystagmography.
• Radiological examination CT/MRI.

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PTA IN MENIERS DISEASE
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CALORIC TEST
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At the end of work up, one should be able to know

• Is true vertigo present?

• Have there been auditory symptoms?

• What is the pattern of onset ?

• What is the duration of the symptoms?

• Are there associated neurologic symptoms?

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NYSTAGMUS

• Involuntary Rhythmic oscillation of eyes.
• Visual impulses regulates the position of the
  eyes in relation to the object of visual
  interest.
• Vestibular impulses regulates the position of the
  eyes in relation to head movement via Vestibulo
  ocular reflex.
• video

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DEGREE OF NYSTAGMUS

• 1st degree It is weak nystagmus and is
  present when patient looks in the direction
  of fast component.
• 2nd degree It is stronger than the 1st
  degree nystagmus and is present when patient
  looks straight ahead,
• 3rd degree It is stronger than 2nd
  degree nystagmus and is present even when
  patient looks in the direction of the slow
  component.
• (Alexander' s law)

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Direction of Head rotation Right
Vestibulo-ocular reflex Slow phase of nystagmus
to LEFT
Increased afferent activity Right vestibular
nucleous
Decreased afferent activity Left vestibular
nucleous
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Lateral Rectus
Lateral Rectus
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• In Irritative/Inflammatory lesion, the vestibular
  nuclei on same side become hyperactive i.e.
• Lesion on Rt. Side will stimulate vestibular
  nuclei on Rt. Side,
• Slow phase of nystgmus will be towards Lt.
• While corrective fast component will bring back
  eyes to Rt., so nystgmus will be to Rt.
• I (Irritative)----I (Ipsilateral).
• While reverse occur in paralytic lesion.
• P (Paralytic)----C (Contralateral).

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CHARACTERISTICS OF PERIPHERAL NYSTAGMUS

• Associated with sensation of vertigo
• Has a latent period
• Unidirectional and horizontal and has a fast and
  slow components except in few cases.
• More marked when looking in direction of fast
  phase.
• Is enhanced by removal of optic fixation either
  in darkness or by using frenzels glasses.
• Fatiguable.

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CHARACTERISTICS OF CENTRAL NYSTAGMUS

• Has no latent period.
• Not fatiguable
• May be direction changing, rotatory or
  disconjugate.
• Not affected by removal of optic fixation.

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SPINNED
PERIPHERAL
CENTRAL
Sudden (Onset) Yes Slow, gradual
Positional Yes No
Intensity Severe ill defined
Nausea/Diaphoresis Frequent Infrequent
Nystagmus Horizontal/ torsional Vertical/ direction changing
Ear Can be present Absent
Duration Paroxysmal Constant
CNS signs Absent Usually present
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PERIPHERAL VERTIGO

• Approximation 95 of ED patients with vertigo.

• Due to dysfunction of one of vestibular organs.

• Asymmetry of input

• Sensation of rotation

• Associated with nausea, pallor and diaphoresis.

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PERIPHERAL (Lesions of end organvestibular
nerve)

• Benign paroxysmal positional vertigo
• Meniere's disease
• Vestibular neuronitis
• Labyrinthitis
• Vestibulotoxic drugs
• Head trauma
• Perilymph fistula
• Syphilis
• Acoustic neuroma

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BPPV

• Benign Paroxysmal Positional Vertigo
• Age 60-70 years
• FM, 21
• Head trauma
• Commonest cause of peripheral vertigo
• Brief violent attacks of vertigo provoked by
  certain head positions
• No auditory symptoms

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Characteristic of BPPV

• Turn head
• After a few seconds delay, vertigo occurs
• Resolves within 1 minute if you dont move
• If you turn your head back, vertigo recurs in the
  opposite direction

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BPPV

• B Benign
• Not a brain tumor
• Can be severe and disabling

• P Paroxysmal
• Episodic, not persistent
• Helpful feature in the differential diagnosis

• P Positional
• Occurs with position of head
• Turning over in bed
• Looking up
• Bending over

• V Vertigo
• An illusion of motion
• The room is spinning

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PATHOPHYSIOLOGY OF BPPV

• Otoliths become detached from hair cells in
  utricle
• Inappropriately enter the posterior semicircular
  canal

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Structure of macula, the sensory end organ of
the utricle and the saccule.
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PHYSIOLOGY

• Normal situation
• As one turns head to the right
• Endolymph moves ?SCC receptors fire ? head
  turning right
• Stop turning head? endolymph stops moving ? SCC
  receptors stop firing ? head has stopped moving

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PATHOPHYSIOLOGY OF BPPV

• BPPV
• Stop turning head ? otoliths keep moving ? drag
  endolymph ? receptors continue to fire
  inappropriately ? head is still moving
• Eyes ? head is NOT moving
• Brain ? room must be spinning in the opposite
  direction

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DIX-HALLPIKE MANEUVER

• The diagnosis of BPPV is generally from the
• history.

• Can confirm the diagnosis of BPPV

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DIX-HALLPIKE MANEUVER
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 testing
6-Reverse of nystagmus on returning to upright
position.
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DIX-HALLPIKE MANEUVER
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EPLEY MANEUVER

• 1. Repeat Hallpike
• Previously performed diagnostic Hallpike test
  tells you the starting position (right or left)

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EPLEY MANEUVER

• 2. Turn head 90 degrees in the other direction

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EPLEY MANEUVER

• 3. Patient rolls onto shoulder, rotates head and
  looks down towards floor

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EPLEY MANEUVER
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MENIERES DISEASE

• Characterized by triad of
• Vertigo
• Tinnitus
• Hearing loss (sensorineural)
• Chronic relapsing illness (? familial)
• Due to a build-up of endolymphatic pressure in
  the labyrinth.
• Investigations
• Pure tone audiogram
• Electrocochleography

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MENIERES DISEASE

• Medical Treatment
• Bed rest
• Fluid and salt restriction
• Vestibular sedatives / vasodilators.
• Systemic steroids / intra tympanic injection.
• Surgical Treatment
• Sac decompression
• Cervical sympathectomy
• Vestibular nerve section
• Labyrinthectomy

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VESTIBULAR NEURONITIS

• Acute unilateral loss of peripheral vestibular
  function
• Voilent attacks of rotatory vertigo, nausea and
  vomiting
• Worsened by head movement
• Followed by slow but gradual recovery over a
  period of 10 days to 03 weeks.
• Occurs in healthy young to middle-aged adults
• Often after respiratory infections
• Hearing is normal.
• Self-limiting

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LABYRINTHITIS

• Viral and bacterial
• Serous or purulent
• Severe rotatory vertigo, vomiting and profound
  sensorineural deafness
• Irritative nystagmus in the initial stage
  followed by paralytic nystagmus.
• IV Antibiotics in the initial stage with
  labyrnthine sedatives
• Mastoidectomy

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VESTIBULOTOXIC DRUGS

• By damaging the inner hair cells of the inner
  ear.
• Aminoglycoside antibiotics particularly
• Streptomycin,
• Gentamicin,
• Kanamycin
• Affect hair cells of the crista ampullaris and to
  some extent those of the maculae.
• Other drugs
• Antihypertensives,
• Labyrinthine sedatives,
• Oestrogen preparations,
• Diuretics,
• Anti microbials (nalidixic acid,metronidazole)
  and
• Antimalarial.

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HEAD TRAUMA

• Head injury may cause concussion of labyrinth,
• Completely disrupt the bony labyrinth or VIllth
  nerve,or cause a perilymph fistula.
• Severe acoustic trauma,such as caused by an
  explosion can also disturb the vestibular end
  organ (otoliths) and result in vertigo.

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PERILYMPH FISTULA

• Perilymph leaks into the middle ear through the
  oval or round window.
• Follow as a complication of stapedectomy,or ear
  surgery when stapes is accidentally dislocated.
• Also result from sudden pressure changes in the
  middle ear e.g barotrauma,diving,forceful
  Valsalva or raised intracranial pressure (weight
  lifting or vigorous coughing).
• Causes intermittent vertigo and fluctuating
  sensorineural hearing loss,sometimes with
  tinnitus and sense of fullness in the ear.

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ACOUSTIC NEUROMA

• Classified in peripheral vestibular disorders as
  it arises from CN VIII within internal acoustic
  meatus.
• Causes only unsteadiness or vague sensation of
  motion.
• Severe episodic vertigo,as seen in the end organ
  disease,is usually missing.
• Other tumours of temporal bone (e.g. glomus
  tumour,carcinoma of external or middle ear and
  secondaries),destroy the labyrinth directly and
  cause vertigo.

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Rehabilitation Plan

• General Fitness Programme
• Systematic exercise programme
• Cawthorne Cooksey exercises

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CAWTHORNE COOKSEY EXERCISES

• A. Resting
• Eye movements
• At first slow then quick, up and down
• From side to side focusing on finger moving from
  the face three feet to one feet.
• Head movements
• At first slow then quick
• Later with eye close
• Bending forward and backwards
• Turning by side to side.

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CAWTHORNE COOKSEY EXERCISES

• B. Sitting
• First two points are as above
• Shoulder shrugging and circling
• Bending forward and picking objects from the
  ground

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CAWTHORNE COOKSEY EXERCISES

• C. Standing
• A-1,2 and B3.
• Changing from setting to standing position, the
  eyes open and closed
• Throwing a ball from hand to hand above eye
  level.
• Changing from sitting to standing and turning
  around in between.

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CAWTHORNE COOKSEY EXERCISES

• D. Moving About
• Walk across the room with eyes open and then
  closed.
• Walk up and down the slope with eyes open and
  then close
• Walk up and down steps with eyes open and then
  close
• Any game involving stoping or stretching and
  aiming such as basket ball.

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PSYCHOLOGICAL SUPPORT
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THANKS