DR AGBONIFO M CONSULTANT E.N.T SURGEON ISTH, IRRUA. EDO STATE. DIZZINESS, VERTIGO & IMBALANCE.

DR AGBONIFO M

CONSULTANT E .N.T SURGEONISTH, IRRUA.EDO STATE.

DIZZINESS, VERTIGO & IMBALANCE

PRETEST ABOUT VERTIGOIT IS ALSO REFFERED TO AS DIZZINESSIT IS AN INNER EAR DISEASEIT IS DEFINED AS HALLUCINATION OF

MOVEMENTA VERY IMPORTANT COMPONENT OF IT IS

NYSTAGMUS

BPPV:MEANS BENIGH PAROXYSMAL

POSITIONAL VERTIGOIT IS THE COMMONEST CAUSE OF

PERIPHERAL VERTIGOIT IS ASSOCIATED WITH HEARING LOSSTREATMENT IS SURGICAL

DIX HALLPIKE TEST IS AN OFFICE PROCEDURE TO DIAGNOSE MENIERE’S DX

MEDICAL TREATMENT FOR VERTIGO INCLUDE THE USE OF BETAHISTINE

CAUSE OF PERIPHERAL VERTIGO INCLUDE MENIERE’S DX

CENTRAL VERTIGO COULD BE CAUSED BY C.V.A

SURGICAL TREATMENT IS THE FIRST LINE OF TREATMENT FOR BPPV

CAUSES OF VERTIGO IS VERTIGO

OUTLINE

INTRODUCTIONANATOMY &PATHOPHYSIOLOGY

(VESTIBULAR APPARATUS)AETIOLOGYCLINICAL FEATURESINVESTIGATIONTREATMENTREHABILITATIONCONCLUSION

INTRODUCTION

For the otolaryngologist the dizzy Pt often presents a diagnostic challenge, therefore the clinical evaluation has the following basic objectives:

It aims to present the basic knowledge and concept of symptom of dizziness

It presents the clinical approach to evaluating the dizzy patient. To differentiate different causes of dizziness, vertigo and imbalance

It explains the skills needed in primary care and secondary care settings of managing a dizzy patient

It aims to bring about positive attitudinal changes in the management of dizzy patients

Introduction cont…

It is a common symptom especially with increasing age

We have to distinguish between VERTIGO andNONVERTIGO

A critical distinction is differentiating vertigo from nonvertigo

Central and peripheral vertigo

Definitions

Vertigo is the true rotational movement of self or the surroundings.

Nonvertigo includes light-headedness, unsteadiness, motion intolerance, imbalance, floating, or a tilting sensation.

This dichotomy is helpful because true vertigo is often due to inner-ear disease, whereas symptoms of nonvertigo may be due to CNS, cardiovascular, or systemic diseases.

Nystagmus is involuntary rapid movt of the eyes.

Definitions cont

It can be horizontal (back & forth ; left & right), vertical (up & down) or rotatory. It has 2 phases ; slow & fast . The slow phase originates from the vestibular system and fast corrective phase from the brain.

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ANATOMY/ PATHOPHYSIOLOGY

MAITENANCE OF BALANCE RELIES UPON

INPUTS FROM

VISUAL(70%)

VESTIBULAR(15%)

PROPRIOCEPTIVE(15%)

PATHOLOGY IN A WIDE VARIETY OF SYSTEMS

MAY GIVE RISE TO DYSEQUILIBRIUM

.

ANATOMY/PATHOPHYSIOLOGY CONT

Vestibular apparatus is made up of

Membranous and bony labyrinth embedded in petrous part of the temporal bone

5 distinct end organs3 semicircular canals: superior, lateral, posterior

2 otolith organs: utricle and saccule

Anatomy

Copyright ©2003 Canadian Medical Association or its licensors

Parnes, L. S. et al. CMAJ 2003;169:681-693

Osseous (grey/white) and membranous (lavender) labyrinth of the left inner ear


There are five openings into area of utricle

Saccule in spherical recess

Utricle in elliptical recess

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Vestibular labyrinth - detects linear and angular head movements

Semicircular canals - angularHair cells organized under cupula

Otolithic organs (utricle, sacule) - linearHair cells attached to a layer of

otoconiaVestibular nerve - superior, inferior

branchAfferent nerve fibers are bipolar -

cell bodies lie within Scarpa’s ganglion


Afferent fibers terminate in the vestibular nuclei in floor of fourth ventricleSuperior vestibular nucleusLateral vestibular nucleusMedial vestibular nucleusDescending vestibular nucleus


Vestibular nuclei project toCerebellumExtraocular nucleiSpinal cordContralateral vestibular nuclei


Superior vestibular nerve: superior canal, lateral canal, utricle

Inferior vestibular nerve: posterior canal and saccule

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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 fx

Disruption of balance between inputs results in vertigo

Goal of treatment: restore balance between different inputs

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Pathophysiology

Vestibular system influences autonomic system

Intimate linkage in brainstem pathways between vestibular and visceral inputs

Alteration of vestibular inputs results in:nausea, vomitingPallorRespiratory/circulatory changes

VERTIGO

CAUSES:VascularEndocrine/Epilepsy℞eceived (℞)TraumaInfection/InflammatoryGrowth (Tumour)Others (Ophthalmologic, Miscellaneous)

CAUSES OF VERTIGOVASCULAR

Hypertension Orthostatic hypotensionSubclavian steal syndromeCarotid-artery diseaseVertebral-basilar artery insufficiencyArrhythmiaAortic stenosisBradycardia

CAUSES OF VERTIGOENDOCRINE

Diabetis mellitus Hypoglcaemia Thyromegaly Hyperthyroidism/Hypothyroidism Salt losing syndrome

EPILEPSY Temporal lobe epilepsy

HAEMATOLOGIC Anemia Polycythemia Leukemia

CAUSES OF VERTIGORECEIVED DRUGS

Streptomycin Kanamycine Diazepam Sedatives Opiates Alcohol Neuroleptics Aspirin Nicotine Caffeine Prochlorperazine

CAUSES OF VERTIGOTRAUMA

Head injuryNeck injuryFracture semicircular canal

CAUSES OF VERTIGO

INFECTIONS/INFLAMMATORY Influenza Herpes zoster oticus Measles Mumps Syphilis , neurosyphilis Encephalitis Meningitis

( see more under otologic causes)

CAUSES OF VERTIGOGROWTHS (TUMOURS)

Posterior fossa tumoursMetastatic tumours to brainAcoustic neuroma (intracranial)Primary intracranial tumors

GLIAL Multiple sclerosis

CAUSES OF VERTIGOOTHERS

Heat strokeTemporomandibular joint syndromeOsteoarthritisStrokeTransient ischemic attacks

OTOLOGIC

CAUSES OF VERTIGOOTOLOGIC

Bening paroxysmal positional vertigo Vestibular neuronitis Acute serous otitis media Acute labyrinthitis Choleasteatoma Purulent otitis media Petrositis Poststapedectomy syndrome Perilymph fistula Meniere’s syndrome Acoustic neuroma (intracranial) Ototoxic drugs Auto-immune ear diseases

TYPES OF VERTIGO

Peripheral Vertigo: BPPV Vestibular neuronitis Ménière disease Auto-immune inner ear disease Labyrinthitis Acoustic neuroma syphilis

Central Vertigo: Migraine Cerebropontine angle tumours Multiple sclerosis Falls Cerebrovascular disease

CLINICAL FEATURES

HISTORY:A patient who presents with dizziness should

be questioned to distinguish true vertigo and nonvertigo. Ask patient to use other words other than dizziness in describing symptom

The rationale for using other words is that patients may use word dizzy nonspecifically to describe vertigo, unsteadiness, generalized weakness, syncope, presyncope, or falling.

Associated symptoms

Sudden onset and vivid memory of vertiginous episodes are often due to inner-ear disease, especially if hearing loss, ear pressure, or tinnitus is also present.

Gradual and ill-defined symptoms are most common in CNS, cardiac, and systemic diseases.

The time course of vertigo is also important.

Episodic true vertigo that lasts for seconds and is associated with head or body position changes is probably due to benign paroxysmal positional vertigo (BPPV).

Vertigo that lasts for hours or days is probably caused by Ménière disease or vestibular neuronitis.

Vertigo of sudden onset that lasts for minutes can be due to brain or vascular disease, especially if cerebrovascular risk factors are present.

The history should include

review of systems (especially head trauma and/or ear diseases) and screening for anxiety and/or depression.

History of prescription medicines, over-the-counter medications, herbal medicines, and recreational drugs (including smoking and alcohol) can help to identify pharmacologically induced syndromes.

Physical examination

General examination should emphasize

vital signs, supine and standing blood-pressure measurement,

evaluation of the cardiovascular and

neurologic systems.

Ear and Neck examinations

Examine the ears for visible external- and/or middle-ear infection and/or inflammation.

Test hearing by using a tuning fork or by whispering.

( Audiometric tests)Examine the neck for range of motion.

Other Tests

Specific examination of the vestibular system, beyond the ears, nose, throat and neurologic examination, is fundamental to the evaluation of the patient with dizziness.

Clinical assessment of the Vestibular system

The Romberg and single leg standing tests

Assessment of gait with eyes open and closed

A search for past pointingEvidence of spontaneous nystagmusEvidence of positional nystagmusThe fistula tests

Office Examination of the Dizzy Patient

Dix-Hallpike ManeuverUsed to provoke nystagmus and

vertigo commonly associated with BPPV

Head turned 45 degrees to maximally stimulate posterior semicircular canal

Head supported and rapidly placed into head hanging position

Frenzel glasses eliminate visual fixation suppression of response

Dix-Hallpike Maneuver

Dix-Hallpike Maneuver

Positive testUp-beating nystagmusNystagmus to the stimulated sideRotary component to the affected earLasts 15-45 secondsLatency of 2-15 secondsFatigues easily

Pneumatic Otoscopy

Positive and negative pressure applied to middle ear

Hennebert’s sign/symptom – nystagmus and vertigo with pressure, alternates with positive and negative pressure

Can be present in patients with perilymphatic fistula, syphilis, Meninere’s disease, SCC dehiscence syndrome

Dynamic Visual Acuity

Used for bilateral vestibular weakness

Visual acuity checked on Snellen chart

Rechecked while rotating head back and forth at 1-2 Hz.

Loss of 2-3 lines considered abnormal

Romberg Test

Patient asked to stand with feet together and eyes closed

Fall or step is positive testEqual sway with eyes open and closed suggests proprioceptive or cerebellar site

More sway with eyes closed suggests vestibular weakness

Romberg Test

Dysdiadochokinesia Testing

Most commonly tested with the hand slapping test

Abnormalities seen in patients with cerebellar dysfunction

Poor sensitivity and specificity

Tandem Gait Test

Patients are asked to walk heal to toe in a straight line or in a circle

Complex function evaluates many aspects of balance

Poor performance seen in cerebellar lesions, but can be seen in many disorders

Poor sensitivity and specificity

Quantitative Vestibular Testing

Diagnosis unclearProlonged symptoms unresponsive to conservative treatment

Screen for central disordersEvaluate prior to surgical ablation procedures

Documentation of vestibular deficits

Electronystagmography (ENG)

Divided into oculomotor tests, positional and positioning tests, and caloric tests

Only vestibular test with the ability to test individual labyrinths separately

Relies on the vestibulo-ocular reflex (VOR) to test the peripheral vestibular function

Mostly a test of HSCC function

Electronystagmography (ENG)

Oculomotor testsAll test eye movements that originate in the cerebellum

Saccadic trackingSmooth pursuit trackingOptokinetic testing

Oculomotor Tests

Saccadic trackingPatients concentrates on a randomly

moving targetLatency – difference in time between

movement of object and eye (150-250 ms)

Velocity – speed of saccade 200-400 degrees/second low end of normal

Accuracy – amount of undershoot/overshoot of target (75-120%)

Smooth Pursuit Test

Tests ability to accurately and smoothly pursue a target

Gain of eyes compared to movement of target

Saccade movements eliminated from calculations

Asymmetrical pursuit highly suggestive of central disorders

Optokinetic Tests

Vestibular system and optokinetic nystagmus allow steady focus on objects

Target is rapidly passed in front of subject in one direction, then the other

Eye movements are recorded and compared in each direction

Asymmetry suggestive of CNS lesionHigh rate of false positive results

Caloric Testing

Established and widely accepted method of vestibular testing

Most sensitive test of unilateral vestibular weakness

Patient positioned 30 degrees from prone (HSCC vertical allowing max stim)

Cold and warm water/air flushed into EAC

Caloric Testing

COWS (cold opposite, warm same) – direction of the nystagmus

Stimulation in 0.002-0.004 Hz range (Head movements in 1-6 Hz range)

Visual fixation should reduce strength of caloric responses 50-70%

% caloric paresis = 100 * [(LC + LW) – (RC + RW)/(LC + LW + RC + RW)]

Posturography

Used to tests integration of balance systemsUseful in quantification of fall riskMost useful in following conditions:

Chronic disequilibrium and normal examsSuspected malingeringSuspected multifactorial disequilibriumPoorly compensated vestibular injuries

INVESTIGATIONS

Audiogram is routinely needed

Electronystagmography

Caloric testing Radiological Investigation

Blood examination

Gadolinium-enhance MRI – pinpoints site of lesion.

Dynamic posturography - quantifies balancing response to induced sways.

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TREATMENT

TREAT THE CAUSE IF KNOWN

MEDICAL

SURGICAL

PHYSICAL THERAPY

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Medical Treatment

SymptomaticSpecific therapyVestibular rehabilitation

Medical TreatmentMedications 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.

Categories of Drugs commonly used in treatment of dizziness

Antihistamines: eg meclizine, stugerone,• Betahistidine (serc)

Anticholinergics: e.g.Scopolamine (Isopto),

glycopyrrolate (Robinul)Phenothiazines : eg Promethazine,

prochlorperazineBenzodiazepines: eg diazepam (Valium) Monoaminergics: eg ephedrine

Vestibular rehabilitation exercises

Semont manoeuvreParticle repositioning manoeuvre (Epley)

Dix-Hallpike manoevreCawthorne exercisesBrandt-Daroff exercises (dispersing

otolithic debris in the semicircular canals)

Lempert, and Hamid maneuvers, among others.



Fig 9: Liberatory manoeuvre of Semont (right ear)

Fig. 9: Liberatory manoeuvre of Semont (right ear).

The top panel shows the effect of the manoeuvre on the labyrinth as viewed from the front and the induced movement of the canaliths (from blue to black). This manoeuvre relies on inertia, so that the transition from position 2 to 3 must be made very quickly.

Photo: Christine Kenney

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.



Particle repositioning manoeuvre (right ear) (Epley)

Particle repositioning manoeuvre (right ear).

Schema of patient and concurrent movement of posterior/ superior semicircular canals and utricle. The patient is seated on a table as viewed from the right side (A). The remaining parts show the sequential head and body positions of a patient lying down as viewed from the top. Before moving the patient into position B, turn the head 45° to the side being treated (in this case it would be the right side). Patient in normal Dix–Hallpike head-hanging position (B). Particles gravitate in an ampullofugal direction and induce utriculofugal cupular displacement and subsequent counter-clockwise rotatory nystagmus. This position is maintained for 1–2 minutes. The patient's head is then rotated toward the opposite side with the neck in full extension through position C and into position D in a steady motion by rolling the patient onto the opposite lateral side. The change from position B to D should take no longer than 3–5 seconds. Particles continue gravitating in an ampullofugal direction through the common crus into the utricle. The patient's eyes are immediately observed for nystagmus. Position D is maintained for another 1–2 minutes, and then the patient sits back up to position A. D = DIRECTION OF VIEW OF LABYRINTH, DARK CIRCLE = POSITION OF PARTICLE CONGLOMERATE, OPEN CIRCLE = PREVIOUS POSITION. ADAPTED FROM PARNES AND ROBICHAUD (Otolaryngol Head Neck Surg 1997;116: 238-43).45 Photo: Christine Kenney

Surgical Care:Surgery is usually reserved for those in whom CRP fails. It is not a first-line treatment because it is invasive and holds the possibility of complications such as hearing loss and facial nerve damage.

Surgical Care:

Options includelabyrinthectomy, posterior canal occlusion, singular neurectomy, Vestibular nerve section, and transtympanic aminoglycoside application.

All have a high chance of vertigo control.

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Conclusions

Vestibular complaints common to ENTThorough evaluation and

understandingDx and treat acute symptomsWean vestibular suppressantsSpecific pharmacotherapy institutedChronic, uncompensated disease

benefits from early VRT

DR AGBONIFO M CONSULTANT E.N.T SURGEON ISTH, IRRUA. EDO STATE. DIZZINESS, VERTIGO & IMBALANCE.

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Transcript of DR AGBONIFO M CONSULTANT E.N.T SURGEON ISTH, IRRUA. EDO STATE. DIZZINESS, VERTIGO & IMBALANCE.