Dizziness, Vertigo & Imbalance

Dizziness, Vertigo & Imbalance

DIZZINESS, VERTIGO & IMBALANCE DR AGBONIFO M C O N S U LT A N T E . N. T S U R G E O N ISTH, IRRUA. E D O S TAT E . PRETEST ABOUT VERTIGO IT IS ALSO REFFERED TO AS DIZZINESS IT IS AN INNER EAR DISEASE IT IS DEFINED AS HALLUCINATION OF

MOVEMENT A VERY IMPORTANT COMPONENT OF IT IS NYSTAGMUS BPPV: MEANS BENIGH PAROXYSMAL POSITIONAL VERTIGO IT IS THE COMMONEST CAUSE OF PERIPHERAL VERTIGO IT IS ASSOCIATED WITH HEARING LOSS TREATMENT IS SURGICAL

DIX HALLPIKE TEST IS AN OFFICE PROCEDURE TO DIAGNOSE MENIERES DX MEDICAL TREATMENT FOR VERTIGO INCLUDE THE USE OF BETAHISTINE CAUSE OF PERIPHERAL VERTIGO INCLUDE MENIERES 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 INTRODUCTION ANATOMY &PATHOPHYSIOLOGY (VESTIBULAR APPARATUS) AETIOLOGY CLINICAL FEATURES INVESTIGATION TREATMENT REHABILITATION

CONCLUSION 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 and NONVERTIGO 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. ANATOMY/ PATHOPHYSIOLOGY 10 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 organs 3 semicircular canals: superior, lateral, posterior 2 otolith organs: utricle and Anatomy Osseous (grey/white) and membranous (lavender) labyrinth of the left inner ear Parnes, L. S. et al. CMAJ 2003;169:681-693

Copyright 2003 Canadian Medical Association or its licensors ANATOMY/PATHOPHYSIOLOGY CONT There are five openings into area of utricle Saccule in spherical recess Utricle in elliptical recess

ANATOMY/PATHOPHYSIOLOGY CONT 15 Vestibular labyrinth - detects linear and angular head movements Semicircular canals - angular Hair cells organized under cupula Otolithic organs (utricle, sacule) linear Hair cells attached to a layer of otoconia

Vestibular nerve - superior, inferior branch ANATOMY/PATHOPHYSIOLOGY CONT Afferent fibers terminate in the vestibular nuclei in floor of fourth ventricle Superior vestibular nucleus Lateral vestibular nucleus Medial vestibular nucleus Descending vestibular nucleus

ANATOMY/PATHOPHYSIOLOGY CONT Vestibular nuclei project to Cerebellum Extraocular Spinal nuclei cord Contralateral vestibular

nuclei ANATOMY/PATHOPHYSIOLOGY CONT Superior vestibular nerve: superior canal, lateral canal, utricle Inferior vestibular nerve: posterior canal and saccule

Pathophysiology 19 Balance requires Normal functioning vestibular system Input from visual system (vestibulo-ocular) Input from proprioceptive system (vestibulospinal) 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 Pathophysiology 20 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 VERTIGO CAUSES: Vascular Endocrine/Epilepsy eceived () Trauma

Infection/Inflammatory Growth (Tumour) Others (Ophthalmologic, Miscellaneous) CAUSES OF VERTIGO VASCULAR Hypertension Orthostatic hypotension Subclavian steal syndrome Carotid-artery disease

Vertebral-basilar artery insufficiency Arrhythmia Aortic stenosis Bradycardia CAUSES OF VERTIGO ENDOCRINE Diabetis mellitus Hypoglcaemia Thyromegaly Hyperthyroidism/Hypothyroidism

Salt losing syndrome EPILEPSY Temporal lobe epilepsy HAEMATOLOGIC Anemia Polycythemia Leukemia CAUSES OF VERTIGO RECEIVED DRUGS

Streptomycin Kanamycine Diazepam Sedatives Opiates Alcohol Neuroleptics Aspirin Nicotine Caffeine Prochlorperazine

CAUSES OF VERTIGO TRAUMA Head injury Neck injury Fracture semicircular canal CAUSES OF VERTIGO INFECTIONS/INFLAMMATORY

Influenza Herpes zoster oticus Measles Mumps Syphilis , neurosyphilis Encephalitis Meningitis ( see more under otologic causes) CAUSES OF VERTIGO

GROWTHS (TUMOURS) Posterior fossa tumours Metastatic tumours to brain Acoustic neuroma (intracranial) Primary intracranial tumors GLIAL Multiple sclerosis CAUSES OF VERTIGO OTHERS

Heat stroke Temporomandibular joint syndrome Osteoarthritis Stroke Transient ischemic attacks OTOLOGIC CAUSES OF VERTIGO OTOLOGIC Bening paroxysmal positional vertigo

Vestibular neuronitis Acute serous otitis media Acute labyrinthitis Choleasteatoma Purulent otitis media Petrositis Poststapedectomy syndrome Perilymph fistula Menieres syndrome Acoustic neuroma (intracranial) Ototoxic drugs Auto-immune ear diseases

TYPES OF VERTIGO Peripheral Vertigo: BPPV Vestibular neuronitis Mnire 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 Mnire 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 bloodpressure 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 pointing Evidence of spontaneous nystagmus Evidence of positional nystagmus The fistula tests Office Examination of the Dizzy Patient Dix-Hallpike Maneuver Used

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 Dix-Hallpike Maneuver

Dix-Hallpike Maneuver Positive test Up-beating nystagmus Nystagmus to the stimulated side Rotary component to the affected ear Lasts 15-45 seconds Latency of 2-15 seconds Fatigues easily Pneumatic Otoscopy

Positive and negative pressure applied to middle ear Henneberts sign/symptom nystagmus and vertigo with pressure, alternates with positive and negative pressure Can be present in patients with perilymphatic fistula, syphilis, Menineres 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 test Equal 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 unclear Prolonged symptoms unresponsive to conservative treatment

Screen for central disorders Evaluate 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 tests All test eye movements that originate in the cerebellum Saccadic tracking

Smooth pursuit tracking Optokinetic testing Oculomotor Tests Saccadic tracking Patients concentrates on a randomly moving target Latency difference in time between movement of object and eye (150250 ms) Velocity speed of saccade 200-400

degrees/second low end of normal Accuracy amount of undershoot/overshoot of target (75- 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 lesion

High 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 systems Useful in quantification of fall risk Most useful in following conditions: Chronic disequilibrium and normal exams Suspected malingering Suspected multifactorial disequilibrium Poorly 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. TREATMENT

58 TREAT THE CAUSE IF KNOWN MEDICAL SURGICAL PHYSICAL THERAPY Medical Treatment 59

Symptomatic Specific therapy Vestibular rehabilitation Medical 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. 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, prochlorperazine Benzodiazepines: eg diazepam (Valium) Monoaminergics: eg ephedrine Vestibular rehabilitation exercises Semont manoeuvre Particle repositioning manoeuvre

(Epley) Dix-Hallpike manoevre Cawthorne exercises Brandt-Daroff exercises (dispersing otolithic debris in the semicircular canals) Lempert, and Hamid maneuvers, among others. Fig 9: Liberatory manoeuvre of Semont (right ear) Parnes, L. S. et al. CMAJ 2003;169:681-693

Copyright 2003 Canadian Medical Association or its licensors 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) Parnes, L. S. et al. CMAJ 2003;169:681-693 Copyright 2003 Canadian Medical Association or its licensors 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 DixHallpike 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 12 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 35 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 12 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 include labyrinthectomy,

posterior canal occlusion, singular neurectomy, Vestibular nerve section, and transtympanic aminoglycoside application. All have a high chance of vertigo control. Conclusions 70

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

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