Vertigo Clinic - ECAB 9788131229729, 9788131239308, 8131239306

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ECAB Clinical Update: Otorhinolaryngology

Vertigo Clinic

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ECAB Clinical Update: Otorhinolaryngology

Vertigo Clinic Dr. Deepak Haldipur Dr. Anita Bhandari Dr. V. Jayakumar Dr. Sreenivasa Murthy TM Dr. Anirban Biswas

Editor Dr. Deepak Haldipur

ECAB Clinical Update: Otorhinolaryngology

A division of Reed Elsevier India Private Limited

Copyright © 2012 Elsevier Mosby, Saunders, Churchill Livingstone, Buerworth Heinemann and Hanley & Belfus are the Health Science imprints of Elsevier. All rights reserved. No part of this publicaon may be reproduced, stored in a retrieval system, or transmied in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, without the prior permission of the copyright holder. Medical knowledge is constantly changing. As new informaon becomes available, changes in treatment, procedures, equipment, and the use of drugs become necessary. The authors, editors, contributors, and the publisher have, as far as possible, taken care to ensure that the informaon given in this text is accurate and up-to-date. However, readers are strongly advised to confirm that the informaon, especially with regard to drug dose/usage, complies with current legislaon and standard of pracce. Opinions expressed in this book are those of the authors and do not necessarily reflect those of Elsevier India Pvt. Ltd., the editors, or sponsors. Elsevier India Pvt. Ltd. assumes no liability for any material published herein. Although all adversing material is expected to conform to ethical (medical) standards, inclusion in this publicaon does not constute a guarantee or endorsement of the quality or value of such product or of the claims made of it by its manufacturer.

ISBN 978-81-312-2972-9 Published by: Elsevier, a division of Reed Elsevier India Private Limited Registered Office: 622, Indraprakash Building, 21 Barakhamba Road, New Delhi - 110001 Corporate Office: 14th Floor, Tower 10B, DLF Cyber City, Phase-II, Gurgaon 122002, Haryana

Typeset at Chitra Computers, Delhi Printed at EIH Unit-Press, Manesar, Gurgaon

ECAB Clinical Update: Otorhinolaryngology ELSEVIER CLINICAL ADVISORY BOARD MEMBERS

Dr. N.N. Mathur MS DNB FRSM MNAMS

Dr. V.P. Sood MS FICS

Director Professor ENT Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi.

Director, Sood Nasal Research Foundaon, Delhi. Ex-HOD, Dept. of ENT, AIIMS, Founder & Past President of All India Rhinology Society.

Dr. Ajit Man Singh

MS FRCS DNB

Senior Consultant ENT, Max Healthcare, New Delhi.

Dr. Anirban Biswas Consultant Neurotologist VERTIGO CLINIC Belle Vue Kolkata, President, Associaon of Otolaryngologists of India.

Dr. K.O. Paulose

DLO FRCS (UK)

Senior Consultant ENT, Jubilee Memorial, Thiruvananthapuram.

Lt. Col. Dr. A. Ravikumar MS DNB DLO (RCS)

Prof. & Head, Dept. of ENT, Sri Ramachandra Medical College & Research Instute. Sri Ramachandra University, Porur, Chennai.

Dr. Abhoya Kumar Kar MS Retd. Professor and Head, Department of ENT, and Head & Neck Surgery MKCG Medical College, Berhampur and GSL Medical College, RMY, Andhra Pradesh. Vising Professor, Annamalai University, Tamil Nadu.

Dr. Kishore Chandra Prasad DLO MS FACS

Dean, Srinivas Instute of Medical Sciences and Research Centre, Ex-Professor & HOD, ENT and Director of Post-Graduate Studies in ENT-Head & Neck Surgery, Kasturba Medical College & affiliated hospitals (Manipal University).

Padma Shri Dr. Mohan Kameswaran MS FRCS DSc FAMS

Padma Shri Dr. Santosh K. Kacker MS FRCS

Director, Delhi ENT Hospital and Research Centre, Delhi. Ex-HOD (Dept. of ENT) and Director, All India Instute of Medical Sciences.

Managing Director, Madras ENT Research Foundaon, Chennai.

Dr. M.V. Kirtane MS DORL Prof. Emeritus, Seth G.S. Medical College and KEM Hospital, Mumbai.

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Contributors Deepak Haldipur MS (ENT) Senior ENT Consultant, Chord Road Hospital Honorable ENT Consultant, Indian Instute of Science Bengaluru, Karnataka Anita Bhandari MBBS MS (ENT) Sr. ENT Surgeon (Fellowship in Neurotology & Otology [Singapore]) Jain ENT Hospital Jaipur, Rajasthan Anirban Biswas Consultant Neurotologist Vergo Clinic   Kolkata, West Bengal

V Jayakumar MD DCH DM (Neuro) Chief Neurologist JK Instute of Neurology Madurai, Tamil Nadu Sreenivasa Murthy TM MBBS DLO DNB Consultant ENT Surgeon Columbia Asia Hospital Yeshwanthpur, Bengaluru, Karnataka

ELSEVIER INDIA Clinical Educaon and Reference Division DIRECTOR SALES MANAGER  CLINICAL SPECIALTIES Vidhu Goel Ravindra Kamble

CONTENT MANAGER Dr. Gautam Das

COVER DESIGNER Milind Majgaonkar

CONTENT DESIGNERS AND EDITORS Ms. Bobby Choudhury Dr. Jayeeta Bhaacharjee Swa Sharma

PRODUCTION DEPARTMENT Sunil Kumar Arvind Booni

EDITORIAL OFFICE Elsevier, a division of Reed Elsevier India Private Limited 14th Floor, Building No. 10B, DLF Cyber City, Phase-II, Gurgaon, Haryana – 122002, India. Telephone: + 91-124-4774444 Fax: + 91-124-4774100 E-mail: [email protected]

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Contents Preface .................................................................................... xi Dr. Deepak Haldipur Vergo—Neurologist’s Perspecve .........................................1 Dr. V Jayakumar Understanding the Process Flow in a Vergo Clinic— From Entry to Exit of a Paent ..............................................28 Dr. Sreenivasa Murthy TM State-of-the-Art Vergo Clinic ...............................................56 Dr. Anirban Biswas Seng Up a Vergo Clinic in a Semi-Urban Center ..............85 Dr. Anita Bhandari

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Preface Gone are the days when vergo was just an ‘add-on’ problem/ case. A er headache, vergo and dizziness are the second most common illnesses of paents. Vergo is not a single disease, but rather a non specific syndrome consisng of various disorders of different origins. Considering the fact that the number of paents suffering from vergo is constantly on the rise, the number of man-hours lost in this suffering is tremendous. Stascs reveal that at least 1 of every 5 paents suffers from vergo a er the age of 60 years and at least half of these paents connue to have recurrent episodes for the rest of their life. This makes the problem very challenging. Doctors of different specializaons, including neurologists, neurootologic specialists, neuro-ophthalmologists, otolaryngologists, head and neck surgeons, ophthalmologists, ENT specialists, and general medicine praconers, aending paents with vergo agree on the fact that the main needs of a paent suffering from vergo are me, empathy, compassion, and keen interest from the treang doctor. Despite a beer understanding of cellular biomechanics of vesbular/balancing system, advances in imaging techniques (computed tomography [CT], magnetic resonance imaging [MRI], single-photon emission computed tomography [SPECT], angiography, etc.), and invesgaons (video-electronystagmography [ENG], brainstem-evoked response audiometry [BERA], vesbularevoked myogenic potenal [VEMP], and electrocochleography), the diagnosis of most syndromes of vergo can only be correctly made by ways of a careful medical history and physical examinaon of the sensory structures of hearing, balance, vision, and propriocepon, together with central nervous system connecons that integrate the sensory informaon produced by these structures.

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Information Preface

International collaboration and dissemination of scientific observaon among researchers has resulted in greater appreciaon of the mulple factors that play a role in the heterogeneous disorders of vergo that affect many of our paents. These innovaons in equipment and scienfic knowledge have spawned greater clinical insight and allowed the development of otoneurology into a recognized and respected subspeciality. The moment of truth seems to have finally arrived. Time has come where vergo has to become a separate speciality, and it is economically viable for a doctor to pracce vergo exclusively, considering the huge populaon of vergo paents that we have in our country. And for that, seng up a vergo clinic becomes a priority. Laboratory tests can now provide precise informaon about labyrinthine, auditory, eye-tracking, visual, and somatosensory funcon. CT scan and nuclear magnec resonance scanning provide detailed anatomic informaon of the inner ear, mastoid, or cerebelloponne angle to locate the pathology. Maneuvers and exercises alongwith pharmacotherapy play a major role in the management of the condion to alleviate the symptoms. With the advent of high-quality microscopes and drills, doing advanced anvergo surgeries has also become a reality. The frequent usage of intratympanic route of drugs administraon has also opened up a new channel of treatment, especially for extremely severe, incapacitang, intractable cases of vergo. This issue brings together 5 authors who have been innovave researchers in this field. These are what we can claim as the first generaon of neurootologists who have focused exclusively on treang vergo. They have provided their experse and insight into applicaon of recent advances in current clinical pracce and future research. The goal of this issue is to highlight the rapid development in the field of vergo during the past 2 decades and the need of creang a vergo clinic. Dr. Deepak Haldipur MS (ENT) Senior ENT Consultant, Chord Road Hospital Honorable ENT Consultant, Indian Instute of Science Bengaluru, Karnataka xii

Vertigo—Neurologist’s Perspective Dr. V Jayakumar Chief Neurologist JK Institute of Neurology Madurai, Tamil Nadu

INTRODUCTION The symptom of ‘vergo’ or dizziness is a common complaint for which paents seek neuro-otological consultaon. The incidence is reported to be 20–30%, increasing with the age.1–3

Unfortunately, the term dizziness and giddiness are o en used by the paents, causing confusion and misunderstanding in the mind of treang physician. These terms are used to encompass the following different condions, viz: 1. Vergo 2. Presyncope 3. Disequilibrium 4. Other condions It is very important to have a clear disncon regarding these condions as they have different diagnosc and therapeuc implicaons.

VERTIGO Vergo refers to ‘an illusion of movement’ usually in the form of a spinning sensaon of either self or the environment. It is a common symptom of vesbular dysfuncon.

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Vesbular dysfuncon could involve either the peripheral vesbular system (semicircular canal and vesbular nerve) or the central vesbular system (vesbular nucleus and its connecons).

PRESYNCOPE Presyncope is o en described as lightheadedness or feeling of near fainng and is o en associated with pallor, sweang, dimness of vision, blackout, and wobbly feeling in the legs. There is no sensaon of movement. Mostly, presyncope occurs in the standing or sing posion, not on lying posion. It o en occurs as a result of decreased cerebral perfusion.

Just like syncope, presyncope is also caused by cardiac disease, cardiac arrhythmias, vasovagal aack, autonomic disorders, postural hypotension, and certain drugs.

Presyncope is also caused by cardiac disease, cardiac arrhythmias, vasovagal attack, autonomic disorders, postural hypotension, and certain drugs.

DISEQUILIBRIUM The term disequilibrium often refers to a feeling of unsteadiness or imbalance o en experienced while standing or walking. There is no feeling of rotaon or impending fainng.

It is a nonspecific symptom as a result of disorders affecng cortex, basal ganglia, cerebellum, spinal cord, and peripheral nerves.

OTHER CONDITIONS CAUSING DIZZINESS Other condions that could produce dizziness include mostly psychiatric disorders like hysterical hypervenlaon, anxiety, panic disorder, and depression.4

Head trauma, hypoglycemic episodes, occasionally chronic fibromyalgia,5 drugs (andepressants and aminoglycosides),6,7 etc, can also produce dizziness and vergo. Most of the surveys indicate the following causes for dizziness8:  Peripheral vesbular disturbance: 40% 2

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Presyncope and disequilibrium: 25% Psychogenic: 15% Central vesbular disturbance: 10%

CLINICAL EVALUATION OF A PATIENT WITH VERTIGO/DIZZINESS As with any other condion in neurology, the success of making the right diagnosis depends on the thoroughness of the history taking, which plays a major role.

The following algorithm is useful at the bedside when paents present with a symptom of dizziness or vergo (Algorithm 1).

HISTORY 1. Exact descripon of the episode: Paent must be allowed to describe the clinical aack in detail with properly placed leading quesons in order to differenate whether it is a real vergo, presyncope, or disequilibrium.

Vertigo precipitated by turning in bed; side-to-side head movement indicates benign paroxysmal vertigo. 2. Mode of onset and duraon:  Benign paroxysmal posional vergo (BPPV) is usually sudden and lasts for few seconds.  Vertebrobasilar transient ischemic aacks (TIAs), Ménière’s disease, etc., lasts for few minutes to hours.  Persistent vertigo occurs in brainstem/cerebellar stroke, demyelinaon, posterior fossa space-occupying lesion (SOL), vesbular neuronis, and psychogenic vergo. 3. Precipitang events:  Vergo precipitated by turning in bed; side-to-side head movement indicates benign paroxysmal vergo.  Dizziness precipitated a er geng up suddenly from lying posture occurs commonly in orthostac hypotension.

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4 Causes  Vertebro basilar vascular disorders  Demyelinating disorder (Multiple sclerosis)  Migraine and vertigo  Epileptic vertigo  Acoustic neuroma

 Vertebro basilar TIA  PICA syndrome (Wallenberg)  AICA syndrome  Cerebellar infarct/hemorrhage  Infarction of the nodulus  Brainstem/pontine infarcts

Algorithm 1. Approach to dizziness or vertigo. AICA: anterior inferior cerebellar artery; BPPV: Benign paroxysmal positional vertigo; PICA: posterior inferior cerebellar artery; TIA: transient ischemic attack

e.g.  BPPV  Vestibular neuronitis/ labrynthitis  Ménière's disease

Peripheral Central

Causes  Panic, anxiety and depression  Phobic postural vertigo  Hypoglycemia  Drugs

Causes  Frontal lobe ataxia  Basal ganglia disorders  Normal pressure hydrocephalus  Cerebrovascular junction anomaly  Cerebellar disorders  Myelopathy – e.g. B12 deficiency  Peripheral neuropathy

Causes  Cardiac disease  Cardiac arrhythmias  Vasovagal attack  Autonomic disorders  Postural hypotension  Drugs

 Symptoms/type of nystagmus  Dix-Hallpike maneuver  Head impulse or head thrust test

Mostly psychogenic and drugs

Indicative of proprioceptive dysfunction

Indicative of decreased cerebral perfusion

Indicative of vestibular dysfunction

Vague sensation

Others

Sensation of unsteadiness

Disequilibrium

Sensation of near fainting

Presyncope

Sensation of spinning

Vertigo

Dizziness/Vertigo

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A sense of imbalance and fear of falling immediately a er standing or while aempng to walk indicate disequilibrium. 4. Associated features:  Severe nausea and voming with severe vergo are o en seen in peripheral vesbular disturbance.  Hearing loss and nnitus are commonly associated with Ménière’s disease, anterior inferior cerebellar artery (AICA) stroke, and acousc schwannoma.  Diplopia, numbness or weakness, unsteadiness of the limbs, dysphagia, dysarthria, etc., indicate vertebrobasilar stroke or brainstem demyelinaon.  Headache occurs commonly in cerebellar hemorrhage, migrainous vergo, posterior fossa SOL.  Abnormal gait and presence of sensory symptoms in relaon to the limbs indicate disequilibrium.  Autonomic symptoms like urinary, erecle dysfuncon, and abnormalies of sweang could be associated with orthostac hypotension. 

Diplopia, numbness or weakness, unsteadiness of the limbs, dysphagia, dysarthria, etc., indicate vertebrobasilar stroke or brainstem demyelination. 5. Others:  Drug intake, symptoms suggesve of psychiatric disorders like anxiety, depression, and panic disorders should also be elicited.  A history of pre-exisng cardiac problem could indicate the possibility of presyncope.

CLINICAL EXAMINATION Clinical examinaon is aimed at evaluang the following aspects to arrive at a diagnosis and to plan for further invesgaons and management. These aspects are very important for the praconer to understand so that a concrete and logical plan for further workup is developed. i. To differenate a peripheral and a central vesbular disorder. ii. Evaluaon of brainstem and cerebellar dysfuncon.

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Table 1. Peripheral Versus Central Vergo Features

Peripheral

Central

Nausea, vomiting, vertigo

More severe

Less

Horizontal and rotatory

Can be in any direction

Spontaneous nystagmus Type

Never purely vertical or rotator Direction

Unidirectional, fast phase May reverse the direction is towards the normal ear, and the amplitude increases in the direction of fast phase. The direction of fast phase does not change in relation to gaze

Visual fixation

Suppresses the nystagmus

No effect

Head movement

Accentuates the nystagmus

No significant change

After a latent period

Immediate

Induced nystagmus (Dix–Hallpike maneuver) Onset Duration

60 seconds

Adaptability

Adaptable

No adaptation

Fatigability

Fatigable

No fatigability

iii. Assessment of gait and propriocepve funcons. iv. Evaluaon of autonomic nervous system.

Central Versus Peripheral Vestibular Dysfunction Vergo occurs as a result of an imbalance between either central or peripheral vesbular system on either side. In general, the severity of vergo, nausea, and voming is more in relaon to peripheral vesbular disorder than in central vesbular disorder.

Nystagmus is a very important physical sign and a detailed analysis is very vital. Nystagmus can be spontaneous or can be induced by certain maneuvers like Dix–Hallpike. The Table 1 outlines certain important features:

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The following 2 important clinical tests are important for the bed-side evaluaon of the vesbular funcon. 1. Dix–Hallpike maneuver 2. Head impulse or head thrust test

Dix–Hallpike Maneuver9 The paent’s head is laterally rotated to 45° and is brought from sing to lying posion rapidly while holding the head and extending it to 20° at the edge of a cot. Head is held in that posion for at least 30 seconds to observe for any nystagmus. The test is repeated on the opposite side. This is a very useful test to detect BPPV and is considered posive when vergo and nystagmus occur. Nystagmus recurs again, but in the opposite direcon, once the paent is made to sit. The detailed evaluaon of the semicircular canal is beyond the scope of this arcle.

Head Impulse or Head Thrust Test10 This is a very useful test to differenate a peripheral vesbular dysfuncon from a central one. Here a very fast, low-amplitude (15–20°), discrete head

Caloric test is also useful to assess vestibular function, it is more useful when it is done with butterfly charting in electronystagmography thrust is given to one side by the examiner to the paent while sing and the paent is asked to concentrate on the examiner’s nose. The test is repeated on the other side.

In normal individuals, because of the intact vesbule-ocular reflex, the subject’s eyes remain focused on the examiner’s nose. On the other hand, if there is a peripheral vesbular dysfuncon, there will be catch-up saccades when the head is turned to the affected side. Although caloric test is also useful to assess the vestibular funcon, it is more useful when it is done with buerfly charng in electronystagmography (ENG). In addion, the other eye-movement abnormalies should also be looked for. For example, the presence of vercal gaze palsy could suggest early progressive supranuclear palsy (Steele–Richardson–Olszewski syndrome), which is also associated with recurrent falls. Similarly,

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the presence of downbeat nystagmus should make us to suspect craniovertebral (CV) juncon anomaly, where the associated oscillopsia can be mistaken for vergo. Further evaluaon of the vesbular system can be done by vesbularevoked myogenic potenals (VEMPs), ENG, rotaonal test, etc.

Evaluation of Brainstem and Cerebellar Dysfunction The presence of squint, swallowing difficulty, nasal regurgitaon, change in voice, diplopia, unsteadiness, and sensory or motor symptoms in addion to vergo suggest the possibility of brainstem and/or cerebellar involvement.

Hence, a detailed examinaon of cranial nerves, especially oculomotor, sixth, seventh, and auditory nerves; palatal movements; and facial or limb sensory loss should be done. In addion, cerebellar signs like nystagmus, finger–nose inco-ordination, heel–knee inco-ordination, dysarthria, dysdiadochokinesia, and gait ataxia should be looked for.

The presence of squint, swallowing difficulty, nasal regurgitation, change in voice, diplopia, unsteadiness, and sensory or motor symptoms in addition to vertigo suggest the possibility of brainstem and/or cerebellar involvement.

Assessment of Gait and Proprioceptive Functions Examinaon of the gait is very important in bringing out cerebellar ataxia, and even peripheral vesbular disorders can cause severe vergo and unsteadiness. However, the typical wide-based cerebellar ataxia can be easily idenfied. In addion, the presence of Parkinson’s features, the typical gait of progressive supranuclear palsy, and normal pressure hydrocephalus (gait apraxia) can also be idenfied.

The detailed sensory examinaon should include the specific tests for propriocepon, namely joint posion and vibraon. Romberg’s sign is suggesve of sensory ataxia, and the paent o en mistakes this for vergo. Further evaluaon of the peripheral nerves and sensory system could be done by nerve conducon, electromyographic (EMG) studies, and evoked potenals studies. 8

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Evaluation of Autonomic Nervous System Examinaon of the autonomic nervous system is important not only in a paent who presents with symptom suggesve of presyncope but also in paents with Parkinson’s features, especially to rule out Shy-Dragger syndrome in addition to patients presenting with pure autonomic neuropathy.

The presence of orthostac hypotension can be considered when there is a reducon of systolic blood pressure of at least 20 mmHg or diastolic blood pressure of 10 mmHg within 3 minutes of standing.11 In addion, pulse rate also should be checked, as failure of increase of heart rate while standing from lying indicates autonomic failure (in the absence of β-blocker intake). Further evaluaon can be done by lt-table test, R–R interval variability, and sympathec skin response studies.

The presence of orthostatic hypotension can be considered when there is a reduction of systolic blood pressure of at least 20 mmHg or diastolic blood pressure of 10 mmHg within 3 minutes of standing.

VERTIGO IN CENTRAL NERVOUS SYSTEM DISORDERS Central vesbular disorders are o en associated with other neurological signs and symptoms.

Vertebrobasilar Vascular Disorders Since the vesbular nucleus has a larger representaon in the brainstem, majority of vertebrobasilar vascular diseases o en manifest with severe vergo in addion to other neurological symptoms and signs. The following are the important conditions presenting with vertigo, which require immediate aenon and treatment. i. Vertebrobasilar TIA ii. Lateral medullary syndrome (Wallenberg syndrome) iii. Anterior inferior cerebellar artery syndrome

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iv. Cerebellar infarct and hemorrhage v. Infarcon of the nodulus of the cerebellum vi. Brainstem/ponne infarcts

Vertebrobasilar Transient Ischemic Attack In vertebrobasilar TIA, the other symptoms like diplopia, dysarthria, disequilibrium, drop attacks, etc, occur in addition to vertigo. Unlike carod artery TIA (where artery-to-artery embolism is mostly involved), in vertebrobasilar TIA, hemodynamic factors are mostly involved.

Lateral Medullary Syndrome (Wallenberg Syndrome)— Posterior Inferior Cerebellar Artery Syndrome Lateral medullary infarcon classically occurs when there is an ischemia in the posterior inferior cerebellar artery (PICA), affecng the lateral medulla.

The symptoms and signs are referable to the structures affected, namely:

Lateral medullary infarction classically occurs when there is an ischemia in the posterior inferior cerebellar artery, affecting the lateral medulla.        

Ipsilateral Horner syndrome—due to sympathec tract involvement. Ipsilateral ataxia—due to inferior cerebellar peduncle involvement. Ipsilateral pain and temperature loss over the face—due to involvement of descending tract of fi h nerve. Contralateral pain and temperature loss over the limbs—due to the involvement of spinothalamic tract. Vergo—due to the involvement of vesbular nucleus. Palatal palsy—involvement of Xth nerve. No limb weakness as pyramidal tracts are not involved. In addion, there are a wide variety of neuro-ophthalmological signs seen. The important features are outlined in the diagram (Figure 1).

Illustrave Case 1: A 70-year-old male presented with an acute onset of vergo and unsteady feeling when he got up from the bed. He was seen by the family doctor who had suggested labrynthine sedave drugs. Over the next few hours, he noced slurring of speech, unsteady feeling while 10

Dorsal

Horner’s syndrome Loss of pain, temperature ipsilaterallyover the face

Sympathetic tract Descending tract of V

Vestibulus nucleus

Inferior cerbellar peduncle

Vertigo

Ataxia, cerebellar signs

Loss of pain, temperature contralaterally

Spinothalamic tract

Tractus solitarius

Palatal palsy

Xth nerve

Inferior olivary nucleus

XIIth nerve

Pyramid



Figure 1. Wallenberg's syndrome — Clinico-anatomical and radiological correlations.

Affected areas

Ventral

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walking, and nasal regurgitaon of feeds with difficulty in swallowing and right facial numbness. He was a known case of hypertension with ischemic heart disease.

Examinaon revealed a BP of 130/90 mmHg and pulse rate 80/min. Neurological examinaon revealed following findings.         

Right Horner syndrome Dysarthric speech Spontaneous horizontal nystagmus—direcon changing with larger amplitude on looking to the right side Dix–Hallpike maneuver and head impulse test negave Right palatal palsy Loss of pain and temperature over right side of the face Loss of pain and temperature over le side of the trunk and limbs Right-sided cerebellar signs (limb incoordinaon) No pyramidal signs

Magnec resonance imaging (MRI) findings were suggesve of PICA infarct (Figures 2 and 3). His echocardiogram revealed le ventricular hypertrophy (LVH) and no intracardiac thrombus. He improved gradually with thrombolytic, antiplatelet, and neuroprotecve drugs along with anhypertensives.

Anterior Inferior Cerebellar Artery Syndrome It may resemble PICA syndrome, but the following points will help in the differenaon:    

Acute onset of deafness—o en due to labrynthine infarcon due to occlusion of internal auditory artery, which is a branch of AICA Tinnitus Facial palsy No limb weakness as pyramidal tracts are not involved Somemes AICA syndrome can be mistaken for Ménière’s disease. The important features are outlined in the diagram (Figures 4 and 5).

Illustrave Case 2: A 52-year-old male, a known diabec, noced acute onset of loss of hearing in the le ear along with severe vergo and voming, for which he was taken to an ENT surgeon, who made a diagnosis of Ménière’s disease and advised prochlorperazine and advised him to have an audiogram done. On the same day evening, he noced benumbed feeling over the le half of the face with a tendency to sway to the le side. 12

MRI – Lateral medullary infarct

MRI – Zoomed view



Figure 2. Wallenberg's (PICA) syndrome.

Horner’s syndrome - Right

Vertigo—Neurologist’s Perspective Jayakumar

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Figure 3. Wallenberg's (PICA) syndrome showing magnetic resonance imaging and anatomical areas of infarct.

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Dorsal cochlear nucleus VIII

Middle cerebellar peduncle

Inferior cerebellar peduncle

Ventral cochlear nucleus VIII

Nerve VIII

Motor nucleus of VII

Spinothalamic tract



Figure 4. Anterior inferior cerebellar artery syndrome anatomical and radiological correlations.

Nucleus of VI

Vertibular nuclei

Spinal nucleus and tract of V

Nerve VII

Nerve VI

Medial lemniscus

Corticospinal tract

Vertigo—Neurologist’s Perspective Jayakumar

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16 Vertigo

Ataxia, cerebellar cigns

Deafness – sensorineural

Loss of pain, temperature ipsilaterally over the face

Loss of pain, temperature over contralateral body and limbs Facial palsy

Figure 5. Anterior inferior cerebellar artery syndrome clinico-anatomical and radiological correlations.

Vertibular nuclei VIII

Ventral cochlear nucleus VIII Inferior cerebellar peduncle Middle cerebellar peduncle

Nerve VIII

Spinal nucleus and tract of V

Nerve VII

Spinothalamic tract

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Figure 6. Magnetic resonance image showing left anterior inferior cerebellar artery infarct.

Figure 7. Magnetic resonance image and anatomical picture showing the area of infarct.

He was brought for neurological consultaon in view of unsteadiness. Neurological examinaon revealed le sensory neural deafness, incoordinaon of the le hand, le facial weakness, pain, and temperature loss over the le side of the face and over the right upper and right lower limb. Magnec resonance imaging showed infarcon in the region supplied by le AIC (Figures 6 and 7). Paent improved with low-molecular-weight heparin and anplatelet drugs along with andiabec drugs and neuroprotecve drugs, although he had a residual le sensory neural hearing loss.

Cerebellar Infarct and Hemorrhage Cerebellar strokes o en present with hyperacute onset of vergo, voming, nuchal pain, occipital headache,12 and severe ataxia. It is very important to differenate cerebellar strokes from other causes of acute vergo as the treatment is vital and life saving.

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Table 2. Cerebellar Strokes Versus Peripheral Vesbular Disorder Features

Cerebellar

Peripheral vestibular

Head impulse test

Intact (no catch-up saccade)

Positive (catch-up saccade)

Nystagmus

Fast component to the side of gaze

Fast component opposite to the side of lesion

Amplitude increases to the side of lesion Patient falls

Nystagmus and falls are to the side of lesion

Amplitude increases opposite to the side of lesion Nystagmus is opposite to the side of lesion, but the fall is toward the side of lesion

Other features

Dysarthria, limb incoordination

Tinnitus and severe vertigo

Certain clues will help when paents present with acute vergo to differenate between cerebellar strokes from peripheral vesbular disorders (Table 2). Most o en, the cerebellar ischemic strokes are embolic in nature. Severe headache and high BP in the context of abovemenoned physical signs should make one to suspect cerebellar hemorrhage. Neuroimaging (MRI) plays a vital role in the diagnosis of cerebellar strokes. Timely thrombolytic therapy in cerebellar infarct and surgical decompression in certain cases will be life saving as even a mild cerebral edema or hemorrhage may cause severe pressure effect in view of the small posterior fossa. Illustrave Case 3: A 33-year-old young male police constable presented with an acute onset of severe vergo, voming, and unsteady feeling, for which he was admied in the nearby hospital and was treated with intravenous (i.v.) fluids and betahisne and prochlorperazine injecon. Since he started developing neurological signs in the form of weakness of the right hand and dysarthria, he was referred for neurological consultaon.

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Figure 8. Magnetic resonance imaging showing left pontocerebellar infarct.

Figure 9. Magnetic resonance imaging showing left pontocerebellar infarct.

Neurological examinaon revealed le Horner syndrome, le palatal palsy, upbeang nystagmus, and le -sided cerebellar signs. Magnec resonance imaging showed le pontocerebellar infarct (Figures 8 and 9). He was treated with thrombolyc, anplatelet, and neuroprotecve drugs. However, his level of consciousness was deteriorang; hence, he was taken for emergency decompression surgery. He recovered

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Figure 10. Computed tomographic scan brain following decompressive surgery.

unevenully in the postoperave period. A repeat computed tomographic (CT) scan showed no midline shi with sufficient expansion of the brain (Figure 10). He gradually improved in the next few weeks and resumed his duty. This case clearly shows that mely and early recognion of cerebellar stroke and an effecve treatment can be life saving. Illustrave Case 4: A 60-year-old male, a known hypertensive, on treatment had profuse sweang and severe vergo when he returned from the toilet a er passing moon. He had not taken anhypertensive drugs on the previous day. There was no h/o chest pain or discomfort. However, he c/o vague nuchal pain.

Neurological examination revealed severe ataxia and horizontal nystagmus with fast component to the side of the gaze. There were no other neurological signs except for mild neck sffness. His BP was found to be 110/70 mmHg, although it used to be usually around 160/100 mmHg even with anhypertensive drugs. In view of the clinical suspicion of cerebellar hemorrhage, an emergency CT and subsequently MRI were done, which confirmed the diagnosis (Figure 11). Although there was a plan for surgical decompression, he improved gradually with conservave treatment with ancerebral edema measures along with anhypertensives. 20

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Jayakumar

Figure 11. Computed tomography (bright area) and magnetic resonance imaging (dark area) showing cerebellar hemorrhage.

Infarction of the Nodulus of the Cerebellum Infarction of the caudal cerebellum, nodulus, and inferior cerebellar hemispherical infarcon can present with isolated severe vergo without much of ataxia, mimicking peripheral vestibular disorder, especially vesbular neuronis.13–15 This possibility should be kept in mind as it may turn out to be a neurological emergency when cerebellar edema compresses the brainstem. Illustrave Case 5: A 70-year-old lady presented with acute onset of severe vergo and voming. She also had mild nnitus. She was treated by an ENT surgeon as vesbular neuronis.

Since her symptoms persisted, she was referred for neurological consultaon. Neurological examinaon showed negave Dix–Hallpike maneuver and head thrust test. She had horizontal nystagmus, whose amplitude was more on looking to the le side. The MRI brain was done in view of cerebellar nystagmus and persistent symptoms, which showed an infarct in the nodulus of the cerebellum (Figure 12). She improved with ancoagulant, anplatelet, and neuroprotecve drugs. This case clearly indicates that infarcon of the nodulus can mimic vesbular neuronis.

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Figure 12. Magnetic resonance imaging showing infarct in the nodulus of the cerebellum.

Brainstem/Pontine Infarcts In addion to the above menoned well-defined syndromes, brainstem infarcts could be patchy and can present with predominantly vergo along with other neurological signs depending on the structures affected.

Demyelinating Disorder (Multiple Sclerosis) Twenty percent of paent with mulple sclerosis can present with vergo when the plaques are near the vesbular nuclei, resembling vesbular neuris, or when the plaques are in the cerebellum, resembling cerebellar infarct.16,17 The vergo is usually sustained, o en associated with other neurological signs like pallor of the opc disc, afferent pupillary defect, and long tract signs.

Magnec resonance imaging and evoked potenals studies may be needed for further evaluaon. Illustrave Case 6: A 40-year-old female came for acute onset of severe vergo of 1-week duraon. There was no headache, voming, or nnitus. Her fundus examinaon revealed le temporal pallor of the opc disc. On retrospecve quesoning, she admied that she was treated for visual loss in the le eye 5 years back, which improved with some injecons. Although

22

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Jayakumar

Figure 13. Magnetic resonance imaging showing right cerebellar and left periventricular plaques.

she did not have any other neurological findings, she was advised to have MRI and evoked potenals studies.

A visual evoked potenal study clearly revealed prolongaon of the P100 latency on the le side. MRI brain with contrast revealed plaques in the cerebellum and periventricular region, suggesve of mulple sclerosis (Figures 13 and 14). She improved well with a course of i.v. methyl prednisolone.

Migraine and Vertigo Twenty-five percent of paents with migraine may present with vergo. Paents with basilar migraine present with vergo, nnitus, and dysarthria followed by typical headache.18,19

The term migrainous vertigo/vestibular migraine is restricted to paents who present with recurrent vergo lasng for seconds to days associated with headache, phonophobia, photophobia, scintillating scotomas, or other aura (Neuhauser criteria).20 Nine percent of paent with migraine have this syndrome. In children (usually 2–4 years of age), a similar syndrome is seen, presenting with episodic vertigo, nausea, and vomiting without headache. Most of the paents respond to drugs for migraine prophylaxis in addion to symptomac usage of labrynthine sedaves.

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Figure 14. Visual evoked potential studies showing prolongation of P100 latency on the left side.

Epileptic Vertigo A rare form of paral seizure may present as an epilepc vergo due to epilepform acvity arising from parts of the cortex that represent the vesbular system, viz., superior lip of the intraparietal sulcus, posterior superior temporal lobe, temporoparietal border areas, V5 area, and le middle frontal gyrus. These episodes usually last for few seconds or minutes.21–23

The diagnosis may be difficult when there are no obvious associated frank clinical seizures like convulsions or psychomotor symptoms. However, an ictal electroencephalogram (EEG) is very useful. Imaging studies may be required to rule out structural lesions. They usually respond to an-convulsants like oxcarbazepine and related drugs.

Acoustic Neuroma Although vergo can occur rarely in simple acousc neuroma, the slow growth of the tumor allows brainstem mechanisms to compensate for the vesbular imbalances. Hence, most of the mes, unilateral hearing loss and nnitus are the common presenng symptoms rather than vergo. However, intratumoral hemorrhage can result in acute vergo.24

Psychogenic Vertigo A variety of somatoform disorders can present with vague non-specific dizziness or vergo. The classical example is ‘phobic postural vergo,’25 24

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Jayakumar

which o en presents with a subjecve postural and gait unsteadiness or vergo and fear of falling, but without real falls and with normal neurological findings, o en triggered by external triggers of other phobic syndromes, and these paents have a compulsive personality. Treatment is focused on treang the underlying psychogenic cause along with symptomac treatment.

CONCLUSION   





   



Vergo or dizziness is a very common symptom in the roune neurological or neuro-otological pracce. It is very important to make a clear differenaon of vergo, presyncope, disequilibrium, and other condions. The analysis of symptoms, type of nystagmus, Dix–Hallpike maneuver, and head thrust/impulse test will help to differenate between peripheral and central vesbular disorders. Vertebrobasilar strokes and brainstem disorders can present with early vergo because of the larger representaon of the vesbular nucleus in the brainstem. In most of the vertebrobasilar strokes (AICA, PICA, etc.), severe vergo and unsteadiness can be easily mistaken for vesbular disorder because of the absence of significant paralysis in view of sparing of pyramidal tracts. It is very important to make an early diagnosis of vertebrobasilar stroke as mely intervenon can save the paent. Anterior inferior cerebellar artery infarct can be mistaken for Ménière’s disease in view of deafness. Infarcon of the nodulus of the cerebellum can present with isolated vergo and may be mistaken for vesbular neuronis. Cerebellar stroke and hemorrhage require early diagnosis as some of them would require emergency surgical decompression to prevent death. Neuroimaging plays a major role in the diagnosis of many of these disorders.

REFERENCES 1. Crespi V. Dizziness and vergo: an epidemiological survey and paent management in the emergency room. Neurol Sci 2004;25(Suppl 1):S24–5. 25

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2. Karatas M. Central vergo and dizziness: epidemiology, differenal diagnosis, and common causes. Neurologist 2008;14:355–64. 3. Colledge NR, Wilson JA, Macintyre CC, MacLennan WJ. The prevalence and characteriscs of dizziness in an elderly community. Age Ageing 1994;23:117–20. 4. Yardley L, Owen N, Nazareth I, Luxon L. Panic disorder with agoraphobia associated with dizziness: characterisc symptoms and psychosocial sequelae. J Nerv Ment Dis 2001;189:321. 5. Rosenhall U, Johansson G, Orndahl G. Otoneurologic and audiologic findings in fibromyalgia. Scand J Rehabil Med 1996;28:225. 6. McKiernan JM, Lowe FC. Side effects of terazosin in the treatment of symptomac benign prostac hyperplasia. South Med J 1997;90:509. 7. Coupland NJ, Bell CJ, Potokar JP. Serotonin reuptake inhibitor withdrawal. J Clin Psychopharmacol 1996;16:356. 8. Kroenke, K, Lucas, CA, Rosenberg, ML, et al. Causes of persistent dizziness. A prospecve study of 100 paents in ambulatory care. Ann Intern Med 1992;117:898. 9. Dix MR, Hallpike CS. The pathology, symptomatology and diagnosis of certain disorders of the vesbular system. Ann Otol Rhinol Laryngol 1952;61:987. 10. Bronstein AM, Lempert T. Dizziness: A Praccal Approach to Diagnosis and Management. Cambridge Clinical Guides. Cambridge, UK: Cambridge University Press, 2007. 11. The Consensus Commiee of the American Autonomic Society and the American Academy of Neurology. Consensus statement on the definion of orthostac hypotension, pure autonomic failure, and mulple system atrophy. Neurology 1996;46:1470. 12. Kumral E, Bogousslavsky J, Van Melle G, et al. Headache at stroke onset: the Lausanne Stroke Registry. J Neurol Neurosurg Psychiatry 1995;58:490–2. 13. Kim HA, Lee H. Isolated vesbular nucleus infarcon mimicking acute peripheral vesbulopathy. Stroke 2010;41:1558–60. 14. Lee H, Sohn SI, Cho YW, et al. Cerebellar infarcon presenng as isolated vertigo: frequency and vascular topographical patterns. Neurology 2006;67:1178–83. 26

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15. Norrving B, Magnusson M, Holtas S. Isolated acute vergo in the elderly; vesbular or vascular disease? Acta Neurol Scand 1995;91:43–8. 16. Frohman EM, Kramer PD, Dewey RB, et al. Benign paroxysmal posioning vergo in mulple sclerosis: diagnosis, pathophysiology and therapeuc techniques. Mult Scler 2003;9:250. 17. Anagnostou E, Mandellos D, Limbitaki G, et al. Posional nystagmus and vergo due to a solitary brachium conjuncvum plaque. J Neurol Neurosurg Psychiatry 2006;77:790. 18. Neuhauser H, Lempert T. Vergo and dizziness related to migraine: a diagnosc challenge. Cephalalgia 2004;24:83–91. 19. Eggers SD. Migraine-related vergo: diagnosis and treatment. Curr Neurol Neurosci Rep 2006;6:106–15. 20. Neuhauser H, Leopold M, von Brevern M, et al. The interrelaons of migraine, vergo, and migrainous vergo. Neurology 2001;56:436–41. 21. Bladin PF. History of “epilepc vergo”: its medical, social, and forensic problems. Epilepsia 1998;39:442–7. 22. Kluge M, Beyenburg S, Fernández G, Elger CE. Epilepc vergo: evidence for vestibular representation in human frontal cortex. Neurology 2000;55:1906–8. 23. Laff R, Mesad S, Devinsky O. Epilepc kinetopsia: ictal illusory moon percepon. Neurology 2003;61:1262–4. 24. Schlieter M, Zoubaa S, Kress B, et al. Hemorrhagic acoustic schwannoma: radiological and histopathological findings. J Neuroradiol 2005;32:210–2. 25. Brandt T. Phobic postural vergo. Neurology 1996;46:1515–9.

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Understanding the Process Flow in a Vertigo Clinic—From Entry to Exit of a Patient Sreenivasa Murthy TM Consultant ENT Surgeon Columbia Asia Hospital Yeshwanthpur, Bengaluru, Karnataka

Vergo is a common complaint which an otorhinolaryngologist needs to assess and manage in his/her daily clinic. Similarly, neurologists, physicians, orthopedicians, and occasionally pediatricians also get paents who seek their help with this complaint. The eology of vergo varies, and the differenal diagnosis is so wide ranging that literally a malfunconing of any system of the body can cause a sensaon of imbalance. Most paents with the unnerving symptom of dizziness/giddiness can be handled by a detailed history, thorough clinical examinaon, and a few invesgaons. In daily pracce, most doctors are hard pressed for me and hence are unable to provide the me required to get details of the history and do a thorough clinical examinaon. This leads to the paent being examined in part and then sent to other specialists and costly invesgaons. A vergo clinic would address paent’s need under one roof. How do we understand a vergo clinic? This can be under 2 headings: infrastructure and operaon. The infrastructure that would be required is: 1. Recepon/customer care/front desk 2. Nursing staon in front of the consultaon chamber 3. Consultaon chamber 4. Invesgaon

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RECEPTION/FRONT DESK OF A CLINIC The recepon is the face of the clinic and needs to be well informed about the processes and programs of the clinic. Dedicated paent care personnel—a couple of the front desk staff need to be idenfied, trained, and made to understand the process of a vergo clinic so that they can iniate the paent into the clinic from the me they receive a phone call for an appointment. It would help most paents if the registraon process can be done on the telephone itself and acvate a file on the paent’s arrival at the clinic. Identify days/time of the day in a week when the clinic can be conducted. It would help both the paent and the physician if dedicated me/day of the week is alloed to these paents to prepare one mentally to address paents.

Dedicated patient care personnel—a couple of the front desk staff need to be identified, trained, and made to understand the process of a vertigo clinic so that they can initiate the patient into the clinic from the time they receive a phone call for an appointment. Once the paent is registered and guided to the first staon. Here, a nurse/junior physician needs to be able to make the inial assessment of the paent, including history and general physical examinaon. It helps to have a quesonnaire made and incorporated into the file, which the paent can fill up with the help of the nurse/physician prior to meeng the consultant. A sample quesonnaire is given in Table 1. On compleng the quesonnaire, the paent can be guided into the consultaon chamber. All paents entering the clinic may not be in a stable condion to undergo the rounes stated above. An occasional paent may need to be aended to as an emergency. It helps to have a protocol to triage a paent with giddiness in the emergency room (ER) to the concerned specialist. The following protocol should help most ER physicians to do the needful (Figure 1). Interviewing the paent on most occasions should guide us to localize the giddiness as being peripheral or central or miscellaneous in eology.

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Table 1. Questionnaire for the Evaluation of a Dizzy Patient Name of the patient: Age: Sex: 1. Ask the patient to describe the sensation, not to use words such as dizzy, giddy, etc. 2. He/she needs to answer the following as ‘yes/no’ a. Do you ever have any of the following sensations? i) Spinning in circles ii) Falling to one side iii) World spinning around you b. The following refer to a typical dizzy spell: i) Do the dizzy spells come in attacks? • How often? • How long? • Date of first spell? ii) Are you free from dizziness between attacks? iii) Does your hearing change with an attack? iv) Are you dizzy mainly when you sit or stand up quickly? v) Are you dizzier in certain positions? • If yes, then which position? vi) Are you nauseated during an attack? vii) Are you dizzy even when lying down? viii) Have you had a recent cold/flu preceding recent dizzy spells? ix) Have you had fullness/pressure/ringing in your ears? x) Have you had pain/discharge in your ear of recent onset? xi) Have you had trouble walking in the dark? xii) Are you better if you sit or lie perfectly still? c. The following refer to other sensations you may have i) Do you blackout or faint when dizzy? ii) Have you had the following: • Severe or recurrent headaches • Any double or blurry vision • Numbness in your face/extremities • Weakness or clumsiness in arms and legs • Slurred or difficult speech • Difficulty swallowing • Tingling around your mouth Contd…

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3. Please list all surgeries he/she has undergone, with approximate dates. 4. Please list all allergies (name of drugs and reactions caused). 5. Please list all medicines he/she currently takes (including pain medicine, non-prescription medicine, sleeping pills, and birth-control pills). 6. Has he/she had any previous testing (like hearing, X-rays, scans, etc)? 7. Any family history of: i.

High blood pressure

ii. Low blood pressure iii. Diabetes iv. Low blood sugar levels v. Thyroid disease vi. Asthma Please list any other diseases that run in the immediate family. 8. Does he/she have any of the following symptoms? i.

Constitutional •

Recent weight change

•

Fever

•

Fatigue

ii. Eyes •

Loss of vision

•

Pain

•

Discharge/tearing

iii. Ear/nose/mouth/throat •

Itchy ears

•

Facial weakness

•

Nasal obstruction

•

Nasal discharge

9. Description of the spell. 10. What are the symptoms that accompany giddiness, when it occurs? 11. Any symptoms of central nervous system disease (like dysarthria, dysphagia, diplopia, hemiparesis, severe localized cephalgia, seizures, and memory loss)? 12. Any accompanying auditory complaints? 13. Dietary habits—vegetarian, eggarian, mixed, non-vegetarian

31

32 Epley maneuver (Class II)

Benign positional peripheral vertigo

+

-

Vestibular neuritis

Ménière’s disease, labyrinthitis

+

Dix-Hallpike maneuver (Class II)

-

Normal tympanic membrane?

Auditory symptoms?

Abnormal tympanic Cerumen? Foreign body membrane? Cholesteotoma Otitis media

Ear examination

-

+

Head trauma?

Normal: · Basilar migraine

+

Normal: · Concussion · Labyrinth concussion

Abnormal: · Temporal fracture · Intracranial blood · Increased intracranial pressure

CT scan (Class I)

Abnormal: · Brain tumor · Vertebrobasilar ischemia · Cerebellar infarct or bleed

CT scan and/or MRI with MRA (Class III)

-

+

Other causes of dizziness

Rule out CNS infection by history physical, or by CT and LP Intravenous antibiotics when indicated (Class I)

Fever?

-

Associated neurological symptoms or physical findings?

True vertigo

Perform history and physical (Class I)

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-

+

Consider drug etiology for symptoms Measure anticonvulsant level (Class II)

+

Figure 1. Clinical pathway—evaluation of the dizzy patient.

CT: computed tomography; CNS: central nervous system; LP: lumbar puncture; MRI: magnetic resonance imaging; EKG: electrocardiography; VS: vital signs; HJ: hemoglobin.



The evidence for recommendations is graded using the following scale. Class I: Definitely recommended. Definitive, excellent evidence provides support. Class II: Acceptable and useful. Good evidence provides support. Class III: May be acceptable, possibly useful. Fair-to-good evidence provides support. Indeterminate: Continuing area of research.

or depression

- Consider thyroid disease, psychiatric causes,

CT scan and/or MRI (Class III)

+

Neurological deficits?

-

+

Consider: Dehydration/hypovolemia Tachy- or brady dysrhythmia Infection/sepsis Labile hypertension

Orthostatic VS Stat Hg Pregnancy testing as indicated (Class III)

New or changed medication? Anticonvulsant use (phenytoin, carbamezapine, etc.)?

-

Dizziness upon standing?

-

EKG (Class III) Possible telemetry admission (Class III)

+

Chest pain or palpitations? Pacemaker? History of cardiac disease?

Abnormal vital signs?

Understanding the Process Flow in a Vertigo Clinic Murthy TM

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Dizziness can be a presenting complaint in many disorders. A considerable number of paents can have mulple causes for their dizziness and accompanied by various symptoms (Figure 2). It would help us to categorize paents of giddiness under one of the following categories.1 

Near-syncope secondary to decreased blood flow to the brain (such as orthostac hypotension and cardiac presyncope): This occurs due to volume depleon, as in paents with voming, loose stools, occult gastrointesnal (GI) bleeds/melena. Paents may guide us to the diagnosis with a past history of cardiac disease, medicaon, and interventions (antihypertensives, pacemaker insertion, or ancoagulants). A large secon of paents vising a vergo clinic are elderly and hence will usually be on medicaons, some of which are known to lead to orthostac hypotension (anhypertensives, an-Parkinsonian drugs, neurolepcs, and ancholinergics). In the elderly, poor condioning and autonomic insufficiency are other causes of orthostac hypotension. What needs to be remembered

Near-syncope secondary to decreased blood flow to the brain occurs due to volume depletion, as in patients with vomiting, loose stools, occult gastrointestinal bleeds/melena.



is that the elderly paent may become dizzy with postural change without significant alteraon in blood pressure (BP).2–5 True vergo: The effort should be toward differenang between peripheral and central causes for vergo. The characterisc feature of peripheral dizziness is the definite sensaon described by paents as a ‘spinning’ or ‘whirling’ feeling or that they or their surroundings are moving in a circular fashion. This experience is brief and their descripon of the event to the point in most paents with peripheral vesbular disorder.6,7

ACCOMPANYING SYMPTOMS OF PERIPHERAL DISEASE Patients with peripheral vertigo have distinctive features of onset, duraon, and accompanying symptoms in relaon to their dizziness. The onset and duraon of each episode of giddiness have an important role

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Accompanying symptoms Vertigo

Hearing loss and/or tinnitus

Brainstem Cerebellar Basal ganglia symptoms

Anxiety Gastrointestinal symptoms Palpitations Breathlessness Angina

Cochlear and/or VIII nerve disorders

Neurological disease

Anemia Cardiovascular disease Thyrotoxicosis Diabetes

Figure 2. The diagnostic value of eliciting associated symptoms in differential diagnosis of vertigo.8 Episode of vertigo

Single Labyrinthitis Multiple sclerosis

Constant Neurological disorders Decompensation Vestibular failure Psychogenic Multiple

Seconds Benign paroxysmal positional vertigo Vertebrobasilar insufficiency Cardiac dysrhythmia Epilepsy

Days Decompensated labyrinthitis

Hours Migraine Ménière's disease

Figure 3. The time course of vertigo in different conditions.12

in aiding us in making a diagnosis. The flowchart (Figure 3) would be a useful guide in arriving at a probable diagnosis. Other aural symptoms such as hearing loss, nnitus, and aural fullness are frequent symptoms of peripheral disease. Posion changes exacerbate the dizziness, and lying 35

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sll decreases the symptoms. Benign posional vergo, for instance, is to be suspected in paents with brief vergo, brought on by a simple posion change such as rolling over in bed. In most aacks, the onset is sudden, and for the most part, paents feel fine between spells. One of the most important informaon that we can obtain from a paent is the duraon of sensaon of vergo. The diagnosc value of elicing associated symptoms in differenal diagnosis of vergo is menoned in Figure 2 The single most useful localizing symptom in a dizzy paent is a unilateral otologic complaint: aural fullness, nnitus, hearing loss, or distoron. By carefully evaluang these complaints, the clinician can frequently localize both the side and the site of the lesion before any examinaon or tesng is done. Frequent causes of unilateral auditory disease with dizziness include endolymphac hydrops, perilymphac fistula, labyrinthis, vesbular neuris, and autoimmune inner ear disease. Patients with central causes of vertigo seldom have nausea and auditory symptoms. They tend to have difficulty in compensang for their vergo.

The single most useful localizing symptom in a dizzy patient is a unilateral otologic complaint: aural fullness, tinnitus, hearing loss, or distortion. Unlike peripheral vergo, central causes of dizziness produce a more variable picture. The sensaon may be described in a variety of ways: spinning, lng, pushed to one side, lightheadedness, clumsiness, or even blacking out. If documented loss of consciousness is present, a peripheral eology of the dizziness is rarely the cause. The other signs of neural dysfuncon that help in localizaon are ataxia, facial weakness, dysarthria, dysphagia, diplopia, hemiparesis, severe localized cephalgia, seizures, and memory loss. The me course of symptoms is more variable from minutes to hours, and the effect of movement or posion change is less predictable. These symptoms lead the clinician to suspect brainstem or corcal rather than labyrinthine sources.9–11 

36

Disequilibrium: It is a sensaon of imbalance when standing or walking—o en secondary to mulple sensory deficits. Paents usually deny any abnormal head sensaon and may refer to their condion as ‘dizziness in the feet.’ Such paents may have impaired motor

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Murthy TM

control. Physical examinaon may reveal decreased visual acuity, peripheral neuropathy (loss of propriocepon), and/or abnormal vesbular funcon.13 Vague lightheadedness other than vertigo, presyncope, or disequilibrium: Paents may describe their complaint as ‘heavyheadedness’ or ‘weird feeling in the head.’ This may occur with psychiatric disorders (anxiety, major depression, and somazaon disorders), hypervenlaon syndrome, encephalopathies, mulsensory dizziness, etc. Hypervenlaon may be associated with lightheadedness, peri-oral and peripheral numbness, ngling, and a sensaon of intense anxiety. Paents with a history of similar episodes or previously diagnosed panic disorder may become hypervigilant to the onset of dizziness symptoms and precipitate recurrent aacks.2,11

One another informaon in the history that can aid us in the diagnosis is age of the paent. Younger paents are more likely to have vesbular disorders, hypervenlaon, mulple sclerosis, and panic aacks. The elderly paent may also have these condions but are more likely than

Younger patients are more likely to have vestibular disorders, hyperventilation, multiple sclerosis, and panic attacks. the younger paent to suffer from stroke, mulsensory dizziness, and neurodegenerative diseases like Parkinson’s.14 Likewise, the elderly vegetarians may suffer from dizziness due to vitamin B12 deficiency.

GENERAL PHYSICAL AND EMOTIONAL HEALTH Many medical condions and emoonal factors can create a sense of dizziness and imbalance. Hypertension, hypotension, atheroscleroc disease, endocrine imbalances, and anxiety states are the common causes of lightheadedness, near-syncope, and/or instability but rarely produce a sense of true vergo. In addion, medicaon side effects and excessive caffeine, nicone, and alcohol intake should be invesgated as a source of dizziness.

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General Physical Examination Once a detailed history is obtained, the clinician needs to evaluate the physical examinaon of the paent and perform a complete head and neck examinaon. This is important as: 1. Dizzy patients frequently have other ear, nose, and throat pathologies. 2. Structural problems of the ear, nose, and throat at mes cause dizziness or indicate a more widespread process. Common findings on the roune examinaon related to dizziness include cerumen impacon, otitis media with effusion, chronic otitis with otorrhea, chronic sinusis with nasal airway obstrucon, and oropharyngeal findings consistent with sleep apnea. Congenital deformies of the pinna, external auditory canal, and face raise the queson of labyrinthine involvement.

Common findings on the routine examination related to dizziness include cerumen impaction, otitis media with effusion, chronic otitis with otorrhea, chronic sinusitis with nasal airway obstruction, and oropharyngeal findings consistent with sleep apnea. 3. The general physical examinaon can expose paents with anemia, postural hypotension, hypertensives, and other ailments, which can add to the discomfort of the paent. It is imperave on our part to examine paent’s BP in supine, sing, and standing posions to diagnose a significant number of postural hypotension paents—a reducon in BP of 20 mmHg in the systole within 2 minutes of standing is significant.2,15,16 At the conclusion of the regular examination, the specialized examinaon for dizziness is performed. Paents are tested with their glasses or contact lenses in place for best corrected vision. The sequence of the examinaon and their interpretaon is as follows (Table 2):

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Table 2. Interpretation of Various Tests to Differentiate between Central and Peripheral Vertigo17–19 Tests

Peripheral vertigo

Central vertigo

Spontaneous nystagmus

Intense, direction-fixed horizontal-rotary nystagmus that is enhanced under Frenzel lenses. Nystagmus intensifies when gazing in the direction of the fast phase (Alexander’s law).

Less-intense, directionchanging horizontal, vertical, torsional, or pendular nystagmus that is diminished under Frenzel lenses.

Gaze nystagmus

Enhancement of peripheral spontaneous nystagmus occurs without direction change when gazing in the direction of the fast phase.

Failure to hold the eye in the eccentric position, the eye drifts toward the midline, followed by refixation saccades toward the target. Gaze-evoked nystagmus is central in origin and always beats in the direction of intended gaze. Causes include drug effect (sedatives, anti-epileptics), alcohol, central nervous system tumors, and cerebellar degenerative syndromes.

Smooth pursuit

—

Cerebellar or brainstem disease can cause saccadic eye tracking in which the patient repeatedly loses the target and then catches up with a small saccade.

Saccades

—

Voluntary saccades (frontal lobe). Involuntary and voluntary saccades (brainstem reticular formation, nuclei of III, IV, and VI cranial nerves). Delayed saccades (cortical and brainstem lesions). Slow saccades (brainstem disease). Inaccurate saccades (overshoots)—cerebellar vermis and fastigial nuclei. Disconjugate movements— involvement of medial longitudinal fasciculus

Fixation suppression

—

Failure of fixation suppression in the presence of adequate visual acuity implies floccular dysfunction

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Head thrust

Head impulse test was — described as a reliable sign of reduced vestibular function in the plane of rotation for the ipsilateral ear.

Headshake

Post-headshake nystagmus is considered a pathologic sign of imbalance in the vestibular inputs in the plane of rotation.

Dynamic visual acuity

Excessive retinal slippage — during head movement is a sign of vestibular dysfunction. Most common cause is bilateral vestibular failure due to ototoxicity or old age.

Dix–Hallpike positioning

Characteristics of classical Atypical positioning nystagmus positioning nystagmus may imply either peripheral or include geotropic torsional central disease. direction, brief latency (5–20 seconds), decline with repeated positioning, 30 seconds or less duration, and reversal on arising.

Static, positional, nystagmus is nonlocalizing by itself and must be interpreted in the light of other physical findings

—

Vertical positional nystagmus is central in origin, implying cranial–cervical or fourth ventricle origin.

Limb coordination

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Dysmetria or dysrhythmia s/o cerebellar cortical disease.

Tragal compression, pneumatic otoscopy, Tullio phenomenon

Consistent eye deviations or nystagmus s/o oval window (fistula, excessive footplate movement), round window (fistula), lateral semicircular canal (fistula), and superior semicircular canal (dehiscence).

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Valsalva maneuver

Eye elevation and intorsion with loud sounds with Valsalva maneuver are suggestive of superior canal dehiscence syndrome.

Cranial–cervical junction abnormalities (Arnold–Chiari malformation in particular) produce vertical downbeat nystagmus with any maneuver that increases intracranial pressure.

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Prolonged nystagmus, vertical nystagmus following horizontal headshake (‘cross coupling’), and disconjugate nystagmus are suggestive of central etiology.

Understanding the Process Flow in a Vertigo Clinic

Hyperventilation action

Irritative nystagmus (toward the affected ear) secondary to elevated pH and increased eighth nerve firing is seen in lesions that affect the vestibular nerve such as petrous apex lesions, acoustic schwannoma, and eighth nerve demyelination.



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The paent is observed for:            

Spontaneous nystagmus Gaze nystagmus Smooth pursuit Saccades Fixaon suppression Head thrust test Headshake test Limb coordinaon Cerebellar funcon test Dix–Hallpike and other posional tests Tragal compression, pneumac otoscopy (fistula test), and Valsalva Hypervenlaon

Dix–Hallpike and other posioning tests rule out benign paroxysmal posional vergo (BPPV) in posterior and horizontal semicircular canals (SCCs). The test varies in the fact that for posterior canal BPPV, paent’s head is hyperextended, with head lted to a side, and for horizontal canal BPPV, paent is in supine posion and head is turned suddenly to one side and then repeated on the opposite side. The nystagmus too varies—for posterior canal BPPV, it is a georotatory nystagmus, and for horizontal canal BPPV, it is horizontal. This is important as the reposioning maneuver also changes for the two condions. Tragal compression, pneumac otoscopy, Tullio phenomenon, and Valsalva maneuver rule out a third window, especially the superior canal dehiscence. At this juncture, in most paents, we would be able to make a diagnosis of the probable eology of their discomfort. Further invesgaons are ordered based on the requirement of the paent.

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INVESTIGATIONS AT OUR DISPOSAL TO ASSESS A PATIENT WITH VERTIGO 1. Roune invesgaons: Blood—complete blood count and blood sugar levels; thyroid funcon test; vitamin B12 assay; and electrolytes— rarely help make a diagnosis.6 2. If suspicious of a cardiovascular cause—electrocardiography (ECG), echocardiography, and Doppler study of vertebral and carod vessels. 3. Vesbular laboratory tesng: It help to document and quanfy abnormalies, aid in diagnosing and localizing vergo as peripheral or central, and determine laterality. Serial evaluaons helps in longterm management, especially paents who have received ototoxic medicaon. 4. Audiological evaluaon: Hearing loss usually localizes the side. Some condions have characterisc audiologic findings, such as

The electronystagmography report will typically comment on spontaneous nystagmus, gaze-evoked nystagmus, saccades, pursuit, optokinetic nystagmus, and positional nystagmus, testing horizontal and sometimes vertical eye movements. the fluctuang low-frequency sensorineural hearing loss (SNHL) of Ménière’s syndrome. Unilateral SNHL should always be further evaluated to rule out retrocochlear pathology, especially if the speech discriminaon score is poor. Roune audiometry should be followed with brainstem-evoked response audiometry (BERA). If BERA is suggesve of retrocochlear pathology and on caloric test the response is poor on the ipsilateral side, neuro-imaging is indicated to rule out the probability of vesbular schwannoma. 5. Electronystagmography (ENG) and caloric tesng: These refer to a combinaon of tests with eye movement recording, which includes a search for vesbular nystagmus, ocular motor screening baery, and caloric tesng. The ENG report will typically comment on spontaneous nystagmus, gaze-evoked nystagmus, saccades, pursuit, optokinec nystagmus, and posional nystagmus, tesng horizontal and somemes vercal eye movements. The ENG may help to quanfy 42

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any spontaneous nystagmus, detect subtle changes of saccadic velocity, or clarify pursuit symmetry, but for the clinician adept at the bedside vesbular and ocular motor examinaon, the informaon gained from this part of the ENG usually adds lile to the evaluaon. The main ulity of the ENG is in caloric tesng. Bithermal caloric tesng is the most widely ulized vesbular laboratory test. It is most useful in assessing unilateral vesbular dysfuncon. The advantage of caloric tesng is that each ear can be smulated individually. 6. Methods of recording eye movements: Caloric and rotaonal chair tesng provides an indirect measure of vesbular funcon based on the eye movements in response to vesbular smulaon. Current tesng focuses on the horizontal vesbulo ocular reflex (VOR) as it is the easiest to smulate and as several reliable methods exist for recording horizontal eye movements. Electro-oculography (EOG) is the most commonly used method because it is simple and non-invasive. Other methods such as video recordings of eye movements and infrared reflecon can be used. Rotaonal tesng

Electro-oculography is the most commonly used method because it is simple and non-invasive. also focuses on the VOR of the horizontal SCCs, because they are easy to smulate and record. Visual–vesbular interacons can be assessed in addion to the same ocular motor screening baery performed prior to caloric tesng. Rotaonal tesng offers several advantages over caloric tesng of the VOR. Rotaonal tesng is ideal for evaluang bilateral vesbular loss because both labyrinths are smulated simultaneously. Diminished funcon, as seen with ototoxic drugs, can be idenfied earlier than with caloric tesng, in which responses have a larger variance. Rotaonal tesng is also more sensive in detecng remaining vesbular funcon. Paents with absent bithermal caloric responses may have recordable or even normal rotaonal-induced nystagmus at high frequencies, detecon of which can have important therapeuc implicaons. Rotaonal tesng is less useful for evaluang unilateral disease. Acute unilateral peripheral lesions may produce an asymmetric gain with rotaonal tesng, parcularly at high speeds where inhibitory cutoff occurs in the remaining intact labyrinth. Lesions in central 43

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vesbular pathways can lead to the same decreased or asymmetric gain seen with peripheral lesions. Increased gain may occur with cerebellar lesions. 7. Radiological imaging: Magnec resonance imaging is useful in paents with suspected central disorders or lesions at the internal auditory canal or vesbulocochlear nerve. Sagial images are used to assess for cerebellar vermis atrophy or a Chiari malformaon. Axial images should be used to scrunize the brainstem as well as look for a vertebral artery dissecon. Gadolinium administraon may reveal an enhancing vesbular schwannoma, meningioma, or microvascular loop (well made out in construcve interference in steady state [CISS] sequences), compressing the vesbular nerve (vesbular paroxysmia). Computed tomography is the modality of choice for evaluang middle ear diseases, trauma, or fibro-osseous disease. High-resoluon thin axial and coronal secons through the temporal bones can assess for superior canal dehiscence as well as

Magnetic resonance imaging is useful in patients with suspected central disorders or lesions at the internal auditory canal or vestibulocochlear nerve. enlarged vesbular aqueducts associated with episodic vergo in the seng of childhood-onset SNHL. 8. Vesbular-evoked myogenic potenals (VEMPs) are a relavely new test that directly measures the modulaon of tonic electromyographic acvity induced by vesbular smulaon. A sound smulus acvates vesbular afferents in the saccule, which then is transmied through inferior part of vesbular nerve to vesbular nucleus to the vesbulospinal tract to the ipsilateral sternomastoid motor nucleus. This reflex produces a brief period of inhibion of motor neuron firing in a tonically acvated sternocleidomastoid (SCM), with a waveform that can be demonstrated through averaging. The amplitude of the response is proporonate to the degree of muscle acvaon during recording and is reduced or abolished in conducve hearing loss but is unaffected by profound sensorineural deafness. VEMPs are parcularly useful for evaluang paents with Tullio phenomenon (imbalance or vergo in response to loud sound). The most common underlying abnormality is a dehiscence of the bony roof of the superior SCC. 44

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9. Posturography: The ENG and rotaon test evaluate vesbule-ocular reflex in the verginous paent without addressing the effects of somatosensory (i.e., propriocepve) and visual influences on equilibrium and paent. In effect, the vesbulospinal tract is not evaluated. Chiefly, the test addresses two major areas: motor control test, which examines the paent’s motor system and the ability of the central nervous system (CNS) to adapt to changing condions, and sensory organizaon test, which examines propriocepve, visual, and vesbular systems working as an integrated whole. Clinically, the types of paent who would be candidates for posturography are: i. Those in whom history indicates imbalance or unsteadiness rather than straighorward vergo ii. Children with delayed motor development iii. Those paents in whom there is an impact of a lesion on the paent’s balance and posture for rehabilitaon planning iv. In whom there is suspected organic vesbular pathology and VOR tesng is non-contributory

The electronystagmography and rotation test evaluate vestibule-ocular reflex in the vertiginous patient without addressing the effects of somatosensory (i.e., proprioceptive) and visual influences on equilibrium and patient.

REHABILITATION The inial assessment helps to idenfy factors that may compromise rehabilitaon efforts. They are: i. Inadequate CNS acvity ii. Poor eye/head stabilizaon iii. Disordered percepon of stability iv. Fluctuang vesbular acvity v. Impaired sensory inputs vi. Psychological dysfuncon vii. Impaired musculoskeletal funcon viii. Impaired balance

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The rehabilitaon plan needs to focus on: i. Correcon of remedial problems—if paent has problems that interfere in rehabilitaon, they need to be corrected, such as visual defects, cataract, joint inflammaons, etc. ii. General fitness program—poorly fit paent will be unable to take part in an acve exercise-based rehabilitaon program, so general fitness needs to be improved slowly but surely. iii. Physical exercise program—to treat musculoskeletal problems such as arthris, retraining in appropriate stance and gait. iv. Psychological assessment—needs to be done, as development of psychological symptoms is common (like anxiety, depression, and phobia) and they need to be addressed with appropriate professional care and therapy. v. Medicaon—most vesbular sedaves have a role only in the acute phase; in chronic paents, it may interfere with rehabilitaon. In such paents, they may be prescribed SOS to aid them connue the exercise regimes.

Medication—most vestibular sedatives have a role only in the acute phase; in chronic patients, it may interfere with rehabilitation. vi. Exercises—customize it to the paents’ needs, which can be done by a pre-rehabilitaon assessment of vesbular deficits, posture, gait, and balance disorders, and then idenfy the best smuli to induce compensaon. These need to be customized based on individuals’ funconal disability. These can be iniated by the physiotherapist and then a home program encouraged. vii. Realisc goals—for family, social, and occupaonal needs—involve the paent in making decision on their limit of ability to perform exercise, including general fitness exercise, and give specific goals, which will help them integrate into the social and occupaonal acvies. viii. Monitoring, feedback, and follow-up—a ready helpline (telephone) is of great help in aiding these paents and movang them through the rehabilitaon.20

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THE DETAILS OF SPECIALIZED EXAMINATIONS FOR GIDDINESS ARE AS FOLLOWS Spontaneous Nystagmus If nystagmus is observed, parcular aenon is paid to the amplitude, direcon, and effect of target fixaon. Lesions of the labyrinth and nerve VIII produce intense, direcon-fixed horizontal-rotary nystagmus that is enhanced under Fresnel lenses. The nystagmus also intensifies when gazing in the direcon of the fast phase (Alexander’s law). This paern can be seen in both irritave (beang toward the affected ear) and destrucve (beang toward the unaffected ear) lesions of the labyrinth, nerve VIII, or (rarely) the vesbular nuclei. In contrast, lesions of the brainstem, cerebellum, and cerebrum cause less-intense, direction-changing horizontal, vercal, torsional, or pendular nystagmus that is diminished under Fresnel lenses. Examples include periodic alternang nystagmus (PAN), congenital nystagmus, and lesions of the midline cerebellum.

Lesions of the brainstem, cerebellum, and cerebrum cause less-intense, direction-changing horizontal, vertical, torsional, or pendular nystagmus that is diminished under Fresnel lenses.

Gaze Nystagmus The ability to maintain eccentric gaze is under control of the brainstem and midline cerebellum, parcularly the vesbulocerebellum (especially the flocculonodular lobes). When these mechanisms fail to hold the eye in the eccentric posion, the eye dri s toward the midline (exponenally decreasing velocity), followed by refixaon saccades toward the target. Such gaze-evoked nystagmus is central in origin and always beats in the direcon of intended gaze. In contrast, enhancement of peripheral spontaneous nystagmus (linear slow component velocity) occurs without direcon change when gazing in the direcon of the fast phase. Causes of gaze-evoked nystagmus include a drug effect (sedaves and an-epilepcs), alcohol, CNS tumors, and cerebellar degenerave syndromes.

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Smooth Pursuit Ask the paent to follow your finger as you slowly move it le and right and up and down. Make sure the paent can see the target clearly and you do not exceed 60° in total arc or 40°/sec. Normal eye tracking of a slowly moving discrete object generates a smooth eye movement that the examiner can easily see. Cerebellar or brainstem disease can cause saccadic eye tracking in which the paent repeatedly loses the target and then catches up with a small saccade. In most cases, abnormal pursuit is non-localizing within the CNS, although ipsilateral loss of pursuit can be ascribed to parietal lobe lesions. The examiner must make sure that the paent can see the target and is aenve to the task.

Saccades Ask the paent to look back and forth between 2 outstretched fingers held about 12 inches apart in the horizontal and vercal plane. Observe for latency of onset, speed, accuracy, and conjugate movement. Saccadic eye movements are refixaon movements that involve the frontal lobes

Cerebellar or brainstem disease can cause saccadic eye tracking in which the patient repeatedly loses the target and then catches up with a small saccade. (voluntary saccades), brainstem reticular formation (voluntary and involuntary saccades), and oculomotor nuclei III, IV, and VI. Delayed saccades are seen in corcal and brainstem lesions, and slow saccades accompany brainstem disease. Inaccurate saccades (especially overshoots) are associated with lesions of the cerebellar vermis and fasgial nuclei. Finally, disconjugate eye movements with slowing of the adducng eye and overshoots of the abducng eye imply medial longitudinal fasciculus pathology frequently associated with mulple sclerosis.

Fixation Suppression Ask the paent to fixate on his or her own index finger held out in front at arm’s length. Unlock the examinaon chair and rotate the paent up to 2 Hz while the paent stares at the finger moving with him/her. The examiner observes for a decrease in the visual–vesbular nystagmus that is evoked during rotaon without ocular fixaon. The modulaon of nystagmus invoked by rotaon is a CNS phenomenon heavily dependent 48

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on the cerebellar flocculus. Failure of fixaon suppression in the presence of adequate visual acuity implies floccular dysfuncon. This test is similar in nature to the fixaon suppression performed a er caloric smulaon during EOG.

Head Thrust Ask the paent to fixate on a target on the wall in front of the paent while the examiner moves the paent’s head rapidly (>2000°/sec2) to each side. The examiner looks for any movement of the pupil during the head thrust and a refixaon saccade back to the target. Either direct observaon of pupillary movement or the use of an ophthalmoscope is employed to document eye movement. Introduced by Halmagyi and Curthoys in 1988, the head impulse test was described as a reliable sign of reduced vesbular funcon in the plane of rotaon for the ear ipsilateral to the head thrust. The observaon of eye movement during the maneuver is a sign of decreased neural input from the ipsilateral ear to the VOR because

The head impulse test was described as a reliable sign of reduced vestibular function in the plane of rotation for the ear ipsilateral to the head thrust. the contralateral ear is in inhibitory ‘saturaon’ and cannot supply enough neural acvity to stabilize gaze. In such instances, the eye travels with the head during the high-velocity movement and a refixaon saccade is necessary to refoveate the target. Bilateral refixaon movements are seen frequently in cases of ototoxicity.

Headshake Tilt the head of the paent forward 30° and shake the head in the horizontal plane at 2 Hz for 20 seconds. Observe for post-headshake nystagmus and note direcon and any reversal. Fresnel lenses are preferred to avoid fixaon. The maneuver may be repeated in the vercal direcon. Postheadshake nystagmus is considered a pathologic sign of imbalance in the vesbular inputs in the plane of rotaon. In most instances, a peripheral cause is idenfied, with the nystagmus directed toward the stronger ear. A small reversal phase is somemes observed. Signs of central eology include prolonged nystagmus, vercal nystagmus following horizontal headshake (‘cross-coupling’), and disconjugate nystagmus.

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Dynamic Visual Acuity Ask the paent to read the lowest (smallest) line possible on a Snellen’s eye chart with best corrected vision (glasses or contact lenses). Repeat the maneuver while passively shaking the paent’s head at 2 Hz and record the number of lines of acuity ‘lost’ during the headshake. Excessive renal slippage during head movement is a sign of vesbular dysfuncon. In the clinical examinaon, the most frequent eology is bilateral vesbular loss related to ototoxicity or aging. Poorly compensated unilateral dysfuncon can also cause loss of dynamic visual acuity but is harder to idenfy with this clinical test. It is important that the examiner shake the paent’s head to avoid pauses, during which the paent can see the target.

Dix–Hallpike Positioning With the examination chair unfolded like a bed, turn the patient’s head 45° to one side while seated and rapidly but carefully have the

Post-headshake nystagmus is considered a pathologic sign of imbalance in the vestibular inputs in the plane of rotation. paent recline. Observe the eyes for nystagmus and, if present, note the following 5 characteriscs: latency, direcon, fague (decrease on repeated maneuvers), habituaon (duraon), and reversal on sing up. A posive maneuver is diagnosc for benign posional vergo, which is thought to be due to otoconial debris either floang (canalithiasis) or fixed (cupulolithiasis) within the posterior SCC of the undermost ear. Characteriscs of classical posioning nystagmus include geotropic torsional direcon, brief latency (5–20 seconds), decline with repeated posioning, 30 seconds or less duraon, and reversal on arising. Atypical posioning nystagmus may imply either peripheral or central disease.

Static Positional Ask the paent to lie sll in 3 posions—supine, le lateral, and right lateral—for 30 seconds and observe for nystagmus. Use of Fresnel lenses is recommended. The presence of a stac posional nystagmus is nonlocalizing by itself and must be interpreted in the light of other physical findings. In general, however, vercal posional nystagmus is central in origin, implying cranial–cervical or fourth ventricle origin. 50

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Limb Coordination Ask the paent to perform a series of coordinaon tasks such as finger– nose–finger, heel–shin, rapid alternang moon, and fine finger moon (counting on all digits). Observe for dysmetria or dysrhythmia. The presence of limb dysmetria or dysdiadochokinesia is a useful indicator of cerebellar corcal disease, which may or may not accompany midline or vesbulocerebellar oculomotor dysfuncon.

Romberg Stance Have the paent stand with feet close together and arms at the side, with eyes open and then eyes closed. Observe for the relave amount of sway with vision present vs absent. The Romberg stance is primarily a test of somatosensaon and propriocepon and not of vesbular input. Paents with compensated bilateral vesbular loss stand normally in both eyes-open and eyes-closed Romberg posion because of adequate propriocepon from the stable support surface. There are 2 ways, however, to make this test more sensive to vesbular deficits—tandem stance and

The Romberg stance is primarily a test of somatosensation and proprioception and not of vestibular input. 3-inch foam. In the tandem stance, the support surface cues are sufficiently altered so that vesbular cues play a greater role in maintaining upright posture. Similarly, when the paent stands on a compliant support surface such as 3-inch foam, somatosensory cues are muted and vesbular cues become more important.

Gait Observation Ask the paent to walk 50 feet in the hall, turn rapidly, and walk back without touching the walls. Observe for iniaon of movement, stride length, arm swing, missteps, and veering and signs of muscle weakness or skeletal abnormality (kyphoscoliosis, limb asymmetry, and limp). There is no such thing as a ‘vesbular gait.’ If a paent suffers an acute unilateral loss of otolithic funcon, the paent will tend to veer toward the side of the lesion. However, a variety of central brainstem and musculoskeletal lesions also produce lateral deviaon during ambulaon. Difficules with gait iniaon and turns and decreased arm swing can be seen in 51

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extrapyramidal disease. Gait ataxia implies cerebellar dysfuncon and is disnctly different from gait deviaon associated with uncompensated peripheral vesbular disease. Finally, exaggerated hip sway, rhythmic deviaons, and an excessive reliance on touching the wall during walking may constute signs of a funconal gait disorder.

SPECIALIZED TESTS Specialized tests are tragal compression, pneumac otoscopy, Tullio phenomenon, and Valsalva maneuver. With Fresnel lenses in place, observe for nystagmus or tonic eye deviaons with symptoms of dizziness under 4 test condions: (1) steady tragal compression to increase pressure in the external auditory canal, (2) posive and negave pressure applied with the pneumac otoscope, (3) presentaon of loud tones via tuning fork or impedance bridge, and (4) increased pressure during breath holding against pinched nostrils or closed glos.

Consistent eye deviations or nystagmus during any of the maneuvers imply abnormal coupling between either the outside atmosphere or the intracranial space and the inner ear. Consistent eye deviaons or nystagmus during any of the preceding maneuvers imply abnormal coupling between either the outside atmosphere or the intracranial space and the inner ear. This can occur with abnormal connecons between the labyrinth and the middle ear or middle fossa at the following sights: oval window (fistula, excessive footplate movement), round window (fistula), lateral SCC (fistula), and superior SCC (dehiscence). In parcular, eye elevaon and intorsion with loud sounds or Valsalva maneuver against pinched nostrils are suggesve of superior canal dehiscence syndrome and have been described by Minor.21,22 In addion, cranial–cervical juncon abnormalies (Arnold–Chiari malformaon in parcular) produce vercal downbeat nystagmus with any maneuver that increases intracranial pressure.

Fukuda Step Test Action Ask the paent to march in place with arms extended and eyes closed for 1 minute. Note the degree of lateral rotaon at the end of the maneuver.

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Most normal subjects deviate 45° toward the affected side. This finding alone, however, is not conclusive for otolith dysfuncon.

Hyperventilation Action Ask the paent to take 20 deep breaths in and out in rapid succession, observe for nystagmus under Fresnel lenses, and record symptoms. Hypervenlaon has 2 effects: (1) cerebrovascular vasoconstricon, and (2) elevaon of blood pH. Vasoconstricon causes lightheadedness and ngling of the hands and lips and may reproduce the symptoms of paents with hypervenlaon syndrome or anxiety. More specifically, irritave nystagmus (toward the affected ear) secondary to elevated pH and increased VIII nerve firing are seen in lesions that affect the vesbular nerve such as petrous apex lesions, acousc schwannoma, and VIII nerve demyelinaon.

Vasoconstriction causes lightheadedness and tingling of the hands and lips and may reproduce the symptoms of patients with hyperventilation syndrome or anxiety.

Mastoid Oscillation Action Place a vibrang source on the mastoid p and observe for nystagmus under Fresnel lenses. Note direcon and waveform and effect of target fixaon with removal of lenses. Mastoid oscillaon acts as an excitatory smulus to both labyrinths and, in some cases of asymmetry, produces a horizontal-rotatory nystagmus toward the stronger ear. In a sense, this nystagmus is similar in origin to that produced by the headshake maneuver.

CONCLUSION The intenon of this chapter is to develop a thought process about evaluaon of dizziness. This can be incorporated in exclusive vergo clinics or in day-to-day pracce. The history should be ‘on the house.’ Give enough me and this will guide you. Most paents with giddiness look very ‘alert and normal’ 53

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and that may tempt us to ‘work them up (invesgate).’ The Dix–Hallpike maneuver, in combinaon with a thorough neurological examinaon, will be more producve than indiscriminate neuro-imaging. The paent, if invesgated for metabolic and hemodynamic causes, may yield results more than imaging. Judicious use of invesgaons and a systemac approach to evaluate giddiness should help us in diagnosing a majority of our paents and help them.

REFERENCES 1. Froehling DA, Silverstein MD, Mohr DN, et al. Does this dizzy paent have a serious form of vergo? JAMA 1994;271:385–8. 2. Kroenke K, Hoffman RM, Einstadter D. How common are various causes of dizziness? A crical review. South Med J 2000;93:160–7. 3. Colledge NR, Barr-Hamilton RM, Lewis SJ, et al. Evaluaon of invesgaons to diagnose the cause of dizziness in elderly people: a community based controlled study. BMJ 1996;313:788–92. 4. Ooi WL, Barre S, Hossain M, et al. Paerns of orthostac blood pressure change and their clinical correlates in a frail, elderly populaon. JAMA 1997;277:1299–304. 5. Mehagnoul-Schipper DJ, Vloet LC, Colier WN, et al. Cerebral oxygenaon declines in healthy elderly subjects in response to assuming the upright posion. Stroke 2000;31:1615–20. 6. Hoffman RM, Einstadter D, Kroenke K. Evaluang dizziness (literature review). Am J Med 1999;107:468–78. 7. Baloh RW. Vergo (review). Lancet 1998;352:1841–6. 8. Luxon LM. The diagnosc value of elicing associated symptoms in differenal diagnosis of vergo. In: Diseases of the Ear 6th ed. London, England: Arnold Publishers 1997. 9. Baloh RW. Dizziness: neurological emergencies (review). Neurol Clin 1998;16: 305–21. 10. Baloh RW. Differenang between peripheral and central causes of vergo (review). Otolaryngol Head Neck Surg 1998;119:55–9. 11. Derebery MJ. The diagnosis and treatment of dizziness (review). Med Clin North Am 1999;83:163–77. 12. Luxon LM. Disorders of balance, assessment and psychological aspects. Figure 14.6: me course of vergo in different vesbular disorders. In: Diseases of the Ear 6th ed. London, England: Arnold Publishers, 1997:222. 13. Pigo DC, Rosko CJ. The dizzy paent: an evidence-based diagnosis and treatment strategy. Emerg Med Pract 2001;3:1–20. 14. Drachman DA. A 69-year-old man with chronic dizziness (case report). JAMA 1998;280:2111–8. 15. Herr RD, Alvord L, Johnson L, et al. Immediate electronystagmography in the diagnosis of the dizzy paent. Ann Emerg Med 1993;22:1182–9.

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16. Walker JS, Barnes SB. Dizziness (review). Emerg Med Clin North Am 1998;16: 845–75. 17. Halmagyi GM, Curthoys IS. A clinical sign of paresis. Arch Neurol 1988;45:737–9. 18. Asawavichiangianda S, Fujimoto M, Mai M, et al. Significance of headshaking nystagmus in the evaluation of the dizzy patient. Acta Otolaryngol Suppl 1999;540:27–33. 19. Minor LB. Superior canal dehiscence syndrome. Am J Otol 2000;21:9–19. 20. Luxon LM. Rehabilitaon and management of balance and vesbular disorders. In: Diseases of the Ear 6th ed. London, England: Arnold Publishers, 1997:233–41. 21. Cremer PD, Minor LB, Carey JP, Sanna CC. Eye movements in paents with superior canal dehiscence syndrome align with the abnormal canal. Neurology 2000;55:1833–41. 22. Hirvonen TP, Carey JP, Liang CJ, Minor LB. Superior canal dehiscence: mechanisms of pressure sensivity in a chinchilla model. Arch Otolaryngol Head Neck Surg 2001;127:1331–6.

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State-of-the-Art Vertigo Clinic Anirban Biswas Consultant Neurotologist Vertigo Clinic, Belle Vue Kolkata, West Bengal

Why is it that vergo clinics are so very rare and why is it that in spite of our regularly hearing of new mulspecialty and superspecialty hospitals coming up in all the lanes and bye lanes of the metropolitan cies and a decent number in all district towns, we praccally never hear of a proper vergo clinic being setup? Vergo is a common disease and according to internaonal stascs 5% of all paents seeking medical advice suffer from some form of balance disorder. As much as 50% of the geriatric populaon is known to have a disorder in the balance system and vergo or imbalance is the second most common complaint in the geriatric populaon. Yet one very rarely hears of a vergo clinic being established. Hospital business is nowadays believed to be one of the most profitable businesses available, there is no dearth of vergo paents, and new hospitals with so-called cung edge technology are sproung in scores daily. But nobody ventures a vergo clinic in any of the hospitals. Vergo paents, just like other paents also need good professional care. Hence, healthcare centers should also stress on establishment of proper vergo clinics so as to avoid shuling between general medical praconers, orthopedic surgeons, ENT specialists, neurologists, cardiologists, ophthalmologists, gastroenterologists (as vergo is somemes accompanied by nausea and voming) and even psychiatrists, and get more or less the same an-vergo drugs in different brand names from all of them along with an advice for a CT scan or MRI of the brain, and an X-ray of the cervical spine–none of which actually test the balance funcon.

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It is rare to find a vergo paent who has not been prescribed anything else but a symptom relieving an-vergo drug which at best just camouflages the symptom of vergo and gives a very false sense of complacency both to the doctor as to the paent. Camouflaging symptoms is no treatment and no treatment is possible unl the underlying cause is diagnosed. Vergo or imbalance is not a disease in itself and is just a symptom of an underlying disease which could be just a trivial self-liming condion like an inflammaon of the vesbular nerve or even a life-threatening condion like a tumor in the brain or some sinister condion like mulple sclerosis, Ménière’s disease, or a brainstem infarct. This form of treatment where an external manifestaon that is a symptom of an underlying disease is treated with symptom-relieving drugs without trying to diagnose the cause of the symptom is unique for the hapless vergo paents and is non-judicious to say the least.

Vertigo or imbalance is not a disease in itself and is just a symptom of an underlying disease which could be just a trivial self-limiting condition like an inflammation of the vestibular nerve or even a life-threatening condition like a tumor in the brain or some sinister condition like multiple sclerosis, Ménière’s disease, or a brainstem infarct. To treat a paent of vergo it is essenal that the underlying cause of the vergo/imbalance is properly diagnosed. Only then can it be actually treated. The diagnosis and management of vergo is a me-consuming affair and requires very specialized setups with specially trained and dedicated manpower. This is precisely why in most advanced countries vergo paents are treated in vergo clinics and by a special class of doctors called neurotologists. This calls for a need to establish vergo clinics both in the semi-urban and urban setups. The treang physicians should be exposed to the proper diagnosing procedures given the exisng infrastructure in their clinics and a proper referral protocol needs to be setup. This would not only go a long way in cung down on the diagnosis me but also save a lot of repeat visits to the hospital and in the long run should also be cost-effecve to the paent.

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A vergo clinic must have three basic things, namely: 



A system of very detailed history taking. As discussed this is a tedious and a very me consuming process and there are two ways of doing it (1) having printed history sheets with quesons and yes/no ck boxes (Appendix 1 and 2), (2) a so ware where all the quesons are pre-entered and a (3) trained receponist who can ask the quesons and fill up the computerized form. There are computerized programs available for this, one of them being the Audio Vesbular Data Management (AVDM) so ware. A setup for the different types of neurotologŝcal tests . This includes both (1) audiological tests like pure tone audiometry with the special tests like tone decay test, short increment sensivity index (SISI) test, alternate binaural loudness balance (ABLB), speech audiometry and glycerol test, brainstem evoked response audiometry (BERA), electrocochleography (ECochG), tympanometry with acousc reflex

All these tests are required because these tests are like small peep windows into the very complex working of the balance system in the brain and it is only by combining the information obtained from the different tests that a mental picture of the functioning of the balance system can be made. tests; (2) vesbular funcon tests like at least one form of oculography either videonystagmography (VNG) or electronystagmography (ENG) preferably both as in some paents VNG is easier and in some ENG is easier, vesbular evoked myogenic potenals (VEMP), cranio-corpography (CCG), stabilometry and other forms of posturography like computerized dynamic posturography. All these tests are required because these tests are like small peep windows into the very complex working of the balance system in the brain and it is only by combining the informaon obtained from the different tests that a mental picture of the funconing of the balance system can be made. Some of these tests are very briefly described below. Most of these tests can be done by specially trained technicians under medical supervision. The medical supervision is very important and the vesbular funcon tests are not something that can be le to insufficiently trained personnel. Interpretaon of the tests is also very much a medical 58

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exercise and must essenally be done by a doctor with special interest in neurotology and sufficient insight and knowledge of the vesbular system. Some of the vesbular funcon tests like VNG and ENG require smulaon of the external auditory meatus which may cause vagal smulaon leading to bradycardia and even cardiac arrest that will require urgent medical management. Moreover, the tests when done cause some degree of vergo or imbalance along with nausea and voming which are not a very pleasant sensaon and the paent feels safe and comfortable when he/she sees a doctor in front. Management of such symptoms should be done only under proper prescripon by qualified clinician. It will not be out of place to menon here that technological advancements take place regularly in neurotological diagnosc instruments and it is very essenal that the vergo clinic keeps on upgrading the instruments as technological improvements take place. It is improper to test a paent with obsolete technology. Modern BERA machines are equipped with a technology

Videonystagmography and electronystagmography require stimulation of the external auditory meatus which may cause vagal stimulation leading to bradycardia and even cardiac arrest that will require urgent medical management.



called chirp that increases the sensivity of the BERA test and so a modern vergo clinic should have facilies of chirp BERA and should not be doing the age-old convenonal BERA. Modern VEMP machines all come equipped with facilies of recfied VEMP and with this technology being available now, the convenonal nonrecfied VEMP is now obsolete. Currently available VNG machines are beer equipped to carry out the very important oculomotor tests which is a very important part of evaluang vesbular funcon and hence machines that do not have this facility is irrelevant in today’s sengs. Proper arrangements for treatment and management of the balance disorder. The mainstay of treatment in many types of balance disorders is some form of physical therapy and not only drug therapy. Hence, the vergo clinic must have provisions of specialized physical therapy that can be carried out by either operaonal therapists or physiotherapists who are specially trained in handling balance disorder paents. A lot of 59

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instruments are now available for carrying out the special physical therapy that is required in balance disorder paents. Some of these are like the balance rehabilitaon unit (BRU) of Interacouscs, or that aached to the posturography units like the stabilometry or computerized dynamic posturography setups. Most posturography instruments are packaged with devices for physical therapy and it is always good if possible and affordable to have such facilies in vergo clinics. No state of the art vergo clinic is complete without a properly trained physician to recognize the symptoms of vergo and appropriately invesgate, or if he feels the need then refer to higher center with more state of the art invesgave facilies to understand the underlying pathology.

THE INFRASTRUCTURAL REQUIREMENTS The minimum civil structure that is required for a vergo clinic is about 4 normal rooms between 100 sq. . and 150 sq. . in size and 2 small soundproof (rather sound-treated) rooms (Figure 1) where special acousc

Most posturography instruments are packaged with devices for physical therapy and it is always good if possible and affordable to have such facilities in vertigo clinics. les (not too costly) have been put on the walls and a false ceiling made with the acousc les. The floor of the soundproof rooms should preferably be made with wooden les if possible and thickly carpeted. One of the 2 soundproof rooms should have the 2 room audiometry facility. One of the soundproof rooms that is the one having the 2-room facility will have to be used for pure tone audiometry and related tests like SISI, TDT, ABLB, etc. and the other soundproof room will be required for the evoked potenal tests like EcochG, ASSR, OAE and BERA tests (Figure 2). This second room should be slightly larger in size preferably 100 sq. . room as the auditory evoked potenal (AEP) machine for BERA, ASSR, EcochG, VEMP, etc. will have to be put here. A single AEP machine connected to a computer can carry out all these tests. A comfortable table for the paent to lie down preferably a 2’ x 6’ paent table (Figure 3), a sing stool, a chair and a complete computer setup with provision for a comfortable place for the computer operator will have to be provided in this room. Space is always a problem in metropolitan cies and so intelligent use of space is very

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Figure 1. A two room sound-treated audiomtery room setup.

important while seng up a vergo clinic. Paent comfort is one of the basic criteria in geng a good result in the auditory evoked potenal and other neurotological tests. This room should preferably be away from places where heavy electrical equipment like pumps or li s are placed. The room where the oculography machine(s) is to be setup be it ENG or beer sll a VNG does not have to be a soundproof room, any ordinary air-condioned room should suffice. The room should be approximately 100–120 sq. . room (Figure 4). If a VNG is to be used then, there should be provisions of hanging a LCD projector from the ceiling or a large (preferably a 60 inch) flatscreen TV monitor on the wall for the visual display during the oculomotor tests (Figure 5). Both together are not required, either the projector or the large TV screen suffices. The room should also have water connecon and a small basin or sink for preparing the hot/cold water for irrigaon in the paent’s ears. If the ready-made caloric irrigators are used then also a water connecon in the room is essenal. If affordable, it is prudent to have both a water caloric irrigator as well as an air caloric irrigator (Figure 6). Not that these are absolutely essenal as the hot and cold water at 44°C and 30°C can be prepared manually quite easily though a bit messy but having them definitely helps and enhances the image of the clinic but they do entail quite a bit of cost. Addional space is required for the doctor’s chamber (Figure 7) which should preferably be a 150–200 sq. . room as most of these balance disorder paents have to be clinically tested for gait and this requires atleast a 10–15 feet of walking space. A 61

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Figure_2. The wall unit for 2 evoked potential machines and an electronystagmography machine and computers.

Figure 3. Positional tests being done during videonystagmography test.

10’ x 10’ room is also required for the posturography test. If space is a constraint then, this room can also be used for craniocorpography. If the balance rehabilitaon unit and other such equipment for balance training has to be installed in the clinic which of course should ideally be done, then

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Figure 4. The setup for patient examination and videonystagmography test.

another room of approximately 100–150 sq. . will be required. These are the minimum space requirements, but provision of a small room for official purposes and record-keeping which can double up as a teaching room for interns and students and of course a very decent paent-waing room (Figure 8) completes the picture. As regards manpower requirements, other than the neurotologist, and an audiological technician, 1 or 2 trained assistants who can operate the machines and a pleasing and compassionate front-desk manager who can take a detailed history from the paent to be fed into the so ware like the one discussed below is all that is necessary to run an effecve vergo clinic.

AUDIO VESTIBULAR DATA MANAGEMENT SOFTWARE Audio vesbular data management is an advanced self-diagnosc so ware, with built in opinion generaon for invesgaons, a quick prescripon pad and self-maintainable drug database. Made with latest fourth-generaon programming language (4GL) language, it’s highly user friendly and very easy to operate. The history taking of the vergo paent is a four page computer screen module, the first page of which is as shown in Figure 9; there are three more pages of history taking.

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Figure 5. Optokinetic tests during videonystagmography test with images projected on the wall from projector.

Figure 6. Preparation for the caloric test during videonystagmography test.

The documentaon of the clinical examinaon of the balance disorder paent is a six page computer screen module (Figure 10). All the different neurotological tests like tympanometry, ENG, VNG, CCG, etc., can be reported using the AVDM so ware. A computer screen from the ENG reporng so ware is shown in Figure 11.

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Figure 7. Neurotologists consultation room.

Figure 8. The patient waiting room.

The page for generating clinical opinion of ENG is shown in Figure 12. The computer screen for reporng findings from CCG tests is shown in Figure 13.

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Figure 9. Computer screen module of history taking of the vertigo patient.

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Figure 10. Computer screen module of clinical examination of the balance disorder patient.

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Figure 11. Electronystagmography reporting software.

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Figure 12. Generation of clinical opinion of electronystagmography.

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Figure 13. Findings reporting from craniocorpography tests.

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Prescripons of all the common neurological diseases can be generated from the ADMS software and the computer screen for generating prescripons is shown in Figure 14. The diagnosis can be done manually or even by using the computer so ware. The computer so ware can make a tentave diagnosis or rather present a selecon of two or three probable diagnoses by compung the inputs in the history taking and clinical test findings. There are many such programs available in the market and the ADMS so ware is just one of the many available. It is always prudent to have such a computerized program for recording paent data, taking a detailed history, documenng the findings of the clinical tests, making a prescripon, generic in reports of the different neurological tests done and recording the follow-up of the paent.

Electronystagmography, videonystagmography cannot be considered sufficient in diagnostic neurotology, and has to be supported by other diagnostic tests that can help us narrow the loci of the lesions and nature of pathology

EQUIPMENT NEEDED IN SETTING UP A VERTIGO CLINIC The diagnosis of a paent with a balance system disorder is rather complex due to the various components of the balance system that include the visual, the propriocepve and the vesbular end organs systems (in addion to a host of other sensory and motor organs, neural pathways in the brain and spinal cord). The ability to differenate between the three basic input systems has been established for many years through the use of the baery of tests used in electronystagmography (ENG). This tool is a must, either as an ENG (or now VNG) for the neurotologist and has been the basic tool in the neurotologist’s armamentarium for ages. ENG/VNG cannot be considered sufficient in diagnosc neurotology, and has to be supported by other diagnosc tests that can help us narrow the loci of the lesions and nature of pathology. Just oculography ENG or VNG is no longer informave enough and other tests have to be used to quantavely and qualitavely assess the vesbular system and localize the lesion causing the vergo/imbalance and then come to an accurate diagnosis. The tests required in a vergo clinic have been enumerated above and just some of

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Figure 14. Prescription generation from the audio vestibular data management software.

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the tests are elaborated below to highlight certain salient features that a doctor who is seng up a vergo clinic needs to be aware of.

THE NEUROTOLOGICAL TESTS The Brainstem Evoked Response Audiometry (BERA) Test It is also called the ABR test or the BSER test. It is an objecve test of hearing that is tradionally used for tesng the structural and funconal integrity of the auditory pathway from the inner ear to the midbrain. Many neurotological disorders that present with vergo or deafness have defects in this poron of the auditory pathway in the brain. This is hence, one of the basic invesgaons in paents suffering from vergo, imbalance, hearing deficit and nnitus. The test is also used to determine the degree of hearing loss objecvity in pediatric paents as well as in difficult to test paents who do not respond reliably to the subjecve tests of hearing like the pure tone audiometry and allied tests.

The brainstem evoked response audiometry test monitors and records the smooth passage of the electrical impulse through the brain. In disorders of the brain involving the auditory pathway, the smoothness of the passage of this electrical impulse gets affected and this abnormality can be picked up by the brainstem evoked response audiometry test. In medical parlance this test is an evoked potenal test where an electrical potenal in response to sound is evoked in the cochlea and this electrical output called ‘acon potenal’ traverses through the auditory pathway to reach the higher areas in the brain where it is processed and the meaning pertaining to the sound interpreted. The BERA test monitors and records the smooth passage of the electrical impulse through the brain. In disorders of the brain involving the auditory pathway, the smoothness of the passage of this electrical impulse gets affected and this abnormality can be picked up by the BERA test. The response is idenfied by peaks (also called waves) that occur typically between 1 ms and 10 ms from the onset of the sound smulus. The BERA peaks are measured and marked tradionally as waves 1, 3, 4, and 5, each wave has an expected latency which is considered as normal and any increase of the latency or absence 73

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of any of the wave/peaks indicates an abnormality in the auditory track i.e., the nerves (neural pathways) that transmit the electrical potenal in the brain. The test however, is a very challenging test as it depends upon a number of variables like the mental and physical state of the paent, unknown levels of noise not only acousc noise but also electrical noise in the vicinity of the instrument, the experience, commitment, dedicaon and the medical insight of the operator of the machine as well as that of the doctor who interprets the test result. Another big challenge in the BERA test is the small response amplitude of the wave peaks at threshold. This makes idenficaon of the BERA waves prey difficult and results in erroneous interpretaon of the results and erroneous esmaon of the hearing threshold. It is due to the same reason that quite o en small tumors in the auditory pathways in the brain remain unidenfied by the BERA test and completely normal BERA findings are obtained in spite of there being a small tumor in the auditory pathway. Correct interpretaon requires an extremely high quality of

Research has shown that the use of the chirp technology results in very significantly increasing the amplitude (approximately 1.5–2 times) of the wave peaks

recording that will be free from arfacts and have robust (high amplitude and easily recognizable) wave peaks. These challenges in BERA have however been largely overcome by modern technology and sophisticated high-end evoked potential machines like, the ‘Interacoustics Eclipse,’ have in-built systems that enhance the sensivity of the BERA test and increases the accuracy of idenficaon of the hearing threshold. This parcular model implements the use of a system called ‘chirp’. Research has shown that the use of the chirp technology results in very significantly increasing the amplitude (approximately 1.5–2 mes) of the wave peaks. This results in increasing the sensivity of the BERA test so that not only small tumors can be idenfied more easily but also helps in idenfying the hearing threshold much more accurately. This reduces the test me and also increases the confidence of the operator. The doctor interpreng the test also finds it much easier and more comfortable. The chirp system uses a technology that manipulates the ming issues of the sound smulus within the cochlea. The 74

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low-frequency sounds are presented to the cochlea a fraction of a millisecond earlier than the high-frequency sounds thereby ensuring that the enre cochlea is smulated together and as one unit thereby, giving a very robust response. In tradional BERA the high-frequency component of the sound smulus smulates the cochlea much earlier than the lowfrequency sounds which results in temporal distoron of the sound in the cochlea that in turn leads to small wave peaks which are quite unidenfiable at threshold. Details and design of the chirp technology may be taken from the publicaons of C. Elberling (2007), Don (2008), etc*. Other modern technologies incorporated in the sophiscated models are monitoring of residual background noise during the recording and having systems by which the quality of the recording can be evaluated online by calculang the evoked response to residual noise rao while the recording is going. These technologies have immensely enhanced the sensivity of the BERA test. Instruments like the Interacouscs Eclipse that have these systems built in are much more sensive than tradional BERA machines.

In traditional Brainstem evoked response audiometry the high-frequency component of the sound stimulus stimulates the cochlea much earlier than the low-frequency sounds which results in temporal distortion of the sound in the cochlea that in turn leads to small wave peaks which are quite unidentifiable at threshold.

THE VESTIBULAR EVOKED MYOGENIC POTENTIAL TEST An Auditory Evoked Potenals system should also be able to perform the vesbular evoked myogenic potenal (VEMP) tests, both cervical as well as ocular. These specific tests of the vesbular end-organs and the VIII cranial vesbular nerve should be part of the neurotologist’s armamentarium (Figures 15 and 16). The VEMP test is an evoked potenal that is used to test the structural and funconal integrity of the saccule and its afferent connecons. The VEMP test is the only test in the vesbulometry test baery that can evaluate the funcon of the saccule and the inferior vesbular nerve. The test works on the principle that when a high-intensity sound smulus is presented to the ear the *Elberling C, Don M, Cebulla M, Stürzebecher E. Auditory steady-state responses to chirp stimuli based on cochlea travelling wave delay. J Acoust Soc 2007;122:2772–85.

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Figure 15. Cervical vestibular evoked myogenic potential test result.

energy transmied into the cochlea through the stapes also smulates the end organ of the saccule whereby the saccule which is a part of the vesbular labyrinth is smulated. This smulaon generates an acon potenal that is an electrical current that passes through the inferior vesbular nerve to the vesbular nucleus and from there to the median longitudinal fasciculus to the motor root of the XIth cranial nerve that is the accessory nerve and from there through the nerve to sternomastoid up to the sternomastoid muscle which is contracted. The VEMP response is actually an electromyography (EMG) recording of the contracon of the sternomastoid muscle brought about by the sound evoked smulaon of the saccule. So, the presence of a normal VEMP implies that the saccule and the inferior vesbular nerve and of course the other constuents of the neural pathway described above are funconing normally. The important parameter in VEMP recordings is the amplitude of contracon of the sternomastoid muscle evoked by the saccular smulaon. The amplitude of contracon of the sternomastoid on the 2 sides is compared by recording the EMG. The difference between the 2 sides should be 35% then the side having the lesser EMG amplitude is considered abnormal. Now, there are many types of VEMP setups available. VEMP usually comes as a part bundled in many low-end evoked potenal machines and is not uncommonly offered to buyers of auditory evoked potenal machines by the manufacturers. Though these machines dish out a VEMP test, yet this is not clinically reliable and the VEMP test data obtained from

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Figure 16. Ocular vestibular evoked myogenic potential test result.

these machines serve no clinical purpose whatsoever and are extremely misleading. They can lead to a wrong diagnosis about saccular funcon as what they test is actually in most cases, an unrecfied VEMP. For the VEMP test data to be clinically reliable, the test has to be a recfied VEMP. So, before purchasing an evoked potenal machine in which the VEMP facilies are there, it is always judicious to ensure that the VEMP supplied is a recfied VEMP and not an unrecfied one. The neurotologist has to read the technical specificaons of the auditory evoked potenal machine and be sasfied that what he is purchasing in the guise of VEMP is actually a recfied VEMP. In the VEMP test the change in contracon of the sternomastoid muscle brought about by the saccular smulaon is measured and the amplitude of contracon of the sternomastoid between the two sides is compared by recording the EMG acvity of the sternomastoid. Measureable VEPMs is generated only on tonically contracted sternomastoid muscle and the VEMP response amplitude is dependent upon the level of pre-smulus EMG acvity of the sternomastoid muscle. If the sternomastoid muscle is tonically strongly contracted, then the VEMP response will be very robust and high in amplitude but if the presmulus contracon of the sternomastoid is not adequately strong, and then the amplitude of the VEMP response will be low irrespecve of saccular funcon. It is hence a vital necessity that the pre-smulus as well as intra-smulus contracon of the sternomastoid muscle is equal on both sides as otherwise; comparing the amplitude of the VEMP response between the le and right sides will have no meaning. Pre-smulus EMG acvity in sternomastoid may not be equal on le and right sides causing grossly erroneous and completely misleading results. It is hence, essenal 77

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that the clinician knows the EMG acvity during VEMP recording. Only the high-end and very sophiscated auditory evoked potenal machines come equipped with the facility where the pre-smulus electromyographic acvity of the sternomastoid can be monitored and documented. Even if the pre-smulus electromyographic acvity of the sternomastoid is not shown online during the VEMP recording (which is available in some high-end evoked potenal machines like ‘Eclipse’ of Interacouscs) yet then, there has to be some electronic mechanism in the VEMP hardware/ so ware by which the VEMP amplitude shown in the final recording has been computed by taking into consideraon the pre-smulus and intrasmulus tonic contracon of the sternomastoid muscle by a process called scaling. This method of VEMP, where the VEMP amplitude is calculated and recorded by taking into consideraon the pre- and intra-smulus tonic contracon of the sternomastoid is what is known as a recfied VEMP. In unrecfied VEMP, the pre-smulus and intra-smulus tonic contracon

This method of vestibular evoked myogenic potential, where the vestibular evoked myogenic potential amplitude is calculated and recorded by taking into consideration the pre- and intra-stimulus tonic contraction of the sternomastoid is what is known as a rectified vestibular evoked myogenic potential. of the sternomastoid muscle is not taken into account and the VEMP recording obtained is irrespecve of the pre-smulus and intra-smulus tonic contracon of the sternomastoid. Figure 17A is a VEMP test done in the ‘Eclipse’ EP25 model of Interacouscs. The poron at the top shows the intra-smulus EMG recording of the tonic contracon of the sternomasod. It clearly shows that the tonic contracon of the sternomastoid is much lesser on the le as compared to that on the right (red colour). The VEMP amplitude is accordingly lesser on the le side (lower part of the picture). The low amplitude of VEMP on the le is hence, not due to saccular disorder but due to an improper test condion where there was a difference in the tonic contracon of the muscle between the le and right sides. Had the intra-smulus EMG of the tonic contracon of the le and right sides not been shown, any clinician would have misdiagnosed this as a saccular

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Figure 17A. Vestibular evoked myogenic potential test done in the ‘Eclipse’ EP25 model of Interacoustics.

hypoacvity on the le side. In such a condion, the VEMP test needs to be repeated with equal contracon of the sternomastoid muscle ensured on both sides. The ‘Eclipse’ model of Interacouscs has an inbuilt facility as a part of the so ware package whereby a visual representaon of the intensity of contracon of the sternomastoid muscle during the test can be shown on a computer screen to be paent undergoing the test. From this visual feedback, the paent can himself/herself make the sternomastoid adequately and equally taut on both sides such that recording with equal tonic contracon of the sternomastoid on the le and right sides is done. This makes the VEMP clinically relevant and without it, the VEMP test becomes clinically irrelevant. Sometimes however, for example due to sffness in the neck, the paent has problems in ensuring equal contracon of the sternomastoid during the VEMP test of the le and right sides. Under such condions, there is a system called VEMP scaling in which the machine automacally records and compares the tonic contracon of the sternomastoid of the two sides and accordingly up or down scales the VEMP amplitude so that the VEMP amplitude recorded is done as a funcon of the equal tonic contracon on both sides. But such facilies are available only in the very high end models like the Eclipse evoked potenal system of Interacouscs and some similar costly models only. Figure 17B is a scaled up version of the same VEMP as Figure 17A where the amplitude of the le side has been scaled up by comparing with the difference in the pre-smulus EMG acvity of the right side.

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Figure 17B. Scaled up version of the same vestibular evoked myogenic potential.

Electrocochleography Although electrocochleography (ECochG) (Figure 18) has been around for many years, for much of that me it was an invasive procedure. With the advent of a peri-tympanic electrode it no longer is invasive and it is now a fast and simple test. Since the invasive technique is no longer necessary the ECochG should become roune within the neurotologic clinic. The diagnosis of endolymphac hydrops, through EcochG ulizing a peritympanic electrode rather than the invasive electrode on the promontory, gives us results that have large amplitudes and good morphology. A dual channels-evoked potentials system, (Figure 19) with the capability of doing not only BERA, ASSR and VEMP but also ECochG becomes necessary. The Labat-evoked potenal machine (Figure 20) that is capable of performing all the auditory evoked potenal tests BERA, ECochG, VEMP, ASSR. The system should have the capability of doing ECochG with good resoluon in order to be able to extract the SP using the non-invasive peri-tympanic electrode.

An Electrocochleography Test Done in the Labat Instrument The advantage of a dual channel-evoked potenals unit would also allow us to simultaneously visualize both an ABR and an EcochG.

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Figure 18. Electrocochleography.

In EcochG the peak AP should correspond to wave 1 of BERA in latency and so whenever in doubt, it is always prudent to carry out a BERA at the same intensity and find out whether the latency of Wave 1 and that of the AP is idencal or not. It is very easy to do so as it does not require any changes of electrodes. The same electrode montage as is required in EcochG, can be used for BERA recording and so wares as in the Labat system, offer us the facility of comparing both on the same screen.

Oculography The term oculography simply means recording of eye movements. Two forms are commonly in use, one is ENG, and the other is VNG. Though ENG is a much cheaper opon, yet VNG is the in thing today due to a lot of clinical advantages. This of course is not to undermine ENG as an oculographic tool, but the higher resoluon of eye movements as obtained in VNG, and the more precise way by which the oculomotor tests can be performed through VNG does make it a beer opon.

Stabilometry An aid to the diagnosis, as well as the rehabilitaon of the paent with a balance system disorder is via stabilometric tesng (Figure 21). The use of a plaorm such as the STABILO SVEP (Figure 22) that follows the French Posturology Associaon guidelines and developed by Dr. Gagey and Dr. Guide should be a must in a modern neurotologic clinic. The tests allow 81

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Figure 19. Dual channels-evoked potentials system.

Figure 20. Electrocochleography test result.

the differenaon of a paent with postural and motor system control pathologies. A er the diagnosc test, a rehabilitaon strategy can be implemented specifically for the paent’s problems by the stabilometry apparatus.

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Figure 21. Stabilometric test result.

Figure 22. Stabilometric testing platform.

The Equitest model of computerized dynamic posturography is a more advanced form of posturography art, which is extremely costly.

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CONCLUSION Neurotologist is an essenal part of the state-of-the-art vergo clinic. Though some technicians are necessary to run the clinic, they are specifically to be used only as machine operators and not as interpreters of the test results which is very much a clinician’s job and not something that a technician is expected or supposed to do. Modern instruments have such excellent so ware that the clinician’s job is now quite simplified and it does not need much of sophiscated manpower and just a couple of trained technicians working under the guidance of the neurotologist should be able to run the show quite effecvely. Just having the best of equipment and the best of infrastructure cannot replace the man behind the machine and it is the neurotologist’s commitment, dedicaon, clinical insight, and clinical acumen that will make or break the success of the vergo clinic.

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Setting Up a Vertigo Clinic in a Semi-Urban Center Anita Bhandari Sr. ENT Surgeon (Fellowship in Neurotology & Otology [Singapore]) Jain ENT Hospital, Jaipur, Rajasthan

Vergo is now recognized to be a major health problem amongst the common populaon affecng all age groups. It is o en not evaluated properly leading to faulty diagnosis and in turn improper treatment. This leads to an overall worsening in the condition of the patient. Seng up a vergo center in the urban and semi-urban sectors makes sense—improving and facilitang the management of the paent and commercially for the clinician. A basic vergo clinic would focus on the evaluaon of balance problems rather than those of hearing. So, the basic equipment required would be: 1. Audiometer 2. Electronystagmography (ENG) and videonystagmograpy (VNG) 3. Single-lens reflex camera with B-mode 4. Convex mirror 5. Computer and printer

AUDIOMETER A well-calibrated digital audiometer with TDH-39 or 49 earphones and adequate masking facilities is an essential requirement. The frequency range should be 250–8000 Hz and intensity range should be 85

ECAB: Otorhinolaryngology

0–120 dB HL. A high frequency audiometer with a range up to 16 KHz would be addionally useful in evaluang paents with high frequency loss and nnitus. Audiometry should be done in an acouscally treated room.

ELECTRONYSTAGMOGRAPHY/ VIDEONYSTAGMOGRAPHY The evaluaon of the vesbulo-ocular reflex along with assessment of the integrity of the smooth pursuit, saccadic, and optokinec system can be done by recording eye movements by electro-oculography. At present 3 types of electro-oculography are in pracce:   

Electronystagmography Videonystagmography Infrared oculography

Electronystagmography involves recording of minute electrical changes in the corneo-renal potenal brought about by eye movements. This potenal has a magnitude of 1 mV and is oriented in the long axis of

The evaluation of the vestibulo-ocular reflex along with assessment of the integrity of the smooth pursuit, saccadic and optokinetic system can be done by recording eye movements by electro-oculography. the eye, the rena being negave and the cornea being posive. VNG records the eye movements by an infrared camera. This informaon is then converted to the digital format. Infrared oculography records eye movements by an infrared light beam which is then documented in the analog form. The ENG/VNG test is capable of identifying, documenting, and quanfying lesions of the vesbulo-ocular system. The clinical tests which can be performed with this equipment include evaluaon of: 1. Spontaneous nystagmus 2. Gaze-induced nystagmus 3. Saccades

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Setting Up a Vertigo Clinic in a Semi-Urban Center

4. 5. 6. 7.



Bhandari

Pendulum tracking Posional and posioning tests Caloric tests Fistula test

The major advantages of ENG include: 1. Allowing recording of eye movements in total darkness and with closed eyelids. 2. Recording and quanfying eye movements which help in idenfying any ocular motor or neurological disorder. 3. It is a standardized procedure with records which allow monitoring of the progress of the disorder. 4. It allows tesng of the vesbular system one side at a me. The disadvantages of ENG include: 1. It assesses only a small part of the balance system and therefore remains a test of low specificity and sensivity.

The ability to record torsional eye movements is one of the major advantages of videonystagmography. It is of utmost importance to understand that the usefulness of electronystagmography/videonystagmography testing depends on test administration and test interpretation. 2. Susceptibility to eye blink artifacts and electromyographic acvity. 3. Torsional eye movements cannot be recorded. The ability to record torsional eye movements is one of the major advantages of VNG. It is of utmost importance to understand that the usefulness of ENG/VNG tesng depends on test administraon and test interpretaon. A proper ENG evaluaon requires trained personnel. A proper ENG evaluaon is not possible without knowledge of neuroanatomy and neurophysiology.

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THE ELECTRONYSTAGMOGRAPHY PROCEDURE Electronystagmography should be done in a room of adequate size allowing enough space for the paent table, ENG machine and computer and a light bar placed about 6 feet away from the head-end of the table. It should be a quiet air-condioned room away from heavy electrical equipment like X-ray machines and cautery machines. As ENG records electrical changes in millivolt, a proper earthing is required. The head-end of the bed should be raised by 30°. The light rod may be mounted on the wall or on a stand.

CRANIOCORPOGRAPHY Craniocorpography (CCG) test involves evaluaon of the vesbulospinal reflex. This test which was developed by Prof. CF Claussen is one of the

Craniocorpography is one of the most efficient, quick, objective and quantitative tests for screening equilibrium function. most efficient, quick, objecve, and quantave tests for screening equilibrium funcon. In this test, a photographic recording of the paent is done while the paent performs a Romberg test, tandem walking, and Unterberger test. The linear and angular displacement and body spin are measured. This test also helps in determining the status of central compensaon.

PROCEDURE AND EQUIPMENT Craniocorpography records the light tracings from light bulbs on the crown of the head on which 3 LED lights are placed. A convex mirror is fied on the ceiling of the room. A camera is placed between the head of the paent and the mirror. A recording of the paent is done while performing Romberg test, tandem walking, and Unterberger test in a darkened room.

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Bhandari

REHABILITATION Rehabilitaon is the most effecve tool for the therapy of vergo and dizziness. Hence, having a room for vesbular rehabilitaon exercises is very useful. A bed with adjustable head-end to perform the posional maneuvers will be required. Other equipment useful for rehabilitaon includes a trampoline, mats, and exercise ball.

REFERENCES 1. Biswas A. In: Clinical Audiovesbulometry Bhalani Publishing House: Mumbai 2009 2. Brandt T. In: Vergo–Its Mulsensory Syndromes 2nd ed. Springer-Verlag: London 2003. 3. Eggers SD. Vergo and Imbalance: Clinical Neurophysiology of the Vesbular System Eggers SDZ, Zee DS, eds. Elsevier Science Ltd, 2009.

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