Non-Surgical Treatment of P. GHOSH AND M. S. ROHATGI

Majority of the cases with dizziness can be treated medically and physiotherapeutically and very few require surgical interventions. In this report one hundred cases of dizziness have been investigated in a busy otolaryngology clinic, diagnosed and treated with drugs and head and neck exercises. The above have been rationalised on a pragmatic basis as to their modes and sites of actions, interactions with various neuropeptides and recalibration of the vestibular subsystem. Above 80% of the cases were benefited by the regimens laid down in this report. An interestingly significant outcome of this study is that the post-treat- ment neuro-otological findings have not altered much even in those patients who have improved and re- sumed their normal activities.

Introduction 'stage of being dysig, meaning stupid fluence or~ the activity of the vesti- or foolish and putting the pragmatic bular nuclei. Thus there are two There is constant interaction aspect of non-surgical treatment of recticulo-vestibular pathways : between the 'phasic' and the 'tonus' dizziness on a rational basis as to the (I) excitatory cholinergic and element and besides havi~.g an sites and modes of actions of different (2) inhibitory monoaminergic. The afferent system, it has also an effec- drugs, their modifying effects on the distribution of nor-epinephrine in tive efferent one, a 'feed-back' and rteuropeptides and, the effect of head the central nervous system is princi- regulating mechanism, that modify and balance exercises with or without pally in the hypothalamus and both the subjective sensation of medications. brainstem reticular system (Vogt, vertigo/imbalance and the objective 1954). The overall activity deperLds findings (Ghosh & Kacker, 1979). Affection of the vestibular sub- upon the balance between these The complexity of the neurones and system, starting from the peripheral transmitters (Eveaton & Goodhill, the synapses in the vestibular 'sub- labyrinth to the cerebral cortex 1968). So dizziness could be due to system' in the central nervous system (temporal lobe and post-central activation of both nor-epinephrine with the co-existence of more than gyrus) leads to dizziness. arid cholinergic reticular areas. one neurotransmitter ir~ a single is the most important manifestation Moreover, the irtterplay between the neurone, multiple pre and post- of vestibular disease. quick-disfiharing and slow-dis- sylxaptic receptors, fast and slow post- charging reticular neurones and synaptic potentials, omnopause neu- Referring to Fig. 1, one can see vestibular nuclei is important (Ghosh rones, reciprocal neuronal units and t[-,at the fibres from the labyrinth and Sen, 1970 ; Ghosh, 1980, 1981). action at sites distant from that of end in the vestibular nuclei and from DizziI).ess would occur when acetyl- release of the transmitters er~ormous- there they relay in the reticular core, choline activation exceeds the capa- ly multiply the problems of assigning eye nuclei (III, IV and VI), dmsa! city of nor-epinephrine system. distir~ct functions to different neuro- nucI.eus of vagus, vomiting centre These are also under the regulation nes and neuropeptides. It has been and chemoreceptor trigger zone, of the inhibitory effects of GABA. electronyst agmographically shown cerebellum (ftoccu]o-nodular lobe that affectiorL of quick and slow- and fastigial nuclei) and temporo- discharging neuronal units in the parietal lobes of cerebral cortex. Habituation to motioal is due to paraxnedian pomine reticular forma- Some fibres (mossy fibres) go directly an enhanced respolLse of the nor- tion are associated with different from the labyrinth via the juxtare- epirLephrine mediated system. The distinct findings on the electronysta- stiform body to the cerebel!um. increased orgalfisation of the neural tagmograph (Ghosh & Kacker, Conversely, cerebral and cerebellar system or mobilization of the enzy- 1979; Ghosh, 1980 & 1981). The fibres converge on the vestibular mes lxecessary for increased nor- psychological aspect of the patient nuclei exertirLg an inhibitory influ- epinephrine activity would be acti- complicates it further. ence. Damage to these enhances vated by repeated exposure to vestibular responses (Ghosh & motion (Wood & Graybiel, 1970, As a clinician, this is a humble Kacker, 1979). 1973). This would alter the balance attempt at recovering from the of activity in the central nervous The neurot~ansmitters, associated system and prevent motion sickness P. Ghosh, Additional Professor, Department of ENT, with vestibular mechanism, are nor- by allowing nor-epiuephrine system All India Institute of Medical Sciences, adrenaline, acety]cho]ine & Gamma to predominate over the acetylcho- New Delhi-110 029, INDIA, Amino Butyric Acid (Fig. 1). Vesti- line system. For the nervous system (formerly, Lecturer in ENT, Faculty of to recalibrate the relationship bet- l~,ledicine, University of Papua New Guinea). bular receptors are cllolinergic. It M. S. Rohatgi, is likely that a cholilzergic transmis- ween visual, proprioceptive and Specialist Ear, Nose and Throat Surgeon, sion to the vestibular neurones cause vestibular sigI~als, repeated head and P.O. Box-228, Maitand vertigo. The cbolinergic reticuIo- eye movemeI~.ts are essential. If the N. S. W. 2320, AUSTRALIA. vestibular pathways enhance the level of nor-epinephrine activity is Reprints request to : activity witl~in the vestibulo-ocular raised by drugs or habituation, or Dr. P. Ghosh, D-34, Ansari Nagar, reflex. The mono-aminergic reticulo- if acetylcholine activity is blocked New Delhi-110029 vestibular pathways activated by by drugs, motion sickness may be India. amphetamine, has an inhibitory in- prevented.

48 Indian Journal of Otolaryngology, Volume 41, No. 2, June, 1989 Won-surgical Treatment of Vertigo--Ghosh & Rohatgi

Material and Methods and PUTATIVE SITES OF ACTION OF ANTIVERTIGINOUS observations DRUGS One hundred cases of vertigo were studied and managed non-surgically. CORTEX The aetiologies were as follows :

Group I : Cervical spine trauma sustained 1-2 years back. The age group was between 20-35 years.

There were 50 cases. HYPOTHAL

Group II : Cervical spondylosis : most of the 25 cases were above 45 years.

Group III: Cupulolithiasis-- 3 cases.

Group IV : Vertebro-basilar insufficiency--9 cases.

Group V : Perilymphatic fistula GABA in the round window--2 cases. PYRDOXINE I Fistulae were closed with fat graft. 9 Mild vertigo persisted for about 3 months and subsequently treated with drugs for 3 months.

Group V1 : Undiasnosed : 11 cases. Age range was 45 to 60 years.

Since facilities for conducting elec- trooculography or optokinetic nys- tagmography are not available in many institutions, reasonable diag- nosis can be and were made by the following : LOWER 1. History. CENTRES 2. Presence and character of spon- taneous nystagmus. 5, 7 LABYRINTH 3. Kopfschuttel (head-shaking) nys- 8 tagmus. 4. Unterberger's test (stepping with hands clasped infront). BLO04 ' SUPPLY I. -- ANTIHISTAMINE~ 5. Positional test. 2. -- ANTIEMETIC PHENOTH|A~|NES 6. . / 3. ~ ANTICHOLINEH~'.~'ICS ~ 4' 7. Cold caloric test with ice-cold 3a -- ADR[NERGIC water. 4. -- VASOD|LATOR$ 8. X-ray cervical spines, internal S* __ DIURETICS 6. -- PSYCHOTHERAPEUTI¢ PRUGS auditory meatus and skull, when 7. -- STEROIDS indicated. 8, ~ ANT|BACTERIAL I* GASA Fig. I. VG - Vestibular ganglion, VN - Vestibular nuclei, RF - Reticular formation, Table I represents the anamnesia, Supprn - Supperssion, NA - Nor-adrenaline, ACtt - Acetylcholine Activa - Activation, CTZ - chemoreceptor Trigger Zone, VC- Vomiting centre, GABA- GammaAmino Butyric which has been tabulated taking the Acid, MR - Med, Rectus, LR - Lateral rectus, Ant - Anterior, Post - Posterior, III& VI-Eye help of available literature and per- nuclei, Fasti - Fastigious nucleus. sonal experience, is helpful in differ- ential diagnosis. In quite a good number of eases, history alone could sient numbness and tingling of face, Spontaneous nystagmus was look- point to tlxe proper diagnosis. In the especially in the periora] region. ed for in sitting and head-erect group with vertebro-basilar insuffi- None of the cases showed any neu- position. This was present in 5 cases ciency, the patients had only tran- rological deficit. of cervical spine trauma, 2 cases of

Indian Journal of Otolaryngology, Volume 41, No. 2, June, 1989 49 °Volt-surgical Treatment of Vertigo--Ghosh & Rohatgi

TABLE I

Dizziness (aetlology and site of pathology;

of sudden onset t hronlc

Below 50 yrs. of age Above 50 yrs. Episodic Non-episodic

D,'ithout cochlear \Vith eochh:ar a) vascular disorders With cochlear Without cochlear I. A~oeiated with symptoms symptoms involving lab) rin- symptoms symptoms fainting or uncon- (a) vestibular (a~ Viral labyrinthiti,. thine blood flow (a) CSO.XIand 1. Positional : scionsness :-- neuronitis ,>f (common) from the vertebro- mastoiditis. (:t~ Cupulolithiasis (a) V. B. insufficiency bacterial, vir~d (b) Bacterial tabvrin- basi!ar system. (b) M~eniere's (BPPV) (T.I.A.) or metabolic thitis (rare) b) Strokes :-cerebral, disease, (Idiopathic, fi)llow- (b) Epilepsy origin. (el Meningitis brain-stem and syphilis and ing head injury & (c) Orthostatic hypo- (b) Tabes dor,ali~. (d/ May follow : cerebellar. Cogan's cfisease vascular episodes tension. (i) Physical activity ~c) Arteriosclerosis. (c Acoustic involving the (d) Carotid arterio- e.g., extreme :d) Hypertensive neurinoma & anterior vestibular sclerosisann carotid exertion, sexual cardiac disease. other C,P-anglc artery), sinus sensitivity. intercourse etc. ~t') diabetes mellitu-. lemons. (b~ Injury to cervical (el Paroxysmal cardiac (ii) Middle ear pressure (d) Ntultiple sprees, arrhythmias. changes e.g. in flying, sclerosis (c'. injury to brain stem (f) Post-inf. cerebellar scuba diving etc. and other stem artery thrombosis. (lib emotional stress lesions including 2. Not associated with (iv) rupture of the round metastatic cancer, faintiug/uncoas- window membrane (di V.B. insufficiency ciousness-- and perilymphatic usually associated (a) psychoneurosis. fistula ht oval with numbness of (b) Diabetes mellitu~. ~indow as followit~ face, sensory dis- (el Hypothyroidism. stapedeetomy. turbance of one (d) Anaemia. or both sides of (el Hypertension. body or slurred (f) Leukaemia. speech. (g) Drugs (ototoxies, 2. Non-Positlonal sedative~, tranqui- (a~ Drugs. lisers etc.) (b) Hyperventilation. (h) Motion sickness. (el Cervical spine (i) Dysequilibrium of trauma, ageing (d) Moenopause. (j) Eye muscle imba- (el Subclavian steal lances. syndrome. (k) Refractive error. (f> Migraine.

cervical spondylosis and 3 cases of been having in 5 of the above eases tenth ones. The rest showed fatigu- vertebro-basilar insuficiency. This in GroupI; 2 of Group II; 2 of able nystagmus towards the under- was not found to be of any localising Group III; 2 of Group V and 2 of most ear, (b) in Group II. 10 cases value. Two cases of Group IV Group VI (both had Kopfschuttel (400/0) showed non-fatiguable type showed vertical (upwards) nystag- nystagmus) and dissimilar type in nystagmu+ and out of these, four mus implicating involvement of both 33 of Group I (including those who cases showed decline after the sixth MLFs (Medial Longitudinal Fasci- had Kopfschuttel nystagmus) and positioning and total decline after ctfli). Then the head was (a) tipped 4 of Group VI, (including those who the ninth ones, (el in Group IlI, all backwards, (b) to the right and (c) had KopfschutteI nystagmm), cor- showed fatiguable nystagmus tow- left, over the shoulders, and (d) for- roborating the widely accepted im- ards tile undermost ear, (d) in wards for about one minute. Two pression that the latter is suggestive Group IV, five cases (about 50%) cases in Group I and 3 cases in of central lesion while the former, showed cla.~sical non-fatiguable tyI_e Group II showed horizontal rotatot T of peripheral lesion. of nystagmu~ towards the upper ear, nystagmus fading away within about (el GroupV, did not show any 15-20 seconds, in b and c positions. Unterberger's test was uot of positional nystagmus and (f) i~t The direction of nystagmus was not much help in localising the lesion ; Group VI three cases (about 25%) helpful in localising the lesion. but it indicated the presence of showed fatiguable type of n3stagmus Kopfschuttel nystagmus (on shaking pathology in the vestibular subsys- towards the undermost ear. tke head sideways around a vertical tem. Positional test revealed the axis for 20 times) was present in 25 following : (a) non-fatiguable nys- Audiometrv was done in all the cases with cervical spondylosis tagmus with direction towards the c'ctses. The following were. the posi- (Group II), 2 cases of V.B. insuffi- upper ear was present in 13 cases iu tive findings : Grou)) 1-- Only 3 ciency (Group IV) and 3 of the Group I (250/o approximately). Out cases showed high frectuency sensori- undiagnosed cases (Group VI). of these, three cases showed decline neural loss. Dynamic ranges between Head shaking produced giddiness in nystagmus after fifth positioning comfortable and uncomfortable levels similar to the one the patients had and total fatigue on the ninth to were not compressed and tone-decay

50 Indian Journal of Otolaryngology, Volume 41, No. 2, June, 1989 Abn-sur¢ical Treatment of Vertigo--Ghosh & Rohatgi

test was negative. Group II~40% who were above 50 years, indicating 1 case showed bilateral hypofime- of them showed high frequency presbyacusis. lion. Group V--Normal reaction. sensori-neural loss in both ears, Group VI--6 were hypofunctioning soggestive of presbyacusis. 30o,/o of Cold caloric test was conducted and 5 normaBy fimctioning. them showed compressed dynamic on all the cases, which showed the range, indicative of presence of following : Group I--I 7 cases show- Therapy consisted of drugs and recruitment. G oup III--- Audio- ed hyperactivity, 3 hypoactivity, head and neck exercises. The drugs merry showed normal . and 30,normal responses. Group II-- that are used in a case of vertigo Group IV--8 of them showed high 11 cases showed hyperactivity and can be rationally tabulated (Table-II frequency sensori-neural loss and 3 out of these 2 showed perversion of and Fig.l). The drugs, commonly out of them showed bilateral tone nystagmus. The rest were normal. used in the present study were : decay, indicating neural lesion. Group III-- Normal reaction., Group V--Both. cases had high fre- Group IV---6 cases were hyperactive (a) Pyridoxine 40 mg TDS. quency sensorineural loss of 30-40 dB. and out of these, 3 showed dissocia- (b) Vasodilators : Cyclandelate- Group VI~8 cases showed bilateral tion and/or perversion of nystagmus, 200 mg. TDS or Q ID. depertdirtg high frequency sensori-neural loss 2 cases showed normal reaction and on the intensity of dizziness and

TAB~II ANTI[VERTIGINOUS DRUGS (Based on Avery's Classification) CLASS ACTION DRUGS A. LABYRINTHINE SUPPR~ANTS I. Antihistamines (1) Vest. Supperssants (Endogran). (a) Cinnarizine 15mgm Q. 6H Anticholinergic (Central). (b) Ylmmrizine 15mgm Q 6H Sedative + Tranquilliser. (c) Dimenhydrinate 50mgm TDS Some enhances sympathetic activity. (d) Promethazine Hydrochlor 25mgm BD Flunarizine acts as a Calcium (e) Meclczine --Channel Blocking Agent. Intrace-- Hydrochlor 25mgm BD llular Calcium is regarded as The (f) Astemizole 10mgm OD physiological link in excitation-respomes coupling. Flunarizine dampens this by inhibiting Influx of Ca-Ion Into the Cells of Crista And Vestibular Neurones (i.e. It Has Both Peripheral and Central Actions) 2. Antiemetics Phenothiazines 2. Supress Central Vest. Pathways. (a) Prochlorperazine I 0mgm TDS Dopaminerglc Blocking Effect. Weak (b) Cinnarizine Antihistamine and Anfi-Cholinergic. (c) Promethazine Hvdrochlor Suppress CTZ~ (Esp. Prochlorperazine) (d) Triflupromazine "Hydrochlor Block Arousal (Reticular) by vest. Stimtdation. 5-10mgm. TDS (e) Trimeprazine Tartarate (f) Cyclizine (Marzine) 3. Antieholinergie (3) Inhibit Central and Peripheral Cholinergic (a) Atropine 0.4mgm I.M. Pathways, Leaning to Blocking cf Para- (b) Scoflatamiae 0.6mgm I.M. Sympathetic System, Depression of Smooth (Transdermal for Muscle Activity, Cerebral and medullary Prophylaxis). Centres. 4. Adrenergic (3a) Depress CTZ + VC. (a) d-Amphetamine 10mgm BD Activate Reti-Vestibular Pathways. (b) Ephedrine 25mgm TDS. Depresses Vest. Naclei. 5. GABA--Xiediated Inhibition (9) Inhibitory Transmitter. (a) Pyridoxine 50mgm BD GABA Fromation Governed by (b) Valproic Acid (Depakene) Pyridoxine-Dependent 15mgm/Kg/daily to 30mgm]Kg/daJly Enzymes (Increase in Cerebellum and Brain in 3 divided doses. Stem). Sodium Valproate Increases The Level of GABA in CNS by Inhibiting the Enzymatic Break Down of GABA. Good in Head Trauma. B. VA~ODILATORS (4) Improve Blood Circulation (a) Histamine Diphosphate 2.75mgm n (Peripheral and Central). Nicotinic 250 ML.N/Saline, 30-60 Drops PeriMin. Acid Reduces Atheroselerosis Also. (b) 5% CO~+95% 03, Breathe For 20 mins, 2-4 Times A Day. (c) Betahistine 30-48mgm./day. (e) Cyclandelate 200mgm 6 hourly (e) Nylidrin 6mgm 8 Hourly

Indian Journal of Otolaryngology, Volume 41, No. 2, June, 1989 51 aVon-surgical Treatment of Vertigo--Ghosh & Rohatgi

CLASS ACTION DRUGS (f) Papaverine 150mgm Capsule BD (.5 mgm/Kgm Body Wt.) (g) Duvad~lan Retard (Isoxsuprine) 40mgm BD. (h) Nicotinic Acid (75mgm TDAC). (i) Perdilatal (Buphemine Hydrochlor) 6mgm Tab. 2TDS (j) Thymoxamine 10 mgm I.V. or 40-100 mgm Orally. (k) Caffeine 150-250mgm TDS. (1) Naftridofuryl (Praxiene) 100mgm TDS.

C. DIURETICS (5) Decrease of Intralabyrinthine Pressure. (a) Acetazolamide 250mgm OD For 2 Carbonic Anhydrase Inhibitor. Decrease Days in every 3 days. Reabsorption of Na, K, CL and-HCO, (b) Hydrochlorthiazide 25mgm 12 Hrly. (K Supplemented if Used for a Long Time. 20 M.Mol/Day). D. PSYCHOTROPICS (6) Modify Subjective Response to Vertigo. 1. Antianxiety Agents Decrease Resting Activity in Vest. Nuclei (a) Diazepam 2-5mgm 8 Hourly. Reticular Faeilitatorv system. (b) Phenobarb 15-45 mgm 8 Hourly. Diazepam Increases GABA-Mediated Inhibiticn. 2. Antidepressants Affect Brain Amine Levels by (a) Amitriptaline 25mgm TDS. Intefering With Their Uptake Into Binding Sites (b) Nortriptyline 10mgm TDS. (Tricyclic Antidepressants)

E. CORTICOSTEROIDS (7) Decrease Labryinthine Oedema-}- Prednisolone 25-100rngm OD. Swelling Due To Virus Infection. Dexamethasone Lessen Damage of Acute Viral Labynthit is if Given Within 24-48 Hrs. F. ANTIBACTERIAL (8) Combat Infection Antibiotics G. CNS-STIMULANTS Cortex & Reticular Activity Xanthine Derivatives e.g. Caffeine-150-250 mgm TDS. H. CNS-METABOLIC STIMULANT Uptake & Utilisation of Glucose & 02 Pyritinol 300-600 mgm daily increased in Cortex & Brainstem. Good after Head Trauma.

Good Combinations : (1) Scopalamine + Dextroamphetamine-- Strongest Antivertiginous Combination. .6 mgm 10 mgm BD (2) Promethazine -t- ,, 25 mgm (3) ,, + Ephedrine 25 mgm TDS. Keywards : CTZ -- Chemoreceptor Trigger Zone. VC -- Vomiting Centre CNS -- Central Nervous System.

(c) pyritinol 300-600 mg. daily. initially and had to discontinue the complain of dizzirtess; 5 cases showed Cinnarizine 25 mg. TDS was manoeuvres. improvement and the rest 5 conti- tried on 10 cases. The above were nued to have symptoms as before, administered for two to three months. No psychotropic drugs viz. diaze- Group II : Out of 25 cases, Acute exacerbations during the treat- pam, was administered routinely 20 cases showed remarkable improve- ment period were managed by since in our experience we found that ment. The remaining 5 cases, had dimenhydrinate, prochlorperazine, this interferes with and delays the improvement to the extent that they and tranquilizers for a few days, recalibrating or learning process that could lead reasonably normal life. depending or~ the responses. Head takes place in the reticular/centrertce- and Neck exercises were prescribed phalic system during the above exe,'- GroupIII : All of them become for six months or more to all the cises. (Ghosh and Kacker, 1979). normal. patients. Initially about 70% of the patients complain of some dizziness The results of treatment were quite Group IV : 6 of them im- on performing the exercises; but encouraging and are as follows: proved and became reasonably they tolerate them subsequemly with active. 3 did not show much improve- pleasure without any induced verti- Group I • 40 of the cases were back ment though they felt somewhat go. Two patients had even vomiting to normal activities and did not better.

,52 Indian Journal of Otolaryngology, Volume 41, No. 2, June, 1989 Non-surg#al Treatment of Vertigo--Ghosh & Rohatgi

Group V : Both the cases became not show any remarkable change epinephrine mediated system as a normal. after non-surgical treatments, yen result of execrise. The former is sub- Group VI: 9 of them improved though there is remarkable subjective stantiated by the fact that tranquili- very well and are leading normal life. improvement. sers reduce and delay this process by The remaining two maintained status depressing the reticular/centerence- quo. phalie system and hence we do not Discussion use these drugs while the patient is Post-treatment neuro-otological undergoing exercises (Ghosh and findings : From the present study it is Kacker, 1979). Any patient com- obvious that the lesions in patients plaining of dizziness should not be Spontaneous horizontal - rotary with dizziness quite often cannot be indiscriminately treated with Steme- nystagmus, where present earlier, precisely localised, though one may" til, Diligan, Valium etc. as a blanket disappeared in 70% of the cases. have reasonable idea as to their cover, since this practice is not only But vertical nystagmus, noted in being peripheral or central (suprase- not helpful in many cases; but Group IV cases, persisted though gmental) in nature. Nevertheless, contrarily, it does harm to many symptomatically they improved re- disturbances eg. upset homeostasis in in the form of delaying the recalibra- markably. Initially and later they the blood circulation and neuro- t-ion I~rocess and at times perpetua- did not have any neurological deficit. transmitters in the vestibular tin.g the symptoms. Pyridoxin en- In about 25% of the cases Kopfschut- 'subsystem', incoming abnormal af- hances the enzymatic reactions that tel nystagmus disappeared. In rest ferent impulses from the periphery increase the concentration of GABA of the cases, though the~e was sub- (as in cervical spondy!osis) to this which inhibits the vestibular sub- jective improvement, Kopf~cbuttel subsystem and cerebellovestibular system leading to subjective impro- nystagmus persisted. Patients with- incoordination etc. can be effectively vement. Pyritinol increases the up- both similar and dissimilar types of managed by non-surgical treatment. take and utilisation of glucose and induced vertigo, following head- The drugs and their rationalised oxygen in the cerebral cortex and shaking, benefited i.e. there was no usages are legion (Fig. 1 and brainstem and is very good for head difference irL their responses to the Table II); but one can choose a few trauma. Vasodilators bring in more treatment between the groups with and treat the patients with gratify- nutrition to the cell of the peripheral peripheral and central lesions. Simi- ing results. The modes of action have and central vestibular apparatus. lar was the behaviour with regards to been tabulated for ready reference Cinnarizine inhibits the influx of fatiguable and non-fatiguable nysta- (Table-II) and the drugs can be calcium-ions into the vestibular cells, gmus on positioning. Both varieties safely instituted. The rationale be- thus, dampening the physiological persisted in all the cases, even in hind head and neck exercises lie in: link in excitation. It also improves those who had subjective improve- i) recalibrating the functional units the blood flow to the vestibular ment. The significant observation is in the central nervous, system and structures, both peripheral and cen- that the neuro-otological findings do ii) enhanced responses in the non- tral.

References 4. Ghosh, P. and Kacker, S. K., 1979: 7. Vogt, M. (1954) : The concentration of Vestibular recruitment and decruitment~ sympthin in different parts of the nervous 1. Avery, G. S. (Editor), 1980: Principle Acta Otolaryngologica, 88: 227-234. system, 07. Physiology 123 : 451-481. and Practice of Clinical Pharmacology and Therapeutics, Sydney and New York~ Adis Press, 349-354. 8. Wood, C. D. and Graybiel, A., 1970 : 2. Eveaton, A. and Goodhill, V. 1968: 5. Ghosh, P. 1980: Inclination of eye- A Theory of motion sickness, based on Comparative sequential studies of effects tracking tracing, Journal of Laryngology pharmacological reaction, Clinical of drugs on the of and Otology 94 • 719-735. Pharmacology and Therapeutics 11 : 621-629 laboratory animals, Acta Otolaryngologica 237 (Suppl) : 1:26. 3. Ghosh, P. and Sen, D. K., 1970 : Nysta- 9. Wood, C. D. and Graybiel, A., 1973 : gmus and Brain lesions, Neurology, 6. Ghosh, P. 1981 : Round peaked nystag- A Theory of motion sickness, Otolaryngo- India, 18 : 236-240. mus, Indian 07. Otolaryngology 33 : 55-58. logic Clinic of Worth America, 6 308-629.

Indian Journal of Otolaryngology, Volume 41, No, 2, June, 1989 53