Auditory System: Clinical and Special Topics

809 Pages·1976·32.64 MB·English

by  E. de Boer

Handbook
of
Sensory Physiology
Volume V/3
Editorial Board
H. Autrum R. Jung W. R. Loewenstein
D.M.MacKay H. 1. Teuber
Auditory System
Clinical and Special Topics
By
E. de Boer W. K. Connor H. Davis J. J. Eggermont R. Galambos
C. D. Geisler G. M. Gerken H. E. von Gierke C. S. Hallpike
E. Hawkins Jr. S. A. Hillyard W. D. Keidel D. E. Parker T. W. Picton
W. Rudmose F. B. Simmons G. Stange C. R. Steele J. Tonndorf
M. E. Wigand F. Zollner
Edited by
Wolf D. Keidel and William D. Neff
With 343 Figures
Springer-Verlag Berlin Heidelberg New York 1976
Wolf D. Keidel
Institut fUr Physiologie und Biokybernetik (formerly I. Physiologisches Institut) der Universitiit 8520 Erlangen,
UniversitiitsstraBe 17 (Germany)
William D. Neff
Center for Neural Sciences and Department of Psychology, Indiana University, Bloomington, Indiana 47401 (USA)
ISBN-13: 978-3-642-66084-9 e-ISBN-13: 978-3-642-66082-5
DOl: 10.1007/978-3-642-66082-5
Library of Congress Cataloging in Publication Data
Main entry under title: Auditory system. (Handbook of sensory physiology; v. Vj3) Biblio
graphy: p. Includes index. 1. Hearing disorders. 2. Hearing. 3. Ear. 4. Electrophysiology.
I. Boer, E. de. II. Keidel, Wolf Dieter. III. Neff, William D. IV. Series. QP351.H34 vol. 5/3
[RF290] 591.1'82'08s [617.8'9] 76-44844
The use of general descriptive names, trade names, trade marks, etc. in this publication, even if the former are
not especially identified, is not to be taken as a sign that such names, as understood by the Trade Marks and
Merchandise Marks Act, may accordingly be used freely by anyone. This work is subject to copyright. All rights
are reserved, whether the whole or part of the material is concerned, specifically those of translation, reprinting,
re-use of iIInstrations, broadcasting, reproduction by photocopying machine or similar means, and storage in
data banks. Under § 54 of the German Copyright Law where copies are made for other than private use, a fee
is payable to the publisher, the amount of the fee to be determined by agreement with the publisher.
© by Springer-Verlag, Berlin' Heidelberg 1976.
Softcover reprint of the hardcover 1s t edition 1976
Contents
Chapter I Sensori-Neural Deafness and Derangements ofthe Loudness Function: their
Nature and Clinical Investigation. By C. S. HALLPIKE. With 32 Figures. 1
Chapter 2 Bone Conduction. By J. TONNDORF. With 28 Figures . . . . . . . .. 37
Chapter 3 Electrical Response Audiometry, with Special Reference to the Vertex Po
tentials. By H. DAVIS. With I Figure . . . . . . . . . . . . . . . . 85
Chapter 4 The Physiological Background of the Electric Response Audiometry. By
W. D. KEIDEL. With 76 Figures. . . . . . . . . . . . . . . . . . . 105
Chapter 5 Clinical Experiences with Evoked Response Audiometry. By. F. ZOLLNER
and G. STANGE. With 16 Figures . . . . . . . . . 233
Chapter 6 Hearing and Equilibrium in Renal Failure. By M. E. WIGAND. With
10 Figures . . . . . . . . . . . . . . . . . . . . . . . . . . . . 279
Chapter 7 Community Response to Noise. By W. K. CONNOR and W. RUDMOSE. With
8 Figures . . . . . . . . . . . . . . . . . . . . . . . . . . . . 307
Chapter 8 Habituation and Attention in the Auditory System. By T. W. PICTON, S. A.
HILLYARD and R. GALAMBOS. With 21 Figures . . . . . . . . . . . . 343
Chapter 9 Mathematical Models of the Mechanics of the Inner Ear. By C. D. GEISLER.
With 6 Figures .......................... 391
Chapter 10 Electrical Stimulation of the Ear in Man. By F. B. SIMMONS. With 2 Figures 417
Chapter II Electrical Stimulation of the Auditory System in Animals. By G. M.
GERKEN. With I Figure . . . . . . . . . . . . . . 431
Chapter 12 Cochlear Mechanics. By C. R. STEELE. With 16 Figures. . . . 443
Chapter 13 On the "Residue" and Auditory Pitch Perception. By E. DE BOER. With
40 Figures. . . . . . . . . . . . . . . . . . . . . . . . . 479
Chapter 14 Infrasound. By H. E. V. GIERKE and D. E. PARKER. With 16 Figures 585
Chapter 15 Electrocochleography. By J. J. EGGERMONT. With 53 Figures. 625
Chapter 16 Drug Ototoxicity. By E. HAWKINS. With 17 Figures. 707
Author Index . 749
Subject Index. 787
List of Contributors
DE BOER, E., Physical Laboratory, ENT Department, Wilhelmina Hospital, University of
Amsterdam, Eerste Helmersstraat 104, Amsterdam -Oud West, The Netherlands
CONNOR, WILLIAM, Tracor Inc., 6500 Tracor Lane, Austin, Texas 78721, USA
DAVIS, HALLOWELL, Central Institute for the Deaf, 818 South Euclid, St. Louis, Missouri
63110, USA
EGGERMONT, J. J., Academisch Ziekenhuis, E.N.T.-Department, Rijnsburgerweg 10, Leiden,
The Netherlands
GALAMBOS, ROBERT, Department of Neurosciences, University of California at San Diego,
La Jolla, California 92037, USA
GEISLER, C. D., Department of Neurophysiology, 283 Medical Science Bldg., University of
Wisconsin, Medical School, Madison, Wisconsin 53706, USA
GERKEN, G. M., The Callier Center for Communication Disorders, The University of Texas
at Dallas, 1966 Inwood Road, Dallas, Texas 75235, USA
VON GIERKE, HENNING, E., 1325 Meadow Lane, Yellow Springs, Ohio 45387, USA (Department
of the Air Force, 6570th Aerospace Medical Research Laboratory (AFSC) , Wright-Patterson
Air Force Base, Ohio 45433, USA)
HALLPIKE, C. S., Fern Lodge, 44 Ashurst Road, West Moors, Dorset, Ferndown 87, 4418, Great
Britain
HAWKINS, JOSEPH E. JR., Kresge Hearing Research Institute, Medical School, The University
of Michigan, Ann Arbor, Michigan 48109, USA
HILLYARD, STEVEN A., Department of Neurosciences, University of California at San Diego,
La Jolla, California 92037, USA
KEIDEL, WOLF D., Institut fiir Physiologie und Biokybernetik der Universitat Erlangen,
8520 Erlangen, Germany
PARKER, D. E., Department of Psychology, Miami University, Oxford, Ohio 45056, USA
PICTON, TERENCE W., University of Ottawa, Hospital General D'Ottawa, 43 Bruyere,
Ottawa, Ontario, Canada, KIN 5C8
RUDMOSE, WAYNE, Tracor Inc., 6500 Tracor Lane, Austin, Texas 78721, USA
SIMMONS, F. BLAIR, Division of Otolaryngology, Stanford University, 300 Pasteur Drive,
Palo Alto, California 94305, USA
STANGE, G., Hals-Nasen-Ohrenklinik der Universitat Freiburg, KillianstraBe 5, 78 Freiburg,
Germany
STEELE, C. R., Department of Aeronautics and Astronautics. Stanford University, Stanford,
California 94306, USA
TONNDORF, JUERGEN, College of Physicians and Surgeons, Columbia University, New York,
N. Y. 10032, USA
WIGAND, M. E., Hals-Nasen-Ohrenklinik der Universitat Erlangen, 8520 Erlangen, Wald
straBe 1, Germany
ZOLLNER, F., Hals-Nasen-Ohrenklinik der Universitat Freiburg, 7800 Freiburg, KillianstraBe 5,
Germany
Chapter 1
Sensori-Neural Deafness and Derangements
of the Loudness Function:
their Nature and Clinical Investigation
*
C. S. HALLPIKE FRS. FRCP. FRCS., Wimborne (Great Britain)
With 32.Figures
Contents
Introduction . . . . . . .
I. Loudness Recruitment: The Nature of the Phenomenon, the Functional Tests
Employed for its Investigation, and its Anatomical and Pathophysiological Me-
chanisms. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 2
A. The Occurrence of Loudness Recruitment in Association with Affections of the
Cochlear End Organs. . . . . . . . . . . . . . . . . . . . . . . . .. 7
B. The Absence of Loudness Recruitment Occurring in Association with Degenera-
tion of the Cochlear Nerve Fibres . . . . . . . . . . . . . . . . . . . . 10
II. Other Tests Employed for the Investigation of the Loudness Function in Sensori
Neural Deafness . . . . . . . . . . . . . . . . 17
A. Determination of the Intensity Difference Limen. . . . . . . . . . . . . . 17
B. BEKESY Audiometry . . . . . . . . . . . . . . . . . . . . . . . . . . 20
C. The SISI (Short Increment Sensitivity Index) of JERGER (JERGER, SHEDD, and
HARFORD, 1959) . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23
D. Determination of The Loudness Discomfort Level (HOOD and POOLE). . . . . 24
E. Middle Ear Impedance Measurements (METz) and their Use for the Determina-
tion of the Reflex Contraction Threshold of the Middle Ear Muscles . . . . . . 25
III. Speech Audiometry: Its Use for the Investigation of Derangement of Speech
Intelligibility Found to Occur in Association with Sensori-Neural Deafness 27
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33
Introduction
Sensori-neural deafness - the nerve or perceptive deafness of the earlier text
books of Otology - is due, with very few exceptions, to organic disorders which
exert their effects, either separately or in combination, upon the sensory cells of
CORTI'S organ or upon the nerve cells or fibres of the peripheral cochlear neurones.
*
Former Director of the Otological Research Unit of the Medical Research Council,
National Hospital for Nervous Diseases, Queen Square, London W.C.I.
2 C. S. HALLPIKE: Sensori-Neural Deafness and Derangements of Loudness Function
In accordance with practice in the United States, the use for this group of the
descriptive title of Sensori-neural Deafness has in recent years become widely
established.
Owing largely to developments in the course of what may be called the
"modern" period of audiology, the subject has acquired new perspectives. The
period in question can be said to have begun with the observations of POHLMAN
and KRANZ (1924) and of FOWLER (1937) on the loudness recruitment phenomenon
which soon lead to the recognition that sensori-neural deafness was characterised
by a variety of complex derangements of the loudness function.
Many new otoneurological test procedures have since been introduced for their
recognition and analysis; these will be described and their principles, practice and
clinical value will be discussed in the light of present experience.
It must be stressed, however, that before the tests can be effectively applied
the diagnosis of sensori-neural deafness first needs to be accurately established.
This diagnosis is largely dependent upon the pure tone audiometric findings.
Here, certain difficulties are well known and arise in particular from cross hearing
and faulty masking. Consideration of these will not be included in this contribution.
I. Loudness Recruitment: The Nature of the Phenome
non, the Functional Tests Employed for its Investigation,
and its Anatomical and Pathophysiological Mechanisms
The diagnosis of sensori-neural deafness, accurately established, has not until
the last two decades provided much insight into particular patterns of organic
damage to the various anatomical elements of the cochlear apparatus. Since then,
however, much progress in this direction has been made. New theoretical concepts
have taken shape, and many new test procedures have been devised. As a result,
it is now possible to effect a serviceable differentiation between the two main
types of sensori-neural deafness: 1. End organ deafness due to organic affections
of the hair cells of Corti's organ. 2. Nerve fibre deafness due to organic affections
of the nerve fibres and cells of the peripheral cochlear neurones. These diagnostik
advances have accrued in large measure from the intensive investigation of certain
derangements of the loudness function, in particular, the loudness recruitment
phenomenon, found to occur in a substantial proportion of cases of sensori-neural
deafness. This will now be considered in some detail.
Early information on the phenomenon of loudness recruitment was provided
in 1924 by POHLMAN and KRANZ. This was followed by the well known investiga
tions of FOWLER (1937) carried out upon subjects suffering from "nerve" deafness.
Fowler was responsible for the introduction of the ABLB (Alternate Biaural
Loudness Balance) test for loudness recruitment which has continued to hold its
place in certain situations, i.e., in subjects with unilateral deafness, as the most
valuable of the many that have been prescribed.
The nature of the phenomenon of loudness recruitment is readily appreciated
from a brief explanation of its demonstration by means of the ABLB test: The
subject wears a pair of telephone receivers each supplied from a pure tone audio-
Loudness Recruitment 3
meter with arrangements for the independent adjustment of the intensity at the
two receivers. The frequency of the stimulus is the same in each receiver and the
tester switches alternately between the two. By this means, two series of intensity
levels are determined, each point of the left ear series being matched for loudness
with a point of the right. ear series. The results are conveniently displayed upon a
ladder diagram of the type used by FOWLER. Fig. 1 illustrates the findings in two
typical cases of unilateral deafness together with their pure tone audiograms.
Case 1 Case 2
Conducting deafness Nerve deafness
Left ear Lef tear
a.0 0 .' -. --. '. --
",'
'" 20
-'!
'c" 40 ~ "-,V ............. r-- --.... 1.0
:.rC.:.i 50 - 1-1 50 .._ _ ..... Right
80 80~~--~--~~~
125 ............................... 8000 125. . .. 8000
R L R L
100 100 100 100
80 /; 80 80 80
- -
50 ~ 50 50 50
":::::::; "
1.0 ~ 40
20 / 20 20 / 20
o 0 0-'- 0
Loudness balance diagrams
Frequency 1000 cps
Fig. 1. (Reproduced by permission of Royal Society of Medicine)
In each case, the test frequency is 1000 Hz at which frequency the audiograms
show a threshold shift for the affected ear of 30 dB. The test starts with a
stimulus of threshold intensity at the right ear; the balancing intensity for the
left ear will, of course, be 30 dB higher. Successive stimuli rising in intensity in
steps of 20 dB are then applied to the right ear, and, for each level, the equal
loudness intensity for the left ear is established by trial, the comparison being
made by switching the stimulus backwards and forwards between the two ears.
The result obtained in Case 1 indicates that the loss of sensitivity, or deafness,
of the affected ear, 30 dB at threshold, remains constant throughout the entire
intensity range. This finding is an unvarying one in conductive deafness and is
4 C. S. HALLPIKE: Sensori-Neural Deafness and Derangements of Loudness Function
open to the straightforward explanation that the obstruction caused by the
middle ear lesion to the passage of sound waves to the inner ear introduces an
attenuation factor, in this case 30 dB, which is constant at all intensities.
A different result is obtained in Case 2. The pure tone audiogram is sub
stantially the same as in Case 1 with a threshold shift at 1000 Hz of 30 dB.
The balancing points at threshold are identical with those of Case 1 with a 30 dB
displacement upwards for the left ear. On ascending the intensity scale, however,
it is found that the sensitivity loss or deafness of the left ear becomes progressively
less until, at 80 dB, equal intensities at the two ears evoke equal sensations of
loudness. In other words, deafness as shown by an elevation of the normal thre
shold is reduced or disappears at high stimulus intensities. This in its simplest
terms constitutes the phenomenon of loudness recruitment.
An alternative form, due to STEINBERG and GARDNER (1937), for the graphic
representation of these results is shown in Fig. 2. It is in common use and has
many advantages. Sound intensities in decibels above the normal threshold are
plotted on the vertical axis for the unaffected ear and on the horizontal axis for
the affected ear. Equal loudness levels for the two ears are plotted on this chart as
_~ __- .--~ __~ __~ B
100 r-
/
80 1----1----1----+---1''-------1
<t) 601---t--t-- H--hrV.::-!
c::
oc:t:l
40 I--+--+-+-+~'-t---I
~
20
I------,I"----,,........,,~+---+-----I
o 20 40 60 80 100
DECIBELS
Fig. 2. (Reproduced by permission of Royal Society of Medicine)
a series of points and the line, AB, passing through the origin, connects the points
which would be obtained in a normal subject. aD is the corresponding line
obtained in Case 1. Here, the sensitivity loss at threshold of the deaf ear is re
a
presented by the displacement of the Point along the base line to the right of the
origin. This sensitivity loss remains constant at higher intensities, and the Line aD
thus lies parallel to AB. EF is the corresponding line obtained in Case 2. As in
Case 1, the same sensitivity loss at threshold is represented by the same dis
placement of the Point E to the right of the origin. At high intensities, however,
the sensitivity loss is progressively reduced and the line EF approaches and
finally coincides with the Line AB.
At the time of FOWLER'S work, the neurological mechanism of loudness
No
recruitment received much attention. Thus, according to LORENTE DE (1937)
quoted by FOWLER (1939), it was considered to be a physiological consequence
Loudness Recruitment 5
of any organic affection which would reduce the number of active neuro-sensory
elements, be they nerve fibres or sensory cells. A similar view seems to have been
accepted by STEVENS and DAVIS (1938). No closer analysis was attempted of the
anatomical basis of loudness recruitment, and the subjects exhibiting it continued
to be included with others within the general category of nerve deafness.
In 1946, the subject was examined afresh by DE BRUi'NE-ALTES who confirmed
the observational data and stressed the need for further studies in which the
results of the clinical tests for loudness recruitment could be correlated with more
exact information upon the underlying structural changes in the cochlear sense
organs and their associated neural pathways, and, in 1948, a substantial body of
information of this kind was presented by DIX, HALLPIKE, and HOOD. This new
information was derived from a detailed clinico-pathological study of subjects
suffering from two different and clearly defined organic affections of the VIII
nerve system, Menieres disease of the labyrinth and acoustic neurofibroma.
In the case of MENIERES disease, it is known from the work of HALLPIKE and
CAIRNS (1938), LINDSAY (1942), ALTMANN and FOWLER (1943) and others that the
primary lesion is one of the endolymph system of the inner ear resulting in damage
to the sensory cells of Corti's organ. The cochlear nerve fibres and ganglion cells
are unaffected, at any rate, until the disease is of long standing.
In the case of acoustic neurofibroma, the observations of HARDY and CROWE
(1936) upon the very early stages in the development of this tumour indicate its
Fig. 3. Cochlea of a human subject showing degeneration of the spiral ganglion cells and
cochlear nerve fibres resulting from tumor pressure upon the VIII nerve. The peripheral
sensory apparatus, including the hair cells of Corti's organ, is well preserved. (Reproduced by
permission of Royal Society of Medicine)