- Email: [email protected]
A THEORY OF NERVE DEAFNESS
83
Preliminary
Communication
A THEORY OF NERVE DEAFNESS THREE types of impairment of hearing are generally
distinguished: (1) Conduction deafness due to loss in the middle ear only, sensitivity for bone conduction being normal. Often caused by thickening of the tympanum or by otosclerosis. in which there is impairment of both air and bone conduction. Associated with degeneration of the sensory cells of the organ of Corti in the inner ear or with other neural damage, such as a tumour of the eighth nerve. (3) Central deafness, which is rare and has no known peripheral origin, being regarded as a central disorder often associated with aphasia. No further mention of this will be made here.
(2) Nerve deafness,
There
seems
to
be
no
mystery about conduction
deafness; the auditory signal is simply attenuated, and this loss may usually be made good with a suitable external amplifier. In nerve deafness, on the other hand, amplification does not make up for the loss, and the defect is not simple attenuation of the signal. The condition has certain rather distinctive features: (1) There is some degree of confusion. The older term " perception deafness ", still sometimes used, indicates this clinical distinction. (2) The deterioration is mainly at the upper end of the frequency spectrum (presbyacusia), hearing for low frequencies often being normal. (3) The audiogram is generally peaky ", a sudden dip (loss of sensitivity) at about 4000 cycles being particularly common. (4) Tinnitus is common, but this may also occur in conduction deafness. (5) The curious phenomenon of loudness recruitment is common. "
.
Recruitment, which is almost certainly found only in deafness, may be described as a shortening of the
nerve
loudness scale.
In
cases
of unilateral
nerve
deafness it may be demonstrated
by applying the same tone to the two ears and asking the patient to balance the intensities for the two ears over a wide Where there is recruitment, the deaf range of intensity. ear will require higher energies at the lower intensities; but, as the level rises, the difference in intensity for loudness balance decreases and may disappear. In conduction deafness the ratio of the two energies will remain constant for loudness balance over the working range of hearing.
Previous work on visual discrimination, where thresholds are supposed to be limited by the effective signalto-noise ratio of the neural systems involved, suggests a possible explanation of nerve deafness. We have visual discrimination as limited the channel by regarded of the the channel system, capacity capacity being a function of the number of fibres available for discrimination and the level of random neural activity, or noise ", tending to mask the signal. Increase in the amount of noise should raise the threshold and tend to produce confusion. Nerve deafness could be due to loss of channel capacity either through loss of functional fibres or through increased noise. These two possibilities give rather different predictions. "
test the hypothesis that nerve deafness is in some due to increased noise masking the auditory signals, we have compared the phenomena of nerve deafness with the effects of noise masking on normal hearing. Their similarity is striking.
To
cases
Fletcher1 found that, when he used thermal noise for masking pure tones, the high tones were primarily affected; in other words, he produced presbyacusia in the normal ear by masking with thermal noise. It is well known that partial sectioning of the cochlear nerve produces presbyacusia in cats2 and also in patients with Meniere’s disease.3 Thus it might be concluded that reduction in channel capacity decreases discrimination of high tones whether this reduction is the result of raised noise or of loss of functional fibres. 1. 2. 3.
Fletcher, H. J. acoust. Soc. Amer. 1938, 9, 275. Wever, E. G., Bray, C. W. J. Psychol. 1937, 3, 101. Neff, W. D. J. comp. physiol. Psychol. 1947, 40, 203. Dandy, W. E. Bull. Johns Hopk. Hosp. 1933, 53, 52 (cited by Wever, ref. 8, p. 243).
Fig.
I-Effects of nerve deafness on differential threshold. No additional masking has been added; tone pips are of same duration as above but following frequencies have been used: 1000, 1500, 2000, 3000, and 4000 cycles per sec. Each of 17 persons used was tested for absolute threshold at the above frequencies and compared with average ear to assess impairment for each frequency. Subjects with the same absolute thresholds (i.e., the same impairment) are grouped together. This grouping is irrespective of frequency-subjects are combined for any frequency for which their absolute thresholds are equal. Thus each subject may appear in several of the curves, at various frequencies. Bone conduction to the mastoid process has been used throughout: we are repeating the experiment for air conduction. As in fig. 1, slope flattens with increasing impairment. It seems possible to estimate effective masking noise for various degrees of nerve deafness by comparing curves in figs. 1 and 2 and selecting those giving best fit.
Fig. 2-Effects of various levels of masking noise on threshold for detecting tone pip lasting 0.01 sec. against continuous tone. Frequency of continuous tone and pip is 1000 cycles per sec. Masking noise reduces slope. Bone conduction was used. Pips slightly rounded to reduce transients.
84
Steinberg and Gardner 4 showed that white noise masking produces recruitment in the normal ear. (In " white " or thermal " random noise all frequencies are present in equal amounts, producing a hissing sound like escaping steam.) Dix, Hallpike, and Hoodfound that recruitment appears to be "
associated with damage to the nerve-endings at the organ of Corti but not with damage to the eighth nerve. This finding is compatible with the hypothesis that neural noise produces recruitment, for disturbance of the nerve-endings (as in Meniere’s disease) would be expected to produce random firing, whereas this is not generally found when fibres are sectioned. When there is marked tinnitus of a particular tone, some loss of hearing is perhaps always found near the corresponding frequency. But although tinnitus is often found with nerve deafness it is not invariably found. We should not expect it if the deafness was due to a tumour of the nerve; but, if the deafness was due to damage of the end-organ, the patient would presumably be aware of his neural -noise as some form of tinnitus. If he is not, some explanation is necessary. The normal person is aware of a surprising amount of selfgenerated sound in a silent room, though he is not normally It is also true that we are not aware of this internal noise. usually aware of irrelevant regular sounds-e.g., the ticking of a clock, and even its chime, when this is familiar, though it may be loud. Perhaps in some cases neural noise is rejected in a similar manner, with the result that, although it may tend to mask wanted sounds, there is no awareness of it as tinnitus, at any rate until attention is called to it. We have found it necessary, on quite other grounds, to postulate a " gate " in sensory discrimination mechanisms.6 to reject abnormally Perhaps this postulated " gate " is raised " high residual noise. The idea of a gate " is important: it is taken over from electronics where the term denotes a threshold introduced into a circuit so that voltages below the gate threshold are rejected. The gate may be raised or lowered or may be fixed. This suggests a possible connection between auditory fatigue and nerve deafness, and they have many features in common. If a sustained noise or tone tends to raise the gate, we should expect recruitment (for only the lowerintensity signals will be affected by the gate) and this is in fact the case. Perhaps some of the results obtained by Hoodwho has done much work on auditory fatigue, might be interpreted on this hypothesis. Further, the neural origin appears to be the same for nerve deafness as for auditory fatigue-between the electro-cochlear activity and the binaural localisation pro8 cess, according to Wever.
If nerve deafness may be caused by raised neural noise a practical conclusion seems to follow. To attempt to raise the wanted signal above the residual noise with a linear amplifier (such as a standard hearing-aid) is likely to overload the ear, for it seems clear that there is no abnormal attenuation in the system. Now, it has been shown by Licklider 9 and discussed by Miller 10 that almost all the information-content of speech is carried by the changeover points, and almost none at the energy peaks; it thus appears possible to prevent overloading, while retaining the necessary information, by using suitable peak clipping in hearing aids. This has been tried but has produced only slight improvement.11 Perhaps in addition it may be necessary to filter out those frequencies where impairment is greatest, because continual stimulation appears, at least in some cases, to increase tinnitus and therefore presumably the amount of neural masking noise. We wish to thank Dr. E. R. F. W. Crossman, Dr. T. S. Littler, Miss Violet Cane, and Prof. O. L. Zangwill for helpful suggestions and advice. We are indebted to Mr. A. S. H. Walford for providing nerve-deaf patients from Addenbrooke’s Hospital. The Medical Research Council gave a grant to one of us (J. G. W.) and a grant for apparatus.
Psychological Laboratory, Cambridge
R. L. GREGORY M.A. Cantab. JEAN G. WALLACE B.Com. Edin.
New Inventions A SIMPLE RESECTOSCOPE MODIFICATIONS of an instrument usually lead to something more complex which requires greater experience in handling. The development of the resectoscope from the days of the Stern/McCarthy ratchet-driven instrument is an example of the complexities which can be superimposed on a machine of
initially simple design. In the past twenty-five
years the demand has been for improvement in vision and illumination, for reduction in the size
examining the possibility that typical nerve deafis due to raised neural noise we have compared differential intensity discrimination (short-tone pips against a continuous tone of the same frequency) over a wide range of intensities and frequencies in (1) nervedeaf ears showing various degrees of impairment and (2) the normal ear in the presence of white noise masking. We should expect the curves relating intensity of the tone pip to the continuous tone to be similar for a nervedeaf ear and a normal ear, subject to added masking noise. By determining the level of noise which produces the best fit of these curves we might hope to estimate the effective level of neurological noise in a nerve-deaf ear showing a given impairment. Preliminary results are fairly encouraging; in particular we find that the curves are similar in general form. These data are shown in 1 and from which 2, figs. comparison may be made. In
ness
4. Steinberg, J. C., Gardner, M. B. J. acoust. Soc. Amer. 1937, 9, 11. 5. Dix, M. R., Hallpike, C. S., Hood, J. D. Proc. R. Soc. Med. 1948, 41, 516. 6. Gregory, R. L., Cane, V. R. Nature, Lond. 1955, 176, 1272. Gregory, R. L. Third London Information Symposium (edited by C. Cherry). 7.
London, 1956. Hood, J. D. Ann. Otol. &c.,
8.
Wever, E. G. Theory
St. Louis, 1955, 64, 507. of Hearing. New York, 1949.
9. Licklider, J. C. R. J. acoust. Soc. Amer. 1946, 18, 429. 10. Miller, G. A. Language and Communication. New York, 1951. 11. Littler, T. S. Personal communication.
Preliminary
Communication
A THEORY OF NERVE DEAFNESS THREE types of impairment of hearing are generally
distinguished: (1) Conduction deafness due to loss in the middle ear only, sensitivity for bone conduction being normal. Often caused by thickening of the tympanum or by otosclerosis. in which there is impairment of both air and bone conduction. Associated with degeneration of the sensory cells of the organ of Corti in the inner ear or with other neural damage, such as a tumour of the eighth nerve. (3) Central deafness, which is rare and has no known peripheral origin, being regarded as a central disorder often associated with aphasia. No further mention of this will be made here.
(2) Nerve deafness,
There
seems
to
be
no
mystery about conduction
deafness; the auditory signal is simply attenuated, and this loss may usually be made good with a suitable external amplifier. In nerve deafness, on the other hand, amplification does not make up for the loss, and the defect is not simple attenuation of the signal. The condition has certain rather distinctive features: (1) There is some degree of confusion. The older term " perception deafness ", still sometimes used, indicates this clinical distinction. (2) The deterioration is mainly at the upper end of the frequency spectrum (presbyacusia), hearing for low frequencies often being normal. (3) The audiogram is generally peaky ", a sudden dip (loss of sensitivity) at about 4000 cycles being particularly common. (4) Tinnitus is common, but this may also occur in conduction deafness. (5) The curious phenomenon of loudness recruitment is common. "
.
Recruitment, which is almost certainly found only in deafness, may be described as a shortening of the
nerve
loudness scale.
In
cases
of unilateral
nerve
deafness it may be demonstrated
by applying the same tone to the two ears and asking the patient to balance the intensities for the two ears over a wide Where there is recruitment, the deaf range of intensity. ear will require higher energies at the lower intensities; but, as the level rises, the difference in intensity for loudness balance decreases and may disappear. In conduction deafness the ratio of the two energies will remain constant for loudness balance over the working range of hearing.
Previous work on visual discrimination, where thresholds are supposed to be limited by the effective signalto-noise ratio of the neural systems involved, suggests a possible explanation of nerve deafness. We have visual discrimination as limited the channel by regarded of the the channel system, capacity capacity being a function of the number of fibres available for discrimination and the level of random neural activity, or noise ", tending to mask the signal. Increase in the amount of noise should raise the threshold and tend to produce confusion. Nerve deafness could be due to loss of channel capacity either through loss of functional fibres or through increased noise. These two possibilities give rather different predictions. "
test the hypothesis that nerve deafness is in some due to increased noise masking the auditory signals, we have compared the phenomena of nerve deafness with the effects of noise masking on normal hearing. Their similarity is striking.
To
cases
Fletcher1 found that, when he used thermal noise for masking pure tones, the high tones were primarily affected; in other words, he produced presbyacusia in the normal ear by masking with thermal noise. It is well known that partial sectioning of the cochlear nerve produces presbyacusia in cats2 and also in patients with Meniere’s disease.3 Thus it might be concluded that reduction in channel capacity decreases discrimination of high tones whether this reduction is the result of raised noise or of loss of functional fibres. 1. 2. 3.
Fletcher, H. J. acoust. Soc. Amer. 1938, 9, 275. Wever, E. G., Bray, C. W. J. Psychol. 1937, 3, 101. Neff, W. D. J. comp. physiol. Psychol. 1947, 40, 203. Dandy, W. E. Bull. Johns Hopk. Hosp. 1933, 53, 52 (cited by Wever, ref. 8, p. 243).
Fig.
I-Effects of nerve deafness on differential threshold. No additional masking has been added; tone pips are of same duration as above but following frequencies have been used: 1000, 1500, 2000, 3000, and 4000 cycles per sec. Each of 17 persons used was tested for absolute threshold at the above frequencies and compared with average ear to assess impairment for each frequency. Subjects with the same absolute thresholds (i.e., the same impairment) are grouped together. This grouping is irrespective of frequency-subjects are combined for any frequency for which their absolute thresholds are equal. Thus each subject may appear in several of the curves, at various frequencies. Bone conduction to the mastoid process has been used throughout: we are repeating the experiment for air conduction. As in fig. 1, slope flattens with increasing impairment. It seems possible to estimate effective masking noise for various degrees of nerve deafness by comparing curves in figs. 1 and 2 and selecting those giving best fit.
Fig. 2-Effects of various levels of masking noise on threshold for detecting tone pip lasting 0.01 sec. against continuous tone. Frequency of continuous tone and pip is 1000 cycles per sec. Masking noise reduces slope. Bone conduction was used. Pips slightly rounded to reduce transients.
84
Steinberg and Gardner 4 showed that white noise masking produces recruitment in the normal ear. (In " white " or thermal " random noise all frequencies are present in equal amounts, producing a hissing sound like escaping steam.) Dix, Hallpike, and Hoodfound that recruitment appears to be "
associated with damage to the nerve-endings at the organ of Corti but not with damage to the eighth nerve. This finding is compatible with the hypothesis that neural noise produces recruitment, for disturbance of the nerve-endings (as in Meniere’s disease) would be expected to produce random firing, whereas this is not generally found when fibres are sectioned. When there is marked tinnitus of a particular tone, some loss of hearing is perhaps always found near the corresponding frequency. But although tinnitus is often found with nerve deafness it is not invariably found. We should not expect it if the deafness was due to a tumour of the nerve; but, if the deafness was due to damage of the end-organ, the patient would presumably be aware of his neural -noise as some form of tinnitus. If he is not, some explanation is necessary. The normal person is aware of a surprising amount of selfgenerated sound in a silent room, though he is not normally It is also true that we are not aware of this internal noise. usually aware of irrelevant regular sounds-e.g., the ticking of a clock, and even its chime, when this is familiar, though it may be loud. Perhaps in some cases neural noise is rejected in a similar manner, with the result that, although it may tend to mask wanted sounds, there is no awareness of it as tinnitus, at any rate until attention is called to it. We have found it necessary, on quite other grounds, to postulate a " gate " in sensory discrimination mechanisms.6 to reject abnormally Perhaps this postulated " gate " is raised " high residual noise. The idea of a gate " is important: it is taken over from electronics where the term denotes a threshold introduced into a circuit so that voltages below the gate threshold are rejected. The gate may be raised or lowered or may be fixed. This suggests a possible connection between auditory fatigue and nerve deafness, and they have many features in common. If a sustained noise or tone tends to raise the gate, we should expect recruitment (for only the lowerintensity signals will be affected by the gate) and this is in fact the case. Perhaps some of the results obtained by Hoodwho has done much work on auditory fatigue, might be interpreted on this hypothesis. Further, the neural origin appears to be the same for nerve deafness as for auditory fatigue-between the electro-cochlear activity and the binaural localisation pro8 cess, according to Wever.
If nerve deafness may be caused by raised neural noise a practical conclusion seems to follow. To attempt to raise the wanted signal above the residual noise with a linear amplifier (such as a standard hearing-aid) is likely to overload the ear, for it seems clear that there is no abnormal attenuation in the system. Now, it has been shown by Licklider 9 and discussed by Miller 10 that almost all the information-content of speech is carried by the changeover points, and almost none at the energy peaks; it thus appears possible to prevent overloading, while retaining the necessary information, by using suitable peak clipping in hearing aids. This has been tried but has produced only slight improvement.11 Perhaps in addition it may be necessary to filter out those frequencies where impairment is greatest, because continual stimulation appears, at least in some cases, to increase tinnitus and therefore presumably the amount of neural masking noise. We wish to thank Dr. E. R. F. W. Crossman, Dr. T. S. Littler, Miss Violet Cane, and Prof. O. L. Zangwill for helpful suggestions and advice. We are indebted to Mr. A. S. H. Walford for providing nerve-deaf patients from Addenbrooke’s Hospital. The Medical Research Council gave a grant to one of us (J. G. W.) and a grant for apparatus.
Psychological Laboratory, Cambridge
R. L. GREGORY M.A. Cantab. JEAN G. WALLACE B.Com. Edin.
New Inventions A SIMPLE RESECTOSCOPE MODIFICATIONS of an instrument usually lead to something more complex which requires greater experience in handling. The development of the resectoscope from the days of the Stern/McCarthy ratchet-driven instrument is an example of the complexities which can be superimposed on a machine of
initially simple design. In the past twenty-five
years the demand has been for improvement in vision and illumination, for reduction in the size
examining the possibility that typical nerve deafis due to raised neural noise we have compared differential intensity discrimination (short-tone pips against a continuous tone of the same frequency) over a wide range of intensities and frequencies in (1) nervedeaf ears showing various degrees of impairment and (2) the normal ear in the presence of white noise masking. We should expect the curves relating intensity of the tone pip to the continuous tone to be similar for a nervedeaf ear and a normal ear, subject to added masking noise. By determining the level of noise which produces the best fit of these curves we might hope to estimate the effective level of neurological noise in a nerve-deaf ear showing a given impairment. Preliminary results are fairly encouraging; in particular we find that the curves are similar in general form. These data are shown in 1 and from which 2, figs. comparison may be made. In
ness
4. Steinberg, J. C., Gardner, M. B. J. acoust. Soc. Amer. 1937, 9, 11. 5. Dix, M. R., Hallpike, C. S., Hood, J. D. Proc. R. Soc. Med. 1948, 41, 516. 6. Gregory, R. L., Cane, V. R. Nature, Lond. 1955, 176, 1272. Gregory, R. L. Third London Information Symposium (edited by C. Cherry). 7.
London, 1956. Hood, J. D. Ann. Otol. &c.,
8.
Wever, E. G. Theory
St. Louis, 1955, 64, 507. of Hearing. New York, 1949.
9. Licklider, J. C. R. J. acoust. Soc. Amer. 1946, 18, 429. 10. Miller, G. A. Language and Communication. New York, 1951. 11. Littler, T. S. Personal communication.