Acta Otolaryngol83: 470474, 1977
PERMANENT EFFECTS OF LOW FREQUENCY VIBRATION ON THE VESTIBULAR SYSTEM E. Aantaa, E. Virolainen and V. Karskela Acta Otolaryngol Downloaded from informahealthcare.com by University of Newcastle on 01/07/15 For personal use only.
From the Department of Otolaryngology, University
of Turku. Turku
I
Finland
(Received March 4, 1976)
Abstract. Among 49 male workers, mean age 30 years, who had been working in conditions of extreme noise and vibration for between 6 months and 10 years vestibular disturbances could be shown (in the form of spontaneous
tineuish between the effects of vibration and " noise on the vestibular system. ~h~ purpose Of this study was to jnvestigate the influence
rotatory tests) in as high as 44.9%. The lesions were believed to have arisen in the peripheral vestibular organ vibration. as a consequence of the low frequency .~
attempt to exclude the influence of noise, only persons with normal hearing were included.
Low frequency vibration can cause irritation in the vestibular system. The symptoms caused by vibration are mainly due to infratones. 49 male workers were studied and in about 45% of them vestibular disturbances of peripheral origin could be demonstrated. Man has a rather good absorbing mechanism against vibration of the earth or floor (Coerman et al., 1960). However, resonance vibration in the skull can also be caused by low frequency vibration of the air. I t is known that vibration, especially below the frequency of 2 Hz, causes irritation in the vestibular system, rather like sea-sickness. Vibration below the frequency of 10 Hz can also irritate the vestibular system. These symptoms caused by vibration are mainly due to infratones. Moreover it has been shown that in many subjects, ordinary noise above 130 dB can cause vertigo and even nystagmus. Even lower noise levels can cause vertigo if the noise is only one-sided (Ades et al., 1957; Bell, 1966; Kryter, 1970). In practice, however, it is not easy to dis-
MATERIAL AND METHODS The present material consisted of two series of subjects. The first series consisted of 49 male workers aged 20 to 52 (mean age 30 years) working in a room where marine diesel engines (10800 h.p.) are tested. They had been exposed to noise and vibration for periods varying from 6 months to 10 years. In their previous employment they had not been exposed to any sort of vibration. None of the subjects had been exposed, either before or during this investigation to carbon monoxide, benzine, trichlorethylene, or other solvents. I t was established that whilst the testing was going on, the whole building vibrated at 2.8 to 21.5 Hz, the amplitude of vibration being as weak as a mere 0.13 to 8.80 pm (Table I). The noise level in the testing room was about 118 dE3 (A). In this room about 18 engines are tested each year, the total proving time of one engine being normally 6 to 12 hours. The control series consisted of 20 female nurses aged 19 to 24 (mean age 20 years). Pro-
Effects of vibration on vestibular system Table I. The vibration of thefloor of the testing room when proving 10800 H . P . marine diesel engines at maximum power
Acta Otolaryngol Downloaded from informahealthcare.com by University of Newcastle on 01/07/15 For personal use only.
Measurements were made with the 1/10 octave filter Frequency (Hz)
(w)
Amplitude
2.5 6.4 8.7 10.0 13.1 15.0 18.0 21.5
0.13 0.38 5.50 1S O 8.80 2.50 2.00 0.38
spective subjects with ear disease, head trauma as well as subjects using medicines were excluded from both series. In all subjects the hearing was normal. A careful case history, and pure tone and speech audiograms were taken at the beginning of the trial. Neuro-otological examinations, including ENG tests and nystagmus observations in a totally dark room with Frenzel's glasses, were made with a one-month interval. Air and bone conduction audiograms were measured by the usual descending-ascending technique. For each subject, speech thresholds and discrimination were determined as described by Palva (1952). A Madsen OB-60 audiometer was used. The rotatory tests were carried out by means of Polman's rotating chair (Polman Mod. 1 1 e 1 1 1) which enables linear adjustment of the acceleration rate from 0.2"/secZon wards. Silver-silverchloride electrodes 7 mm in diameter were employed. The two recording electrodes were located on the skin near the temporal canthi of the lids of both eyes. and the earth electrode was placed on the skin of the forehead. The electrodes were fixed with adhesive tape and electrode jelly was utilized to improve the contact. An a.c. condensercoupled amplifier, time constant 2 sec, upper limit 70 Hz, was utilized for the recording. All recordings were performed in darkness.
471
The subject's head was fixed tilted 30 degrees forward from the vertical, and the eyes were closed. The threshold of acceleration was measured by the following method. The subject was accelerated for 90 sec at a rate of 0.2"/sec2, beginning to the right. He was then decelerated at the same rate. 120 seconds after stopping, the same procedure was repeated, but this time in the opposite direction. This procedure was continued by accelerating the subject at a rate of 0.4"/sec2 and then 0.6"/ sec2 and finally Io/sec2. The total amplitude during the acceleration of I"/sec2 up to the final velocity of 60"/sec was also recorded and calculated. The first post-rotatory nystagmus was measured after an abrupt stop (0.3 sec). Before the stop the velocity of rotation was maintained at 60"/sec during 120 sec. The total amplitude of nystagmus was calculated. Any spontaneous or positional nystagmus was recorded in a dark room while the subject was lying in a supine position and in both lateral positions. The nystagmus was recorded both with closed eyes and with eyes open. The nystagmus was considered pathological when the speed of the slow phase exceeded 7 degrees per second. The caloric test was performed ad modum Hallpike with the following exceptions. The irrigation time was only 30 sec. The induced nystagmus was recorded for 70 sec with the subject's eyes closed. At the 70th second, the
Table 11. Nysttigmus findings rind caloric reactions in subjects ex-posed to vibration
Spontaneous nystagmus Spontaneous nystagmus+ lowered caloric excitability Lowered caloric excitability N o nystagmus. normal caloric reactions Total
No. of subjects
Per cent
10
20.4
2 10
4. I 20.4
27
55. I
49
100.0
472
E. Aantaa e t al.
Acta Otolaryngol Downloaded from informahealthcare.com by University of Newcastle on 01/07/15 For personal use only.
Table 111. The thresholds of angular crcceleration during rotatory tests
tions. The nystagmus findings and caloric reactions in persons exposed to vibration are shown in Table 11. In 10 subjects (20.4%) Control series s0.4"/sec2 20 (100%) there was spontaneous nystagmus in all posiVibration series s0.4"/sec2 35 (71.5%) 14 (28.5%) tions recorded. In 2 subjects (4.1 %) there was >0.4"/sec2 spontaneous nystagmus and lowered caloric excitability. In 27 subjects (55.1 %) ENGfindings were considered normal and among subject was asked to open his eyes and to fix these subjects there was also no head-shaking his gaze on a fixation light, situated about 2 nystagmus observed with Franzel's glasses in metres away, directly in front of him. For each a totally dark room. irrigation the frequency of nystagmus and The thresholds of angular acceleration are angular velocity of the slow nystagmus phase shown for both series in Table 111. In control was calculated during the culmination phase, series the thresholds in both directions (right both before and after opening the eyes. The and left) were equal to or less than 0.4"/s2. In result was considered as "canal paresis" (low35 subjects (71.5%) exposed to vibration the ered excitability) when reactions before the thresholds were the same as in the control fixation were 20% weaker in one ear than in series but in 14 (28.5%) the thresholds were the other. The ocular fixation index was calmore than 0.4"/s2.With the method and equipculated according to Demanez & Ledoux ment adopted in this laboratory the limit of (1970). normal threshold is 0.4"/sz (Virolainen, 1972). The total amplitudes of the nystagmic slow OF1= amplitudexfrequency (eyes open) phase during acceleration at a rate of one dex 100% amplitudexfrequency (eyes closed) gree/s2, from an angular velocity of V/sec to 60"/sec in both series, are shown in Table IV. OF1 was considered normal if it was lower In the control series the mean values both to than 50%. the right (106") and to the left (103") are statistically significantly higher than the corThe optokinetic nystagmus of the subject responding mean values of subjects exposed to was investigated at 30", 40", 50" and 60"/sec to vibration (to the right 86" and to the left 72"). the right and to the left alternately. The mean total (summed) amplitudes of the All these recordings were made by means of Elema Mingograph ENG. The same type of electrode and the same pattern of fixating the electrodes were used as before. Table IV. The totcil crmplitudr of the sloit, phase of the nystagmus o n accelerating at a rmte of one tiegreelsec' f r o m a speed of Oo/ RESULTS sec t o 60"lsec. Comparison brtitqeen control The air and bone conduction values were Jeries and thr subject5 e.rposrci to vibrcition better than 10 dB at each frequency studied in all subjects exposed to vibration. The discrimination ability of subjects was established as 100 per cent. I n the neuro-otological examination there was no sign of any lesion of other cranial nerves. In control series there was neither spontaneous nystagmus nor abnormal caloric reacAi Ili O t o l e r v n ~ d83
Mean values are expressed
in
degrees ~~~~
Mean S . D . 7' Acceleration to the right Control series Vibration series Acceleration to the left Control series Vibration series
106
86
42 39
2 11s
72
43 32
3729
P
0.05 0.001
Effects qf vihrrrtion on vestibular system Table V . Mecin toter1 arnplitudes of thc ,first posf-rotutory nystagriius t o the right r i n d lefi after ( i n cihrupt stop .from ei speed of'6O0/.s(v.. Cornpiirison betwven control series and the subjects who hcive herri exposed t o t3ihrrrtion Mean values expressed in degrees
Acta Otolaryngol Downloaded from informahealthcare.com by University of Newcastle on 01/07/15 For personal use only.
Mean S.D. T First post-rotatory nystagmus, to the right Control series Vibration series First post-rotatory nystagmus, to the left Control series Vibration series
77
45 39
3 613
'17
49 49
1335
101
P
0.001
slow phase of the first post-rotatory nystagmus to the right and left after an abrupt stop from a velocity of 60"/sec are shown in Table V . In the control series the mean total amplitude of right-beating nystagmus was 113" which, statistically, is significantly higher (p
PERMANENT EFFECTS OF LOW FREQUENCY VIBRATION ON THE VESTIBULAR SYSTEM E. Aantaa, E. Virolainen and V. Karskela Acta Otolaryngol Downloaded from informahealthcare.com by University of Newcastle on 01/07/15 For personal use only.
From the Department of Otolaryngology, University
of Turku. Turku
I
Finland
(Received March 4, 1976)
Abstract. Among 49 male workers, mean age 30 years, who had been working in conditions of extreme noise and vibration for between 6 months and 10 years vestibular disturbances could be shown (in the form of spontaneous
tineuish between the effects of vibration and " noise on the vestibular system. ~h~ purpose Of this study was to jnvestigate the influence
rotatory tests) in as high as 44.9%. The lesions were believed to have arisen in the peripheral vestibular organ vibration. as a consequence of the low frequency .~
attempt to exclude the influence of noise, only persons with normal hearing were included.
Low frequency vibration can cause irritation in the vestibular system. The symptoms caused by vibration are mainly due to infratones. 49 male workers were studied and in about 45% of them vestibular disturbances of peripheral origin could be demonstrated. Man has a rather good absorbing mechanism against vibration of the earth or floor (Coerman et al., 1960). However, resonance vibration in the skull can also be caused by low frequency vibration of the air. I t is known that vibration, especially below the frequency of 2 Hz, causes irritation in the vestibular system, rather like sea-sickness. Vibration below the frequency of 10 Hz can also irritate the vestibular system. These symptoms caused by vibration are mainly due to infratones. Moreover it has been shown that in many subjects, ordinary noise above 130 dB can cause vertigo and even nystagmus. Even lower noise levels can cause vertigo if the noise is only one-sided (Ades et al., 1957; Bell, 1966; Kryter, 1970). In practice, however, it is not easy to dis-
MATERIAL AND METHODS The present material consisted of two series of subjects. The first series consisted of 49 male workers aged 20 to 52 (mean age 30 years) working in a room where marine diesel engines (10800 h.p.) are tested. They had been exposed to noise and vibration for periods varying from 6 months to 10 years. In their previous employment they had not been exposed to any sort of vibration. None of the subjects had been exposed, either before or during this investigation to carbon monoxide, benzine, trichlorethylene, or other solvents. I t was established that whilst the testing was going on, the whole building vibrated at 2.8 to 21.5 Hz, the amplitude of vibration being as weak as a mere 0.13 to 8.80 pm (Table I). The noise level in the testing room was about 118 dE3 (A). In this room about 18 engines are tested each year, the total proving time of one engine being normally 6 to 12 hours. The control series consisted of 20 female nurses aged 19 to 24 (mean age 20 years). Pro-
Effects of vibration on vestibular system Table I. The vibration of thefloor of the testing room when proving 10800 H . P . marine diesel engines at maximum power
Acta Otolaryngol Downloaded from informahealthcare.com by University of Newcastle on 01/07/15 For personal use only.
Measurements were made with the 1/10 octave filter Frequency (Hz)
(w)
Amplitude
2.5 6.4 8.7 10.0 13.1 15.0 18.0 21.5
0.13 0.38 5.50 1S O 8.80 2.50 2.00 0.38
spective subjects with ear disease, head trauma as well as subjects using medicines were excluded from both series. In all subjects the hearing was normal. A careful case history, and pure tone and speech audiograms were taken at the beginning of the trial. Neuro-otological examinations, including ENG tests and nystagmus observations in a totally dark room with Frenzel's glasses, were made with a one-month interval. Air and bone conduction audiograms were measured by the usual descending-ascending technique. For each subject, speech thresholds and discrimination were determined as described by Palva (1952). A Madsen OB-60 audiometer was used. The rotatory tests were carried out by means of Polman's rotating chair (Polman Mod. 1 1 e 1 1 1) which enables linear adjustment of the acceleration rate from 0.2"/secZon wards. Silver-silverchloride electrodes 7 mm in diameter were employed. The two recording electrodes were located on the skin near the temporal canthi of the lids of both eyes. and the earth electrode was placed on the skin of the forehead. The electrodes were fixed with adhesive tape and electrode jelly was utilized to improve the contact. An a.c. condensercoupled amplifier, time constant 2 sec, upper limit 70 Hz, was utilized for the recording. All recordings were performed in darkness.
471
The subject's head was fixed tilted 30 degrees forward from the vertical, and the eyes were closed. The threshold of acceleration was measured by the following method. The subject was accelerated for 90 sec at a rate of 0.2"/sec2, beginning to the right. He was then decelerated at the same rate. 120 seconds after stopping, the same procedure was repeated, but this time in the opposite direction. This procedure was continued by accelerating the subject at a rate of 0.4"/sec2 and then 0.6"/ sec2 and finally Io/sec2. The total amplitude during the acceleration of I"/sec2 up to the final velocity of 60"/sec was also recorded and calculated. The first post-rotatory nystagmus was measured after an abrupt stop (0.3 sec). Before the stop the velocity of rotation was maintained at 60"/sec during 120 sec. The total amplitude of nystagmus was calculated. Any spontaneous or positional nystagmus was recorded in a dark room while the subject was lying in a supine position and in both lateral positions. The nystagmus was recorded both with closed eyes and with eyes open. The nystagmus was considered pathological when the speed of the slow phase exceeded 7 degrees per second. The caloric test was performed ad modum Hallpike with the following exceptions. The irrigation time was only 30 sec. The induced nystagmus was recorded for 70 sec with the subject's eyes closed. At the 70th second, the
Table 11. Nysttigmus findings rind caloric reactions in subjects ex-posed to vibration
Spontaneous nystagmus Spontaneous nystagmus+ lowered caloric excitability Lowered caloric excitability N o nystagmus. normal caloric reactions Total
No. of subjects
Per cent
10
20.4
2 10
4. I 20.4
27
55. I
49
100.0
472
E. Aantaa e t al.
Acta Otolaryngol Downloaded from informahealthcare.com by University of Newcastle on 01/07/15 For personal use only.
Table 111. The thresholds of angular crcceleration during rotatory tests
tions. The nystagmus findings and caloric reactions in persons exposed to vibration are shown in Table 11. In 10 subjects (20.4%) Control series s0.4"/sec2 20 (100%) there was spontaneous nystagmus in all posiVibration series s0.4"/sec2 35 (71.5%) 14 (28.5%) tions recorded. In 2 subjects (4.1 %) there was >0.4"/sec2 spontaneous nystagmus and lowered caloric excitability. In 27 subjects (55.1 %) ENGfindings were considered normal and among subject was asked to open his eyes and to fix these subjects there was also no head-shaking his gaze on a fixation light, situated about 2 nystagmus observed with Franzel's glasses in metres away, directly in front of him. For each a totally dark room. irrigation the frequency of nystagmus and The thresholds of angular acceleration are angular velocity of the slow nystagmus phase shown for both series in Table 111. In control was calculated during the culmination phase, series the thresholds in both directions (right both before and after opening the eyes. The and left) were equal to or less than 0.4"/s2. In result was considered as "canal paresis" (low35 subjects (71.5%) exposed to vibration the ered excitability) when reactions before the thresholds were the same as in the control fixation were 20% weaker in one ear than in series but in 14 (28.5%) the thresholds were the other. The ocular fixation index was calmore than 0.4"/s2.With the method and equipculated according to Demanez & Ledoux ment adopted in this laboratory the limit of (1970). normal threshold is 0.4"/sz (Virolainen, 1972). The total amplitudes of the nystagmic slow OF1= amplitudexfrequency (eyes open) phase during acceleration at a rate of one dex 100% amplitudexfrequency (eyes closed) gree/s2, from an angular velocity of V/sec to 60"/sec in both series, are shown in Table IV. OF1 was considered normal if it was lower In the control series the mean values both to than 50%. the right (106") and to the left (103") are statistically significantly higher than the corThe optokinetic nystagmus of the subject responding mean values of subjects exposed to was investigated at 30", 40", 50" and 60"/sec to vibration (to the right 86" and to the left 72"). the right and to the left alternately. The mean total (summed) amplitudes of the All these recordings were made by means of Elema Mingograph ENG. The same type of electrode and the same pattern of fixating the electrodes were used as before. Table IV. The totcil crmplitudr of the sloit, phase of the nystagmus o n accelerating at a rmte of one tiegreelsec' f r o m a speed of Oo/ RESULTS sec t o 60"lsec. Comparison brtitqeen control The air and bone conduction values were Jeries and thr subject5 e.rposrci to vibrcition better than 10 dB at each frequency studied in all subjects exposed to vibration. The discrimination ability of subjects was established as 100 per cent. I n the neuro-otological examination there was no sign of any lesion of other cranial nerves. In control series there was neither spontaneous nystagmus nor abnormal caloric reacAi Ili O t o l e r v n ~ d83
Mean values are expressed
in
degrees ~~~~
Mean S . D . 7' Acceleration to the right Control series Vibration series Acceleration to the left Control series Vibration series
106
86
42 39
2 11s
72
43 32
3729
P
0.05 0.001
Effects qf vihrrrtion on vestibular system Table V . Mecin toter1 arnplitudes of thc ,first posf-rotutory nystagriius t o the right r i n d lefi after ( i n cihrupt stop .from ei speed of'6O0/.s(v.. Cornpiirison betwven control series and the subjects who hcive herri exposed t o t3ihrrrtion Mean values expressed in degrees
Acta Otolaryngol Downloaded from informahealthcare.com by University of Newcastle on 01/07/15 For personal use only.
Mean S.D. T First post-rotatory nystagmus, to the right Control series Vibration series First post-rotatory nystagmus, to the left Control series Vibration series
77
45 39
3 613
'17
49 49
1335
101
P
0.001
slow phase of the first post-rotatory nystagmus to the right and left after an abrupt stop from a velocity of 60"/sec are shown in Table V . In the control series the mean total amplitude of right-beating nystagmus was 113" which, statistically, is significantly higher (p
