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Audiovestibular dysfunction in alcohol dependence. Are we worried?
American Journal of Otolaryngology–Head and Neck Medicine and Surgery 27 (2006) 225 – 228 www.elsevier.com/locate/amjoto
Original contributions
Audiovestibular dysfunction in alcohol dependence. Are we worried? Roshan K. Verma, MSa, Naresh K. Panda, MS, DNB, FRCS Eda,T, Debasish Basu, MDb, Meena Raghunathan, MSc, PhDa,F a
Department of Otolaryngology, Postgraduate Institute of Medical Education and Research, Chandigarh, India b Department of Psychiatry, Postgraduate Institute of Medical Education and Research, Chandigarh, India Received 14 July 2005
Abstract
Purpose: To study the audiovestibular function in patients of long-term alcohol dependence and compare these changes with social users of alcohol and complete abstainers. Material and methods: This was a prospective study of 20 randomly selected patients of long-term alcohol dependence fulfilling International Statistical Classification of Diseases, 10th Revision criteria of alcohol dependence. Audiovestibular function in this group was compared with social user of alcohol and complete abstainers. Results: Statistically significant elevations of thresholds were found at higher frequencies (4000 and 8000 Hz ) in the alcohol-dependent group ( P b .001). Alcohol-dependent patients had elevated thresholds at 4 and 8 kHz. Brainstem-evoked response audiometry showed prolongation of latencies of waves I, III, and V alone with interpeak latencies of I-III and III-V. One third of alcohol-dependent patients had abnormal electronystagmographic (ENG) findings. Abnormal ENG findings were only seen in alcohol-dependent patients with vertigo. There was no significant correlation between duration of alcohol dependence and abnormal ENG. Conclusions: Elevated thresholds at higher frequencies can be the only abnormality in alcoholdependent patients. Presence of vertigo in alcohol-dependent patient may be associated with abnormal ENG findings. There is no correlation of duration of dependence and ENG abnormalities. D 2006 Elsevier Inc. All rights reserved.
1. Introduction Alcohol has since long been considered ototoxic, affecting the audiovestibular functions, both at the peripheral and central sites. Reports on the effect of long-term alcohol ingestion on the audiovestibular systems are conflicting. Nordahl [1] found the incidence of sensorineural loss in 14 of 83 institutionalized alcoholics, but 9 of 14 cases had history of significant noise exposure in the past. Spitzer and Ventry [2] reported hearing to be normal in their study. Niedziellska et al [3] reported sensorineural loss in 22 of 30 long-term alcoholics and no otoacoustic emission in 19 of 30 cases. Chu et al [4] and MacLeod et al [5] found abnormal auditory brainstem responses (ABR) responses to
be more common in alcoholics with neurological abnormalities such as Wernicke-Korsakoff syndrome. The abnormalities were in the form of prolonged I-III, I-V, and III-V interval. Alcohol was also found to have depressant effect on vestibular functions both at the peripheral and central sites [6]. However, there is no study evaluating the effect of alcohol in patients of long-term alcohol dependence. This study was therefore designed to evaluate audiovestibular functions in patients of long-term alcohol dependence and to compare the findings with milder alcoholics and complete abstainers of alcohol to increase the confidence and broaden the prospects of the present study.
2. Material and methods T Corresponding author. Department of Otolaryngology, Postgraduate Institute of Medical Education and Research, Chandigarh, India. E-mail address: [email protected] (N.K. Panda). F Deceased. 0196-0709/$ – see front matter D 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.amjoto.2005.09.005
Twenty randomly selected patients of long-term alcohol dependence fulfilling International Statistical Classification of Diseases, 10th Revision (ICD-10) criteria of alcohol
226
R.K. Verma et al. / American Journal of Otolaryngology – Head and Neck Medicine and Surgery 27 (2006) 225 – 228
Table 1 Mean pure tone thresholds (dB) in various groups 250 Alcohol-dependent Control 1 (social user) Control 2 (complete abstainer)
R L R L R L
500
1000
2000
4000
8000
AC
BC
AC
BC
AC
BC
AC
BC
AC
BC
AC
22.25 21.50 15.67 15.33 15.33 12.33
15.75 14.40 6.33 8.00 7.33 6.33
21.25 20.50 16.00 14.33 14.00 13.67
16.50 14.40 7.67 8.67 8.68 7.33
21.75 20.90 20.33 25.67 14.00 13.67
17.85 16.15 14.63 18.33 9.33 9.00
23.25 23.65 18.00 15.33 12.57 15.00
18.50 17.90 9.33 10.00 9.00 9.67
33.00 34.00 18.33 24.67 16.33 14.00
27.50 25.78 9.00 11.33 9.67 9.33
38.50 33.25 17.67 24.00 19.00 17.67
dependence of more than 2 years and undergoing deaddiction program were selected as subject group. The patients for the study group were referred from the deaddiction center of our hospital. Similar age-matched controls were selected. Control 1 were those who were social users of alcohol and did not fulfill ICD-10 criteria of alcohol dependence. Control 2 were those who had abstained from alcohol throughout their life. An informed consent was taken from all the patients. A detailed medical and otologic history and physical, otolaryngological, and neuro-otologic examination were undertaken in all the patients. A qualified neurologist evaluated the study subjects to look for any alcohol-related neurological disease or Wernicke-Korsakoff syndrome. Patients with confounding factors affecting hearing, such as noise exposure, head injury, ototoxic drug history, syphilis, and so on, were excluded during patient selection. Alcoholdependent patients had abstained from alcohol for at least 1 week before undergoing the study. Each of these cases was then subjected to battery of audiovestibular tests. These were: Pure tone audiometry and special test of hearing were done on dual clinical/diagnostic audiometer (Amplaid 309; Amplifon BPA Division, Milan, Italy) calibrated as per the American National Standard Institute. Auditory brainstem-evoked responses were recorded using Nicolet Compact (Nicolet Biomedical Instruments, Madison, WI) and electrodiagnostic system. Pure tone clicks at an intensity of 85 and 100 dB with masking noise in contralateral ear were delivered at the rate of 11 clicks per second with bandwidth filter adjusted between 150 and 3000 Hz. Total number of clicks delivered was 2000 clicks. Minimum of 2 trials were conducted for each run to ensure the reproducibility of the results. The ABR responses were considered prolonged when the latencies exceeded the mean F 2 SD of the normal controls. Fitzgerald and Hallpike Bithermal cold caloric test was performed in the Vestibular laboratory of the department. It was done by irrigating each ear with 250 mL saline for 40 seconds at 448C and 308C. The resulting nystagmus was recorded using dual-channel AC electronystagmography (nystagmorite ENG machine). The machine was calibrated before each recording. The unilateral weakness and directional preponderance were calculated by using
Jongkees formula. The normal for unilateral weakness was less than 20%, and for directional preponderance, it was less than 25%. 3. Results All the patients in this study were in the age group of 30 to 60 years. Mean age of the patients in the alcoholdependent group was 44.65 years, 47.60 in control I and 45.20 in control group 2 ( P N.05). The average duration of alcohol intake in the alcohol-dependent group was 23.55 years, and the average duration of dependence was 11.85 years, whereas in control group 1, the average duration of intake was 16 years. Twenty percent of the patients had audiovestibular complaints at the time of presentation in the form of hearing loss, vertigo, tinnitus, and aural fullness. None of the patients had spontaneous or gaze-induced nystagmus. Neuro-otologic examination was normal in all of these patients. None of the patients had alcohol-related neurological disease or Wernicke-Korsakoff syndrome; 65% had elevated liver enzymes at presentation. Pure tone audiometry showed abnormal results in 50% (10/20) of cases. Twenty-five percent (5/20) of patients had flat sensorineural hearing loss, and 25% (5/20) had highfrequency loss (Table 1). Hearing threshold was found to be 5 to 10 dB higher at all frequencies in the alcohol-dependent group when compared with control 1, whereas thresholds were found to be 15 to 20 dB higher at all frequencies when compared with control group 2. Statistically significant elevations of thresholds were found at higher frequencies (4000 and 8000 Hz) in the alcohol-dependent group ( P b .001). (Table 2). Speech audiometry and special test of hearing such as tone decay and discrimination scores were found to be normal in all the 3 groups. Table 2 Frequency distribution of elevated thresholds at various frequencies
Low frequency Middle frequency High frequency
v 2, df = 2
Alcoholicdependent, n = 20
Control 2 (social user), n = 15
Control 2 (abstainer), n = 15
5
0
0
8.333
.015
4
0
0
6.527
.038
9
2
1
12.954
.001
P
R.K. Verma et al. / American Journal of Otolaryngology – Head and Neck Medicine and Surgery 27 (2006) 225 – 228
227
Table 3 Mean ABR values
Alcohol-dependent
R L R L R L
Control 1 (social user) Control 2 (abstainer)
Amplitude (mA)
Latency (ms)T
I
V
I
III
V
I-III
III-V
I-V
0.37 0.36 0.31 0.23 0.28 0.23
0.55 0.53 0.54 0.39 0.33 0.51
1.59 1.54 1.51 1.49 1.49 1.49
3.69 3.71 3.69 3.65 3.58 3.60
5.63 5.62 5.53 5.47 5.51 5.50
2.06 2.13 2.13 2.09 2.11 2.05
1.82 1.86 1.81 1.77 1.83 1.83
4.00 4.02 3.94 3.90 3.91 3.87
T P N .05.
3.1. Auditory brainstem-evoked response The auditory brainstem responses were studied in detail to note any abnormalities. Any increase of mean latency and interpeak latency of more than 2 SD of the normal values was taken as abnormal. Abnormal ABR was seen in 40% patients (8/20). The mean of various ABR values is shown in Table 3. In the alcohol-dependent group, the mean absolute latency of waves III and V and interpeak latency of I-V were found to be prolonged. ABR was considered abnormal when the absolute latency and the interpeak latency exceeded (mean of control group 2 F2 SD). Absolute latency of wave I was prolonged in 2 patients, wave III in 2 patients, and wave V in 4 patients in the study group. Again, interpeak latency of I-III was found prolonged in 4 patients, III-V in 3 patients, and I-V in 3 patients in the study group (Table 4). The mean absolute latency of both wave V and the mean interpeak latency of I-V were prolonged in the alcohol-dependent group compared with social users and abstainers with no statistical significance ( P N .05). 3.2. Vestibular functions Bithermal cold caloric response recorded by ENG revealed abnormal response in 30% (6/20) of patients. None of the patients in the 2 control groups showed abnormal responses. Fifteen percent (3/20) of patients had unilateral weakness, 2 had right-sided weakness, and 1 patient had leftsided weakness. Directional preponderance was seen in 15% (3/20) of patients, and all the patients had right-sided preponderance. The average values of each ENG parameter (latent period [LP], total duration [TD], total number of beats [TB], and maximum speed of slow component [MSS]) were
Table 4 Distribution of latency prolongation in all the 3 groups Alcohol-dependent, n = 20 Control 1 (social user), n = 15 Control 2 (abstainer), n = 15 P
I
III
V
I-III
III-V
I-V
2
2
4
4
3
3
0
1
0
1
0
0
0
0
0
0
0
0
N .1
N .1
N .1
N .1
N .1
N .1
within normal limits and clinically insignificant ( P N.05). Comparing the average values of each ENG parameter (LP, TD, TB, and MSS) among the alcohol-dependent patients presenting with or without vertigo, we found LP to be prolonged, TB to be reduced, TD of nystagmus to be reduced, and slowing of maximum phase of slow component in the alcohol-dependent patients with vertigo. This was, however, not statistically significant (Table 5). 4. Discussion Alcohol is an ototoxic drug, affecting both the auditory and vestibular functions both at the peripheral and central sites. Paucity of well-planned studies evaluating the audiovestibular functions in long-term alcoholics has prompted the present study. Unlike the other studies, we have compared the audiovestibular findings in the long-term alcoholic fulfilling ICD-10 criteria of alcohol dependence with the social user of alcohol not fulfilling ICD-10 criteria for alcohol dependence (control 1) and complete abstainer of alcohol (control 2). This study design, therefore, increased the confidence limit in the present report. Twenty percent of our patients presented with audiovestibular symptoms such as hearing loss, tinnitus, vertigo, and aural fullness at the time of presentation. On the contrary, Spitzer and Ventry [2] reported absence of audiovestibular symptoms at presentation in their study. Elevation of pure tone thresholds of more than 30 dB was considered as hearing loss in our study. On evaluation of pure tone audiometry, we found abnormal results in 50% of the cases. Twenty-five percent of patients had sensorineural hearing loss, and 25% had high-frequency hearing loss. In contrast, Nordahl et al [1] reported sensorineural hearing loss in 17 of 83 institutionalized alcoholics. Montauti and Paterni [7] quoted a higher incidence; 15 of 16 of their patients had bilateral symmetrical sensorineural loss. Spitzer and Ventry [2] found hearing to be within normal limits in 15 long-term alcoholic patient. On further evaluation, we found statistically significant elevation of thresholds at higher frequencies. Nine of 20 patients had highfrequency hearing loss in the study group. On the contrary, only 2 of 15 in control 1 and 1 of 15 in control 2 had highfrequency loss. Elevated thresholds at higher frequencies may thus be the only abnormality on pure tone audiogram in
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Table 5 Showing comparison of ENG results of vertigo cases in alcohol dependents LP (s) RCC LCC RHC LHC
TB
TD of nystagmus (s)
MSS (8/s)
V4
NV
P
V4
NV
P
V4
NV
P
V4
NV
P
17.00 14.25 13.25 17.75
12.94 12.19 12.44 13.06
.08 .29 .37 .08
222.50 242.00 200.00 176.75
229.56 257.13 235.06 208.56
.87 .69 .66 .30
177.50 197.75 186.00 171.75
185.88 217.00 206.13 189.00
.71 .38 .08 .31
17.58 18.80 15.20 18.22
22.26 23.11 19.58 20.01
.12 .20 .16 .58
*P N .05. V indicates vertigo; NV, no vertigo; RCC, right cold calorie; LCC, left cold calorie; RHC, right hot calorie; LHC, left hot calorie.
alcohol-dependent patients. Wolff and Gross [8], on the basis of study of histopathology of temporal bones, have shown bowing of Reissner membrane in the upper basal turn of cochlea, necrosis of cells in organ of Corti, and atrophy of spiral ganglion cells in the basal turn. These changes in the basal turn of the cochlea could explain the hearing loss at 4 and 8 kHz. Brainstem-evoked responses were found to be abnormal in 8 (40%) of 20 of the patients. Mean absolute latency of the waves III and V and mean interpeak latency of I-V were found to be prolonged. Surprisingly, none of the patients with abnormal ABR had Wernicke-Korsakoff syndrome or alcohol-related neurological disease. Abnormal ABR may thus be seen in alcoholics even without any neurological abnormality. There are plenty of reports in the literature of abnormal ABR findings in alcoholics with associated neurological disease in the form of Wernicke-Korsakoff syndrome, cerebellar degeneration, and cerebellar ataxia. Abnormal ABR in patients of alcohol dependence could be due to neuronal loss and demyelination in peripheral end organs and central auditory pathway caused by long-term alcohol intake. Evaluation of nystagmus with ENG did not show any abnormalities in either group. However, some interesting findings were noted in patients presenting with vertigo. These patients had prolonged LP, reduced TB, reduced TD of nystagmus, and the slowing of maximum phase of slow component. This has not been reported earlier. In contrast, Sasa et al [6] reported abnormal ENG results in a higher percentage of patients on bithermal stimulation. Victor and Adams [9] attributed abnormal ENG results in long-term alcoholics to be due to deficiency of thiamine, leading to degenerative changes in the olivary nucleus and mamillary
bodies. Wolff and Gross [8] reported loss of neurons in the vestibular ganglion cells and atrophy of crista with features of obliterative arteritis that could explain the vestibular hyporesponse seen in some cases of alcohol-dependent patients, causing peripheral vestibular damage. To conclude, alcohol-dependent patients have elevated thresholds at high frequencies, that is, at 4 and 8 kHz. This may have future implications as these patients could have early onset of presbyacusis. Brainstem-evoked responses may also be abnormal in approximately 20% patients without any clinical symptoms. In addition, alcohol-dependent patients with symptoms of vertigo may show abnormalities on ENG. However, there is no correlation between duration of alcohol dependence and abnormalities on ENG. References [1] Nordahl T. Examination of hearing in alcoholics. Acta Otolaryngol Suppl 1964;188:362 - 70. [2] Spitzer JB, Ventry IM. Central auditory dysfunction among chronic alcoholics. Arch Otolaryngol 1980;106:224 - 9. [3] Niedziellska G, Kalska E, Kusa W. Hearing loss in chronic alcoholics. Ann Univ Mariae Curie Sklodowska [Med] 2001;56:99 - 101. [4] Chu NS, Squires KC, Starr A. Auditory brainstem evoked response in chronic alcoholics patients. Electroencephalogr Clin Neurophysiol 1982;54:418 - 25. [5] MacLeod JG, Tuck RR, Feary PA, Chan. Brainstem evoked response in chronic alcoholics. J Neurol Neurosurg Psychiatry 1985;48:1107 - 12. [6] Sasa M, Takori S, Matsuoka I, et al. Peripheral and central vestibular disorder in alcoholics. Arch Otolaryngol 1981;230(1):93 - 101. [7] Montauti G, Paterni F. Rilievi audiometrici negli alcolists cronici. Boll Mal Orecch 1965;83:500 - 4. [8] Wolff D, Gross MM. Temporal bone findings in chronic alcoholics. Arch Otolaryngol 1968;87:350 - 8. [9] Victor M, Adams RD. On the etiology of the alcoholic neurologic disease, with special reference to nutrition. Am J Clin Nutr 1961;9:3.
Original contributions
Audiovestibular dysfunction in alcohol dependence. Are we worried? Roshan K. Verma, MSa, Naresh K. Panda, MS, DNB, FRCS Eda,T, Debasish Basu, MDb, Meena Raghunathan, MSc, PhDa,F a
Department of Otolaryngology, Postgraduate Institute of Medical Education and Research, Chandigarh, India b Department of Psychiatry, Postgraduate Institute of Medical Education and Research, Chandigarh, India Received 14 July 2005
Abstract
Purpose: To study the audiovestibular function in patients of long-term alcohol dependence and compare these changes with social users of alcohol and complete abstainers. Material and methods: This was a prospective study of 20 randomly selected patients of long-term alcohol dependence fulfilling International Statistical Classification of Diseases, 10th Revision criteria of alcohol dependence. Audiovestibular function in this group was compared with social user of alcohol and complete abstainers. Results: Statistically significant elevations of thresholds were found at higher frequencies (4000 and 8000 Hz ) in the alcohol-dependent group ( P b .001). Alcohol-dependent patients had elevated thresholds at 4 and 8 kHz. Brainstem-evoked response audiometry showed prolongation of latencies of waves I, III, and V alone with interpeak latencies of I-III and III-V. One third of alcohol-dependent patients had abnormal electronystagmographic (ENG) findings. Abnormal ENG findings were only seen in alcohol-dependent patients with vertigo. There was no significant correlation between duration of alcohol dependence and abnormal ENG. Conclusions: Elevated thresholds at higher frequencies can be the only abnormality in alcoholdependent patients. Presence of vertigo in alcohol-dependent patient may be associated with abnormal ENG findings. There is no correlation of duration of dependence and ENG abnormalities. D 2006 Elsevier Inc. All rights reserved.
1. Introduction Alcohol has since long been considered ototoxic, affecting the audiovestibular functions, both at the peripheral and central sites. Reports on the effect of long-term alcohol ingestion on the audiovestibular systems are conflicting. Nordahl [1] found the incidence of sensorineural loss in 14 of 83 institutionalized alcoholics, but 9 of 14 cases had history of significant noise exposure in the past. Spitzer and Ventry [2] reported hearing to be normal in their study. Niedziellska et al [3] reported sensorineural loss in 22 of 30 long-term alcoholics and no otoacoustic emission in 19 of 30 cases. Chu et al [4] and MacLeod et al [5] found abnormal auditory brainstem responses (ABR) responses to
be more common in alcoholics with neurological abnormalities such as Wernicke-Korsakoff syndrome. The abnormalities were in the form of prolonged I-III, I-V, and III-V interval. Alcohol was also found to have depressant effect on vestibular functions both at the peripheral and central sites [6]. However, there is no study evaluating the effect of alcohol in patients of long-term alcohol dependence. This study was therefore designed to evaluate audiovestibular functions in patients of long-term alcohol dependence and to compare the findings with milder alcoholics and complete abstainers of alcohol to increase the confidence and broaden the prospects of the present study.
2. Material and methods T Corresponding author. Department of Otolaryngology, Postgraduate Institute of Medical Education and Research, Chandigarh, India. E-mail address: [email protected] (N.K. Panda). F Deceased. 0196-0709/$ – see front matter D 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.amjoto.2005.09.005
Twenty randomly selected patients of long-term alcohol dependence fulfilling International Statistical Classification of Diseases, 10th Revision (ICD-10) criteria of alcohol
226
R.K. Verma et al. / American Journal of Otolaryngology – Head and Neck Medicine and Surgery 27 (2006) 225 – 228
Table 1 Mean pure tone thresholds (dB) in various groups 250 Alcohol-dependent Control 1 (social user) Control 2 (complete abstainer)
R L R L R L
500
1000
2000
4000
8000
AC
BC
AC
BC
AC
BC
AC
BC
AC
BC
AC
22.25 21.50 15.67 15.33 15.33 12.33
15.75 14.40 6.33 8.00 7.33 6.33
21.25 20.50 16.00 14.33 14.00 13.67
16.50 14.40 7.67 8.67 8.68 7.33
21.75 20.90 20.33 25.67 14.00 13.67
17.85 16.15 14.63 18.33 9.33 9.00
23.25 23.65 18.00 15.33 12.57 15.00
18.50 17.90 9.33 10.00 9.00 9.67
33.00 34.00 18.33 24.67 16.33 14.00
27.50 25.78 9.00 11.33 9.67 9.33
38.50 33.25 17.67 24.00 19.00 17.67
dependence of more than 2 years and undergoing deaddiction program were selected as subject group. The patients for the study group were referred from the deaddiction center of our hospital. Similar age-matched controls were selected. Control 1 were those who were social users of alcohol and did not fulfill ICD-10 criteria of alcohol dependence. Control 2 were those who had abstained from alcohol throughout their life. An informed consent was taken from all the patients. A detailed medical and otologic history and physical, otolaryngological, and neuro-otologic examination were undertaken in all the patients. A qualified neurologist evaluated the study subjects to look for any alcohol-related neurological disease or Wernicke-Korsakoff syndrome. Patients with confounding factors affecting hearing, such as noise exposure, head injury, ototoxic drug history, syphilis, and so on, were excluded during patient selection. Alcoholdependent patients had abstained from alcohol for at least 1 week before undergoing the study. Each of these cases was then subjected to battery of audiovestibular tests. These were: Pure tone audiometry and special test of hearing were done on dual clinical/diagnostic audiometer (Amplaid 309; Amplifon BPA Division, Milan, Italy) calibrated as per the American National Standard Institute. Auditory brainstem-evoked responses were recorded using Nicolet Compact (Nicolet Biomedical Instruments, Madison, WI) and electrodiagnostic system. Pure tone clicks at an intensity of 85 and 100 dB with masking noise in contralateral ear were delivered at the rate of 11 clicks per second with bandwidth filter adjusted between 150 and 3000 Hz. Total number of clicks delivered was 2000 clicks. Minimum of 2 trials were conducted for each run to ensure the reproducibility of the results. The ABR responses were considered prolonged when the latencies exceeded the mean F 2 SD of the normal controls. Fitzgerald and Hallpike Bithermal cold caloric test was performed in the Vestibular laboratory of the department. It was done by irrigating each ear with 250 mL saline for 40 seconds at 448C and 308C. The resulting nystagmus was recorded using dual-channel AC electronystagmography (nystagmorite ENG machine). The machine was calibrated before each recording. The unilateral weakness and directional preponderance were calculated by using
Jongkees formula. The normal for unilateral weakness was less than 20%, and for directional preponderance, it was less than 25%. 3. Results All the patients in this study were in the age group of 30 to 60 years. Mean age of the patients in the alcoholdependent group was 44.65 years, 47.60 in control I and 45.20 in control group 2 ( P N.05). The average duration of alcohol intake in the alcohol-dependent group was 23.55 years, and the average duration of dependence was 11.85 years, whereas in control group 1, the average duration of intake was 16 years. Twenty percent of the patients had audiovestibular complaints at the time of presentation in the form of hearing loss, vertigo, tinnitus, and aural fullness. None of the patients had spontaneous or gaze-induced nystagmus. Neuro-otologic examination was normal in all of these patients. None of the patients had alcohol-related neurological disease or Wernicke-Korsakoff syndrome; 65% had elevated liver enzymes at presentation. Pure tone audiometry showed abnormal results in 50% (10/20) of cases. Twenty-five percent (5/20) of patients had flat sensorineural hearing loss, and 25% (5/20) had highfrequency loss (Table 1). Hearing threshold was found to be 5 to 10 dB higher at all frequencies in the alcohol-dependent group when compared with control 1, whereas thresholds were found to be 15 to 20 dB higher at all frequencies when compared with control group 2. Statistically significant elevations of thresholds were found at higher frequencies (4000 and 8000 Hz) in the alcohol-dependent group ( P b .001). (Table 2). Speech audiometry and special test of hearing such as tone decay and discrimination scores were found to be normal in all the 3 groups. Table 2 Frequency distribution of elevated thresholds at various frequencies
Low frequency Middle frequency High frequency
v 2, df = 2
Alcoholicdependent, n = 20
Control 2 (social user), n = 15
Control 2 (abstainer), n = 15
5
0
0
8.333
.015
4
0
0
6.527
.038
9
2
1
12.954
.001
P
R.K. Verma et al. / American Journal of Otolaryngology – Head and Neck Medicine and Surgery 27 (2006) 225 – 228
227
Table 3 Mean ABR values
Alcohol-dependent
R L R L R L
Control 1 (social user) Control 2 (abstainer)
Amplitude (mA)
Latency (ms)T
I
V
I
III
V
I-III
III-V
I-V
0.37 0.36 0.31 0.23 0.28 0.23
0.55 0.53 0.54 0.39 0.33 0.51
1.59 1.54 1.51 1.49 1.49 1.49
3.69 3.71 3.69 3.65 3.58 3.60
5.63 5.62 5.53 5.47 5.51 5.50
2.06 2.13 2.13 2.09 2.11 2.05
1.82 1.86 1.81 1.77 1.83 1.83
4.00 4.02 3.94 3.90 3.91 3.87
T P N .05.
3.1. Auditory brainstem-evoked response The auditory brainstem responses were studied in detail to note any abnormalities. Any increase of mean latency and interpeak latency of more than 2 SD of the normal values was taken as abnormal. Abnormal ABR was seen in 40% patients (8/20). The mean of various ABR values is shown in Table 3. In the alcohol-dependent group, the mean absolute latency of waves III and V and interpeak latency of I-V were found to be prolonged. ABR was considered abnormal when the absolute latency and the interpeak latency exceeded (mean of control group 2 F2 SD). Absolute latency of wave I was prolonged in 2 patients, wave III in 2 patients, and wave V in 4 patients in the study group. Again, interpeak latency of I-III was found prolonged in 4 patients, III-V in 3 patients, and I-V in 3 patients in the study group (Table 4). The mean absolute latency of both wave V and the mean interpeak latency of I-V were prolonged in the alcohol-dependent group compared with social users and abstainers with no statistical significance ( P N .05). 3.2. Vestibular functions Bithermal cold caloric response recorded by ENG revealed abnormal response in 30% (6/20) of patients. None of the patients in the 2 control groups showed abnormal responses. Fifteen percent (3/20) of patients had unilateral weakness, 2 had right-sided weakness, and 1 patient had leftsided weakness. Directional preponderance was seen in 15% (3/20) of patients, and all the patients had right-sided preponderance. The average values of each ENG parameter (latent period [LP], total duration [TD], total number of beats [TB], and maximum speed of slow component [MSS]) were
Table 4 Distribution of latency prolongation in all the 3 groups Alcohol-dependent, n = 20 Control 1 (social user), n = 15 Control 2 (abstainer), n = 15 P
I
III
V
I-III
III-V
I-V
2
2
4
4
3
3
0
1
0
1
0
0
0
0
0
0
0
0
N .1
N .1
N .1
N .1
N .1
N .1
within normal limits and clinically insignificant ( P N.05). Comparing the average values of each ENG parameter (LP, TD, TB, and MSS) among the alcohol-dependent patients presenting with or without vertigo, we found LP to be prolonged, TB to be reduced, TD of nystagmus to be reduced, and slowing of maximum phase of slow component in the alcohol-dependent patients with vertigo. This was, however, not statistically significant (Table 5). 4. Discussion Alcohol is an ototoxic drug, affecting both the auditory and vestibular functions both at the peripheral and central sites. Paucity of well-planned studies evaluating the audiovestibular functions in long-term alcoholics has prompted the present study. Unlike the other studies, we have compared the audiovestibular findings in the long-term alcoholic fulfilling ICD-10 criteria of alcohol dependence with the social user of alcohol not fulfilling ICD-10 criteria for alcohol dependence (control 1) and complete abstainer of alcohol (control 2). This study design, therefore, increased the confidence limit in the present report. Twenty percent of our patients presented with audiovestibular symptoms such as hearing loss, tinnitus, vertigo, and aural fullness at the time of presentation. On the contrary, Spitzer and Ventry [2] reported absence of audiovestibular symptoms at presentation in their study. Elevation of pure tone thresholds of more than 30 dB was considered as hearing loss in our study. On evaluation of pure tone audiometry, we found abnormal results in 50% of the cases. Twenty-five percent of patients had sensorineural hearing loss, and 25% had high-frequency hearing loss. In contrast, Nordahl et al [1] reported sensorineural hearing loss in 17 of 83 institutionalized alcoholics. Montauti and Paterni [7] quoted a higher incidence; 15 of 16 of their patients had bilateral symmetrical sensorineural loss. Spitzer and Ventry [2] found hearing to be within normal limits in 15 long-term alcoholic patient. On further evaluation, we found statistically significant elevation of thresholds at higher frequencies. Nine of 20 patients had highfrequency hearing loss in the study group. On the contrary, only 2 of 15 in control 1 and 1 of 15 in control 2 had highfrequency loss. Elevated thresholds at higher frequencies may thus be the only abnormality on pure tone audiogram in
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Table 5 Showing comparison of ENG results of vertigo cases in alcohol dependents LP (s) RCC LCC RHC LHC
TB
TD of nystagmus (s)
MSS (8/s)
V4
NV
P
V4
NV
P
V4
NV
P
V4
NV
P
17.00 14.25 13.25 17.75
12.94 12.19 12.44 13.06
.08 .29 .37 .08
222.50 242.00 200.00 176.75
229.56 257.13 235.06 208.56
.87 .69 .66 .30
177.50 197.75 186.00 171.75
185.88 217.00 206.13 189.00
.71 .38 .08 .31
17.58 18.80 15.20 18.22
22.26 23.11 19.58 20.01
.12 .20 .16 .58
*P N .05. V indicates vertigo; NV, no vertigo; RCC, right cold calorie; LCC, left cold calorie; RHC, right hot calorie; LHC, left hot calorie.
alcohol-dependent patients. Wolff and Gross [8], on the basis of study of histopathology of temporal bones, have shown bowing of Reissner membrane in the upper basal turn of cochlea, necrosis of cells in organ of Corti, and atrophy of spiral ganglion cells in the basal turn. These changes in the basal turn of the cochlea could explain the hearing loss at 4 and 8 kHz. Brainstem-evoked responses were found to be abnormal in 8 (40%) of 20 of the patients. Mean absolute latency of the waves III and V and mean interpeak latency of I-V were found to be prolonged. Surprisingly, none of the patients with abnormal ABR had Wernicke-Korsakoff syndrome or alcohol-related neurological disease. Abnormal ABR may thus be seen in alcoholics even without any neurological abnormality. There are plenty of reports in the literature of abnormal ABR findings in alcoholics with associated neurological disease in the form of Wernicke-Korsakoff syndrome, cerebellar degeneration, and cerebellar ataxia. Abnormal ABR in patients of alcohol dependence could be due to neuronal loss and demyelination in peripheral end organs and central auditory pathway caused by long-term alcohol intake. Evaluation of nystagmus with ENG did not show any abnormalities in either group. However, some interesting findings were noted in patients presenting with vertigo. These patients had prolonged LP, reduced TB, reduced TD of nystagmus, and the slowing of maximum phase of slow component. This has not been reported earlier. In contrast, Sasa et al [6] reported abnormal ENG results in a higher percentage of patients on bithermal stimulation. Victor and Adams [9] attributed abnormal ENG results in long-term alcoholics to be due to deficiency of thiamine, leading to degenerative changes in the olivary nucleus and mamillary
bodies. Wolff and Gross [8] reported loss of neurons in the vestibular ganglion cells and atrophy of crista with features of obliterative arteritis that could explain the vestibular hyporesponse seen in some cases of alcohol-dependent patients, causing peripheral vestibular damage. To conclude, alcohol-dependent patients have elevated thresholds at high frequencies, that is, at 4 and 8 kHz. This may have future implications as these patients could have early onset of presbyacusis. Brainstem-evoked responses may also be abnormal in approximately 20% patients without any clinical symptoms. In addition, alcohol-dependent patients with symptoms of vertigo may show abnormalities on ENG. However, there is no correlation between duration of alcohol dependence and abnormalities on ENG. References [1] Nordahl T. Examination of hearing in alcoholics. Acta Otolaryngol Suppl 1964;188:362 - 70. [2] Spitzer JB, Ventry IM. Central auditory dysfunction among chronic alcoholics. Arch Otolaryngol 1980;106:224 - 9. [3] Niedziellska G, Kalska E, Kusa W. Hearing loss in chronic alcoholics. Ann Univ Mariae Curie Sklodowska [Med] 2001;56:99 - 101. [4] Chu NS, Squires KC, Starr A. Auditory brainstem evoked response in chronic alcoholics patients. Electroencephalogr Clin Neurophysiol 1982;54:418 - 25. [5] MacLeod JG, Tuck RR, Feary PA, Chan. Brainstem evoked response in chronic alcoholics. J Neurol Neurosurg Psychiatry 1985;48:1107 - 12. [6] Sasa M, Takori S, Matsuoka I, et al. Peripheral and central vestibular disorder in alcoholics. Arch Otolaryngol 1981;230(1):93 - 101. [7] Montauti G, Paterni F. Rilievi audiometrici negli alcolists cronici. Boll Mal Orecch 1965;83:500 - 4. [8] Wolff D, Gross MM. Temporal bone findings in chronic alcoholics. Arch Otolaryngol 1968;87:350 - 8. [9] Victor M, Adams RD. On the etiology of the alcoholic neurologic disease, with special reference to nutrition. Am J Clin Nutr 1961;9:3.