Download Factors Causing Hearing Impairment

J Am Acad Audiol 6 : 387-395 (1995)
Factors Causing Hearing Impairment :
Some Perspectives from Europe
Agnete Parving
Abstract
This review concentrates on factors causing permanent hearing impairment in childhood,
described in some European studies. The emphasis is on comparative studies, based on
strict criteria and terminology upon which longitudinal changes in the pattern of factors causing hearing impairment can be demonstrated in well-defined cohorts of children . The high
proportion of 20-39 percent of unknown causes of permanent hearing impairment in childhood reflects a general lack of knowledge about causative factors and systematic etiologic
evaluation within pediatric audiology. Future surveillance programs, including examination
procedures directed towards causative factors, may see a reduction of the "unknown" category and ultimately may result in prevention of permanent hearing impairment in childhood.
Some factors causing hearing impairment in adults are mentioned, including recent studies
that show organic toxic solvents as a factor. As well, some controversial findings concerning the relationship between hearing impairment and endocrine disorders such as
hypothyroidism and diabetes mellitus are briefly reported . It is concluded that future developments and research in the etiologic field within pediatric and adult audiology may contribute
to the delineation of yet unknown damaging factors or reduction of the effect of factors causing hearing impairment - a disorder that ultimately results in adverse effects on the quality
of life in all age groups .
Key Words:
Adults, childhood, etiology, hearing impairment
hroughout life, the hearing organ, with
its different anatomical areas, may be
T affected by numerous factors, resulting
in a hearing disorder with an abnormal function
of the auditory system . The loss of auditory sensitivity - which in clinical terms is hearing
impairment (HI) - may result in reduced abilities of the individual (hearing disability) or in
adverse effects on life (hearing handicap) (e .g .,
Davis, 1987). A relationship has been established between HI and numerous damaging factors, based on experimental, epidemiologic, and
clinical case-control studies, but also by removal
of agents resulting in primary prevention in the
population or in the individual subject .
Factors causing hearing disorders differ
according to geography, gender, age, and individual susceptibility to exposed factors. This
"Department of Audiology, Bispebjerg Hospital, Copenhagen, Denmark
Reprint requests : Agnete Parving, Department of
Audiology, Bispebjerg Hospital, DK 2400 Copenhagen NV,
Denmark
contribution describes some European aspects
related to causes of HI . The etiologic classification of HI in this report will be divided
according to hearing disorders in childhood, concentrating on permanent HI to such a degree
that it requires intervention . Deliberately, no
comments and considerations are presented concerning aspects of otitis media with effusion
and all its implications for pediatric audiology.
In this context, the reader is referred to
Chalmers et al (1989) and Haggard and Hughes
(1991) .
The second part will focus on adults, that is,
individuals above the age of 18 years. This section considers studies supporting organic toxic
solvents as damaging factors for the hearing
organ and describes some controversial findings in subjects with hypothyroidism and diabetes mellitus .
HEARING IMPAIRMENT IN CHILDREN
M
odem pediatric audiology accepts that hearing loss in children is a sign/symptom that
should be considered the result of any damaging
Journal of the American Academy of Audiology/Volume 6, Number 5, September 1995
factor(s) affecting the hearing organ. Thus, the
diagnostic evaluation consists of two major steps:
(1) assessment of the HI, its severity, and site of
lesion; and (2) evaluation of the causative factors) .
Within most European countries, children,
upon identification of a permanent HI, will be
entered into a surveillance program aimed
toward a longitudinal follow-up of the intervention and its effect, especially on the child's
speech and language development, social adjustment, and communication skills (European Federation of Audiological Societies, 1993). A
diagnostic evaluation program (individualized for
each child), including thorough history, (computed tomography/magnetic resonance imaging [MRI] scan), serologic, ophthalmologic, X-ray
(CT/MR-scan), pediatric, and genetic examinations, has reduced the category "unknown cause"
to only 11 percent in an epidemiologically welldefined cohort born between 1970-1980 (Parving, 1984). Additional or new information on
causative factors in the individual child may
add to, modify, or change the etiologic diagnosis
in the single child; consequently, the etiologic
evaluation should be considered a longstanding and dynamic process. These statements are
supported by the data in Table 1, which demonstrate the longitudinal aspects of an etiologic
evaluation . It should be mentioned that all etiologies are based on strict criteria, and to some
degree account for the sensitivity/specificity of
different diagnostic procedures . Note that in
1987 an additional 21 children are included in
the cohort, reflecting the delayed identification
of children with congenital HI (Parving, 1983,
1984, 1988).
Table 1
Time of Data Collection
Lack of uniform worldwide accepted description of, and criteria for, defining causative diagnosis limits the possibility for comparative
studies, both within and between countries.
Often the small numbers of subjects in the welldefined reported samples exclude valid statistical
analysis and conclusions. An approach toward
a diagnostic category based on the interaction
between time at insult, causation, and expression has been proposed (Davidson et al, 1988)
and implemented (Parving, 1993a), and may
solve some of the problems within future comparative and longitudinal investigations . In
addition, appropriate sampling of well-defined
cohorts based on strict terminology and definition of hearing level is a prerequisite for valid
information on the distribution of etiologic factors causing HI .
The diagnostic evaluation reflects some
important qualitative (i.e., medical audit) aspects'
of the pediatric audiologic services offered locally.
On a national basis, such data could result in an
appropriate planning for allocation of resources
within this field. Exchange of information and
international collaboration may result in primary
prevention of HI, such as vaccination programs
or genetic counselling.
1980-1990 Cross-sectional Data
In a geographically well-defined cohort of
children born between 1980-1990 and provided
with hearing aids, the prevalence rate of different
factors causing the HI was described. The proportion of the etiologies within the sample was
calculated as shown in Table 2 (Parving, 1993a) .
Cohort Born 1970-1980
1982
Program
Etiologies
N
Fetal infection
Hereditary hearing loss
(no associated abnormalities)
Natal/neonatal complications
Ototoxic drugs
Meningitis
Various genetic syndromes
Chromosomal aberrations
Malformations of ears
Meniere's disease
Otitis media sequelae
Unknown cause
Total
19
32
16
27
16
14
2
3
6
2
2
1
2
18
16
32
117
27
2
3
9
2
2
2
4
Revision 1987
N
%
N
22
43
19
37
20
50
14
36
16
14
14
10
- 31
22
23
138
17
24
19
12
117
11
5
16
8
2
Hearing Impairment/Parving
Table 2 Prevalence Rate (1/1000) of Different
Factors Causing HI (N = 181), Calculated on
Basis of Total Age-matched Target Group
(N = 95,912)
Prenatal causes
Inheritance
Fetal infection
Malformation
Perinatal causes
Postnatal causes
Otitis media
Meningitis
Unknown cause
N
Prevalence Rate
(1/1000)
Proportion of
Etiology (%)
99
84
9
6
17
28
22
6
37
1 .03
0 .88
0 .09
0 .06
0 .17
0 .29
0 .23
0 .06
0 .38
55
46
5
3
9
15
12
3
20
Table 3
Cross-sectional Longitudinal Data
from the Copenhagen Area
Cohort
Prenatal causes
Genetic
Fetal infection
Malformation
Perinatal causes
Postnatal causes
Otitis media
Meningitis
Head injury
Unknown cause
Cohort
1970-1980
(N = 186)
1980-1990
(N = 181)
N
N
95%
Cl
94
65
25
4
27
12
5
6
51
69
27
6
15
7
-
99
84
9
55
85
9
NS
S
S
17
28
22
6
9
15
-
NS
49
26
37
20
NS
1
S = significant, NS = not significant .
The causative factors in this sample were categorized according to Davidson et al (1988) . The
table shows that prenatal causes are most frequent, and that inheritance is the overall dominating factor accounting for 46 percent .
Perinatal and postnatal factors account for 9
percent and 15 percent, respectively. Twenty
percent had not been classified as to etiology at
the time of data collection (January 1992).
When performing cross-sectional longitudinal comparisons based on retrospective data,
the definitions and criteria for the comparison
must be identical in order to evaluate true differences in the causes of hearing disorders in children . However, a change in prevalence due to a
cohort effect (e .g., rubella epidemic) may change
the overall prevalence and thus influence and
change the proportion of different causes within
the sample . In addition, the period of sampling
and the age of the children, that is, the time of
evaluation, is crucial, especially in small samples, and should always be considered .
With this in mind, a comparison of two
cohorts of children provided with hearing aids
and born between 1970-1980 (evaluated January 1982) and 1980-1990 (evaluated January
1992) shows an increase in the prevalence of 23
percent, that is, 1.5/1000 in the 1970-1980 cohort
(N = 186/121,544 age-matched children) and
1.9/1000 in the 1980-1990 cohort (N =181/95,912
age-matched children). The change may in part
be due to changes in the criteria for provision of
hearing aids . However, when controlling for that
factor, a true increase in the prevalence of 19 percent was demonstrated . The increase resulted
in changes in the pattern of factors causing HI,
as shown in Table 3 . There was a significantly
higher proportion of HI caused by inheritance
in the 1980-1990 cohort, whereas there was a significant reduction in the proportion of etiologies associated with fetal infections . These
inversely related changes result in no significant
changes overall in the prevalence of prenatal
causes, but emphasize that a more detailed evaluation of the causes in the different categories
according to time of insult is necessary. This
development in the causes of HI throughout a
10-year period in the described area is compatible with the increase of immigrants in the target population, having different cultural and
religious backgrounds (Parving, 1993a, b) . Thus,
the results seem to document the strong relationship between demography and disease.
Some additional longitudinal information on
the causes of HI can be obtained from a cohort
of subjects born between 1960-1970, who were
living in Copenhagen (data collection in January 1991). Any comparative analysis to the
cohorts born between 1970-1980 and 1980-1990
is vulnerable due to the age factor. For valid comparison, the 1960-1970 cohort should have been
evaluated in January 1972, and the retrospective sampling based on clinical records results
in prevalence underestimates and lack of information (Parving and Christensen, 1993). A
reanalysis of the data can, however, control for
the criterion "provision of hearing aids," and
thus a sample of N =125 was evaluated and categorized according to Davidson et al (1988) . The
population of those between 20-30 years in 1991
comprised N = 110,504, yielding an estimate of
1 .1/1000 adults provided with a hearing aid.
Due to the shortcomings in the original sampling,
the prevalence rate may represent a substantial
underestimate, but it may also reflect the changing attitude towards hearing aid rehabilitation,
Journal of the American Academy of Audiology/Volume 6, Number 5, September 1995
which became increasingly more acceptable
throughout the 1970s and 1980s due to improvements in both the technical and cosmetic aspects
of hearing instruments .
The causes of the HI in the 1960-1970 cohort
are listed in Table 4. To facilitate comparison of
information on the longitudinal cross-sectional
data, the causes of the HI in the birth cohorts
of the 1970s and 1980s cohorts are also included .
Due to uncertainty concerning the 1960-1970
cohort, no comparative statistical analysis has
been included .
Some Additional European Data
In 1977, the member countries of the European Community performed a survey of a cohort
of hearing-disabled children born in 1969 (Martin et al, 1981). The survey had many objectives, including to "determine the cause of
deafness" and "define the size of the group in
which the cause is reported to be unknown."
The survey demonstrated that, among those
with sensorineural HI, the cause could be
ascribed to fetal rubella infection in 16 percent,
varying from 12-20 percent between countries,
while genetic causes accounted for only 9 percent
of the HI . Although the survey was confined
according to geography and birth cohort, and the
criteria for hearing level (>_ 50 dB HI in the better hearing ear averaged across the audiometric frequencies of 500, 1000, and 2000 Hz) was
strictly defined, the most reliable result obtained
is - according to the present author's evaluation - the proportion of 42 percent of unknown
etiology of the HI . Based on the survey, it was
recommended that there should be more detailed
research into the etiology of the HI in children
with a supposed unknown cause.
Table 4
Prenatal
Genetic
Fetal infection
Malformation
Perinatal
Postnatal
Otitis sequelae
Meningitis
Head injury
Unknown
390
10-Year Birth Cohorts
1960s
(N = 125)
1970s
(N = 186)
1980s
(N= 181)
N
N
%
N
94
84
9
6
27
12
22
6
49
51
99
55
15
7
17
28
9
15
26
37
20
55
49
2
4
25
14
3
8
3
31
44
65
25
4
20
11
5
6
1
25
Recent epidemiologic figures on HI in childhood from two European countries (England
and Denmark) have shown that the prevalence
rate of 2/1000 of children with permanent HI,
requiring hearing aids in identical birth cohorts,
is fairly similar within both the compared health
authority districts within countries and also
between the two countries (Davis and Wood,
1992 ; Parving 1993b; Davis and Parving, 1994).
A direct comparison between the proportion of
different diagnostic categories could not be performed between countries. However, when family history and the neonatal intensive care unit
status of the children were considered significant,
differences in the factors causing HI were found
between the two countries. This was not the
case, however, between districts within the same
country (Parving, 1993a ; Davis and Parving,
1994).
Although a European survey has not been'
carried out, numerous data on the etiology of
hearing disorders in children have been reported
from several European countries and districts
(e .g ., Kankkunen, 1982 ; Newton, 1985 ; Das,
1988 ; Hirsch, 1988 ; Lenzi and Zaghis, 1988 ;
Dias and Andrea, 1990 ; van Rijn and Cremers,
1991 ; Vanniasegaram et al, 1993). An attempt
has been made - whenever allowed by the
available data - to organize some of the reported
etiologies according to generally recognized categories (Davidson et al, 1988). The result may
be seen in Table 5. It is important to understand that major differences in the inclusion
criteria, definition of samples, age of the children,
and definition of hearing level are present,
thereby excluding a detailed direct comparative analysis . A cautious interpretation supports
the notion that prenatal causes are most frequent
in different parts of Europe with genetic factors,
dominating and varying from 20-46 percent
within the samples listed in Table 5 . Although
this is not new information, it is important due
to the rapid development of the field of molecular genetics . Future research within this area
may provide clinicians with additional valuable
information, probably resulting in a reduction
of unknown cause and improved counselling
and prevention of genetic HI (O'Malley and Ledley, 1993 ; Ryan et al, 1993).
In Table 6, the frequency of unknown cause
in some European studies suggests that the category comprises 20-39 percent of all individuals with HI . Although this represents an
improvement compared to the 42 percent
reported in the European survey (Martin et al,
1981), the high proportion of unknown cause in
Hearing Impairment/Parving
Table 5
Factors Causing Hearing Impairment in Childhood*
Newton, 1985
(N= 111 ;
> 25 dB HL)
N
Prenatal
Genetic factors
Fetal infection
Malformations
Various
Perinatal
Postnatal
Otitis media sequelae
Meningitis
Measles/mumps
Ototoxicity
Various
van Rijn, 1989
(N = 162
? 35 dB HL)
N
%
43
33
15
N
46
64
9
2
14
14
5
15
9
11
6
8
1
3
4
1
Dias and Andrea, 1990
(N = 1024x;
dB HL ?)
201
93
26
19
143
50
52
41
16
Vanniasegera m, et al 1993
(N= 101 ;
>_ 50 dB HL)
N
33
14
16
40
8
16
2
4
1
48
16
8
1
*The table should be read in conjunction with Table 6.
'In 10 subjects with conductive and 93 with perceptive HI, the etiology is known but not categorized .
the samples supports the idea of a general ignorance about factors causing damage to the hearing organ in childhood.
111
1977-1980
39
been reported (Church and Gerking, 1988), and
the ototoxicity and teratogenic effects of drugs
are now often considered (Barr, 1982 ; Scott and
Griffiths, 1994). Finally, noise exposure, even
from infant toys (Jerger, 1994), or from the environment, may represent a hazard to the hearing of children. In fact, fetal noise exposure has
been suggested as a causative factor (Lalande et
al, 1986); however, the supportive evidence is
scarce and fairly speculative.
To the author's knowledge, a causal relationship between fetal infection with human
immunodeficiency virus and HI has not yet been
established, but some reports demonstrate auditory dysfunction in HIVaffected subjects (Real
et al, 1987 ; Birchall et al, 1992). Since the virus
is neurotropic, a fetal viral infection may affect
the hearing organ and cause auditory dysfunction, resulting in a prenatal cause of HI . However, a sensorineural HI in HIV-infected subjects
may be caused by other infectious agents or by
sequels from encephalitis/meningitis; thus, the
auditory dysfunction may be categorized as postnatal. Future research within this problem may
support the speculations .
1568
Not defined
32
Concluding Remarks
162
1960-1975
34
1024
Not defined
27
181
1980-1990
20
101
Not defined
29
It seems likely that significant differences are
present in the prevalences of causes of childhood
HI among the European countries, considering the
differences in the national child populations.
However, in order to further document this, identical definitions and strict criteria for etiologic
diagnosis, including intrinsic and extrinsic factors,
Future Etiologic Perspectives
A constant clinical awareness towards etiologic diagnosis may yield additional or new
information on future diseases causing HI in children . Through such diligence, a likely relationship between HI and fetal alcohol syndrome has
Table 6 Proportion (%) of Unknown Cause
in Different European Reports
Investigated
(N)
Martin et al, 1981
(EEC)
Kankkunen,1982
(Sweden)
Parving, 1984, 1988
(Denmark)
Newton, 1985
(England)
Lenzi and Zaghis, 1988
(Italy)
van Rijn, 1989
(Holland)
Dias and Andrea, 1990
(Portugal)
Parving, 1993
(Denmark)
Vanniasegaram
et al, 1993 (England)
Birth
Unknown
Cohorts Category
(YO
(°/0)
2988
1969
42
179
1970-1980
16
117/138
1970-1980 11/17
Journal of the American Academy of Audiology/Volume 6, Number 5, September 1995
should be introduced . The sensitivity and specificity of diagnostic tests and procedures should be
evaluated, etiologic diagnostic programs implemented, and performance ensured of all pediatric units. As true changes in the causes of HI
have been documented over time, a continuous
monitoring of the causes should be performed, and
this may result in preventative measures, nationally and internationally.
CAUSES OF HEARING IMPAIRMENT
INADULTS
umerous factors, intrinsic and extrinsic N known and unknown - may affect the
hearing organ in adults and result in permanent,
predominantly sensorineural HI throughout
life . The strong correlation between HI and age,
gender (intrinsic factors), noise exposure, otitis
media, and ototoxic drugs (extrinsic factors) has
long since been established and known, and will
not be concentrated upon in this context (e .g .,
reviews by Davis, 1987 ; Henderson et al, 1993 ;
Nadol, 1993 ; Scott and Griffiths, 1994). Throughout the last decade, lifestyle factors, such as
diet, alcohol, and smoking, have also been emphasized (e .g ., Axelsson and Lindgren, 1985 ; Sikora
et al, 1986 ; Dengerink et al, 1987 ; Stephens et
al, 1991); however, the findings are controversial and much disputed, and it seems fair to
state that major uncertainties still exist concerning lifestyle and HI .
Solvent Exposure and HI
Continuous exposure to organic toxic solvents has been accepted as a factor causing
damage to the brain, resulting in cognitive dysfunctions or even severe degrees of dementia
(Axelsson et al, 1980 ; Hein et al, 1990). This relationship has in some European countries been
recognized by the political and administrative
authorities, and may be based on legislation
resulting in compensation, if the exposure can
be ascribed to the occupational environment .
An involvement of cranial nerves after
organic solvent exposure has been demonstrated,
including vestibular function (Odkvist et al,
1980, 1987). Moreover, an accumulation of animal (e .g ., Pryor et al, 1987 ; Sullivan et al, 1989 ;
Johnson, 1994) and human studies (Barregard
and Axelsson, 1984 ; Jacobsen et al, 1993 ; Morata
et al, 1993) support the notion that toxic solvents
represent a factor contributing to the development of HI . The exact mechanisms behind the
damaging effect of organic solvents or solvents
in combination with other damaging factors is
392
not fully understood, but a synergistic effect in
rats between noise and organic solvents has
been supported (Johnson, 1994), whereas an
additive effect in humans has been suggested
(Jacobsen et al, 1993 ; Morata et al, 1993).
Among Brazilian workers within printing
and painting manufacturers, a case-control study
demonstrated significant differences between
the prevalence of high-frequency HI in unexposed subjects (i .e ., 8%), combined noise and
toluene exposure (i .e ., 53%), noise only exposure (i .e ., 26%), and organic solvent only exposure (i.e ., 18%) . The study estimated an adjusted
relative risk of HI 4 times greater for the noise
group, 11 times greater for the combined noise
and solvent exposure group, and 5 times greater
for the solvent only exposure group (Morata et
al, 1993).
In a Danish epidemiologic study, the relationship between self-assessed hearing problems and occupational exposure to solvents was
investigated using a cross-sectional design with
3284 participating male subjects, aged 53-74
years. The study demonstrated that exposure to
organic solvents for 5 years or more resulted in
an adjusted relative risk for HI of 1 .4 (95% CI
1.1-1 .9) without exposure to noise. The factors
adjusted for were age, noise trauma, chronic
middle ear infection, and a family history of HI .
The prevalence of HI was 24 percent in subjects not exposed to organic solvents, and the
attributable risk from solvent exposure was 9.6
percent. Exposure less than 5 years had no effect
on hearing ability. In contrast to the study by
Morata et al (1993), the Danish study showed
no additional effect from organic solvents to
noise exposure, which was by far the most hazardous factor to hearing ability.
Although some controversies between the
mentioned studies exist, it seems likely that a
moderate adverse effect on hearing sensitivity
in humans is caused by toxic organic solvents,
which should be accounted for and prevented in
the working environment.
Disorders in Endocrine Glands
Hypothyroidism
Since 1907, a relationship between acquired
hypothyroidism and reduced hearing sensitivity has been claimed (Kemp, 1907), often based
on single case stories or upon small, uncontrolled samples treated with L-thyroxine, demonstrating improvements in hearing sensitivity
(Ritter and Lawrence, 1960 ; Sachdev and Hall,
1975). These findings have been disputed (de Vos,
Hearing Impairment/Parving
1963 ; Post, 1964), and, more recently, case-control studies in subjects above and below the age
of 60 years have failed to demonstrate an effect
of thyroid hormone on the hearing ability in
subjects with acquired hypothyroidism (Parving
et al, 1983, 1986). In addition, no evidence for
a causal relationship between hypothyroidism
and hearing disability was found using an epidemiologic approach (Parving et al, 1993).
Experimental animal studies showing morphologic and functional abnormalities cannot
be disregarded; however, many animal experiments have concentrated on congenital hypothyroidism, which originates in the developing ear
and thus is completely different from hypothyroidism acquired in adulthood. Thus, no morphologic or specific histologic abnormalities were
demonstrated in the temporal bones from elderly
subjects dying with untreated myxoedema (Parving et al, 1986 ; Hald et al, 1991), and, in addition,
no deposition of neutral or acid glycosaminoglycans could be found in postmortem examinations of the brain from two subjects (Hald et
al, 1991). However, as the thyroid gland is an
essential regulator of cellular metabolism, the
claimed relationship between hypothyroidism
and HI based on treatment with L-thyroxine
may be due to improved cellular mechanisms in
the organ of Corti, or in the neurogenic tissue
of the cochlear nerve, or in a combination of these.
The continuing demonstration of improvements
in hearing ability in hypothyroid patients upon
treatment should perhaps be explained by a
better cooperation in psychoacoustic testing,
when the patient is euthyroid, and thus in a better, general health condition . Although the
pathoanatomical literature is scarce on this subject, the hypothesized functional relationship
between HI and acquired hypothyroidism in
adults is strongly supported by preliminary findings showing a lack of morphologic and histologic
abnormalities in the temporal bones and brains
from such patients .
Diabetes Mellitus
The claim of a causal relationship between
HI and diabetes mellitus is also controversial in
clinical, epidemiologic, and histologic studies
(e .g., Jorgensen and Buch, 1961 ; Friedmann et
al, 1975 ; Taylor and Erwin, 1978 ; Gibbin and
Davis, 1981 ; Parving et al, 1990, 1993 ; Ferrer et
al, 1991 ; Triana et al, 1991 ; Rust et al, 1992).
Some of the conflicts derived from clinical studies may be ascribed to the pronounced heterogeneity of diabetic patients in the investigations
and/or to lack of strict criteria for HI and/or to
less sophisticated techniques for assessment of
hearing disorders in the past .
In a case-control study including only subjects with long- and short-term insulin-dependent diabetes mellitus, pure-tone audiometry
failed to demonstrate a relationship between
HI and diabetes mellitus when adjusted for age
and sex, whereas the results of auditory brainstem response showed prolonged latencies of
the I-V intervals in 40 percent of the long-term
patients and in 5 percent of the short-term
patients (Parving et al, 1990). This supported
previous findings by Donald et al (1981) and
Fedele et al (1984), and a subsequent study
including MRI and neuropsychological testing
showed signs of damage to the central nervous
system and supported the hypothesis of a diabetic encephalopathy (Collier et al, 1988 ;
Pozzessere et al, 1988) including the central
auditory pathways (Dejgaard et al, 1991). However, so far, histologic studies of the brains, temporal bones, or central auditory pathways from
the investigated subjects have not been reported,
and the causal relationship between diabetes
mellitus and HI - whatever the site of lesion should still be a subject for future investigations and dispute .
Concluding Remarks
Concerning factors causing HI in adults,
the intentions were to briefly summarize some
evidence for extrinsic factors, such as toxic
organic solvents that are likely to cause damage
to the hearing organ, and point out the highly
controversial findings within hypothyroidism
and diabetes mellitus, to which some of the
author's own research has contributed. Other
investigations, both mentioned and unmentioned, are highly acknowledged by the author,
who apologizes for both deliberate exclusions
of references and for ignorance.
Future developments and research in the etiologic field within pediatric and adult audiology
may contribute to the delineation of yet unknown
damaging factors or reduction of the effect of factors causing HI, a disorder that ultimately
results in adverse effects on the quality of life
in all age groups .
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