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_________________________________________________________________
Record: 23
Author(s): Becker DP; Grossman RG; McLaurin RL; Caveness WF
Title: Head injuries--panel 3.
Language: ENG
Source: Arch Neurol; 1979 Nov 16. Vol 36 Issue 12 P 750-8
CY: UNITED STATES
ISSN: 0003-9942
Pub Type: JOURNAL ARTICLE
Journal Code: 80K
Journal Subset: A; M
MeSH Heading: Aerospace Medicine:*. Brain Injuries:CO/*DI/TH.
Accidents, Aviation:PC. Brain Damage, Chronic:CO. Cerebral Palsy:ET.
Cerebrospinal Fluid. Cerebrospinal Fluid Shunts. Certification.
Epilepsy:ET. Fistula. Hematoma, Subdural:ET. Hydrocephalus:ET. United
States.
Check Tag(s): Human
UI: 80064433
EM: 8003
Database: Comprehensive MEDLINE with FullTEXT with MeSH
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_________________________________________________________________
Record: 7
Author(s): Cullen SA; Drysdale HC; Mayes RW
Author's Address: RAF Department of Aviation Pathology, RAF Institute
of Health and Medical Training, Halton, Buckinghamshire.
Title: Role of medical factors in 1000 fatal aviation accidents: case
note study.
Language: ENG
Source: BMJ; 1997 May 31. Vol 314 Issue 7094 P 1592
CY: ENGLAND
ISSN: 0959-8138
Pub Type: JOURNAL ARTICLE
Journal Code: BMJ
Journal Subset: A; M; X
MeSH Heading: Accidents, Aviation:*CL. Acute Disease:*. Chronic
Disease:*. Alcoholic Intoxication. Central Nervous System Diseases.
Great Britain. Heart Diseases. Check Tag(s): Human
UI: 97329699
EM: 9709
Database: Comprehensive MEDLINE with FullTEXT with MeSH
Section: Papers
ROLE OF MEDICAL FACTORS IN 1000 FATAL AVIATION ACCIDENTS: CASE NOTE
STUDY
Sudden illness in flight is said to cause 1.5% of fatal general
aviation accidents.[1] This study reviews the experience from the
United Kingdom.
Methods and results
We reviewed the findings of 1000 consecutive accidents between 1956
and 1995 for which a consultant from our department either performed
or attended the necropsies. Medical or toxicological factors caused or
were a contributory cause in 47 accidents (table 1). Cardiac disease
in the pilot was the most common factor. In one case the collapse of a
front seat passenger in a light aircraft was thought to have
distracted the pilot and caused the accident. The other medical causes
in private pilots included nine cases of alcohol intoxication and
three definite suicides. Central nervous system disorders contributed
to seven accidents; three pilots were thought to have had epileptic
fits, one had encephalitis, one a pituitary tumour, one haemorrhage
from a cerebellar arteriovenous malformation, and one with a history
of migraine radioed a report of visual disturbances and numbness
before his crash.
Comment
Finding disease in the crew does not mean that it is the cause of the
accident. Usually it is a coincidental finding. The main problems of
interpretation are that the signs of trauma are superimposed on the
disease process and that the victims often have such serious injuries
that meaningful examination of their organs is impossible. For
example, we know of a case where a young helicopter pilot collapsed on
his way to his aircraft. He was admitted to hospital where he died of
a haemorrhage into a cerebral metastasis from a minute testicular
teratoma. Had he died while flying his brain would probably have been
severely traumatised. Even if the tumour had been found it would have
been difficult to determine if the haemorrhage caused the accident or
was caused by it.
The history of the flight and accident is essential for accurate
interpretation of pathological findings in aviation accidents. In this
series most of the pilots had cardiac disease. Often there are no
signs of acute changes and pathologists rely entirely on history.
Haemorrhage into an atheromatous plaque has been seen occasionally,
and in these cases staining for iron showed the presence of
haemosiderin laden macro-phages suggesting that there had been
previous bleeds into the plaque. This contrasts with the bleeding
caused by direct trauma to the heart which is adventitial rather than
within the plaque and has no demonstrable haemosiderin.
The commonest cause of incapacitation in flights not resulting in
accidents is neurological disorders.[2,3] However, neurological
disorders were under represented in our series, probably because of
the difficulty in postmortem diagnosis and the severe cerebral damage
that often occurs in aviation accidents.
The 2.4% rate of alcohol intoxication in private pilots is comparable
with that reported elsewhere[4] but is much less than the third of
private pilots quoted in the British Medical Association booklet
Alcohol and accidents.[5] Interestingly, five pilots were clearly
drinking while flying as the remains of spirit bottles were found in
the wreckage. One of these cases may have been suicide and in three
others in which the pilot was not intoxicated we are certain that the
pilot took his own life.
We thank Professor J K Mason and Drs P J Stevens, A J C Balfour, and I
R Hill for their meticulous case notes and accident analysis.
Funding: None.
Conflict of interest: None.
Correspondence to: Dr Cullen.
1 Booze CE Sudden in-flight incapacitation in general aviation. Aviat
Space Environ Med 1989;60:332-5.
2 McCormick TJ, Lyons TJ. Medical causes of in-flight incapacitation:
USAF experience 1978-1987. Aviat Space Environ Med 1991;62:884-7.
3 Froom P, Benbassat J, Gross, M, Ribak J, Lewis BS. Air accidents,
pilot experience, and disease related in-flight sudden incapacitation.
Aviat Space Environ Med 1988;59:278-81.
4 Kuhlman JJ, Levine B, Smith ML, Hordinsky JR. Toxicological findings
in Federal Aviation Administration general aviation accidents. J
Forensic Sci 1991;.36:1121-8.
5 Morgan D, ed. The BMA Guide to Alcohol and Accidents. London: BMA,
1989.
(Accepted 29 November 1996)
Table 1 Role of medical factors in fatal aviation accidents
Legend for Chart:
A - Category
B - Total accidents
C - Medical factors, Cardiac
D - Medical factors, Other
E - Medical factors, Total (%)
A B C D E
Glider 67 6 2 8 (12)
Private 375 9 17 26 (7)
Commercial 114 4 1 5 (4)
Military 407 3 5 8 (2)
Parachutists, hang gliders 37 0 0 0
Total 1000 22 25 47 (4.7)
~~~~~~~~
By S. A. Cullen, H. C. Drysdale, R. W. Mayes , S. A. Cullen,
consultant pathologist , H. C. Drysdale, consultant pathologist and R.
W. Mayes, principal toxicologist
RAF Department of Aviation Pathology, RAF Institute of Health and
Medical Training, Halton, Buckinghamshire HP22 5P
RAF Department of Aviation Toxicology, RAF Institute of Health and
Medical Training
_________________
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Item Number: 97329699
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_________________________________________________________________
Record: 9
Author(s): Wilmshurst P
Title: Brain damage in divers [editorial; comment] [see comments]
Language: ENG
Source: BMJ; 1997 Mar 8. Vol 314 Issue 7082 P 689-90
CY: ENGLAND
ISSN: 0959-8138
Pub Type: COMMENT; EDITORIAL
Journal Code: BMJ
Journal Subset: A; M; X
MeSH Heading: Brain Injuries:*ET. Diving:*IN. Decompression
Sickness:ET. Check Tag(s): Human
CM: Comment on: BMJ 1997 Mar 8;314(7082):701-5
Comment in: BMJ 1997 Jun 14;314(7096):1761; discussion 1761-2
UI: 97226144
EM: 9706
Database: Comprehensive MEDLINE with FullTEXT with MeSH
Section: Editorial
BRAIN DAMAGE IN DIVERS
Diving itself may cause brain damage --but we need more evidence
Diving involves risk of neurological injuries. These may arise from
decompression illness (a label which recognises the difficulty in
distinguishing clinically decompression sickness due to gas nucleation
from gas invasion caused by pulmonary barotrauma), anoxia (caused by
near drowning), and the toxic effects of high partial pressures of
breathing gases. The possibility that divers and others working in
hyperbaric conditions may acquire neuropsychological damage without a
clear history of a precipitating event is worrying. Since 1978 five
international meetings have discussed this possibility, but no
consensus exists whether diving per se causes brain damage.
Much of the evidence of functional abnormalities in divers with no
history of decompression illness is anecdotal. Many reports describe
findings in mixed groups of divers, some with and some without prior
decompression illness.[1 2] The most quoted study involved a snapshot
assessment of intellectual function in Australian abalone divers,[3]
with no assessment of change over time and no controls. The
psychological assessment probably failed to reflect the
characteristics of these particular individuals, and their dive
practices.
the brains and spinal cords of unaffected divers which resemble the
abnormalities found after decompression illness.[4 5] Retinal
fluorescein angiography in divers with no history of decompression
illness has demonstrated vasculopathy, which may be a marker for
neurovascular injury.[6] Concern is heightened by evidence of long
term injuries to other organs, such as crippling dysbaric
osteonecrosis in divers and caisson workers years after hyperbaric
exposure.
When neurological damage occurs in divers the prime suspects are gas
bubbles. Gas nucleation is generally accepted to be the initiating
event in most of the syndromes collectively known as decompression
sickness. However, free gas does not invariably lead to decompression
sickness. Doppler ultrasound can detect "silent" bubbles in the venous
blood of many asymptomatic divers. Most bubbles are filtered out by
the pulmonary capillaries. It was once believed that a critical amount
of gas nucleation was required before decompression sickness occurred.
We now know that this may be true for extreme decompressions in
individuals without intracardiac or pulmonary right to left shunts,
but in those with a shunt a relatively small bubble load can result in
paradoxical gas embolism.[7 8]
Decompression sickness can affect many systems, but the serious
effects are neurological. There is usually abrupt or rapid evolution
of a focal central neurological deficit (or deficits). The injury may
be mild or severely disabling; it may be permanent or resolve
spontaneously or with treatment with oxygen and recompression;
episodes may recur. Clinically the spectrum of neurological
decompression sickness resembles that of thromboembolic
cerebrovascular disease, with one exception: decompression sickness
commonly affects the spinal cord. This difference may be explained by
the considerable gas load in the cord at the end of many dives
compared with the gas content of an equivalent weight of brain tissue.
The greater blood flow to the brain means that more gas bubbles
embolise the brain, but more dissolved gas is available to amplify
embolic bubbles in the cord. Conceivably recurrent subclinical
decompression sickness may result in a condition analogous to
multi-infarct dementia with gas embolism rather than thromboembolism
as the initiator.
There are other neurological insults. During many normal dives
neurological effects occur from variations in gas partial pressures.
Every depth change of 7 m produces change in ambient pressure
equivalent to a trip between sea level and the top of Mount Everest.
The narcotic effects of nitrogen at depths of 30 m or less are well
described. Narcosis is reversed by ascent but can repeated exposure
cause target organ damage like repeated alcohol intoxication? Other
breathing gases are also not inert at high partial pressures. Oxygen
is neurotoxic. Very deep dives, during which mixtures containing
helium are breathed, can result in the high pressure neurological
syndrome, which causes excitatory effects including tremor, myoclonus,
and convulsions. Repeated insults might produce permanent harm.
Until recently investigational techniques were too insensitive to
detect neurological abnormalities in "normal" divers or even in those
with clinical effects from decompression illness[9]. Magnetic
resonance imaging seems to offer greatest promise. Reul and colleagues
found more hyperintense subcortical white matter lesions in the brains
of sport divers than in non-diving controls.[10] The difference was
due to a subgroup of divers who had multiple brain lesions. In this
issue Knauth and colleagues report that multiple brain lesions on
magnetic resonance scans in sport divers occur exclusively in those
with large right to left shunts (presumed to be patent foramen ovale,
though some may be small atrial septai defects or pulmonary
arteriovenous shunts) (p 701).11
These observations are consistent with the well documented role of
shunts in the pathogenesis of overt decompression illness by means of
paradoxical gas embolism but extend this role to subclinical injury.
This is plausible. Decompression illness is a spectrum. It may be so
mild that divers do not seek treatment.[8] Divers who have had
decompression illness and in whom we find a large shunt often
recollect mild neurological symptoms after earlier dives which they
did not consider important at the time. The fact that the illness can
be mild adds plausibility to studies showing an increased prevalence
of subclinical lesions in divers with a large shunt but also cautions
against accepting data uncritically from studies in which subjects
were self selected.[10 11]
The results of magnetic resonance scans in others exposed to
hyperbaric conditions have not been entirely consistent. Caisson
workers also have an increased prevalence of brain lesions.[12]
Professional divers do not,[13] even though necropsy evidence of
pathological injury is commoner than in sport divers.[5] Magnetic
resonance imaging does not always reveal abnormalities in cases of
dear neurological decompression illness.[14] These apparent
contradictions may be due to differences in imaging techniques,
methods of subject recruitment, and confounding variables.
Interestingly, magnetic resonance findings do not correlate with the
results of psychometric tests or electroencephalograms.[12 13] Further
investigation into the possibility that diving per se causes brain
damage is required, but we must not forget that evidence of
pathological change is not proof of functional deficit.
1 Vaernes RJ, Eidsvik S. Central nervous dysfunctions after near miss
accidents in diving. Aviat Space Environ Med 1982;53:803-7.
2 Todnem K, Nyland H, Skiedsvoll H, Svihus R, Rinck P, Kambestad BK,
et al. Neurological long term consequences of deep diving. Br J Indust
Med 1991;48:258-66.
3 Edmonds C, Boughton J. Intellectual deterioration with excessive
diving (punch drunk divers). Undersea Biomed Res 1985; 12:321-6.
4 Palmer AC, Calder IM, Hughes JT. Spinal cord degeneration in divers.
Lancet 1987;ii:1365-6.
5 Palmer AC, Calder IM, Yates PO. Cerebral vasculopathy in divers.
Neuropathol Appl Neurobiol 1992;18:113-24.
6 Polkinghorne PJ, Sehmi K, Cross MR, Minassian D, Bird AC. Ocular
fundus lesions in divers. Lancet 1988;ii:1381-3.
7 Moon RE, Camporesi EM, Kisslo JA. Patent foramen ovale and
decompression sickness in divers. Lancet 1989;i:513-4.
8 Wilmshurst PT, Byrne JC, Webb-Peploe MM. Relation between
interatrial shunts and decompression sickness in divers. Lancet
1989;ii:1302-6.
9 Halsey MJ, Elliott DH, eds. Diagnostic techniques in diving
neurology. London: Medical Research Council Decompression Sickness
Panel, 1987.
10 Reul J, Weis J, Jung A, Willmes K, Thron A. Central nervous system
lesions and cervical disc herniations in amateur divers. Lancet
1995;345:1403-5.
11 Knauth M, Ries S, Pohtmann S, Kerby T, Forsting M, Daffertshofer M,
et al. Multiple brain lesions in sport divers: the role of a patent
foramen ovale. BMJ 1997;314:701-5.
12 Fueredi GA, Czarnecky DJ, Kindwall EP. MR findings in the brains of
compressed-air tunnel workers: relationship to psychometric results.
AJNR 1991;12:67-70
13 Todem K, Skeidsvoll H, Svihus R, Rinck P, Riise T, Kambestad BK, et
al. Electroenceph Clin Neurophysio11991 ;79:322-9.
14 Warren LP, Djang WT, Moon RE, Camporesi EM, Sallee DS, Anthony DC,
et al. Neuroimaging of scuba diving injuries to the CNS. AJR
1988;151:1003-8.
~~~~~~~~
By Peter Wilmshurst
Consultant cardiologist, Royal Shrewsbury Hospital, Shrewsbury SY3 8XQ
_________________
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_________________________________________________________________
Record: 10
Author(s): Chen TJ; Chen SS; Hsieh PY; Chiang HC
Author's Address: Department of Physiology, Institute of Public
Health, Kaohsiung Medical College, Taiwan, Republic of China.
Title: Auditory effects of aircraft noise on people living near an
airport.
Language: ENG
Source: Arch Environ Health; 1997 Jan-Feb. Vol 52 Issue 1 P 45-50
CY: UNITED STATES
ISSN: 0003-9896
Pub Type: CLINICAL TRIAL; JOURNAL ARTICLE
Journal Code: 6YO
Journal Subset: A; M
MeSH Heading: Aircraft:*. Hearing Loss, Noise-Induced:CL/*DI. Noise,
Transportation:*AE. Adult. Audiometry. Auditory Threshold. Evoked
Potentials, Auditory. Middle Age. Random Allocation. Residence
Characteristics. Check Tag(s): Comparative Study; Female; Human; Male;
Support, Non-U.S. Gov't
Abstract: Two groups of randomly chosen individuals who lived in two
communities located different distances from the airport were studied.
We monitored audiometry and brainstem auditory-evoked potentials to
evaluate cochlear and retrocochlear functions in the individuals
studied. The results of audiometry measurements indicated that hearing
ability was reduced significantly in individuals who lived near the
airport and who were exposed frequently to aircraft noise. Values of
pure-tone average, high pure-tone average, and threshold at 4 kHz were
all higher in individuals who lived near the airport, compared with
those who lived farther away. With respect to brainstem
auditory-evoked potentials, latencies between the two groups were not
consistently different; however, the abnormality rate of such
potentials was significantly higher in volunteers who lived near the
airport, compared with less-exposed counterparts. In addition, a
positive correlation was found between brainstem auditory-evoked
potential latency and behavioral hearing threshold of high-frequency
tone in exposed volunteers. We not only confirmed that damage to the
peripheral cochlear organs occurred in individuals exposed frequently
to aircraft noise, but we demonstrated involvement of the central
auditory pathway.
UI: 97192038
EM: 9705
Database: Comprehensive MEDLINE with FullTEXT with MeSH
AUDITORY EFFECTS OF AIRCRAFT NOISE ON PEOPLE LIVING NEAR AN AIRPORT
ABSTRACT. Two groups of randomly chosen individuals who lived in two
communities located different distances from the airport were studied.
We monitored audiometry and brainstem auditory-evoked potentials to
evaluate cochlear and retrocochlear functions in the individuals
studied. The results of audiometry measurements indicated that hearing
ability was reduced significantly in individuals who lived near the
airport and who were exposed frequently to aircraft noise. Values of
pure-tone average, high pure-tone average, and threshold at 4 kHz were
all higher in individuals who lived near the airport, compared with
those who lived farther away. With respect to brainstem
auditory-evoked potentials, latencies between the two groups were not
consistently different; however, the abnormality rate of such
potentials was significantly higher in volunteers who lived near the
airport, compared with less-exposed counterparts. In addition, a
positive correlation was found between brainstem auditory-evoked
potential latency and behavioral hearing threshold of high-frequency
tone in exposed volunteers. We not only confirmed that damage to the
peripheral cochlear organs occurred in individuals exposed frequently
to aircraft noise, but we demonstrated involvement of the central
auditory pathway.
Exposure to noise of sufficient level and duration can produce hearing
loss and many nonauditory effects, including some adverse
noise-related physiological changes (e.g., cardiovascular effects,
performance and behavioral effects, sleep disturbance, communication
interference[1-5]). The most severe effect is the noise-induced damage
to the delicate structures in the human ear designed to perceive
sound.
The sensorineural hearing loss that affects the ability to hear at
frequencies around 4 kHz has long been recognized as chronically
noise-induced hearing loss (NIHL),[6-9] which is generally agreed to
be the result of a degeneration of the outer and inner hair
cells.[10,11] The results of animal studies have demonstrated that the
early effects of noise may involve the cochlea; degeneration of
central auditory connections likely occur at a later stage.[12]
However, the previous findings about the effects of environmental
noise exposure on hearing loss remain controversial.[13-17]
During past decades, gradually increasing aircraft traffic provoked a
heightened public concern about air-craft-noise pollution in areas
located around airports. Given that systematic investigations of the
auditory effects of potentially severely damaging high-frequency
aircraft noise were not available in Taiwan, we undertook some studies
during the past 3 y and detected some marked deleterious effects of
aircraft noise in airport employees and school-age children.[6,7]
During recent years, Taiwanese who live near airports have
demonstrated frequently against irritating aircraft noise, which they
claim has affected their health and daily activities. According to
Baxter et al.,[14] however, individuals who lived near an airport
were, under normal circumstances, in no danger of suffering permanent
noise-induced hearing damage.[14] In view of the controversy, we
sought to determine the effects of high-frequency aircraft noise on
auditory pathway function and hearing in people who resided near an
airport. We also attempted to establish regression equations for
predicting the degree of hearing loss under certain circumstances.
Material and Method
According to the day-night level (DNL) contours (obtained from the
Environmental Protection Agency of Taiwan) around Kaohsiung airport,
three residential areas located in the second largest city in Taiwan
that neighbored Kaohsiung airport were chosen for this investigation.
The aircraft noise exposure is uniform in these areas (DNL > 75 dB).
The airport is located in a suburban area of this industrial port, and
it serves both domestic and international flights that number
approximately 150/d. Each day approximately 10 flights depart each
hour during the time interval from 7 A.M. to 10 P.M. The highest
values measured during overflights approached 86.8 dBA. According to
our previous survey, the prevalence of high-frequency hearing loss was
41.9% in airport employees,[6] and mild hearing loss was experienced
by 10.1% of children who attended school near the airport. In this
study, a residential area located farther from the airport than the
three residential areas mentioned earlier served as a control. There
was no highway, railroad, or factory in any of the residential areas
studied.
All volunteers in the residential areas were asked randomly to
participate in the study, provided they had lived in the area for at
least 1 y. All volunteers were examined physically and
neurootologically. Data gathered included sex, age, occupation,
portion of day spent at home, use of ototoxic drugs, occurrence of
head trauma, pathological problems of the outer and middle ear, and
radiological signs of retrocochlear involvement. Subjects with any
problem that influenced their ability to hear were excluded.
We measured audiometry and brainstem auditory-evoked potentials
(BAEPs) in all participants to evaluate cochlear and retrocochlear
functions. Audiometry analysis was used to measure hearing thresholds
at various fixed-frequency pure tones, thus yielding a test of
cochlear function. The BAFP records, which were made on the scalp in
response to sounds, were assumed to arise from the nerve tracts and
nuclei of the ascending brainstem auditory pathways, indicating
central auditory transmission (i.e., reflection of retrocochlear
function). A summary of this technique was described previously in
detail.[7] All measurements were performed while the subject was at
home and after he or she had rested for at least 10 h. The mean
behavioral hearing threshold of each ear at 0.5 kHz, 1 kHz, and 2 kHz
was calculated from audiograms and was referred to as pure tone
average (PTA); the mean hearing threshold at 4 kHz, 6 kHz, and 8 kHz
was referred to as the high pure tone average (HPTA).[6,7] Various
classes of hearing loss were suggested, based on PTA values, including
the frequencies required most for speech recognition (Table 1).[18]
The rates of hearing loss (permanent threshold shift) in our
participants were estimated in accordance with this classification. In
addition, latencies of BAFPwaves I, III, and V, as well as the I-III,
III-V, and I-V interpeak latencies indicating neural transmission
times, were calculated. Abnormality was defined as a latency 2
standard deviations greater than the mean value in volunteers who
lived a considerable distance from the airport.
Variables retained for analysis were (a) behavioral hearing threshold
to pure tone (i.e., PTA, HPTA, and threshold at 4 kHz); (b)
abnormality rate from audiometry; (c) absolute latencies of waves I,
III, and V; (d) I-III, III-V, and I-V interpeak latencies; and (e)
abnormal BAEP rate. The two groups of residents were compared.
Differences in thresholds and latencies were tested for statistical
significance by Student's t test, and abnormality rates were analyzed
by the chi-square test. Furthermore, BAFP latencies were collated with
various behavioral hearing measures, yielding correlation coefficients
(Pearson's r), slopes, and intercepts for equations that predicted
hearing loss from BAEP latency data.
Results
There were 175 persons available for participation in this study; 83
lived near the airport (group A), and 93 individuals resided farther
from the airport (group B). Sex, age, job, noise exposure at the
workplace, portion of day spent at home, and location of residence for
the two groups are summarized in Table 2. Neither sex (tested by
chi-square) nor age distribution (Student's t test, stratified age by
10 y tested by chi-square) were significantly different between the
two groups. There were significantly more unemployed subjects in group
A than in group B (chi-square); therefore, the amount of time spent at
home was significantly different between the two groups, and
significantly more participants in group A stayed in their homes > 9
h/d. The number of subjects who suffered from noise exposure (i.e., >
80 dB 4 h/d for > 1 y) at the workplace was not significantly
different between the two groups (chi-square). Traffic noise caused by
motor vehicles in the residential areas was not significantly
different in the two groups. There were 56.6% and 57.6% of subjects in
groups A and B, respective[y, who lived in quieter areas (i.e., homes
with driveways); the remaining subjects lived in noisier areas (i.e.,
houses near crossroads and adjacent to two- or four-way streets).
Values of PTA, HPTA, and threshold at 4 kHz were significantly higher
in group A subjects who lived near the airport than in group B
subjects (Table 3). The distribution of hearing thresholds in the
better ear of participants is listed in Table 4 and accords with Bess
classification (Table 1). The hearing thresholds of the majority
(93.5%) of group B participants were within normal limits, but only
31.3% of group A subjects exhibited normal limits. The rate of hearing
impairment was 68.7% in group A and 6.5% in group B (chi-square, p <
.01).
Differences in mean peak and interpeak latencies of BAEP recordings
were not significant statistically between the two groups (Table 5).
Only peaks III and V and I-III interpeak latencies in the left ear
were significantly different. Brainstem auditory-evoked potential
abnormalities were detected, however, in 44.6% of group A, compared
with 14.1% of group B (chi-square, p< .01).
The behavioral hearing threshold was correlated significantly with
individual BAEP latencies in group A (Table 6), which included more
individuals with significant hearing loss, compared with group B. The
BAEP latency appeared to be better related to hearing thresholds at
high-tone, rather than at low-tone frequencies. In an attempt to
predict hearing loss from BAEP latencies (Table 7), we compared
latencies of wave V (the prominent component wave) and interpeak I-V
(indication of auditory central conduction) with various behavioral
measures and derived a set of linear regression equations, correlation
coefficients (r), slopes, and intercepts (Table 7). Both wave V and
interpeak I-V latencies were highly significantly related to hearing
thresholds at 4 kHz, 6 kHz, and 8 kHz, as well as to HPTA.
Discussion
Currently, noise is a noticeable problem in residential areas,
especially in Taiwan. Major environmental noise sources are frequently
noisy airports and/or busy roads. Most investigators of environment
noise focus attention on the nonauditory and adverse physiological
effects to the cardiovascular system,[1,2,4,5,19,20] even though
hearing damage is the most serious consequence of noise exposure.
It is well known that airport noise constitutes a very serious threat
to public health. In the past, we have drawn attention to the effects
of high-frequency aircraft noise on the function of central acoustic
pathways and hearing ability. The results of our previous studies have
demonstrated that (a) both peripheral cochlear organs and central
auditory pathways were damaged in airport employees, and the degree of
auditory damage coincided with job patterns[6]; and (b) damage to
peripheral cochlear organs was confirmed in school-age children,
although involvement of the central auditory pathway could not be
verified.[7] Intermittent exposure to aircraft noise and greater
distance between school and airport might account for milder noise
effects in school-age children. We attempted, therefore, to complete
systematic research on the auditory effects of high-frequency aircraft
noise in Taiwan. Following our investigations of airport employees and
schoolchildren, we determined that a community located near an airport
should be studied next.
As described in earlier studies,[6,7] the mechanism of chronic
noise-induced hearing loss (NIHL) involves damage to the outer hair
cells of the basal turn of the cochlea via long-term noise
exposure[21-23] (i.e., a noise-related hearing deficit is commonly a
drop of "notch" at 4 kHz). With continued exposure to noise,
audiometric thresholds are not only lowered at 4 kHz but also decline
significantly between 1 kHz and 3 kHz, with a concomitant decrease in
speech intelligibility.[24,25] In addition to cochlear lesions, damage
to the central auditory pathway has also been suggested.[6,26-28] The
major contribution to BAEP originates in the basal turn of the
cochlea, primarily in the 2 kHz to 5 kHz region.[21,29-31] Therefore,
the site affected by noise and the sources of BAEP along the cochlear
basilar membrane are similar.[21]
In the present study, distribution of age, sex, and noise exposure at
the workplace or at home was not significantly different between the
two groups. The audiometry measurements indicated that hearing ability
was significantly worse in individuals who resided near an airport.
All values of PTA, HPTA, and threshold at 4 kHz were higher in
individuals exposed to aircraft noise frequently, and the abnormality
rate, which was based on PTA values, was also significantly higher in
these participants. The relatively greater hearing loss at high
frequencies in group A, as demonstrated by their HPTA values and
thresholds at 4 kHz, concurred with the relatively high prevalence of
NIHL in this same group, which was exposed more frequently to aircraft
noise. Furthermore, differences in PTA abnormalities evidenced that
hearing loss in group A exceeded that experienced in group B. These
indices show that long-term exposure to aircraft noise affects the
hearing threshold both at high frequencies, as well as at lower
frequencies, which are relevant to speech intelligibility.
Although prolongation in peak and interpeak latencies did not occur
consistently in group A, the BAEP abnormality rate in this group was
increased significantly. These observations, however, did not confirm
whether central transmission did or did not affect people exposed to
aircraft noise for extended periods. This uncertainty would likely be
resolved if we were to increase the size of the study population.
The slopes of linear regression equations were all positive,
indicating a positive correlation between BAFP latency and behavioral
hearing threshold (i.e., as BAEP latency was prolonged, behavioral
hearing threshold increased). The threshold in the higher frequency
regions (i.e., 2 kHz-8 kHz) was correlated strongly with BAEP latency,
thus reaffirming the relevance of the 2 kHz-5 kHz interval to BAEP. In
addition, this result confirmed the observations of Coats and
Martin,[29] who, in 1977, found a strong relationship between
behavioral threshold at 8 kHz and BAEP. It is not unreasonable,
therefore, to predict NIHL from BAEP latency because a typical NIHL
usually affects the hearing threshold at frequencies that exceed 4
kHz.
A comparison was made between the findings for schoolchildren and the
present volunteers; an age effect was evident in our volunteers. The
audiograms revealed significantly higher hearing thresholds for both
groups in the current study, compared with schoolchildren (Fig. 1).
The age effect also influenced presentation of BAEP for volunteers who
had longer latencies. Moreover, age seemed to influence the cochlear
organs by increased values of PTA, HPTA, and threshold at 4 kHz, as
well as by the prolongation of BAEP wave I, HPTA, but its effect on
the central auditory transmission was not evident from our studies.
Although Baxter[14] concluded that people who lived near a military
airport were in no danger of suffering permanent hearing damage from
aircraft noise, he suggested that this might change if the frequency
of flights increased.[14] In addition, Wu et al.[32] suggested that
air-craft-noise exposure in Taiwan did not appear to affect the
hearing thresholds of schoolchildren. This result is contrary to that
of our previous study of schoolchildren.[7] Wu et al.[32] divided
students from two schools into high- and low-noise exposure groups,
respectively, based on environmental noise measurements.
Unfortunately, these two groups differed in size and were not
comparable. This shortcoming and different airport/ school
environmental factors contributed to the discrepancy. In the current
study, the study population lived near a busy international airport,
and a statistically significant association was noted between aircraft
noise exposure and prevalence of NIHL. In addition to confirmation of
damage to the cochlear organs, involvement of the central auditory
pathways should also be considered, given that a positive correlation
was observed between BAEP latency and hearing threshold at higher
frequencies in the group that lived closest to the airport.
* * *
This study was supported by a grant from the National Science Council
(NSC83-0421 -B-037-002Z) of Taiwan.
Submitted for publication July 5, 1995; revised; accepted for
publication June 25, 1996.
Requests for reprints should be sent to Dr. Shun-Sheng Chen,
Department of Neurology, Kaohsiung Medical College, Kaohsiung 807,
Taiwan, Republic of China.
Table 1.--Classes of Hearing Impairments and Their Possible Effects on
Speech Intelligibility
Legend for Chart:
A - Classification of hearing impairment
B - PTA (dBHL)
C - Possible effects on speech understanding
A B C
Within normal limits < 27 No significant difficulty
with faint speech
Mild hearing loss 27-40 Difficulty only with
faint speech
Moderate hearing loss 41-55 Frequent difficulty with
normal speech
Moderately severe 56-70 Frequent difficulty with
hearing loss loud speech
Severe hearing loss 71-90 Can understand only
shouted or amplified speech
Profound hearing loss > 91 Usually cannot understand
even amplified speech
Notes: PTA = pure tone average, and HL: hearing level.
Table 2.--Distribution of Sex, Age, Job, Duration of Time Spent at
Home, and Residence Location for Groups A and B
Legend for Chart:
A - Characteristic
B - Group A (near airport)
C - Group B (farther from airport)
A B C
Total subjects 83 92
Sex
Male 27 (32.53) 27 (29.35)
Female 56 (67.47) 65 (70.65)
Age (y)
x +/- SD 45.43 +/- 13.55 43.51 +/- 9.2
Range 17-70 23-67
Employed[*]
Yes 49 (59.04) 84 (91.30)
None 34 (40.96) 8 (8.70)
Noise exposure at
workplace (> 80 dB
4 h/d) 18/49 (36.73) 34/84 (40.48)
Duration at home (h)[*]
1-8 3 (3.61) 14 (15.22)
9-16 35 (42.17) 66 (71.74)
17-24 45 (54.22) 12 (13.04)
Residence
Quiet 47 (56.62) 53 (57.60)
Noisy 36 (43.37) 39 (42.39)
Notes: Values in table are numbers of subjects, except for age, which
is expressed in y. Values within parentheses are percentages.
* p < .01, Student's t test or chi-square test.
Table 3.--Comparisons of Pure Tone Average, High Pure Tone Average,
and Hearing Threshold at 4 kHz between Participants of Two Different
Residential Areas
Legend for Chart:
A - Group
B - n
C - Ear
D - Pure tone average
E - High pure tone average
F - 4-kHz hearing threshold
A B C D
E F
A 83 Right 35.81 +/- 13.46[*]
36.47 +/- 21.96[*] 34.64 +/- 19.91[*]
Left 35.60 +/- 12.63[*]
36.49 +/- 20.20[*] 33.67 +/-18.08[*]
B 92 Right 23.30 +/- 8.36
21.90 +/- 11.02 19.51 +/- 10.06
Left 21.68 +/- 4.90
21.82 +/- 10.35 18.91 +/-9.46
Notes: Right versus Left: paired Student's t test -- no significant
difference in either group.
* Group A versus B: p < .01, Student's t test.
Table 4.--Distribution of Hearing Threshold in the Better Ear of
Individuals (According to the Classification Shown in Table 1)
Legend for Chart:
A - Pure tone average (dBHL)
B - Group A (n = 83)
C - Group B (n = 92)
A B C
< 27 26 (31.33) 86 (93.48)
27-40 39 (46.99) 6 (6.52)
41-55 14 (16.87) 0
56-70 3 (3.61) 0
71-90 0 0
> 91 1 (1.20) 0
Notes: Values shown are numbers of subjects; values within parentheses
are percentages.
Table 5.--Mean Peak and Interpeak Latencies (msec) of Brainstem
Auditory Evoked Potentials in Two Groups of Participants
Legend for Chart:
A - Group
B - n
C - Ear
D - Latencies (msec), I
E - Latencies (msec), III
F - Latencies (msec), V
G - Latencies (msec), I-III
H - Latencies (msec), III-V
I - Latencies (msec), I-V
A B C D E F
G H I
A 83 Right 1.94 +/- 0.17 4.05 +/- 0.28 5.93 +/- 0.32
2.11 +/- 0.26 1.88 +/- 0.20 3.99 +/- 0.32
Left 1.92 +/- 0.17 4.08 +/- 0.30[*] 5.95 +/- 0.33[a]
2.16 +/- 0.27[a] 1.87 +/- 0.25 4.03 +/- 0.32
B 92 Right 1.91 +/- 0.14 3.98 +/- 0.24 5.86 +/- 0.29
2.07 +/- 0.23 1.88 +/- 0.19 3.95 +/- 0.29
Left 1.89 +/- 0.15 3.97 +/- 0.21 5.86 +/- 0.23
2.08 +/- 0.21 1.89 +/- 0.15 3.97 +/- 0.25
Notes: Right versus Left: paired Student's t test--no significant
difference in either group.
* p < .01, group A versus B, Student's t test.
a p < .05, group A versus B, Student's t test.
Table 6.--Description of Behavioral Hearing Threshold at Various Tone
Frequencies Correlated Significantly with BAEP Latency
Legend for Chart:
A - Latency
B - Tone frequency (Hz)
A B
I Threshold of 4k[*], HPTA[*]
III Threshold of 0.5k[*], 2k, 4k, 6k, 8k, and
PTA[*], HPTA
V Threshold of 2k[*], 4k, 6k, 8k, and HPTA
I-III Threshold of 2k[*], 4k, 6k, 8k, and HPTA
III-V --
I-V Threshold of 4k, 6k, 8k, and HPTA
Notes. PTA: pure tone average, HPTA = high pure tone average, and BAEP
= brainstem auditory evoked potentials. *p < .05 (all others: p <
.01).
Table 7.--Correlation Analysis of Brainstem Auditory Evoked Potential
(BAEP) Latency with Behavioral Measures (n = 166 Ears from 83
Residents in Group A)
Legend for Chart:
A - Behavioral measure of audiometry
B - BAEP absolute and interpeak latencies
C - Correlation coefficient (r)
D - p
E - Slope (dB/ms)
F - Intercept (dB)
A B C D E F
Threshold of 0.5k V .14 NS -- --
I-V .08 NS -- --
Threshold of 1 k V .11 NS -- --
I-V .05 NS -- --
Threshold of 2k V .17 <.05 7.98 -16.83
I-V .12 NS -- --
Threshold of 4k V .33 <.01 19.36 -80.88
I-V .24 <.01 14.47 -23.87
Threshold of 6k V .37 <.01 25.18 -112.05
I-V .31 <.01 21.60 -49.07
Threshold of 8k V .32 <.01 23.89 -104.18
I-V .26 <.01 20.54 -44.61
Pure tone average V .15 NS -- --
I-V .09 NS -- --
High pure tone average V .36 <.01 22.81 -99.04
I-V .28 <.01 18.87 -39.19
Note. NS = not significant.
GRAPH: Fig. 1. Mean values and standard deviations (downward bars) of
pure tone average (PTA), high pure tone average (HPTA), and threshold
of 4 kHz in children and present volunteers. a children attending
school near an airport, b children as controls, c people living around
an airport, and d controls.
References
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~~~~~~~~
By TSAN-JU CHEN Department of Physiology; SHUN-SHENG CHEN Department
of Neurology; PEI-YIN HSIEH Institute of Public Health Kaohsiung
Medical College Kaohsiung, Taiwan, Republic of China; HORN-CHE CHIANG
School of Public Health Kaohsiung Medical College Kaohsiung, Taiwan,
Republic of China
_________________
Arch Environ Health is copyrighted. Text may not be copied without the
express written permission of the publisher except for the imprint of
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software. Text is intended solely for the use of the individual user.
Source: Arch Environ Health.
Item Number: 97192038
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_________________________________________________________________
Record: 19
Author(s): Rotondo G; Maniero G; Toffano G
Author's Address: Postgraduate School of Aerospace Medicine,
University of Rome, Italy.
Title: New perspectives in the treatment of hypoxic and ischemic brain
damage: effect of gangliosides.
Language: ENG
Source: Aviat Space Environ Med; 1990 Feb. Vol 61 Issue 2 P 162-4
CY: UNITED STATES
ISSN: 0095-6562
Pub Type: JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
Journal Code: 9JA
Journal Subset: M
MeSH Heading: Brain Damage, Chronic:*TH. Cerebral Anoxia:*TH. G(M1)
Ganglioside:*AD. Gravitation. Nerve Regeneration:DE. Space Flight.
Check Tag(s): Animal; Human
Abstract: Aircrews operating at high G forces and altitudes may be
exposed to both physiological and physical stresses capable of
inducing brain hypoxia. A potential therapeutic tool for the treatment
of flight personnel, monosialoganglioside (GM1) has been found to
reduce deficits and enhance repair following CNS injury. A survey of
experimental evidence concerning the effects of GM1 in the acute phase
of CNS injury supports its proposed application for aerospace
medicine.
Refs: 20
CAS Registry #: 37758-47-7
CU: 90
UI: 90179654
EM: 9006
Database: Comprehensive MEDLINE with FullTEXT with MeSH
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the OMIKK account, user s1089547.main.emed. Neither EBSCO or OMIKK are
responsible for the content of this e-mail.
_________________________________________________________________
Record: 29
Author(s): Pirozzi L
Title: [Aeromedical problems in cranio-vertebral injuries]
Transliterated Title: Problemi aeromedicinei traumatismi
cranio-vertebrali
Language: ITA
Source: Minerva Med; 1975 Mar 10. Vol 66 Issue 18 P 869-78
CY: ITALY
ISSN: 0026-4806
Pub Type: JOURNAL ARTICLE
Journal Code: N6M
Journal Subset: M
MeSH Heading: Aerospace Medicine:*. Brain Injuries:*. Skull
Fractures:*. Spinal Injuries:*. Wounds and Injuries:DI/*TH. Accidents,
Aviation. Engraving and Engravings. Fractures.
Check Tag(s): Human
Abstract: Impact between the brain and the cristae of the base
normally results as a consequence of inertia when an obstacle is hit,
followed by contusion, or intra-, sub- or extradural haematoma. The
skull itself may be briken (usually at the interpilasters or the weak
points of the pilasters) or dented. Denting resulted in the depression
of a circular fragments or fragments, with compression of the dura
mater or brain; this, in turn, may be contused, lacerated or even
crushed. Spinal crash fractures usually involve the lumbar region.
Neck fractures are rare. The picture may be one of clinical silence
(local pain) or marked neurological involvement. Damage to the cord is
expressed in the form of shock, complete flaccid para- or tetraplegia,
complete loss of sensation below the lesion, loss of deep and
superficial reflexes, urinary retention and rectal incontinence.
Treatment is rendered complicated by profuse scalp haemorrhages,
respiratory insufficiency requiring orotracheal intubation and
assisted respiration, convulsions, which should be handled with care,
since ordinary anti-epilepsy products may mask the onset of
hypertension and haematoma. Swelling should be reduced with
cortisones. Diuretics may be too brusque and lead to intracerebral
haematoma. In the case of spinal injuries, particular care should be
excercised in shifting the patient and conveying him to hospital.
Where high neck lesions are suspected, the possibility of damage to
the originating segments of the phrenic nerve must be borne in mind.
UI: 75138420
EM: 7508
Database: Comprehensive MEDLINE with FullTEXT with MeSH
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responsible for the content of this e-mail.
_________________________________________________________________
Record: 31
Author(s): Reinhardt RF; Clarke NB
Title: Aviation psychiatry and the Navy special board of flight
surgeons.
Language: ENG
Source: Int Psychiatry Clin; 1967 Winter. Vol 4 Issue 1 P 121-31
CY: UNITED STATES
ISSN: 0020-8426
Pub Type: JOURNAL ARTICLE
Journal Code: GU1
Journal Subset: M
MeSH Heading: Aerospace Medicine:*. Mental Disorders:*EP. Military
Psychiatry:*. Naval Medicine:*. Adult. Brain Damage, Chronic:EP.
Hysteria. Paranoid Disorders:EP. Phobic Disorders. Schizophrenia:EP.
Syncope:EP. Tic Disorders. Vision Disorders:EP.
Check Tag(s): Human; Male
CU: 97
UI: 67219050
EM: 6711
Database: Comprehensive MEDLINE with FullTEXT with MeSH
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the OMIKK account, user s1089547.main.emed. Neither EBSCO or OMIKK are
responsible for the content of this e-mail.
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