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15

Hearing Loss in Singers

and Other Musicians

Robert Thayer Sataloff, Joseph Sataloff, and Brian McGovern

Singers and other musicians depend on good hearing

to match pitch, monitor vocal quality, and provide

feedback and direction for adjustments during

perfor-mance The importance of good hearing among

per-forming artists has been underappreciated Although

well-trained musicians are usually careful to protect

their voices or hands, they may subject their ears to

unnecessary damage and thereby threaten their

musi-cal careers The ear is a critimusi-cal part of the musician’s

“instrument.” Consequently, it is important for

sing-ers to undsing-erstand how the ear works, how to take care

of it, what can go wrong with it, and how to avoid

hearing loss from preventable injury

Causes of Hearing Loss

The classification and causes of hearing loss have

been described in detail in standard textbooks of

otolaryngology and previous works by the authors,1,2

and they will be reviewed only briefly in this

chap-ter Hearing loss may be hereditary or nonhereditary,

and either form may be congenital (present at birth)

or acquired There is a common misconception that

hereditary hearing loss implies the presence of the

problem at birth or during childhood In fact, most

hereditary hearing loss occurs later in life All

oto-laryngologists know families whose members begin

to lose their hearing in their third, fourth, or fifth

decade, for example Otosclerosis, a common cause

of correctable hearing loss, often presents when

peo-ple are in their 20s or 30s Similarly, the presence of

deafness at birth does not necessarily imply

heredi-tary or genetic factors A child whose mother had

rubella during the first trimester of pregnancy or was exposed to radiation early in pregnancy may be born with a hearing loss This is not of genetic etiology and has no predictive value for the hearing of the child’s siblings or future children Hearing loss may occur because of problems in any portion of the ear, the nerve between the ear and the brain, or the brain Understanding hearing loss requires a basic knowl-edge of the structure of the human ear

Anatomy and Physiology of the Ear

The ear is divided into 3 major anatomical divisions: the outer ear, the middle ear, and the inner ear.The outer ear has 2 parts: (1) the trumpet-shaped

apparatus on the side of the head, the auricle or pinna,

and (2) the tube leading from the auricle into the

tem-poral bone, the external auditory canal The opening of the tube is called the meatus.

The middle ear is a small cavity in the temporal bone

in which 3 auditory ossicles, the malleus (hammer), incus (anvil), and stapes (stirrup), form a bony bridge

from the external ear to the inner ear (Figure 15–1) This bony bridge is held in place by muscles and liga-

ments The tympanic membrane or eardrum stretches

across the inner end of the external ear canal, rating the outer ear from the middle ear The middle-ear chamber normally is filled with air and connects

sepa-to the nasopharynx through the eustachian tube The

eustachian tube helps to equalize pressure on both sides of the eardrum

The inner ear is a fluid-filled chamber divided into

2 parts: (1) the vestibular labyrinth, which functions

as part of the body’s balance mechanism, and (2) the

cochlea, which contains thousands of minute, sensory,

hairlike cells (Figure 15–2) responsible for beginning

the electrical stimulation to the brain The organ of

Corti functions as the switchboard for the auditory

system The eighth cranial (acoustic) nerve leads

from the inner ear to the brain, serving as the

path-way for the electrical impulses that the brain will

interpret as sound

Sound begins from a source that creates vibrations

or sound waves in the air somewhat similar to the

waves created when a stone is thrown into a pond

The pinna collects these sound waves and funnels

them down the external ear canal to the eardrum The

sound waves then cause the eardrum to vibrate

These vibrations are transmitted through the middle

ear over the bony bridge or ossicular chain formed by

the malleus, incus, and stapes The vibrations in turn

cause the membranes over the openings to the inner

ear to vibrate, causing the fluid in the inner ear to be

set in motion The motion of the fluid in the inner ear

displaces the hair cells, which in turn excite the nerve

cells in the organ of Corti, producing electrochemical

impulses that are transmitted to the brain along the

acoustic nerve As the impulses reach the brain, we

experience the sensation of hearing

Establishing the Site of Damage

in the Auditory System

The cause of a hearing loss, like that of any other ical condition, is determined by obtaining a detailed history, making a thorough physical examination, and performing various clinical and laboratory tests

med-An audiogram provides a “map” of hearing and details the levels at which sound is detected at vari-ous frequencies When a hearing loss is identified, an attempt is made to localize the point along the audi-tory pathway where the difficulty has originated Every attempt to determine whether the patient’s hearing loss is conductive, sensorineural, central, functional, or a mixture of these is made However, sometimes these distinctions can be difficult to make

In particular, it is very difficult to distinguish sensory from neural lesions

Details of the otologic history, physical examination, and test protocols are detailed in many otolaryngol-ogy texts Medical evaluation of a patient with a sus-pected hearing problem includes a comprehensive history; complete physical examination of the ears, nose, throat, head, and neck; assessment of the cranial nerves, including testing the sensation in the external auditory canal (Hitselberger sign); audiogram (hear-

Figure 15–1 Cross section of the ear The semicircular canals are part of the balance

system.

Figure 15–2 Cross-section of the organ of Corti A Low magnification B Higher magnification.

ing test); and other tests, as indicated Recommended

additional studies may include computed

tomog-raphy (CT), magnetic resonance imaging (MRI),

dynamic imaging studies such as single-photon

emission computed tomography (SPECT), position

emission tomography (PET), specialized hearing

tests such as brainstem evoked response

audiom-etry (ABR or BERA), electronystagmography (ENG),

computerized dynamic posturography (CDP),

oto-acoustic emissions, immittance measures, central

auditory processing testing, and a variety of blood

tests for the many systemic causes of hearing loss

All patients with hearing complaints deserve a

thor-ough examination and comprehensive evaluation to

determine the specific cause of the problem and to

rule out serious or treatable conditions that may be

responsible for the hearing impairment Contrary to

popular misconceptions, not all cases of

sensorineu-ral hearing loss are incurable So “nerve deafness”

should be assessed with the same systematic vigor

and enthusiasm as conductive hearing loss

Conductive Hearing Loss

In cases of conductive hearing loss, sound waves are

not effectively transmitted to the inner ear as a result

of some mechanical defect in the outer or middle

ear The outer and middle ear normally enhance and

transfer sound energy to the inner ear or cochlea In

a purely conductive hearing loss, there is no damage

to the inner ear or the neural pathway; rather, the

damage lies in the external canal or the middle ear

Patients diagnosed as having conductive hearing

loss have a much better prognosis than those with

sensorineural loss, because modern techniques make

it possible to cure or at least improve the vast majority

of cases in which the damage occurs in the outer or

middle ear Even if they are not improved medically

or surgically, these patients stand to benefit greatly

from a hearing aid, because what they need most is

amplification They are not bothered by distortion

and other hearing abnormalities that may occur in

sensorineural hearing losses

Some more common types of conductive hearing

loss may result from a complete or partial

block-age of the outer ear, which will interfere with sound

transmission to the middle ear Outer ear problems

include birth defects, total occlusion of the external

auditory canal by wax, foreign body (eg, a piece of

cotton swab or ear plug), infection, trauma, or tumor

Large perforations in the tympanic membrane may

also cause hearing loss, especially if they surround

the malleus However, relatively small, central

per-forations usually do not cause a great deal of hearing impairment Hearing loss from middle ear dysfunc-tion is the most common cause of conductive hear-ing loss and may cause a hearing decrease of up to

60 decibels It may occur in many ways The dle ear may become filled with fluid because of eustachian tube dysfunction The fluid restricts free movement of the tympanic membrane and ossicles, thereby producing hearing loss Middle-ear conduc-tive hearing loss may also be caused by ossicular abnormalities These include fractures, erosion from disease, impingement by tumors, congenital malfor-mations, and other causes However, otosclerosis is among the most common This hereditary disease afflicts the stapes and prevents it from moving in its normal piston-like fashion in the oval window Hear-ing loss from otosclerosis can be corrected through stapes surgery, a brief operation under local anesthe-sia, and it is usually possible to restore hearing

mid-Sensorineural Hearing Loss

The word sensorineural was introduced to replace the ambiguous terms perceptive deafness and nerve deaf- ness The term sensory hearing loss is applied when

the damage is localized to the inner ear and auditory nerve The cochlea has approximately 15 000 hearing nerve endings (hair cells) Those hair cells, and the nerve that connects them to the brain, are susceptible

to damage from a variety of causes Neural hearing loss

is the correct term to use when the damage is in the auditory nerve proper, anywhere between its fibers

at the base of the hair cells and the auditory nuclei This range includes the bipolar ganglion of the eighth cranial nerve Other common names for this type of

loss are nerve deafness and retrocochlear hearing loss

These names are useful if applied appropriately and meaningfully, but too often they are used improperly.Although at present it is common practice to group together both sensory and neural components, it has become possible through advanced diagnostic tech-niques to attribute a predominant part of the dam-age, if not all of it, to either the inner ear or the nerve This separation is advisable because the prognosis and the treatment of the 2 kinds of impairment differ For example, in all cases of unilateral sensorineural hearing loss, it is important to distinguish between a sensory and neural hearing impairment, because the

neural type may be due to a tumor called an acoustic neuroma, which could become life-threatening if left

untreated Cases that we cannot identify as either sensory or neural and cases in which there is damage

in both regions we classify as sensorineural.

There are various and complex causes of

sensori-neural hearing loss, but certain features are

charac-teristic and basic to all of them Because the histories

obtained from patients are so diverse, they contribute

more insight into the etiology than into the

classifi-cation of a cause Sensorineural hearing loss often

involves not only loss of loudness but also loss of

clar-ity The hair cells in the inner ear are responsible for

analyzing auditory input and instantaneously coding

it The auditory nerve is responsible for carrying this

complex coded information Neural defects such as

acoustic neuromas (benign tumors of the auditory

nerve) are frequently accompanied by severe

dif-ficulties in discriminating sounds and words

effec-tively, although the actual hearing threshold for

differences in sounds may not be greatly affected

Sensory deficits in the cochlea are often associated

with distortion of sound quality, distortion of

loud-ness (loudloud-ness recruitment), and distortion of pitch

(diplacusis) Diplacusis poses particular problems

for musicians, because it may make it difficult for

them to tell whether they are playing or singing

cor-rect pitches This symptom is also troublesome to

conductors Keyboard players and other musicians

whose instruments do not require critical tuning

adjustments compensate for this problem better than

singers, string players, and the like In addition,

sen-sorineural hearing loss may be accompanied by

tin-nitus (noises in the ear) and/or vertigo However, it

is possible to have these auditory symptoms and not

demonstrate a hearing loss on a routine audiogram

Hearing loss may be present at frequencies between

or above those usually tested and can be detected

with special audiometers that test all (or nearly all)

of the frequencies from 125 to 12 000 Hz Special

ultrahigh-frequency audiometers are available

com-mercially and can measure hearing thresholds up to

20 000 Hz An evaluation of this hearing range can

show damage that could not be detected at routinely

tested frequencies

Sensorineural hearing loss may be due to a great

number of conditions, including exposure to ototoxic

drugs (including a number of antibiotics, diuretics,

and chemotherapy agents), hereditary conditions,

systemic diseases, trauma, and noise, among other

causes Most physicians recognize that hearing loss

may be associated with a large number of hereditary

syndromes2,3 involving the eyes, kidneys, heart, or

any other body system; but many are not aware that

hearing loss also accompanies many, very common

systemic diseases Naturally, these occur in

musi-cians as well as others The presence of these systemic

illnesses should lead physicians to inquire about

hearing and to perform audiometry in selected cases Problems implicated in hearing impairment include

Rh incompatibility, hypoxia, jaundice, rubella, mumps, rubeola, fungal infections, meningitis, tuberculosis, sarcoidosis, Wegener granulomatosis, vasculitis, his-tiocytosis X, allergy, hyperlipoproteinemia, syphilis, hypothyroidism, hypoadrenalism, hypopituitarism, renal failure, autoimmune disease, coagulopathies, aneurysms, vascular disease, multiple sclerosis, infesta-tions, diabetes, hypoglycemia, cleft palate, and others.2

Prolonged exposure to very loud noise is a mon cause of hearing loss in our society Noise-induced hearing loss is seen most frequently in heavy industry However, occupational hearing loss caused

com-by musical instruments is a special problem, as cussed below

dis-Mixed Hearing Loss

For practical purposes, a mixed hearing loss should be

understood to mean a conductive hearing loss panied by a sensory, neural (or a sensorineural) loss

accom-in the same ear However, the claccom-inical emphasis is

on the conductive hearing loss, because available therapy is so much more effective for this disorder Consequently, the otologic surgeon has a special interest in cases of mixed hearing loss in which there

is primarily a conductive loss complicated by some sensorineural damage In a musician, curing the correctable component may be sufficient to convert hearing from unserviceable to satisfactory for perfor-mance purposes

Functional Hearing Loss

Functional hearing loss occurs as a condition in which the patient does not seem to hear or to respond, yet the handicap is not caused by any organic pathol-ogy in the peripheral or central auditory pathways The hearing difficulty may have an entirely psycho-logical etiology, or it may be superimposed on some mild organic hearing loss, in which case it is called a

functional or a psychogenic overlay Often, the patient

has normal hearing, but the secondary gain from a hearing loss, even if it is not organic, motivates the patient to behave as though he or she has a legitimate hearing loss In some cases, the patient may not even realize that the loss is nonorganic A careful history usually will reveal some hearing impairment in the patient’s family or some personally meaningful ref-erence to deafness that generated the patient’s psy-chogenic hearing loss The important challenge for the clinician in such a case is to classify the condition

properly, so that effective treatment can be initiated

Functional hearing loss occurs not only in adults, but

also in children This diagnosis should be considered

whenever hearing problems arise in musicians under

great pressure regardless of age, including young

prodigies

Central Hearing Loss (Central Dysacusis)

In central hearing loss, the damage is situated in the

central nervous system at some point in the brain

between the auditory nuclei (in the medulla

oblon-gata) and the cortex Formerly, central hearing loss

was described as a type of “perceptive deafness,” a

term now obsolete

Although information and research about central

hearing loss has developed, it remains complex and

unclear Physicians know that some patients cannot

interpret or understand what is being said and that

the cause of the difficulty is not in the peripheral

mechanism but somewhere in the central nervous

system In central hearing loss, the problem is not a

lowered pure-tone threshold but the patient’s

abil-ity to interpret what he or she hears Obviously, it

is a more complex task to interpret speech than to

respond to a pure-tone threshold; consequently, the

tests necessary to diagnose central hearing

impair-ment must be designed to assess a patient’s ability to

handle complex information

Psychological Consequences

of Hearing Loss

Performing artists are frequently sensitive,

some-what “high-strung” people who depend on

physi-cal perfection in order to practice their crafts and

earn their livelihoods Any physical impairment that

threatens their ability to continue as musicians may

be greeted with dread, denial, panic, depression, or

similar responses, which may be perceived as

exag-gerated, especially by physicians who do not

special-ize in caring for performers In the case of hearing

loss, such reactions are common even in the general

public Consequently, it is not surprising that

psycho-logical concomitants of hearing loss in musicians are

seen in nearly all cases

Many successful performers are communicative

and gregarious and anything that impairs their

abil-ity to interact in their usual manner can be

problem-atic Their vocational hearing demands are much

greater than those required in most professions, and

often musicians’ normal reactions to hearing loss

are amplified by legitimate fears about interruption

of their artistic and professional futures The lems involved in accurately assessing the disability associated with such impairments are addressed below in the discussion of occupational hearing loss

prob-in musicians

Occupational Hearing Loss

Performing artists are required to accurately match frequencies over a broad range, including frequen-cies above those required for speech comprehension Even mild pitch distortion (diplacusis) may make it difficult or impossible for musicians to play or sing in tune Elevated high-frequency thresholds may lead

to excessively loud playing at higher pitches and to

an artistically unacceptable performance, which may end the career of a violinist or conductor, for example

It is extremely important for singers and other cians to be protected from hearing loss However, the musical performance environment poses not only critical hearing demands, but also noise hazards Review of the literature reveals convincing evidence that music-induced hearing loss occurs, but there is

musi-a clemusi-ar need for ongoing resemusi-arch to clmusi-arify incidence, predisposing factors, and methods of prevention It

is interesting to note that, in direct contrast to many other publications, Johnson and Sherman evaluated

60 orchestra members and 30 nonmusicians from 250

to 20 000 Hz and found no substantive differences.4

This study suggested that there is no additional risk

to hearing as a result of exposure to orchestral music Similarly, Schmidt and colleagues showed that the students of Rotterdam Conservatory did not show any decreased hearing loss when compared to a group of medical students of the same age, despite the music students’ exposure to music.5

As mentioned previously, noise exposure can cause both temporary and/or permanent hearing loss In a study to evaluate temporary threshold shift

in performers and listeners, Axelsson and Lindgren determined that the performers showed less of a shift than the audience did.6 It was surmised by the authors that this may be explained by pre-exposure hearing levels The performers had poorer hearing levels than listeners did before being exposed to the study noise Another interesting finding was that the male listeners showed more of a temporary shift than the females The authors suggested that exposure to live pop music should be limited to 100 dBA or less for no more than 2 hours When symphony orches-tra musicians from the Royal Danish Theater were studied, Ostri et al found that 58% of the 95 subjects demonstrated a hearing loss when using 20 dB HL

as the “normal” cutoff value The male subjects were

more affected by noise exposure than the female

sub-jects.7 The authors concluded that symphonic music

does indeed cause hearing loss In 2014, Schmidt

et al8 studied the hearing levels of 182 professional

symphony orchestra musicians with varying degrees

of exposure time and intensity For most of the

musi-cians tested, the level of hearing loss was less than

expected based on the 1999 International

Organiza-tion for StandardizaOrganiza-tion’s measure for predicting

permanent threshold shifts based on duration and

intensity of noise exposure.9 Although the level of

hearing loss was generally less than predicted, they

found that the ears with the highest exposure (above

90.4 dBA and a mean exposure time of 41.7 years)

had an additional threshold shift of 6.3 dB compared

to musicians with the lowest exposure In 1992,

McBride et al set out to determine whether noise

exposure affected the classical musician.10 Contrary

to other studies, audiograms showed no significant

differences between participants of the same sex and

age They did prove that the musicians were exposed

to high doses of noise, which do pose an occupational

hazard Drake-Lee studied 4 heavy-metal musicians

before and after performance.11 It was determined

that exposure does cause a temporary threshold shift

with a maximum effect at lower frequencies An

arti-cle by Bu in 1992, examined hearing loss in Chinese

opera orchestra musicians.12 Bu discovered that the

incidence of hearing loss in this group was

exceed-ingly high and apparently associated with the types

of instruments used.12 Bu has suggested measures

to combat the noise exposure other than the use of

ear protectors, such as percussion musicians seated 1

meter lower than the other musicians in order to

bet-ter preserve hearing of the instrumentalists around

them.12 However, such suggestions have a variety of

drawbacks and practical limitations

Occupational hearing loss is usually bilateral,

fairly symmetrical, sensorineural hearing impairment

caused by exposure to high-intensity workplace noise

or music This subject has been discussed in this text,

and specifically with regard to musicians in a

previ-ous review, in general in detail elsewhere.13 Music is

one of the professions that can produce a somewhat

asymmetrical hearing loss in selected cases

It has been well established that selected

sym-phony orchestra instruments, popular orchestras,

rock bands, and personal stereo headphones

pro-duce sound pressure levels (SPL) intense enough

to cause both temporary and permanent hearing

loss Such hearing loss may also be accompanied

by tinnitus and may be severe enough to interfere

with performance, especially in violinists The

vio-lin is the highest-pitched string instrument in tine use The amount of hearing loss is related to the intensity of the noise, duration and intermittency

rou-of exposure, total exposure time over months and years, and other factors Rosanowski and Eysholdt published a case study on a violinist with bilateral tinnitus.14 They recorded peak sound pressure levels

of over 90 dB The violinist showed a 20-dB drop in hearing between 2 and 8 kHz on the side with which the violin rests (left) This phenomenon (asymmetry)

is produced by the head shadow, the same nism that causes asymmetrical hearing loss in rifle shooters The authors point out the potential hazard

mecha-of other auditory symptoms (ie, tinnitus) as a result

of noise exposure In their 1999 study of hearing, nitus, and exposure to amplified recreational noise, Metternich and Brusis found a very high risk of tin-nitus even when subjects were exposed to short dura-tions of amplified music.15 This risk appears to be greater than the risk of permanent hearing loss from the same exposure

tin-Various methods have been devised to help protect the hearing of performers For example, many sing-ers and other musicians (especially in rock bands) wear ear protectors They may not feel comfortable wearing ear protection during a performance but may take precautionary measures during practice Ear protectors have changed tremendously over the years, and there are more sophisticated and suitable models available now that cater to the musician The importance of using new, more appropriate ear pro-tectors for professional musicians should be stressed, especially because the previously unappreciated relationship between orchestral music exposure and noise-induced hearing loss has become clear In their 1983 publication, “The Hearing of Symphony Orchestra Musicians,” Karlsson et al determined that the criteria used to evaluate noise exposure in indus-try must be different from the criteria used to assess acoustic instrument levels in symphonic music.16

This complex issue is discussed later in this chapter Singers need to be made more aware of the hazards

of noise exposure and find ways to avoid or reduce its effects whenever possible They should also be careful to avoid exposure to potentially damaging avocational noise such as loud music through head-phones, chainsaws, snowmobiles, gunfire, motorcy-cles, and power tools Hoppmann has reviewed the hazards of being an instrumental musician, including hearing loss, and he emphasizes the need for a team approach to comprehensive arts-medicine diagnosis and care.17 Noise exposure has a cumulative effect, and exposure to these other types of noise just com-pounds the damage to a performer In his article

entitled, “Binaural hearing in music performance,”

Donald Woolford evaluated the effects of hearing

impairment on performance and found no direct

cor-relation between degree of hearing impairment and

level of performance.18

Clinical observations in the authors’ practice

sug-gest that the rock performance environment may be

another source of asymmetrical noise-induced

hear-ing loss, a relatively unusual situation because most

occupational hearing loss is symmetrical Rock

sing-ers and instrumentalists tend to have slightly greater

hearing loss in the ear adjacent to the drum and

cym-bal, or the side immediately next to a speaker, if it is

placed slightly behind the musician Various

meth-ods have been devised to help protect the hearing

of rock musicians For example, most of them stand

beside or behind their speakers, rather than in front

of them In this way, they are not subjected to peak

intensities, as are the patrons in the first rows

The problem of occupational hearing loss among

classical singers and other musicians is less

obvi-ous but equally important In fact, in the United

States, it has become a matter of great concern and

negotiation among unions and management

Vari-ous reports have found an increased incidence of

high-frequency sensorineural hearing loss among

professional orchestra musicians as compared to the

general public, and sound levels within orchestras

have been measured between 83 and 112 dBA, as

discussed below The size of the orchestra and the

rehearsal hall are important factors, as is the

posi-tion of the individual instrumentalist within the

orchestra Players seated immediately in front of the

brass section appear to have particular problems,

for example Individual classical instruments may

produce more noise exposure for their players than

assumed In their study entitled “Hearing

assess-ment of orchestral musicians,” Kahari et al reported

that male musicians have a more pronounced

high-frequency hearing loss than females exposed to the

same musical noise.19 They also noted that

percus-sion and woodwind players demonstrated a slightly

more pronounced hearing loss than musicians of

large string instruments

Because many singers and instrumentalists

prac-tice or perform 4 to 8 hours a day (sometimes more),

such exposure levels may be significant An

interest-ing review of the literature may be found in the report

of a clinical research project on hearing in classical

musicians by Axelsson and Lindgren.20 They also

found asymmetrical hearing loss in classical

musi-cians, greater in the left ear This is a common

find-ing, especially among violinists A brief summary of

most of the published works on hearing loss in cians is presented below

musi-In the United States, various attempts have been made to solve some of the problems of the orches-tra musician, including placement of Plexiglas barri-ers in front of some of the louder brass instruments; alteration in the orchestra formation, such as eleva-tion of sections or rotational seating; changes in spacing and height between players; use of special-ized musicians, ear protectors; and other measures These solutions have not been proven effective, and some of them appear impractical, or damaging to the performance The effects of the acoustic environ-ment (concert hall, auditorium, outdoor stage, etc)

on the ability of music to damage hearing have not been studied systematically Recently, popular musi-cians have begun to recognize the importance of this problem and to protect themselves and educate their fans Some performers are wearing ear protectors regularly in rehearsal and even during performance,

as noted in the press in 1989.21 In a 5-year study of the health of 377 professional orchestra musicians, Ackermann et al reported that 64% of the musicians who responded to the survey used earplugs at least intermittently They also highlighted the need for hearing protection by reporting that “For average reported practice durations (2.1 hour per day, 5 days

a week), 53% would exceed accepted permissible daily noise exposure in solitary practice, in addition

to sound exposure during orchestral rehearsals and performance.”22(p8) Considerable additional study is needed to provide proper answers and clinical guid-ance for this very important occupational problem

In fact, a review of the literature on occupational hearing loss reveals that surprisingly little informa-tion is available on the entire subject Moreover, all

of it is concerned with instrumentalists; few similar studies in singers were found In 2008, Hamdan et

al recorded the transient-evoked otoacoustic sions (TEOAEs) of 23 normal hearing singers and found them to be less robust than those of the control group These results suggest subtle cochlear dysfunc-tion possibly resulting from increased noise exposure during practice and performance The authors pro-pose using TEOAE measurement as a tool to identify ears as “at risk for music-induced hearing loss.”23

emis-Study of the existing reports reveals a variety of approaches Unfortunately, neither the results nor the quality of the studies is consistent Nevertheless, familiarity with the research already performed pro-vides useful insights into the problem In 1960, Arnold and Miskolczy-Fodor studied the hearing of 30 pia-nists SPL measurements showed that average levels

were approximately 85 dB SPL, although periods of

92 to 96 dB SPL were recorded.24 The A-weighting

network was not used for sound level measurements

in this study No noise-induced hearing loss was

iden-tified The pianists in this study were 60 to 80 years of

age; and, in fact, their hearing was better than normal

for their age Flach and Aschoff,25 and later Flach,26

found sensorineural hearing loss in 16% of 506 music

students and professional musicians, a higher

per-centage than could be accounted for by age alone,

although none of the cases of hearing loss occurred

in students Hearing loss was most common in

musi-cians playing string instruments Flach and Aschoff

also noticed asymmetrical sensorineural hearing loss

worse on the left in 10 of 11 cases of bilateral

sensori-neural hearing loss in instrumentalists.25 In one case

(a flautist), the hearing was worse on the right In

4% of the professional musicians tested, hearing loss

was felt to be causally related to musical noise

expo-sure Histories and physical examinations were

per-formed on the musicians, and tests were perper-formed

in a controlled environment This study also included

interesting measurements of sound levels in a

profes-sional orchestra Unfortunately, they are reported in

DIN-PHONS, rather than dBA

In 1968, Berghoff 27 reported on the hearing of 35

big band musicians and 30 broadcasting (studio)

musicians Most had performed for 15 to 25 years,

although the string players were older as a group and

had performed for as many as 35 years In general,

they played approximately 5 hours per day

Hear-ing loss was found in 40- to 60-year-old musicians

at 8000 and 10 000 Hz Eight musicians had

sub-stantial hearing loss, especially at 4000 Hz Five out

of 64 (8%) cases were felt to be causally related to

noise exposure No difference was found between

left and right ears, but hearing loss was most

com-mon in musicians who were sitting immediately

beside drums, trumpets, or bassoons Sound level

measurements for wind instruments revealed that

intensities were greater 1 meter away from the

instru-ment than they were at the ear canal Unfortunately,

sound levels were measured in PHONS Lebo and

Oliphant studied the sound levels of a symphony

orchestra and two rock-and-roll orchestras.28 They

reported that sound energy for symphony orchestras

is fairly evenly distributed from 500 to 4000 Hz, but

most of the energy in rock-and-roll music was found

between 250 and 500 Hz The SPL for the symphony

orchestra during loud passages was approximately

90 dBA For rock-and-roll bands, it reached levels

in excess of 110 dBA Most of the time, during rock

music performance, sound energy was louder than

95 dBA in the lower frequencies; symphony tras rarely achieved such levels However, Lebo and Oliphant made their measurements from the audi-torium, rather than in immediate proximity to the performers.28 Consequently, their measurements are more indicative of distant audience noise exposure than that of the musicians or audience members in the first row In 2008, O’Brien, Wilson, and Bradley29

orches-studied orchestral SPLs They found the musicians

at the greatest risk of sustained noise exposure to

be the principal trumpeter, first and third hornists, and principal trombonist They also noted the high-est peak SPLs in the percussion and timpani sec-tions Rintelmann and Borus studied noise-induced hearing loss in rock-and-roll musicians, measuring SPL at various distances from 5 to 60 ft from center stage.30 They studied 6 different rock-and-roll groups

in 4 locations and measured a mean SPL of 105 dB Their analysis revealed that the acoustic spectrum was fairly flat in the low- and mid-frequency region and showed gradual reduction above 2000 Hz They also detected hearing loss in only 5% of the 42 high school and college student rock-and-roll musicians they studied The authors estimated that their exper-imental group had been exposed to approximately

105 dB (SPL) for an average of 11.4 hours a week for 2.9 years

In 1970, Jerger and Jerger studied temporary threshold shifts (TTSs) in rock-and-roll musicians.31

They identified TTSs greater than 15 dB in at least one frequency between 2000 and 8000 Hz in 8 of 9 musi-cians studied prior to performance and within 1 hour after the performance Speaks and coworkers32 exam-ined 25 rock musicians for threshold shifts, obtaining measures between 20 and 40 minutes following per-formance In this study, shifts of only 7 to 8 dB at 4000 and 6000 Hz were identified TTSs occurred in about half of the musicians studied Six of the 25 musicians had permanent threshold shifts Noise measurements were also made in 10 rock bands Speaks et al found noise levels from 90 to 110 dBA Most sessions were less than 4 hours, and actual music time was gener-ally 120 to 150 minutes The investigators recognized the hazard to hearing posed by this noise exposure

In 1972, Rintelmann, Lindberg, and Smitley studied the effects of rock-and-roll music on humans under laboratory conditions.33 They exposed normal hear-ing females to rock-and-roll music at 110 dB SPL in a sound field They also compared subjects exposed to music played continuously for 60 minutes with others

in which the same music was interrupted by 1 ute of ambient noise between each 3-minute musical selection At 4000 Hz, they detected mean TTSs of

min-26 dB in the subjects exposed to continuous noise, and

22.5 dB in those exposed intermittently Both groups

required approximately the same amount of time for

recovery TTSs sufficient to be considered potentially

hazardous for hearing occurred in slightly over 50%

of the subjects exposed to intermittent noise and in

80% of subjects subjected to continuous noise

A study by Samelli et al34 in 2012, compared

dif-ferent areas of the auditory pathway of professional

pop/rock musicians with that of nonmusicians The

participants included 16 young male pop/rock

musi-cians who had been performing for at least 5 years,

and a group of age-matched peers Although the

researchers found damage to the peripheral auditory

system evidenced by higher pure-tone thresholds and

smaller TEOAE amplitudes, they found no damage to

the central auditory nervous system The researchers

assessed the central auditory system using auditory

brainstem response (ABR) testing Both groups were

within the normal range However, the group of pop/

rock musicians had earlier neural responses to the

acoustic stimuli, suggesting better or faster

process-ing of acoustic information Samelli et al attribute this

to musical training providing improved processing

of acoustic information and improved spontaneous

attention to sound While their speculation might be

correct, the findings also could be explained by mild

hyperacusis associated with noise-induced

senso-rineural impairment Alternatively, it might be that

their superior hearing performance was present from

birth and predisposed them to choose careers as

musi-cians The findings also could be irrelevant clinically

In 1972, Jahto and Hellmann35 studied 63

orches-tra musicians playing in contemporary dance bands

Approximately one-third of their subjects had

mea-surable hearing loss, and 13% had bilateral

high-frequency loss suggestive of noise-induced hearing

damage They also measured peak SPL of 110 dB

(the A scale was not used) They detected potentially

damaging levels produced by trumpets, bassoons,

saxophones, and percussion instruments In contrast,

in 1974, Buhlert and Kuhl36 found no noise-induced

hearing loss among 17 performers in a radio

broad-casting orchestra The musicians had played for an

average of 20 years and were an average of 30 years

of age In a later study, Kuhl37 studied members of

a radio broadcasting dance orchestra over a period

of 12 days The average noise exposure was 82 dBA

He concluded that such symphony orchestras were

exposed to safe noise levels, in disagreement with

Jahto and Hellmann.35 Zeleny et al studied members

of a large string orchestra with intensities reaching

104 to 112 dB SPL.38 Hearing loss greater than 20 dB

in at least one frequency occurred in 85 of 118 subjects

(72%), usually in the higher frequencies Speech quencies were affected in 6 people (5%) Conversely,

fre-in 2007, Reuter and Hameroshoi39 found no evidence

of TTSs or changes in otoacoustic emissions for 12 normal hearing symphony orchestra musicians, both before and after rehearsals

In 1976, Siroky et al reported noise levels within

a symphony orchestra ranging between 87 and 98 dBA, with a mean value of 92 dBA.40 Audiometric evaluation of 76 members of the orchestra revealed

16 musicians with hearing loss, 13 of them rineural Hearing loss was found in 7.3% of string players, 20% of wind players, and 28% of brass play-ers All percussionists had some degree of hearing loss Hearing loss was not found in players who had performed for fewer than 10 years but was present

senso-in 42% of players who had performed for more than

20 years This study needs to be reevaluated in sideration of age-matched controls At least some of the individuals reported have hearing loss not caus-ally related to noise (eg, those with hearing levels of

con-100 dB HL in the higher frequencies) In a ion report, Folprechtova and Miksovska also found mean sound levels of 92 dBA in a symphony orches-tra with a range of 87 to 98 dBA.41 They reported that most of the musicians performed between 4 and 8 hours daily They reported the sound levels of vari-ous instruments as seen in Table 15–1

compan-A study by Balazs and Gotze, also in 1976, agreed that classical musicians are exposed to potentially damaging noise levels.42 The findings of Gryczynska and Czyzewski supported the concerns raised by other authors.43 In 1977, they found bilateral normal

Table 15–1 Sound Levels of Various Instruments

Instrument Sound Level (dBA)

hearing in only 16 of 51 symphony orchestra

musi-cians who worked daily at sound levels between 85

and 108 dBA Five of the musicians had unilateral

normal hearing; the rest had bilateral hearing loss

In 2009, a team of researchers from the University

of Sydney began a large-scale comprehensive health

study of 377 professional orchestra musicians The

Sound Practice Project evaluated the health of

musi-cians from 8 professional orchestras over a 5-year

period Although the focus was on physical and

psy-chological impacts of the profession, they found that

the majority of subjects were exposed to noise that

exceeded daily acceptable levels.22

In 1977, Axelsson and Lindgren studied factors

increasing the risk for hearing loss in pop

musi-cians.44 They reported that aging, length of exposure

per musical session, long exposure time in years,

military service, and listening to pop music with

headphones all had a statistically significant

influ-ence on hearing They noted that the risk and severity

of hearing loss increase with increasing duration of

noise exposure and increasing sound levels In pop

music, the exposure to high sound levels was felt to

be limited in time, and less damaging low

frequen-cies predominated

Also in 1977, Axelsson and Lindgren published an

interesting study of 83 pop musicians and noted a

significant incidence of hearing loss.45 They

reana-lyzed previous reports investigating a total of 160

pop musicians, which identified an incidence of only

5% hearing loss In their 1978 study, Axelsson and

Lindgren tested 69 musicians, 4 disk jockeys, 4

man-agers, and 6 sound engineers.46 To have hearing loss,

a subject had to have at least 1 pure-tone threshold

exceeding 20 dB HL at any frequency between 3000

and 8000 Hz Thirty-eight musicians were found to

have sensorineural hearing loss In 11, only the right

ear was affected; in 5, only the left ear was affected

Thirteen cases were excluded because their hearing

loss could be explained by causes other than noise

Thus, 25% of the pop musicians had

sensorineu-ral hearing loss probably attributable to noise The

most commonly impaired frequency was 6000 Hz,

and very few ears showed hearing levels worse than

35 dB HL After correction for age and other factors,

25 (30%) had hearing loss as defined above Eleven

(13%) had hearing loss defined as a pure-tone

audio-metric average greater than 20 dB HL at 3000, 4000,

6000, and 8000 kHz in at least one ear Of these 11,

7 (8%) had unilateral hearing loss The authors

con-cluded that it seemed unlikely that sensorineural

hearing loss would result from popular music

pre-sented at 95 dBA with interruptions and with

rela-tively short exposure durations and low-frequency

emphasis Axelsson and Lindgren published ther articles on the same study.47,48 They also noted that TTS measurements in pop music environments showed less shift in musicians than in the audience They also found that female listeners were more resistant to TTS than males In a follow-up study

fur-to their 1975 work, published in 1977,44,45 Axelsson and Eliasson re-evaluated 53 out of the original 83 pop/rock musicians they had studied.49 Their find-ings indicate a rather slow progression of hearing loss The authors were surprised to find that hear-ing remained so stable and fell within 20 dB of origi-nal thresholds They surmised that this presentation may have something to do with the stapedius reflex, but this theory has yet to be proven In our opinion, this finding is a manifestation of the asymptotic pat-tern seen in noise-induced hearing loss (NIHL) from other sources and is not surprising In a 2001 follow-

up study to a 1979 assessment done by Axelsson and Lindgren (published in 1981),20 Kahari et al re-eval-uated 56 of the original 139 orchestral musicians in Sweden.50 Interestingly, 16 years later, those studies showed no significant decreases in pure-tone thresh-old The male participants continued to demonstrate

a greater hearing loss than the females in the frequency range

high-In 1981, Westmore and Eversden studied a phony orchestra and 34 of its musicians.51 They recorded SPL for 14.4 hours Sound levels exceeded

sym-90 dBA for 3.51 hours and equaled or exceeded

110 dBA for 0.02 hours In addition, there were brief peaks exceeding 120 dBA They interpreted their audiometric testing as showing noise-induced hear-ing loss in 23 of 68 ears Only 4 of the 23 ears had

a hearing loss greater than 20 dB HL at 4000 Hz There was a “clear indication” that orchestral musi-cians may be exposed to damaging noise However, because of the relatively mild severity, they specu-lated that, “it is unlikely that any musician is going

to be prevented from continuing his artistic career.”

In Axelsson and Lindgren’s 1981 study, sound level measurements were performed in 2 theaters, and 139 musicians underwent hearing tests.20 Sound levels for performances ranged from 83 to 92 dBA Sound levels were slightly higher in an orchestra pit, although this

is contrary to the findings of Westmore.51 Fifty-nine musicians (43%) had pure-tone thresholds worse than expected for their ages French hornists, trumpeters, trombonists, and bassoonists were found to be at increased risk for sensorineural hearing loss Asym-metric pure-tone thresholds were common in musi-cians with hearing loss and in those still classified

as having normal hearing The left ear demonstrated greater hearing loss than the right, especially among

violinists Axelsson and Lindgren also found that the

loudness comfort level was unusually high among

musicians Acoustic reflexes also were elicited at

com-paratively high levels, being pathologically increased

in approximately 30% TTSs were also identified,

supporting the assertion of noise-related etiology

Also, in 1983, Lindgren and Axelsson attempted

to determine whether individual differences of TTS

existed after repeated controlled exposure to

nonin-formative noise and to music having equal frequency,

time, and sound level characteristics.52 They studied

10 subjects who were voluntarily exposed to 10

min-utes of recorded pop music on 5 occasions On 5 other

occasions they were exposed to equivalent noise

Four subjects showed almost equal sensitivity in

measurements of TTS, and 6 subjects showed marked

differences, specifically, greater TTS after exposure to

the nonmusic stimulus This research suggests that

factors other than the physical characteristics of the

fatiguing sound contributed to the degree of TTS

The authors hypothesized that these factors might

include the degree of physical fitness, stress, and

emotional attitudes toward the sounds perceived

The authors concluded that high sound levels

per-ceived as noxious cause greater TTS than high sound

levels that the listener perceived as enjoyable

In 1983, Karlsson and coworkers published a

report with findings and conclusions substantially

different from those of Axelsson and others.53

Karls-son et al investigated 417 musicians, 123 of whom

were investigated twice at an interval of 6 years

After excluding 26 musicians who had hearing loss

for reasons other than noise they based their

con-clusions on the remaining 392 cases Karlsson et al

concluded that there was no statistical difference

between the hearing of symphony orchestra

musi-cians and those of a normal population of similar

age and sex.53 Their data revealed a symmetric dip

of 20 dB HL at 6000 Hz in flautists and a 30 dB HL left

high-frequency sloping hearing loss in bass players

Overall, a 5-dB HL difference between ears was also

found at 6000 and 8000 Hz, with the left side being

worse Although Karlsson and coworkers concluded

that performing in a symphonic orchestra does not

involve an increased risk of hearing damage, and that

standard criteria for industrial noise exposure are not

applicable to symphonic music, their data are similar

to previous studies Only their interpretation varies

substantially

In 1984, Woolford studied SPLs in symphony

orchestras and hearing.54 Woolford studied 38

Aus-tralian orchestral musicians and measured SPLs

using appropriate equipment and technique He

found potentially damaging sound levels, consistent with previous studies Eighteen of the 38 musicians had hearing losses Fourteen of those had threshold shifts in the area of 4000 Hz, and 4 had slight losses

at low frequencies only

Johnson et al studied the effects of instrument type and orchestral position on the hearing of orchestra musicians.55 They studied 60 orchestra musicians from 24 to 64 years in age, none of whom had symp-tomatic hearing problems The musicians underwent otologic histories and examinations and pure-tone audiometry from 250 through 20 000 Hz Unfor-tunately, this study used previous data from other authors as control data In addition to the inherent weakness in this design, the comparison data did not include thresholds at 6000 Hz There appeared to be

a 6000-Hz dip in the population studied by Johnson

et al, but no definitive statement could be made The authors concluded that the type of instrument played and the position on the orchestra stage had no signifi-cant correlation with hearing loss, disagreeing with findings of other investigators In another paper pro-duced from the same study,56 Johnson et al reported

no difference in the high-frequency thresholds (9000–

20 000 Hz) between musicians and nonmusicians Again, because he examined 60 instrumentalists, but used previously published reports for comparison, this study is marred This shortcoming in experimen-tal design is particularly important in high-frequency testing during which calibration is particularly dif-ficult and establishment of norms on each individual piece of equipment is advisable

In their 1986 article entitled, “The level of the cal loud sound and noise induced hearing impair-ment,” Ono et al determined the importance of measuring the cumulative effects of noise over long periods of time on a single individual They devel-oped a compact noise dosimeter designed to evalu-ate long-term and varied exposure called “Noise Badge.”57

musi-In 1987, Swanson et al studied the influence of jective factors on TTS after exposure to music and noise of equal energy,58 attempting to replicate Lind-gren and Axelsson’s 1983 study Swanson’s study used 2 groups of subjects, 10 who disliked pop music, and 10 who liked pop music Each subject was tested twice at 48-hour intervals One session involved exposure to music for 10 minutes The other session involved exposure to equivalent noise for 10 minutes Their results showed that individuals who liked pop music experienced less TTS after music than after noise Those who disliked the music showed greater TTS in music than in noise Moreover, the group that

sub-liked pop music exhibited less TTS than the group

that disliked the music These findings support the

notion that sounds perceived as offensive produce

greater TTS than sounds perceived as enjoyable

A particularly interesting review of hearing

impair-ment among orchestra musicians was published by

Woolford et al in 1988.59 Although this report

pre-sents only preliminary data, the authors have put

forward a penetrating review of the problem and

interesting proposals regarding solutions, including

an international comparative study They concluded

that among classical musicians the presence of

hear-ing loss from various etiologies includhear-ing noise has

been established, that some noise-induced hearing

impairments in musicians are permanent (although

usually slight), and that efforts to reduce the intensity

of noise exposure can be successful

In addition to concern about hearing loss among

performers, in recent years there has been growing

concern about noise-induced hearing loss in

audi-ences Those at risk include not only people at rock

concerts, but also people who enjoy music through

stereo systems, especially modern personal

head-phones Concern about hearing loss from this source

in high school students has appeared to the lay press

and elsewhere.60,61 Because young music lovers are

potentially performers, in addition to other reasons,

this hazard should be taken seriously and

investi-gated further

In 1990, West and Evans studied 60 people aged

15 to 23 years at the University of Keele, looking for

hearing loss caused by listening to amplified music.62

They found widening of auditory bandwidths to be

a sensitive, early indicator of noise-induced hearing

loss that was detectable before threshold shift at 4000

or 6000 Hz occurred They advocated the use of

fre-quency resolution testing and high-resolution Békésy

audiometry for early detection of hearing

impair-ment West and Evans found that subjects extensively

exposed to loud music were significantly less able to

differentiate between a tone and its close neighbors

Reduced pitch discrimination was particularly

com-mon in subjects who had experienced TTS or tinnitus

following exposure to amplified music

In 1991, van Hees published an extensive thesis

on noise-induced hearing impairment in orchestral

musicians.63 He agreed that noise levels were

poten-tially damaging in classical and wind orchestras

Unlike other researchers, van Hees found it more

useful to classify the instruments by orchestral zone,

rather than by instrument or instrument group

However, he found a much greater incidence of

hear-ing loss among both symphony and wind orchestra

musicians than was reported in previous literature

In contrast to previous investigators, he also did not find evidence of asymmetric hearing loss in violinists and cello players

In 1991, the musicians of the Chicago Symphony Orchestra were evaluated by Royster, Royster, and Killion Subjects were given individual dosimeters, and 68 measurements were made during various rehearsals and performances More than half of the musicians had audiograms consistent with NIHL and showed a high prevalence of “notch” patterns.64 The authors measured Leq values and hearing thresh-old levels on 32 musicians and found that pure-tone thresholds between 3 and 6 kHz correlated to the measured equivalent sound level (Leq), which was determined to range from 79 to 99 dBA SPL.63

In their 1998 evaluation of choir singers and ing loss, Steurer and colleagues made some unusual discoveries that warrant additional research The authors discovered that low-frequency hearing, in particular 250 Hz to 1 kHz, was most affected in these subjects.65 They were not able to explain the demonstrated hearing losses below 100 Hz but have speculated that there may be increased endolym-phatic pressure when singing that could account for the loss in this range

hear-Reviewing these somewhat confusing and tradictory studies reveals that a great deal of impor-tant work remains to be done to establish the risk

con-of hearing loss among various types con-of musicians, the level and pattern of hearing loss that may be sus-tained, practical methods of preventing hearing loss, and advisable programs for monitoring and early diagnosis However, a few preliminary conclusions can be drawn First, the preponderance of evidence indicates that noise-induced hearing loss occurs in both pop and classical musicians and is causally related to exposure to loud music Second, in most instances, especially among classical musicians, the hearing loss is not severe enough to interfere with speech perception Third, the effects of mild high-frequency hearing loss on musical performance have not been established Fourth, it should be possible to devise methods to conserve hearing in performing artists without interfering with their performance

In 1991, Chasin and Chong reported on an ear tection program for musicians.66 They provide an interesting discussion of the use of ear protectors in musicians, although several aspects of their paper are open to challenge In particular, their assertion that some vocalists (particularly sopranos) have self-induced hearing loss caused by singing has not been substantiated

pro-Legal Aspects of Hearing Loss

in Singers and Musicians

The problem of hearing loss in musicians raises

numerous legal issues, especially the implications of

occupational hearing loss, and hearing has become

an issue in some orchestra contracts Traditionally,

workers’ compensation legislation has been based on

the theory that workers should be compensated when

a work-related injury impairs their ability to earn a

living Ordinarily, occupational hearing loss does not

impair earning power (except possibly in the case of

musicians and a few others) Consequently, current

occupational hearing loss legislation broke new legal

ground by providing compensation for interference

with quality of life — that is, loss of living power

Therefore, all current standards for defining and

compensating occupational hearing loss are based on

the communication needs of the average speaker, and

losses are usually compensated in accordance with

the recommendations of the American Academy of

Otolaryngology.13 Because music-induced hearing

loss appears to rarely affect the speech frequencies,

it is not compensable under most laws However,

although a hearing loss at 3000, 4000, or 6000 Hz with

preservation of lower frequencies may not pose a

problem for a boilermaker, it may be a serious

prob-lem for a violinist Under certain circumstances, such

a hearing loss may even be disabling Because

profes-sional instrumentalists require considerably greater

hearing acuity throughout a larger frequency range,

we must investigate whether the kinds of hearing

loss caused by music are severe enough to impair

performance If so, new criteria must be established

for compensation for disabling hearing impairment

in musicians, in keeping with the original intent of

the workers’ compensation law

There may also be unresolved legal issues

regard-ing hearregard-ing loss not caused by noise in professional

musicians Like people with other disabilities,

numer-ous federal laws protect the rights of those with

hearing impairment In the unhappy situation in

which an orchestra must release a hearing-impaired

violinist who can no longer play in tune, for example,

legal challenges may arise In such instances, and in

many other circumstances, an objective assessment

process is in the best interest of performers and

man-agement Objective measures of performance are

already being used in selected areas for singers, and

they have proven beneficial in helping the performer

assess dispassionately certain aspects of performance

quality and skill development Such technologic

advances will probably be used more frequently

in the future to supplement traditional subjective assessment of performing artists for musical, scien-tific, and legal reasons

Ear Protectors for the Musician

Current ear protectors offer a much more suitable solution to noise protection than their predecessors There are several models available that cater to musi-cians and their specific requirements The design strategy has improved to allow more accurate music and speech perception at lower intensity levels Vari-ous models provide differing attenuation levels rang-ing from 9 to 25 decibels These protectors are custom fitted to the individual and thus provide better per-formance than preformed in-the-ear hearing protec-tors They can be purchased through an audiologist

or hearing aid dispenser

Noise Exposure and the Audience

The focus of this chapter thus far has been on the musician and noise exposure A few more recent studies have looked at the effects of noise on an audi-ence In particular, Gunderson, Moline, and Cata-lano, in a 1997 publication, evaluated the effect of noise exposure on employees of urban music clubs Average sound levels ranged from 94.9 to 106.7 dBA Only 16% of the employees used ear protection.67 The authors recommended the development of a hear-ing conservation program for this often overlooked population Similarly, in 1998, Sataloff, Hickey, and Robb evaluated noise levels at an outdoor rock con-cert Results showed audience exposure to levels of

119 dBA These studies indicate that future efforts need to focus on hearing conservation not only for the performer, but for audiences as well.68

Treatment of Occupational Hearing Loss in Singers and Other Musicians

For a complete discussion of the treatment of ing loss, the reader is referred to other sources1 and

hear-to standard ohear-tolaryngology texts Most cases of sorineural hearing loss produced by aging, heredi-tary factors, and noise cannot be cured When they involve the speech frequencies, modern, properly adjusted hearing aids are usually extremely helpful However, these devices are rarely satisfactory for musicians during performance More often, appro-

sen-priate counseling is sufficient The musician should

be provided with a copy of his or her audiogram and

an explanation of its correspondence with the piano

keyboard Unless a hearing loss becomes severe,

this information usually permits musicians to make

appropriate adjustments For example, a conductor

with an unknown high-frequency hearing loss will

call for violins and triangles to be excessively loud If

he or she knows the pattern of hearing loss, this error

may be reduced Musicians with or without hearing

loss should routinely be cautioned against

avoca-tional loud noise exposure without ear protection

(hunting, power tools, motorcycles, etc) and ototoxic

drugs In addition, they should be educated about

the importance of immediate evaluation if a sudden

hearing change occurs When diplacusis (pitch

distor-tion) is present, compensation is especially difficult,

especially for singers and string players Auditory

retraining may be helpful in some cases Hopefully,

electronic devices will be available in the future to

help this problem, as well

Conclusion

Good hearing is of great importance to musicians, but

the effects on performance of mild high-frequency

hearing loss remain uncertain It is most important

to be alert for hearing loss from all causes in

perform-ers, to recognize it early, and to treat it or prevent its

progression whenever possible Musical instruments

and performance environments are capable of

pro-ducing damaging noise Strenuous efforts must be

made to define the risks and nature of music-induced

hearing loss in musicians, to establish damage-risk

criteria, and to implement practical means of noise

reduction and hearing conservation

Singers depend on their hearing almost as much

as they do on their voices It is important not to take

such valuable and delicate structures as our ears for

granted Like the voice, the ear must be understood

and protected if a singer is to enjoy a long, happy, and

successful career

References

1 Sataloff J, Sataloff RT Hearing Loss 3rd ed New York,

NY: Marcel Dekker; 1993.

2 Sataloff RT, Sataloff J Occupational Hearing Loss 2nd ed

New York, NY: Marcel Dekker; 1993.

3 Konigsmark BW, Gorlin RJ Genetic and Metabolic

Deaf-ness Philadelphia, PA: WB Saunders; 1976.

4 Johnson DW, Sherman RE, Aldridge J, Lorraine A Extended high frequency hearing sensitivity: a norma-

tive threshold study in musicians Ann Otol Rhinol yngol 1986;95(2, pt 1):196–202.

5 Schmidt JM, Verschuure J, Brocaar MP Hearing loss

in students at a conservatory Audiology 1994;33(4):

185–194.

6 Axelsson A, Lindgren F Temporary threshold shift after

exposure to pop music Scand Audiol 1978;7(3):127–135.

7 Ostri B, Eller N, Dahlin E, Skylv G Hearing

impair-ment in orchestral musicians Scand Audiol 1989;18(4):

concert J R Soc Med 1992;85(10):617–619.

12 Bu G [Prevention of noise induced hearing loss in

musicians of Chinese opera.] Zhonghua Er Bi Yan Hou

Ke Za Zhi 1992;27(2):73–75, 124.

13 Cocchiarella L, Andersson GBJ Guides to the tion of Permanent Impairment 5th ed Chicago, IL: AMA Press; 2001:245–275.

Evalua-14 Rosanowski F, Eysholdt U [In situ sound pressure measurement in a professional violinist with bilateral

tinnitus Laryngorhinootologie 1996;75(9):514–516.

15 Metternich FU, Brusis T [Acute hearing loss and

tin-nitus caused by amplified recreational music rhinootologie 1999;78(11):614–619.

Laryngo-16 Karlsson K, Lundquist PG, Olaussen T The hearing

of symphony orchestra musicians Scand Audiol 1983;

19 Kahari KR, Axelsson A, Hellstrom PA, Zachau G

Hear-ing assessment of classical orchestral musicians Scand Audiol 2001;30(1):13–23.

20 Axelsson A, Lindgren F Hearing in classical musicians

Acta Otolaryngol Suppl 1981;(377):3–74.

21 Time September 29, 1989:78.

22 Ackermann BJ, Kenny DT, O’Brien I, Driscoll TR Sound Practice — improving occupational health and safety for professional orchestral musicians in Austra-

lia Front Psychol 2014;5:973.

23 Hamdan A, Abouchacra K, Zeki A, Zatoun G sient-evoked otoacoustic emissions in a group of pro- fessional singers who have normal pure-tone hearing

Tran-thresholds Ear and Hearing 2008;29(3):360–377.

24 Arnold GE, Miskolczy-Fodor F Pure-tone thresholds of

professional pianists Arch Otolaryngol 1960;71:938–947.

25 Flach M, Aschoff E [On the question of occupationally

related hearing difficulties in musicians.] Z Laryngol

Rhinol Otol 1966;45:595–605.

26 Flach M [Hearing musicians from the otologic

view-point.] Monatsschr Ohrenheilkd Laryngorhingol 1972;9:

424–432.

27 Berghoff F Höbrleistung und berufsbedingte

Hörsch-ädigung des Orchestermusikers mit einem Beitrag zur

Pathophysiologie des Larmtraumatischen

Hörscha-dens 1968, Dissertation Cited in Axelsson A,

Lind-gren F Hearing in classical musicians Acta Otolaryngol

Suppl 1981;(377):3–74.

28 Lebo CP, Oliphant KP Music as a source of acoustic

trauma Laryngoscope 1968;72(2):1211–1218.

29 O’Brien I, Wilson W, Bradley A Nature of orchestral

noise J Acoustic Soc Am 2008;124(2):926–939.

30 Rintelmann WF, Borus JF Noise-induced hearing loss

and rock and roll music Arch Otolaryngol 1968;88:

377–385.

31 Jerger J, Jerger S Temporary threshold shift in

rock-and-roll musicians J Speech Hear Res 1970;13:221–224.

32 Speaks C, Nelson D, Ward WD Hearing loss in

rock-and-roll musicians J Occup Med 1970;12:216–219.

33 Rintelmann WF, Lindberg RF, Smitley EK Temporary

threshold shift and recovery patterns from two types

of rock and roll music presentations J Acoust Soc Am

1972; 51:1249–1255.

34 Samelli A, Matas C, Carvallo R, et al Audiological and

electrophysiological assessment of professional pop/

rock musicians Noise Health 2012;14(56):6–12.

35 Jahto K, Hellmann H [The problem of acoustic trauma

in orchestra musicians.] HNO 1972;20(1):21–29.

36 Buhlert P, Kuhl W Höruntersuchungen im freien

Schall-feld zum Altershörverlust Acustica 1974;31:168–177.

37 Kuhl W Keine Gehörschädigung durch Tanzmusik,

simfonische Musik und Maschinengeräusche beim

Rundfunk Kampf dem Larm 1976;23(4):105–107.

38 Zeleny M, Navratilova Z, Kamycek Z, et al [Relation of

hearing disorders to the acoustic composition of

work-ing environment of musicians in a wind orchestra.]

Cesk Otolaryngol 1975;24(5):295–299.

39 Reuter K, Hammershoi D Distortion product

opto-acoustic emission of symphony orchestra musicians

before and after rehearsal J Acoustic Soc Am 2007;121:

327–336.

40 Siroky J, Sevcikova L, Folprechtova A, et al

Audiologi-cal examination of musicians of a symphonic orchestra

in relation to acoustic conditions [Czech] Cesk

Otolar-yngol 1976;25(5):288–294.

41 Folprechtova A, Miksovska O [The acoustic conditions

in a symphony orchestra.] Pracov Lek 1978;28:1–2.

42 Balazs B, Gotze A [Comparative examinations between

the hearing of musicians playing on traditional

instru-ments and on those with electrical amplifications.]

[Czech] Ful-orr-gegegyogyaszat 1976;22:116–118.

43 Gryczynska D, Czyzewski I [Damaging effect of music

on the hearing organ in musicians.] Otolaryngol Pol

1977;31(5):527–532.

44 Axelsson A, Lindgren F Factors increasing the risk for

hearing loss in “pop” musicians Scand Audiol 1977;6:

49 Axelsson A, Eliasson A, Israelsson B Hearing in pop/

rock musicians: a follow-up study Ear Hear 1995;16(3):

245–253.

50 Kahari KR, Axelsson A, Hellstrom PA, Zachau G ing development in classical orchestral musicians: a

Hear-follow-up study Scand Audiol 2001;30(3):141–149.

51 Westmore GA, Eversden ID Noise-induced hearing

loss and orchestral musicians Arch Otolaryngol 1981;

107(12):761–764.

52 Lindgren F, Axelsson A Temporary threshold shift

after exposure to noise and music of equal energy Ear Hear 1983;4(4):197–201.

53 Karlsson K, Lundquist PG, Olaussen T The hearing of

symphony orchestra musicians Scand Audiol 1983; 12:

257–264.

54 Woolford DH Sound pressure levels in symphony orchestras and hearing Preprint 2104 (B-1), Australian Regional Convention of the Audio Engineering Society, September 25–27, 1984; Melbourne, Australia.

55 Johnson DW, Sherman RE, Aldridge J, Lorraine A Effects of instrument type and orchestral position on hearing sensitivity for 0.25 to 20 kHZ in the orchestral

musician Scand Audiol 1985;14:215–221.

56 Johnson DW, Sherman RE, Aldridge J, et al Extended high frequency hearing sensitivity A normative thresh-

old study in musicians Ann Otol Rhinol Laryngol 1986;

95:196–202.

57 Ono H, Deguchi T, Ino T, et al [The level of the musical

loud sound and noise induced hearing impairment.] J UOEH 1986;8(suppl):151–161.

58 Swanson SJ, Dengerink HA, Kondrick P, Miller CL The influence of subjective factors on temporary thresh- old shifts after exposure to music and noise of equal

energy Ear Hear 1987;8(5):288–291.

59 Woolford DH, Carterette EC, Morgan DE Hearing

impairment among orchestral musicians Music cept 1988;5(3):261–284.

Per-60 Gallagher G Hot music, high noise, and hurt ears Hear

J 1989;42(3):7–11.

61 Lewis DA A hearing conservation program for

high-school level students Hear J 1989;42(3):19–24.

62 West PD, Evans EF Early detection of hearing damage

in young listeners resulting from exposure to amplified

music Br J Audiol 1990;24:89–103.

63 van Hees OS Noise Induced Hearing Impairment in Orchestral Musicians Amsterdam, Holland: University

of Amsterdam Press; 1991.

64 Royster JD, Royster LH, Killion MC Sound exposures

and hearing thresholds of symphony orchestra

musi-cians J Acoust Soc Am 1991;89(6):2793–2803.

65 Steurer M, Simak S, Denk DM, Kautzky M Does choir

singing cause noise-induced hearing loss? Audiology

1998;37(1):38–51.

66 Chasin M, Chong J An in situ ear protection program

for musicians Hearing Instrument 1991;42(12):26–28.

67 Gunderson E, Moline J, Catalano P Risks of ing noise-induced hearing loss in employees of urban

develop-music clubs Am J Ind Med 1997;31(1):75–79.

68 Sataloff RT, Hickey K, Robb J Rock concert audience

noise exposure: a preliminary study J Occupat Hear Loss 1998;1(2):97–99.

16

Endocrine Function

Timothy D Anderson, Dawn D Anderson, and

Robert Thayer Sataloff

Endocrine problems are worthy of special attention

The human voice is extremely sensitive to

endocrino-logic changes, with many endocrine changes

occur-ring in the voice throughout the normal human life

cycle, in addition to the potential for derangements

of these complex systems at any time The

laryn-gologist caring for voice patients must be familiar

with the broad range of normal changes, as well

as the potential for hormonal imbalances, that may

affect the voice in order to recognize them promptly

and generate appropriate treatment and referrals

Although accurate diagnoses of problems

involv-ing the endocrine system often can be made by the

otolaryngologist through a comprehensive history,

physical examination, and appropriate laboratory

investigations, the value of a good endocrinologist

interested in consulting in the care of professional

voice users cannot be overestimated As in other

areas of professional voice care, recognizing

abnor-malities and prescribing therapy can be challenging

Otolaryngologists are encouraged strongly to enlist

the services of an endocrinologist who is interested

in arts-medicine and to assist in his or her education

in the special problems of professional voice users

Unfortunately, the more we learn about endocrine

disorders, the more complex these systems appear,

and hormonal effects on the voice are poorly studied

and understood

Sex Hormones

Voice changes associated with sex hormones are

encountered commonly in clinical practice and have

been investigated more than have the voice effects of

most other hormonal changes The status of the voice

as a secondary sexual characteristic is well lished, and through the work of doctors Jean and Beatrice Abitbol and others, the status of the larynx

estab-as a sex-hormone responsive organ hestab-as been sized.1–4 In an elegant demonstration, the Abitbols showed that superficial laryngeal and vaginal smears both exhibited significant changes throughout a woman’s normal menstrual cycle Surprisingly, the smears from cervix and larynx were indistinguish-able at each phase of the cycle This work has been supported by localization of estrogen, progesterone, and androgen receptors in both the mucosa and deeper tissues of the larynx,4–11 although other stud-ies have failed to find these receptors and propose other mechanisms by which the larynx is affected by hormonal changes, such as differential expression of various growth factors.12–14

empha-The voice changes in response to changing sex mones throughout life The initial and most dramatic changes occur in both males and females at puberty

hor-In females, cyclic voice and laryngeal changes occur with each menstrual cycle, and a second permanent change occurs at menopause Males undergo a more dramatic initial pubertal voice change, but then have relatively stable circulating levels of sex hormones across their life span and undergo fewer subsequent voice changes

Males

Puberty is the process of sexual development that lasts between 2 and 5 years and normally begins at age 12 to 17 It is still not known what triggers the onset of puberty In males, it seems as if the pituitary

gland becomes less sensitive to the suppressive effects

of testosterone on the release of

gonadotrophic-releasing hormone This causes escalating levels of

circulating testosterone that reach adult levels by the

end of puberty.15 These high testosterone levels are

maintained until senescence, when they gradually

drop The initial physical sign of puberty is

enlarge-ment of the testes This is followed by rapid growth,

increases in muscle mass especially in the chest and

shoulder girdle, and development of male secondary

sex characteristics The development of hair in the

axilla, face, and groin is initiated by adrenal

andro-gens and then facilitated by the presence of high

lev-els of testosterone and dihydrotestosterone (DHT)

Although DHT was thought to be the primary active

form of testosterone, it is now clear that both

testos-terone and DHT interact in a complex manner, often

binding to the same receptor complex but mediating

different cellular effects through poorly understood

mechanisms.16,17 Disorders of normal development

occur with any disturbances in the production,

receptors or effects of testosterone, DHT, or

adre-nal androgens Although no pathologic process has

been ascribed to high levels of natural testosterone,

exogenous administration of pharmacologic doses

of sex steroids has significant effects on both males

and females Anabolic steroids can cause testicular

atrophy, acne, voice changes, hirsutism, psychologic

changes, and severe heart problems Because these

drugs do have the potential to increase lean body

mass and athletic performance in both men18–20 and

women,21 they are widely available for illicit use by

both professional and recreational atheletes.22 Use

of exogenous androgens has been banned in every

major competitive sport and should be strongly

dis-couraged, especially in professional voice users In

both males and females, these drugs may cause

per-manent lowering and coarsening of the voice

Puberty’s effect on the male larynx is to increase

the size and mass of the intrinsic cartilages of the

lar-ynx, with formation of a prominent Adam’s apple

The muscles and ligaments of the larynx also become

bulkier and change shape contributing to the drop in

fundamental frequency of the voice.23 These changes

occur at variable rates and require constant

retun-ing of the delicate voice production mechanisms

until pubertal development has ceased While this

retraining occurs, voice breaks and uncontrolled

pitch changes can cause considerable embarrassment

to the affected adolescent male

The most obvious derangement of the normal

pubertal voice changes is exemplified by castrati

When castrato singers were in vogue, castration of

males at about age 7 or 8 resulted in failure of

puber-tal laryngeal development due to lack of the normal amounts of testosterone The lack of circulating tes-tosterone led to delayed closure of bony growth cen-ters and tall stature with large lung capacities The combination of immature larynges and exceptional power produced voices in the alto or soprano range that boasted a unique quality of sound that cannot be replicated in any other way.24 The use of castrati in religious music continued from the 16th century until

1903, when it was officially banned by Pope Pius X.25

The presence of high levels of androgens has been hypothesized to be causally related to the increased incidence of coronary heart disease and atheroscle-rosis in men as compared to women This suggests that there may have been at least some advantage to being a castrato However, in an interesting study, Nieschlag and coworkers compared the life span

of 50 famous castrati born between 1581 and 1858 with 50 intact, equally famous male singers born during the same period and found no trend toward increased longevity in castrati.26 This may point to the cardioprotective effects of estrogen instead of adverse cardiovascular effects of androgens

Failure of male voice change at puberty is mon Medical causes of hormonal deficiencies include Kallmann syndrome, cryptorchidism, delayed sexual development, Klinefelter syndrome, and Fröhlich syndrome.27 In these cases, the persistently high-pitched voice may be the complaint that brings the patient to medical attention In some ways, these dis-orders can mimic castration For example, patients with Klinefelter syndrome become tall at puberty and have long legs and gynecomastia They have small testes that do not produce sperm In patients in whom the levels of circulating testosterone are very low, pubic hair is absent, and the voice remains soprano Voice changes may be less dramatic in patients with Klinefelter syndrome in whom more testosterone is produced Patients with low circulating androgen levels can achieve a normal male fundamental fre-quency with the administration of exogenous testos-terone.28 Professional singers with hypoandrogenism should be warned that the posttherapy singing voice may be substantially altered, and may no longer be perceived as a “professional-level” voice.29 It should

uncom-be recognized that medical or surgical castration is still occasionally required therapeutically in adult males, particularly in the treatment of prostate or tes-ticular cancer In such cases, the mild increase in fun-damental frequency of the speaking voice that occurs physiologically with aging may be accelerated, but survival considerations must take precedence over vocal concerns Rarely, the larynx may fail to respond

to hormonal changes at the time of puberty, and an

infantile larynx and soprano voice may be seen in a

male with normal secondary sex characteristics and

testosterone levels It is hypothesized that there is an

androgen receptor abnormality confined to the

lar-ynx in these cases, and exogenous androgen

admin-istration has not resulted in further voice change in

these patients After puberty, sex-hormone-related

problems are encountered uncommonly in men

Although there appears to be a correlation between

sex hormone levels and depths of male voices (higher

testosterone and lower estradiol levels in basses than

in tenors),30,31 the most important hormonal

consid-erations in males occur during puberty.23 The most

common hormonal problems encountered in

postpu-bertal males are probably those related to ingestion of

anabolic steroids, as discussed earlier Use of

testos-terone in middle-aged and elderly men has become

much more widespread since the development of

topically administered testosterone The diagnosis

and treatment of “low-T” is currently under scrutiny,

and the US Food and Drug Administration (FDA) has

recently pointed out that slow decline in levels of

testosterone in older men are normal, and has urged

that health-care providers only use testosterone in

those patients with recognized disorders of the

tes-ticles or pituitary due to the risk of adverse effects,

especially heart attack and stroke.32 Interestingly, the

voice change in elderly men seems to be related more

strongly to estrogen than testosterone levels, so

tes-tosterone supplementation of male singers may be

ineffective in avoiding senescent voice changes.33

Females

The female professional voice user must weather

multiple changes in the milieu of her sex hormones

during her life At puberty, estrogen and

progester-one levels rise, secondary sex characteristics develop,

and the menstrual cycle is established Throughout

a woman’s reproductive life, the female voice

pro-fessional has cyclic changes in the relative serum

concentration of estrogen and progesterone that

may cause important laryngeal changes The rapid

physical and physiologic changes that occur

dur-ing pregnancy also have the potential to affect the

professional voice user Voice changes of pregnancy

may be similar to those encountered premenstrually

or mimic those produced by exogenous androgens

They are occasionally perceived as desirable by the

patient In some cases, alterations produced by

preg-nancy are permanent.32,33 After the climacteric, serum

levels of estrogen and progesterone fall while

tes-tosterone levels remain relatively stable, once again

affecting the larynx

Androgenic medications should be avoided in female singers, if there are any reasonable therapeu-tic alternatives Clinically, these drugs are now used most commonly to treat endometriosis or (illicitly) to enhance athletic performance.21,34 Exogenous andro-gens cause unsteadiness of the female voice, rapid changes of timbre, and lowering of fundamental voice frequency.34–40 These changes often are irre-versible, and can occur within weeks of initiation of androgens It should be stressed that these changes can occur even with “bio-identical” hormones, which many patients regard as more natural and therefore more safe It also appears that the timing of androgen exposure is important, with early childhood andro-gen exposure from adrenocortical tumors causing only rare vocal virilization.41 In the past, voices with androgenic damage have been considered “ruined.”

In our experience, voices are altered permanently, but not necessarily ruined Through a slow, meticulous retraining process, it has been possible in some cases

to return singers with androgenic voice changes to

a professional singing career However, their “new voice” has fewer high notes and fuller low notes than before androgen exposure

Puberty

The trigger causing the onset of puberty in females

is not known Gradual increases in estrogen and gesterone are seen with eventual establishment of a normal menstrual cycle with cyclic hormonal changes that can affect the voice.42,43 Secondary sexual matu-ration is dependent on several factors besides normal hormonal changes Normal menstrual cycles require adequate energy stores and caloric intake.44 This is particularly important in dancers, gymnasts, and other athletes who maintain a very low body weight and body fat and may experience delayed menarche

pro-or secondary amenpro-orrhea Secondary amenpro-orrhea also has been observed in normal weight athletes with inadequate caloric intakes In some women, once training is reduced, normal cycling can resume, although sequelae of delayed menarche or second-ary amenorrhea can be observed throughout the woman’s life Because maximal bone mass is accu-mulated by age 25 to 30, osteoporosis can be particu-larly severe if sexual maturation is delayed

Because initial pituitary hormone secretion occurs

at night, adequate sleep also is essential in cents to initiate puberty Once sexual maturity is attained, gonadotropin secretion is independent of sleep Finally, optic exposure to sunlight is essential for normal timing of sexual development Blind ado-lescents have delayed menarche Decreased exposure

adoles-to sunlight is thought adoles-to be capable of delaying

devel-opment in humans, although experimental evidence

is lacking In females, although estrogen and

proges-terone are the primary sex hormones, adrenal and

ovarian androgens and other pituitary hormones also

play an essential role (Table 16–1) The female voice

undergoes changes during puberty with a decrease

in fundamental frequency of about one-third of an

octave.45 Changes in the resonance properties of the

upper airways contribute to the change from a

dis-tinctively childlike voice to an adult female voice

Because the pubertal changes in the vocal instrument

are not as large or rapid as those in the male, obvious

voice breaks and register changes are unusual

None-theless, maintenance of a professional singing voice

during these changes can be difficult and requires

constant adjustments in technique and expectations

to avoid the development of maladaptive behaviors

Disorders of puberty are rare, but they occur more

commonly in females than males Voice complaints

are not a common feature of these disorders in

females with the exception of processes with a

rela-tive excess of androgens Abnormalities of pubertal

development can be divided into delayed maturation

and precocious puberty As the initial sign of puberty

should be formation of breast buds, delayed sexual

maturation is identified by failure of breast budding

by age 13 or sexual hair growth that precedes breast

budding by more than 6 months The differential

diagnosis for delayed puberty includes premature

ovarian failure (as seen in Turner syndrome),

inad-equate gonadotropin-releasing hormones (GnRH)

secretion from the hypothalamus (as in Kallmann

syndrome), inadequate gonadotropin (luteinizing

hormone [LH] and/or follicle-stimulating hormone

[FSH]) secretion, and inadequate body fat (anorexia

nervosa or excessive exercise) Theoretically, heavy

marijuana use could delay puberty as marijuana

blocks the release of GnRH from the hypothalamus,

preventing normal gonadotropin secretion,44 but no human cases have been reported

Precocious puberty is defined as the onset of breast budding before age 8 There are many potential causes of precocious puberty Physicians caring for the voice are most likely to see precocious puberty

as a result of androgen excess, as these conditions carry the risk of irreversible deepening and coars-ening of the voice at an early age One representa-tive disorder is congenital adrenal hyperplasia as a result of an incomplete 21-hydroxylase deficiency 21-Hydroxylase is an enzyme that converts proges-terone to desoxycorticosterone during the synthesis

of cortisol in the adrenal gland Minor deficiencies in this enzyme lead to accumulation of adrenal andro-gens, which produce premature adrenarche In addi-tion to the premature development of pubic and axillary hair, prolonged exposure to adrenal andro-gens can cause virilization of the voice With early diagnosis and continuous adequate treatment, vocal virilization can be avoided.46,47

Females can suffer significant vocal problems from ingesting anabolic steroids Marked virilization

of the voice is common and is usually irreversible Physicians must be familiar with these side effects, because virilizing agents are not only used by women bodybuilders,34 but are also prescribed for postmeno-pausal sexual dysfunction and other problems Such treatments may substantially masculinize and “age”

a voice and may end a vocal career Patients with virilization have higher baseline scores on the voice handicap index, and complain because they are fre-quently mistaken for a man on the telephone.47 Risks must be weighed carefully against benefits before such medication is prescribed, and the voice care-fully monitored in voice professionals during ther-apy Female-to-male transsexuals are a special case where virilizing effects of androgens on the voice are desirable Cases of female-to male-transsexual pro-

Table 16–1 Sequence of Female Puberty24

Sign Age (years) Hormone

Adult breast development 12.5–15 Progesterone Sexual hair growth (initiation) 10.5–11.5 Androgens Adult sexual hair pattern 13.5–16 Androgens

fessional voice users continuing to successfully work

have been reported.48

Menstrual Cycle

Probably the most common hormonal voice

com-plaints in female voice professionals are related to

the normal hormonal fluxes encountered during the

menstrual cycle Although voice changes associated

with the normal menstrual cycle may be difficult to

quantify,49–52 there is no question that they occur

Most of the ill effects are seen in the immediate

menstrual period and are known as laryngopathia

pre-menstrualis This condition is common and is caused

by physiologic, anatomic, and psychologic

altera-tions secondary to endocrine changes The

subjec-tive symptoms are characterized by decreased vocal

efficiency, loss of the highest notes in the voice, vocal

fatigue, slight hoarseness, and some muffling of the

voice; it is often more apparent to the singer than to the listener Submucosal hemorrhages in the larynx are more common in the premenstrual period.52,53

Singers used to be excused from singing in European opera houses during premenstrual and early men-strual days (called grace days) This practice is not followed in the United States and is no longer prac-ticed widely in Europe Voice dysfunction similar to laryngopathia premenstrualis is also relatively com-mon at the time of ovulation.54

Familiarity with the normal ovarian cycle is helpful

in understanding these problems (Figure 16–1) The cycle begins with the menstrual period and ends just prior to the next menses The first portion of the cycle

is known as the follicular phase It is characterized

by gradually increasing levels of estrogen and low levels of progesterone The follicular phase normally occupies the first 14 days of the cycle, but is variable Ovulation begins the luteal phase, which continues

Figure 16–1. Normal ovarian cycle FSH = follicle-stimulating hormone; LH = luteinizing hormone.

for 14 days Progesterone levels increase during the

first half of luteal phase Estrogen decreases but rises

again slightly premenstrually

The cause of menstrual cyclic dysphonia remains

incompletely understood The combined activity of

estrogen/progesterone in the premenstrual period

causes venodilatation by relaxing smooth muscles,

thereby increasing blood volume These changes

result in engorgement of vocal fold blood vessels and

vocal fold edema In addition, polysaccharides break

down into smaller molecules in the vocal folds and

bind water, increasing fluid accumulation

Vasodila-tation also causes changes in nasal patency and

self-perception (audition) In addition, the premenstrual

hormonal environment decreases gastric motility,

exacerbating laryngopharyngeal reflux Abdominal

bloating and cramps impair effective support In

addition, Abitbol et al1 showed a strong correlation

between premenstrual dysphonia and luteal

insuffi-ciency The incidence of premenstrual hoarseness is

unknown, but anecdotally it appears to be significant

in about one-third of women Although most authors

and clinicians have been more impressed with

pre-menstrual voice changes than with those occurring

during midcycle, at least one author has suggested

that voice changes occurring at the time of

ovula-tion may actually be more prominent.2 In a survey

of female singers regarding premenstrual symptoms,

the most frequent general symptom was abdominal

bloating, and the most frequent voice symptom was

difficulty singing high notes.55 Other commonly

reported vocal symptoms were changes in voice

qual-ity and impairment in flexibilqual-ity A study of vocally

untrained young women revealed no spectrographic

changes in the voice through the menstrual cycle,56

although other studies have reported cyclic

hoarse-ness or even periodic aphonia during the

premen-strual period of nonsingers.57–59 Speech dysfluencies

have also been reported to occur more frequently in

the premenstrual period.60

Although ovulation inhibitors have been shown to

mitigate some of these symptoms,51 in rare patients,

older birth control pills containing more androgenic

progesterones were reported to alter voice range

and character deleteriously after only a few months

of therapy.61–64 Current formulations of oral

contra-ceptives use much lower hormone doses and voice

changes have not been reported.65 Indeed, many

women find that the oral contraceptives decrease

vocal fluctuations and stabilize the voice.66 When oral

contraceptives are used, the voice should be

moni-tored closely Androgenic progesterone-containing

oral contraceptives are still available in some

coun-tries and may cause permanent masculinization of

the voice Oral contraceptives marketed in the United States generally do not contain these progesterones Under crucial performance circumstances, oral con-traceptives can be used to alter the time of men-struation While common in athletes, the effects of this manipulation on the voice are unknown When cyclical voice changes are incapacitating, endocrino-logic or gynecologic assessment and appropriate hor-monal therapy certainly should be considered.The hormonal cycle is also associated with men-strual cramping, or dysmenorrhea Cramps occur in approximately one-half to three-quarters of menstru-ating women, and about 10% are disabled for 1 to 3 days monthly.64,67 Muscle cramping associated with menstruation causes pain and compromises abdomi-nal contraction This undermines support and makes singing or projected speech (acting and public speak-ing) difficult Dysmenorrhea is also associated with diarrhea and low back pain, which further impair support It also may be accompanied by fatigue, headache, dizziness, emesis, nausea, all of which are distracting and potentially impair technique and performance Menstrual cramps seem to be due to uterine contraction mediated by local prostaglandin release Hence, prostaglandin inhibitors such as ibu-profen are prescribed commonly for dysmenorrhea The combination of such drugs with capillary fragil-ity and other hormonally mediated vascular changes puts a professional voice user at higher risk of vocal hemorrhage.53 Medications that impair coagulation should therefore be avoided The development of the selective cyclooxygenase-2 (COX-2) inhibitors offers

an alternative to nonsteroidal anti-inflammatory drugs (NSAIDs) The selective COX-2 inhibitors are marketed as not causing anticoagulation or gastric complications Dysmenorrhea pain relief has been documented with celecoxib,68 offering a potentially safer alternative for professional voice users, although these medications are not widely used by gynecolo-gists for this purpose

The hormonal cycle also is associated in some women with premenstrual syndrome (PMS) This syndrome may include emotional lability, depres-sion, anxiety, irritability, decreased concentration ability, abdominal bloating, edema, nausea, diar-rhea, palpitations, water and salt retention, and other changes that may affect voice performance adversely Insomnia occurs commonly, as well, and subsequent sleep deprivation may further impair voice function

In controlled, double-blind studies, fluoxetine zac, Lilly) has been shown to reduce the psychiatric symptoms associated with severe premenstrual dys-phoric disorder, especially when taken only during the premenstrual period.69,70 Interestingly, further

(Pro-studies have shown improvements in physical

symp-toms including bloating, breast tenderness, and

head-ache with intermittent dosing of fluoxetine.71 The

manufacturer is now marketing fluoxetine under the

name Serafem with specific labeling for premenstrual

use Although no information has been published on

the effects of fluoxetine on premenstrual dysphonia,

the reduction in physical symptoms may be helpful

in facilitating voice performance More study on the

use of this medication is required before its use can be

recommended strongly for voice professionals Oral

contraceptives are also frequently helpful in

mitigat-ing premenstrual symptoms and are widely used for

this purpose

One common disorder of the menstrual cycle is

polycystic ovary syndrome (PCOS) Anovulation

and physiologic androgen excess can lead to marked

virilization Although hirsutism, oily skin, and acne

are most common, androgen-mediated vocal changes

can also occur Treatment of PCOS is evolving

con-stantly, but oral contraceptives, spironolactone, and

metformin are often able to control some of the

symptoms.72 In obese patients with PCOS (80% of

patients), weight loss is one of the most effective

treatments

Endometriosis commonly presents as severe

dysmenorrhea Ectopic areas of endometrial tissue

respond to the hormones regulating the normal

men-strual cycle and undergo a normal cycle of

prolifera-tion and shedding (menstruaprolifera-tion) on the surface of

pelvic or abdominal organs The pathophysiologic

mechanism resulting in endometriosis is unknown

Control of endometriosis symptoms can sometimes

be obtained with use of oral contraceptive agents or

other medications Hormonal intrauterine devices

(IUDs) are highly effective in controlling

endome-triosis symptoms Danazol (Danocrine, Samofi) is no

longer used widely due to significant side effects and

high cost Danazol induces a high-androgen,

low-estrogen hormonal environment that can coarsen and

lower the voice.73 Leuprolide acetate, while effective,

causes a hypoestrogenism similar to menopause that

also may be harmful to voice strength and quality

Because leuprolide acetate causes medical

meno-pause it should not be used for more than 6 months

even in patients without professional voice needs,

because it causes significant osteoporosis as well as

other symptoms of menopause The estrogen

sup-pression caused by leuprolide acetate is sufficiently

great that it should rarely be used in voice

profes-sionals Laparoscopy with ablation of the areas of

endometriosis may provide months of symptom

control but does not commonly result in a

perma-nent cure In patients in whom all visible disease can

be treated, the 5-year recurrence rate is 20% If oral contraceptives and hormonal IUD are ineffective,

we frequently recommend that voice professionals undergo early laparoscopy for definitive diagnosis and surgical control in order to avoid the long-term use of potential voice-altering medications

Sexual Activity

Many myths and unproven admonitions are gated by performers regarding the effects of sexual activity on performance Many professional perform-ers believe that coitus prior to a performance is detri-mental Similar prohibitions on sexual activity before athletic competition are widespread A few studies in the sports medicine literature have been performed

promul-to determine whether sexual activity can affect letic performance Sztajzel et al found a very slight difference in heart rate recovery following exercise

ath-in a group of male patients 2 hours after sexual ity.74 This difference disappeared in a second test performed 10 hours after sexual activity.75 An earlier study in male athletes failed to show a difference in performance 12 hours after sexual activity.76 Unfor-tunately, there are no more recent studies about the effects of sexual activity on athletic performance, and

activ-no studies at all regarding the effects of sexual activity

on the voice There are several limitations in applying the limited information about athletic performance

to voice professionals All of the studies above were performed using male subjects There is no pub-lished study detailing the effects of sexual activity

on the athletic or vocal performance of females It is not known whether studies on athletic performance are applicable to vocal performance More research

is required to answer the questions about the vocal effects of sexual activity

Multiple methods of contraception are available and effective In the female voice professional, barrier methods or nonhormonal IUD (Paragard, Duramed) are probably the safest choice as no hormonally active medications are taken Patients taking oral contracep-tives must be monitored carefully for voice changes, and androgenic compounds should obviously be avoided Medroxyprogesterone acetate (Depo-Pro-vera, Pharmacia, and Upjohn) is a long-acting pro-gestational agent that is administered by injection every 3 months Medroxyprogesterone acetate causes adverse changes in the lipoprotein profile, probably accelerates osteoporosis, and has been associated with depressive episodes Depo-Provera induces a hypoestrogenic state that may cause voice changes similar to those encountered during menopause

Other progestin-only contraceptive choices include

subcutaneous implants (Implanon, Merck) and

pro-gestin-only oral contraceptive pills Standard oral

contraceptive pills are highly effective, and contain

both estrogen and progesterone Alternatives include

trans-cutaneous patches (Ortho-Evra, Ortho-McNeil)

and vaginal rings (Nuva-Ring, Merck) Although

most modern IUDs are hormone eluting, there is

minimal systemic absorption and the hormone

effects are imperceptible Potential voice effects of

hormonal IUDs have not been studied, but are

con-sidered unlikely

Infertility

Treatment for infertility often involves

pharmaco-logical manipulation of sex hormone levels

Admin-istration of estrogen, progesterone, FSH, LH, and

other hormonally active or hormonally related

com-pounds are required frequently Female professional

voice users should be informed completely regarding

potential side effects of the medications prescribed

to treat their infertility, especially those with

poten-tial androgenic effects Both subjective and objective

changes in the voice during in Vitro Fertilization

(IVF) therapy have been observed.77 Close

collabora-tion between the infertility specialist and a physician

experienced in the care of voice professionals should

be encouraged to minimize voice changes

Pregnancy

The rapid physical changes that occur during

preg-nancy can cause significant voice changes High levels

of progesterone decrease lower esophageal sphincter

tone and gastric motility, and higher intra-abdominal

pressures tend to exacerbate laryngopharyngeal

reflux Morning sickness with vomiting during the

first trimester also exposes the larynx to stomach

con-tents Abdominal distention during the later stages

of pregnancy interferes with abdominal muscle

func-tion and properly supported singing Any singer

whose abdominal support is compromised

substan-tially should be discouraged from singing until the

abdominal impairment has resolved In some singers,

this may occur as early as the fourth or fifth month,

but some women can support adequately and may

sing safely into their ninth month of pregnancy The

individual variations are due to the size and position

of the uterus, the size of the woman, the severity of

reflux, weight gain, and other factors

Laryngopathia gravidarum is a rare voice disorder

of pregnancy that is often associated with

preeclamp-sia.78–80 Like preeclampsia, the etiology of this

dis-order is incompletely understood The progressive hoarseness in laryngopathia gravidarum is due to edema of the superficial layer of the lamina propria, and it generally resolves rapidly after parturition.79,81

Severe cases of laryngopathia gravidarum have been reported, including one patient with a marginal pre-pregnancy airway who required tracheotomy.79,82

Less dramatic but similar changes in the vocal folds have been demonstrated in normal pregnancies, sug-gesting that laryngopathia gravidarum is an exagger-ated pathologic presentation of normal physiologic changes during pregnancy.83

Breastfeeding causes high levels of circulating prolactin, which suppress the normal female sex hormones In women who breastfeed exclusively, circulating levels of estrogen and progesterone are similar to those found during menopause As the frequency of breastfeeding diminishes, prolactin levels fall, and the normal menstrual cycle resumes Although breastfeeding has the potential to cause voice symptoms similar to those found in either menopause or prolactin-secreting pituitary tumors, voice changes are uncommon due to the relatively short period of amenorrhea (generally less than

1 year) Common symptoms encountered during breastfeeding include loss of libido and mucosal changes including mucous membrane dryness Cur-rent American Academy of Pediatrics guidelines continue to strongly recommend exclusive breast-feeding for 6 months and continuation of breastfeed-ing for at least another 6 months.84 With adequate hydration and good technique, most female voice professionals should have no vocal complaints due

to breastfeeding

Menopause

After age 35, the process of oocyte maturation and ovulation becomes increasingly inefficient and irreg-ular Because the ovaries are the major producers

of estrogen and progesterone, as menopause gresses, the serum levels of these hormones gradu-ally decrease Early in the process of menopause, estrogen and progesterone levels are maintained by ever-increasing levels of pituitary FSH The remain-ing oocytes become increasingly resistant to FSH, and hormone levels eventually decrease substantially The increasing ovarian resistance to FSH and LH first causes irregular menses, which progresses to anovu-lation and cessation of menstruation The period of waning ovarian function is the climacteric, and the

pro-cessation of menses is termed menopause The mean

age at which menopause occurs is 51, with 25% of women reaching menopause before age 45 and 95%

by age 55.44 After menopause the ovary continues

to be a hormonal organ Continuing LH stimulation

causes the ovary to produce the androgens

andro-stenedione and testosterone Androandro-stenedione is

con-verted to the estrogen estrone in fatty tissue, linking

the circulating estrogen levels to body weight

Abit-bol separates postmenopausal women into 2 types:

Reubens and Modiglianis.3 Women of the Reubens’

type have plenty of peripheral fat, and endogenous

estrogens therefore provide some protection against

the physiologic changes of menopause Modigliani

types have little endogenous estrogen and are more

vulnerable both to the effects of unopposed

ovar-ian androgens and to the physiologic menopausal

changes due to low estrogens In the United States,

Reuben types predominate, but management of the

menopausal professional voice user must be tailored

to the individual patient, as discussed below

Symptoms of the climacteric include night sweats,

insomnia and sleep deprivation, hot flashes,

geni-tal atrophy, laryngeal mucosal changes, and other

alterations Cardiovascular disease, osteoporosis,

and other changes also become more common as

menopause progresses Isenberger et al investigated

the possible connections between the reproductive

system and the singing voice.85 They studied

sing-ers with amenorrhea and found that common vocal

complaints among these singers included a crack in

the voice; the larynx could not make a smooth

tran-sition between chest and head voice; breathiness/

weakness; an inability to phonate on certain pitches;

a lack of flexibility or inability to sing certain scales

and/or arpeggios quickly and easily; and an

inabil-ity to adequately support tones These complaints

are similar to those reported by perimenopausal

women.86–88 In addition to the hormonal changes,

women entering or in menopause also have to deal

with age-related factors that affect the voice They

include decrease in lung power, atrophy of laryngeal

muscles, stiffening of laryngeal cartilages, vocal fold

thickening, a loss of elastic and collagenous fibers,

and other factors discussed in Chapter 13 The vocal

correlates may include breathiness, decrease in

over-all vocal range (especiover-ally upper range), change in

characteristics of the vibrato, development of a

trem-olo, decreased breath control, vocal fatigue, and pitch

inaccuracies.86–89 After menopause, voices typically

drop in fundamental frequency because the ovary

secretes little or no estrogen, but continues to secrete

androgen

It should be remembered that cessation of

men-strual periods is often a late sign of hormonal changes

The most prominent menopausal hormonal change

is a 10- to 20-fold drop in estradiol levels.90 In some

cases, hypoestrogenic voice changes may precede interruption of menses, and it may be desirable to start estrogen replacement even before menstrual periods become irregular or stop Hormone replace-ment therapy (HRT) may be helpful in some singers,91

although other studies have failed to show any vocal benefit from hormone replacement therapy In recent years, hormone replacement therapy has been viewed with a much more critical eye The number of meno-pausal women being treated with HRT has dropped, and the intensity of therapy has been reduced greatly Estrogen replacement to premenopause levels is no longer accepted and should not be a goal of therapy Both sequential and continuous HRT using estrogen and progesterone have been shown to be safe vocally, although continuous therapy is generally preferred Care must be taken to keep progesterone doses low, and this medication may even be omitted if no uterus

is present Due to increased risk of myocardial tion and stroke, late initiation of HRT is no longer recommended There are many potential benefits of estrogen replacement, including not only increased vocal longevity, but also avoidance of osteoporosis, cardiovascular disease, and other systemic problems However, there are also potential risks, including

infarc-an increased incidence of endometrial carcinoma, breast cancer, and venous thrombosis Interest-ingly, cutaneously delivered estrogens do not seem

to increase the risk of venous thromboembolism It

is recommended strongly that singers approaching menopause be referred to a gynecologist specializing

in the treatment of menopause for appropriate seling and careful consideration of the potential risks and benefits of HRT A good resource for referrals in the United States is the North American Menopause Society database (http://www.menopause.org)

coun-Thyroid Hormones

The thyroid gland regulates protein synthesis and sue metabolism through the production of thyroid hormones under the control of thyroid-stimulating and thyrotropin-releasing hormones Thyroid hor-mone is also necessary for numerous other normal functions, including growth Disorders of the thy-roid gland can cause laryngeal dysfunction either through hormone effects or due to local effects on the recurrent laryngeal nerves This topic is discussed in greater detail in Chapter 17

tis-Thyroid hormone production is under lamic and pituitary control The hypothalamus releases thyrotropin-releasing hormone (TRH), which stimu-lates the pituitary production of thyroid-stimulating

hypotha-hormone (TSH) TSH then acts directly on the

thy-roid gland to increase the synthesis and release of the

thyroid hormone thyroxine Thyroxine is produced

in the thyroid gland by binding of organic iodine to

tyrosine Two forms of thyroxine exist in the body,

tri-iodothyroxine (T3) and tetra-iodothyroxine (T4)

T4 is the primary hormone released by the thyroid

gland; it is then converted by the liver and kidney to

the more active form, T3 Both T3 and T4 are

exten-sively protein bound in the serum, primarily by

thy-roid-binding globulin and albumin Only unbound

hormone is active Free thyroxine inhibits the release

of both TSH and TRH, providing feedback inhibition

to maintain stable levels of free thyroid hormone

Thyroid hormone binds to intranuclear receptors that

bind directly to DNA, changing gene expression

Thyroid disorders are extremely common in

clini-cal practice and are reviewed more extensively in

Chapter 17 It has been estimated that 1.4% of women

in the United States have low thyroid function

(hypo-thyroid), and approximately 4% of adult Americans

have thyroid nodules.92 Hypothyroidism is more

common in the elderly and often produces symptoms

mistaken for aging changes In general,

hypothyroid-ism causes lethargy, muscle weakness, weight gain,

temperature intolerance, dry skin, brittle hair,

con-stipation, menstrual irregularities, muscle cramps,

neurological dysfunction, and dysphonia

Hypothy-roidism is a well-recognized cause of voice

disor-ders.93–97 Up to 80% of patients with hypothyroidism

may have voice complaints, with the frequency of

voice problems increasing with more severe

hypo-thyroidism.98 Hoarseness, vocal fatigue, muffling of

the voice, loss of range, and a feeling of a lump in

the throat may be present even with mild

hypothy-roidism Even when thyroid function tests are within

the low-normal range, this diagnosis should be

con-sidered, especially if thyroid-stimulating hormone

levels are in the high-normal range or are elevated

Thyroid evaluation also may require other blood

tests, ultrasound, uptake scans, fine needle biopsy,

and additional studies not discussed in this book

The mechanism of voice changes associated with

hypothyroidism is not completely understood,

espe-cially in cases of mild hypothyroidism More than 30

years ago, Ritter demonstrated an increased level of

acid mucopolysaccharides submucosally in the vocal

folds in hypothyroidism.94 These excess

mucopoly-saccharides probably act to increase the osmolality of

the lamina propria, increasing its fluid content This

results in effectively increased vocal fold mass and

decreased vibration In some cases, changes similar

to Reinke’s edema may be apparent In severe

hypo-thyroidism with myxedema, these changes are more

profound and may be associated with decreased muscle strength and even vocal fold paralysis Hypo-thyroidism also can cause other symptoms impacting professional voice users, including nasal stuffiness, rhinorrhea, and pharyngeal dryness.96 Treatment for hypothyroidism depends on the etiology In most cases, if neoplasia is not present, thyroid replacement

is sufficient However, numerous functions ing voice) should be monitored closely, and otolaryn-gologists who do not work frequently with thyroid disease certainly should consider collaborative man-agement with an endocrinologist With appropriate treatment voice changes associated with hypothy-roidism should be reversible Although changes that occur with hypothyroidism may mimic Reinke’s edema in some cases, hypothyroidism is no more common in patients with isolated Reinke’s edema than in age- and sex-matched populations.99

(includ-Although hyperthyroidism is less common than hypothyroidism, it can produce similar voice dis-turbances.96 Symptoms of hyperthyroidism include heat intolerance, sweating, palpitations, weight loss, tremors, and weakness Mild hyperthyroidism usu-ally does not cause voice problems In more severe cases, muscle weakness, dehydration, and tremor all contribute to voice changes Physiologic changes in laryngeal structure also may occur Fulminant hyper-thyroidism, or thyrotoxicosis, causes serious medical symptoms that can be both very unpleasant and life threatening Management of thyrotoxicosis includes beta-adrenergic blockade to decrease the cardiac symptoms as well as medical intervention to decrease the release of thyroid hormone Oral administration

of large quantities of iodine is used in many cases,

as thyroid uptake of iodine temporarily inhibits the release of formed thyroid hormone and can decrease the size and vascularity of a toxic goiter Propylthio-uracil or methimazole also blocks thyroid hormone synthesis and release They are effective over a longer term than iodine Definitive treatment of hyperthy-roidism may require thyroid ablation with radioac-tive iodine or total thyroidectomy

The close anatomic relation between the thyroid gland and the recurrent and superior laryngeal nerves places these nerves at risk when the thyroid gland is involved with structural or inflammatory disorders Structural thyroid disorders including tumors and benign goiters may interfere with voice by stretching the nerves, causing vocal fold paresis or paralysis,

or by invasion or compression of the larynx or chea Large thyroid masses also can affect voice by impairing vertical laryngeal motion Inflammatory disorders of the thyroid gland can cause neuropraxia

tra-of the recurrent or superior laryngeal nerves The

most common inflammatory disorder of the thyroid

is Hashimoto’s thyroiditis, an autoimmune disorder

Other forms of thyroiditis are less common but also

can affect the neural supply of the larynx Similar

problems may arise consequent to surgery of the

thyroid gland.99 Transient changes in the quality of

a professional voice user’s instrument are expected

after thyroid surgery, but permanent changes are

rare, especially when the surgery is performed with

nerve monitoring by an experienced thyroid surgeon

In one study of 12 professional singers undergoing

thyroidectomy, all returned to performance after a

mean recovery of 9 weeks (range 0.5–8 months).100,101

Pituitary Hormones

The pituitary and hypothalamus are both important

in regulating a host of endocrine functions In

addi-tion to regulating the secreaddi-tion of sex and thyroid

hormones as discussed previously, the hypothalamic-

pituitary system controls the levels of growth

hor-mone (GH), prolactin, oxytocin, antidiuretic horhor-mone

(ADH), and cortisol via adrenocorticotropic hormone

(ACTH) Professional voice users may develop

prob-lems due to either deficiency or excess of these

hor-mones Disorders leading to deficiency in hormones

from the pituitary are rare, and voice changes are

not always prominent symptoms Pituitary hormone

excess, normally from functional adenomas of the

pituitary, is more common As symptoms generally

are insidious in onset and often nonspecific, an astute

physician with interest in voice disorders may be the

first to suspect and diagnose a pituitary adenoma

Treatment of pituitary adenomas is primarily by

sur-gical resection, although medications are available for

some types of tumors Multiple surgical approaches

have been described, although transphenoidal

micro-surgery is used most commonly Sublabial

transsphe-noidal approaches can disrupt sensory innervation to

the upper lip and alveolus, causing transient speech

compromise lasting several months.102 Voice

pro-fessionals should be warned about this potentially

troublesome surgical complication Transnasal

endo-scopic techniques are therefore encouraged in voice

professionals

Prolactin

Prolactin-secreting tumors occur with equal frequency

in men and women, but they are often diagnosed

earlier in women High levels of prolactin inhibit the

normal LH surge that triggers ovulation; so women

with prolactinomas most often present with

amen-orrhea, infertility, and galactorrhea Voice symptoms are similar to those that occur premenstrually in some women Men generally complain only of decreased libido Voice changes are not prominent in men

Growth Hormone

Excess growth hormone causes acromegaly mon symptoms include coarse facial features with overgrowth of the mandible and frontal bossing, enlargement of hands and feet, muscle weakness, headache, arthralgias, paresthesias, and goiter In addition to changes in the nasopharyngeal airway and oral cavity, the larynx itself is altered The car-tilaginous larynx widens and grows; the vocal folds become thickened, dropping the fundamental voice frequency and coarsening the voice.103 Death from respiratory causes is 3 times more likely in acrome-galic patients than in matched controls.104 Although much of the upper respiratory compromise is due to macroglossia and hypertrophy of pharyngeal soft tis-sue, cases of slowly progressive laryngeal obstruction requiring tracheotomy have been reported.103 The cri-coarytenoid joints may become fixed in acromegalics and there has been speculation that acromegalic patients may be more prone to develop arytenoid dislocations than other patients Laryngoceles are more common in these patients and may contribute

Com-to respiraCom-tory difficulties.105

Acromegaly may be treated by surgery, radiation therapy, or medications Many patients require a combination of treatment modalities Medications used to control acromegaly are primarily somatosta-tin analogues, many of which are now available in long-acting formulations Pituitary surgery has been reported to result in normalization of vocal funda-mental frequency within a few weeks of surgery.103

Other physical changes often are permanent

Adrenocorticotropic Hormone (ACTH)

Decreased production of ACTH causes falling levels

of cortisol, a life-threatening condition Symptoms include weakness, anorexia, and weight loss in the early stages; hypotension, vomiting, diarrhea, and personality changes often occur later Without treat-ment, mortality approaches 80% Treatment involves prompt replacement of glucocorticoids

Increased levels of ACTH cause Cushing’s disease Other states of glucocorticoid excess result in similar symptoms but are collectively termed Cushing’s syn-drome Women are 5 times more likely than men to develop Cushing’s disease, most often between the ages of 25 and 45 Common symptoms include truncal

and facial obesity, osteoporosis, hypertension,

vir-ilization of females, diabetes mellitus, and

psycho-logical changes Amenorrhea is common in women

Voice changes are more prominent in women than

men and can range from mild changes similar to

premenstrual voice changes to severe, irreversible

virilization of the voice Professional voice users

with long-standing glucocorticoid excess also may

develop sequelae from diabetes, as discussed below

Treatment is directed at the underlying cause of

the glucocorticoid excess and can range from

pitu-itary surgery or radiation in patients with

ACTH-secreting tumors to minimizing chronic use of

medicinal glucocorticoids

Diabetes

Diabetes mellitus is one of the most common

medi-cal conditions affecting Americans Associated with

obesity, type II diabetes is a state of relative insulin

resistance Chronically elevated blood glucose levels

and high serum insulin levels cause a wide range

of complications Because diabetes is so prevalent,

laryngologists must be particularly familiar with

its laryngeal manifestations In addition to the

com-monly recognized problems of polyuria, polydipsia,

and polyphagia, diabetes is well known to cause

xerostomia, xerophonia, hearing loss, microvascular

disease, and neuropathies Microvascular occlusion

results in ischemia and even tissue death,

includ-ing muscle atrophy and diabetic retinopathy

Neu-ropathy leads to gradual loss of fine motor control,

which may be noticed early by a professional voice

user In advanced states, neuropathy may even cause

vocal fold paralysis.106 Neuropathies also involve

the sensory nerves and can impair tactile

informa-tion needed for voice control In addiinforma-tion to causing

other control problems, sensory deficits may impair

or destroy the person’s ability to sing “by feel” rather

than “by ear” in noisy environments In addition,

diabetes mellitus is associated with an increased rate

of infection, generalized fatigue, edema, poor wound

healing, and other health problems that may impair

voice function It is common for the laryngologist

attuned to laryngeal manifestations of systemic

dis-ease to be the first physician to diagnose diabetes

Maintenance of good vocal health, technique, and

hygiene is essential in individuals with diabetes

Weight loss, dietary changes, and aerobic exercise can

control mild cases of diabetes For more serious cases,

maintaining good control of blood glucose levels is

essential The wide variety of medications available

for diabetics makes close supervision by an

endocri-nologist desirable Consistent maintenance of blood glucose levels within the normal range can slow or prevent the development of many of the complica-tions of long-term diabetes

Other Hormone Dysfunctions

Other endocrine disturbances may alter the voice, as well For example, thymic abnormalities can lead to feminization of the voice.107 Pancreatic dysfunction may result in xerophonia (dry voice), as occurs in patients with diabetes mellitus The voice effects of some endocrine systems or hormones have not been studied adequately For example, despite the wide-spread use of melatonin to combat jet lag and other sleep disorders, little is known about its physiologic effects Care must be taken before recommending hormonally active medications (including selected alternative medications) to professional voice users, because minor changes in the structure or function

of the larynx can have dire consequences in this population

Conclusion

Hormone imbalances and dysfunction commonly affect the voice, and dysphonia may be the presenting symptom of serious systemic disease Laryngologists must be alert constantly for hormonal dysfunction in patients with voice complaints Collaboration with

a skilled endocrinologist interested in the problems

of singers, actors, and other voice professionals is invaluable

References

1 Abitbol J, deBrux J, Millot G, et al Does a hormonal vocal cord cycle exist in women? Study of vocal pre- menstrual syndrome in voice performers by video- stroboscopy glottography and cytology on 38 women

J Voice 1989;3:157–162.

2 Higgin MB, Saxman JH Variations in vocal frequency

perturbation across the menstrual cycle J Voice 1989;

3:233–243.

3 Abitbol J, Abitbol P, Abitbol B Sex hormones and the

female voice J Voice 1999;13(3):424–446.

4 Marsigliante S, Muscella A, Resta L, Storelli Human larynx expresses isoforms of the oestrogen receptor

Cancer Lett 1996;99:191–196.

5 Voelter CH, Kleinsasser N, Joa P, et al Detection of

hormone receptors in the human vocal fold Eur Arch Otorhinolarngol 2008;265:1239–1244.

6 Brunings JW, Schepens JJ, Peutz-Kootstra CJ, Kross,

KW The expression of estrogen and progesterone

receptors in the human larynx J Voice 2013;27(3):

376–380.

7 Wu D, Jiang JJ, Fang R, Swinarski K, Cui X G

pro-tein-coupled estrogen receptor 1 expression in human

vocal fold Laryngoscope 2013;123:948–951.

8 Bianchini C, Patore A, Pelucchi S, et al Sex hormone

receptor levels in laryngeal carcinoma: a comparison

between protein and RNA evaluations Eur Arch

Oto-rhinolarngol. 2008:265:1089–1094.

9 Ferguson BJ, Hudson WR, McCarty KS Jr Sex

ste-roid receptor distribution in the human larynx and

laryngeal carcinoma Arch Otolaryngol Head Neck Surg

1987;113:1311–1314.

10 Marsigliante S, Leo G, Resta L, Storelli C Steroid

receptor status in malignant and non-malignant

lar-ynx Ann Oncol 1992;3(5):387–392.

11 Newman SR, Bulter J, Hammond EH, Gray SD

Pre-liminary report on hormone receptors in the human

vocal fold J Voice 2000;14(1):72–81.

12 Schneider B, Cohen E, Stani J, et al Towards the

expression of sex hormone receptors in the human

vocal fold J Voice 2006;21(4):502–507.

13 Cohen E, Kolbus A, Trotsenburg M, et al

Immuno-histochemical examinations of sex hormone

recep-tors in benign vocal fold lesions Folia Phoniatr Logop

2009;61:259–262.

14 Nacci A, Fattori B, Basole F, et al Sex hormone

recep-tors in vocal fold tissue: a theory about the influence

of sex hormones in the larynx Folia Phoniatr Logop

2011;63:77–82.

15 Lee PA, Migeon CJ Puberty in boys: correlation of

plasma levels of gonadotropins (LH, FSH),

andro-gens (testosterone, androstenedione,

dehydroepi-androsterone and its sulfate), estrogens (estrone

and estradiol) and progestins (progesterone and

17 hydroxyprogesterone J Clin Endrocrinol Metab

1975;41: 556–562.

16 Porto CS, Lazari MF, Abreau LC, Bardin CW,

Gun-salus GL Receptors for androgen-binding proteins:

internalization and intracellular signaling J Steroid

Biochem Mol Biol 1995;53:561–565.

17 Oliver VL, Poulios K, Ventura S, Hayes JM A novel

androgen signaling pathway uses

dihydrotestoster-one , but not testosterdihydrotestoster-one, to activate the EGF receptor

signaling cascade in prostate stromal cells Br J

Phar-macol 2013;170(3):592–601.

18 Isidori AM, Giannetta E, Greco EA, et al Effects of

testosterone on body composition, bone metabolism,

and serum lipid profile in middle aged men: a

meta-analysis Clin Endocrinol (Oxf) 2005;63(3):280–293.

19 Zajac Z, Wilk M, Soca T, Maszczyk A, Chycki J Effects

of growth hormone and testosterone on aerobic and

anaerobic fitness, body composition and lipoprotein

profile in middle-aged men Ann Agric Environ Med

2014;21(1):156–160.

20 Hartgens F, Kulpers H Effects of androgenic-anabolic

steroids in athletes Sports Med 2004;34(8):513–554.

21 Bermon S, Vilain E, Fenichel P, Ritzen M Women with hyperandrogenism in elite sports: scientific and ethi-

cal rationales for regulating J Clin Endocrinol Metab

2015;100(3):828–830.

22 Wood RI, Stanton SJ Testosterone and sport: current

perspectives Horm Behav 2012;61(1):147–155.

23 Harries ML, Walker JM, Williams DM, Hawkins S, Hughes IA Changes in the male voice at puberty

Arch Dis Child 1997;77:445–447.

24 Brodnitz F The age of the castrato voice J Speech Hear Disord 1975;40:291–295.

25 Smith AM Eunuchs and castrations: JAMA faces the music JAMA 1991;266:655–656.

26 Nieschlag E, Nieschlag S, Behre HM Lifespan and

29 King A, Ashby J, Nelson C Effects of testosterone

replacement on a male professional singer J Voice

2001; 15(4):553–557.

30 Meuser W, Nieschlag E Sexuell hormone und

stim-mlage des mannes Dtsch Med Wochenschr 1977;102:

261–264.

31 Evans S, Neave N, Wakelin D, Hamilton C The tionship between testosterone and vocal frequencies

rela-in human males Physiol Behav 2008;93:783–788.

32 Testosterone and Other Anabolic Androgenic Steroids (AAS): FDA Statement-Risks Associated with Abuse and Dependence http://www.fda.gov/safety/med watch/safetyinformation/safetyalertforhumanmed icalproducts/ucm526151.htm Accessed November

28, 2016.

33 Gugatschka M, Kiesler K, Obermayer-Pietsch B, et

al Sex hormones and the elderly male voice J Voice

2010; 24(3):369–373.

34 Strauss RH, Mariah T, Liggett MS, Lanese RR Anabolic steroid use and perceived effects in ten-weight-trained

women athletes JAMA 1985;253(19):2871–2873.

35 Damsté PH Virilization of the voice due to anabolic

steroids Folia Phoniatr (Basel) 1964;16:10–18.

36 Damsté PH Voice changes in adult women caused by

virilizing agents J Speech Hear Disord 1967;32:126–132.

37 Saez S, Francoise S Récepteurs d’androgènes: mise en évidence dans la fraction cytosolique de muqueuse normale et d’épithéliomas pharyngólaryngés humains

C R Acad Sci (Paris) 1975;280:935–938.

38 Vuorenkoski V, Lenko HL, Tjernlund, P Vuorenkoski

L, Perheentupa J Fundamental voice frequency ing normal and abnormal growth, and after androgen

dur-treatment Arch Dis Child 1978;53:201–209.

39 Arndt HJ Stimmestrungen nach Behandlung mit

androgenen und anabolen Hormonen Munch Med Wochenschr 1974;116:1715–1720.

40 Bourdial J Les troubles de la voix provoqués par la

thérapeutique hormonale androgène Ann Otolaryngol Chir Cervicofac 1970;87:725–734.

41 Grisa L, Leonel ML, Goncalves MIR, et al Impact of

early postnatal androgen exposure on voice

develop-ment PLoS One 2012;7(12):e50242.

42 Flach M, Schwickardi H, Simen R Welchen Einfluss

haben Menstruation and Schwangerschaft auf die

augsgebildete Gesangsstimme? Folia Phonatr (Basel)

1968; 21:199–210.

43 von Deuster CV Irreversible Stimmestrung in der

Schwangerscheft HNO 1977;25:430–432.

44 Beckmann CRB, Ling FW, Barzansky BM, et al

Obstet-rics and Gynecology Baltimore, MD: Williams and

Wilkins; 1995.

45 Amir O, Biron-Shental T The impact of hormonal

fluctuations on female vocal folds Curr Opin

Otolar-yngol Head Neck Surg 2004;12:180–184.

46 Furst-Recktenwald S, Dorr HG, Rosanowski F

Andro-glottia in a young female adolescent with congenital

adrenal hyperplasia and 21-hydroxylase deficiency J

Ped Endocrinol Metab 200;13(7):959–962.

47 Nygren U, Nystrom HF, Falhammar H, et al Voice

problems due to virilization in adult women with

congenital adrenal hyperplasia due to 21-hydroxylase

deficiency Clin Endocrinol 2013;79:859–866.

48 Damrose E Quantifying the impact of androgen

ther-apy on the female larynx Auris Nasus Larynx 2009; 36:

110–112.

49 van Gelder L Psychosomatic aspects of endocrine

dis-orders of the voice J Commun Disord 1974;7:257–262.

50 Schiff M The influence of estrogens on connective

tis-sue In: Asboe-Hansen G, ed Hormones and Connective

Tissue Copenhagen, Denmark: Munksgaard Press;

1967: 282–341.

51 Wendler J Zyklusabhngige leistungsschwankungen

der Stimme und ihre Beeinflussung durch

Ovulation-shemmen Folia Phoniatr (Basel) 1972;24:259–277.

52 Lacina O Der Einfluss der Menstruation auf die

Stimme der Singerinnen Folia Phoniatr (Basel) 1968;20:

13–24.

53 Abitbol J Vocal cord hemorrhages in voice

profession-als J Voice 1988;2(3):261–266.

54 Raj A, Gupta B, Chowdhury A, Chadha S A study of

voice changes in various phases of menstrual cycle

and in postmenopausal women J Voice 2010;24(3):

363–368.

55 Davis CB, Davis ML The effects of premenstrual

syndrome (PMS) on the female singer J Voice 1993;

7(4):337–353.

56 Silverman EM, Zimmer CH Effect of the menstrual

cycle on voice quality Arch Otolaryngol 1978;104:7–10.

57 Frable MA Hoarseness, a symptom of premenstrual

tension Arch Otolaryngol 1962;75:66–68.

58 Valenta LJ Cyclic laryngeal edema with aphonia

Let-ter to the Editor Ann Int Med 1975;82(1):62–63.

59 Higgins MD, Saxman JH Variations in vocal

fre-quency perturbation across the menstrual cycle J

Voice 1989; 3(3):233–243.

60 Silverman EM Speech fluency fluctuations during the

menstrual cycle J Speech Hear Res 1975;18:202–206.

61 Pahn J, Goretzlehner G Stimmestrungen durch

hor-monale Kontrazeptiva Zentralbl Gynakol 1978;100:

NY: The Voice Foundation; 1978:3:86.

64 Wentz AC Dysmenorrhea, premenstrual syndrome

and related disorders In: Jones HW, Wentz AC,

Bur-nett LS, eds Novak’s Textbook of Gynecology Baltimore,

MD: Williams and Wilkins; 1988:240–262.

65 La FMB, Howard DM, Ledger W, Davidson JW, Jones

G Oral contraceptive pill containing drospirenone and the professional voice: an electrolaryngographic

analysis Logoped Phoniatr Vocol 2009;34:11–19.

66 Amir O, Biron-Shental T, Muchnik C, Kishon-Rabin

L Do oral contraceptives improve vocal quality?

Lim-ited trial on low-dose formulations Obstet Gynecol

2003;101(4):773–777.

67 Andersch B, Milsom I An epidemiologic study of

young women with dysmenorrhea Am J Obstet col 1982;144:655–660.

68 Daniels S, Robbins J, West CR, Nemeth MA Celecoxib

in the treatment of primary dysmenorrhea: results from two randomized, double blind, active- and

placebo-controlled, crossover studies Clin Ther 2009;

70 Diegoli MS, da Fonseca AM, Diegoli CA, Pinotti

JA A double-blind trial of four medications to treat

severe premenstrual syndrome Int J Gynaecol Obstet

1998;62(1):63–67.

71 Steiner M, Romano SJ, Babcock S, et al The efficacy

of fluoxetine in improving physical symptoms

asso-ciated with premenstrual dysphoric disorder BJOG

2001;108(5):462–468.

72 Guzick D Polycystic ovary syndrome:

symptomatol-ogy, pathophysiolsymptomatol-ogy, and epidemiology Am J Obstet Gynecol 1998;179(6, pt 2):S89–S93.

73 Baker J A report on alterations to the speaking and singing voices of four women following hormonal

therapy with virilizing agents J Voice 1999;13:496–507.

74 Sztajzel J, Periat M, Marti V, Krall P, Rutishauser W Effect of sexual activity on cycle ergometer stress test parameters, on plasmatic testosterone levels and

on concentration capacity J Sports Med Phys Fitness

77 Amir O, Lebi-Jacob N, Harari O The Effect of in vitro

fertilization treatment on women’s voice J Voice 2014;

28(4):518–522.

78 Bhatia PL, Singh MS, Jha BK Laryngopathia

gravi-darum Ear Nose Throat J 1981;60:408–412.

79 Hoing R, Seitzer D Clinical aspects of laryngopathia

gravidarum Laryngol Rhinol Otol (Stuttg) 1988; 67(11):

564–566.

80 Brimacombe J Acute pharyngolaryngeal oedema and

pre-eclamptic toxaemia Anaesth Intensive Care 1992;

20(1):97–98.

81 von Deuster C Irreversible vocal changes in

preg-nancy HNO 1977;25(12):430–432.

82 Laitinen K Life-threatening laryngeal edema in a

pregnant woman previously treated for thyroid

car-cinoma Obstet Gynecol 1991;78(5, pt 2):937–938.

83 Baptista-La FM, Sundberg J Pregnancy and the

sing-ing voice: reports from a case study J Voice 2012; 26(4):

431–439.

84 Section on Breastfeeding, American Academy of

atrics Breastfeeding and the use of human milk

Pedi-atrics 2012;129:e827–e841.

85 Isenberger H, Brown WS, Rothman H Effects of

menstruation on the singing voice Part II: further

developments in research In: Transcripts of the Twelfth

Symposium: Care of the Professional Voice New York,

NY: The Voice Foundation; 1983:117–123.

86 D’haeseleer E, Depypere H, Claeys S, et al The

im-pact of menopause on vocal quality Menopause

2011;18(3): 267–272.

87 Friedman AD The impact of menopause on the

voice: past, present and future Menopause 2011;18(3):

248–250.

88 Nebdes-Laureano J, Ferriani RA, reis RM, et al

Com-parison of fundamental voice frequency between

menopausal women and women at menacme

Maturi-tas 2006;55:195–199.

89 Hollien H “Old Voices”: What do we really know

about them? J Voice 1987;1(1):2–17.

90 Khaw K The menopause and hormone replacement

therapy Postgrad Med J 1992;68:615–623.

91 D’haeseleer E, Depypere H, Claeys S, van Bosel J,

van Lierde K The menopause and the female larynx,

clinical aspects and therapeutic options: A literature

review Maturitas 2009;64:27–32.

92 Larson PR The thyroid In: Wyngaarden JB, Smith

LH, eds Cecil’s Textbook of Medicine Vol 2 18th ed

Philadelphia, PA: WB Saunders; 1988:1315–1344.

93 Ritter FN The effect of hypothyroidism on the larynx

of the rat Ann Otol Rhinol Laryngol 1964;73:404–416.

94 Ritter FN Endocrinology In: Paparella M, Shumrick

D, eds Otolaryngology Vol 1 Philadelphia, PA: WB

Saunders; 1973:727–734.

95 Michelsson K, Sirvio P Cry analysis in congenital

hypothyroidism Folia Phoniatr (Basel) 1976;28:40–47.

96 Gupta OP, Bhatia PL, Agarwal MK, et al Nasal ryngeal and laryngeal manifestations of hypothyroid-

pha-ism Ear Nose Throat J 1977;56(9):10–21.

97 Malinsky M, Chevrie-Muller C, Cerceau N Étude clinique et électrophysiologique des altérations de

la voix au cours des thyrotoxioses Ann Endocrinol (Paris) 1977;38:171–172.

98 Mohammadzadeh A, Heydari E, Azizi F Speech

impairment in primary hypothyroidism J Endocrinol Invest 2011;34:431–433.

99 White A, Sim DW, Maran AGD Reinke’s oedema and

thyroid function J Laryngol Otol 1991;105:291–292.

100 Timon CI, Hirani SP, Epstein R, Rafferty MA gation of the impact of thyroid surgery on vocal tract

Investi-steadiness J Voice 2010;24(5):610–613.

101 Randolph GA, Sritharan N, Song P, et al ectomy in the professional singer-neural monitored

Thyroid-surgical outcomes Thyroid 2015;25(6):665–671.

102 Viswanath N, Rosenfield DB, Baskin DS, Wieber SJ Transient speech compromise following sublabial transsphenoidal surgery: a case report and findings

of a small preliminary study Ear Nose Throat J 2000;

79(4):286–289.

103 Williams RG, Richards SH, Mills RG, Eccles R Voice

changes in acromegaly Laryngoscope 1994;104: 484–487.

104 Murrant NJ, Gatland DJ Respiratory problems in

acromegaly J Laryngol Otol 1990;104:52–55.

105 Motta S, Ferone D, Colao A, et al Fixity of vocal

chords and laryngocele in acromegaly J Endocrinol

1997; 20:672–674.

106 Sommer DD, Freeman JF Bilateral vocal cord

paraly-sis associated with diabetes mellitus: case reports J Otolaryngol 1994;23(3):169–171.

107 Imre V Hormonell bedingte Stimmestrungen Folia Phoniatr (Basel) 1968;20:394–404.

17

The Vocal Effects of Thyroid

Disorders and Their Treatment

Julia A Pfaff, Hilary Caruso-Sales, Aaron Jaworek, and

Robert Thayer Sataloff

Anatomical Considerations

The thyroid gland, one of the largest endocrine glands

in the body, is a butterfly-shaped gland laying in the

anterior neck usually at the level of the second to

fourth tracheal cartilages The gland is composed of

2 lateral lobes joined by a central isthmus, with each

lobe measuring approximately 4 cm cranial-caudal,

1.5 cm transverse, and 2 cm anterior-posterior

Occa-sionally, a pyramidal lobe is present cranially

repre-senting the remnant pathway as the thyroid gland

descended from the foramen cecum near the tongue

base to the gland’s final resting place in the lower

neck Attached to the posterolateral surface of the

thyroid gland are the superior and inferior

parathy-roid glands The superior glands are most commonly

located at the level of the cricothyroid joint,

approxi-mately 1 cm above the intersection of the recurrent

laryngeal nerve (RLN) and the inferior thyroid artery

in a plane deep to the RLN The inferior parathyroid

glands are more variable in location but are found

most commonly on the posterolateral aspect of the

thyroid capsule in close association with the inferior

pole of the thyroid The inferior parathyroid glands

are often located in a plane superficial to the RLN.1

The main arterial supply to the thyroid gland is

derived from the superior thyroid artery (STA),

which is a branch of the external carotid artery, and

the inferior thyroid artery (ITA) which is a branch of

the thyrocervical trunk The thyroid ITA artery is a

single unpaired persistent embryologic vessel seen

in approximately 1.5% to 12% of the population that

variably feeds the inferior thyroid isthmus.1 Venous

drainage of the thyroid includes the superior, dle, and inferior thyroid veins The superior thyroid artery and vein travel in close association within the superior pole vascular pedicle, while the middle and inferior thyroid veins travel without arteries and drain into the internal jugular vein, and the internal jugular or brachiocephalic vein, respectively The principal innervation of the thyroid itself is via the autonomic nervous system, including parasympa-thetic fibers from the vagus nerve and sympathetic fibers from the superior sympathetic chain.1

mid-The thyroid lobes are in close proximity to 2 vical branches of the vagus nerve on each side that innervate the larynx — the recurrent laryngeal nerve (RLN) and the superior laryngeal nerve (SLN) This anatomical relationship has important implications for laryngeal function in the setting of thyroid disor-ders and following thyroid or parathyroid surgery The RLN provides motor innervation to all intrinsic laryngeal muscles except the cricothyroid muscle, which receives motor innervation from the exter-nal branch of the SLN (EBSLN) The RLN supplies sensation to the vocal folds and subglottic larynx, upper esophagus, and trachea as well as parasym-pathetic innervation to the lower pharynx, larynx, trachea, and upper esophagus The internal branch

cer-of the SLN (IBSLN) supplies sensation to the lower pharynx, supraglottic larynx, and base of tongue, and supplies special visceral afferents to epiglottic taste receptors The anatomy is covered in greater detail elsewhere in this book

The SLN begins its course by branching from the upper vagus nerve, descending medial to the carotid

sheath, and eventually dividing into internal and

external branches approximately 2 to 3 cm above the

superior pole of the thyroid gland The IBSLN

con-tinues traveling medially to the carotid artery and

eventually enters the posterior aspect of the

thyro-hyoid membrane to innervate the supraglottis The

EBSLN is often classified according to its relationship

with the STA, traveling closely with the artery and

eventually piercing the inferior constrictor to supply

the cricothyroid muscle The STA and superior pole

are often described as variable landmarks and many

classifications of the anatomical course of the EBSLN

have been depicted.2 In particular, the course of the

EBSLN with respect to the inferior constrictor and

the nerve’s point of entry into the inferior

constric-tor muscle vary, with the nerve lying either

super-ficial or deep to the muscle itself The importance of

classifying the location of the EBSLN should not be

overlooked as injury to this nerve, particularly

dur-ing thyroidectomy, can lead to vocal dysfunction

Cernea et al proposed a classification system based

on the level above the superior pole of the thyroid at

which the EBSLN crosses the STA.3 They classified

a nerve to be “at risk” during thyroid surgery if the

EBSLN crossed within 1 cm or less of the superior

pole Cernea type 1 nerves cross the STA 1 cm or more

above the superior pole, type 2a cross a distance <1 cm

above the superior pole and type 2b cross below the

upper border of the thyroid Hence, Cernea types 2a

and 2b are considered “at risk” during thyroid

sur-gery Cernea also described type Ni nerves when the

EBSLN could not be located.3–5

Kierner et al proposed a modification of the Cernea

classification Kierner added a fourth variant

capa-ble of explaining the Cernea type Ni In fact, Kierner

types 1 through 3 correspond with Cernea types 1, 2a,

and 2b, respectively Kierner type 4, however,

corre-sponds with an EBSLN that does not cross the

supe-rior thyroid artery (STA) and, instead, runs dorsally

until its termination at the cricothyroid muscle.6

The Friedman classification system is based on

the relationship between the EBSLN and the

infe-rior pharyngeal constrictor muscle According to

the Friedman classification, a type 1 nerve descends

superficial to the inferior pharyngeal constrictor until

the cricothyroid is reached Type 2 involves neural

penetration of the lower portion of the constrictor

muscle, and type 3 involves descent of the EBSLN

deep to the constrictor muscle throughout its course

Based on this classification, Friedman claimed that

application of a nerve stimulator at the inferior

con-strictor-cricothyroid junction would indicate whether

the EBSLN was located deep to the inferior

constric-tor Absence of a stimulation response would imply a

Friedman type 1 nerve (equivalent to Cernea types 2a and 2b and Kierner types 2 and 3), requiring further dissection for nerve identification.7

Block et al classified the EBSLN according to whether

it passes between, superficial to, or deep to the rior thyroid artery and its branches5 (Figure 17–1) Block type A involves the EBSLN lying on the infe-rior constrictor, running medial to the STA Type B involves an EBSLN running deep to the inferior con-strictor (ie, Friedman type 3), while types C and D classify the EBSLN as crossing between the branches

supe-of the STA Finally, type E involves the EBSLN ing below the apex of the superior thyroid pole (ie, Cernea type 2b and Kierner type 3).5

cross-The embryologic origin of the RLN gives it a unique anatomical course On the right, the RLN branches from the vagus nerve and loops around the subclavian artery at the level of the innominate artery It then ascends in the neck, traveling from lateral to medial in an oblique course, crossing the inferior thyroid artery and eventually approaches the trachoesophageal groove behind the common carotid artery On the left, the RLN arises from the vagus nerve just below the aortic arch and loops medially under the aorta It then emerges from underneath the aor-tic arch and enters the thoracic inlet in a paratracheal position, coursing upward along the tracheoesopha-geal groove, ultimately crossing the distal branches of the inferior thyroid artery Eventually, each recurrent laryngeal nerve enters the larynx between the infe-rior cornu of the thyroid cartilage and the arch of the cricoid, branching after laryngeal penetration in two-thirds of cases In the remaining one-third of cases, the RLN branches prior to its laryngeal entry point.1

In 0.5% to 1% of the population, the RLN does not follow its anticipated course in association with the great vessels.1 Instead, it arises from the vagus nerve at the level of the thyroid gland and enters the larynx directly close to the superior thyroid vessels Known as a nonrecurrent RLN, this anomaly is found exclusively on the right side (except in patients with transposition of the great vessels) and is associated with an anomalous retro-esophageal right subclavian artery The nonrecurrent RLN places the nerve at higher risk during thyroid surgery as it is not located

in the expected anatomical location.1

Thyroid Dysfunction and Physiology

The thyroid gland is responsible for the production

of 2 major metabolic hormones known as thyroxine (T4) and triiodothyronine (T3) These hormones play critical roles in the regulation of the body’s basal

metabolic rate Overproduction of thyroid hormone

results in hyperthyroidism, while underproduction

results in hypothyroidism Complete absence of

these hormones can cause a 40% to 50% decrease in

basal metabolic rates, while overproduction can lead

to a basal metabolic rate 60% to 100% above the

nor-mal level.8

The thyroid gland is composed of follicles

consist-ing of a colloid matrix that contain a large molecule

called thyroglobulin The colloid contains various

amino acids and molecules of iodine involved in the

production of thyroid hormone Formation of thyroid

hormones requires the enzyme peroxidase, which is

responsible for the oxidation of iodine The oxidized

iodine is then combined with the amino acids to form

thyroid hormone, which is stored in the follicle until

its release.8 Occasionally, patients can form

antibod-ies to thyroglobulin and peroxidase, which disrupt

the formation of thyroid hormone This can lead to

enlargement and nodularity of the gland, and

even-tually, a benign hypothyroid state known as

Hashi-moto’s (autoimmune) thyroiditis

Thyroid hormones are released from the gland

in response to thyroid-stimulating hormone (TSH)

from the pituitary Ninety-seven percent of thyroid

hormone released from the gland is in the form of

thyroxine (T4), which is later converted its active

form, triiodothyronine (T3) in the tissues.8 When the

level of circulating thyroid hormone is sufficient, it inhibits the pituitary from releasing more TSH Like-wise, when circulating hormone is low, it signals the pituitary to release more TSH This process, known

as negative feedback inhibition, is an important regulatory pathway in maintaining basal metabolic rate and a euthyroid state Some patients may form antibodies to the TSH receptor that result in its acti-vation and overstimulation of the release of thyroid hormone In this disease process, negative feedback inhibition is lost, resulting in an overt state of hyper-thyroidism known as toxic goiter, thyrotoxicosis, or Grave’s disease Thyroid blood tests are helpful in clinical evaluation (Table 17–1)

Thyroid dysfunction affects approximately 15% of the population with a female-to-male predominance

of 4:1, making it an exceedingly common endocrine disorder that is second only to diabetes mellitus.9,10

Because of its often indolent initial signs and toms, thyroid dysfunction may go unrecognized in some patients for many years, leading to advanced disease at presentation and a reduced quality of life

symp-at the time of diagnosis.9 Signs and symptoms of hyperthyroidism include excessive sweating, heat intolerance, heart palpitations, weight loss despite

an increased appetite, diarrhea, anxiety, insomnia, palmar hyperhidrosis, tremors, skin thickening (especially in the pretibial region), hyperreflexia,

Figure 17–1. Anatomical variants of the course of the external branch of the superior laryngeal nerve (EBSLN) (Illustration

by Casey Fisher, DO.)

irritability, and occasionally protrusion of the orbits

known as exophthalmos Voice users may present

with the complaint of an audible vocal tremor On

physical examination, hyperthyroidism may be

asso-ciated with tachycardia and other heart arrhythmias,

most commonly atrial fibrillation Signs and

symp-toms of hypothyroidism include fatigue, depression,

weight gain, constipation, impaired fertility, cold

intolerance, hyporeflexia, bradycardia, periobital

puffiness, nonpitting edema, muffling of the voice,

and thinning of the hair and nails Thyroid gland

enlargement may be found on examination of both

hypo- and hyperthyroid patients

Vocal Dysfunction and Thyroid Disease

In addition to the systemic signs and symptoms

described above, voice disorders are among the most

frequent presenting complaints in patients with

thy-roid disease McIvor et al demonstrated that up to

one-third of patients with thyroid disease enced dysphonia at the time of presentation.11 Kada-kia et al described similar findings, which included symptoms of tremulous voice, breathy or gravelly quality, and loss of range.12 Heman-Ackah et al found

experi-that 47.4% of patients who presented to their gology practice with vocal fold paresis were found

laryn-to have underlying undiagnosed thyroid disease, including benign disease (29.9%), thyroiditis (7.8%), hyperthyroidism (3.6%), and malignancy (1.6%).13

Benign Thyroid Disease

Benign thyroid disease is an important consideration

in patients with vocal dysfunction because patients with hypothyroidism have been shown to score lower in vocal self-assessment, clinical evaluation of voice, and Voice-Related Quality of Life (V-RQOL).14

In a study of 67 women with benign thyroid disease, patients with vocal complaints had lower scores in all assessments, including vocal self-assessment, speech

Table 17–1 Common Laboratory Tests Utilized in the Assessment of Thyroid Disorders

Thyroxine binding

globulin (TBG) Produced in the liver 1 of 3 main proteins bound

to circulating T3 and T4

Low/high (TSH, free T4 usually normal, but total T4 and T3 may

be abnormal)

Low = gene defects (inherited),

hyperthyroidism, renal disease, liver disease, systemic illness, Cushing’s syndrome, malnutrition, medications

High = hypothyroidism, liver disease,

pregnancy

Thyroglobulin (TG) Prohormone for T3 and

T4 produced and used entirely within thyroid tissue

Elevated Marker for recurrence of well-differentiated

thyroid cancers, may be elevated in:

hyperthyroidism, subacute thyroiditis, thyroid adenomas

Antithyroglobulin

antibody Autoimmune marker for thyroid disease (can

interfere with thyroglobulin levels)

Present Well-differentiated thyroid cancer,

Hashimoto’s thyroiditis (40%–80%), Grave’s disease (50%–70%), nonthyroid autoimmune disease (40%), chronic urticaria, pregnancy (10%–15%), up to 10% of healthy individuals

Antithyroid

peroxidase antibody Autoimmune marker for thyroid disease

Present Hashimoto’s thyroiditis (90%–99%),

Grave’s disease (50%–80%), nonthyroid autoimmune disease (40%), pregnancy (10%–15%)

Thyroid-stimulating

immunoglobulin (TSI) TSH receptor antibody promotes production of

thyroid hormone

Present Grave’s disease (>90%), Hashimoto’s

thyroiditis (<20%), toxic multinodular goiter (<50%)

Thyrotropin

binding inhibitory

immunoglobulin (TBII)

TSH receptor antibody inhibits production of thyroid hormone

Present Grave’s disease (70%), Hashimoto’s

thyroiditis (20%–30%), toxic multinodular goiter (15%)

Note Abnormal values should be interpreted with free T4 and/or T3 levels to determine if clinical versus subclinical hyper- or hypothyroid

and language pathologist assessment using a visual

analog scale, and the V-RQOL questionnaire.14 Much

of the voice dysfunction associated with benign

thy-roid disease is thought to be attributable to increased

hyalurionic acid concentrations in the vocal folds as

a result of a state of hypothyroidism The increase

in hyaluronic acid concentration leads to fluid

reten-tion and thickening of the vocal folds called

laryn-geal myxedema.14 These patients may present with

hoarseness characterized by lowered vocal pitch and

decreased vocal clarity despite a relatively normal

laryngeal examination.15 The histological changes

in the vocal folds develop rapidly in the setting of

hypothyroidism, and they can even be observed in

the period of transient hypothyroidism following

thyroidectomy with voice changes appearing as

early as 36 to 48 hours postoperatively.15 The human

larynx has also been shown to demonstrate thyroid

hormone receptors, TR alpha and beta, among the

fibrous lamina propria, cartilage, and glandular

ele-ments These receptors may also contribute to the

his-tologic and physiologic voice changes seen in thyroid

dysfunction.16 With thyroid hormone replacement

therapy, hypothyroidism can be reversed with an

improvement in voice outcomes.17 Birkent et al

dem-onstrated that 24 hypothyroid women treated with

thyroid hormone replacement therapy resulting in a

euthyroid state achieved a significant improvement

in vocal fundamental frequency from a pretreatment

average of 223.48 ± 36.10 Hz to 237.64 ± 38.31 Hz.18

Advanced Thyroid Disease

Advanced disease at diagnosis may increase the risk

of persistent or worsened voice disorders after

treat-ment.11 This is true especially among patients with

large goiter, hyperthyroidism, toxic goiter, and

thy-roid malignancy In a study by McIvor et al, 9 out of

27 patients with large, compressive goiters presented

with complaints of dysphonia Of the 12 patients

who presented with isolated nodules, only 2

dem-onstrated similar complaints.11 Other authors have

demonstrated similar findings, indicating that a

thy-roid mass of larger than 5 cm is a predictor of

worsen-ing postoperative voice outcomes,19 and up to 17% of

substernal goiters are associated with some degree

of recurrent nerve injury.20

In some instances of mulitnodular goiter with

preoperative dysphonia, improvement of vocal

dys-function has been reported after excision of the

goi-ter.11,19,21 In these instances, the recurrent laryngeal

and external branch of the superior laryngeal nerves

were preserved intraoperatively and the muscles

they innervate demonstrated normal EMG findings

after thyroidectomy The postoperative ment in vocal function is thought to be attributable

improve-to relief of local compression on the laryngeal nerves, improved vibration of the vocal folds, and relief of any upper airway obstruction.19,21

Hyperthyroidism and toxic goiter, even when treated preoperatively, are often associated with negative voice outcomes In a study comparing 12 patients with nontoxic goiter and 8 with toxic goiter,

Watt-Boolsen et al demonstrated that preoperative

voice dysfunction resolved following thyroidectomy

in the nontoxic group but persisted postoperatively among individuals with toxic goiter.22

Many patients with malignant disease have operative dysphonia which is a poor prognostic indicator Advanced disease with preoperative neu-ral involvement often results in permanent vocal dysfunction.20 In a study conducted by Caroline et

pre-al, 35% of patients undergoing thyroid surgery had malignant disease and were found to have unilateral

or bilateral laryngeal nerve paresis on preoperative EMG, none of which improved postoperatively.19

Patients with a postoperative diagnosis of adenoma demonstrated no change on postoperative laryngeal EMG, while all patients with a diagnosis of thyroid-itis alone improved.19

Clinical Evaluation of Thyroid Disease

Once a thyroid disorder or nodule is suspected or covered, clinical work-up should begin with a thor-ough history and physical examination, including a videostroboscopic laryngeal examination to assess vocal fold motion Elements of the history predict-ing malignancy may include rapid growth of the thy-roid, progressive hoarseness, a history of childhood head and neck irradiation or total body irradiation, a family history of thyroid cancer, or history of a syn-drome associated with thyroid cancer (eg, multiple endocrine neoplasia syndromes, Cowden syndrome)

dis-in a first-degree relative Suspicion for malignancy

on physical examination may be supported by vocal fold paresis/paralysis, cervical lymphadenopathy, and fixation of the thyroid gland to surrounding structures (eg, skin, thyroid cartilage, trachea).The American Thyroid Association (ATA) has provided recommendations regarding indications for biopsy and additional workup (eg, serology and imaging) in the evaluation of a thyroid nodule (Fig-ure 17–2).23 Diagnostic thyroid ultrasound should be considered in all patients with a suspected thyroid nodule or other thyroid abnormality on physical examination Often, an incidental thyroid nodule is

Figure 17–2. Revised American Thyroid Association Management Guidelines for Patients with Thyroid Nodules and Differentiated Thyroid Cancer The publisher for this copyrighted material is Mary Ann Liebert, Inc publishers.