Tinnitus: characteristics, causes, mechanisms, and treatments.

Abstract

Tinnitus-the perception of sound in the absence of an actual external sound-represents a symptom of an underlying condition rather than a single disease. Several theories have been proposed to explain the mechanisms underlying tinnitus. Tinnitus generators are theoretically located in the auditory pathway, and such generators and various mechanisms occurring in the peripheral auditory system have been explained in terms of spontaneous otoacoustic emissions, edge theory, and discordant theory. Those present in the central auditory system have been explained in terms of the dorsal cochlear nucleus, the auditory plasticity theory, the crosstalk theory, the somatosensory system, and the limbic and autonomic nervous systems. Treatments for tinnitus include pharmacotherapy, cognitive and behavioral therapy, sound therapy, music therapy, tinnitus retraining therapy, massage and stretching, and electrical suppression. This paper reviews the characteristics, causes, mechanisms, and treatments of tinnitus.

Full text

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REVIEW
J Clin Neurol 2009;5:11-19
Copyright ⓒ 2009 Korean Neurological Association 11
Print ISSN 1738-6586 / On-line ISSN 2005-5013
10.3988/jcn.2009.5.1.11


Tinnitus: Characteristics, Causes, Mechanisms, and Treatments

Byung In Han, MDa; Ho Won Lee, MDb; Tae You Kim, MDc; Jun Seong Lim, MDd; Kyoung Sik Shin, MDe
aDo Neurology Clinic, Willis Medical Network, Daegu, Korea
Deptartment of bNeurology, Brain Science and Engineering Institute, Kyungpook National University School of Medicine, Daegu, Korea
cWillis Hospital, Willis Medical Network, Busan, Korea
Department of dNeurology, Sung Ae Hospital, Seoul, Korea
eJeil Neurology Clinic, Willis Medical Network, Daejeon, Korea

Received November 28, 2008
Revised February 13, 2009
Accepted February 13, 2009

Correspondence
Byung In Han, MD
Do Neurology Clinic,
Willis Medical Network,
637 Jungang-dearo, Jung-gu,
Daegu 700-440, Korea,
Tel +82-53-252-2225
Fax +82-53-289-6502
E-mail han-byungin@hanmail.net


Tinnitus-the perception of sound in the absence of an actual external sound-represents a symptom
of an underlying condition rather than a single disease. Several theories have been proposed to
explain the mechanisms underlying tinnitus. Tinnitus generators are theoretically located in the
auditory pathway, and such generators and various mechanisms occurring in the peripheral au-
ditory system have been explained in terms of spontaneous otoacoustic emissions, edge theory,
and discordant theory. Those present in the central auditory system have been explained in terms
of the dorsal cochlear nucleus, the auditory plasticity theory, the crosstalk theory, the somato-
sensory system, and the limbic and autonomic nervous systems. Treatments for tinnitus include
pharmacotherapy, cognitive and behavioral therapy, sound therapy, music therapy, tinnitus re-
training therapy, massage and stretching, and electrical suppression. This paper reviews the char-
acteristics, causes, mechanisms, and treatments of tinnitus.


Key Wordsaa tinnitus, discordant theory, tinnitus retraining therapy.

J Clin Neurol 2009;5:11-19

Introduction

Tinnitus is defined as a phantom auditory perception-it is a
perception of sound without corresponding acoustic or me-
chanical correlates in the cochlea.1 Tinnitus represents one of
the most common and distressing otologic problems, and it
causes various somatic and psychological disorders that in-
terfere with the quality of life.2 A population-based study of
hearing loss in adults aged 48 to 92 years found that tinnitus
had a prevalence of 8.2% at baseline and an incidence of 5.7%
during a 5-year follow-up.3 The prevalence of tinnitus increases
with age.4
Tinnitus also represents a common symptom among chil-
dren with hearing loss.5 Tinnitus is a subjective phenomenon
that is difficult to evaluate objectively, with it being measur-
ed, quantified, and described only based on the responses of
patients. Although tinnitus can have many different causes, it
most commonly results from otologic disorders, with the most
common cause believed to be noise-induced hearing loss.6
The various therapeutic approaches to tinnitus have produced
mixed results, and hence it is generally assumed that tinnitus
has diverse physiological causes.7
Clinical Manifestations

Characteristics of tinnitus
The sound perceived by those with tinnitus can range from a
quiet background noise to a noise that is audible over loud
external sounds. Tinnitus is generally divided into two cate-
gories: objective and subjective. Objective tinnitus is defined
as tinnitus that is audible to another person as a sound ema-
nating from the ear canal, whereas subjective tinnitus is au-
dible only to the patient and is usually considered to be de-
void of an acoustic etiology and associated movements in the
cochlear partition or cochlear fluids. Many physicians use the
term tinnitus to designate subjective tinnitus and the term so-
matosound to designate objective tinnitus.6
The sounds associated with most cases of tinnitus have
been described as being analogous to cicadas, crickets, winds,
falling tap water, grinding steel, escaping steam, fluorescent
lights, running engines, and so on. It is believed that these
types of perception result from abnormal neuronal activity at
a subcortical level of the auditory pathway.6,8
The pattern characterizing tinnitus is related to the library
of patterns stored in auditory memory and also, via the lim-

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12 J Clin Neurol 2009;5:11-19
bic system, associated with emotional states.9 The charac-
teristics of tinnitus are generally unrelated to the type or sever-
ity of any associated hearing impairment, and thus the latter of-
fers little diagnostic value.6 Most tinnitus patients match their
tinnitus to a pitch above 3 kHz.10 The tinnitus characterizing
Meniere’s disease, described as roaring, matches a low-fre-
quency tone that is usually from 125 to 250 Hz.11 However, tin-
nitus in the advanced “burned-out” stage of Meniere’s dis-
ease is often higher in pitch and tonal in quality.12
Most patients with both tinnitus and hearing loss report
that the frequency of the tinnitus correlates with the severity
and frequency characteristics of their hearing loss, and that
the intensity of the tinnitus is usually less than 10 dB above
the patient’s hearing threshold at that frequency.6 Some pa-
tients who have central auditory processing disorders and
have difficulties understanding speech in noise report experi-
encing tinnitus even though their pure-tone audiometric
thresholds are normal.8,13
Less prevalent forms of tinnitus, such as those involving
well-known musical tunes or voices without understandable
speech, occur among older people with hearing loss and are
believed to represent a central type of tinnitus involving rever-
beratory activity within neural loops at a high level of pro-
cessing in the auditory cortex.8,14
Somatic tinnitus is a type of subjective tinnitus in which
the frequency or intensity is altered by body movements such
as clenching the jaw, turning the eyes, or applying pressure to
the head and neck.15 Reports that tinnitus is louder upon awak-
ening suggest the involvement of somatic factors, such as
bruxism. Reports that tinnitus vanishes during sleep but re-
turns within a few hours further suggest that psychosomatic
factors, such as neck muscle contractions occurring in an
upright position or jaw clenching, play etiological roles.16
Because objective tinnitus (which is audible to another
person) represents the semantic opposite of subjective tinnit-
us, a better nosological approach might be to use the term
somatosound instead of objective tinnitus irrespective of whe-
ther the sounds are audible to others, reserving the term tinn-
itus for the perception of sound in the absence of any acous-
tic source. Thus, “tinnitus” would describe cases previously
diagnosed as subjective tinnitus.6 Objective tinnitus might be
vascular or mechanical in origin. Objective tinnitus of vascul-
ar origin could be a referred bruit from stenosis in the carotid
or vertebrobasilar system. Objective mechanical tinnitus is due
to abnormal muscular contraction of the nasopharynx or mid-
dle ear, as can occur in palatal myoclonus.17 Pulsatile tinnitus
can also manifest subjectively as an increased awareness of
blood flow in the ear. Indeed, the cause of somatosensory pul-
satile tinnitus syndrome is not vascular, with the syndrome de-
riving from cardiac-synchronous somatosensory activation of
the central auditory pathway or the failure of somatosensory-
auditory central nervous system (CNS) interactions to sup-
press cardiac somatosounds.18 Pulsatile tinnitus superimpos-
ed on steady tinnitus could result from the pulsation of blow
flow with the spiral capillary of the basilar membrane.19

Associated symptoms
The most common associated symptoms or subjective dis-
comforts involve concentration difficulties, insomnia, and de-
creased speech discrimination.20 The annoyance of tinnitus is
not correlated with the acoustic characteristics, but there is a
significant correlation with psychological symptoms.21 The
difference between simply perceiving tinnitus and being an-
noyed or distressed by it depends exclusively on the activation
of the limbic and autonomic nervous systems.8 Most patients
with significant tinnitus have difficulty falling asleep due to
the accompanying anxiety, which also causes difficulties in
returning to sleep during periods of wakefulness during the
night.8
There is pronounced neuronal activity in the auditory path-
ways during sleep due to the auditory system continuously
monitoring the sound environment.8 Common detrimental ac-
tivities and/or conditions include noise exposure, being locat-
ed in a quiet place, emotional stress, loss of sleep, and physi-
cal exhaustion.22 Annoyance, depression, and interference with
sleep are more common and the tinnitus is louder in patients
with Meniere’s disease than in those with tinnitus deriving
from other etiologies.22 Furthermore, the successful control of
vertigo in patients with Meniere’s disease can lead to them
focusing more on their tinnitus and hence becoming more
distressed by this condition.12
The strength of the reaction to tinnitus is therefore deter-
mined by its significance and by past experience-the actual
intensity and characteristics of the sound are of secondary im-
portance.23

Natural course
Noise-induced tinnitus can be acute or chronic. Acute tinnitus
can last from a few minutes to a few weeks after noise expo-
sure.24 In some cases, tinnitus has a gradual onset and several
years can pass before an intermittent, low-intensity tinnitus
becomes bothersome.25 Spontaneous remission by natural ha-
bituation is experienced by more than three-quarters of suffer-
ers. Habituation occurs within the CNS, whereas adaptation
involves a peripheral sensory organ.8 For those in whom the
condition worsens, the tinnitus intensity increases over time
but its pitch tends to remain stable.22 If tinnitus persists for
more than 2 years, it is considered permanent and irreversi-
ble.26 However, chronicity is not associated with a favorable
response to treatment.27

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www.thejcn.com 13
Causes and Pathophysiology

Causes
Tinnitus does not represent a disease itself but instead is a
symptom of a variety of underlying diseases. Otologic causes
include noise-induced hearing loss, presbycusis, otosclerosis,
otitis, impacted cerumen, sudden deafness, Meniere’s disease,
and other causes of hearing loss. Neurologic causes include
head injury, whiplash, multiple sclerosis, vestibular schwan-
noma (commonly called an acoustic neuroma), and other cer-
ebellopontine-angle tumors. Infectious causes include otitis
media and sequelae of Lyme disease, meningitis, syphilis, and
other infectious or inflammatory processes that affect hearing.
Tinnitus is also a side effect of some oral medications, such as
salicylates, nonsteroidal anti-inflammatory drugs, aminoglyco-
side antibiotics, loop diuretics, and chemotherapy agents (e.g.,
platins and vincristine). Temporomandibular-joint dysfunction
and other dental disorders can also cause tinnitus. However, in
many cases no underlying physical cause is identifiable.28 For
many years, hearing loss has been understood to be the most
common cause of tinnitus,29 and population-based data indi-
cate that excessive noise exposure represents the second most
common cause of tinnitus. However, about 40% of patients
cannot identify any cause associated with tinnitus onset.26
Any pathologic lesion in the auditory pathway or any re-
duction in auditory nerve function has the potential to pro-
duce tinnitus.19 The location of the hearing problem (i.e., in the
middle ear or in the inner ear) and the otologic disorder caus-
ing the hearing loss do not appear to influence the etiologic
potential.6 Interestingly, most patients with tinnitus complain
about a sensation of fullness or blockage in the middle ear,
suggesting a problem with middle ear pressure or increased
impedance of the ossicular chain.30
Unilateral high-frequency hearing loss combined with poor
speech discrimination suggests the presence of a tumor, usual-
ly a vestibular schwannoma/acoustic neuroma or a meningio-
ma.28 Bilateral subjective tinnitus requires assessment of hear-
ing and can be associated with presbycusis, noise-induced
hearing loss, endolymphatic hydrops, and a vascular labyrin-
thine lesion.21 However, most cases of unilateral tinnitus are
not associated with life-threatening otologic disease.6

Trigger factors
Small temporary changes in the outer hair cells (OHCs) fol-
lowing noise exposure can trigger the emergence of tinnitus
by increasing the gain of the central auditory system.8 In gen-
eral, tinnitus represents a threshold phenomenon for which any
one factor, such as chronic progressive hearing loss, is insuf-
ficient to elicit its emergence-two or more trigger factors (i.e.,
psychosocial stress, noise exposure, and somatic factors) can
act synergistically to produce symptomatic tinnitus.15 About
75% of new cases are related to emotional stress as the trigger
factor rather than to precipitants involving cochlear lesions.8

Pathophysiology
Tinnitus represents a symptom of diverse pathologies. It is
proposed that all levels of the nervous system are, to varying
degrees, involved in tinnitus manifestation.1,31

Peripheral auditory system

Spontaneous otoacoustic emissions
Spontaneous otoacoustic emissions (SOAEs), first discover-
ed by Kemp,32 are small acoustic signals presumed to be ge-
nerated by the electromotile activity of the OHCs of the coch-
lea and propagated into the external auditory canal.33 SOAEs
produced by the cochlea can be perceived as tinnitus.34 SOAEs
are usually inaudible, but they can become audible due to
instability.35 These atypical SOAEs are much more prevalent
in the higher frequency range and can appear at sound pres-
sure levels up to 55 dB SPL in the ear canal.36 Tinnitus due to
SOAEs is mild and is more common in subjects with normal
hearing and in those with only middle ear disorders.37 SOAEs
decrease as hearing loss progresses, and hence these otoa-
coustic emissions are not likely to cause tinnitus when a
hearing loss of 35 dB or more is present.38 However, SOAEs
cannot fully explain the mechanism of tinnitus since aspirin
largely abolishes SOAEs without improving tinnitus.39

Edge theory
Edge theory, also known as contrast theory, proposes that
tinnitus is induced by increased spontaneous activity in the
edge area,40 which represents a transition from OHCs in the
organ of Corti with relatively normal morphology and func-
tion on the apical (i.e., low-frequency) side of a lesion to OHCs
toward the basal side that are missing or have a pathologic
appearance and poor functionality.19 Edge theory can be ex-
plained by discordant theory.9

Discordant theory
According to discordant theory, tinnitus is induced by the dis-
cordant dysfunction of damaged OHCs and intact inner hair
cells (IHCs) of the organ of Corti. Intense noise and ototoxic
agents initially damage OHCs in the basal turn of the cochl-
ea, and subsequently, if continued or repeated, affect IHCs-
this is due to IHCs being more resistant to such damage.9
IHCs are the receptor cells for sound transduction, and almost
all afferent fibers in the auditory nerve (95%) innervate IHCs.8
In contrast, OHCs work as mechanical amplifiers, enhancing
weak sounds by providing up to 50 dB, which can be evalu-

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Tinnitus Review
14 J Clin Neurol 2009;5:11-19
ated by measuring otoacoustic emissions.8 In almost all situ-
ations OHCs are damaged more than IHCs, which results in
the disinhibition of neurons in the dorsal cochlear nuclei
(DCNs).8 Spontaneous activity is increased when neurons in
the DCN receive excitation from IHCs but not from the dam-
aged OHCs, and this is perceived as tinnitus.8 Normally there
is a small gap between the top of the cilia of the IHCs and the
bottom of the tectorial membrane, but in the area in which
OHCs are affected but IHCs are intact, the tectorial mem-
brane might touch the IHC cilia, thus causing the IHCs to de-
polarize.41 The OHCs normally recover with a few days, but
this can be delayed for up to a few months.42,43 Therefore, it is
hypothesized that tinnitus represents a consequence of a cen-
tral gain adaptation mechanism when the auditory system is
confronted with a hearing loss.44 Discordant theory explains
why many individuals with tinnitus have normal hearing if
there is only partial damage to OHCs, since up to 30% of
OHCs can be damaged without inducing hearing loss.45 OHCs
die at a rate of approximately 0.5% per year beginning during
the first years of life, and OHC-induced hearing loss does
not usually appear before the end of the fifth decade of life.8
Discordance is absent in totally deaf individuals with comple-
te damage to both OHCs and IHCs, and hence tinnitus is not
induced. If there is increased gain within the CNS, tinnitus is
present even in deaf subjects.23 Similarly, noise-induced tin-
nitus is caused by discordant damage between OHCs and
IHCs.41 Two types of noise-induced tinnitus have been iden-
tified: tonal and complex. Tonal tinnitus results from discor-
dant dysfunction of OHCs and IHCs manifesting in a single
area, whereas complex tinnitus results from multiple areas of
discordance.46 When patients clearly have the central type of
tinnitus, such as after transection of the auditory nerve, the
OHC concept is not applicable and alternative mechanisms
need to be considered.23

Central auditory system

The dorsal cochlear nucleus
The DCN has been implicated as a possible site for the gen-
eration of tinnitus-related signals owing to its tendency to
become hyperactive following exposure to tinnitus-inducing
agents such as intense sound and cisplatin.47 OHC damage
triggers plastic readjustments in the DCN, resulting in DCN
hyperactivity.48 It is hypothesized that a reduction in auditory-
nerve input leads to disinhibition of the DCN and an increase
in spontaneous activity in the central auditory system, which
manifests as tinnitus.49 This mechanism could explain the tem-
porary ringing sensation that can follow exposure to loud
sound.50 The plastic readjustments in the DCN are slow and
lead to tinnitus with a delayed onset. IHC damage prevents
hyperactivity in the DCN.51

Auditory plasticity theory
According to auditory plasticity theory, damage to the cochlea
enhances neural activity in the central auditory pathway.52
Auditory plasticity emerges as a consequence of the aberrant
pathway, and tinnitus might be considered to be the auditory
system analog to phantom limb sensations in amputees.53 Tin-
nitus might be generated in the temporal lobe in the auditory
association cortex54 and inferior colliculus.55 The ability of some
individuals to modulate tinnitus by performing voluntary so-
matosensory or motor actions is probably attributable to plastic
changes involving the development of aberrant connections
between the auditory and sensory-motor systems in the brains
of these patients.56

Crosstalk theory
According to crosstalk theory, when auditory nerve fibers are
intact and some other cranial nerves are damaged, artificial
synapses (called crosstalk) can develop between individual au-
ditory nerve fibers, resulting in the phase-locking of the spon-
taneous activity of groups of auditory neurons. In the ab-
sence of external sounds, this creates a neural pattern that re-
sembles patterns evoked by actual sounds.57 These cranial
nerves are sensitive to compression at the root entry zone,
where they are covered by myelin. Nerve compression causes
crosstalk between nerve fibers, and the breakdown of the
myelin insulation of the nerve fibers establishes ephaptic cou-
pling between them. This notion is applied to the cochlear-
vestibular nerve, which is covered by central myelin for most
of its length and hence is vulnerable to compression from
blood vessels or tumors impinging upon the nerve (e.g., ves-
tibular schwannoma). Such compression and consequent ep-
haptic coupling might lead to tinnitus if synchronization of the
stochastic firing in the cochlear nerve is perceived as sound.57

Somatosensory system
The activity of the DCN is also influenced by stimulation of
nonauditory structures;47 however, the somatosensory system
is the only nonauditory sensory system that appears to be re-
lated to tinnitus (e.g., in temporomandibular-joint syndrome and
whiplash).49 Somatic tinnitus can develop from activation of
latent oto-somatic interaction.16 Somatic (craniocervical) tinni-
tus, like otic tinnitus, is caused by disinhibition of the ipsilater-
al DCN, which is mediated by nerve fibers whose cell bodies
lie in the ipsilateral medullary somatosensory nuclei. These
neurons receive inputs from the nearby spinal trigeminal tract,
the fasciculus cuneatus, and the facial, vagal, and glossophar-
yngeal nerve fibers innervating the middle and external ears.49
Pain signals from the cochlea carried by the cochlear C fi-

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Han BI et al.

www.thejcn.com 15
bers could also be interpreted by the CNS as tinnitus.58 It is fur-
ther hypothesized that somatic tinnitus is due to central cross-
talk within the brain, because certain head and neck nerves
enter the brain near regions known to be involved in hearing.57

Limbic and autonomic nervous systems
The aforementioned theories cannot explain why some people
suffer from tinnitus while others do not. More than 80% of
those perceiving tinnitus for the first time do not associate the
sound with any negative meaning and experience spontane-
ous habituation. However, if the first perception of tinnitus
induces high levels of annoyance or anxiety by association
with unpleasant stimuli or with periods of stress and anxiety,
tinnitus mightlead to high levels of annoyance or anxiety. At
the unconscious level, tinnitus can increase progressively with-
out the patient being aware, resulting in enhanced activity in
the limbic and autonomic nervous systems. In such situa-
tions, tinnitus emerges as a clinically significant problem.8

Treatments

Tinnitus treatments can be divided into two categories: 1)
those aimed at directly reducing the intensity of tinnitus and
2) those aimed at relieving the annoyance associated with tin-
nitus. The former include pharmacotherapy and electrical sup-
pression,59 and the latter include pharmacotherapy, cognitive
and behavioral therapy, sound therapy, habituation therapy,60
massage and stretching, and hearing aids.

Pharmacotherapy
Extensive reviews of randomized clinical trials have revealed
that only nortriptyline, amitriptyline, alprazolam, clonazepam,
and oxazepam are more beneficial than placebo.59,61 Dobie et
al. reported that nortriptyline were statistically superior to
placebo, although placebo was also effective.62 Podoshin et al.
reported that amitriptyline was superior to placebo with re-
spect to sleep disturbance and interference with activities.63
Johnson et al. reported that alprazolam was more effective
than placebo in reducing tinnitus intensity.64 Lechtenberg and
Shulman noted that clonazepam and oxazepam were effective
in more than 50% of tinnitus cases.65 However, when patients
stopped taking either of these drugs, tinnitus recurred to its
prior level or a worse level.65 The only medication providing
a reliable reduction of tinnitus is intravenous lidocaine, and
there is a close association between the effects of lidocaine
and oral carbamazepine.66 Intravenous lidocaine produces a
change in the neural activity in the right temporal lobe in the
auditory association cortex.54 Unfortunately, lidocaine cannot
be used clinically because it must be injected, its effects are
of short duration, and it frequently produces adverse side
effects.61 Tocainide, an oral antiarrhythmic drug closely re-
lated to lidocaine, is not beneficial.67 Tinnitus due to SOAEs
can be diminished by aspirin.68 A recent 3-month randomized
clinical trial involving 50 patients found that acamprosate, a
drug used in the treatment of alcoholism, was more benefi-
cial than placebo.69 Flecainide, mexiletine, betahistine, carba-
mazepine, ginko extract, amylobarbiturate, baclofen, lamotri-
gine, misoprostol, zinc, cinnarizine, flunarizine, caroverine, ep-
erisone, and melatonin are no more beneficial than placebo.59
Diazepam and flurazepam significantly change the tinnitus
intensity.61

Cognitive and behavioral therapy
Cognitive therapy focuses on how one thinks about tinnitus
and on the avoidance of negative ideation, whereas behav-
ioral therapy uses the systematic desensitization approach that
is applied to many phobias.70 Cognitive therapy involves teach-
ing patients to cope with their tinnitus by replacing negative
thinking with more positive thinking. Cognitive therapy in-
cludes counseling and cognitive restructuring. Counseling
should include 1) informing patients that it is unlikely that their
annoyance with tinnitus will improve dramatically, 2) inform-
ing patients about the usefulness of tinnitus self-help groups,
3) helping patients to minimize the time devoted to activities
and/or conditions in which the tinnitus intensity is increased
and to maximize the time devoted to activities and/or condi-
tions in which the tinnitus intensity is decreased, and 4) stress-
ing the avoidance of noise exposure, since noise-induced
hearing loss and tinnitus are related.22 Cognitive restructur-
ing involves changing thoughts associated with tinnitus. In this
context, patients are encouraged to accept the idea that tin-
nitus does not deserve all the attention it gets.71 Behavioral
therapy focuses on positive imagery, attention control, and re-
laxation training.70 Positive imagery involves focusing thou-
ghts on something pleasant, thereby diverting thoughts from
tinnitus. Patients begin with pleasant visual images (e.g., lying
on a beach) and auditory images (e.g., the sound of waves or
wind through the leaves).70 Attention control involves moving
attention away from the tinnitus when it is bothersome. This
process might begin by placing two pictures next to one ano-
ther and then presenting two acoustic stimuli (e.g., a fan noise
and conversational speech) emanating from an adjacent room.
Next, a picture and the tinnitus are paired, followed by the
pairing of a thought and the tinnitus.70 Relaxation training uses
a guided protocol to teach participants to apply progressive
muscle relaxation, involving tensing and relaxing the arms,
face, neck, shoulders, abdomen, legs, and feet.70

Sound therapy
Sound therapy uses sounds found in natural settings, including