Tinnitus Retraining Therapy
for patients with tinnitus
and decreased sound tolerance
Pawel J. Jastreboff, PhD, ScD*,
Margaret M. Jastreboff, PhD
Tinnitus and Hyperacusis Center, Department of Otolaryngology,
Emory University School of Medicine, 1365A Clifton Road, NE, Atlanta, GA 30322, USA
Tinnitus is a common otologic symptom that can cause annoyance and
interference with everyday activities. Most patients describe their tinnitus as
ringing, hissing, buzzing, cricket-like, or escaping steam . Tinnitus is often
described as a constant, intermittent, or ﬂuctuating complex sound. It has
been proposed that tinnitus is a phantom auditory perception, ie, the per-
ception of a sound without any corresponding auditory/vibratory activity in
the cochlea [2,3].
Tinnitus should be diﬀerentiated from somatosounds, which are typi-
cally generated by structures in, or adjacent to the ear and evoke normal vibra-
tory activity of the basilar membrane in the cochlea. Occasionally, sounds
originating from distant sites of the human body, such as those generated by
artiﬁcial heart valves, can be perceived as well [4,5]. Spontaneous otoacoustic
emissions are a speciﬁc type of recordable somatosounds originating from the
cochlear outer hair cells (OHC) [6,7].
Although tinnitus is experienced by 15% to 20% of the population, only
a small number of people seek medical help . The degree of annoyance,
distress level, anxiety, sleep problems, emotional reactions, difﬁculties with
concentration, and interference with work and everyday activities varies
among patients [1,4,9]. Tinnitus is more prevalent in the elderly, although it
may affect people of all ages, including children [10–14].
The majority of tinnitus patients have an associated hearing loss, however,
approximately 20% to 30% of patients have normal hearing . Tinnitus is
frequently accompanied by decreased sound tolerance [16–18]. Tinnitus and
Otolaryngol Clin N Am
36 (2003) 321–336
* Corresponding author.
E-mail address: firstname.lastname@example.org (P.J. Jastreboff).
0030-6665/03/$ - see front matter Ó2003, Elsevier Science (USA). All rights reserved.
hearing loss are both well recognized and properly addressed in the literature
[1,8,19–21]. On the contrary, decreased sound tolerance has been neglected
and has not been properly addressed as a signiﬁcant health issue despite the
fact that it can create a high level of discomfort and may have a profound
impact on a patient’s life. In extreme cases, patients’ lives are controlled by
avoidance of sound, which often prevents them from normal social inter-
actions and everyday activities [17,22]. Decreased sound tolerance is present
when a subject exhibits negative reaction (eg, discomfort, pain, annoyance,
dislike, fear, etc) as a result of exposure to a sound which would not evoke
similar reaction in an average listener . In most cases, decreased sound
tolerance results from the combination of hyperacusis and misophonia.
Occasionally, misophonia, or mild hyperacusis, is the only problem, but severe
hyperacusis is always accompanied by misophonia.
Hyperacusis reﬂects an abnormally strong ampliﬁcation occurring within
the auditory pathways during sound exposure [2,17,23]. Consequently,
neuronal activity evoked by a bothersome sound is similar to the one in-
duced by a signiﬁcantly higher sound level in normal subjects. Patients
frequently experience physical discomfort and their reactions depend on the
physical characteristics of the sound (spectrum and peak sound level). The
activation of the limbic and autonomic nervous systems occurs only sec-
ondarily. The connections of these systems with the auditory pathways, as
well as their tonic level of activation, are normal.
Misophonia, or strong dislike of sounds (from the Greek word ‘‘miso’’–
hate), originates from an abnormal activation of the limbic and autonomic
nervous systems by a sound in the presence of a normally functioning
auditory system [17,23]. When fear is the dominant evoked emotion, miso-
phonic patients are described as phonophobic. In misophonia, the degree of
reactions is only partially determined by the physical characteristics of
a sound, while it depends signiﬁcantly on a patient’s past experience, the
context in which the sound occurs, and the patient’s psychological proﬁle.
Tinnitus may be associated with Me
`re’s disease, presbycusis, otitis,
otosclerosis, ototoxicity, vestibular schwannoma, autoimmune hearing loss,
as well as in hormonal changes of pregnancy and menopause [1,8,19,24,25].
Hyperacusis can coexist with tinnitus or be associated with medical con-
ditions such as Williams syndrome, Ramsay Hunt syndrome, Bells’ palsy,
Lyme disease, perilymphatic ﬁstula, migraines, head injury, and as a side
effect of withdrawal from benzodiazepines [18,26–38].
The most frequent advice oﬀered to patients with decreased sound
tolerance is to avoid noise, the advice which unfortunately results in gradual
worsening of this problem. In the past, many methods have been tried for
tinnitus with variable outcomes. These modalities of treatment include coun-
seling, medications such as antidepressants, anticonvulsants, antianxiety,
local anesthetics and vasodilators, surgery, masking techniques, psychologic
approaches, biofeedback, acupuncture, hyperbaric oxygen chamber ther-
apy, and temporomandibular joint treatment [4,5,39–41].
322 P.J. Jastreboff, M.M. Jastreboff /Otolaryngol Clin N Am 36 (2003) 321–336
Tinnitus Retraining Therapy (TRT) was proposed in the late 1980s and
was ﬁrst published in 1990 . It is a method based on the neurophysiological
model of tinnitus and decreased sound tolerance, aimed at inducing and
sustaining habituation of reactions, and perception to intrusive tinnitus
and/or to external sounds. The habituation is achieved as a result of
modiﬁcation of the neural connections linking the auditory with the limbic
and autonomic nervous systems. TRT, although not a cure for tinnitus,
provides relief in a signiﬁcant number of sufferers and is effective in most
patients with decreased sound tolerance.
Outline of the neurophysiological model of tinnitus
and decreased sound tolerance
The neurophysiological model of tinnitus provides the theoretical basis of
studying tinnitus and decreased sound tolerance, as well as their treatments.
The following are the crucial postulates of the model: (1) in cases of
clinically-signiﬁcant tinnitus, in addition to the auditory system, various
systems of the brain, particularly the limbic and autonomic nervous systems,
are involved in processing tinnitus-related and sound-evoked neuronal
activities; (2) sustained overactivation of the sympathetic part of the auto-
nomic nervous system is largely responsible for the behavioral manifestation
of tinnitus-induced problems; (3) functional connections between diﬀerent
systems in the brain are developed and governed by the principles of
conditioned reﬂexes; (4) by inducing and sustaining habituation (ie, passive
extinction) of these reﬂexes, it is possible to remove the negative impact of
tinnitus and decreased sound tolerance on a patient’s life [17,42].
Note that formal deﬁnition of habituation is identical with the deﬁnition of
the passive extinction of conditioned reﬂexes, ie, ‘‘The decline of a conditioned
response following repeated exposure to the conditioned stimulus’’ . In
most instances tinnitus-related neuronal activity originates within the pe-
ripheral structures of the auditory system and is detected and processed within
the auditory pathways. In approximately 80% of cases, the tinnitus-related
neuronal activity undergoes the process of natural habituation at a sub-
conscious level, and since it is not linked with any danger or other signiﬁcant
information which needs to be monitored, it is easily habituated .
Many hypotheses and theories exist regarding mechanisms of tinnitus
origin. Recent research favors the theory of discordant damage or dys-
function of OHC and inner hair cell (IHC) systems proposed in 1990 [2,45].
This hypothesis postulates that tinnitus-related neuronal activity is gen-
erated in the dorsal cochlear nucleus as a result of unbalanced activity
transmitted by type I and type II auditory nerve ﬁbers. Speciﬁcally, when
OHC are damaged or dysfunctional, while inner hair cells are reasonably
intact, activity in type I ﬁbers is normal, while activity in type II ﬁbers is absent
or decreased . The discordant dysfunction theory may provide explanation
323P.J. Jastreboff, M.M. Jastreboff /Otolaryngol Clin N Am 36 (2003) 321–336
to a number of questions regarding tinnitus (eg, why 20% of tinnitus patients
have normal hearing and why tinnitus is absent in 27% of totally deaf people).
Perception of tinnitus is actually an indicator of a positive phenomenon
occurring within the auditory system, which adapts to a speciﬁc physiological
condition, including peripheral or central dysfunctions. An interesting mani-
festation of this compensatory action is provided by an experiment in which 80
subjects without prior tinnitus were placed into an anechoic chamber .
Within 5 minutes, 94% of them developed tinnitus, which disappeared once
they returned to normal auditory environment. The investigation of single
neurons activity in the auditory pathways and auditory evoked potentials
after cochlear damage or restricted sound input, may provide an explanation
for this phenomenon. Under these conditions, the sensitivity of a signiﬁcant
proportion of neurons within the auditory pathways increases, while the
ampliﬁcation of the auditory signals also increases. Consequently, ongoing
spontaneous activity normally blocked from being perceived and representing
the ‘‘code of silence,’’ is perceived as tinnitus.
When the perception of tinnitus is associated with negative reinforcement
such as strong emotions and traumatic experiences, the limbic system is acti-
vated, leading to the activation of the autonomic nervous system (Fig. 1).
Fig 1. A block diagram of the neurophysiologic model of tinnitus and decreased sound
tolerance. Note multiple functional connections between involved systems crucial in the
development of conditioned reﬂex arcs.
324 P.J. Jastreboff, M.M. Jastreboff /Otolaryngol Clin N Am 36 (2003) 321–336
Physiological and psychological, reactions, reﬂecting activation of these
systems (eg, increased level of stress-related hormones, blood pressure, sleep
problems, anxiety, etc), act as a negative reinforcement for the conditioned
reﬂex arc linking auditory with the limbic and autonomic nervous systems,
which leads to enhancement of tinnitus signal and prevention of extinction of
this reﬂex (ie, prevention of habituation). Consequently, the cascade of nega-
tive reactions (eg, anxiety, depression, tension), which are present in most
patients with signiﬁcant tinnitus, starts to develop and a vicious circle is
It is of interest that tinnitus severity is not related to the psychoacoustical
characteristics of tinnitus, and treatment outcomes cannot be predicted by
psychoacoustical measures. These observations support the postulate that
the eﬀects of tinnitus on an individual depend on the extent of activation of
the limbic and autonomic nervous systems and not on the level of activation
within the auditory pathways. If the limbic and autonomic nervous systems
are not activated by the tinnitus signal, the person is experiencing tinnitus
without any associated disturbances. Moreover, perception of tinnitus in
these cases is limited. This results from a brain limitation that prevents pro-
cessing of more than one task that requires full attention . As perception
of a sound involves attention, this would hinder perception of other sounds
or performing other tasks. It needs to be mentioned that the auditory system
receives and processes a large volume of acoustic information, however,
only a small fraction of this information reaches the level of conscious
Processing of sound-induced modiﬁcations of the neuronal activity
includes detection, based on pattern recognition, enhancement or suppres-
sion of signals, and evaluation and comparison with patterns already stored
in memory. Most of these processes occur at the subconscious level and
activation resulting from exposure to familiar and unimportant sounds is
blocked at this level without any activation of the limbic and autonomic
nervous systems. On the other hand, new sounds evoke an orientation
reaction and activate the limbic and autonomic nervous systems, preparing
us for action. Once these sounds are evaluated as unimportant, they are
habituated, do not evoke reactions, and are not perceived. If, however,
a sound is classiﬁed as important requiring attention and some action,
neuronal networks become tuned to a speciﬁc pattern of this sound-induced
neuronal activity, the signal is enhanced, the limbic and autonomic ner-
vous systems are activated, and this sound is consciously perceived and
monitored. Repeated appearance of the sound linked to reinforcement
(particularly negative), will further strengthen the ability to detect this
particular signal, and will result in enhancement of reactions evoked by this
sound. Note that the selection and categorization of a sound as an un-
important one, that needs to be habituated, have to occur at the
subconscious level. Thus, if tinnitus is categorized as an unimportant and
familiar signal, it undergoes automatic habituation, and the tinnitus-related
325P.J. Jastreboff, M.M. Jastreboff /Otolaryngol Clin N Am 36 (2003) 321–336
neuronal activity does not spread to the limbic and autonomic nervous
systems, and to higher cortical auditory areas where it would be perceived.
The situation is diﬀerent when tinnitus has been linked with negative
factors and consequently it has been classiﬁed as a signal requiring at-
tention, monitoring, and preparation for a potential action. In such cases,
tinnitus-related neuronal activity will be treated in the same manner as
activity evoked by a familiar important sound, its detection will be enhanced,
the neuronal signal will be ampliﬁed, and transferred to the limbic and
autonomic nervous systems, resulting in behaviorally observed tinnitus-
The strength of any neuronal signal is related to the diﬀerence between
this signal and background neuronal activity. By applying this principle to
tinnitus and enriching the environment by additional sound will cause
decrease of the strength of tinnitus signal, leading to reduction of the
autonomic nervous system reactions, and promoting passive extinction of
the conditioned reﬂex (ie, habituation of reactions).
While attempting to induce habituation, the plasticity of the brain should
be sustained at a normal level. Benzodiazepines (Alprazolam, Diazepam,
Lorazepam, Clonazepam), frequently prescribed to tinnitus patients, impair
brain plasticity and reduce, or even prevent, the ability to learn [48–56]. As
brain plasticity and learning skills are absolutely crucial for TRT, or any
other habituation-based therapy, benzodiazepines are counterproductive
and are contraindicated for patients undergoing TRT.
Sounds used to decrease tinnitus signal strength have to follow speciﬁc
requirements. Obviously, they should not evoke anxiety or annoyance, as
these would enhance activation of the limbic and autonomic nervous sys-
tems, and consequently counteract the process of habituation. Two addi-
tional precautions need to be considered: First, suppression of tinnitus
perception, commonly incorrectly labeled as ‘‘masking,’’ should be avoided
as counterproductive for habituation. Suppression of tinnitus removes
the signal that needs to be habituated, and consequently habituation
is prevented. Second, sound levels close to the threshold of detection should
be avoided as well, in order to avoid the inﬂuence of stochastic resonance
[57,58], a phenomenon that enhances the strength of weak signals when
additional low level of broadband noise is added.
It is important to recognize the presence of two types of habitua-
tion: habituation of reaction (Fig. 2) and habituation of perception (Fig. 3).
Different neuronal networks and brain centers are involved in these
phenomena. The goal of TRT is to achieve habituation of reaction, which is
the weakening and disappearance of functional connections between the
auditory pathways, and the limbic/autonomic nervous systems. In this case,
patients may still perceive tinnitus, however, they are not bothered by it.
Habituation of perception is a secondary, but an inevitable consequence of
sufﬁciently strong habituation of reaction, and should not be the primary
goal of the treatment. Consequently, patients are aware of their tinnitus only
326 P.J. Jastreboff, M.M. Jastreboff /Otolaryngol Clin N Am 36 (2003) 321–336
a small percentage of the time. Without prior habituation of reaction,
habituation of perception will not occur, and patients will embark on an
endless search for the ‘‘Holy Grail’’ of ‘‘golden silence.’’
Finally, the systems and mechanisms outlined above for tinnitus are the
same for misophonia, where the tinnitus-related neuronal activity is replaced
by activity evoked by external sounds . For hyperacusis, it is necessary to
include the mechanisms of abnormally high ampliﬁcation of sound-evoked
mechanical vibration by OHC system and/or sound-induced neuronal ac-
tivity by central auditory pathways. Both mechanisms will yield a high level
of the neuronal signal, even when sound levels would be acceptable for
a normal listener.
Implementation of the neurophysiological model in TRT
The initial interview and the audiological evaluation provide information
needed during medical evaluation, for the selection of speciﬁc variant of
the treatment, and during the retraining counseling. Although tinnitus,
decreased sound tolerance and hearing loss are distinctively diﬀerent and
well-deﬁned problems, many patients confuse them. For example, some
Fig 2. Habituation of reaction reﬂects lack of activation of the autonomic nervous system by
the tinnitus-related neuronal activity or activity evoked by external sounds.
327P.J. Jastreboff, M.M. Jastreboff /Otolaryngol Clin N Am 36 (2003) 321–336
patients blame their tinnitus for the diﬃculty to understand speech, despite
the fact that in reality coexisting high-frequency hearing loss is responsible
for this problem. Others overprotect their ears from sounds under normal
conditions and claim to have signiﬁcant decreased sound tolerance, even
though in reality they have normal sound tolerance, and their behavior
reﬂects avoidance of sound when their tinnitus loudness increases during
and after exposure to louder sound, a commonly observed phenomenon.
Actually, by sound overprotection, these patients may induce hyperacusis and
The main goals of the initial interview are to: (1) identify patients’
complaints and associated problems; (2) determine the impact of tinnitus/
decreased sound tolerance on the patient’s life; (3) assess the emotional status
and the degree of distress; (4) evaluate the presence and duration of
the consequences of sound exposure on tinnitus/decreased sound tolerance;
(5) obtain information for proper counseling and TRT approach; and (6)
establish a reference base for future assessment of treatment outcome.
Patients are also asked to evaluate their problems by using numerical or
analog scales, and list of activities aﬀected by a speciﬁc problem. This
structured interview is performed with assistance of speciﬁc forms [60,61].
A medical evaluation by an otolaryngologist is directed toward
identifying medical conditions that may cause, contribute to, or have
Fig 3. Habituation of perception reﬂects lack of activation of the high auditory cortical centers.
328 P.J. Jastreboff, M.M. Jastreboff /Otolaryngol Clin N Am 36 (2003) 321–336
impact on the treatment. Audiological evaluation should include a pure tone
audiogram with speech discrimination, and loudness discomfort levels
(LDL). The frequencies tested should include the 12 kHz frequency since in
many cases tinnitus pitch is above 8 kHz. LDLs allow to evaluate the
patient’s tolerance to sound and assess the presence of hyperacusis and
misophonia. Additional tests include pitch and intensity matching, minimal
suppression (‘‘masking’’) levels for tinnitus, and distortion product oto-
All patients undergo retraining counseling tailored to their speciﬁc
category and speciﬁc version of sound therapy, with or without wearable
instruments. Tabletop sound machines and avoidance of silence are recom-
mended to all patients, who are furthermore advised to avoid tinnitus
suppression (‘‘masking’’) and ear overprotection. It needs to be stressed that
sounds used for sound therapy should never induce annoyance or dis-
comfort of any type.
Based on the medical and audiological evaluation results, coupled with
the information obtained during the initial interview, patients can be
classiﬁed into one of the following ﬁve categories (Table 1):
Category 0 consists of patients with relatively weak or recent (less than 2
months duration), tinnitus. These patients usually do not have signiﬁcant
hearing loss or hyperacusis, and sound exposure does not cause prolonged
worsening of their tinnitus. Sound therapy is implemented by using tabletop
sound machines. There is no need for wearable sound generators, unless the
patient insists on using one.
Category 1 consists of patients with disturbing tinnitus without any
associated signiﬁcant hearing loss or hyperacusis. Worsening of tinnitus
following prolonged exposure to sound is absent. The following points are
discussed during the retraining counseling: (1) There is no medical problem
which can be linked to tinnitus, and our evaluation assured that this is a case.
Tinnitus perception typically results from the auditory system working very
well, and compensating to the presence of a small irregularity in the
functioning of the cochlea or auditory nerve; (2) Tinnitus is not a real sound:
it is perception of neural activity, and as such, it is governed by diﬀerent
The category of the treatment and instrumentation
0 Tinnitus weak or short lasting No instruments
1 Bothersome tinnitus Sound generators
2 Tinnitus and hearing loss Combination instruments or hearing aids
3 Hyperacusis with or without tinnitus
Without hearing loss Sound generators
With hearing loss Combination instruments, or sound
generators followed by hearing aids
4 Hyperacusis or tinnitus with
Sound generators or combination
329P.J. Jastreboff, M.M. Jastreboff /Otolaryngol Clin N Am 36 (2003) 321–336
principles than activity evoked by sounds; (3) Tinnitus-related neuronal
activity is a weak signal and its impact on the patient’s life depends on the
brain’s interpretation of this signal; (4) It is impossible at present to repair
a damaged cochlea, however, it is possible to modify the way the brain detects
and responds to the signal by retraining of neural connections; (5) The brain
is a very plastic organ and undergoes constant functional reconﬁguration. It
is possible to train the brain to ﬁlter out the signal, and thus, prevent it from
activating the limbic and autonomic nervous systems (habituation of tinnitus-
evoked reactions), and avoid reaching the high cortical level involved in
conscious perception (habituation of tinnitus perception); (6) There is no
relationship between tinnitus and progressive hearing loss; tinnitus does not
cause hearing loss, and hearing loss does not cause tinnitus, despite the fact
that tinnitus is more prevalent in people with hearing loss.
Sound therapy is implemented by using a tabletop sound machine and
a wearable sound generator, which is set at ‘‘mixing’’ or ‘‘blending’’ point. At
this level, patients can still perceive separately tinnitus and sound from the
sound generators, but these two perceptions start to intertwine, interact,
blend, and mix together. Sound generators are used as long as possible during
the waking hours and the level of sound stays the same throughout the day.
Category 2 patients have signiﬁcant hearing loss and tinnitus, however,
hyperacusis and prolonged worsening of symptoms after sound exposure, are
absent. Mechanisms of tinnitus distress are explained in the same manner
as for Category 1. For sound therapy, combination instruments are recom-
mended. These devices consist of a high-quality hearing aid and a sound
generator, which provide both ampliﬁcation of enriched background sounds,
and decrease the impact of ‘‘strain to hear.’’ If, due to ﬁnancial constrains or
speciﬁcs of hearing loss, combination instruments are not possible, then
enriched sound background, further ampliﬁed by hearing aids, is utilized.
Category 3 patients have signiﬁcant hyperacusis, although tinnitus, hearing
loss may or may not be present. Prolonged worsening of hyperacusis or
tinnitus after sound exposure is not present. Counseling focuses on issues
related to potential mechanisms responsible for hyperacusis and misophonia,
which in the case of signiﬁcant hyperacusis, is inevitable. Speciﬁcally, the
following points are presented during a counseling session: (1) the auditory
system works in automatic gain control manner (ie, the sensitivity of the
system is adjusted continuously to an average level of sound, eg, the gain
increases when the level of external sound decreases). This process involves
several levels of the auditory system, with OHC, and subconscious levels of the
auditory neural pathways playing a dominant role; (2) malfunction of these
systems could lead to overampliﬁcation of sound-induced signal and manifest
at the behavioral level as hyperacusis; and (3) by continuous presence of a low-
level sound, it is possible to turn down enhanced gain within the auditory
system, and thus, decrease, or even eliminate hyperacusis. Mechanisms of
tinnitus are discussed brieﬂy, as tinnitus frequently decreases signiﬁcantly
once improvement in hyperacusis takes place. Sound generators are used
330 P.J. Jastreboff, M.M. Jastreboff /Otolaryngol Clin N Am 36 (2003) 321–336
when there is no associated hearing loss, while combination instruments are
used when hearing loss is present. The sound of instruments is set at a
comfortable level that does not induce annoyance. The level of the sound can
be changed when the patient moves to a noisier environment.
Category 4 patients typically exhibit hyperacusis as a dominant com-
plaint, and exhibit prolonged worsening of hyperacusis/tinnitus follow-
ing exposure to sound. Note that strong misophonia or phonophobia can
evoke eﬀects very similar to those observed in Category 4 and a detailed
interview is needed to diﬀerentiate these problems. Sound generators are
recommended as a main part of sound therapy in this category and usu-
ally response to treatment is slow. Since Category 4 patients tend to be
oversensitive persons, it is suggested that they start using their sound
generators for a week without switching them on, in order to habituate
somatosensory input from the ear canal.
Several issues related to the implementation of TRT need to be em-
phasized: (1) TRT does not require the use of wearable instruments in all
patients since they are only part of sound therapy, making its implementation
easier and assuring better compliance; (2) Patients are not always compliant
and may reject instrumentation, or insist on using sound generators while
having signiﬁcant subjective hearing loss. While this is not optimal, in the
majority of cases, treatment can still be eﬀective; (3) The previously men-
tioned categories provide general approach guidance, and patients might be
on the border of two categories. Diagnosis and recommendations depend on
the dominant problem, but when hyperacusis is present, it needs to be treated
ﬁrst; (4) Patients may change category during treatment. For example,
patients with signiﬁcant hyperacusis, hearing loss and tinnitus are initially
treated as Category 3, and later when hyperacusis subsides they are treated as
Category 2. Consequently, they are treated ﬁrst with sound generators, and
later with hearing aids, if combination instruments are not applicable.
It is helpful to have an enriched sound environment not only during the day,
but during the night as well. It has been reported that the auditory system
remains very active up to the level of inferior colliculi even during full surgical
anesthesia . Substantial processing of the tinnitus-related neuronal activity
occurs at and below this level, and sound used during the night may act by
weakening tinnitus signal. Furthermore, the majority of tinnitus patients have
sleeping problems secondary to the tinnitus , and for them the sound
exposure during the night is always recommended. The continuous, mild level
of sound from tabletop sound machines decreases the difference between the
tinnitus signal and normally quiet surroundings, which is important when
patients are in a very shallow phase of the natural cycle of sleep.
Hyperacusis treatment requires desensitization procedures by exposing
patients to continuous low level of sound over a period of months. The sound
level, provided in most cases by wearable sound generators or combination
instruments, is adjusted as needed by the patient and is kept below the level
that evokes annoyance or discomfort. Additional sounds provided by tabletop
331P.J. Jastreboff, M.M. Jastreboff /Otolaryngol Clin N Am 36 (2003) 321–336
sound machines, nature’s sounds, radio, television, etc, can be utilized as well.
The avoidance of silence and continuous exposure to background sound is
even more important for hyperacusis than for tinnitus patients. Desensitiza-
tion used for hyperacusis follows general principles of the neurophysiological
model of tinnitus, and it is a part of standard TRT protocol [4,16,59,63,64].
The process of desensitization involves gradual decrease of use of ear
protection. Overprotection of hearing, by systematic decrease of average
sound level reaching the auditory system, results in enhancement of tinnitus
and hyperacusis. The progress of recovery from hyperacusis is monitored
carefully by LDL measurements and follow-up interviews, which include
detailed review of affected activities.
The misophonic component, however, cannot be removed by desensiti-
zation and there is a necessity for use of a separate approach. Recognizing
the similarity of the neural networks involved in tinnitus and misophonia,
and involvement of conditioned reﬂexes, a method based on the active
extinction of conditioned reﬂexes is promoted [65,66]. This involves sys-
tematic exposure of patients to sounds associated with a pleasant situa-
tion, and gradual increase of the sound levels .
Basic desensitization produces decrease of hyperacusis relatively fast.
Typically, patients with pure hyperacusis show prompt response to treatment
and prompt recovery. Many patients accept the maximal levels of sound
allowed for testing LDLs without experiencing any discomfort. Misophonia
might take longer to respond, depending on how strongly the conditional
reﬂex arcs have been established. In a signiﬁcant number of patients, it is
possible to achieve not only improvement, but even cure of decreased sound
tolerance. It is important to recognize that if only hyperacusis is treated
without recognition and treatment of misophonia, results are unpredictable
and recovery might take a long time or even treatment might be unsuccessful.
Since decreased sound tolerance frequently results from a combination of
hyperacusis and misophonia/phonophobia, it is crucial to assess the presence
and the degree of both entities [18,63], and treat them properly [17,59,67].
To achieve tinnitus habituation, it is necessary to retrain the feedback
loops that have formed between the auditory, limbic, and autonomic
nervous systems. Since tinnitus is present all the time, these connections are
being continuously enhanced and may induce a high level of reactions. In
order to counteract this enhancement, counseling at regular follow-up visits
is very important.
Although there are no published randomized, well-controlled studies
evaluating the eﬀectiveness of TRT, there is a growing number of clinical
reports documenting the eﬀectiveness of this method. With the present
version of TRT, tinnitus improvement is usually seen at the third month
332 P.J. Jastreboff, M.M. Jastreboff /Otolaryngol Clin N Am 36 (2003) 321–336
following initiation of treatment, with deﬁnite improvement by the sixth
month . The majority of patients achieve a high level of tinnitus control
in 12 months after initiation of treatment [63,64,68,69]. In the past, we advised
patients to follow the TRT protocol for approximately 18 months in order
to prevent relapses. In cases of signiﬁcant improvement, we have not seen
relapse of tinnitus during the past 12 years. At present, the recommended
duration of treatment in fully compliant patients is at least 12 months.
The results of the treatment using TRT are very satisfactory showing
signiﬁcant improvement in over 80% of cases [70–74]. In a recent study, it
was reported that patients had sustained a high level of tinnitus control
4 years after completion of treatment .
Our experience has revealed the following: (1) TRT is applicable for all
types of tinnitus, as well as for decreased sound tolerance, with signiﬁcant
improvement of tinnitus occurring in over 80% of the cases, and at least
equal success rate for decreased sound tolerance. (2) TRT can provide cure
for decreased sound tolerance. (3) TRT does not require frequent clinic
visits and has no side eﬀects; however, (4) Special training of health
providers involved in this treatment is required for this treatment to be
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