by Myriam Westcott, Audiologist
Acoustic shock disorder (ASD) is an involuntary response to a sound perceived as traumatic (usually a sudden, unexpected loud sound heard near the ear), which causes a specific and consistent pattern of neurophysiological and psychological symptoms. These include aural pain/fullness, tinnitus, hyperacusis, muffled hearing, vertigo and other unusual symptoms such as numbness or burning sensations around the ear. Typically, people describe acoustic shock as feeling like they have been stabbed or electrocuted in the ear. If symptoms persist, a range of emotional reactions including post traumatic stress disorder, anxiety and depression can develop.
Call centre staff using a telephone headset are vulnerable to ASD because of the increased likelihood of exposure, close to their ear(s), of sudden unexpected loud sounds randomly transmitted via the telephone line. In the early 1990s, co-inciding with the rapid growth of call centres in Australia, increasing numbers of employees were reporting ASD symptoms. A similar pattern was being noticed overseas. As a result, a number of audiologists, scientists and occupational health experts began to research ASD.
A study of ASD symptoms in 103 call centre operators exposed to 123 acoustic incidents is reviewed. The proposed neurophysiological mechanism of ASD is discussed, in particular tonic tensor tympani syndrome (TTTS) and temporomandibular disorder (TMD). An understanding of TTTS provides insight into the neurophysiological basis of tinnitus and hyperacusis escalation, in association with high levels of emotional trauma and anxiety. Audiological assessment, diagnosis, rehabilitation and workplace management of ASD is discussed.
The potential severity and persistence of ASD symptoms have significant clinical and medico-legal implications. With the rapid growth of call centres around the world, professionals providing tinnitus and hyperacusis therapy are increasingly likely to encounter some or all of the cluster of ASD symptoms in their clients.
Acoustic shock is an involuntary response to a sound perceived as traumatic (acoustic incident), which causes a specific and consistent pattern of neurophysiological and psychological symptoms (1). The degree of trauma is influenced by the psychological context of the workplace and/or environment where the acoustic incident exposure occurred. Acoustic shock symptoms are usually temporary, but for some the symptoms can be persistent, escalate and result in a permanent disability. The term acoustic shock disorder (ASD) is used to identify this persistent symptom cluster.
An acoustic incident is any sound that is perceived as threatening, usually a sudden/unexpected/loud sound heard near the ear. The sound is rarely loud enough or present for long enough to cause a noise induced hearing loss. Examples include explosions, telephone faults, scream in the ear.
Call centre staff using a telephone headset are vulnerable to ASD because of the increased likelihood of exposure, close to their ear(s), to an acoustic incident randomly transmitted via the telephone line. In the early 1990s, co-inciding with the rapid growth of call centres in Australia, increasing numbers of employees were reporting acoustic shock symptoms (2). A similar pattern was being noticed overseas (3, 4).
In a more general clinical population, any clients who have developed tinnitus and hyperacusis, particularly following exposure to a sudden unexpected loud sound or associated with a highly traumatic experience, may report at least some of these symptoms (5).
ASD causes a specific and consistent pattern of neurophysiological and psychological symptoms. Initial symptoms include a severe startle reaction, often with a head and neck jerk, and a shock/trauma reaction with symptoms of disorientation, distress, shakiness, crying, headache, fatigue. A severe ASD can lead to Post Traumatic Stress Disorder (PTSD). Other symptoms can include pain/blockage/pressure/tympanic fluttering in the ear; pain/burning/numbness around the ear/jaw/neck; tinnitus, hyperacusis and phonophobia; mild vertigo and nausea; headache; and subjective muffled/distorted hearing. ASD generally does not result in a hearing loss, although if present it tends not to follow the typical high frequency pattern of a noise induced hearing injury but affects low and mid frequency sensorineural hearing (1, 2).
Typically, people describe acoustic shock as feeling like they have been stabbed or electrocuted in the ear. The symptoms are involuntary, unpleasant and frightening; they can range from mild to severe; and be of short, temporary duration or persistent. If symptoms persist, a range of emotional reactions including trauma, anxiety and depression can develop.
As ASD symptoms are subjective, they are easily misunderstood, misdiagnosed or not believed. An inadequate understanding of the symptoms often exacerbates anxiety, and can lead to confusion and distress. The long term symptoms of severe ASD are consistent with severe hyperacusis, or category 4 according to the Tinnitus Retraining Therapy (TRT) system of classification. Some of the most severe cases of hyperacusis seen in my clinic are those with ASD.
Milhinch and Doyle (2) carried out the first large scale study of ASD, using data from a number of audiological clinics and from the files of a large call centre operator. A total of 103 people, including 91 females and 12 males, were exposed to 123 acoustic incidents in the period 1994 to 1999.
Pain was the most frequent symptom, reported by 95%. Of these, 81% reported ear pain, 11% pain in the neck or jaw, and 7% facial pain. Tinnitus was reported by 50%, usually accompanied by other symptoms, but in 6% it was the only symptom. Loss of balance was reported by 48%. The most distressing and durable symptom tended to be hyperacusis, reported by 32%.
Other symptoms reported included headaches (32%), facial numbness (9%), a burning feeling in the ear or face (5%), tingling (3%), a feeling of pressure or fullness in the ear (11%), an echo, or hollow feeling in the ear (18.4%) and muffled/distorted hearing (18.4%).
In some cases all symptoms resolved within a few hours or days. In other cases symptoms persisted for months or indefinitely. In the long term, 10% developed a range of emotional reactions including anxiety, depression, hypervigilance, anger and feelings of vulnerability.
Repeated acoustic incident exposure exacerbated an individual's vulnerability to ASD, as well as the degree and persistence of their injury. Pre-existing stress/anxiety, as well as fear of repeated incident exposure, also appeared to increase vulnerability to ASD, with a ripple effect observed amongst other staff members (6).
Call centre staff are therefore particularly vulnerable: the workplaces are often large, open plan environments with high levels of ambient noise, requiring the operator to turn up the volume of their headset, increasing vulnerability to acoustic incident exposure. Additionally, the workplace environment is potentially stressful: the job requirements are often competitive, monitored and repetitive, with the calls made frequently unwelcome
The initial physiological symptoms of acoustic shock are considered to be a direct consequence of excessive, involuntary middle ear muscle contractions. While the stapedial reflex is an acoustic reflex triggered by high volume levels, the tensor tympani reflex is a startle reflex (6, 7) which is exaggerated by high stress levels. The tensor tympani muscle contracts immediately preceding the sounds produced during self-vocalisation, suggesting it has an established protective function to loud sounds (1), assists in the discrimination of low frequency sounds (8), and is involved in velopharyngeal movements (8).
TTTS was originally described by Dr I. Klockhoff (9-12), and has been proposed by Patuzzi, Milhinch and Doyle (13) and Patuzzi (7) as the neurophysiological mechanism causing most of the persistent ASD symptoms. TTTS is an involuntary condition where the centrally mediated reflex threshold for tensor tympani muscle activity becomes reduced as a result of anxiety and trauma, so it is continually and rhythmically contracting and relaxing, aggravated by intolerable sound exposure1. This appears to initiate a cascade of physiological reactions in and around the ear, which can include: tympanic membrane flutter; alterations in ventilation of the middle ear cavity leading to a sense of blockage or fullness, as well as muffled/echoey/distorted hearing; irritation of the trigeminal nerve innervating the tensor tympani muscle, leading to frequent neuralgic pain; and symptoms consistent with temporomandibular disorder (TMD).
An exaggerated startle reflex and hypervigilance are listed as symptoms of PTSD (DSM-IV, D.5), and individuals with PTSD have been shown to produce heightened autonomic responses (eg increased heart rate) to acoustic stimuli that would not be expected to produce a startle response. My clinical observation of over 85 ASD clients shows that once TTTS has become established, auditory hypervigilance and an exaggerated startle reflex can lead to the escalation of hyperacusis, where the range of sounds that elicit this involuntary response increases to include more everyday sounds. These sounds become increasingly intolerable when TTTS symptoms are exacerbated following exposure. Phonophobia, headache, fatigue, anxiety, and depression can result, particularly if an inadequate explanation or diagnosis of TTTS symptoms is not offered.
A subsequent acoustic incident exposure can therefore lead to a highly enhanced startle response, so that repeated acoustic incidents significantly enhance ASD vulnerability. The persistent pain caused by TTTS can become further exacerbated in a process of central pain sensitisation.
While acoustic shock is usually triggered by an acoustic incident, in some cases, ASD symptoms can develop as a result of cumulative exposure to sustained headset use, without a specific acoustic incident being identified, apparently as a result of triggering the established protective function of the tensor tympani muscle.
Ramirez et al (14) aimed to explore the anatomical and physiological connections in TMD patients with secondary aural symptoms and the central and peripheral mechanisms involved. The authors carried out an extensive peer-reviewed literature search, using data from (12), 436 patients in 49 papers, to analyse aural symptoms (otalgia, tinnitus, vertigo, subjective hearing loss and aural fullness) exacerbated by dysfunctional mouth and jaw dynamics. They proposed a range of muscular, bone communication and neural scenarios to explain this relationship, placing emphasis on tensor tympani muscle involvement and trigeminal nerve dysfunction.
According to Ramirez et al, at a peripheral level TTTS appears to trigger a series of physiological reactions in and around the ear from tympanic membrane tension and alterations in middle ear ventilation. The tensor tympani muscle is innervated by the motor portion of the mandibular branch of the trigeminal nerve, and the authors consider that TTTS can lead to, and in an efferent pathway be caused by, an abnormal stimulation of the trigeminal nerve. This can lead to a chronic irritation of the trigeminal nerve, as well as other cranial and cervical sensory nerves of the ear and periauricular region. Central sensitisation can develop from the resultant chronic pain, leading to an expansion of the perceived peripheral pain and resulting in the typical symptoms of severe TMD.
The research carried out by Ramirez et al (14) shows the aural symptoms associated with TMD and their neurophysiological consequences are at least partially a consequence of TTTS. These aural symptoms and the typical pattern with TMD of chronic, severe myofascial pain; numbness, tingling and burning in and around the ear; escalation and trigger point development in the neck, shoulder and arm and central pain sensitisation are identical to those observed in my clients with severe ASD, and support the proposal that TTTS is the neurophysiological mechanism of ASD. However, ASD clients do not generally have temporomandibular joint (TMJ) dysfunction, unless it is part of a secondary escalation pattern. A hypothesis is presented that TMD can develop when TTTS is caused by an ASD, albeit with a different aetiologic pathway and without TMJ dysfunction.
ASD is beginning to be recognised as a legitimate and discreet disorder, and can be readily misdiagnosed as TMD stemming from TMJ dysfunction. From a differential diagnosis perspective, TMJ dysfunction can lead to TTTS symptoms and escalate to TMD. While central pain sensitisation is common with TMD caused by TMJ dysfunction, the aural symptoms do not tend to escalate and hyperacusis is not usually present.
With ASD, TTTS is associated with hyperacusis: the symptoms are triggered or exacerbated by exposure to sound perceived as intolerable, and the primary cause is related to an anxiety/trauma response to sound. Clinically, TTTS appears to be triggered by the anticipation as well as the perception of sounds considered to be highly threatening and/or intolerable. There is little known and much to research in understanding this aetiologic pathway.
Hyperacusis escalation is common with ASD so that an increasing range of sounds become intolerable, with a corresponding escalation in TTTS symptoms, potentially leading to TMD. For this reason, a detailed history is essential in tracking the order of development and escalation of symptoms, and their relationship to acoustic incidents/headset use, prior to making a responsible and considered diagnosis of ASD.
Rapid referral for a comprehensive audiological assessment provides reassurance, and can help control an escalation of symptoms and limit the development of hyperacusis. History taking should document immediate and persistent symptoms since the acoustic incident exposure; prior acoustic incident exposures; and prior otological and psychological history. Significant malingering is rare in ASD clients, in my experience. Most clients are bewildered, frightened or angered by their symptoms and desperate to recover.
For clients with severe ASD, listening to sounds via headphones during a hearing assessment can be highly threatening and often leads to a significant increase in symptoms, which can persist for days. I consider that frequent audiological testing should not be carried out for these clients. Suprathreshold audiological testing should be limited and loudness discomfort testing, in particular acoustic reflex testing due to the volume levels required, is contraindicated. Some ASD clients have unfortunately had their symptoms permanently exacerbated as a result of a traumatic response to acoustic reflex testing.
On examination of the affected ear, the ear canal and tympanic membrane generally appear healthy and normal. ASD symptoms are subjective, so an experienced clinician makes a diagnosis on the basis of a thorough case history noting the pattern of symptoms; their onset, persistence and escalation; and their link with exposure to intolerable (or difficult to tolerate) sounds. If they have developed in association with acoustic incident exposure and/or hyperacusis is present, it is likely that they are a result of TTTS. The symptoms are remarkably consistent.
TTTS symptoms can be readily confused with outer/middle/inner ear pathology, and an ENT specialist opinion is required to exclude this possibility. If severe vertigo is reported a perilymph fistula needs to be excluded.
ASD management and rehabilitation
A clear diagnosis and explanation of TTTS symptoms has considerable therapeutic benefit.
The most distressing and persistent ASD symptoms tend to be aural pain and hyperacusis. Sharp stabbing aural pain and numbness/burning in and around the ear are consistent with trigeminal nerve irritation. If pain levels are severe, treatment for trigeminal neuralgia, TMD and/or referral to a pain management clinic is indicated. Hyperacusis desensitisation therapy and massage of the muscular trigger points around the neck and shoulder will reduce TTTS symptoms, but progress can be slow once symptoms become entrenched.
Referral for psychological/psychiatric treatment of anxiety, depression and PTSD is indicated, as needed.
In call centres, rapid referral for ASD diagnosis and management can help control a ripple effect in other staff.
With the identification of ASD, output limiters in headset equipment have been developed to restrict maximum volume levels transmitted down a telephone line. However, ASD continues to occur despite their use. In my opinion, they are of benefit primarily to help reduce the probability of an initial acoustic incident exposure. The dominant factors of an acoustic incident leading to ASD appear related to the sudden onset, unexpectedness and impact quality of loudish sounds outside the person's control near to the ear(s), rather than to high volume levels alone. If TTTS develops, because of the vulnerability of further escalation to acoustic incidents at lower volume levels, it is impossible to give a 100% guarantee of protection.
With severe ASD, TTTS symptoms can be involuntarily aggravated by the mere placement of a headset over the ears in the workplace. I consider an ASD client should not return to headset or telephone duties on either ear until the symptoms have fully resolved. A graded return to work can then be carried out with handset use initially on the opposite ear.
The potential severity and persistence of ASD symptoms have significant clinical and medico-legal implications. With the rapid growth of call centres around the world, professionals providing tinnitus and hyperacusis therapy, as well as general practitioners, ENT specialists, occupational physicians, TMD specialists, neurologists and trauma psychologists/psychiatrists, are increasingly likely to encounter some or all of the cluster of ASD symptoms in their clients.
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