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Perspective

Mourning for Silence: Bereavement and Tinnitus—A Perspective

by
Dirk De Ridder
1,*,
Berthold Langguth
2 and
Winfried Schlee
3
1
Section of Neurosurgery, Department of Surgical Sciences, University of Otago, Dunedin 9016, New Zealand
2
Department of Psychiatry and Psychotherapy, University of Regensburg, 93053 Regensburg, Germany
3
Institute for Information and Process Management, Eastern Switzerland University of Applied Sciences, 9000 St. Gallen, Switzerland
*
Author to whom correspondence should be addressed.
J. Clin. Med. 2025, 14(7), 2218; https://doi.org/10.3390/jcm14072218
Submission received: 24 January 2025 / Revised: 8 March 2025 / Accepted: 18 March 2025 / Published: 25 March 2025
(This article belongs to the Section Otolaryngology)
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Abstract

:
Tinnitus is defined as the conscious awareness of a tonal or composite noise for which there is no identifiable corresponding external acoustic source, which becomes tinnitus disorder when the phantom sound is associated with suffering and/or disability. There is only limited knowledge about the time course of tinnitus disorder. Bereavement science has identified four different trajectories: resilience, recovery, chronic, and delayed. The question arises whether these four trajectories exist in tinnitus as well if one considers tinnitus as the loss of silence (at will). To verify whether these four trajectories exist, short-term tinnitus progression was analyzed retrospectively using an Ecological Momentary Assessment (EMA) approach, extracting the data from patients who started using the TrackYourTinnitus (TYT) app (version 1, Ulm University, 2013) from the start of their tinnitus perception. Four patients were identified retrospectively via the TYT app with acute tinnitus, and the bereavement trajectories were reconstructed based on EMA. In conclusion, this perspective suggests that the four known bereavement trajectories may exist in tinnitus, and prospective evaluations of larger samples are warranted to confirm or disprove this analogy between bereavement and tinnitus, in which tinnitus is conceived as the loss of (controllable) silence.

1. Introduction

Tinnitus has been defined as the conscious awareness of a tonal or composite noise for which there is no identifiable corresponding external acoustic source, which becomes tinnitus disorder when associated with emotional distress, cognitive dysfunction, and/or autonomic arousal, leading to behavioral changes and functional disability [1]. In other words, “tinnitus” describes the auditory or sensory component, whereas “tinnitus disorder” reflects the auditory component with associated suffering [1]. These definitions are based on an analogy of pain [2,3] and adapted from definitions already in use in the DSM-V and ICD11 for pain [1]. Both tinnitus and pain have similar neurophilosophical (Darwinian and Bayesian), anatomical (lateral, medial and descending pathways), pathophysiological (thalamocortical dysrhythmia), clinical (entirely subjective, wind-up, and hypersensitivity), and treatment (psychology, medication, neuromodulation, and surgery) characteristics [4,5,6,7,8], permitting the definitions’ alignment. As in tinnitus, in pain, there is a sensory component and a suffering component [8,9], leading to the classification of Somatic Symptom Disorder in the DSM-5, previously known as pain disorder. However, in contrast to pain, in which the ICD 11 classification recognizes seven subgroups [10,11], no subgroups have yet been defined despite multiple statistical attempts. This may mean that either tinnitus is not as heterogeneous as once thought from a ‘pathophysiological’ point of view, or some crucial aspects are missing. In tinnitus, large-scale ‘clinical’ heterogeneity has resulted in problems of standardizing diagnosis, management, and treatment. Four main dimensions have been described for tinnitus heterogeneity: 1. perception; 2. risk factors/comorbidities; 3. distress/suffering; and 4. treatment responses [12]. However, this assumes that all tinnitus is inherently static in nature, which it is not. Tinnitus can change over time, which means a fifth dimension needs to be added to clinical heterogeneity. Looking at the natural evolution of tinnitus, it has been shown that while in 80% of patients it is relatively static, in 20% of patients, tinnitus can disappear within 4 years, and in those 80% in whom it persists, in 10%, it can improve, and in 10%, it can worsen [13]. This suggests that at least four different trajectories exist: recovery, delayed worsening, and stability (resilient or chronic), further adding to the heterogeneity of tinnitus. The prevalence of tinnitus in the general population is estimated at 14.4% [14]. Whereas about 80% of people who have tinnitus can cope with it and can lead normal lives, for about 20% of people, tinnitus is associated with suffering [14,15].
For individuals exposed to work-related noise, prevalence is estimated at 23.3% [16]. In the military, 6–7% of soldiers develop tinnitus after deployment [17]. Depending upon the circumstances, traumatic events may contribute to the onset of tinnitus [18,19,20,21]. In veterans, the prevalence of severe and very severe tinnitus (= tinnitus disorder) is significantly higher, and this is related to PTSD. Indeed, veterans with tinnitus, but without PTSD, typically report predominantly mild tinnitus, whereas veterans with PTSD typically report moderate, severe, or very severe tinnitus, and this is associated with increased anxiety and depression [22]. Among PTSD-affected soldiers, the prevalence of tinnitus is over 50% [23]. PTSD is considered a psychological injury, and while tinnitus is a symptom, its onset may be connected in memory to the injury, thereby evincing the capacity to exacerbate the trauma’s effects [20].
Tinnitus and depression are comorbid, as evidenced in veterans [22], but also in the general public [24]. Whereas acute tinnitus is comorbid with anxiety and insomnia, chronic tinnitus is more often associated with depression [25].
This suggests that tinnitus perception may change over time [26,27], associated with changes in the neural signature of tinnitus in the brain, which also changes over time [28]. Most studies that aimed to investigate the time course of tinnitus assumed a common progression. However, based on bereavement science, it can be hypothesized that patients may follow any of four trajectories describing grief due to bereavement [29]. This means that tinnitus can be conceptualized to lead to the feeling of bereavement or loss of a bygone era in which there was no phantom sound, an era characterized by silence that could be controlled at will. Thus, tinnitus may lead to the feeling of mourning for the loss of silence, and hence researchers in the tinnitus field may learn something from bereavement science.
Bereavement science demonstrates that there are four trajectories to trauma and grief: 1. resilience, 2. recovery, 3. chronic dysfunction, and 4. delayed trauma [29]. These trajectories are similar for prolonged grief disorder, PTSD, and depression [30], i.e., when a close family member dies, people are either resilient to prolonged grief, PTSD, and depression, or recover from all four or not [30]. Considering that PTSD and depression are comorbid to tinnitus in ± 25% of people [24], it can be hypothesized that if tinnitus is considered as a trauma or the bereavement of controllable silence, these four trajectories could also exist in tinnitus and help to distinguish between tinnitus and tinnitus disorder.
Resilient people continue to thrive irrespective of trauma or loss. Their normal functioning is not or only mildly disrupted. In recovery, people’s daily functioning is initially moderately or severely disrupted, but over 1 to 2 years there is the gradual normalization of functioning. Chronic dysfunction is characterized by the severe disruption of normal functioning from the beginning, which does not improve over time. Delayed trauma leads initially to mild or moderate disruption of normal functioning, which after a delay worsens progressively to severe interference [29].
The question is whether these trajectories also exist in tinnitus. But irrespective of this, researchers in the tinnitus field can learn from bereavement science that tinnitus heterogeneity may be linked to these different trajectories, which means the tinnitus field may benefit from a similar stratification.

2. Methods and Materials

To verify whether these 4 trajectories may possibly exist, as posited in this perspective, we explored tinnitus progression retrospectively using Ecological Momentary Assessment (EMA), a commonly used research method that aims to assess phenomena with a focus on ecological validity and to help both the user and the researcher observe these phenomena over time. One phenomenon that benefits from this capability is chronic tinnitus. TrackYourTinnitus (TYT) (version 1, Ulm University, 2013) is an EMA-based mobile crowdsensing platform designed to provide more insights into tinnitus by repeatedly assessing various dimensions of tinnitus, including perception (i.e., perceived presence).
Using the TrackYourTinnitus database, 4 patients were retrospectively retrieved who started charting tinnitus loudness and tinnitus annoyance almost from day 1 of developing tinnitus.
The TrackYourTinnitus study was conducted according to the guidelines of the Declaration of Helsinki and approved by the Institutional Ethics Committee of the University of Regensburg (protocol number: 15-101-0204) dated 26 August 2015.

3. Results

Of the four patients who charted tinnitus from the acute setting, one was defined as being resilient (1572), one as following a quick recovery trajectory (4479), one as following a chronic trajectory (721), and one as having a delayed trajectory (677) (see Figure 1 and Table 1). Since people who use the TYT app are not required to provide all the requested data, the demographic and clinical data are only partial (see Table 1). Their ages were between 42 and 62 years old, three of four people were male, and the miniTQ score varied from five to twenty-three (from no distress to most severe distress). The resilient trajectory is associated with the absence of distress. Recovery occurred in the patient who initially had the most severe distress, which also is seen in the delayed trajectory. The chronic trajectory was observed in the patient with severe distress, but not the most severe distress and also not moderate nor the absence of distress (obviously).

4. Discussion

Tinnitus is well known as a heterogenous disorder with multiple hypothesized subtypes [33]. Many researchers and clinicians have tried to classify these subtypes according to their clinical profiles, etiologies, and response to treatment, with little success [33]. The occurrence of overlapping tinnitus subtypes suggests that the disorder exists along a continuum of severity, with no clear distinct boundaries [33]. From a mechanistic point of view, the unified, personally unique tinnitus percept has been described as an emergent property of partially overlapping, dynamically changing, interacting brain networks, each representing a different clinical aspect of the unified, individualized tinnitus percept [34], suggesting that the interaction of these separate networks determines the phenomenology of tinnitus, ultimately leading to a dimensional spectrum, rather than categorical subtypes [33]. The question is whether there exists one common trajectory all patients go through, or whether multiple different trajectories exist?
Based on this small exemplary data sample of tinnitus patients who filled out an EMA form using the TrackYourTinnitus app from the early stages of acute tinnitus shows that the four trajectories known in bereavement science may also be present in patients with tinnitus (Figure 2, Table 2). Thus, conceptually, in tinnitus, we may see the 4 suggested trajectories.

4.1. Resilience (±70–80%) [30]

Resilience is defined as the capacity of a dynamic system to adapt successfully to disturbances that threaten system function, viability, or development [35]. Applied to neuroscience, it is defined as the ability to cognitively or emotionally cope with stress, trauma, or adversity without long-term negative consequences. Psychological resilience is present in 80% of people with bereavement [30] and PTSD [36]. This is similar to the 85% of patients who have tinnitus, but do not suffer from it [14,15]. Resilience has a protective effect on tinnitus handicap, as indexed by the THI, and neuroticism has a negative effect [37]. Thus, people with high psychological resilience will tolerate the presence of tinnitus better, which is in keeping with bereavement science. Resilience may not have a direct or indirect influence on tinnitus loudness [38]. However, resilience influences annoyance directly, as does neuroticism on tinnitus annoyance and severity [38,39]. The protective effect of high resilience is associated with better emotional health and reduced depression, anxiety, and somatic symptom severity, which, in turn, are associated with a less distressing tinnitus [40]. Based on the natural history of tinnitus, it can be estimated that resilience and recovery is indeed present in 80% of people with tinnitus [13]. This is similar to what is known about trauma. Meta-analyses have shown that around 80% of trauma-exposed people are resilient to or recover from trauma, whether it is related to major traumatic events [36], floods [41], war zones [42], or pandemics [43]. This is also similar to prolonged grief disorder [44], although the incidence of the latter varies between 10% [45] and 40% [46], which may be due to the very low certainty level of the evidence for the pooled prevalence of Prolonged Grief Disorder (PGD) and its symptoms [47].

4.2. Recovery (±10–20%) [30]: Normal Transient Suffering

Suffering is normal in bereavement, and when resilience does not prevent the impact of suffering on normal functioning, it can lead to transient disability. However, this can be followed by recovery, taking 1–2 years [29,48,49]. In tinnitus, in about 20% of patients the THI score improves by twenty points, and about 50% by seven points (=Minimal Clinically Important Difference, MCID) over a period of 1–6 years. As the patients did seek treatment, so it cannot be concluded whether this is solely based on spontaneous recovery [27]. However, natural evolution demonstrates that after 4 years, 20% of people with tinnitus no longer have it, and in the 80% of patients who still have tinnitus, in 10% there is an improvement [13]. Furthermore, complete recovery from tinnitus is possible even in chronic cases [50].

4.3. Chronic (±5%) [30]: Pathological Persistent Suffering = Tinnitus Disorder

Chronic suffering as expressed as prolonged grief and PTSD symptoms, and depression is present in 5% of bereaved patients [30]. This is similar in magnitude to the global prevalence of tinnitus disorder (2.3%) [14]. The risk factors for these bereaved patients who are chronically suffering are neuroticism [51,52] and insomnia [53], whereas social support is protective [51]. Comorbid anxiety, depression, and PTSD result in more grief [54]. In tinnitus, the risk factors for bothersome tinnitus are also neuroticism and insomnia [13,55] and also include hearing difficulties, ototoxic medication, and work noise exposure [13,55]. It is important that tinnitus loudness is not the principal determinant of whether people suffer chronically, but rather their personality characteristics, sleep behaviors, and hearing difficulties.

4.4. Delayed (±5%) [30] Tinnitus Disorder

The delayed worsening of bereavement is rare, and it is unclear whether this really exists [56]. In tinnitus, this is also unknown. Delayed tinnitus has been hypothesized to exist in those with noise trauma [57,58] according to evidence based on rat studies [59]. Mechanistically, this may be related to an inflammatory response that develops progressively in the auditory system associated with noise trauma [60]. From a theoretical perspective, a second mechanism could involve patients who could initially cope with the tinnitus but are exposed to emotional stress for other reasons. When the extra stressors occur, they may experience worsening of pre-existing tinnitus and tinnitus severity [61]. Usually, this will only result in transient worsening or fluctuation, but if the stressors are severe or repetitive, this could lead to persistent worsening. A summary of these four categories can be found in Table 2.
In all these trajectories, temporarily fluctuations may occur, when people suffer more and/or perceive the phantom sound louder, but this worsening is only transient and commonly associated with any extra non-specific stressors. Indeed, ‘suffering’ is processed in the brain in the medial pathway, which is non-specific, i.e., it is the same for tinnitus, pain, or any other stimulus, and overlaps with the stress network [8,9,62,63]. Thus, any stress may worsen tinnitus-associated suffering. Furthermore, stress changes the sensory gain via increased alpha2 noradrenergic receptor activation [64], which could make patients perceive tinnitus louder. Stress that transiently worsens tinnitus can be social, e.g., work- or family-related; associated with physical stress, such as surgeries or infections; or psychological. Stress may exacerbate both tinnitus loudness and tinnitus-associated suffering transiently via its effect on the medial network, which colocalizes with the salience network (insula, ACC) in cognitive neuroscience [9,65]. Normally after the stressor is removed, the patients will recover to their previous state. However, more chronic stress may create longer-lasting worsening by its immune dysfunction-inducing effect [66], and its interference with the triple network may reflect a double hit as well [67], which has been posited to be crucially involved in tinnitus processing [63]. It is indeed known that stress in general can worsen the tinnitus percept [61,68,69].
Stress increases daily energy expenditure by 30%, as does immune activation, and when stress results in insomnia, this may add another 30% extra energy expenditure [70]. This will lead to fatigue and mental exhaustion. Consequently, it is unsurprising that fatigue is associated with higher tinnitus-related distress [71].
  • Is there a theoretical framework for this analogy?
There exist multiple brain-based theoretical models of tinnitus and tinnitus disorder. No coherent encompassing model exists yet that integrates different tinnitus models, such as the gain model [72], the neuroinflammation model [73], the multiple network model [74], the imbalance model [8], the Bayesian brain models [75,76], and the triple network model [63]. As seen from the variations in the Bayesian brain model, it can be proposed that when auditory deafferentation occurs, with or without hearing loss [77], this will result in auditory uncertainty about what occurs in the changing environment [76]. When this auditory deprivation is not deemed salient, no tinnitus will be generated [78], yet when the brain does consider the lack of auditory input as salient, it follows a better-safe-than-sorry approach and fills in the missing auditory information by generating the sound itself, thereby reducing auditory uncertainty [4]. As such, tinnitus can be seen as an uncertainty disorder [79], which can generate stress and suffering in people who are genetically or epigenetically prone. Reducing auditory uncertainty via a filling-in mechanism may explain the development of tinnitus [76]. We now propose that the based on this theoretical foundation, tinnitus may generate a feeling of bereavement of the ‘loss of silence’ at will. Everybody who develops tinnitus may initially perceive bereavement as the feeling of loss of silence at will, but depending on individual coping mechanisms this may result in different trajectories that are akin to what has been theorized in the bereavement literature [56]. Indeed, when hearing loss is associated with neuroticism, sleep deprivation, work noise exposure, or ototoxic drugs, this increases the risk for developing bothersome tinnitus [13], which could evolve into a disorder, i.e., tinnitus with suffering, when bother turns into anxiety and depression. As such, tinnitus is the outcome of a resilient or recovery trajectory, and tinnitus disorder is the consequence of a chronic or delayed trajectory. In essence, the perceived distress or intrusiveness associated with tinnitus may theoretically reflect maladaptive coping with auditory uncertainty. In other words, not accepting that there may never be silence (at will) anymore can lead to tinnitus disorder, which is similar to not accepting that the loss of a loved one is forever, leading to complicated grief or prolonged grief disorder. From this point of view, the acceptance of bereavement, i.e., the ‘loss of silence’, is inversely proportional to perceived intrusiveness, distress, or suffering.
  • What drives certain patients to follow one trajectory, and others a different one?
Resilience is the default response to the development of tinnitus, as it occurs in 80% of people with tinnitus. Resilience is based on genetic and epigenetic factors that involve the nervous system, the immune system, and the endocrine system [80], all involved in integrated and concerted responses to internal and external stressors [66]. Indeed, for PTSD, it has been shown that if someone has the risk genes for PTSD, a single incidence of exposure to trauma is sufficient to trigger the development of PTSD by activating PTSD risk gene expression [81,82]. However, also some people without the risk genes develop PTSD after trauma. This has been linked to epigenetic tagging, e.g., via the methylation of the same genes, turning normal genes into functional risk genes [81]. Epigenetic tagging can for example occur as a consequence of an extreme stressor in early childhood, such as any form of severe childhood adversity. But epigenetic modifications can result from other causes, such as toxins, medication, diet, psychological or physical stress, and trauma [9]. In other words, with the risk genes for poor resilience, a person may end up on a trajectory that differs from the resilience trajectory, such as the chronic distress trajectory or the delayed trajectory. But a person without those risk genes may still end up on the chronic or risk trajectory if there have been epigenetic modifications to the resilience genes due to early childhood adversity, psychological or physical trauma, intoxications, poor diet, medication, etc., resulting in a double hit [81,82]. In other words, people without risk genes require two traumas for PTSD to develop. An analogy of tinnitus would be that hearing loss only triggers tinnitus if certain risk genes are present, or if two hits occur, in which the first hit triggers the epigenetic tagging of the tinnitus risk genes, and the second hit subsequently triggers tinnitus. This has been suggested in people with polymorphism for the COMT gene. COMT Val158Met polymorphism can increase susceptibility to the clinical manifestation of tinnitus in those people with hearing loss [83]. However, this does not result in suffering. For this, another polymorphism may be essential. BDNF Val66Met polymorphism can result in suffering with the associated worsening of tinnitus loudness perception [84]. This may need to be seen from a broad perspective. Some genetic polymorphisms are associated with clinical features. The genes associated with tinnitus and hearing loss overlap partially, but some are different [85]. Also, personality characteristics such as neuroticism are genetically determined [86,87], as is long and short sleep duration [88], and insomnia [89]. All these factors increase the risk for people with tinnitus to follow the chronic suffering trajectory. Neuroticism is indeed a risk factor for chronic grief/distress [51] and tinnitus distress [90,91]. Some polymorphisms associated with neuroticism overlap with the genes involved in resilience, suggesting that indeed genetic and epigenetic influences partially determine which trajectory a person will follow once tinnitus occurs [92]. Considering that neuroticism genes also overlap with anxiety and depression risk genes [87], this may explain why people with genetic risk genes for neuroticism may have an increased risk of developing tinnitus disorder (= the trajectory of chronic distressed tinnitus) [13,37,39]. Insomnia is also a risk factor for developing the chronic trajectory. Insomnia can lead to immune dysfunction [70,93,94], triggering a long-term neuroinflammatory pathology which is known to be associated with most chronic neurological and psychiatric disorders, including anxiety [95], depression [95], tinnitus [73,96,97], and PTSD [98,99].
In summary, tinnitus, pain, PTSD, and PGD may share a common pathophysiological mechanism, in which genetic and environmental (epigenetic) factors determine whether low-grade neuroinflammation turns an acute symptom, such as pain, tinnitus, stress, or loss, in a chronic state, resulting in chronic pain, chronic tinnitus, PTSD, and PGD (= complicated grief). This may be mediated or worsened via the sleep problems common to all these pathologies. The analogy involving these four disorders is summarized in Figure 3, based on the proposed very similar pathophysiological mechanisms involved in chronic pain [9], chronic tinnitus, PTSD [100], and bereavement [101].
  • Are these trajectories clinically meaningful?
The four different trajectories may require different management and treatment approaches, suggesting that incorporating these trajectories in studies may be highly relevant to help combat the heterogeneity of populations included in studies, as well for individual patients seen in the clinic. These trajectories do suggest that it may even be useful to create different tinnitus management programs and treatment centers for the different trajectories. Whereas those with resilience do not require treatment, patients on the recovery trajectory may benefit from simple short-term audiological/ENT or psychological management to facilitate the natural recovery process. On the other hand, those on the chronic and delayed trajectories may require long-term multidisciplinary help involving multidisciplinary tinnitus centers with neurology/neurosurgery/psychiatry/psychology and ENT/audiology collaboration. People on the chronic trajectory may require multimodal approaches, such as a combination of CBT, medication, and/or neuromodulation for comorbid suffering involving sleep problems, anxiety, and depression. This may need to be maintained if, for example, the chronic trajectory is due to factors that are not sufficiently addressed or cannot be addressed such as neuroticism, ototoxic medication, a loud workplace, and progressive hearing loss. The delayed group is especially intriguing as it can be envisioned that timely CBT or multimodal treatment could prevent the transition from tinnitus to tinnitus disorder.
Whereas resilience is related to well-characterized genes [80,92], complicated grief (chronic and delayed trajectories) after the loss of a spouse is linked to different gene variants [101], especially related to inflammation, e.g., via IL6-174 SNP [102] and the gene variants that downregulate interferon 1 immune responses [103]. This has resulted in a model that suggests that bereavement trajectories differ based on a genetically and epigenetically induced proinflammatory state [101], analogous to what has been proposed for tinnitus [73,97].
Different genes have been linked to the development of tinnitus and tinnitus disorder, strongly suggesting that the clinical distinction between tinnitus and tinnitus disorder is reflected in a different genetic structure [104,105]. The rare genetic variants associated with tinnitus disorder include those related to neural activity (e.g., ANK2, NAV2, and TMEM132D), inflammation (e.g., TSC2), metabolism (e.g., AKAP9), and calcium channel function (CACNA1E) [104,105]. As tinnitus disorder is typical for chronic and delayed trajectories, it may be of relevance to look at inflammation-related genes, as neuroinflammation is involved in tinnitus, complicated grief, anxiety [96], and depression [95]. These variants differ from the common variants found in tinnitus GWAS, highlighting the distinct genetic underpinnings for tinnitus disorder compared to those of tinnitus alone. Furthermore, some genes involved in tinnitus disorder such as TMEM132 have also been associated with anxiety [106,107], explaining that these gene variants are relevant for tinnitus disorder. In summary, it can be proposed that some gene variants make people vulnerable to develop tinnitus in the setting of auditory uncertainty related to deafferentation, and having some other extra, but different gene variants may determine whether tinnitus results in associated suffering (tinnitus disorder) due to neuroinflammatory processes.
As a consequence, involving geneticists and pharmacologists, especially for treating people who follow the chronic or delayed trajectory should be arranged. For example, genetic studies show that six druggable genes (TLR4, MMRN1, BRAF, ACVR1B, NOS2, and GPX1) are already being explored for drug development targeting neuroticism [86], which may be used in the early treatment of people at risk of following the chronic trajectory. For example, TLR4 is targeted by cyclobenzaprine [86], which is currently used to treat tinnitus [108], NOS2 can be targeted by dexamethasone and gingko biloba [73], which are also already used to treat tinnitus [109]. NOS2 can also be targeted by arginine, miconazole, and minocycline [86], which could theoretically be repurposed for the treatment of tinnitus. And GPX1 is targeted by cannabidiol, but also glutathione and selenium [86], which are readily available. Thus, understanding the genetic and non-genetic risk factors for these trajectories could potentially lead to more personalized management and treatment approaches in people suffering from tinnitus.
A weakness of this perspective is that it could be a self-fulfilling prophecy by specifically searching for the expected trajectories. While this could be a correct assumption, this is the case with all theoretical models. Another weakness is that tinnitus tracking was of a short duration. Consequently, what is fitted to the chronic trajectory in this representative case may still be the recovery trajectory in the long term.
  • How do we move forward?
Ideally, a large prospective long-term follow up dataset needs to be developed that tracks many patients with tinnitus from day 1 for at least 1 year longitudinally for tinnitus loudness, tinnitus-associated distress/suffering, and disability, in which, subsequently, data-driven cluster analysis is performed to extract the statistically independent trajectories.
Once this stratification is performed, genetic and epigenetic studies may add to the clinical data by helping to develop personalized treatment approaches for patients. This may require multidisciplinary tinnitus centers, analogous to what already exists for pain.

5. Conclusions

If tinnitus is addressed from the point of view that tinnitus represents the loss of silence (at will), and thus bereavement, it can be theorized that the canonical four trajectories of bereavement may exist in tinnitus. And even though this study is based on little data, the four trajectories that exist in bereavement are compatible with the tinnitus trajectories. It is evident that all the trajectories may fluctuate in the long term, with ups and downs depending on the non-tinnitus-related extra stressors transiently worsening tinnitus loudness and annoyance. Recognizing these trajectories may result in the more personalized management and treatment of tinnitus. Further prospective studies looking at larger samples may prove or disprove this theoretical perspective.

Author Contributions

Conceptualization, D.D.R.; methodology, D.D.R. and W.S.; software, W.S.; data curation, W.S.; writing—original draft preparation, D.D.R.; writing—review and editing, W.S. and B.L.; visualization, D.D.R.; supervision, D.D.R., W.S. and B.L.; project administration, D.D.R. All authors have read and agreed to the published version of the manuscript.

Funding

This manuscript received no external funding.

Institutional Review Board Statement

This TrackYourTinnitus study was conducted according to the guidelines of the Declaration of Helsinki and approved by the Institutional Ethics Committee of the University of Regensburg (protocol number: 15-101-0204) dated 26 August 2015.

Informed Consent Statement

Informed consent incorporated in the TrackYourTinnitus application was obtained from all the subjects involved in this study.

Data Availability Statement

Data are available from W.S. on reasonable request.

Conflicts of Interest

The authors declare no conflict of interest.

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Figure 1. Trajectories of patients with tinnitus. Red line = tinnitus loudness; black line = tinnitus distress.
Figure 1. Trajectories of patients with tinnitus. Red line = tinnitus loudness; black line = tinnitus distress.
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Figure 2. Schematized trajectories of tinnitus evolution based on bereavement science.
Figure 2. Schematized trajectories of tinnitus evolution based on bereavement science.
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Figure 3. Similar pathophysiological mechanisms underpin chronic pain, chronic tinnitus, PTSD and PGD, in which genetic vulnerability and environment-induced epigenetic changes introduce proinflammatory state that turns the acute symptom into a chronic persistent state.
Figure 3. Similar pathophysiological mechanisms underpin chronic pain, chronic tinnitus, PTSD and PGD, in which genetic vulnerability and environment-induced epigenetic changes introduce proinflammatory state that turns the acute symptom into a chronic persistent state.
Jcm 14 02218 g003
Table 1. Demographic and clinical characteristics of the four patients.
Table 1. Demographic and clinical characteristics of the four patients.
User ID1572
Resilient		4779
Recovery		721
Chronic		677
Delayed
age55626242
sexmalemalefemalemale
miniTQ5 (no distress)23 (most severe)15 (severe)20 (most severe)
tinnitus sideright earright earinside headboth ears, worse in left ear
description of tonehigh-frequency whistlehigh-frequency tonecricketstone
vertigoNAnoNANA
hearing problemNAnoNANA
hearing aidsNAnoNANA
headacheNAnoNANA
psychiatric treatmentNAnoNANA
medicationNAnoNANA
Questionnaires used: TSCHQ = Tinnitus Sample Case History Questionnaire [31] and miniTQ = mini Tinnitus Questionnaire) [32], NA = data Not Available.
Table 2. Bereavement trajectories applied to tinnitus.
Table 2. Bereavement trajectories applied to tinnitus.
TrajectoryBereavementTinnitus (Loss of Silence)
Resilience:Minimal disruption in daily functioningTinnitus causes minimal disruption in daily functioning
Low levels of distress or grief symptomsAcceptance of tinnitus as a non-threatening aspect of their sensory experience
Adaptive coping skillsIndividuals adapt very quickly to the presence of tinnitus using adaptive coping skills
Recovery:Intense emotional pain early onInitially high levels of annoyance, anxiety, or emotional pain
Gradual improvement in mood and functioningGradual reduction in distress as habituation occurs or therapeutic interventions are successful to reduce tinnitus
Effective use of support systems and coping mechanismsReturn to a baseline sense of control over life.
Chronic grief:Long-lasting emotional pain and difficulty adjusting to life without the deceased personOngoing feelings of frustration, anxiety, depression, or despair that tinnitus will never go away
Interference with daily functioning and relationships.Difficulty habituating to the sound, with tinnitus dominating attention and mental space.
May indicate complications such as Prolonged Grief Disorder (PGD).May indicate co-occurring conditions such as anxiety disorders or depression.
Delayed grief:Initial avoidance or suppression of grief.Initial minimization, suppression, or unawareness of the emotional impact of tinnitus
Emotional pain emerging months or even years after the loss.Distress emerging later, often triggered by life stressors, increased tinnitus loudness, or reduced coping resources
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De Ridder, D.; Langguth, B.; Schlee, W. Mourning for Silence: Bereavement and Tinnitus—A Perspective. J. Clin. Med. 2025, 14, 2218. https://doi.org/10.3390/jcm14072218

AMA Style

De Ridder D, Langguth B, Schlee W. Mourning for Silence: Bereavement and Tinnitus—A Perspective. Journal of Clinical Medicine. 2025; 14(7):2218. https://doi.org/10.3390/jcm14072218

Chicago/Turabian Style

De Ridder, Dirk, Berthold Langguth, and Winfried Schlee. 2025. "Mourning for Silence: Bereavement and Tinnitus—A Perspective" Journal of Clinical Medicine 14, no. 7: 2218. https://doi.org/10.3390/jcm14072218

APA Style

De Ridder, D., Langguth, B., & Schlee, W. (2025). Mourning for Silence: Bereavement and Tinnitus—A Perspective. Journal of Clinical Medicine, 14(7), 2218. https://doi.org/10.3390/jcm14072218

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