From: Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2009 Jun;31(3):381-2

To investigate the association between cervical curvature and cervical sympathetic symptoms, the clinical data of 318 patients with cervical spondylosis who underwent surgical treatment in our department between July 2003 and December 2007 were retrospectively analyzed. All patients were divided into group without sympathetic symptoms (n = 284) and group with sympathetic symptoms (n = 34). The curvatures of both groups on cervical lateral radiographs were measured using Borden method and statistical analysis was performed.

The incidence of abnormal cervical curvature in group with cervical sympathetic symptoms were 67.6% (23/34), which was significantly higher than that in group without cervical sympathetic symptoms (50.7%, 144/284). Cervical curvature abnormality may be an independent factor that affects the cervical sympathetic symptoms.

In Zhonghua Wai Ke Za Zhi. 2008 Sep 15;46(18):1424-7, Treatment and mechanism of cervical spondylosis with sympathetic symptoms concluded: The sympathetic nerve fibers distributed in the cervical posterior longitudinal ligament maybe another one significant factor causing sympathetic symptom of cervical spondylosis.

Posterior Cervical Sympathetic Syndrome is a condition that is characterized by a host of cranial symptoms, such as headaches, abnormal functions of the eyes and the ears, and psychological and mental disorders. This syndrome usually appears after neck injuries, inflammation, or neoplasm.”

Sympathetic symptoms related to the neck may include; vertigo, disequilibrium, tinnitus, scotomata, decreased vision, dysphagia, dysphonia, cough, anxiety and asthenia.

History: In 1925, Jean Alexandre Barre, M.D., a French neurologist, and in 1928, Yong-Choen Lieou, a Chinese physician, each independently described a syndrome with a variety of symptoms thought to be due to a dysfunction in the posterior cervical sympathetic nervous system (a group of nerves located near the vertebrae in the neck). The posterior cervical sympathetic syndrome became known as Barre-Lieou Syndrome.

In a case documented in Vertebrogenic autonomic dysfunction-subjective symptoms published in The Journal of the CCA. 1981 Jun;25(2): 51-7,

Mrs. F. presented with neck pain and headaches. She had sustained a whiplash injury 2 years previously and her symptoms had cleared with chiropractic therapy. Her present symptoms had recurred 2 months prior to her consultation here. She complained of a constant, moderate to severe upper cervical ache which radiated into the occipital-frontal regions. The cephalalgia occurred daily and intensified in the midafternoon. She reported associated dizziness and difficulty in focusing her eyes. She could not clearly focus on close objects and stated that while driving, the windshield seemed to move back and forth in relation to her eyes. She was constantly squinting in an effort to see clearly. She had been seen by an optometrist 3 weeks previously with negative findings.

On examination, cervical extension, right side-bending and left rotation were painful and limited. There was palpable paravertebral muscle spasm and restriction of motion in the upper cervical articulations. Trigger points were found here which reproduced the cephalalgia.

Cervicogenic autonomic dysfunction was objectivated with the following manoeuvres:

1. Triggers: Firm pressure over the right lamina of C2 precipitated an immediate bout of blurred vision and diplopia.
2. Resisted Motion: Resisted cervical extension (with the head fixed so as to exclude vestibular motion) resulted in an episode of “swooning” and vertigo.
3. Cervical Torsion: The patient’s head was fixed by an assistant (so as to exclude vestibular motion) and the torso was rotated, flexed, extended, side-bent and circumducted under the immobilized cranium. These manoeuvres precipitated vertigo.

From: PLoS ONE. 2009;4(3):e5026. Epub 2009 Mar 27

Tinnitus is a frequent condition with high morbidity and impairment in quality of life. The pathophysiology is still incompletely understood. Electromagnetic fields are discussed to be involved in the multi-factorial pathogenesis of tinnitus, but data proofing this relationship are very limited. Potential health hazards of electromagnetic fields have been under discussion for long. Especially, individuals claiming themselves to be electromagnetic hypersensitive suffer from a variety of unspecific symptoms, which they attribute to electromagnetic fields exposure. The aim of the study was to elucidate the relationship between electromagnetic field exposure, electromagnetic hypersensitivity and tinnitus using a case-control design.

Tinnitus, the perception of sound in the absence of an external sound, is a frequent disorder of auditory perception, which is very difficult to treat. Tinnitus as a phantom perception of a meaningless sound has to be differentiated from auditory hallucinations which mainly occur in the context of psychiatric diseases and are characterized by e.g. the perception of voices. About 10–20% of the adult population experiences some degree of tinnitus. Many learn to ignore the sounds and experience no major effects, but for about 1 in 100 adults, the noise interferes significantly with daily life. In those patients, tinnitus is frequently associated with neuropsychiatric co-morbidity such as depression, anxiety or sleep disorders, which underlines the clinical and socio-economic importance.

Even if the pathophysiology of tinnitus remains incompletely understood, there is growing evidence that dysfunctional neuroplastic processes in the brain are involved. In particular, it is assumed that tinnitus might be the correlate of maladaptive neuroplastic changes due to distorted sensory input. Accordingly functional imaging studies demonstrated neuroplastic alterations in the central auditory system. However tinnitus related alterations of neural functioning are not limited to the central auditory system, but also encompass non-auditory regions such as frontal and limbic areas.

There has been an ongoing debate, whether tinnitus might be related to exposure to electromagnetic fields. One previous study found a tinnitus prevalence of 14% in a sample of electromagnetic hypersensitive subjects. Whereas electromagnetic hypersensitivity per se is not a proxy variable for electromagnetic field exposure, substantial evidence from electrophysiological studies has shown electromagnetic fields and especially mobile phone emissions to influence cognitive function and neuronal processing in the central auditory system. These might represent potential mechanisms by which electromagnetic fields could contribute to the development of tinnitus. However, two recent epidemiological studies from a student and a the general population, respectively, did not demonstrate a significant relationship between mobile phone use and tinnitus.

Besides the hypothesized involvement in the generation of tinnitus, electromagnetic field exposure has also been related to a variety of unspecific health symptoms (e.g., dizziness, fatigue, headache, sleep disturbances, etc.). Despite a huge amount of studies investigating the health impact of electromagnetic fields, no clear relationship between electromagnetic field exposure and these unspecific health symptoms could be established and the majority of provocation studies failed to demonstrate such a relationship. Based on the fact that some individuals suffer from a variety of symptoms, which they attribute to electromagnetic fields exposure, whereas the overwhelming majority does not experience any symptoms under the same electromagnetic field exposure, the concept of “subjective electromagnetic hypersensitivity” evolved. This subjective electromagnetic hypersensitivity is characterized by health complaints, which interfere with daily living and are subjectively attributed to electromagnetic fields of named emission sources (e.g., mobile phone base stations, hot spots, TV-sets, etc.). Very recent data from an epidemiological case-control study suggest that this subjective electromagnetic hypersensitivity is characterized by dysfunctional cognitions, reduced discrimination ability for sensory stimuli and increased sensitivity of a cortical network encompassing the anterior cingulate and insular cortex.

Due to the large sample size, the detailed clinical and neurobiological characterization and the control group, which was matched for age, gender and either living surroundings or workplace (as very rough proxies for electromagnetic field exposure), this study population was well suited to investigate the relationship between tinnitus, subjective electromagnetic hypersensitivity and electromagnetic field exposure. In detail, we addressed the following questions: 1.) Do subjective electromagnetic hypersensitive people suffer more often from tinnitus than controls? 2.) Are there clinical characteristics that point to potential common pathological mechanisms?

With the failure to prove a causal relationship between electromagnetic field exposure and symptoms in subjectively electromagnetic hypersensitive patients, research is focusing increasingly on neuronal mechanisms involved in symptom formation. Recent results suggest an individual vulnerability of these patients against environmental stressors especially affecting the autonomic nervous system. A pilot study investigating possible alterations of central nervous system excitability found evidence for alterations of the glutamatergic system, which may be an indicator of reduced adaptation abilities of these patients. These results have been replicated in a larger study population underlining the robustness of these findings. Furthermore, specific dysfunctional cognitions dealing with different aspects of electromagnetic fields were identified to play a pivotal role in the generation of subjective electromagnetic hypersensitivity. The importance of these cognitive processes is supported by the efficacy of cognitive behavioral therapy for the treatment for electromagnetic hypersensitivity. In addition, functional imaging revealed the involvement of anterior cingulate and insular cortex in symptom generation. These areas, which are part of a neural network conveying distress and avoidance in pain perception, seem also to play a pivotal role in subjective electromagnetic hypersensitivity or other functional somatic syndromes like e.g. multiple chemical sensitivity. With respect to tinnitus, the increased prevalence in electromagnetic hypersensitive patients could be due to the increased sensitivity of this cortical distress network, which has been repeatedly shown to be involved in the pathophysiology of tinnitus.

The dysfunctional over-activation of this cortical neural network might be related to a disturbed representation of external and internal perceptions, which in turn could explain the reduced ability to discriminate real from sham electromagnetically evoked stimuli of electromagnetic hypersensitive patients as well as in subjects experiencing tinnitus.

Taken together these results point to a shared pathophysiology of subjective electromagnetic hypersensitivity and tinnitus. It may be hypothesized that these changes represent a key feature of somatoform disorders, which should be addressed in future studies.

In conclusion, this study has shown that tinnitus is much more frequent among subjective electromagnetic hypersensitive patients whereas there is no hint for a relationship between tinnitus and exposure to electromagnetic fields. Rather, the correlation between tinnitus and electromagnetic hypersensitivity might be due to an individual vulnerability. Neurobiological characteristics of this increased vulnerability such as an oversensitive cortical distress network and an impaired discrimination ability for electromagnetically evoked sensory stimuli might be involved in the pathophysiology of both tinnitus and electromagnetic hypersensitivity and possibly also in other related perception disorders. Nevertheless, this hypothesis derived from our epidemiological study has to be confirmed in further studies by e.g. intervention studies aiming for a normalization of the postulated over-activated distress network in subjectively electromagnetic hypersensitive (e.g. cognitive behavioral therapy, which has been shown to be successful in electromagnetic hypersensitivity and tinnitus patients).

From: BMC Neurosci. 2009 Feb 19;10(1):11. [Epub ahead of print]

Patients that suffer from chronic tinnitus complain of an ongoing perception of a phantom sound in the absence of any physical source for it. About 5-15 % of the population in western societies experience a phantom tinnitus sound and 1-3% of the population suffer from severe tinnitus that affects their daily life and is accompanied in 50 % of the cases by depression, in 40 % of the cases by insomnia and about 20% of the patients complain of an important decrease in their quality of life. Unfortunately, the underlying mechanisms responsible for the tinnitus perception is currently not known. Tinnitus therapies typically concentrate on coping with the tinnitus but there is no therapy that reliably reduces the perception of tinnitus.

Tinnitus is often accompanied by damage to the peripheral hearing system and a series of plastic changes in the central auditory system are observed in parallel to that. It is thought that a deafferentation of the hearing system triggers a series of reorganization processes at all levels of the auditory system. Indeed, abnormal neuronal activity in tinnitus has been demonstrated for the auditory nerve fibers, the dorsal cochlear nucleus, the inferior colliculus, the primary and the secondary auditory cortex. Furthermore, it has been found that a dissection of the auditory nerve in tinnitus patients does not lead to relief in tinnitus and most of the patients still experience tinnitus after surgery. Thus, there is an agreement that the tinnitus phantom sound is generated in the central nervous system – most likely as a result of the reorganization that is going on in the auditory system after hearing loss.

However, there are also studies that demonstrated tinnitus-related cortical abnormalities outside the auditory system. Using methods as different as Positron Emission Tomography (PET), Voxel Based Morphometry (VBM) and Magnetoencephalography (MEG) differences in cortical activity have been shown for the frontal cortex, the parietal lobe, mesial posterior regions and the subcollosal region including the nucleus accumbens. As hypothesized earlier by Jastreboff it might be that tinnitus is generated within the auditory system while non-auditory regions are involved in encoding the conscious percept well as the emotional evaluation of it. This idea also fits with a recently established model of the global neuronal workspace by Deheane and colleagues. This group suggests the existence of workspace neurons that are located mainly in the parietal lobe, the frontal, the cingulate cortex and the sensory systems. In order to form a conscious percept of a stimulus, two conditions are required: First, neuronal activity of the sensory cortex of the respective modality. Second, an entry into the global neuronal workspace and thus long-range coupling between the widely distributed workspace neurons. According to this model, coupling within this frontoparietal-cingulate network is needed for conscious perception (i.e. awareness of the stimulus). Activity of the sensory areas without this coupling would remain preconscious.

Different brain regions need to communicate with each other in order to integrate information, perform their specific function and distribute information to other brain areas. It has been suggested that this communication is performed by neuronal synchronization between those brain areas and the functional importance of this interareal coupling has been shown in several studies. In this literature, the terms ’coherence’, ’synchrony’, and ’coupling’ are used with slightly different connotations. To avoid misunderstandings the authors want to use the term ’coupling’ throughout this manuscript to describe the functional interaction between distant Neuronal Cell Assemblies.

The importance of long-range functional coupling has been shown recently by many authors in different fields of neuroscience. For instance, Supp et al. demonstrated different patterns of long-range coupling in the gamma band between visually presented familiar and unfamiliar objects and Miltner et al. found enhanced gamma band coupling during associative learning. Melloni et al. used different masks to manipulate whether a test stimuli was visible or invisible to the participants. They found significant differences of gamma phase locking between the ’visible’ and the ’invisible’ condition. Hummel and Gerloff showed an increase of alpha band coupling between occipital and left central areas correlates with behavioral performance in a visuotactile integration task. Uhlhaas and colleagues reviewed abnormal neuronal coupling in a
large variety of brain disorders, namely schizophrenia, epilepsy, autism, Alzheimer‘s disease and Parkinson‘s disease. In a behavioral experiment, Gross et al. showed that changes in the inter-regional coupling vary with changes of the behavioral task demands.

To the best of our knowledge there is currently no study on long-range functional coupling in chronic tinnitus. In previous studies the authors investigated abnormal power changes in the spontaneous activity of tinnitus patients and found an increase in delta power (<4 Hz) and a decrease in alpha-power (8-12 Hz). These changes were most prominent in the temporal region, however abnormalities were also found in the left frontal and right parietal cortex. This already suggested a frequency-specific long-range cortical network, however no measure of functional coupling was applied. In another study using Magnetoencephalography to describe power changes in the temporal cortex the authors showed an increase of gamma band activity in chronic tinnitus patients. However, these changes were only calculated for time windows around slow-wave peaks and the authors did not investigate long-range coupling. Theoretically, power changes of Neuronal Cell Assemblies and coupling between them can be completely independent and thus the authors were not able to deduce knowledge about inter-regional coupling from these studies.

With the present study the authors aimed to investigate inter-areal functional coupling of spontaneous activity in tinnitus patients and to compare them with normal controls. Functional coupling was measured in a broad frequency range from 1 to 90 Hz by means of phase locking analysis. The authors used a phase locking method described by Lachaux et al., which measures the phase difference between two recorded signals to quantify whether this phase difference is constant over time. A perfect coupling of the two signals results in a constant phase difference and is operationalized with a phase locking value of one. Lower values indicate weaker phase locking and the value of zero reflects no phase coupling at all.

Here, the authors first present substantial differences in the resting-state long-range functional coupling in chronic tinnitus sufferers. Specifically, two networks of different architectures and anti-correlated activity primarily account for the group differences. First, tinnitus patients are characterized by a decrease of phase couplings in the alpha frequency. Second, they display enhanced phase coupling in the 48-54 Hz gamma range. In both the tinnitus and the control group, there was a significant negative correlation between the alpha and the gamma network activity, suggesting an interplay of alpha and gamma coupling on an individual level. Furthermore, the duration of tinnitus seems to have an impact on the network architecture. In patients with tinnitus of short duration, gamma network changes are concentrated on the left temporal cortex. In contrast in the group with longer tinnitus duration, this network appears more widespread distributed over the entire cortex with lower impact of temporal areas.

Because the source montage that the authors used in this study covers only main areas of interest in the cortex, the authors are not able to interpretation of the precise location of the coupled sources. This is also because of technical constraints that are inherent to the inverse modeling used in MEG. However, the rough coverage of the brain however does not diminish the frequency-specific findings reported here. Also, the authors analyzed the power spectra of all sources to check whether they match with findings that were reported elsewhere. Power spectra analysis of spontaneous resting-state data (eyes open) in tinnitus usually shows a reduction of alpha power and an enhancement of slow-wave power. In this study, the alpha reduction was most pronounced for the temporal areas and to a smaller amount in the parietal and poster regions. The enhancement of the slow-wave power was localized mainly in the left temporal cortex. Overall, the alpha reduction was stronger than the enhancement of the slow-waves. In the additional material to this paper the authors report the grand average power spectrum over all sources and the power spectra of all source locations of the current analysis. The effects that the authors found in earlier studies were also observed in this analysis. Additionally, there was a slight increase in gamma power that was also found in another study of our group. Furthermore, the additional file 3 gives a graphical illustration of the alpha power distribution (9-12 Hz) over the sources for the tinnitus and the control group. Occipital alpha power in resting state recordings with eyes open is usually smaller than in recordings with eyes closed. With this source montage, occipital alpha power is largely represented by the PCC-source. There was no significant group difference in the alpha power of this source.

In this study, the authors found evidence for abnormal functionality in long-range cortical networks between tinnitus and control participants in the resting state, which are specific to the alpha and gamma frequency band. A general interaction between alpha and gamma power in the brain has already been postulated earlier. It is assumed that alpha directly or indirectly reflects an intrinsic mechanism that prevents the build-up of gamma coupling within neural cell assemblies during deprivation from input. Functionally, such a mechanism appears to be necessary, as strongly interconnected excitatory oscillators would have a natural tendency to synchronize their activity. A deficiency of this mechanism is putatively an important prerequisite for the emergence of phantom perceptions. Their finding suggests that this relationship between alpha and gamma frequency is not limited to local power changes, but also might apply to interareal phase coupling.

The authors found that the inter-regional coupling of the alpha and gamma frequency bands discriminate well between the tinnitus and the control participants. Participants with a tinnitus perception are characterized by a decrease of long-range alpha coupling and an increase of long-range gamma coupling. Even though the discrimination of 83 % is not sensitive enough to use it as an objective diagnostic tool for tinnitus, this is a strong argument that long-range couplings play an important part in the neuronal mechanisms associated with the tinnitus perception.

Here the authors propose a tinnitus model that integrates this finding with current knowledge on the tinnitus. On a first level the tinnitus is generated within the central auditory system and is most likely a result of reorganization processes triggered by damage to the hearing system. This is supported by numerous studies that show functional reorganization of the auditory system in tinnitus patients. On a second level, abnormal coupling with higher-order brain regions outside the auditory system underlies its conscious perception. The authors assert that both levels are necessary for an ongoing perception of the tinnitus phantom sound.

Even though the alpha and gamma coupling discriminated well between tinnitus and control participants an association between the long-range coupling and the subjective degree of tinnitus distress was lacking. In an earlier study – also with resting-state recordings in the MEG - the authors found moderate correlations of the subjective tinnitus rating with alpha power decrease in temporal regions. It is likely that the authors investigated two different neuronal mechanisms: One mechanism that is involved in the general perception of tinnitus and the other mechanism that is associated with tinnitus distress. The former study reported an association between temporal power changes and tinnitus distress. The current study on long-range coupling discriminated well between tinnitus perception and no tinnitus perception. Both mechanisms do not necessarily have to be associated.

With respect to tinnitus duration the authors found that longer-lasting tinnitus (> 4 years) accompanies marked changes in the pattern of the gamma network compared to shorter-lasting tinnitus. The most obvious difference between long and short lasting tinnitus is a decrease in importance of the left temporal part of the network, i.e. there are fewer connections formed within this brain region. On the other side, functional connections between non-auditory areas are increased in tinnitus of longer duration. Based on the data that the authors present here the authors cannot decide whether this is only a change of functional coupling or whether structural changes also occur. A study using diffusion tensor imaging could help to clarify this question.

Notwithstanding whether the change in the network architecture is structural or functional, the results offer an explanation for a so far unresolved riddle in treating chronic tinnitus with Transcranial Magnetic Stimulation: It has been shown in a series of clinical studies that the efficacy of TMS treatment strongly depends on the duration of tinnitus. In these studies shorter tinnitus duration predicts better treatment outcome for therapeutical application of Transcranial Magnetic Stimulation applied while the treatment efficacy declines with longer duration of tinnitus. A tinnitus duration of 3 to 4 years seems to represent the turning point and patients below this point benefit only little from the treatment. The intriguing detail about this is that TMS is traditionally applied to the left temporal cortex. In the light of our findings these negative treatment effects make sense: as the gamma network shows a major hub in the left temporal cortex of patients with short tinnitus duration, stimulation of this region exhibits a potentially great impact on this network. However, since the gamma network is more widespread in patients with a long history of tinnitus, the impact of the stimulation to the
left hemisphere is largely reduced. This idea of an alteration of the tinnitus-related neural network over time was hypothesized earlier and the data that the authors presented here are the first experimental support for this idea.

Here the authors demonstrate for the first time alterations in the long-range network during spontaneous activity in tinnitus patients. The results can be described by an overall decrease of coupling in the alpha frequency band together with an increase of gamma coupling. This pattern of phase coupling discriminates with a high percentage (83 %) the tinnitus patients from the healthy controls. Here the authors suggest a tinnitus model that incorporates 1) altered activity of the central auditory system that most likely generates the tinnitus sound and 2) the coupling across distant brain regions that is needed for a conscious perception of the tinnitus sound.

From: BMC Health Serv Res. 2009 Feb 11;9(1):29. [Epub ahead of print]

Subjective tinnitus is the involuntary perception of the concept of a sound without the presence of an external source. It is a chronic condition that is highly prevalent, especially among hearing impaired individuals. Studies show a prevalence of 10% to 20% in the general population and among hearing impaired individuals prevalence has been estimated at 75% to 80%. Of the Dutch population at least 2 million individuals suffer from some form of tinnitus, 340,000 individuals indicate to hear the tinnitus continuously and 60,000 individuals claim to be severely impaired in their daily activities. Among severe sufferers it causes disability associated with severe affective problems, major declines in concentration, sleeping difficulties, hypersensitivity to sounds and problems in re-directing attention. The combination of these complaints makes them feel exhausted and frustrated resulting in diminished quality of life. Tinnitus is known to occur as a concomitant of almost all the dysfunctions that involve the human auditory system and it is postulated that the aetiology of tinnitus is diverse and that different activation circumstances can be present. Little is known about the pathophysiology and there is no known drug or curative therapy at present though considerable research effort has been expended in this regard.

In many cases tinnitus sufferers are referred to different caregivers in a nonstandardized way, and often receive insufficient and sometimes inappropriate treatment. This may comprise prescribing a drug that is not proven to be effective, or informing the patients that not much can be done to improve the situation. Especially in those individuals suffering from a moderate to severe tinnitus, incorrect information and delay of appropriate treatment is expected to increase psychological strain, aggravation of tinnitus severity and prolongation of the referral trajectory. Since tinnitus sufferers seek help in various areas of health care without receiving appropriate treatment, they are financially burdening the system superfluously. In absence of a proven cure or uniformly effective treatment, tinnitus are is often fragmentised and costly.

As for most health problems in the Dutch population, the general practitioner is the initial professional to consult for patients with tinnitus. In most cases, within six months after onset of subjective tinnitus the individual consults his general practitioner, but one quarter of the respondents wait several years until they seek help. In the official Dutch general practitioner patient information letter on tinnitus, it is stated that there is not much that can be done to alleviate complaints. Another frequently consulted specialist is the ENT physician. Treatment possibilities include removal of cerumen, medication, and audiological rehabilitation. Generally, the effects of these treatments are disappointing.

A recent study by El Refaie et al (2004) shows that functional and social handicap in tinnitus sufferers is significantly reduced, and quality of life improves significantly, as a result of attendance at a specialised tinnitus clinic. Specialised clinics for chronic disorders such as tinnitus and chronic pain have been proven to be most effective in treatment. Similarities between tinnitus and chronic pain in terms of cognitive and behavioural mechanisms have been suggested recently and a similar treatment could be effective for the tinnitus population. As in chronic pain, multidisciplinary specialised treatment is more effective in ameliorating severe tinnitus complaints than monodisciplinary treatments. A retrospective pilot study, by the applicants of this proposal, in the Tinnitus Centre Limburg (TCL) shows significant improvements in 71% of the patients. Intrusiveness of the tinnitus ameliorates in 85% of the subjects and 78% experiences improvement in emotional distress caused by the tinnitus.

The objective of this study is to examine the effectiveness, costs and cost effectiveness of a comprehensive multidisciplinary treatment provided by a specialised tinnitus centre. Treatment is based on a stepped care approach, tailored to individual needs, with key elements from cognitive behavioural therapy, education, relaxation techniques, attention diversion, exposure in daily live situations, and tinnitus retraining therapy.

The following research questions were formulated:

1. What are the effects on generic quality of life of comprehensive specialized tinnitus care as provided by a specialised tinnitus centre, as compared to usual care?

2. What are the effects on health, in terms of negative affect, tinnitus beliefs, fear of the tinnitus, and tinnitus annoyance, of comprehensive specialized tinnitus care as provided by a specialised tinnitus centre, as compared to usual care?

3. What are the costs to health care and to society of treatment provided by a specialised tinnitus centre in the Dutch health care system as compared to usual care?

4. What is the cost effectiveness of treatment provided by a specialised tinnitus centre in the Dutch health care system as compared to usual care?

This study will provide information on whether a comprehensive, multidisciplinary treatment is more effective and efficient care for tinnitus patients. The results will also show whether the specialised treatment improves quality of life and patient satisfaction. If the intervention is proven to be effective, implementation of the intervention is considered and anticipated. First results are not expected before the beginning of 2010.

Trial Registration The trial has been registered at ClinicalTrial.gov. The trial registration number is NCT00733044.

From: BMC Ear Nose Throat Disord. 2008 Nov 3;8(1):7 [Epub ahead of print]

Tinnitus retraining therapy is aimed at removing negative associations of the tinnitus signal to enable the natural habituation process to occur. The goal is to achieve this through retraining counseling and sound therapy. Retraining counseling is a crucial part of tinnitus retraining therapy; it teaches patients the components of the neurophysiological model of tinnitus and encourages them to reclassify their tinnitus as a neutral signal. Sound therapy is assumed to facilitate tinnitus habituation by decreasing the strength of tinnitus signal. The tinnitus retraining therapy protocol requires that the patient adheres to the regimen for 12-24 months (typically attending for seven sessions over that time), except for patients experiencing weak tinnitus, which hearing aids little impact on everyday life.

Since the first description of tinnitus retraining therapy in the 1990s, clinicians have modified and customised the method of tinnitus retraining therapy to suit their practice and their patients. A simplified form of tinnitus retraining therapy hearing aids been used at Ealing Primary Care Trust (PCT) Audiology Department since 2005. This is different from tinnitus retraining therapy in the type and (shorter) duration of retraining counseling. Although the counseling used in simplified tinnitus retraining therapy also aims to get the patient to reclassify tinnitus as a neutral stimulus, it is different from the counseling used in tinnitus retraining therapy in the following ways: (1) there is no teaching about basic functions of the auditory system; (2) there is no presentation of the basics of brain function and the interactions of various systems of the brain; (3) there is no explanation of the theoretical basis of habituation based on the Jastreboff neurophysiological model; and (4) the duration of the initial counseling of simplified tinnitus retraining therapy is 30 minutes in comparison to 90 minutes for the initial tinnitus retraining therapy counseling.

Sound therapy for simplified tinnitus retraining therapy is the same as for the tinnitus retraining therapy except for patients in Jastreboff’s “category one”. Patients in this category have bothersome tinnitus, but no hearing loss, and no decreased sound tolerance. In simplified tinnitus retraining therapy, they are issued with a bedside/tableside sound generator but, in contrast to tinnitus retraining therapy, wearable sound generators (Wsound generator) are not offered unless the patient asks for them (for more details, see the procedures). The entire simplified tinnitus retraining therapy takes between 3 and 24 months (2-8 sessions). The first appointment lasts about 30 minutes, and then the patient is seen for follow ups (30 minutes) as required at 1 month, 2 month, 3 month, and 6 month intervals.

The aims of this observational study were: (1) to assess the effectiveness of simplified tinnitus retraining therapy, as carried out at Ealing PCT Audiology Department during 2005 and 2006 and (2) to determine the extent to which the success of simplified tinnitus retraining therapy is affected by the duration of tinnitus, the patient’s age, the use of hearing aids, and the use of sound generators.

Educational retraining counseling is generally regarded as an important component of tinnitus retraining therapy. The counseling in tinnitus retraining therapy is intended to explain the mechanisms underlying the tinnitus, based on the Jastreboff neurophysiological model, and to remove negative associations with the tinnitus. This is regarded as important for allowing habituation to the tinnitus to occur. The counseling used in Ealing PCT Audiology Department was also intended to reduce negative associations with the tinnitus, but was shorter in duration and simplified. The simplified counseling did not include any teaching about the interactions of various systems of the brain, there was no explanation of the Jastreboff neurophysiological model, and the duration of the initial counseling was only 30 minutes. The sound therapy used with simplified tinnitus retraining therapy for each patient category was essentially the same as for tinnitus retraining therapy, except that Wsound generators were not recommended to patients who exhibited tinnitus with no hearing loss and no decreased sound tolerance. However, Wsound generators were fitted to the patients who showed particular interest in making use of such devices.

Tinnitus retraining therapy is an established method of treating tinnitus patients and typically results in a decline (improvement) in Tinnitus Handicap Inventory scores of 25 to 35 points after 12-24 months of treatment. Studies on the psychometric adequacy of the Tinnitus Handicap Inventory questionnaire suggest that a decline in Tinnitus Handicap Inventory score of 20 points or more can be considered as a statistically significant improvement in perceived tinnitus handicap. Our results revealed that the Tinnitus Handicap Inventory score declined by approximately 45 points (SD= 22) after 3-24 months of simplified tinnitus retraining therapy. The cause of the greater mean effect in our study in comparison with earlier studies of tinnitus retraining therapy is not clear. It might reflect individual differences in the patients, differences in the way that patients were selected for inclusion in the studies, or individual differences in the clinicians’ personality and attitude. In any case, our results indicate that simplified tinnitus retraining therapy can produce benefits comparable to those produced by tinnitus retraining therapy.

The effectiveness of a substantially simplified version of tinnitus retraining therapy was assessed through an uncontrolled retrospective study on 42 patients seen at Ealing PCT Audiology Department during the period 2005-2006. Simplified tinnitus retraining therapy differs from tinnitus retraining therapy in the type and (shorter) duration of the counseling but is similar to tinnitus retraining therapy in the application of sound therapy. Although we did not include a control group to assess the extent to which patients would have improved without treatment, our results revealed that simplified tinnitus retraining therapy was successful in reducing tinnitus handicap. Tinnitus Handicap Inventory and VAS scores for tinnitus loudness, annoyance and effect on life declined (improved) significantly over a period of 3 to 23 months for patients who received simplified tinnitus retraining therapy. The mean decline of Tinnitus Handicap Inventory score was 45 (SD= 22) and the difference between pre- and post-treatment scores was statistically significant. The mean decline of the VAS score was 1.6 (SD= 2.1) for tinnitus loudness, 3.6 (SD= 2.6) for annoyance, and 3.9 (SD= 2.3) for effect on life. The differences between pre and post treatment VAS scores were statistically significant in all cases. The amount of improvement in Tinnitus Handicap Inventory scores tended to be greater for patients who used sound generators as a part of their treatment, but was not significantly associated with duration of tinnitus and age.

From: Prog Brain Res. 2007;166:215-9

In treating patients with temporomandibular joint (TMJ) dysfunction it was noticed that tinnitus and vertigo were common in such patients and there was also muscular tension in jaw and neck. During treatment of these patients it was also noted that injection of lidocaine in a jaw muscle reduced not only their muscular problems but also that the tinnitus was reduced while the local anesthetic was active. Evaluation of 39 patients with disabling tinnitus, and all suffered from tinnitus, revealed that 10 of them had bilateral tinnitus and TMJ disorders revealed that pain in the face, temples or jaw occurred often among these patients. Many of such patients had also symptoms of cervical spine disorders, head, neck and shoulder pain, and limitations in side bending and rotation were also frequent complaints. One-third of these patients could influence tinnitus by jaw movements and 75% could trigger vertigo by head or neck movements. Treatment of jaw and neck disorders in 24 patients with Ménière’s disease had a beneficial effect on not only their episodic vertigo but also on their tinnitus and aural fullness. At the 3-year follow-up, intensity of all symptoms were significantly reduced.

From: Pain Res Manag. 2006 Autumn;11(3):197-9

Whiplash trauma can result in injuries that are difficult to diagnose. Diagnosis is particularly difficult in injuries to the upper segments of the cervical spine (craniocervical joint complex). Studies indicate that neck injuries in that region may be responsible for the cervicoencephalic syndrome, as evidenced by headache, balance problems, vertigo, dizziness, eye problems, tinnitus, poor concentration, sensitivity to light and pronounced fatigue. Consequently, diagnosis of lesions in the craniocervical joint region is important.

Functional magnetic resonance imaging is a radiological technique that can visualize injuries of the ligaments and the joint capsules, and accompanying pathological movement patterns. Three severely injured patients that had been extensively examined without any findings of structural lesions were diagnosed by functional magnetic resonance imaging to have injuries in the craniocervical joint region. These injuries were confirmed at surgery, and after surgical stabilization the medical condition was highly improved. It is important to draw attention to the urgent need to diagnose lesions and dysfunction in the craniocervical joint complex and also improve diagnostic methods in whiplash injuires.

From: HNO. 2008 Jul;56(7):673-7 Article in German

The causes of tinnitus, vertigo, and hearing disturbances may be pathological processes in the cervical spine – neck and temporomaxillary joint. In these cases, tinnitus is called somatosensory tinnitus. For afferences of the cervical spine, projections of neuronal connections in the cochlear nucleus were found. A reflex-like impact of the cervical spine on the cochlear nucleus can be assumed. The tinnitus treatment concept of the Charité University Hospital in Berlin involves the cooperation of ENT specialists with many other disciplines in an outpatient clinic. A standardized examination protocol has been established, and physical therapy has been integrated into the interdisciplinary tinnitus treatment. For tinnitus modulating therapy of muscular trigger points, local anesthetics as well as self-massage or treatment by a physiotherapist or osteopath are useful.

This is a first post in a new category – Tinnitus. There has been evidence of a relationship between tinnitus and the neck along with temporomadibular dysfunction (tmj or tmd), which will also be a new category in the near future.