Auditory nerve compression: a forgotten treatable cause for tinnitus

Dirk De Ridder

doi:10.1136/jnnp.2009.178855

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Auditory nerve compression: a forgotten treatable cause for tinnitus

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Don't forget to look for a cause in tinnitus
Dirk De Ridder
Published on: 31 August 2010
Forget auditory nerve compression as a treatable cause for tinnitus
Robert L. Folmer
Published on: 23 August 2010
VESTIBULAR PAROXYSMIA
Sabino G. Echebarria
Published on: 7 May 2010

Published on: 31 August 2010
Don't forget to look for a cause in tinnitus
- Dirk De Ridder, neurosurgeon
I thank the editor for the opportunity to respond to a letter to the editor entitled 'Forget auditory nerve compression as a treatable cause for tinnitus' by Dr Folmer.
It states that in my editorial comment reality concerning tinnitus is distorted and, more specifically, that 1. many effective, non-surgical, non-pharmacologic management strategies are available and helpful for patients who experience tinnitus; 2. audit...
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I thank the editor for the opportunity to respond to a letter to the editor entitled 'Forget auditory nerve compression as a treatable cause for tinnitus' by Dr Folmer.
It states that in my editorial comment reality concerning tinnitus is distorted and, more specifically, that 1. many effective, non-surgical, non-pharmacologic management strategies are available and helpful for patients who experience tinnitus; 2. auditory nerve compression is an exceedingly rare cause of tinnitus; 3. therefore, microvascular decompression surgery for tinnitus should be undertaken in a similarly miniscule number of cases.
Based on his own work on tinnitus, Dr Folmer quotes 'proof' that many effective, non-surgical, non-pharmacologic management strategies are available and helpful for patients who experience tinnitus. These papers however do not seem to scientifically support his claims. One of the papers1 does not contain any data but only explains a flowchart that terminates in two endpoints: 1.'Employ management strategies and reassess at 1, 6 and 12 months' or 2. 'Reassure patient that condition is harmless'. These management strategies consist of individualized (as it should be) counseling and sound treatments. In other words, explaining how tinnitus develops combined with passive or active sound treatment, i.e. hearing aids or sound generators. In essence this is a variation of tinnitus retraining therapy or cognitive behavioral therapy plus sound treatment. The results of the second paper referenced2, dealing with the efficacy of ear-level devices, show exactly the same improvement without and with sound treatment 2, thus suggesting a placebo effect or effect of the counseling and therefore underscoring his rather surprising claim 'proven' efficacy. Furthermore, the claimed improvements might be statistically significant, but seem clinically irrelevant. The VAS intensity improves from 7.06/10 to 6.47/10, with most responses on the questionnaires improving from 3.4 to 3 (table 3, Folmer 2002)3. Moreover, the tinnitus associated depression scores remain unchanged in 112, worsen in 58 and improve in 28 patients, an outcome that would probably not satisfy neither patients nor tclinicians. Furthermore, these results are obtained in a way that is most likely non-sustainable at a population level. A first intake consultation takes 4 hours, and a follow up 2 hours, suggesting that only 2 patients can be evaluated per an eight-hour working day 3. This means that, following this treatment approach, for the 40.000.000 US citizens suffering from tinnitus 3, 1000 tinnitus specialists would spend 20.000 days, i.e. more than 60 years, just to do the first consultation. Thus Dr Folmer's statement that many effective and helpful treatments are available for people suffering from tinnitus, might be a distorted overoptimistic view of reality, and unrealistic to perform in routine clinical practice.
Everybody agrees that microvascular compressions are an uncommon cause for tinnitus. An epidemiological analysis demonstrates that the known incidences of other microvascular compression syndromes such as trigeminal neuralgia, hemifacial spasm, and glossopharyngeal neuralgia are related to the length of their respective CNS segments. Based on these data it has been estimated that microvascular compressions of the eighth cranial nerve result in an incidence of tinnitus of approximately 8/100.0004 , i.e. potentially more than 3000 patients in the US each year develop tinnitus based on a microvascular compression. For these patients it is known that the longer the tinnitus exists the worse the results of the surgical decompression5, and 4 years might be a treatment limiting factor6. Furthermore it is known that when no surgical decompression is performed a progressive deterioration of the nerve's integrity develops, as evidenced by a prolonging IPL I-III interval, and that this is associated with worsening of tinnitus intensity7. Therefore it is important to learn how to select this rare subgroup of causally treatable patients from the vast majority of unfortunately yet untreatable patients, before irreversible damage settles in. Thus it is essential that scientific journals publish reports, even on small amounts of patients, of successful treatments in very well selected specific subgroups. This will increase our understanding of how to better delineate tinnitus subgroups. If you do not look for it, you will not find it, and thus will not be able to treat it.
According to Dr Folmer we should leave a patient with a causally treatable tinnitus undiagnosed and untreated. The consequence of this attitude would be to stop any diagnosis in medicine and instead just apply some cognitive behavioral treatment for better accepting fate in life. This fatalistic philosophy progressively lost its grip on Western Society since the 12the century and especially since the scientific revolution of the 17th century. The concept 'Forget auditory nerve compression as a treatable cause for tinnitus' thus represents an unsustainable concept which is incompatible with contemporary medicine, even more so as it has become clear that there are many different subgroups of tinnitus and thus that there exists not one treatment, albeit individually adapted, that fits all.
If you only have a hammer, everything looks like a nail. The approach towards tinnitus treatment is rapidly evolving away from this concept. In this respect, the Tinnitus Research Initiative, promoting international multidisciplinary collaborations among clinicians and between clinicians and basic scientists has developed a flowchart (www.tinnitusresearch.org), permitting to separate tinnitus in its many subgroups, one of which is microvascular compressions. Specific treatments are being developed for each of the subgroups. This requires specialized tinnitus centers in which a truly multidisciplinary approach is available, combining the expertise of audiologists, psychologists, neurologists, psychiatrists, ENT surgeons and neurosurgeons.
It can therefore only be hoped that health care providers base their treatment approaches not only on statistics, but on the clinical relevance of the data and the proposed treatment and the practical reality of it. Moreover, progress and not personal, albeit well meant, opinions should guide the future of tinnitus treatments. Only by developing new treatments, and perfecting existing ones and their indications, will one day many effective (probably diverse) strategies become available and helpful for patients who experience tinnitus. These might, or might not, include surgical, pharmacologic options. For the time being, let us not forget that a limited amount of patients can already 'really' be helped, for instance in the case of microvascular compressions.
1. Folmer RL, Martin WH, Shi Y. Tinnitus: questions to reveal the cause, answers to provide relief. J Fam Pract 2004;53(7):532-40.
2. Folmer RL, Carroll JR. Long-term effectiveness of ear-level devices for tinnitus. Otolaryngol Head Neck Surg 2006;134(1):132-37.
3. Folmer RL. Long-term reductions in tinnitus severity. BMC Ear Nose Throat Disord 2002;2(1):3.
4. De Ridder D, Moller A, Verlooy J, Cornelissen M, De Ridder L. Is the root entry/exit zone important in microvascular compression syndromes? Neurosurgery 2002;51(2):427-33; discussion 33-4.
5. Moller MB, Moller AR, Jannetta PJ, Jho HD. Vascular decompression surgery for severe tinnitus: selection criteria and results. Laryngoscope 1993;103(4 Pt 1):421-7.
6. De Ridder D, Vanneste S, Adriaenssens I, Lee AP, Plazier M, Menovsky T, et al. Microvascular decompression for tinnitus: significant improvement for tinnitus intensity without improvement for distress. A 4-year limit. Neurosurgery;66(4):656-60.
7. De Ridder D, Heijneman K, Haarman B, van der Loo E. Tinnitus in vascular conflict of the eighth cranial nerve: a surgical pathophysiological approach to ABR changes. Prog Brain Res 2007;166:401-11.
Conflict of Interest:
None declared
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Conflict of Interest:
None declared.
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Published on: 23 August 2010
Forget auditory nerve compression as a treatable cause for tinnitus
- Robert L. Folmer, Research Investigator
Dr. De Ridder overstates reality in the title of his editorial, "Auditory nerve compression: a forgotten treatable cause for tinnitus" and distorts reality in the text of the commentary. Examples of distortion include: there are no effective treatments available for most cases of tinnitus; auditory nerve compression is a common cause of tinnitus; carbamazepine and microvascular decompression surgery are viable treatment...
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Dr. De Ridder overstates reality in the title of his editorial, "Auditory nerve compression: a forgotten treatable cause for tinnitus" and distorts reality in the text of the commentary. Examples of distortion include: there are no effective treatments available for most cases of tinnitus; auditory nerve compression is a common cause of tinnitus; carbamazepine and microvascular decompression surgery are viable treatment options for tinnitus. The realities are: 1) many effective, non-surgical, non-pharmacologic management strategies are available and helpful for patients who experience tinnitus; 2) auditory nerve compression is an exceedingly rare cause of tinnitus; 3) therefore, microvascular decompression surgery for tinnitus should be undertaken in a similarly miniscule number of cases. Support for this conservative use of surgery comes from an article written by De Ridder et al (2007): "The outcome of operations for tinnitus, moving the blood vessel off the nerve (microvascular decompression operations, MVD) is less successful than microvascular decompression operations for other vascular conflict syndromes." I agree, so let's stop recommending this surgery for tinnitus, because it is more likely to harm patients than to help them. Reports of efficacy for the procedure claimed by Moller et al (1993) and Dr. Jannetta were, in polite terms, overly optimistic. In his 2010 JNNP commentary, De Ridder proclaims the importance of articles by Nam et al (2010) and Brantberg (2010) that describe a "unique form of tinnitus in contrast to most other kinds of tinnitus is responsive to pharmacological (and surgical) treatment." The problem with this statement: it gives readers (including patients and clinicians) the false impression and false hope that carbamazepine or microvascular decompression surgery are likely to help. The total number of patients in the study by Nam et al (2010) plus the total in the study by Brantberg (2010) is five. Far-reaching treatment recommendations cannot be made on the basis of five patients. Carbamazepine is an anticonvulsant that might reduce tinnitus (or a patient's reaction to it) in the same way that benzodiazepines or barbiturates can in some cases. However, medications of this type - or surgery - should not be the first considerations for tinnitus treatment. Instead, I recommend that clinicians familiarize themselves with different types of tinnitus management strategies that have proven effective for hundreds of patients and present little or no risk of side effects or catastrophic outcomes (for example, see Folmer 2002; Folmer et al, 2004; Folmer & Carroll, 2006; Goebel et al, 2006; Henry et al, 2008; 2009; 2010).
REFERENCES
De Ridder D, Heijneman K, Haarman B, van der Loo E. Tinnitus in vascular conflict of the eighth cranial nerve: a surgical pathophysiological approach to ABR changes. Prog Brain Res. 2007;166:401 -411.
Folmer RL. Long-term reductions in tinnitus severity. BMC Ear Nose and Throat Disorders 2002;2:3. http://www.biomedcentral.com/1472-6815/2/3
Folmer RL, Carroll JR. Long-term effectiveness of ear-level devices for tinnitus. Otolaryngol Head Neck Surg. 2006;134(1):132-137.
Folmer RL, Martin WH, Shi, Y. Tinnitus: Questions to reveal the cause, answers to provide relief. J Fam Pract. 2004;53(7):532-540.
Goebel G, Kahl M, Arnold W, Fichter M. 15-year prospective follow-up study of behavioral therapy in a large sample of inpatients with chronic tinnitus. Acta Otolaryngol Suppl. 2006;556:70-79.
Henry JA, Zaugg TL, Myers PJ, Kendall CJ, Michaelides EM. A triage guide for tinnitus. J Fam Pract. 2010;59(7):389-393.
Henry JA, Zaugg TL, Myers PJ, Kendall CJ, Turbin MB. Principles and application of educational counseling used in progressive audiologic tinnitus management. Noise Health. 2009;11(42):33-48.
Henry JA, Zaugg TL, Myers PJ, Schechter MA. Using therapeutic sound with progressive audiologic tinnitus management. Trends Amplif. 2008;12(3):188-209.
Moller MB, Moller AR, Jannetta PJ, Jho HD. Vascular decompression surgery for severe tinnitus: selection criteria and results. Laryngoscope. 1993;103(4 Pt 1):421-427.
Conflict of Interest:
None declared
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Conflict of Interest:
None declared.
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Published on: 7 May 2010
VESTIBULAR PAROXYSMIA
- Sabino G. Echebarria, NEUROLOGIST- BASQUE HEALTH SERVICE-OSAKIDETZA/ NEUROLOGY AREA - H.SAN ELOY ( BARKALDO-BIZKAIA )DISTR
- Other Contributors:
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Vestibular paroxysmia has been defined classically by series of rotational to-and-fro vertigo, precipitated or modulated by head position.Then , descriptional basis of the clinical picture may be disclosed if vertigo may be associated to hipoacusis and tinitus or not.
In the case of pure tinnitus description , the loud / low pitch sound of the tinnitus may be defined as paroxysmal tinnitus. Ethilogical purposes...
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Vestibular paroxysmia has been defined classically by series of rotational to-and-fro vertigo, precipitated or modulated by head position.Then , descriptional basis of the clinical picture may be disclosed if vertigo may be associated to hipoacusis and tinitus or not.
In the case of pure tinnitus description , the loud / low pitch sound of the tinnitus may be defined as paroxysmal tinnitus. Ethilogical purposes have been described considering neurovascular compression : a vascular compression of the eight cranial nerve , defined in up to 65 % of samples ( vascualr loops in the internal auditory canal ) . Mechanisms have been proposed , such as ectopic discharges / conduction block ( vestibular hypofunction / excitation ). Recent findings enhance the role of amygdalohippocampal , cochlear and temporal cortex in tinnitus pathogenesis .What should be discerned is the concurrent importance of ephaptic transmission in a solely description / plus or not central mechanisms derived of such condition.
References: -Strupp M et al. Acute vestibulopathy. Curr Opin neurol 2001 ; 14: 11-20.
Conflict of Interest:
None declared
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