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How to cite this article Oliveira CA, Negreiros JR J, Cavaicante IC, Bahmad JR F, Venosa AR. The cause of objective tinnitus provoked by palatal and middle-ear myoclonus may be identified by magnetic resonance imaging of the central nervous system in the Guilliain-Mollaret triangle or it may be idiopathic. The production of objective tinnitus by myoclonus has been reported in the literature as being related to palatal [1-4] or middle-ear myoclonus [5-9].
The tensor tympani muscle (TTM) and the stapedius muscle (SM) are involved in middle-ear myoclonus.
The TVPM increases tension in the soft palate and opens the eustachian tube when it contracts.
This brief review of anatomy and physiology provides important notes: The TVPM and the TTM both are supplied by the fifth cranial nerve, and both have insertions in the cartilaginous portion of the eustachian tube. In 1983, Rock [10] described some patients who were able to provoke objective tinnitus by forcefully closing their eyelids (forceful eyelid closure syndrome). In 1981, Klochoff [9] described patients with TTM contractions due to severe emotional distress and anxiety. We present two cases of objective tinnitus caused by myoclonus, neither of which is accompanied by a documentable lesion in the central nervous system. A 40-year-old woman came to us complaining of bilateral clicks heard continuously in both ears and starting suddenly 4 years previously. At otomicroscopy, we could see movement of the manubrium of the malleus and of the posterior quadrant of the tympanic membrane synchronous with the noises in both ears, although they were stronger in the left. The results of neurological examination, MRI with gadolinium enhancement of the brain, and computed tomography of the temporal bones were normal. On follow-up, patient 1 stated that the clicks again were bothering her and, indeed, they could be heard by the examiner when he put his ear close to the patient's ear.
At otomicroscopy, no movement could be seen in either side, even though the clicks were evident.
Some reports cite objective tinnitus associated with a previous episode of facial paralysis [8] and report high-frequency continuous objective tinnitus cured by sectioning of the SM tendon [7]. The first case that we presented herein clearly shows the occurrence of both palatal and TTM myoclonus synchronous with the noises.
Stapedial reflex was present in the right ear of patient 1 and was absent in the left (worse) ear. Further evidence of repeated opening and closing of the eustachian tube caused by the TVPM myoclonus is offered in our second case: Even though the tympanic membrane was perforated, we still could see rhythmical movements of the needle of the impedance bridge, probably indicating repeated pressure and volume changes in the middle ear (see Fig. What seems to be clear is that at least part of the noise is caused by the slapping together of the eustachian tube walls, as stated by Pulec et al.
From a practical standpoint, one must always search for both palatal (TVPM) and middle-ear (TTM) myoclonus in patients with tinnitus symptoms. This research was presented in part at the Twenty-Ninth Neurootological and Equilibriometric Society Congress, Bad Kissingen, Germany, March 14-l7, 2002. If you need to see a larger view please click on any picture, use back button on browser to return to this page.
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The tensor veli palatini muscle (TVPM) and the levator veli palatini muscle (L VPM) are involved in palatal myoclonus.
The TIM arises from the cartilaginous part of the eustachian tube, the adjacent part of the greater wing of the sphenoid, and from its 20- to 25-mm-Iong semicanal; its tendon inserts in the neck of the malleus. The L VPM elevates the soft palate and probably assists in the opening of the eustachian tube by the TVPM.
In contrast, the SM and the L VPM are supplied by different cranial nerves and by the pharyngeal plexus, and neither has insertions in the cartilaginous portion of the eustachian tube. These patients had hearing losses in the lower frequencies, whereas hearing was normal in the higher frequencies. Most often, palatal myoclonus is related to documentable lesions in the central nervous system (Guilliain-Mollaret triangle).
Still unclear is whether middle-ear and palatal myoclonus are different entities or usually appear together. The origin of the sounds also is in doubt: Are they produced by the eustachian tube walls slapping together or by TTM contractions or by both, and is the SM important in the production of the tinnitus? With all the aforementioned uncertainties, treatment of this condition is certainly open to discussion. We discuss these cases in light of the previously described literature and some ideas our own.
Nasoendoscopy with a 4-mm zero-degree rigid endoscope (Storz Endoscopy of America Inc ., Culver City, CA) showed movement of the soft palate synchronous with the sounds and revealed stronger pulses on the left side. We could see the TTM contracting rhythmically after exposure, but the SM was totally quiet.
At otomicroscopy, movement of the posterior quadrant of the tympanic membrane-but not of the manubrium of the malleus-could be seen in both ears. Audiometry showed conductive hearing loss in the left ear compatible with the tympanic membrane defect (Fig.
His impression was that movements of the tubal muscles caused the noises reported in tinnitus. These symptoms seem to be different from the clicking noise we have discussed and probably are associated with synkinesis of the facial muscles (tinnitus triggered by closing the eyes) and SM.
Section of both TTM tendons did not eliminate the clicking but rendered it much weaker and tolerable to the patient and her bed partner.
However, during surgery, we watched the SM under the microscope for a long time and did not witness any contraction of this muscle. Both muscles are supplied by the fifth cranial nerve and belong to the same group of muscles. It is our contention that most cases of myoclonus will have a cause somewhere in the Guilliain-Mollaret triangle. From the literature, one can perceive the following unanswered questions: (1) Are palatal and middle-ear myoclonus different entities or do they usually appear together?
The first muscle originates from the edge of the greater wing of the sphenoid bone, adjoining petrosphenoidal fissure, and lateral wall of the eustachian tube. The TTM pulls the malleus medially, increasing tension in the tympanic membrane, and the SM pulls the stapes footplate away from the oval window. In 1995, the same author [11] studied 428 patients who had no complaint of tinnitus and found retraction of the manubrium and posterior middle one-third of the tympanic membrane in 107 patients (25%) under the microscope during forceful eyelid closure. These authors showed that their patients heard sounds immediately after the onset of electrical activity in the region of the eustachian tube walls.
Tympanometry showed right and left middle-ear volume variations synchronous with the clicks.
We sectioned the TTM tendon, after which the woman noticed remarkablly diminished tinnitus on completion of the procedure; however, after 2 weeks, the symptom had returned. The boy had many infections in this ear and eventually experienced a perforation of the tympanic membrane, which was central and dry at the time of examination. Air-bone gap on the left is probably due to the tympanic membrane perforation and is not related to the tinnitus. Since then, most reports on this subject refer to palatal myoclonus and follow Politzer's ideas [1-5, 11].
Severe emotional distress and anxiety have been reported as causes of rhythmical TTM contractions and are said to be cured by relaxation techniques and section of the TTM tendon [9]. However, also clear is that the palatal myoclonus is an important component of the clicks: After section of the TTM, we still observed wavy movement of the posterior quadrant of the tympanic membrane at otomicroscopy, which was confirmed by the impedance bridge. Possibly the absence of recordable reflex in the left ear was due to the strong rhythmical contraction of the TTM masking the reflex, but we cannot exclude the possibility of SM myoclonus not seen during surgery.


Patient 1 had a repeat examination 3 days before this writing, results of which showed no abnormalities in the Guilliain-Mollaret triangle. SM contribution to the clicks is possible but unlikely because it is supplied by a different cranial nerve (nerve VII) and it is a small muscle (four times smaller than the TTM semicanal). Section of the TTM is an easy and safe procedure and may solve the problem (as in patient 1). Affected patients must be followed up closely, because such lesions may become apparent at a later date. Palatal myoclonus as a cause of objective tinnitus: A report of six cases and a review of the literature. Impedance Fluctuation and a "Tensor Tympani Syndrome." In RL Penha, W Pizarro (eds), Proceedings of the Fourth International Symposium on Acoustic Impedance Measurement. The SM arises from the pyramidal process, and its tendon inserts in the neck of the stapes. He also found increased impedance at maximum compliance during forceful eyelid closure in 75% (321 patients) . They hypothesised that the noises were caused by the slapping of the eustachian tube walls as they closed. Nasoendoscopy with the rigid 4-mm zero-degree endoscope (Storz) showed palatal movements (as described in patient 1) on both sides, although they were stronger on the left side. Few reports, however, refer to middle-ear myoclonus, and the source of the noises is said to be the TTM rhythmical contractions [6,11 ,12]. This outcome probably represents the repeated opening of the eustachian tube by the TVPM myoclonus, and the clicking probably originates from the slapping together of the tube walls when closing, as stated by Pulec et al. Nonetheless, in more than 20 years of practice in Brazil, we have seen only two cases of idiopathic palatal and middle-ear myoclonus.
The TTM also has insertions in the cartilaginous eustachian tube and could contribute to tubal opening.
If such a procedure is insufficient to cure the disorder, clonazepam might help but may not be tolerated and may lead to habit formation.
In 2000, Jero and Salmi [5] stated that palatal myoclonus may be idiopathic, but this is extremely rare. After the second procedure, the patient was much improved for 2 months, although she still could hear the clicks in both ears. The tensor tympani muscle tendon has been cut on both sides; therefore, the volume oscillations are due to the tensor veli palatini muscle myoclonus opening the eustachian tube repeatedly. In the right ear, he also had clicks that were less intense and not as easily provoked by the aforementioned maneuvers. As the left tympanic membrane had a large central perforation, these oscillations of volume and pressure are due to the tensor veli palatini muscle myoclonus opening the eustachian tube repeatedly. Some reports suggest simultaneous rhythmical contractions of the SM as part of middle-ear myoclonus.
Also clear is that TTM myoclonus produces noise in the middle ear when vibrating the ossicular chain. Botulinum toxin injected in the TVPM certainly would work but might cause palatal dysfunction and would have to be repeated for a lifetime; the eustachian tube probably would malfunction as well. The second muscle arises from the inferior surface of the apex of the petrous bone medial to the eustachian tube, and its tendon merges with the upper and posterior surface of the palatal aponeurosis. The patient was placed on clonazepam for 2 weeks, after which she reported a decrease in the noises; however, she discontinued the medicine because of excessive drowsiness.
The intact tympanic membrane on both sides prevented any pressure variation large enough to be recorded. The noises in the left ear were easily heard by the examiner without getting close to the patient.
Our plan is to perform a tympanoplasty in the left ear and to section the TTM tendon at the same time.
We present two cases of idiopathic palatal and middle-ear myoclonus and discuss these cases in light of the literature and of some ideas of our own. When last seen I week before the writing of this article, she was on no medication and stated that the clicks were perfectly tolerable and that she did not wish further medication.
The superior cerebellar peduncle joins the dentate and the red nuclei, and the olivodentate tract joins the dentate nucleus and the inferior olive. These authors believed that the great majority of palatal myoclonus cases have a documentable lesion in the aforementioned structures.
Working with monkeys in 1984, Fitzgerald [3] showed that lesions in the inferior olivary tract caused palatal myoclonus. Their hypothesis was that the continuous sound was caused by tetanic contractions of the TTM and SM muscles.



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