Endoscopic Assessment of the Isthmus Tympanicum and Tensor Tympani Fold and their Relationship with Mastoid Pneumatization in Chronic Otitis Media.

OBJECTIVES: To endoscopically evaluate the patency of the isthmus tympanicum and integrity of the tensor tympani fold as routes of ventilation of the attic and mastoid in chronic otitis media (COM) and to assess their effects on mastoid pneumatization. MATERIALS AND METHODS: Sixty patients with COM were categorized into two groups: (1) Group A: 36 patients with tympanic membrane perforation (2) Group B: 24 patients with limited attic disease of whom 14 patients had attic retraction pockets and 10 with limited attic cholesteatoma. A multislice computed tomography scan of the temporal bone was performed for each patient to assess the degree of mastoid pneumatization. Notably, either myringoplasty or tympanomastoid surgery was performed in all patients. An endoscope was inserted into the middle ear for evaluation of the isthmus tympanicum and tensor fold area. RESULTS: The isthmus tympanicum was patent in most ears (83.3%) of group A, whereas it was blocked in most ears (83.3%) of group B. The tensor fold was complete in 77.8% of ears in group A and 83.3% of ears in group B. It was observed that 94.1% of ears with patent isthmus in both groups had normal mastoid pneumatization and 5.9% of ears had poorly pneumatized mastoid. By contrast, 7.7% of ears with blocked isthmus tympanicum had normal mastoid pneumatization and 92.3% had poor mastoid pneumatization. Normal mastoid pneumatization was observed in 50% of ears in both groups with complete tensor fold, and 83.3% of ears with an incomplete tensor fold. CONCLUSION: A significant correlation was observed between COM with limited attic disease and obstruction of the isthmus tympanicum. Obstruction of isthmus tympanicum was associated with poor mastoid pneumatization. Furthermore, an incomplete tensor fold was associated with well pneumatized mastoid.

First emerging objective experimental evidence of hearing impairment following subarachnoid haemorrhage; Felix culpa, phonophobia, and elucidation of the role of trigeminal ganglion.

Objective: The exact mechanism of phonophobia induced by subarachnoid hemorrhage (SAH) has not been understood well. This subject was investigated. Material and methods: This study was conducted on 25 rabbits. They divided into three groups: Five as control, five as SHAM, 20 as SAH group. All animals objected to 85 dB impulse noise by daily periods, and their phonophobic score values were examined by daily periods for 20 days. Their brains, trigeminal ganglia were extracted bilaterally. The normal and degenerated neuron densities of trigeminal ganglia were examined by stereological methods and compared with phonophobia scores. Results: Phonophobic score was 19-17, mean live neuron density (LND) of the trigeminal ganglia was 16.321 ± 2.430/mm3, and degenerated neuron density (DND) was 1.15 ± 0.120/mm3 in animals of control groups (n = 5). The phonophobic score was 17-14, LND: 14.345 ± 1.913/mm3, DND of the trigeminal ganglia was 1.150 ± 0.110/mm3 in SHAM group (n = 5). The phonophobic score was 14-8, LND: 12.987 ± 1.966/mm3, mean DND of the trigeminal ganglia was 2.520 ± 510/mm3 in animals with high phonophobia scores (n = 6). The phonophobic score was 7-4, LND: 9.122 ± 1.006, mean DND of the trigeminal ganglia was 5.820 ± 1.610/mm3, in animals with fever phonophobia scores (n = 9). Conclusion: An inverse relationship between DND trigeminal ganglion (TGG) and phonopobic score was found. The paralysis of tensor tympani muscle owing to trigeminal ganglia ischemia may be responsible for phonophobic clinical state in animals with SAH. In addition, there seems to be an important concern for the verbal component of GCS in SAH. These two important findings have not been published previously.

An Integrative Model Accounting for the Symptom Cluster Triggered After an Acoustic Shock.

Acoustic shocks and traumas sometimes result in a cluster of debilitating symptoms, including tinnitus, hyperacusis, ear fullness and tension, dizziness, and pain in and outside the ear. The mechanisms underlying this large variety of symptoms remain elusive. In this article, we elaborate on the hypothesis that the tensor tympani muscle (TTM), the trigeminal nerve (TGN), and the trigeminal cervical complex (TCC) play a central role in generating these symptoms. We argue that TTM overuse (due to the acoustic shock), TTM overload (due to muscle tension), and ultimately, TTM injury (due to hypoxia and "energy crisis") lead to inflammation, thereby activating the TGN, TCC, and cortex. The TCC is a crossroad structure integrating sensory inputs coming from the head-neck complex (including the middle ear) and projecting back to it. The multimodal integration of the TCC may then account for referred pain outside the ear when the middle ear is inflamed and activates the TGN. We believe that our model proposes a synthetic and explanatory framework to explain the phenomena occurring postacoustic shock and potentially also after other nonauditory causes. Indeed, due to the bidirectional properties of the TCC, musculoskeletal disorders in the region of the head-neck complex, including neck injury due to whiplash or temporomandibular disorders, may impact the middle ear, thereby leading to otic symptoms. This previously unavailable model type is experimentally testable and must be taken as a starting point for identifying the mechanisms responsible for this particular subtype of tinnitus and its associated symptoms.

Tensor veli palatini electromyography for monitoring Eustachian tube rehabilitation in otitis media.

BACKGROUND: The pathogenesis of otitis media is related to Eustachian tube dysfunction. The tensor veli palatini muscle actively opens the Eustachian tube and promotes middle-ear ventilation. This study describes a technique for paratubal electromyography that uses a surface, non-invasive electrode able to record tensor veli palatini muscle activity during swallowing. METHODS: Twenty otitis media patients and 10 healthy patients underwent tensor veli palatini electromyography. Activity of this muscle before and after Eustachian tube rehabilitation was also assessed. RESULTS: In 78.5 per cent of patients, the electromyography duration phase and/or amplitude were reduced in the affected side. The muscle action potential was impaired in all patients who underwent Eustachian tube rehabilitation. CONCLUSION: This study confirmed that Eustachian tube muscle dysfunction has a role in otitis media pathogenesis and showed that muscle activity increases after Eustachian tube rehabilitation therapy.

[The modern view of the clinical significance of tensor tympani muscle].

The objective of the present work was analyse the modern views of the role of tensor tympani muscle in the development of otic pathology. In this context, the authors discuss tenotomy of the middle ear muscles for the treatment of Meniere's disease, diagnostics and clinical aspects of middle ear myoclonus, and tonic tensor tympani syndrome.

Functional evaluation of paratubal muscles using electromyography in patients with chronic unilateral tubal dysfunction.

Eustachian tube dysfunction is closely related to the development of otitis media and result from several factors including inflammation within the nasal cavity and nasopharynx, adenoid hypertrophy, cleft palate and nasopharyngeal carcinoma. To some extent, eustachian tube dysfunction may be related to weakness of the paratubal muscles, such as the tensor veli palatini and levator veli palatini muscles. The aim of the study is to find out myogenic factors in eustachian tube dysfunction using electromyography (EMG), and to evaluate the clinical feasibility of EMG. Ten patients with unilateral eustachian tube dysfunction were included in this study. The healthy side of each patient was used as a control. EMG tests on paratubal muscles were conducted under the view of a 30° endoscope or fiberoptic laryngoscope. EMG on the tensor veli palatini showed decreased amplitudes on the affected side in one patient during phonation. EMG on the levator veli palatini showed decreased amplitudes on the affected side in two patients during both deglutition and phonation, one patient during phonation only, and two patients during deglutition only. The only patient who had decreased amplitude on EMG of the tensor veli palatini also had decreased amplitude on EMG of the levator veli palatini. In conclusion, although it is generally accepted that the tensor veli palatini plays a major role in opening the eustachian tube, reduced activity of the levator veli palatini may be related to eustachian tube dysfunction. When assessing eustachian tube function, EMG is useful for evaluating myogenic factors.

Tenotomy of the middle ear muscles causes a dramatic reduction in vertigo attacks and improves audiological function in definite Meniere's disease.

CONCLUSIONS: Because the presented data reveal an immediate and persistent reduction of vertigo and a clear improvement in hearing function and functional scales, we conclude tenotomy to be effective in unilateral, definite Meniere's disease - laying the foundation for future prospective, randomized controlled trials. OBJECTIVES: This study compares the unique long-term results of tenotomy of the stapedius and tensor tympani muscles in definite Meniere's disease refractory to medical treatment and presents a hypothesis on why tenotomy seems effective. METHODS: This was an interventional cohort study. The study sample comprised 30 patients (15 males, 15 females; average age 57 ± 13.1 years) with definite Meniere's disease (AAO-HNS criteria, 1995). Patients were evaluated pre- and postoperatively using pure tone audiometry, AAO-HNS questionnaires regarding vertigo attacks, functional level scores, and tinnitus, and were followed up for 2-9 years. Postoperative values were calculated for the patient collective as a whole and consequently divided into three equal postoperative terms of 3 years each. RESULTS: A statistically significant improvement of inner ear hearing levels postoperatively (p = 0.041) and a major reduction in vertigo attacks in all groups (p < 0.001) with complete absence of attacks in 26/30 patients was noted. Results remained constant up to 9 years postoperatively. Although tinnitus persisted, the intensity was lower overall (p = 0.013).

Scleraxis is required for differentiation of the stapedius and tensor tympani tendons of the middle ear.

Scleraxis (Scx) is a basic helix-loop-helix transcription factor expressed in tendon and ligament progenitor cells and the differentiated cells within these connective tissues in the axial and appendicular skeleton. Unexpectedly, we found expression of the Scx transgenic reporter mouse, Scx-GFP, in interdental cells, sensory hair cells, and cochlear supporting cells at embryonic day 18.5 (E18.5). We evaluated Scx-null mice to gain insight into the function of Scx in the inner ear. Paradoxical hearing loss was detected in Scx-nulls, with ~50% of the mutants presenting elevated auditory thresholds. However, Scx-null mice have no obvious, gross alterations in cochlear morphology or cellular patterning. Moreover, we show that the elevated auditory thresholds correlate with middle ear infection. Laser interferometric measurement of sound-induced malleal movements in the infected Scx-nulls demonstrates increased impedance of the middle ear that accounts for the hearing loss observed. The vertebrate middle ear transmits vibrations of the tympanic membrane to the cochlea. The tensor tympani and stapedius muscles insert into the malleus and stapes via distinct tendons and mediate the middle ear muscle reflex that in part protects the inner ear from noise-induced damage. Nothing, however, is known about the development and function of these tendons. Scx is expressed in tendon progenitors at E14.5 and differentiated tenocytes of the stapedius and tensor tympani tendons at E16.5-18.5. Scx-nulls have dramatically shorter stapedius and tensor tympani tendons with altered extracellular matrix consistent with abnormal differentiation in which condensed tendon progenitors are inefficiently incorporated into the elongating tendons. Scx-GFP is the first transgenic reporter that identifies middle ear tendon lineages from the time of their formation through complete tendon maturation. Scx-null is the first genetically defined mouse model for abnormal middle ear tendon differentiation. Scx mouse models will facilitate studies of tendon and muscle formation and function in the middle ear.

[Tensor veli palatini and tensor tympani muscles: anatomical, functional and symptomatic links]. / Tensores del velo del paladar y del martillo: vínculos anatómicos, funcionales y sintomáticos.

INTRODUCTION AND OBJECTIVES: Temporomandibular disorders are associated with symptoms such as tinnitus, vertigo, sensation of hearing loss, ear fullness and otalgia. The connection and dysfunction of the tensor tympani and tensor veli palatini muscles seems to be associated with the aforementioned symptoms. We seek to demonstrate and explain this connection through the morphometry of these structures. METHODS: We studied 22 paired blocks and 1 left side of human temporal bone. Digital measurements were made of the tensor tympani muscles and stapes. RESULTS: The average length of the stapedial muscle was 5.8 mm SD 0.61, and that of the tensor tympani was 19.69 mm SD 1.07. Anatomical connections were found in all the samples between the tensor veli palatini muscles through a common tendon. CONCLUSIONS: There is a need for an interdisciplinary management between physician and specialized dentist in cases of craniofacial pain.

Activation of middle-ear muscles by transcranial magnetic stimulation.

OBJECTIVES: To evaluate the reliability of transcranial magnetic stimulation in eliciting admittance changes due to activation of middle-ear muscles. METHODS: Admittance changes induced by transcranial magnetic stimulation at the inion were evaluated in eight normal subjects, two subjects with prelingual deafness and 22 patients suffering from other otological disorders characterised by absence of acoustic reflex. RESULTS: Responses showed a predominant negative peak in normal ears. Two small positive components, one preceding and the other following the negative deflection, were less consistently elicited. Only a positive wave was detected in otosclerotic subjects. Patients with tympanic membrane perforation or previous tympanoplasty with ossicular discontinuity did not show any response. CONCLUSIONS: Transcranial magnetic stimulation is able to activate both stapedius and tensor tympani muscles. In conjunction with admittance audiometry, it may represent a method of exploring the mechanics of the middle ear when acoustic reflex testing is not reliable. It can be helpful in the confirmation of stapes fixation when a severe to profound hearing loss is present.

The effect of auditory stimulation on the tensor tympani in patients following stapedectomy.

CONCLUSION: We believe that a tensor tympani reflex, in response to loud sound, is present in a minority of people, although its functional significance with regard to sound transmission is questionable. The absence of startle response in our stapedectomized subjects makes us question whether the tensor component of the startle response is large enough to be identified by manometry. OBJECTIVES: This study was organized to examine reflex activity to stimulation by loud sound or by startle in the tensor tympani. Although many previous studies have been carried out, results have been contradictory, and methodological flaws have rendered the interpretations questionable. PATIENTS AND METHODS: Stapedectomized patients were invited to take part in the study. Thirteen patients underwent testing by extratympanic manometry, using a standard tympanometer. Responses were observed during repeated stimuli with loud sound at 500, 1000, 2000 and 4000 Hz to the ipsilateral and contralateral ears, and with an air jet against the closed eye. A control group was also studied for the startle test. RESULTS: Three clear ipsilateral (23%) and two clear contralateral (14%) responses to auditory stimuli were seen in the 13 patients. We found responses to startle stimuli in none of our study group and eight (42%) of control ears.

Reversed ipsilateral acoustic reflex pattern.

OBJECTIVE: To determine the characteristics and possible origin of reversed ipsilateral acoustic reflex. STUDY DESIGN: Retrospective. SETTING: University hospital. PATIENTS: Sixty-three ears in 52 patients (mean age 37.6 years) with unilateral or bilateral sensorineural hearing loss and 45 age- and sex-matched persons as controls. METHODS: Audiometry and impedance audiometry examinations were studied retrospectively. Hearing test records were investigated, and patients with unilateral or bilateral sensorineural hearing loss were included. Forty-five age- and sex-matched persons served as controls. The ipsilateral and contralateral acoustic reflex patterns of these patients were investigated. Reflex-forming acoustic thresholds and latencies of ipsilateral reversed (positive) reflexes were compared with ipsilateral negative (upward) reflexes. RESULTS: The ipsilateral acoustic reflexes of 18 of 63 ears with sensorineural hearing loss were absent, and the remaining 45 were reversed (positive). A significant difference was found between ipsilateral reversed and ipsilateral negative acoustic reflex thresholds (p < .001) and latencies (p < .001). No statistically significant differences were found between ipsilateral and contralateral negative reflex latencies. CONCLUSIONS: The reversed acoustic reflex pattern is not an artifact but a physiologic event. This reflex does not appear to be related to stapedius or tensor tympani muscle contraction. We believe that the etiology of the reversed reflex is related to the system that contains the tympanic membrane, malleus, and incus and their ligaments but not the middle ear muscles.

Músculo tensor del tímpano: músculo masticatorio extraño / Tensor tympani muscle: strange chewing muscle

Con este trabajo se pretende alertar al medico y al odontólogo en el entendimiento y la integración del manejo interdisciplinario para la detección de síntomas de oido comunes en patologías diferentes, brindando mayores herramientas en la fase conservadora de la terapia para esta sintomatología compartida. La fisiología del músculo tensor del tímpano y su funcionalidad en el oído medio ha sido velada aun cuando su disfunción y relaciones anatómicas están explicando un grupo de síntomas óticos confusos a la evaluación clínica convencional. Los músculos del oído medio comparten un origen embriológico y funcional común con los músculos masticatorios y faciales. En este artículo se pretende hacer énfasis en la dimensión neurológica y anatómica de la funcionalidad (individual y compartida) de estos músculos entre si y el sistema estomatognático. La tonicidad aumentada de este músculo deja de ser un fenómeno sin conexiones lógicas,ofreciendo a su actividad normal o disfuncional el protagonismo que se merece y redefiniendo su funcionalidad e importancia en la comprensión de los síntomas óticos referidos muy en común con síntomas de otras patologías de origen extra-ótico. El tinitus, vértigo, sensación de oído tapado, hipoacusia, hiperacusia y la otalgia son síntomas que al evaluanoser primarios de patologías en oído, deben ser descartados por el medico y relacionados con patologías vecinas que pueden producirlos. Ya existe la necesidad de entender los desordenes temporomandibulares y la sintomatología referida cráneo-facial desde una perspectiva neurofisiológica y músculo-esquelética comprendida en el sistema estomatognático. En la práctica diaria se observa con frecuencia una sintomatología común para los síntomas oticos y los desordenes temporomandibulares que se deben entender bajo una perspectiva amplia, anatómica, neuroanatómica y clínica

This work seeks to alert medical and odontological staff to understanding and using interdisciplinary handling for detecting different pathologies’ common otic symptoms. It offers better tools for this shared symptomatology during therapy’s conservative phase. Tensor tympani muscle physiology and function in the middle ear have been veiled, even when their dysfunction and anatomical relationships may explain a group of confused otic symptoms during conventional clinical evaluation. Middle ear muscles share a common embryological and functional origin with chewing and facial muscles. This article emphasizes that these muscles share a functional neurological and anatomical dimension with the stomatognathic system; these muscles’ increased tonicity ceases to be a phenomenon having no logical connections. It offers functionality and importance in understanding referred otic symptoms in common with other extra-otical symptom pathologies. Tinnitus, vertigo, otic fullness sensation, hyperacusia, hypoacusia and otalgia are not only primary hearing organ symptoms. They should be redefined and related to the neighboring pathologies which can produce them. There is a need to understand temporomandibular disorders and craniofacial referred symptomatology from neurophysiologic and muscle-skeletal angles contained in the stomatognathic system. Common symptomatology is frequently observed in otic symptoms and temporomandibular disorders during daily practice; this should be understood by each discipline from a broad, anatomical and clinical perspective

Tensor tympani muscle: strange chewing muscle.

This work seeks to alert medical and odontological staff to understanding and using interdisciplinary handling for detecting different pathologies common otic symptoms. It offers better tools for this shared symptomatology during therapy s conservative phase. Tensor tympani muscle physiology and function in the middle ear have been veiled, even when their dysfunction and anatomical relationships may explain a group of confused otic symptoms during conventional clinical evaluation. Middle ear muscles share a common embryological and functional origin with chewing and facial muscles. This article emphasizes that these muscles share a functional neurological and anatomical dimension with the stomatognathic system; these muscles increased tonicity ceases to be a phenomenon having no logical connections. It offers functionality and importance in understanding referred otic symptoms in common with other extra-otical symptom pathologies. Tinnitus, vertigo, otic fullness sensation, hyperacusia, hypoacusia and otalgia are not only primary hearing organ symptoms. They should be redefined and related to the neighboring pathologies which can produce them. There is a need to understand temporomandibular disorders and craniofacial referred symptomatology from neurophysiologic and muscle-skeletal angles contained in the stomatognathic system. Common symptomatology is frequently observed in otic symptoms and temporomandibular disorders during daily practice; this should be understood by each discipline from a broad, anatomical and clinical perspective.

Tonic contractions of the tensor tympani muscle: a key to some non-specific middle ear symptoms? Hypothesis and data from temporal bone experiments.

CONCLUSIONS: The results of this study show that in clinical practice it will not be easy to diagnose tonic contractions of the tensor tympani muscle and only a combination of findings will be helpful. Based on these experimental results a clinical study will be started which should clarify the diagnostic relevance of indicators of tonic tensor muscle contractions. OBJECTIVES: There are indications from the literature and from personal experience that tonic contractions of the tensor tympani muscle may play a role in some ear symptoms, such as fullness, certain cases of tinnitus, slight hearing loss or Ménière's disease-like findings. In order to prove this theory we looked for indicators, either visual or functional, to help clinically diagnose the functional state of the muscle, particularly its tonic contraction. MATERIAL AND METHODS: Experiments simulating tensor contractions were carried out on temporal bone specimens. Traction was applied either to the isolated muscle, to its tendon or to the malleus neck. Effects were observed either visually via an endoscope or by impedance audiometry using multiple-frequency tympanometry. RESULTS: During simulated tensor traction the aspect of the tympanic membrane changed slightly, i.e. there was some inward movement of the umbo. However, such effects were only identifiable during the pulling action or by directly comparing the "contracted" and "relaxed" states. Tympanometry revealed a decrease in the peak amplitudes and a shift in the middle ear resonance towards higher frequencies during contractions.

[New aspects of the mechanics of the auditory tube]. / Neue Aspekte zur Mechanik der Tuba auditiva.

The aim of the present article is to describe the mechanical components of the auditory tube and the role of these components in auditory tube function. Particular attention will be given to those aspects which have not been sufficiently dealt with in the past, such as the role of the isthmus region, the function of the lateral mucosal folds, the significance of the of the surfactant proteins and the pathophysiology of the patulous auditory tube. Special attention is given to the tensor veli palatini muscle and its physiology. Because of its isometric contraction, the function of this muscle depends on so-called hypomochlia changing the direction of its force. In the context of this article, the three hypomochlia involved are the pterygoid hamulus, Ostmann's fatty tissue and the medial pterygoid muscle. The so-called "Eppendorf-maneuver" is depicted for the first time.

The reversed ipsilateral acoustic reflex: clinical features and kinetic analysis.

OBJECTIVE: The reversed ipsilateral acoustic reflex (RIAR) has been the subject of few studies in the past literature and the nature of this "reflex" response is not yet completely understood. It can be observed in different diseases, all of which result from inactivity of the stapedial reflex (SR). We aimed to investigate the occurrence of the RIAR in different diseases. MATERIAL AND METHODS: An extensive clinical investigation of the RIAR was carried out. RESULTS: The RIAR was found to be present in 100% of ears lacking an effective SR arc. Its amplitude is modulated by the air pressure level in the external ear canal whilst its sign is constantly positive and never reverses. CONCLUSION: Kinetic analysis of the RIAR suggests the existence of a single underlying phenomenon while the interaction of the RIAR with the SR may explain the complex morphology frequently observed in the normal ipsilateral acoustic reflex.

["Irritative" pathology of the external auditory canal and decreased sound sensation]. / Patología "irritativa" del conducto auditivo externo y disminución de la sensación sonora.

We have not found in the literature an explanation for the intermittent and transient decreased lesser hearing sensation in patients with dysesthesia of the external auditory canal (EAC). In this paper we offer a possible explanation for it. Our hypothesis is that the stimulation of the sensory fibers of the trigeminal and facial nerves in the EAC is able to increase the stiffness of the ossicular chain by means of a reflex stimulation of malleus and stapes muscles. This intermittent and transient increase of the ossicular stiffness could explain the intermittent and transient decrease of hearing sensation in these patients.

Patología "irritativa" del conducto auditivo externo y disminución de la sensación sonora / Dysesthesia of the external auditory canal and decreased hearing sensation

En la literatura no hemos encontrado una explicación para la disminución intermitente y transitoria de la sensación sonora en pacientes con patología "irritativa" del conducto auditivo externo (CAE). En este artículo ofrecemos una posible explicación. Hipotetizamos que la estimulación de las fibras sensitivas de los nervios trigémino y facial en el CAE es capaz de producir un aumento de la rigidez de la cadena osicular a través de la estimulación refleja de los músculos del martillo y el estribo. Este aumento intermitente y transitorio de la rigidez provocaría la disminución intermitente y transitoria de la sensación sonora en estos pacientes (AU)

We have not found in the literature an explanation for the intermittent and transient decreased lesser hearing sensation in patients with dysesthesia of the external auditory canal (EAC). In this paper we offer a possible explanation for it. Our hypothesis is that the stimulation of the sensory fibers of the trigeminal and facial nerves in the EAC is able to increase the stiffness of the ossicular chain by means of a reflex stimulation of malleus and stapes muscles. This intermittent and transient increase of the ossicular stiffness could explain the intermittent and transient decrease of hearing sensation in these patients (AU)