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3 Physiology ofthePeripheral andCentral Hearing System
53
sounds presented from the ipsilateral side of the head are dominant in the lateral efferent and send excitatory projections to the contralateral inferior colliculus. On the contrary, MOC sends excitatory projections from the contralateral side of the head to the inferior colliculus on the same side. These results show that the contra­lateral side of the brain dominates the sound source to the inferior colliculus [9, 18].
3.6.2.4 Inferior Colliculus
This is the main receiving station of the pathway originating from the auditory nuclei in the brainstem. It is the primary place where sound identication and local­ization information is collected. It is organized tonotopically, and the frequency mapping of bers with the same characteristic frequency, but from different nuclei in the same tonotopic order, is managed here in the auditory pathway. Although the medial geniculate is the obligatory transition zone for all auditory inputs entering the body, the projection of some neurons may bypass the inferior colliculus. Inhibition of inferior colliculus cells ensures sustained responses to complex signals over a wide range of stimulus intensities. This inhibition reduces transmembrane resistance, increases temporal accuracy in rapid temporal uctuations, and may pro­vide frequency selectivity [9, 6164].
3.6.2.5 The Medial Geniculate Body
Specically, this is a thalamic relay within the auditory system. It receives afferent input from the inferior colliculus and transmits it to the cerebral cortex. It has very dense reciprocal connections with the cortex. It is divided into three parts: ventral, dorsal, and medial. It projects to the center of the auditory cortex. The ventral part sharpens frequency resolution and is a specialized region for advanced analysis in hearing. It has very dense reciprocal connections with the auditory cortex, making it a functional unit of the cortex. The dorsal and medial parts receive a lot of input (except for the auditory system), but it has the characteristic of being a seldom used pathway that projects widely to the primary auditory cortex [9, 11, 13].
Apart from the auditory response, the somatosensory has multimodal interac­tions in visual stimuli, which allows us to have responses that can change as a result of learning. While the dorsal part is particularly involved in novel stimuli, the ven­tral part, due to its close relationship with the amygdala, allows responses to danger­ous stimuli that evoke fear [9, 18].
3.6.3 The Auditory Cortex
Located bilaterally in the superior temporal gyrus of the right and left temporal lobes, extending to the lateral sulcus and transverse temporal gyrus (Heschl’s gyrus), the auditory cortex is the region where the basic and highest-level processes related to hearing take place. The tonotopically organized auditory cortex, which includes Brodmann areas 41 and 42, receives direct input from the contralateral ear via the medial geniculate body and enables recognition of basic elements such as pitch and loudness [9, 11, 13]. It is responsible for the analysis of heard sounds and their
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adaptation according to the characteristics of the incoming auditory stimuli. When recognizing speech features, neurons in the cerebral cortex use ipsilateral and con­tralateral spectral information [11].
The primary auditory cortex (PAC) or core area, Brodmann area 41, is located in the posteromedial part of Heschl’s gyrus. The PAC is surrounded by areas embed­ded in the sulci called the belt and parabelt. The auditory stimulus is rst analyzed in this central region and then directed to the belt and parabelt areas. The PAC and some belt areas are tonotopically organized. The area surrounding the PAC is called the secondary auditory cortex or the auditory association area. While unilateral destruction of the PAC results in mild hearing loss in the contralateral ear, destruc­tion of both cortices greatly reduces hearing sensitivity. Destruction of the second­ary auditory cortex (belt and parabelt areas) results in an inability to interpret the meaning of sounds [9, 11, 13, 18].

3.7 Conclusion

In summary, the perception of sound stimuli involves a nely tuned sequence of events, beginning with the capture and conduction of sound waves by the outer and middle ear, followed by the conversion of these waves into electrical signals by the inner ear. This process underscores the complexity of the auditory system and the importance of each component in the overall function of hearing. Disorders at any stage can lead to hearing loss, underscoring the need for a thorough understanding of the system for effective diagnosis and treatment.

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57
Eustachian Tube: AnOverview
ZeynelÖztürk, NurayBayar Muluk, andGabrielaKopacheva-Barsova

4.1 Introduction

As a complicated anatomical structure, the Eustachian tube (ET) (also called the pharyngotympanic or auditory tube) plays a critical role in maintaining homeostasis in the middle ear. It begins in the middle ear and continues medially before opening just behind the inferior turbinate; the bony lateral third passes through the squamous and petrous parts of the temporal bone. Two-thirds of the medial brocartilage forms the torus tubarius, a mucosal elevation that opens into the nasopharynx. When one yawns, sneezes, swallows, or performs the Valsalva maneuver—all of which apply positive pressure—the levator and tensor veli palatine muscles contract, open­ing the tube [1].
When the ET is unable to perform any of the above three functions, the condition is called Eustachian tube dysfunction (ETD). It can be classied as acute if it occurs within 3months or as chronic if it occurs after that time. Fullness or “popping” in the ear, decreased hearing, tinnitus, autophony, otalgia, and imbalance are symp­toms of ETD, which affect 1% of the population. Dilatative ETD, patulous ETD, and barotrauma-induced ETD are the three main types [24].
4
Gabriela Kopacheva-Barsova was deceased at the time of publication.
Z. Öztürk Faculty of Medicine, Department of Otorhinolaryngology, Nişantaşı University, Istanbul, Turkey
Baypark Hospital, Istanbul, Turkey
N. Bayar Muluk (*) Faculty of Medicine, Department of Otorhinolaryngology, Kirikkale University, Kirikkale, Turkey
G. Kopacheva-Barsova (Deceased) Faculty of Medicine, Department of Otorhinolaryngology, Cyril and Methodius University of Skopje, Skopje, Republic of North Macedonia
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024 M. T. Kalcioglu et al. (eds.), Otology Updates, Comprehensive ENT,
https://doi.org/10.1007/978-3-031-76173-7_4
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Z. Öztürk et al.

4.2 Eustachian Tube Anatomy

The ET is composed of cartilage and bone. The adult ET extends inferiorly, anteriorly, and medially from the middle ear and measures approximately 36mm. The lateral one­third, which is 12mm in length, is bony and originates from the anterior wall of the middle ear cavity; the medial two-thirds, which is 24mm in length, is brocartilagi­nous and enters the posterolateral wall of the nasopharynx. The tube opens near the posterior end of the inferior turbinate, approximately 1.25cm behind and just below it.
The bony portion is broad at the tympanic orice. The narrowest part of the ET is the isthmus; it gradually narrows as it passes through the temporal bone at the juncture of the squamous and petrous parts [5].
A posteromedially oriented cartilaginous plate forms the cartilaginous portion. The cartilage forms the anterior curvature of a short ange at the nasopharyngeal orice. Fibrous tissue constitutes the remainder of the anterolateral wall. At the isthmus, the brocartilaginous portion of the tube ends laterally as the apex and continues with the bony portion, whereas the torus, where the brocartilaginous tube broadens and ends medially, lies below and elevates the nasopharyngeal muco­sal surface. The Rosenmüller fossa is a recess just behind this elevation; it is often the site of nasopharyngeal carcinoma and occult primary tumors [5].
A potential slit-like space between the greater wing (ala major) of the sphenoid bone and the petrous portion of the temporal bone secures the cartilaginous ET to the skull base [5].
The ET has a nearly triangular lumen with a vertical diameter of 2–3mm and a horizontal diameter of 3–4mm. Unlike the bony portion, which is continuously open, the brocartilaginous portion remains closed until swallowing, yawning, or vigorous ination causes it to open.
The length of the ET in the newborn is about 18mm. Compared to the adult ET, it is typically atter, less angular, and about half the size. While the cartilaginous portion lies inferiorly, the bony portion is more elongated and larger in diameter [5].
The respiratory epithelium, consisting of mucosal glands, goblet cells, and colum­nar ciliated cells, lines the ET at its nasopharyngeal opening. The bony portion of the tube is where the respiratory epithelium meets the mucosa of the middle ear.
The posterior wall of the ET has a more extensive mucosal surface and more mucosal folds (microturbines) in pediatric specimens compared to adult specimens, according to a study by Ozturk etal. In addition to contributing to the development of ET dysfunction, these microturbines may play a critical clearing and protective role in children, according to their ndings [3].
4.3 Eustachian Tube Function andPhysiology
Below are the physiological functions of the ET specied in three bullet points:
• Controls airow or pressure in the middle ear.
• Protects the middle ear from pressure and secretions from the nose and throat.
• Cleans the nasopharynx of middle ear secretions.
4 Eustachian Tube: AnOverview
61
4.3.1 Control ofAirflow or Pressure
At rest, the ET is compressed and there may be a slight negative pressure in the middle ear. Routine air pressure is maintained by repeated opening of the ET [5].
When a person swallows or yawns, the tensor veli palatini muscle contracts and opens the ET.ET dysfunction is a consequence of cleft palate, which is caused by a defect in the function due to the anatomic defect in the tensor veli palatini muscles. The role of the levator veli palatini muscle remains to be determined. Some have questioned its role in opening the ET [5].
The effectiveness of ET ventilation is lower in children than in adults. Middle ear disease is more common in children, and other contributing factors include over­sized adenoids and recurrent upper respiratory tract infections. However, the decreasing incidence of otitis media from infancy to adulthood shows that ET func­tion improves as children develop.
Due to the regular opening of the ET, middle ear pressure typically remains sta­ble in the range of +50mm to 50mm H2O.However, forces outside or above this range are not always indicative of middle ear disease [5]. The middle ear can absorb approximately 1mm of gas or air per day. The mastoid air cell system is accounted as the gas source and reservoir of the middle ear [5]. At rest, the ET remains closed. Thus, the nasopharynx serves to attenuate sudden loud sounds before they reach the middle ear [5].
Patulous ET is a rare but serious condition characterized by an abnormally patent Eustachian line. The patient often expresses dissatisfaction with ear fullness and autophony, which are symptoms of hearing loss. Rapid weight loss, which can lead to shrinkage of the ET, is believed to exacerbate the problem [5].
The ET conducts normal middle ear secretions to the nasopharynx via the muco­ciliary transport system and repeated active opening and closing of the tube pas­sages [5]. Reux of nasopharyngeal secretions into the tube, which can cause otorrhea, can occur when there is a disruption in the closed middle ear system, including after mastoid surgery or a ruptured tympanic membrane [5].
In addition, blowing one’s nose too hard can cause pressure to build up in the nasal airway and nasopharynx, causing secretions from the nose to get stuck in the middle ear. Otitis media with effusion (OME) has now been linked to laryngopha­ryngeal reux (LPR). Pepsinogen was found in 84% of OME by Al-Saab etal., with
1.86–12.5 times higher concentrations than the serum [6].
It is believed that nasopharyngeal secretions that reach the middle ear cavity with LPR through ET can sometimes result in otorrhea when the closed middle ear sys­tem is disrupted as in the perforation of the tympanic membrane or after a mastoid­ectomy procedure [5].

4.4 Eustachian Tube Dysfunction

Otitis media with effusion (OME), atelectasis of the middle ear, and chronic otitis media with tympanic membrane perforation appear to be caused by persistent ET dysfunction [1]. It is common practice for surgical procedures to address
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Z. Öztürk et al.
complications resulting from ET dysfunction rather than the problem itself. Sedlmaier etal. documented the results of laser ablation toward the posterior por­tion of the nasopharyngeal orice of the tubal ostium [7]. In the presence of patho­logical signs such as tubal tonsillar, restricted ET orice, or adenoids, ET function was optimized in 70% of patients [5].
In 2011, Poe etal. presented the results of a pilot clinical study evaluating the efcacy and safety of ET balloon dilatation. According to their ndings, patients with long-term OME, who could not self-insufate their ET by Valsalva maneuver, swallowing, or yawning, appeared to benet from cartilaginous ET dilatation and there were no signicant side effects [8].
Among children with intractable chronic obstructive ET dysfunction, a great majority as high as 80% showed clinical symptom relief after balloon dilation ther­apy according to a study by Tisch etal. [9].
Adults with persistent dilatory ET dysfunction may nd temporary relief with balloon dilatation, according to a retrospective study by Satmis and van der Torn. There was a statistically signicant improvement in patients’ ET Dysfunction Questionnaire (ETDQ-7) scores at 1 and 3months following surgery. The air– bone gap also improved postoperatively. Approximately 43% and 48% of partici­pants reported being satised at the rst and second follow-up visits, respectively [10].
According to a literature review by Mehta etal., only 11–18% of patients with chronic ET dysfunction showed clinical improvement after intranasal corticosteroid monotherapy. Buteyko breathing and intranasal corticosteroid treatment relieved symptoms in half of the chronic patients in one study [11].
With the utilization of tissue engineering in the regeneration of mastoid air cells (MACs), Kanemaru etal. investigated the altered function of the ET [12]. They found that the ET portion and middle ear gas exchange were improved by tissue­engineered regeneration of MACs [5].
Using transnasal video endoscopy in a sample of 33 adults, Alper etal. found that individuals with a history of middle ear disease but otherwise healthy middle ears had less soft palate elevation during swallowing. This correlates with a wider ET orice and rotation of the medial lamina, suggesting impaired ET function and an increased risk of otitis media [5, 13].
ET dysfunction treatment is explained in detail in Chap. 29.
4.5 Epidemiology ofEustachian Tube Dysfunction
Recent research has shown that for every pediatric clinic visit for ET dysfunction, there are 0.77 adult visits, indicating that the prevalence is higher in children than in adults. As one of the known consequences of ET dysfunction, OME affects nearly 90% of children before they enter school [14]. ET dysfunction is diagnosed in approximately 1% of adults. Men are typically diagnosed before the age of 20, while women tend to be diagnosed later in life. To date, there is no evidence of a statistically signicant seasonal variation [15].
4 Eustachian Tube: AnOverview
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4.6 Etiology ofEustachian Tube Dysfunction
In barotrauma-induced ET dysfunction, middle ear pressure is not adequately regu­lated because the ET does not open in response to changes in ambient pressure. Patients may have normal otoscopy and tympanometry results due to increased air pressure in certain situations, such as deep sea diving or descending from a high altitude. Repeated equalization efforts caused by elevated atmospheric pressure cause local irritation and mucosal edema of the ET mucosa. This makes it difcult to be open and transparent in the future. The goal of treating baro-challenge ET dysfunction with oral or topical decongestants is to reduce mucosal edema and local tissue hyperemia, which, in turn, shrinks the nasopharyngeal mucosa and improves ET patency [1].
An overly patent ET causes patulous ET dysfunction because the tube does not close properly at rest, allowing the nasopharynx and middle ear to communicate continuously. Autophony, characterized by repetitive “snifng” to reduce self­vocalization, is a sign of this [1].
An episode of rhinitis, upper respiratory tract infection, or gastroesophageal reux syndrome may cause inammation and mucosal edema, leading to orice obstruction and dysfunction and resulting in dilatory ET dysfunction. It is important to rule out malignancies such as nasopharyngeal cancer, when a patient presents with unilateral obstruction. Benign causes of obstruction such as adenoid hypertro­phy or complications following adenoidectomy should also be considered [1]. A common symptom caused by harmful pressure buildup in the middle ear is ear full­ness [1618].
4.7 Evaluation oftheEustachian Tube
Tympanic insufation may demonstrate active negative pressure, and negative rest­ing middle ear pressures may be inferred from a type C tympanogram. A complete hearing evaluation must include tuning fork testing with Rinne’s and Weber’s tuning forks and pure-tone audiometry [1].
Using a scoring system, the ETDQ-7 attempts to screen for the severity of ET dysfunction as reported by the patient. The seven questions range from “no prob­lem” (a score of 1) to “severe problem” (a score of 7). ET dysfunction is present if the mean score is >2.0 [19].
4.8 How toApproach Eustachian Tube Malfunction
The most likely cause of ET dysfunction determines the course of treatment [1]:
Reducing acid production in the body and adopting a healthier lifestyle are the mainstays of treatment for gastroesophageal reux disease. Possible options include proton pump inhibitors and other anti-acid medications. If possible, try to make lifestyle changes to eliminate allergens. Nasal corticosteroids and antihistamines