Overview of Head & Neck Clinical Anatomy
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OVERVIEW OF HEAD & NECK CLINICAL ANATOMY Editors Gülay AÇAR Aynur Emine ÇİÇEKCİBAŞI Lyon 2025
OVERVIEW OF HEAD & NECK CLINICAL ANATOMY Editors Gülay AÇAR Aynur Emine ÇİÇEKCİBAŞI Lyon 2025
Overview of Head & Neck Clinical Anatomy Editors • Assoc. Prof. Dr. (MD) Gülay AÇAR • Orcid: 0000-0002-9524-5056 • Prof. Dr. (MD) Aynur Emine ÇİÇEKCİBAŞI • Orcid: 0000-0002-1373-3065 Cover Design • Motion Graphics Book Layout • Motion Graphics First Published • October 2025, Lyon e-ISBN: 978-2-38236-911-1 DOI: 10.5281/zenodo.17362830 copyright © 2025 by Livre de Lyon All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without prior written permission from the Publisher. The author or authors of the relevant section are responsible for any copyright infringement that may occur due to the images and graphics used in the book. The editor or publisher does not assume responsibility in this regard. Publisher • Livre de Lyon Address • 37 rue marietton, 69009, Lyon France website • http://www.livredelyon.com e-mail • [email protected]
I PREFACE It is clear that developmental anatomy is a vital, ever-changing and intricate field of knowledge for clinicians. Its value lies in its ability to preserve human life, improve well-being, and enhance quality of life. It is not uncommon for medical students to find learning about cranial anatomy and embryology challenging. In response, academicians are continually striving to simplify the understanding of head and neck clinical anatomy. The comprehension of anatomical variations constitutes an indispensable component of anatomical knowledge, being of particular relevance to medical imaging and to the diverse clinical departments. Furthermore, surgeons who understand the anatomy of the head and neck can perform surgery safely and precisely to optimise health restoration and minimise morbidity. This book provides an up-to-date overview of head anatomy, from basic medical sciences to clinical practices, through eleven chapters written by academics and researchers. While the book chapters are primarily intended to help undergraduate medical students understand head and neck anatomy and recognise its value in clinical applications for diagnosis and treatment, I am sure clinicians will also find them useful for updating and refreshing their knowledge. We would like to express our sincere gratitude to all the authors who contributed to the preparation of this book and to the publishing team who provided technical support, in recognition of the fact that scientific production is a collective effort. Editors Assoc. Prof. Dr. (MD) Gülay AÇAR Prof. Dr. (MD) Aynur Emine ÇİÇEKCİBAŞI Necmettin Erbakan University, Faculty of Medicine, Department of Anatomy
III CONTENTS PREFACE I 1CHAPTER I. DEVELOPMENTAL ANATOMY OF THE SKULL Sümeyye ÖZDEMİR & Gülay AÇAR CHAPTER II. LIGHT-REFRACTING STRUCTURES: CLINICAL 25ANATOMY OF THEOPTICAL MEDIA OF THE EYE Muhammed ErtuğrulÖZBEY&AynurEmine ÇİÇEKCİBAŞI CHAPTER III. FUNCTIONAL AND CLINICAL ANATOMY OF THE LACRIMAL APPARATUS 57 SümeyraDOĞMUŞ CHAPTER IV. ANATOMY AND CLINICAL SIGNIFICANCE OF THE INFERIOR ORBITAL FISSURE 75 İrfanAKYILDIZ CHAPTER V. ANATOMY AND CLINICAL SIGNIFICANCE OF THE NASAL CAVITY 83 BurakŞEN CHAPTER VI. PRESERVATION RHINOPLASTY 97 YaserSaidÇETIN CHAPTER VII. ANATOMY AND CLINICAL SIGNIFICANCE OF THE EUSTACHIAN TUBE 105 ZeynepSenaCOŞAR&AynurEmineÇİÇEKCİBAŞI CHAPTER VIII. THE COCHLEA: ANATOMY, DEVELOPMENT, VARIABILITY AND CLINICAL IMPLICATIONS 123 RukiyeSOYAL CHAPTER IX. ANATOMICAL AND CLINICAL PERSPECTIVES ON THE EXTERNAL AUDITORY CANAL 139 SümeyraDOĞMUŞ CHAPTER X. ANATOMY AND CLINICAL SIGNIFICANCE OF THE MAJOR SALIVARY GLANDS 151 BurakŞEN&GülayAÇAR CHAPTER XI. MAXILLA AND CLINICAL ANATOMY 169 EnesPOLAT
DEVELOPMENTAL ANATOMY OF THE SKULL 7 forms the uncinate process (processus uncinatus). The second ethmoturbinal forms the middle nasal concha (concha nasalis media), the third forms the superior nasal concha (concha nasalis superior), and the fourth and fifth contribute to the structures of the supreme nasal concha (concha nasalis suprema). These structures are embryologically derived from the ethmoid bone (9). The maxilloturbinal fold, located just beneath the ethmoturbinals, gives rise to the inferior nasal concha; however, this structure is not of ethmoidal origin. The grooves between the ethmoturbinal folds form the meatuses of the nose (meatus nasi) and their associated recesses. The superior extension of the groove between the first and second ethmoturbinals develops into the frontal recess (recessus frontalis), while its inferior extension gives rise to the ethmoidal infundibulum (infundibulum ethmoidale), the semilunar hiatus (hiatus semilunaris), and the middle nasal meatus (meatus nasi medius). The second groove forms the superior meatus (meatus nasi superior), and the third groove develops into the supreme meatus (meatus nasi suprema) (10, 11). The primordial maxillary and the anterior ethmoidal cells begin to develop from the ethmoidal infundibulum at approximately the 16th week of intrauterine life. At birth, the maxillary sinus has a volume of about 6–8 cm³. The sinus enlarges rapidly during the first three years, grows at a slower rate between 3 and 7 years, and then accelerates again between 7 and 12 years until it reaches its adult size. The ethmoidal sinus (sinus ethmoidalis) expands through the pneumatization of adjacent bones. Newly formed air spaces in this region are named after the bones into which they extend. When ethmoidal air cells extend into the frontal bone, the frontal sinus (sinus frontalis) develops. This structure is rarely observed before the age of 2. The development of the frontal sinus is usually completed at 16–18 years in males and 12–14 years in females (10,11).
8 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY Tablo 2.1. Embryological features of paranasal sinus development Sinus / Structure Onset (Intrauterine / Postnatal) Developmental Process Completion / Key Notes Ethmoturbinal structures 7th–8th week (intrauterine) Formation of 5–6 ethmoturbinal folds along the lateral nasal wall; the first four contribute to the development of the ethmoid bone . 1st ethmoturbinal: agger nasi cells and uncinate process; 2nd: middle nasal concha; 3rd: superior nasal concha; 4th–5th: supreme nasal concha. Maksilloturbinal 7th–8th week (intrauterine) Develops beneath the ethmoturbinals; forms the inferior nasal concha , but is not of ethmoidal origin. Contributes to the formation of meatuses and recesses. Maxillary sinus 16th week (intrauterine) Develops from the ethmoidal infundibulum; volume at birth ~6–8 cm³. Rapid growth during the first 3 years; slower growth between 3–7 years; accelerated growth between 7–12 years until adult size is reached. Ethmoidal sinus Late fetal period Expands through pneumatization of surrounding bones; newly formed air cells are named after the bones into which they extend. Extension into the frontal bone gives rise to the frontal sinus. Frontal sinus Rarely before 2 years Forms through pneumatization of the frontal bone by ethmoidal air cells. Development usually completed at 16–18 years in males and 12–14 years in females. Sphenoidal sinus 3rd month (fetal) Nasal mucosa migrates to the posterior nasal capsule; the cartilaginous recess → ossiculum Bertini → fuses with the body of the sphenoid to form the cavity. No significant growth until age 3; pneumatization begins thereafter, reaching the pterygoid canal (canalis nervi pterygoidei) by 6–7 years. In advanced pneumatization, the anterior clinoid process (processus clinoideus anterior) and the pterygoid process (processus pterygoideus) may also be pneumatized. Note: The timings and developmental processes of embryological growth are compiled from the literature (Bolger, 2001; Scuderi et al., 1993).
DEVELOPMENTAL ANATOMY OF THE SKULL 9 Unlike other paranasal sinuses, the sphenoidal sinus follows a distinct developmental course. At the 3rd month of fetal life, the nasal mucosa shifts toward the posterior portion of the nasal capsule. As a result, a structure known as the “cartilaginous recess” forms within the nasal cavity. The bony structure surrounding this cartilage gradually develops into what is called the ossiculum Bertini. Around the age of 3, the intervening cartilaginous tissue disappears, and the ossiculum Bertini attaches to the body of the sphenoid, thereby transforming the cavity into the sphenoidal sinus (10). The sphenoidal sinus does not show significant enlargement before the age of 3. Pneumatization begins thereafter, progressing posteriorly, laterally, and inferiorly. By approximately 6–7 years of age, the expansion of the sphenoidal sinus reaches the pterygoid canal. If pneumatization continues, the anterior clinoid process and the pterygoid process may also become pneumatized (10,11). 3. Anatomy of the Paranasal Sinus Bones 3.1.AnatomyoftheFrontalBone The frontal bone consists of three main parts: the squamous part (squama frontalis), the orbital part (pars orbitalis), and the nasal part. The squamous part is the largest and widest portion of the frontal bone; its anterior surface is convex, whereas its posterior surface is concave. This region forms the forehead and the superior portion of the orbits. On the anterior surface of the squamous part, on both sides of the midline, lie rounded prominences called the frontal tuberosities (tuber frontale). Below these, the curved structures where the eyebrows are located are known as the superciliary arches (arcus superciliaris). The flat area between the superciliary arches is called the glabella, and the eyebrows lie just anterior to this structure (6). The inferior border of the superciliary arch forms the supraorbital margin, a sharp edge that constitutes the superior boundary of the orbit. Laterally, this margin projects as the zygomatic process (processus zygomaticus), which plays an important role in protecting the eye. Along the supraorbital margin, two important foramina or notches may be present: the frontal notch (incisura frontalis) medially and the supraorbital notch (incisura supraorbitalis) laterally. These structures serve as passageways for vessels and nerves, such as the frontal nerve (nervus frontalis) and the supraorbital nerve (nervus supraorbitalis) (7). The orbital part forms the floor of the orbits and has a direct relationship with the orbital cavity. The nasal part supports the nasal bridge and associated
10 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY structures. Together, these three parts define the distinct structural and functional features of the frontal bone. The zygomatic process located laterally on the squamous part forms the articulation between the frontal bone and the zygomatic bone. This articulation contributes to the lateral walls of the facial skeleton. The posterior margin of the zygomatic process creates a ridge known as the temporal line (linea temporalis), which continues to join the parietal bone, thereby delineating the boundaries of the temporal region (1, 12). The nasal part is a small region located at the inferior midline of the squamous part. Within this part, a notch articulates with the nasal bone, the frontal process of the maxilla (processus frontalis maxillae), and the lacrimal bone. The midpoint of this junction is termed the nasion. From the margin of the nasal part that articulates with the nasal bone, a downward projection called the nasal spine extends. The nasal spine joins with the nasal crest (crista nasalis) and the perpendicular plate of the ethmoid bone (lamina perpendicularis ossis ethmoidalis), contributing to the structure of the nasal septum (12). The internal surface of the squamous part (facies interna) is concave, and along the midline lies a groove known as the groove for the superior sagittal sinus (sulcus sinus sagittalis superioris). This groove narrows inferiorly to form the frontal crest (crista frontalis), which terminates inferiorly at the foramen cecum (foramen caecum). The foramen is sometimes a blind recess and only rarely an open passage, in which case it may transmit the emissary vein (vena emissaria). On either side of the groove for the superior sagittal sinus, small depressions termed granular foveolae are observed, representing impressions made by the arachnoid granulations (12). The orbital part consists of two thin and flat bony plates that contribute to the formation of the orbital roof. Between these plates lies the ethmoidal notch (incisura ethmoidalis), a U-shaped indentation that opens posteriorly. Along the margins of this notch are small pits called ethmoidal pits , which are connected to the ethmoidal air cells. On the external surface of the orbital part is the lacrimal fossa (fossa glandulae lacrimalis), which houses the lacrimal gland, and the trochlear fovea (fovea trochlearis), which serves as the attachment site for the cartilaginous trochlea (cartilago trochlearis). On the internal surface are the cerebral impressions (impressiones gyrorum), which accommodate the gyri of the brain, and the cerebral ridges (juga cerebralia), corresponding to the sulci of the brain (12). The ethmoidal notch articulates with the cribriform plate (lamina cribrosa) of the ethmoid bone . Along the margins of this notch are small pits known as the ethmoidal fossae (foveolae ethmoidales). Similar pits are also present on the ethmoid bone itself. In the cranial skeleton, these pits are positioned opposite
DEVELOPMENTAL ANATOMY OF THE SKULL 11 each other, forming the ethmoidal air cells. Furthermore, grooves extending transversely along this border unite with corresponding grooves on the ethmoid bone, creating foramina that transmit vessels and nerves. These foramina are referred to as the anterior and posterior ethmoidal foramina (foramen ethmoidale anterius and foramen ethmoidale posterius), which establish communication between the nasal cavity and the orbit (12). At the anterior end of the ethmoidal notch and on either side of the nasal spine lie openings called the frontal sinus apertures (apertura sinus frontalis). Through these apertures, the frontal sinus is accessed. The sinus is typically divided into two chambers by a septum known as the septum of the frontal sinuses (septum sinuum frontalium), which usually deviates slightly to one side. The air-filled frontal sinus is lined with mucosa and drains into the middle nasal meatus via the nasofrontal canal (canalis nasofrontalis). In male individuals, the frontal sinus is generally larger, and the superciliary arches in the anterior region are more prominently developed (12). The thick and serrated posterior border of the squamous part is called the parietal margin (margo parietalis). This margin articulates with the parietal bones (ossa parietalia) to form the coronal suture (sutura coronalis). The portion of the parietal margin close to the zygomatic process articulates with the sphenoid bone and is therefore termed the sphenoidal margin (margo sphenoidalis) (1). 3.2.AnatomyoftheSphenoidBone The sphenoid bone is located in the cranial base (basis cranii), positioned between the anterior portions of the temporal bones (ossa temporalia) bilaterally and the basilar part of the occipital bone (pars basilaris ossis occipitalis). This bone consists of a central body, paired pterygoid processes extending inferiorly, and the greater and lesser wings, which project laterally (1). The sphenoidal sinus lies within the body of the sphenoid bone and is divided into chambers by one or more septa known as the sphenoidal septa (septum sinuum sphenoidalium). On the anterior surface of the body are the openings of the sphenoidal sinus (apertura sinus sphenoidalis). At the midline of the anterior portion of the corpus, a vertical ridge extending inferiorly is called the sphenoidal crest (crista sphenoidalis), whereas posteriorly there is the sphenoidal rostrum (rostrum sphenoidale), which articulates with the superior margin of the vomer (12). On the superior surface of the corpus, the flat area between the lesser wings is termed the jugum sphenoidale. Projecting anteriorly from the jugum is the ethmoidal spine (spina ethmoidalis). Posterior to this lies the prechiasmatic
12 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY sulcus (sulcus prechiasmaticus), a transverse groove uniting with the optic canals (canales optici). The sella turcica occupies the central upper surface of the body as a saddle-shaped depression formed between two prominences. Its anterior part is the tuberculum sellae, its posterior part the dorsum sellae, and between them lies the hypophyseal fossa (fossa hypophysialis), which houses the pituitary gland (glandula hypophysialis). Lateral projections from the tuberculum sellae are termed the middle clinoid processes (processus clinoidei medii), while those on the dorsum sellae are called the posterior clinoid processes (processus clinoidei posteriores) (12). On the posterior superior surface of the corpus is the clivus, a sloping surface that articulates with the occipital bone. The orbital plate of the frontal bone articulates with the anterior border of the lesser wing. The posterior border of the lesser wing contributes to the formation of the superior orbital fissure (fissura orbitalis superior). The posterior extremities of both lesser wings project as the anterior clinoid processes. Inferomedial to the anterior clinoid process lies the carotid sulcus (sulcus caroticus), whose lateral boundary is marked by the sphenoidal lingula (1). The greater wing consists of four distinct surfaces: the cerebral surface (facies cerebralis), the temporal surface (facies temporalis), the maxillary surface (facies maxillaris), and the orbital surface (facies orbitalis). In addition, it has four borders: the zygomatic border (margo zygomaticus), the frontal border (margo frontalis), the parietal border, and the squamous border (margo squamosus) (12) The cerebral surface, which is the internal surface, is in contact with the gyri of the brain and contributes to the boundaries of the superior orbital fissure (fissura orbitalis süperior). The squamous border articulates with the squamous part of the temporal bone (pars squamosa ossis temporalis). Posterior to the superior orbital fissure lies the foramen rotundum. Further posteriorly is the foramen ovale, an oval-shaped opening through which the emissary vein, accessory meningeal artery (arteria meningea accessoria), mandibular nerve (nervus mandibularis), and occasionally the lesser petrosal nerve (nervus petrosus minor) pass. Medial to the foramen ovale, the foramen venosum may sometimes be observed, while posterolateral to it is the foramen spinosum, which transmits the middle meningeal artery (arteria meningea media) (12). The orbital surface, which forms part of the posterior and lateral wall of the orbit, contributes to the formation of the superior orbital fissure medially
DEVELOPMENTAL ANATOMY OF THE SKULL 13 and, together with the maxilla, to the inferior orbital fissure (fissura orbitalis inferior) inferiorly (1). From the inferior aspect of the sphenoid body, the pterygoid processes project downward bilaterally. Each pterygoid process consists of two thin plates: the medial plate and the lateral plate. The notch between these two laminae is known as the pterygoid notch (incisura pterygoidea). Passing through the pterygoid process to the pterygopalatine fossa (fossa pterygopalatina) is the pterygoid canal. Furthermore, the pterygopalatine groove (sulcus pterygopalatinus) on the anterior surface of the pterygoid process joins with the groove of the same name on the palatine bone to form the greater palatine canal (canalis palatinus major) (1). At the inferoposterior end of the medial plate lies a posterolateral projection called the pterygoid hamulus. On its medial side is a groove known as the groove of the hamulus (sulcus hamuli pterygoidei). The leaf-like vaginal process (processus vaginalis) articulates with the ala of the vomer (ala vomeris) and the sphenoidal process of the palatine bone (processus sphenoidalis ossis palatini). The grooves in this region, together with the palatine bone and vomer, form the palatovaginal canal (canalis palatovaginalis) and the vomerovaginal canal (canalis vomerovaginalis) (1). 3.3.AnatomyoftheEthmoidBone The ethmoid bone is a structure composed predominantly of thin bony lamellae. It forms the superior and posterior regions of the nasal cavity as well as part of the anterior cranial base. Superiorly, it is situated within the ethmoidal notch of the frontal bone . Structurally, the ethmoid bone consists of four main parts: the cribriform plate, the perpendicular plate, and the paired ethmoidal labyrinths (labyrinthi ethmoidales) (12). The cribriform plate, which covers the ethmoidal notch, contains numerous small foramina known as the cribriform foramina (foramina cribrosa) through which the fibers of the olfactory nerve (nervus olfactorius) pass. The crista galli projects upward from the anterosuperior portion and terminates laterally in the alae of the crista galli (alae cristae galli) (12). Inferior to the cribriform plate lies the perpendicular plate, which forms the superior and posterior portions of the nasal septum. It articulates inferiorly with the vomer and anteroinferiorly with the septal cartilage (cartilago septi nasi). This structure may exhibit deviations that vary between individuals. Along the
14 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY superior portions of its lateral walls, shallow grooves corresponding to branches of the olfactory nerve may be observed (1). On either side, the ethmoidal labyrinths represent characteristic components of the ethmoid bone . On the lateral surface of this complex bony mass lies a smooth plate known as the orbital plate, which contributes to the medial wall of the orbit. Medial to the orbital plate are the anterior, middle, and posterior ethmoidal air cells, which are air-filled and lined with mucosa. Some posterior ethmoidal cells may extend toward the lateral wall of the sphenoidal sinus, where they are referred to as Onodi cells (cellulae Onodi). At the junction with the frontal bone , the anterior ethmoidal foramen and the posterior ethmoidal foramen open into the orbit (1). On the medial surface of the ethmoidal labyrinth are curved bony projections known as the middle nasal concha and the superior nasal concha. Occasionally, a second superior nasal concha, termed the supreme nasal concha, may be observed in the upper posterior region. The superior nasal concha is usually directed posteriorly and is the smallest of the conchae; it can therefore be identified only when viewed from the posterior aspect of the nasal cavity. The middle nasal concha is more prominent, articulating anteriorly with the maxilla and posteriorly with the perpendicular plate of the palatine bone (lamina perpendicularis ossis palatini). Within the nasal cavity, the superior borders of the conchae attach to the lateral wall, whereas their inferior borders project freely into the cavity. Immediately below the superior nasal concha lies the superior nasal meatus, and beneath the middle nasal concha lies the middle nasal meatus (12). When the middle nasal concha is lifted upward, a prominent bulging structure on the lateral nasal wall, the ethmoidal bulla (bulla ethmoidalis), becomes visible. From the anteroinferior aspect of this structure extends a curved bony projection directed posteriorly and inferiorly, known as the uncinate process (Figure 3.3.3). In cadaveric or in vivo examinations, the funnel-shaped depression located between the uncinate process and the ethmoidal bulla is identified as the ethmoidal infundibulum. Into this anatomical structure open the frontal sinus, the maxillary sinus, and the anterior ethmoidal cells. The ethmoidal infundibulum is connected to the middle nasal meatus via a narrow slit-like passage termed the hiatus semilunaris. The middle nasal meatus is one of the principal drainage pathways, receiving the openings of the frontal sinus, the anterior and middle ethmoidal cells, and the maxillary sinus. In addition, the blind recess situated between the superior nasal concha and the sphenoid body is known as the sphenoethmoidal recess (recessus sphenoethmoidalis) (1).
DEVELOPMENTAL ANATOMY OF THE SKULL 15 4. Paranasal Sinuses The paranasal sinuses are paired, air-filled cavities that develop during the embryonic period through the invagination of the nasal mucosa into the adjacent bony structures. Their inner surface is lined with ciliated respiratory epithelium, continuous with that of the nasal mucosa. In newborns, the sinuses are not yet fully developed and usually contain fluid; they gradually become air-filled with age and typically complete their maturation after puberty (1). The anatomy of the paranasal sinuses is among the most variable regions in the human body. These variations may differ markedly across ethnic groups, between sexes, and even between the right and left sides of the same individual (13). The sinuses communicate with the nasal cavity through various ostia located in the lateral nasal wall, thereby allowing aeration (12, 14). In humans, there are four paired major paranasal sinuses: the ethmoidal sinüs consisting of anterior, middle, and posterior groups; the sphenoidal sinus; the frontal sinus; and the maxillary sinüs. Although their size and shape vary among individuals, the total volume of these cavities is generally considered to be approximately 80 cm³ (1). In addition, less common accessory sinus formations are present. Examples include the interfrontal sinus (sinus interfrontalis) and small nasal cells located in the frontal and ethmoidal regions. Clinically important anatomical variants of the ethmoidal sinuses include the agger nasi cell (cellula aggeri nasi), Haller’s cell (cellulae ethmoidales infraorbitales), and the Onodi cell (cellula ethmoidalis posterior extending toward the sphenoidal sinus). Such accessory structures should be carefully considered during procedures like endoscopic sinus surgery, as these anatomical variations may increase the risk of infection and lead to complications during surgical interventions (12). 4.1.EthmoidalSinus The ethmoidal air cells develop as invaginations of the nasal cavity (cavitas nasalis) that extend posteriorly, and this process is completed by early adolescence, when the sinus reaches adult size (15). The average length of the ethmoidal sinus ranges between 4 and 5 cm, while its height is typically around 2.5–3 cm (16). In newborns, only a limited number of aerated cells are present, whereas in adults the number frequently exceeds 15 (17). The cellulae ethmoidales that constitute the ES are classified into three major groups: anterior cells (cellulae anteriores), middle cells (cellulae mediae), and posterior cells (cellulae posteriores). The anterior and middle ethmoidal
16 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY cells usually open into the middle nasal meatus, while the posterior ethmoidal cells may open into the superior nasal meatus, the sphenoethmoidal recess, or directly into the nasal cavity (cavitas nasi) (18, 1, 15). Due to its complex anatomical structure, the ES is also referred to as the ethmoidal labyrinth (17). The basal lamella separates the anterior and posterior ethmoidal cells. Within the labyrinth, the number of anterior cells (3–7) generally exceeds that of the posterior cells (2–4), although the latter are larger in volume (19). The most posteriorly located ethmoidal cells are of considerable anatomical and clinical importance due to their close relationship with the optic nerve. This association was first described by Adolf Onodi in 1903, and these cells have since been termed Onodi cells in the literature (1). Found in approximately 8–14% of cases, they are significant because of their relationship with the optic nerve and the internal carotid artery (arteria carotis interna). The presence of an Onodi cell markedly increases the risk of optic nerve injury, particularly during endoscopic sinus surgery (15, 20, 1). Anatomical variability among these cells is substantial. Among the anterior ethmoidal cells, the largest and most prominent is the ethmoidal bulla, which lies deep and superolateral to the middle nasal concha (21). The size of the ethmoidal bulla varies among individuals: it may be larger or smaller than normal, and in rare cases, it may be absent. Enlargement of the ethmoidal bulla can influence the course of the anterior ethmoidal artery (arteria ethmoidalis anterior) and may also narrow the ostium of the maxillary sinus, thereby leading to functional obstruction (Alsaied, 2017). Superiorly, the ethmoidal bulla communicates with the middle nasal meatus via its opening (21). The blood supply of the ES is provided by the sphenopalatine artery (arteria sphenopalatina), the anterior ethmoidal artery, and posterior branches, while its neural innervation is derived from the anterior and posterior ethmoidal nerves (nn. ethmoidales anterior et posterior) and the pterygopalatine ganglion (ganglion pterygopalatinum) (1). 4.1.1.AnatomicalVariantsoftheEthmoidalAirCells Agger Nasi Cell The agger nasi cell (cellula aggeri nasi) is the most anterior and often one of the largest ethmoidal air cells. It is located in the frontal recess region, adjacent to the anterior wall of the frontal sinus. Anatomically, it constitutes an important component of the frontal recess and frontal sinus drainage pathway. Positioned just anterior to the uncinate process, the agger nasi cell can partially or completely influence frontal sinus drainage depending on its size (22).
DEVELOPMENTAL ANATOMY OF THE SKULL 23 28. Cakur B, Sümbüllü MA, Yılmaz AB. A retrospective analysis of sphenoid sinus hypoplasia and agenesis using dental volumetric CT in Turkish individuals. Diagn Interv Radiol. 2011;17(3). 29. Fujii K, Chambers SM, Rhoton AL Jr. Neurovascular relationships of the sphenoid sinus: a microsurgical study. J Neurosurg. 1979 Jan;50(1). 30. Meloni F, Mini R, Rovasio S, Stomeo F, Teatini GP. Anatomic variations of surgical importance in ethmoid labyrinth and sphenoid sinus: a study of radiological anatomy. Surg Radiol Anat. 1992;14(1). 31. Kazkayası M, Karadeniz Y, Arıkan OK. Anatomic variations of the sphenoid sinus on computed tomography. Rhinology. 2005;43(2). 32. Unal B, Bademci G, Bilgili YK, Batay F, Avci E. Risky anatomic variations of sphenoid sinus for surgery. Surg Radiol Anat. 2006;28(2). 33. DeLano MC, Fun FY, Zinreich SJ. Relationship of the optic nerve to the posterior paranasal sinuses: a CT anatomic study. AJNR Am J Neuroradiol. 1996;17. 34. Evans JJ, Kenning TJ. Endoscopic and keyhole cranial base surgery. Cham: Springer; 2019. 35. Earwaker J. Anatomic variants in sinonasal CT. Radiographics. 1993 Mar;13(2). 36. Lee WT, Kuhn FA, Citardi MJ. 3D computed tomographic analysis of frontal recess anatomy in patients without frontal sinusitis. Otolaryngol Head Neck Surg. 2004 Sep;131(3). 37. Stammberger HR, Kennedy DW; Anatomic Terminology Group. Paranasal sinuses: anatomic terminology and nomenclature. Ann Otol Rhinol Laryngol Suppl. 1995;167:7-16
25 CHAPTER II LIGHT-REFRACTING STRUCTURES: CLINICAL ANATOMY OF THE OPTICAL MEDIA OF THE EYE MUHAMMED ERTUĞRUL ÖZBEY1 & AYNUR EMİNE ÇİÇEKCİBAŞI2 1(M.D.), Necmettin Erbakan University, Faculty of Medicine, Department of Anatomy, Konya/TÜRKİYE E-mail: [email protected] ORCID: 0009-0004-0162-2351 2(M.D. Prof.), Necmettin Erbakan University, Faculty of Medicine, Department of Anatomy, Konya/TÜRKİYE E-mail: aynur[email protected] ORCID: 0000-0002-1373-3065 1. Introduction The refraction of light within the eye’s optical media is essential for forming a clear image on the retina. The cornea, aqueous humor, lens, and vitreous humor each have distinct refractive indices, causing incoming light rays to bend according to Snell’s Law.
26 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY Figure 1. Illustration showing how light changes direction when passing between media of different refractive indices. The incident, refracted, and normal rays are depicted to demonstrate the relationship defined by Snell’s law, which governs the optical behavior of transparent structures in the eye. The cornea is the eye’s first and most powerful refractive surface, directing incoming light rays toward the lens. Following the cornea, the aqueous humor—a clear fluid located in the anterior chamber—contributes to the eye’s optic pathway with minimal additional refraction. The lens adjusts the direction of light rays by altering its shape to form a focused image on the retina; its refractive index varies dynamically with accommodation. Behind the lens, the vitreous humor—a gel-like substance—fills the space between the retina and the lens, sharing a refractive index similar to that of the aqueous humor, which produces minimal light deviation. Covering the corneal surface, the tear film provides a smooth refractive interface and maintains transparency. These varying refractive indices of the ocular media allow light to bend appropriately, resulting in a sharp retinal image. The resulting inverted image on the retina is detected by photoreceptors—rod and cone cells—whose photochemical signals are transmitted through the optic nerve to the cerebral cortex, where perceptual processes reconstruct the visual scene (1).
LIGHT-REFRACTING STRUCTURES: CLINICAL ANATOMY OF THEOPTICAL . . . 27 Figure 2. Anatomical illustration of the optical media responsible for light refraction within the eye, including the cornea, aqueous humor, lens, and vitreous body. These structures collectively maintain the precise focusing of incoming light onto the retina, ensuring visual clarity and optical integrity. The eye’s optical media play a critical role in both surgical and diagnostic procedures within the head and neck region. Optical imaging techniques—such as optical coherence tomography, confocal microscopy, and fluorescence imaging— enable rapid, non-invasive assessment of tissue morphology and early detection of lesions (2). Furthermore, understanding the anatomical properties of these media provides essential guidance for surgical planning, helping surgeons identify critical structures, optimize surgical margins, and perform more precise interventions. 2. Embryology of the Eye Eye embryology is a highly coordinated and intricate process that influences both head and neck morphology and visual function. The eye develops through interactions with the neuroectoderm, surface ectoderm, and periocular mesenchyme, which are derived from neural crest and mesodermal cells. The eye field is initially located on the anterior neural plate; it is then guided by transcription factors and signaling pathways toward lens induction, optic vesicle formation, and the subsequent development of the optic cup. The inner and outer layers of the optic cup differentiate into the neural retina and retinal pigment epithelium, whereas the lens vesicle detaches from the surface ectoderm to form lens fibers and the capsule. During these stages, processes such as embryonic fissure closure, development of the hyaloid vascular system,
28 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY and the formation of the corneal epithelium and stroma ensure the transparency and refractive integrity of the optical media. Errors at any point in this sequence can lead to congenital anomalies—including coloboma, aniridia, and microphthalmia—that compromise ocular form and function (3). Figure 3. Embryological development of the eye. Developmental stages from the optic vesicle to the mature lens, showing the formation and regression of the hyaloid artery and the development of the pupillary membrane. 3. Histology and Physiology of the Optical Media of the Eye The cornea, aqueous humor, lens, and vitreous humor possess specialized histological features that preserve transparency and ensure proper optical function (2). A clear understanding of the microscopic organization of these structures is essential for comprehending how they transmit and focus light while maintaining intraocular homeostasis. Table 1. Thicknesses and refractive indices of the eye’s light-refracting structures.
LIGHT-REFRACTING STRUCTURES: CLINICAL ANATOMY OF THEOPTICAL . . . 29 3.1.Cornea A transparent, avascular tissue located at the anterior and central surface of the eye, serving as the primary refractive structure that focuses incoming light onto the retina (2). The average central corneal thickness is 0.52–0.55 mm, increasing to approximately 0.65 mm at the periphery. This distribution helps maintain the optimal refractive power. The corneal diameter measures approximately 11–12 mm horizontally and 10–11 mm vertically (4-5). Histologically, it is composed of six distinct layers (6). Table 2. Thicknesses and refractive indices of the corneal layers. Epithelial Layer: A multilayered, non-keratinized squamous epithelium that provides a protective barrier against environmental irritants and contributes to the smoothness of the cornea. Bowman’s Membrane: A thin, acellular layer located beneath the epithelium, enhancing the mechanical strength and resilience. Stroma: The thickest corneal layer, composed predominantly of regularly arranged collagen fibers, which ensures transparency and primary light refraction of the cornea (4-5). Dua’s Layer: This layer was first described in 2013. As it is a recently identified structure, further research is needed to clarify its anatomical and functional significance fully. A thin, transparent, and mechanically robust preDescemet’s layer that is situated between the corneal stroma and Descemet’s membrane. It contributes to the structural integrity of the cornea and serves as an essential surgical landmark, providing a clear plane for precise dissection (6).
30 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY Descemet’s Membrane: A specialized basement membrane located between the stroma and endothelium, providing structural support. Endothelial Layer: A monolayer of cuboidal cells lining the posterior corneal surface, regulating stromal hydration to maintain transparency and optical clarity (4-5). At the cornea-sclera junction lies the limbus, a transitional zone rich in stem cells that supports epithelial regeneration and preserves optical integrity. Protecting the limbus is particularly important during surgery or trauma. The cornea-sclera interface also maintains stromal organization, ensuring both optical clarity and mechanical stability (4). Understanding corneal anatomy is essential for surgical planning, trauma management, and refractive procedures. Figure 4. Histological structure of the corneal layers. Microscopic illustration showing the detailed organization of the cornea, including the epithelium, Bowman’s layer, stroma, Dua’ layer, Descemet’s membrane, and endothelium. The anterior segment of the eye comprises the anterior and posterior chambers, which help refract light and maintain an optimal optical pathway between the cornea and the lens. The iris separates the anterior and posterior chambers, and both spaces are filled with aqueous humor. The anatomy of these chambers can vary with age, refractive errors, and pathological conditions, making a detailed biometric assessment crucial for surgical planning (2).
LIGHT-REFRACTING STRUCTURES: CLINICAL ANATOMY OF THEOPTICAL . . . 31 3.2.AqueousHumor A transparent, watery fluid in the anterior segment of the eye that occupies the space between the cornea and the lens, and contributes to optical clarity and physiological homeostasis. Histologically, it is composed predominantly of water (~98%), with small amounts of electrolytes, glucose, and amino acids (2). Figure 5. Anterior and posterior chambers of the eye. Illustration showing the anterior and posterior chambers separated solely by the pupil, highlighting their relative positions to the iris, lens, and cornea. Aqueous humor is continuously produced by the nonpigmented epithelial cells of the ciliary body at a rate of 2–3 µL/min. It flows from the posterior chamber through the pupil into the anterior chamber, helping regulate intraocular pressure. The majority of aqueous humor drains through the trabecular pathway into Schlemm’s canal, located at the anterior chamber angle. A smaller portion exits via the uveoscleral pathway, passing through the ciliary muscle and sclera into the extracellular spaces. Impaired production, circulation, or drainage of aqueous humor can lead to several ocular diseases (2). 3.3.Lens The lens is a transparent, biconvex structure situated between the posterior chamber and the vitreous body, playing a crucial role in focusing light onto the retina. Anatomically, it contains a central nucleus, a surrounding cortex, and a lens capsule. The anterior surface of the lens is convex, whereas the posterior surface is relatively flat.
32 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY The lens achieves transparency and precise refractive function through a highly organized cellular architecture. A monolayer of metabolically active epithelial cells lines the anterior surface of the lens, maintaining homeostasis and serving as a source of stem cells for the continuous production of new fiber cells. In the equatorial region, these epithelial cells differentiate into elongated, anucleate fiber cells, which progressively accumulate in the center of the lens to form the nucleus (3,7). The lens is suspended by zonular fibers, which connect peripherally to the lens capsule and are supported by the ciliary body. These fibers stabilize the lens and facilitate focusing. Accommodation depends on changes in zonular fiber tension. When the ciliary muscle contracts, the zonules relax, causing the lens to thicken and enabling near vision. Conversely, when the muscle relaxes, the zonules stretch, allowing the lens to flatten for distance vision. This dynamic lens structure adjusts optical power to maintain image clarity and plays an important role in the eye’s overall refractive system, working together with the structures of the anterior and posterior segments (2-3). Figure 6. Histological structure of the lens and ciliary body. Microscopic illustration showing the detailed organization of the lens, including the lens capsule, epithelium, and fiber arrangement, along with the ciliary body. This figure highlights the anatomical features involved in accommodation and the regulation of lens curvature.
LIGHT-REFRACTING STRUCTURES: CLINICAL ANATOMY OF THEOPTICAL . . . 39 polyangiitis and presents as stromal erosion with inflammation. In both conditions, early detection and prompt treatment with systemic or topical immunosuppressants are crucial to prevent irreversible stromal thinning and vision loss. Stromal scars and opacities commonly result from corneal trauma, chemical burns, or severe infections. They feature disruption of the organized collagen lamellae within the corneal stroma. This process also activates fibroblasts, causing a loss of corneal transparency and reduced visual acuity. Clinically, patients often report decreased vision and photophobia. Management depends on the scar’s depth and its effect on vision: superficial scars may be monitored or treated with laser-based procedures, while deeper stromal lesions might require lamellar or penetrating keratoplasty (2,4). 4.1.4.Descemet’sMembraneDiseases · Descemetocele (protrusion of Descemet’s cells in deep ulcers) · Posterior polymorphous dystrophy (PPMD) · Traumatic tears (Haab lines – in congenital glaucoma) Descemetocele is a severe corneal ulcer marked by the exposure of Descemet’s membrane. In this condition, most of the corneal epithelium and stroma are lost, leaving only Descemet’s membrane and the endothelium intact. Clinically, a thin, transparent area of the cornea is visible, and the risk of corneal perforation is extremely high. Management requires urgent intervention, usually with intensive topical antibiotics. When there is an imminent risk of perforation, surgical procedures such as penetrating keratoplasty or lamellar patch grafting are performed to restore corneal integrity. Posterior Polymorphic Dystrophy (PPMD) is a rare, usually inherited corneal disorder that primarily affects Descemet’s membrane and the corneal endothelium. Histopathologically, PPMD features endothelial cell polymorphism and focal thickening of Descemet’s membrane, which may lead to corneal edema, mild visual disturbances, or, in severe cases, significant vision loss. The condition is often asymptomatic and is found incidentally during routine eye exams. Diagnosis mainly relies on slit-lamp biomicroscopy, which reveals characteristic endothelial changes, with confirmation possible through specular or confocal microscopy of the endothelium. Treatment is mostly symptomatic, such as using hypertonic saline drops for mild edema. In advanced or visionthreatening situations, endothelial keratoplasty—like DSAEK or DMEK—may be needed.
40 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY Haab lines are thin, linear breaks in Descemet’s membrane, commonly seen in patients with congenital glaucoma. These breaks result from chronically elevated intraocular pressure (IOP) during neonatal or early childhood, causing the corneal stroma to stretch. Typically, these tears form a circular or arc-shaped pattern, mainly in the peripheral cornea, and usually do not directly affect visual acuity. Diagnosis is made through slit-lamp biomicroscopy, which shows the characteristic lines, and treatment mainly focuses on managing the underlying glaucoma (2,4). 4.1.5.EndothelialLayerDiseases · Fuchs endothelial dystrophy · CHED (Congenital hereditary endothelial dystrophy) · Iatrogenic endothelial insufficiency (post-surgery) · Endothelial keratitis (associated with HSV, CMV) · Endothelial cell loss due to intraocular surgery or trauma Fuchs endothelial dystrophy (FED) is a progressive disorder of the corneal endothelium that usually appears after middle age and often affects both eyes. The loss of endothelial cells causes corneal edema and stromal thickening, which leads to blurred vision and increased sensitivity to light. Clinically, the disease is marked by the presence of focal endothelial excrescences, commonly known as guttae. A slit-lamp examination may show stromal edema and epithelial microcystic changes. Treatment varies based on how severe the disease is; early stages can be managed with hypertonic saline drops and efforts to reduce corneal hydration, while advanced cases often require endothelial keratoplasty, such as Descemet Membrane Endothelial Keratoplasty (DMEK) or Descemet Stripping Automated Endothelial Keratoplasty (DSAEK). Congenital Hereditary Endothelial Dystrophy (CHED) is a rare, congenital corneal dystrophy characterized by corneal edema caused by dysfunction of the corneal endothelial cells. It most commonly affects both eyes and is inherited in an autosomal recessive pattern. Clinically, CHED presents at birth or in early childhood with a diffusely cloudy cornea, photophobia, and decreased visual acuity. Diagnosis is mainly made through slit-lamp examination, which typically shows increased corneal thickness and thickening of the Descemet’s membrane. Treatment options are limited, and in cases of severe edema with significant vision loss, surgical procedures such as endothelial keratoplasty (DSEK or DMEK) may be necessary.
LIGHT-REFRACTING STRUCTURES: CLINICAL ANATOMY OF THEOPTICAL . . . 41 Iatrogenic endothelial insufficiency is usually caused by damage or dysfunction of corneal endothelial cells due to corneal or anterior segment surgery, such as cataract removal, corneal transplant, or trauma to the anterior segment. Patients may present with signs like corneal swelling, blurry vision, and opacities. Diagnosis is confirmed by evaluating endothelial cell density and shape using slit-lamp examination and specular microscopy. The severity of endothelial damage guides treatment: mild cases may improve with conservative options like hypertonic saline or anti-edema eye drops, whereas severe cases impacting vision often require endothelial keratoplasty, including Descemet Stripping Automated Endothelial Keratoplasty (DSAEK) or Descemet Membrane Endothelial Keratoplasty (DMEK). Endothelial keratitis is an inflammatory condition of the corneal endothelium, usually caused by a viral infection. Herpes Simplex Virus (HSV)-induced endothelial keratitis shows symptoms such as corneal edema, keratic precipitates, and mild nearby stromal inflammation, often following a previous epithelial HSV infection. Cytomegalovirus (CMV)-related endothelial keratitis is marked by ongoing inflammation in the anterior chamber and a gradual loss of endothelial cells, especially in immunocompetent people. Patients typically experience blurred vision, sensitivity to light, and corneal swelling. Diagnosis relies on clinical signs and is confirmed through PCR testing of the aqueous humor to identify the virus and direct treatment. Management includes topical and systemic antivirals for HSV, while CMV infections are treated with topical ganciclovir or systemic valganciclovir, based on how severe the disease is. Both intraocular surgical procedures and ocular trauma can cause direct or indirect loss of corneal endothelial cells. During procedures such as phacoemulsification, vitrectomy, or trabeculectomy, endothelial cell density may decrease due to mechanical trauma, ultrasound energy, and oxidative stress, which can potentially lead to corneal edema and blurred vision. Likewise, penetrating injuries or contusion-type trauma can damage the endothelial layer, resulting in long-term corneal decompensation. Clinical evaluation relies on specular microscopy to measure endothelial cell density and assess cellular morphology, including pleomorphism and polymegathism. Treatment options depend on the severity and may include topical hypertonic agents, postoperative edema control, or, in advanced cases, endothelial transplantation, such as Descemet’s Stripping Automated Endothelial Keratoplasty (DSAEK) or Descemet Membrane Endothelial Keratoplasty (DMEK) (2,4).
42 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY 4.1.6.DiseasesThatCanAffectAllCornealLayers Certain corneal diseases can involve all layers of the cornea rather than being limited to just one. In advanced bacterial, fungal, or viral keratitis, the infection often starts in the epithelium and can spread through the stroma to the endothelium, potentially causing severe vision loss. Chemical burns, especially those caused by alkali agents, can quickly damage the entire corneal thickness, leading to deep scarring and opacities. Advanced dystrophies and degenerations, like macular or granular dystrophy, mainly affect the stroma but may eventually involve all layers. Traumatic injuries and procedures can also weaken the full thickness of the cornea, depending on how severe and how they occur. Additionally, secondary keratopathy related to tear film problems, such as in dry eye syndrome or Sjögren’s syndrome, can affect both superficial and deeper corneal structures (2,4,9). 4.2.LensDiseases Among the ocular refractive components, the lens is unique in providing dynamic focusing, a function that depends on its transparency and flexibility. Therefore, pathological changes in its structure can cause optical aberrations and notable image distortion. Lens disorders include a wide range, from congenital anomalies and metabolic issues to degenerative, traumatic, and systemic diseases. Like the cornea, the lens can be anatomically divided into its capsule, epithelium, and fiber layers, a framework that improves understanding of structure–function relationships and their clinical implications (2). 4.2.1.Cataract Cataract is defined as a pathological loss of lens transparency and is the leading cause of reversible blindness worldwide. The condition results from protein aggregation—primarily involving crystallins—along with capsular changes and metabolic disturbances, which eventually cause opacification within the normally clear lens. Clinically, cataracts decrease visual acuity and impair contrast sensitivity, color discrimination, and glare resistance, significantly affecting daily activities like reading and night driving. Anatomically, the specific location of the opacity leads to different subtypes: nuclear cataracts, associated with central lens sclerosis and hardening; cortical cataracts, characterized by peripheral wedge-shaped opacities; and posterior subcapsular cataracts, which cause rapidly progressive central vision loss. Recognizing these patterns is vital
LIGHT-REFRACTING STRUCTURES: CLINICAL ANATOMY OF THEOPTICAL . . . 43 for determining the best timing for surgery and for customizing intraocular lens implantation. Although most cataracts are age-related degenerative processes, they can also result from congenital anomalies, metabolic diseases, ocular trauma, or secondary to systemic and ocular conditions. Therefore, cataract should not be viewed merely as an aging disease but as a condition with a wide range of clinical and etiological factors. · Age-Related (Senile) Cataract · Congenital Cataract · Secondary Cataract · Traumatic Cataract · Metabolic Cataract Age-related (senile) cataracts develop gradually due to degenerative changes in lens proteins and oxidative stress. They are classified as nuclear sclerosis, cortical, or posterior subcapsular, and typically cause slowly progressive blurred vision, reduced contrast sensitivity, and glare, especially at night. Congenital cataracts appear at birth or early childhood, often resulting from genetic mutations, metabolic disorders, or intrauterine infections. They may present with a white pupillary reflex and carry a risk of amblyopia. Opacities may affect the lens capsule and cortex. Secondary cataracts occur after trauma, uveitis, steroid therapy, or ocular surgery. Posterior subcapsular opacities along the visual axis can cause blurring and glare, along with fibrosis and cellular proliferation within the capsule. Traumatic cataracts result from direct or indirect eye injuries. Capsular disruption can produce irregular cortical opacities. Sudden vision loss, photophobia, and halos are common, and careful surgical planning is necessary due to zonular or capsular weakness. Metabolic cataracts are linked to systemic conditions such as diabetes or galactosemia. Abnormal glucose or galactose metabolism causes osmotic stress and protein aggregation in the lens, leading to refractive changes and image distortion. All cataract types are diagnosed through slit-lamp biomicroscopy to evaluate the location and density of opacities. Significant visual impairment is usually treated surgically, commonly with phacoemulsification or extracapsular lens extraction, followed by intraocular lens implantation, considering capsular integrity, zonular status, and any potential anterior segment abnormalities (2,7).
44 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY 4.2.2.Lensdislocation Lens dislocation refers to the abnormal movement of the crystalline lens from its normal position along the optical axis. It is classified as subluxation, indicating partial displacement, or luxation, indicating complete displacement. · Lens Subluxation · Lens Luxation · Genetic Syndromes Lens subluxation refers to a partial displacement of the lens, usually caused by zonular weakness or damage. This condition is common in Marfan syndrome, homocystinuria, and after ocular trauma. It may present with refractive errors, such as myopia, astigmatism, and halos. Lens luxation is the complete displacement of the lens and can occur in the anterior or posterior chamber. Posterior luxation results in displacement into the vitreous cavity, whereas anterior luxation often causes acute glaucoma and photophobia. Understanding the anatomy of the lens capsule and zonules is vital for surgical planning. The extent of zonular damage influences lens stability during intraocular lens (IOL) implantation. In partial subluxation, the lens can often be preserved or treated with specialized zonule-supported IOL techniques. In complete luxation, lens removal and appropriate IOL placement are typically necessary. A threedimensional understanding of lens and anterior segment anatomy is crucial for minimizing complications and enhancing refractive outcomes (2,7). Certain genetic syndromes compromise the integrity of the zonular fibers, leading to lens subluxation or luxation. · Marfan Syndrome: Fibrillin-1 mutations weaken zonules, typically causing superior-temporal lens subluxation. Visual impairment and refractive changes may appear early in life. · Weill-Marchesani Syndrome: Zonules are short and thick, often resulting in inferior lens subluxation due to microspherophakia. Patients usually have short stature and short limbs. · Ehlers-Danlos Syndrome: Collagen abnormalities decrease zonular elasticity, contributing to lens instability. Recognizing these genetic contexts is essential for surgical planning. Preoperative assessment should include evaluating lens stability, the extent and
LIGHT-REFRACTING STRUCTURES: CLINICAL ANATOMY OF THEOPTICAL . . . 45 direction of zonular weakness, and potential vitreous complications. Combining anatomical findings with the patient’s clinical phenotype helps determine the surgical approach and minimizes the risk of intraoperative issues (2,7,10). 4.2.3.Presbyopia Presbyopia is an age-related functional disorder of the optical system, characterized by a gradual decline in the lens’s ability to accommodate for near vision. With aging, lens elasticity decreases, and the coordination between the ciliary muscle and zonules weakens, resulting in difficulty focusing on close objects. The lens becomes stiffer and slightly thicker over time, which limits dynamic changes in anterior and posterior curvature. These structural changes reduce transverse and anterior-posterior shape adjustments, decreasing accommodative capacity. Patients typically present with blurred near vision, eye strain, and difficulty reading. Symptoms often become noticeable in the early to mid-40s. Surgical or optical correction considers lens status, anterior segment measurements, and pupil dynamics. Advanced surgical options include multifocal or accommodative intraocular lenses, which aim to restore both near and distance vision by compensating for the loss of lens elasticity. Understanding these changes is crucial for effective treatment planning (2,7). 4.2.4.LensImmunologyandInflammation The lens is transparent and avascular, features that usually make it immunologically “ignored.” While these traits enhance optical function, they also increase the eye’s risk of inflammatory reactions after trauma, surgery, or rare infections. The lens capsule, a semipermeable membrane around the fibers, acts both as a physical barrier and an immunological buffer. · Lens Infections · Lens Protein-Induced Immune Reactions Lens infections are typically bacterial, although fungal agents may rarely be involved. Disruption of the lens capsule permits pathogens to contact the vitreous and anterior chamber, triggering an intense inflammatory response. Early detection and treatment are vital for preserving vision and preventing postoperative complications. Exposure of lens proteins after luxation or capsular disruption can provoke significant immune responses. Clinically, this
46 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY appears as intraocular inflammation after phacoemulsification or, in rare cases, lens-induced uveitis (2,7). 4.2.5.LensMetabolismandItsRelationshipwithSystemicDisorders The lens maintains a very delicate metabolic balance to keep transparency and optical function. Since lens cells do not have blood vessels, nutrients and waste products are exchanged through passive and active transport via the aqueous humor. As a result, systemic metabolic problems can directly disturb lens stability, leading to protein denaturation, osmotic stress, and damage to lens fibers. In diabetes mellitus, high glucose levels in the lens cause sorbitol buildup and osmotic swelling, resulting in cortical cataracts. Similarly, inherited metabolic disorders like galactosemia can cause early lens clouding and congenital cataracts. This metabolic sensitivity makes the lens a window into systemic disease and is an important factor in surgical planning, affecting both cataract development and the risk of complications (2,7). 4.3.AqueousHumorDiseases Aqueous humor is a transparent fluid produced by the ciliary body and drained through the trabecular meshwork and Schlemm’s canal. It is essential for maintaining optical clarity, intraocular pressure, and the metabolic balance of the anterior segment. Disruptions in the balance between aqueous humor production and drainage can lead to changes in intraocular pressure, which are linked to various eye conditions. The most notable pathology is glaucoma, which can be primary, secondary, or congenital. Aqueous humor imbalance may also result from inflammation, trauma, iatrogenic factors, systemic diseases, or medications, all of which can threaten visual outcomes if not addressed promptly (2,7). For ophthalmologists, a thorough understanding of aqueous humor physiology and pathology is therefore crucial. Both medical and surgical treatments must be customized to target the specific cause of dysfunction, making the concept of aqueous humor fundamental to clinical ophthalmology. Glaucoma is a group of disorders in which the dynamics of aqueous humor and the biology of the optic nerve converge, making clinical anatomy central to both diagnosis and surgical decision-making. · Primary Glaucomas Open-Angle Glaucoma (POAG) Angle-Closure Glaucoma (PACG)
LIGHT-REFRACTING STRUCTURES: CLINICAL ANATOMY OF THEOPTICAL . . . 47 Congenital (Pediatric) Glaucoma · Secondary Glaucomas Uveitic Glaucoma Pigmentary Glaucoma Pseudoexfoliative Glaucoma Neovascular Glaucoma Traumatic Glaucoma · Aqueous Humor Production Disorders Hyposecretory / Hyposecretory Glaucoma Hypersecretory / Ciliary Adenoma · Non-Glaucomatous Trabecular Obstruction Inflammatory (post-uveitic trabeculitis) Hemorrhagic / Vascular Post-Surgical (pseudophakic or aphakic glaucoma) Rare Toxic / Drug-Induced Causes In POAG, the trabecular meshwork and Schlemm’s canal appear clinically open. However, microscopic changes—including the accumulation of extracellular matrix within the trabecular beams, endothelial dysfunction, and reduced permeability of the juxtacanalicular tissue—gradually limit aqueous drainage. This resistance, along with the pressure transmitted through the lamina cribrosa, impairs axoplasmic transport and ultimately causes the loss of retinal ganglion cells. PACG results from anatomical predispositions, such as a shallow anterior chamber, a thickened lens, or an anterior iris insertion. These factors promote pupillary block, where increasing posterior chamber pressure causes the iris to bow forward, obstructing the trabecular meshwork. Acute attacks present with severe ocular pain, corneal edema, and systemic symptoms, while chronic forms can lead to synechiae and permanent closure. Laser peripheral iridotomy or lens extraction relieves the block by removing the anatomical barrier 2,11). Congenital (pediatric) glaucoma results from developmental anomalies of the trabecular meshwork, which lead to impaired drainage of aqueous humor. During prenatal development, the anterior chamber angle normally matures in coordination with the trabecular meshwork, Schlemm’s canal, and ciliary body; incomplete development of these structures causes elevated intraocular pressure (IOP) and increased mechanical stress on the cornea and sclera. Clinically, distinctive signs include buphthalmos (enlarged eye), corneal edema, and
48 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY Haab’s striae. Developmental defects often affect the entire anterior chamber angle and may be associated with malformations of the iris or angle structures, as seen in the Axenfeld-Rieger complex. Surgical treatment aims to improve aqueous outflow through angle-opening procedures such as trabeculotomy or goniotomy. Careful evaluation of anterior chamber anatomy, corneal elasticity, and individual variations in the angle is therefore crucial. Early diagnosis and anatomically guided surgery are vital for achieving optimal IOP control and good visual outcomes (11). In secondary forms, the underlying pathology disrupting aqueous humor flow varies. Inflammatory cells and proteins may obstruct the trabecular meshwork in uveitis, pseudoexfoliative fibrils can accumulate in Schlemm’s canal, pigment granules shed from the iris may block flow in pigmentary glaucoma, and VEGF-driven fibrovascular membranes can seal off the angle in neovascular glaucoma. Traumatic angle recession and retained lens material after surgery can also increase intraocular pressure. Glaucoma is not simply a pressure disorder but a spectrum of conditions reflecting both static and dynamic relationships within the anterior segment, the trabecular meshwork microstructure, and the optic nerve head anatomy. The aim of surgical treatment is to restore normal aqueous outflow or to create alternative drainage routes. Hyposecretory glaucoma is a rare condition caused by functional or anatomical failure of the ciliary body, rather than the typical mechanisms of increased aqueous outflow resistance or overproduction. Causes include decreased metabolic activity of the ciliary epithelium, post-surgical damage, inflammatory atrophy, and advanced ocular trauma. Reduced aqueous humor production can impair optic nerve perfusion, even when intraocular pressure is low or normal. Patients often exhibit hypotonic signs such as corneal edema, a shallow anterior chamber, and choroidal folds, which may lead to maculopathy. Chronic ischemic changes in the optic nerve head can mimic glaucomatous optic neuropathy. Atrophy or scarring of the ciliary epithelium is a key feature. Histology reveals epithelial cell loss and stromal fibrosis. The main goal is to preserve ciliary function and control inflammation if present. Cycloplegics (agents that paralyze the ciliary muscle) and topical steroids may be helpful in some cases. In advanced disease, managing complications related to low aqueous pressure becomes critical. A thorough clinical and anatomical understanding guides surgical strategies aimed at preserving or supporting ciliary structures. Accurate assessment of the anatomical and functional state of the ciliary body is essential for effective management of hyposecretory glaucoma.
LIGHT-REFRACTING STRUCTURES: CLINICAL ANATOMY OF THEOPTICAL . . . 55 4. Krachmer JH, Mannis MJ, Holland EJ. Cornea. 3rd ed. 3 vols. Philadelphia: Elsevier Mosby; 2011. 5. Levin LA, Petersen S, editors. Adler’s physiology of the eye. 12th ed. Philadelphia: Elsevier; 2020. 6. Dua HS, Faraj LA, Said DG, Gray T, Lowe J. Human cornea has a sixth layer: Dua’s layer. Ophthalmology. 2013;120(9):1778-1785. 7. Kanski J, Bowling B. Clinical ophthalmology: a systematic approach. 8th ed. Philadelphia: Elsevier; 2015. 8. Charles S. Vitreous microsurgery. 5th ed. Philadelphia: Wolters Kluwer; 2018. 9. Ambati KR, Mannis MJ, Holland EJ. Ocular surface disease: cornea, conjunctiva and tear film. 1st ed. Philadelphia: Saunders/Elsevier; 2013. 10. Rimoin DL, Connor JM, Pyeritz RE, Korf BR, Emery AEH. Emery’s Elements of Medical Genetics. 14th ed. Philadelphia: Elsevier; 2022. 11. Ritch R, Shields MB, Krupin T, editors. The glaucomas. 2nd ed. St. Louis: Mosby; 1996. 12. Azar DT. Refractive surgery. 3rd ed. Philadelphia: Elsevier; 2019.
57 CHAPTER III FUNCTIONAL AND CLINICAL ANATOMY OF THE LACRIMAL APPARATUS Sümeyra DOĞMUŞ (PT, PhD. Can.), Necmettin Erbakan University, Faculty of Medicine, Department of Anatomy, Konya/Turkey E-mail: fzt.smyr[email protected] ORCID: 0009-0005-7673-1293 1. Introduction The structures involved in the secretion of tears and their transportation from the ocular surface to the inferior nasal meatus within the nasal cavity are collectively referred to as the lacrimal apparatus. The components of the lacrimal apparatus include the lacrimal gland, accessory lacrimal glands, excretory ductules, lacrimal puncta, lacrimal canaliculi, lacrimal sac, and nasolacrimal duct. (1) After being produced, tears travel along the edges of the eyelids and accumulate at the medial canthus. Through muscle contraction, blinking, and capillary action, they pass into the lacrimal puncta and then proceed into the lacrimal canaliculi. Subsequently, they pass through the lacrimal sac and the nasolacrimal duct, ultimately reaching the inferior nasal meatus. (1) 2. Historical Information About the Lacrimal Apparatus and Its Surgery Italian anatomist Giovanni Battista Morgagni (1682-1771), known as the father of anatomical pathology, was one of the first to describe the lacrimal drainage system. In his work Adversaria Anatomica Omnia, published in 1718, Morgagni stated that the lacrimal drainage system lacked valves and that the flow within it was bidirectional. German anatomist Johann Gottfried Zinn (1727-1759) was among the first to describe the complete anatomical course of the lacrimal drainage system. (2)
58 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY Lorenz Heister (1683-1758) was the first to classify disorders of the lacrimal system, while Percival Pott (1714-1788), an English surgeon and one of the founders of orthopedics, was the first to author texts on lacrimal system disorders. (2) Austrian ophthalmologist Joseph Hasner (1819-1892) elucidated the mechanical processes of tear drainage and developed surgical procedures for lacrimal fistulas. The plica lacrimalis at the most inferior part of the lacrimal drainage system is named Hasner’s valve. Modern dacryocystectomy (DCT) was first described by Rudolph Berlin in 1868. Berlin emphasized that DCT was the primary surgical intervention for untreatable epiphora and the best method for protecting against corneal abscess and cataracts. (2) The first endoscopic intranasal dacryocystorhinostomy (DCR) was performed on cadavers by Dale H. Rice in 1988, while Peter John Wormald introduced the mechanical and powered DCR technique in 2002. (3) Conjunctivodacryocystorhinostomy (CDCR) was first introduced by Von Hoffman in 1904 as a procedure involving the opening of the lacrimal sac and suturing it to the conjunctiva. (4) In 1965, Lester Jones refined the CDCR procedure by placing Jones tubes to alleviate upper lacrimal system obstructions. (5) 3. Embryology of the Lacrimal Apparatus At the beginning of the 5th week of the prenatal period, the medial and lateral nasal processes become visible, forming the nasal pit. By the end of the 6th week, the lateral nasal processes begins to fuse with the maxillary processes, giving rise to the nasolacrimal groove. (6) In Carnegie stage 16, part of the classification system used to describe specific periods of human embryonic development, epithelial cells within the nasolacrimal groove thicken, forming the nasolacrimal lamina, the primordium of the lacrimal system. By Carnegie stage 19, the nasolacrimal lamina separates from the surface ectoderm, initiating the formation of the lacrimal cord. The lateral portion of the lacrimal cord, close to the surface ectoderm, bifurcates to form the canaliculi. (7) By Carnegie stage 20, the nasal cartilages become prominent, and the lacrimal cord is located laterally to the nasal capsule. At Carnegie stage 22, the proximal portion of the lacrimal system has begun to differentiate, though a lumen has not yet formed. The mesenchymal tissue surrounding the canalicular primordium has condensed. By Carnegie stage 23, the morphology of the lacrimal system is well-developed, and the lateral portion of the lacrimal cord
FUNCTIONAL AND CLINICAL ANATOMY OF THE LACRIMAL APPARATUS 59 differentiates proximally into the upper and lower canaliculi and distally into the lacrimal sac. The medial portion of the lacrimal cord extends caudally and laterally towards the inferior meatal lamina. (8) The development of the lacrimal gland also begins at Carnegie stage 23, arising from solid epithelial buds in the superolateral conjunctival fornix, surrounded by mesenchymal condensation. The orbital lobe of the gland forms during the first two months, while the palpebral lobe develops later from secondary buds. (9) The lacrimal gland is ectodermal in origin and undergoes branching morphogenesis, similar to other exocrine glands, to reach functional maturity. (10) Postnatally, it continues to develop for 3-4 years. (9) Developmental abnormalities in this region often occur after the 4th month of gestation and may lead to agenesis of any part of the lacrimal drainage system, formation of supernumerary puncta lacrimalia, or lacrimal fistulas. (9) In most newborns, the distal end of the nasolacrimal duct is covered by a mucosal membrane that typically opens within a few weeks, enabling normal drainage. However, in about 4% of newborns, this membrane remains closed, causing obstruction. This obstruction can result in epiphora or, less commonly, dacryocystitis. (11) 4. Anatomy of the Lacrimal Apparatus The structures that make up the lacrimal apparatus include the lacrimal gland, accessory lacrimal glands (Krause and Wolfring glands), excretory ductules, lacrimal puncta, lacrimal canaliculi, lacrimal sac, and nasolacrimal duct. (1) The lacrimal gland and accessory lacrimal glands form the secretion system, while the other structures make up the drainage system. Tears produced by the lacrimal gland and accessory lacrimal glands are spread across the surface of the cornea and conjunctiva via the excretory ductules. The tears enter the lacrimal punctum, flow into the lacrimal canaliculus, and then move into the lacrimal sac, finally draining into the inferior meatus of the nasal cavity through the nasolacrimal duct. The lacrimal puncta and lacrimal canaliculus form the proximal part of the drainage system, with their lumen lined by multilayered cubic epithelium, while the lacrimal sac and nasolacrimal duct form the distal part of the drainage system, with their lumen lined by multilayered columnar epithelium. The primary function of the structures that make up the lacrimal apparatus is to maintain adequate moisture on the cornea and conjunctiva and to drain excess tears into the inferior meatus of the nasal cavity and the nasopharynx. (12)
60 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY 4.1.LacrimalGland The lacrimal gland is a tubuloacinar exocrine gland responsible for tear secretion, located in the superolateral aspect of the orbit, within the fossa for the lacrimal gland of the frontal bone. The gland is anatomically divided into two distinct parts by the tendon of the levator palpebrae superioris muscle and the Whitnall ligament. The larger, superior portion is referred to as the orbital part, while the smaller, inferior portion is termed the palpebral part. (12,13) The superior surface of the orbital part is attached to the periorbita, whereas its inferior surface is anchored to the tendon of the levator palpebrae superioris. The posterior aspect is related to the orbital fat. The superior surface of the palpebral part lies in contact with the levator palpebrae superioris muscle, while its inferior surface extends to the lateral half of the superior conjunctival fornix. (1) The lacrimal gland measures approximately 20 mm in length and 12 mm in width. The thickness of the orbital part is around 5 mm, whereas the palpebral part measures approximately 3 mm in thickness. Structurally, the gland consists of multiple lobules separated by loose connective tissue. (14) The lacrimal gland is composed of three distinct cell types: acinar cells, ductal cells, and myoepithelial cells. Acinar cells, which constitute approximately 80% of the glandular structure, form lumina that coalesce into excretory ducts lined by cuboidal ductal cells. Whereas salivary glands contain a large number of ductal cells, the lacrimal gland is characterized by a relatively sparse ductal cell population. The ducts are organized as intralobular and interlobular channels. (13) Acinar cells are primarily responsible for the synthesis of proteins such as lysozyme and lactoferrin. (15) Ductal cells, accounting for approximately 10-12% of the gland, function primarily to modify the primary fluid (tears) produced by the acinar cells by secreting additional electrolytes and water. Myoepithelial cells, exhibiting a characteristic stellate morphology, are situated between the acinar and ductal cells and the basal lamina. Among the exocrine glands, myoepithelial cells are found exclusively in the lacrimal gland, salivary glands, and mammary glands. (13) The neural regulation of lacrimal gland function exhibits a highly complex organization. The initial step in this regulatory process involves the activation of sensory nerves located within the cornea and conjunctiva. The second step entails the efferent activation of parasympathetic and sympathetic nerves, followed by the third step, which is the stimulation of acinar and ductal cells. The final step culminates in the secretion of proteins, electrolytes, and water. The cornea and conjunctiva are richly innervated with sensory nerve endings, and their activation
FUNCTIONAL AND CLINICAL ANATOMY OF THE LACRIMAL APPARATUS 61 leads to both fluid secretion from the lacrimal gland and vasodilation. The increased blood flow resulting from vasodilation further enhances secretory activity. The lacrimal gland is innervated by both the sympathetic and parasympathetic nervous systems; however, the parasympathetic system serves as the primary regulator of glandular secretion. Following stimulation of sympathetic and parasympathetic fibers, neurotransmitters are released to modulate glandular secretion. The primary parasympathetic neurotransmitters involved in this regulation are acetylcholine and vasoactive intestinal peptide (VIP), whereas the principal sympathetic neurotransmitter is norepinephrine. (13) The lacrimal gland receives innervation from the trigeminal nerve, the facial nerve, and the superior cervical ganglion of the sympathetic system. Sensory input from the gland is transmitted via the lacrimal nerve, a branch of the ophthalmic division of the trigeminal nerve. Parasympathetic secretomotor fibers originate from the lacrimal nucleus, located in the upper part of the superior salivatory nucleus within the pons, and travel through the intermediate nerve portion of the facial nerve. These fibers continue along the greater petrosal nerve, subsequently joining the deep petrosal nerve of the sympathetic system to form the nerve of the pterygoid canal (Vidian nerve). After synapsing in the pterygopalatine ganglion, postganglionic fibers establish a connection with the maxillary nerve via a communicating branch, continue into the zygomatic nerve, and then course within the zygomaticotemporal branch. Through another communicating branch, fibers join the lacrimal nerve of the ophthalmic division to ultimately reach the lacrimal gland and initiate secretion. (9,16) Sympathetic system activity generally decreases tear production but maintains the basal secretion necessary for ocular surface homeostasis. Sympathetic fibers arise from the superior cervical ganglion of the sympathetic trunk, travel along the internal carotid plexus, and reach the lacrimal gland. (12) One of the principal functions of the lacrimal gland is the synthesis of proteins that are secreted into the tear fluid. These proteins serve to protect the cornea and conjunctiva from bacterial invasion and contribute to the regulation of epithelial tissue functions. (15) Tear fluid is composed primarily of water, with small proportions of salts (~1%), proteins (~0.6%), and a very minor fraction of lipids (~0.1%). (12) The lacrimal gland receives its arterial supply from the lacrimal artery, a branch of the ophthalmic artery; the recurrent meningeal artery, a branch of the lacrimal artery; and the infraorbital artery, a branch of the maxillary artery. Venous drainage occurs via the superior ophthalmic vein, which subsequently empties into the cavernous sinus. (19)
62 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY 4.2.AccessoryLacrimalGlands The accessory lacrimal glands include the Krause and Wolfring glands. The Krause glands are small, numerous glands situated primarily in the superior conjunctival fornix, with additional glands in the inferior conjunctiva. In contrast, the Wolfring glands are fewer and are located along the superior tarsal border. (1) The Krause and Wolfring glands are structurally and histologically similar to the lacrimal gland, yet their innervation differs. Unlike the lacrimal gland, the accessory lacrimal glands do not receive parasympathetic innervation. Another distinction is that while the lacrimal gland produces reflex tears, the accessory lacrimal glands primarily secrete basal tears. (17) The rate of basal tear production is approximately 1 µl/min, with the majority of it evaporating. With age, basal secretion decreases, and elderly individuals may not exhibit symptoms even in cases of drainage system obstruction. (18) 4.3.ExcretoryDuctules These are small ducts, approximately 12 in number, that begin from the lacrimal gland. The orbital part of the gland contains 4-5 ducts, which converge with ducts from the palpebral part of the gland to drain tears into the lateral half of the superior conjunctival fornix. The 7-8 ducts located in the palpebral part open separately. Excess tears accumulate in the lacus lacrimalis and are reflexively moved to the punctum lacrimale due to the opening and closing of the eyelids. (1) 4.4.LacrimalPunctum The lacrimal puncta are located approximately 6 mm lateral to the medial canthus of the eye, one on the papilla lacrimalis of the upper and lower eyelids separately. Their diameter is approximately 0.2-0.3 mm. When the eyelids are open, the lower lacrimal punctum is seen 1 mm laterally from the upper lacrimal punctum, and when the eyelids are closed, the lacrimal puncta come into contact with each other and open into the lacrimal canaliculi. (12) Embryologically, the maxillary process develops faster than the lateral nasal process, causing the inferior lacrimal punctum to be located 0.5-3 mm more temporally than the superior lacrimal punçtum. (19) 4.5.LacrimalCanaliculi The superior lacrimal punctum gives rise to the superior lacrimal canaliculus, while the inferior lacrimal punctum gives rise to the inferior lacrimal canaliculus.
FUNCTIONAL AND CLINICAL ANATOMY OF THE LACRIMAL APPARATUS 63 The superior lacrimal canaliculus travels vertically for approximately 2 mm upwards, then changes direction medially and continues horizontally for about 6-10 mm. The superior lacrimal canaliculus is generally slightly shorter than the inferior canaliculus and progresses toward the lacrimal sac with an inclination of 25°-30°. The inferior lacrimal canaliculus travels downward for approximately 2 mm at an angle of 10°-15°, followed by another 6-10 mm horizontally. (12,20) The deep part of the orbicularis oculi muscle’s palpebral portion is known as the Horner’s muscle. The temporal 4/5 of the horizontal portion of the canaliculi is encircled by the Horner’s muscle, while the remaining 1/5 of the canaliculus turns posteriorly without contact with the muscle. Additionally, the temporal 4/5 portion of the horizontal canaliculus contains denser elastic fibers, while the nasal 1/5 contains fewer elastic fibers. This arrangement is significant in the lacrimal drainage pump system. The diameter of the canaliculi ranges from 0.3 to 0.6 mm and can expand up to 1 mm due to their elastic fiber structure. (19) The superior lacrimal canaliculus and inferior lacrimal canaliculus merge in 90% of cases to form a common canaliculus. In the remaining lower percentage of cases, each canaliculus continues separately. (11) If the canaliculi enter the lacrimal sac without forming a common canaliculus, they do so through one or two openings. If they form a common canaliculus, they enter the lacrimal sac through a small diverticulum on the lateral wall of the sac, known as the Maier sinus, and then progress within the lacrimal sac. (21) The Maier sinus is more prominent when the eyelids are closed. (19) The common canaliculus is approximately 3 mm in length and is more often a continuation of the inferior lacrimal canaliculus. All canaliculi are lined with stratified squamous epithelium and then transition into cylindrical epithelium as they continue. (20) When the eyelids close, the distal part of the canaliculi constricts due to the action of the orbicularis oculi muscle (referred to as the Horner’s muscle), exerting pressure on the tear fluid, a phenomenon known as the Venturi effect. When the eyelids open, the muscle relaxes, causing the canal lumen to widen, and the tears are absorbed. This is referred to as the Bernoulli effect. The inferior lacrimal canaliculus serves as the primary route for draining tears from the conjunctiva, with approximately 80-90% of the tear fluid being drained through this pathway. Even a minor dysfunction at this level of the lacrimal drainage system can lead to pathological tear flow. (12) 4.6.LacrimalSac The lacrimal sac is located in the fossa sacci lacrimalis, which is formed by the processus frontalis of the maxilla and the os lacrimale, and is situated in the
64 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY antero-medial part of the orbit. The anterior boundary of the fossa sacci lacrimalis is formed by the crista lacrimalis anterior (maxilla), while the posterior boundary is formed by the crista lacrimalis posterior (os lacrimale). In the center of the fossa is the sutura lacrimomaxillaris, the point of union between the maxilla and the os nasale. (1,19) The bone at this sutural site is thinner and can be easily perforated during surgical procedures. (19) The lacrimal sac is cone-shaped, and its lateral surface is covered by the fascia lacrimalis. This fascia is a continuation of the periorbita between the crista lacrimalis anterior and crista lacrimalis posterior. The posterior part of the lacrimal sac is covered by the fascia of the Horner muscle. The anterior portion of the external surface of the fascia lacrimalis is covered by the medial canthal tendon. (1,19) The anterior extension of this ligament lies in front of the lacrimal sac and terminates at the crista lacrimalis anterior. The posterior extension is located between the periorbita and the lacrimal sac, separating the two, and terminates at the crista lacrimalis posterior. (11) The lacrimal sac is lined with stratified cylindrical epithelium. (22) Unlike the lacrimal canaliculi, it expands when the eyelid is closed and contracts when the eyelid is open. The horizontal diameter of the lacrimal sac is 1-2 mm and can vary due to pressure effects. (23) Its diameter decreases towards the distal end, where it continues as the nasolacrimal duct. The length of the sac is approximately 12.5 mm. (12) The upper part of the lacrimal sac is referred to as the fundus. 4.7.NasolacrimalDuct The nasolacrimal duct is located within a bony channel formed by the maxilla, lacrimal bone, and inferior nasal concha. (1) The upper part of the duct is the intraosseous portion, which is approximately 12 mm long and 1 mm in diameter. The lower part is the membranous portion, also referred to as the intrameatal section. The intrameatal section is approximately 5 mm long and travels within the nasal mucosa, opening into the inferior nasal meatus. (21,24) At the opening site, there is a mucosal fold known as the Hasner valve. The nasolacrimal duct follows a postero-infero-lateral course along the lateral wall of the nasal cavity. The projection on the facial skeleton corresponds to the line extending from the medial corner of the eye to the second molar tooth. (12) Six morphological types of the upper part of the nasolacrimal duct, known as the lacrimal sulcus, have been described: 1)”S” shaped (11.3% occurrence frequency) 2) Boat-shaped (upper and lower parts narrower than the middle), observed in 1.6% of cases.
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75 CHAPTER IV ANATOMY AND CLINICAL SIGNIFICANCE OF THE INFERIOR ORBITAL FISSURE İrfan AKYILDIZ (PhD.Can.) Necmettin Erbakan University,Faculty of Medicine, Department of Anatomy, Konya/Turkey E-mail: [email protected] ORCID: 0000-0002-1756-2793 1. Introduction The orbit is essentially the bony cavity that houses the eye and its accessory structures. Located on both sides of the nose, the orbit is an important structure formed by the walls and surfaces created by the union of the bones in the facial skeleton. In addition to housing many neurovascular structures, the orbit is the attachment site for the muscles surrounding the eye. Furthermore, it protects the eye from external factors and provides the volume relationship necessary for coordinated movement between the eyes (1). Within the orbit, the optic canal, superior orbital fissure, inferior orbital fissure, and common tendinous ring are present, which allow the passage of neurovascular structures. At the same time, the supraorbital foramen, anterior ethmoidal foramen, posterior ethmoidal foramen, and zygomaticofacial foramen located around the orbit are structures through which blood vessels and nerves pass during their course (2). 2. Embryology of the Orbit During the fourth week of embryogenesis, the formation of the neural tube initiates a chain reaction, and bone tissue development begins after the fifth week. The basal plate, formed by the fusion of cartilaginous structures, joins with the periotric capsule to form the sphenooccipital region. This region is divided into two areas: the pars ethmoidalis and the pars orbitotemporalis. The ethmoid bone and inferior nasal concha develop from the ethmoid part, while
76 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY the sphenoid body, sella turcica, greater wing, and lesser wing develop from the orbitotemporal part (3). The bones forming the orbit develop from the mesoderm layer. The inner walls of the orbit develop from the lateral nasal process. At the same time, the frontal process of the maxilla, the nasal bone, the lacrimal bone, and parts of the ethmoid bone also originate from the lateral nasal process. Part of the sphenoid bone attaches to the skull base at the rear. The fissure between the orbital surface of the sphenoid bone and the presphenoid allows the optic nerve to pass through .The orbit is not fully developed after birth. For this reason, the eyes appear more prominent than in adults. The medial walls of the orbit begin to become parallel to each other with age. The outer walls show a 90° angle difference (4). 2. Anatomy of the Orbit The orbit, which resembles a prism with its base in front and apex behind, has an approximate volume of 27 ml. The orbit reaches its maximum volume 1 cm behind the lateral edge. The orbit, with its apex approximately 5 cm behind, is a passage point for many vessels and nerves. Its inner walls run almost parallel to each other, with a distance of about 2.5 cm between them. The width of the orbit is 4 cm, and its height is 3.5 cm. These two inner walls are divided by the ethmoid sinuses. The lateral walls of the orbit run from the outside to the inside at a 45° angle to the inner walls, converging at the center at the back (5,6). It is formed by seven bones: the orbit, ethmoid bone, frontal bone, lacrimal bone, maxilla, palatine bone, sphenoid bone, and zygomatic bone. The anterior third of the lateral wall of the orbit is formed by the zygomatic bone, while the posterior two-thirds are formed by the greater wing es of the sphenoid bone. The section at the apex of the orbital cone is called the “orbital apex” (5). The opening in front of the orbit, called the aditus orbitae, is referred to as the orbital rim. The upper part of the orbit is called the supraorbital margin, the lower part is called the infraorbital margin, the outer edge is called the lateral margin, and the inner edge is called the medial margin (7). 3. Inferior Orbital Fissure The inferior orbital fissure extends along the inferolateral aspect of the orbit, formed by the greater wing of the sphenoid bone posteriorly, the zygomatic bone laterally, the sphenoid body medially, a short portion of the palatine bone, and the maxilla anteriorly, separating the lateral wall from the floor posteriorly.
ANATOMY AND CLINICAL SIGNIFICANCE OF THE INFERIOR ORBITAL FISSURE 77 The foramen rotundum opens into it, and immediately above it, it continues with the lower end of the superior orbital fissure (4,5). The inferior orbital fissure connects the orbit with the pterygopalatine fossa. It also provides a connection between the infratemporal fossa and the orbit, and between the temporal fossa and the orbit. The inferior orbital fissure opens toward the posterolateral direction of the orbital floor. This fissure allows the passage of several neurovascular structures. These are the infraorbital artery, infraorbital nerve, zygomatic nerve, inferior branch of the inferior ophthalmic vein, and orbital branches of the pterygopalatine ganglion (4,5). 3.1.BoneStructuresFormingtheInferiorOrbitalFissure The inferior orbital fissure is formed posterolaterally by the greater wings of the sphenoid bone, laterally by the zygomatic bone, medially by the sphenoid body and a short segment of the palatine bone, and anteriorly by the maxilla. The medial margin of the greater wings of the sphenoid bone forms the inferior margin of the superior orbital fissure and the posterolateral margin of the inferior orbital fissure (4,5). The serrated posteromedial border of the zygomatic bone articulates superiorly with the greater wing of the sphenoid bone via the sphenozygomatic suture and inferiorly with the orbital surface of the maxilla. Between the articular surfaces, there is a small free surface on the posteromedial border that forms the lateral border of the inferior orbital fissure (5). The lateral edge of the orbital surface of the palatine bone forms the border of the inferior orbital fissure below and behind, while the maxilla forms its anterior border (8). 3.2. Neurovascular Structures Passing Through the Inferior Orbital Fissure Some blood vessels and neural structures in the skull pass through the inferior orbital fissure during their course. 3.2.1.BranchesOriginatingfromthePterygopalatineGanglion The pterygopalatine ganglion, a parasympathetic ganglion belonging to the facial nerve, is located in the pterygopalatine fossa. Parasympathetic, sympathetic, and sensory fibers arrive at the pterygopalatine ganglion and branch out. The thin orbital branches, composed of sensory and sympathetic fibers, pass through the inferior orbital fissure and enter the orbit. Sensory fibers
78 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY go to the periosteum covering this area, while sympathetic fibers go to the orbital muscle. Some fibers also pass through the posterior ethmoidal foramen to reach the posterior (5). 3.2.2.InfraorbitalArtery The infraorbital artery originates from the maxillary artery; it frequently appears together with the posterior superior alveolar artery. It can be considered a continuation of the third part of the maxillary artery. It passes anteriorly and enters the orbit through the inferior orbital fissure. Within the orbit, it travels along the orbital floor, first along the infraorbital sulcus and then along the infraorbital canal, exiting the orbit via the infraorbital foramen together with the infraorbital nerve. It then reaches the surface beneath the infraorbital head of the levator labii superioris muscle (5,9). 3.2.3.InfraorbitalNerve The infraorbital nerve originates from one of the main branches of the maxillary nerve. After the inferior orbital fissure, the maxillary nerve continues as the infraorbital nerve.After the inferior orbital fissure, it proceeds anteriorly along the orbital floor into the infraorbital sulcus. The infraorbital nerve passes from the infraorbital canal on the anterior surface of the orbit to the maxillary bone. This canal ends at the foramen infraorbitale, where the infraorbital nerve emerges onto the surface. This exit point may be located below the orbit and lateral to the nasal cavity (4,5,9). The infraorbital nerve gives off branches as it progresses along its course. Both the middle and anterior superior alveolar nerves originate within the orbit. The palpebral branches ascend from beneath the orbicularis oculi muscle to innervate the lower eyelid. The nasal branches of the infraorbital nerve extend toward the skin of the external part of the nose. Finally, the superior labial branches descend beneath the levator labii superioris muscle. (5,9) 3.2.4.ZygomaticNerve The zygomatic nerve, a branch of the maxillary division of the trigeminal nerve, occurs in the pterygopalatine fossa. This nerve carries cutaneous fibers originating from the pterygopalatine ganglion and post-synaptic parasympathetic fibers. These final fibers, originating from the superior salivatory nucleus and passing through the major petrosal branch of the facial nerve, terminate in the lacrimal gland. It enters the orbit through the inferior orbital fissure and
ANATOMY AND CLINICAL SIGNIFICANCE OF THE INFERIOR ORBITAL FISSURE 79 branches into the zygomaticotemporal and zygomaticofacial nerves at an angle of approximately 20° to 40° along the orbital floor. The zygomaticotemporal nerve then passes through the zygomaticotemporal foramen on the temporal surface of the zygomatic bone and enters the temporal fossa (5,10). 3.2.5.InferiorOphthalmicVeins It originates as a venous network in the anterior part of the orbital floor and medial wall. It receives veins from the inferior rectus muscle, inferior oblique muscle, lacrimal sac, and some eyelids, extends backward in the lower part of the orbit, and divides into two branches. One of these passes through the inferior orbital fissure and joins the pterigoid venous plexus, while the other enters the cranium through the superior orbital fissure and ends in the cavernous sinus through a separate opening or, more commonly, together with the superior ophthalmic vein (5). 3.2.6.OrbitalisMuscle This muscle, composed of smooth muscle fibers, closes the inferior orbital fissure and is innervated by the sympathetic system (5). 3.3.ConnectionsandAdjacenciesoftheInferiorOrbitalFissure The lower orbital fissure connects to important surrounding structures due to its location. It also acts as a bridge between other structures. The pterygopalatine fossa is located immediately behind the top of the orbit, at the junction of the inferior orbital fissure and the pterygomaxillary fissure. This fossa is bounded by the body of the sphenoid bone, the base of the pterygoid process, the anterior surface of the greater wing, the infratemporal surface of the maxilla, the perpendicular lamina of the palatine bone, and the orbital and sphenoid processes. The pterygopalatine fossa connects to the orbit via the inferior orbital fissure, to the nasal cavity via the sphenopalatine foramen, and to the infratemporal fossa via the pterygomaxillary fissure. The terminal branches of the maxillary nerve, pterygopalatine ganglion, and maxillary artery are found in the pterygopalatine fossa (4,5). The pterygomaxillary fissure is a narrow gap located at the junction of the anterior and medial walls of the infratemporal fossa. It serves as a connection between the infratemporal fossa and the pterygopalatine fossa. It allows the passage of branches of the maxillary artery and vein (4,5).
80 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY The temporal fossa connects to the infratemporal fossa via a canal extending between the zygomatic arch externally and the infratemporal crest, which is part of the greater wings of the sphenoid bone internally (4,5). The infratemporal fossa is an irregular wedge-shaped depression located on the inner side and below the zygomatic arch. The inferior orbital fissure, located on the upper edge of the anterior wall, connects the orbit to the fossa (4,5). The infraorbital canal is one of the canals on the orbital surface of the maxilla and opens just below the orbital rim, which contains the eye and related structures. It transmits the infraorbital nerve, both of which enter this canal from the infraorbital sulcus and exit via the infraorbital foramen after passing through the maxillary sinus (4,5) 4. The Clinical Significance of the Inferior Orbital Fissure Orbital fractures are usually “blow-out” fractures caused by increased intraorbital pressure due to trauma to the orbit. In indirect blow-out fractures, the lowest wall of the orbit, which is the weakest wall, fractures in front of the inferior orbital fissure when the eye is directly impacted. Orbital fat tissue and sometimes the inferior rectus muscle and inferior oblique muscle herniate through the resulting opening. The integrity of the orbital aditus is usually preserved. In direct blow-out fractures, the trauma strikes directly toward the orbital aditus, fracturing its lower edge, followed by a fracture of the orbital floor; herniation may not occur (11,12). Many approaches to the skull base encounter or are very close to the inferior orbital fissure. Trauma, tumors, infections located near the superior orbital fissure, foramen rotundum, pterygopalatine fossa, infratemporal fossa, and temporal fossa may also affect the inferior orbital fissure (13). 5. Conclusion The orbit is an important region where structures that affect many functions are located or pass through. In addition, the lower orbital fissure is important for understanding and treating potential functional losses, as it allows the passage of neurovascular structures, requiring detailed knowledge of its embryological development and anatomy. Furthermore, knowing the anatomical structure of the orbit and the inferior orbital fissure is important for creating a safe corridor during surgical procedures.
ANATOMY AND CLINICAL SIGNIFICANCE OF THE NASAL CAVITY 87 wall (8). The floor of the cavitas nasi is formed by the lamina horizontalis of the os palatinum and the proc. palatinus of the os maxilla. This part also forms the hard palate, known as the palatum durum. The openings of the incisive canals are located near the nasal septum, at the beginning of the nasal cavity and behind the vestibule of the nose. The incisive canals open into the incisive foramen (for.) in the oral cavity (8). The medial wall of the cavitas nasi is formed by the septum nasi, which consists of cartilage anteriorly and bone posteriorly. The septum nasi is covered by a membrane. As can be understood from this, the septum nasi consists of three parts: the pars cartilaginea, the pars membranacea, and the pars ossea. The pars cartilaginea is formed by the cartilago septi nasi, and the pars ossea is formed by the vomer and the lamina perpendicularis belonging to the os ethmoidale (8). The lateral wall of the cavitas nasi is more complex and wider than the other walls. This wall is formed by the lamina perpendicularis belonging to the palatine bone, the lamina medialis of the pterygoid process belonging to the sphenoid bone, the lacrimal bone, the inferior nasal concha (CNI), the middle nasal concha (CNM), and the superior nasal concha (CNS) (7). The nasal conchae curve inward and downward to form the roof of the nasal meatus. These conchae divide the cavitas nasi into four different passages: the inferior nasal meatus, the middle nasal meatus, the superior nasal meatus, and the sphenoethmoidal recess. The sphenoid sinus opens into the sphenoethmoidal recess located in the superoposterior part of the CNS. The posterior ethmoidal sinuses open into the superior nasal meatus, located between the middle nasal concha and the superior nasal concha (7). The cellulae ethmoidales medii, cellulae ethmoidales anteriores, maxillary sinus, and frontal sinus open into the meatus nasi medius, which is located below the CNM (5). The oval-shaped bulge formed by the cellulae ethmoidales medii is called the bulla ethmoidalis. The slit immediately below the bulla is called the hiatus semilunaris and ends at the infundibulum ethmoidale. The ductus nasolacrimalis opens into the inferior nasal meatus (8). The osteomeatal complex is located on the lateral wall of the nose and is formed by the convergence of several important structures. This complex consists of the uncinate process, frontal recess, semilunar hiatus, ethmoidal infundibulum, ethmoidal bulla, and maxillary sinus ostium. The drainage of the ethmoidal sinus, frontal sinus, and maxillary sinus passes through this complex. Any thickening or variation in the mucosal layer observed in this clinically important region may result in recurrent infections, obstruction, and stasis in the sinuses draining here (9). Concha bullosa (CB) is the most common anatomical variation of the osteomeatal complex (10).
88 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY 3.2.2.NasalCirculation The nose is supplied by branches of the facial artery, maxillary artery, and ophthalmic artery (11). The nasal cavity is supplied primarily by the sphenopalatine artery, a branch of the maxillary artery, branches of the facial artery, and the posterior ethmoidal artery and anterior ethmoidal artery, which are branches of the ophthalmic artery. A large part of the roof of the nasal cavity is supplied by the anterior lateral nasal branches of the anterior ethmoidal artery and the posterior lateral nasal branches of the sphenopalatine artery; the posterosuperior part of the roof is supplied by branches of the posterior ethmoidal artery. The anterior septal branches, originating from the anterior ethmoidal branch of the ophthalmic artery, supply the upper part of the nasal septum. The descending branches of the anterior septal branches join the Kiesselbach plexus. They also supply the anterior part of the nasal septum. The posterior ethmoidal artery, a branch of the ophthalmic artery, together with the descending palatine artery and posterior septal branches originating from the sphenopalatine branch of the maxillary artery, and the septal branches originating from the superior labial branch of the facial artery, supply the upper part of the nasal septum. The rr. septales of the superior labial artery, the rr. septales, and the descending palatine artery are arteries that are part of the Kiesselbach plexus (7). The posterior ethmoidal artery originating from the ophthalmic artery and the anterior lateral nasal branches originating from the anterior ethmoidal branch of the ophthalmic artery supply the roof of the nasal cavity. The descending palatine artery originating from the maxillary artery additionally supplies the inferior nasal meatus (7). The sphenopalatine artery is known as the artery of epistaxis (nosebleed). This artery also forms the majority of the anastomoses in the Kiesselbach plexus. Nosebleeds are most frequently seen in this region (7). The veins of the nasal region form a rich submucosal venous plexus. The plexuses accompany the arteries and drain into the veins, taking the same names as the arteries (8). 3.2.3.LymphaticDrainageoftheNose Lymphatic vessels originating from the vestibulum nasi drain into the submandibular nodes, while the lymphatic vessels from the rest of the cavitas nasi drain into the superior deep cervical nodes (8). The posterior part of the lower wall of the nose drains into the parotid lymph nodes (7).
ANATOMY AND CLINICAL SIGNIFICANCE OF THE NASAL CAVITY 89 3.2.4.NervousInnervationoftheNose The general sensation of the cavitas nasi mucosa is provided by branches originating from the anterior alveolar nerve (n. maxillaris) (which also provides sensation to the inferior concha nasalis with the MNI), the nasociliary nerve (n. opthalmicus) (which provides sensation to the outer part of the nasal wall and the septum nasi. ), the pterygoid canal nerve (Vidian nerve), the ramus nasalis of the pterygopalatine nerve (which innervates the posterior-superior part of the CNS and the general sensation of the nasal septum), the anterior palatine nerve (which innervates the general sensation of the CNM and CNI) and the nasopalatine nerve (which innervates the middle part of the nasal septum) (5). The olfactory nerve receives the sense of smell from the olfactory region. The fibers of the olfactory nerve pass through the holes in the cribriform plate and reach the anterior cranial fossa. Here, they first form the olfactory bulb and then form the olfactory tract. Some fibers of the olfactory nerve change neurons in the olfactory bulb, while others change neurons in the olfactory tract (7). 4. Nose Clinic 4.1.NasalSeptumDeviations This refers to the deviation of the nasal septum from the median plane, either acquired or congenital. The incidence range has been reported as 40-45% (10). Traumas occurring during birth and the inconsistent development of bone and cartilage tissues can also be added to the causes of nasal septum deviation. The most common cause, however, is anatomical variations of the osteometal complex (12). Fundamentally, it involves wear and dislocation of cartilage and bone structures (13). Nasal septum deviation is classified into four different types based on its shape. Type 1: Deviated to the right or left (to one side), Type 2: Resembling a “C” shape, Type 3: S-shaped, Type 4: Crest or isolated spinlike. The angle between the crista galli and the deviated tip is called the angle of deviation (13). The most important consequence of septal deviations is nasal obstruction. Despite being deviated on one side, there is concha hypertrophy on the opposite side of the deviation. If the deviation touches the lateral wall of the nose, contact-type headache develops. Ulceration, bleeding, and dryness of the mucosa may be seen due to changes in airflow caused by the deviation. Impaired mucociliary activity may predispose to sinusitis. Anterior rhinoscopy is crucial
90 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY in diagnosing nasal septal deviations. Deviations in the caudal part of the nose can be visualized by lifting the tip of the nose upward using a finger. Endoscopy is used to diagnose posterior deviations. Cottle classification can also be used to determine the localization of deviations (14). 4.2.ConchaBullosa Concha bullosa is defined as the pneumatization of the concha nasalis media. It is the second most common anatomical variation within the osteomeatal complex (4-80%). It is thought to be formed by the spread of anterior ethmoidal and, to a lesser extent, posterior ethmoidal air cells. Unilateral concha bullosa is more common than bilateral concha bullosa. It can be easily detected with radiological images (CT) (13). Concha bullosa adversely affects mucociliary activity and narrows the cavitas nasi. As a result, diseases of the maxillary sinus and secondary infections may occur. If an abnormally large concha nasalis medius is encountered during nasal endoscopy, concha bullosa is suspected. To confirm the diagnosis, the degree of aeration in the concha is determined by CT. To relieve the obstruction, the lateral edge of the concha is excised endoscopically (13). 4.3.ConchaHypertrophy This is a variant anatomical abnormality commonly found in the inferior nasal concha. It increases resistance in the nasal airway and causes nasal obstruction. Obstructions caused by turbinate hypertrophy are divided into two types based on bone structure or mucosa. Vasomotor and allergic rhinitis develop after mucosal hypertrophy. It is usually bilateral. It is treated with nasal corticosteroid sprays, antihistamines, corticosteroid injections, mast cell stabilizers, immunotherapy, and topical decongestants. If the obstruction is severe, surgical treatment is recommended (13). 4.4.AccessoryCellsAroundtheEthmoidSinus 4.4.1.AggerNasiCell It refers to pneumatization located in the upper-anterior part of the attachment site of the lateral wall of the concha nasalis medius (15). They are anterior ethmoidal air cells localized in the anterior-superior part of the hiatus semilunaris located on the lateral wall of the nose (16). They extend anteriorly within the os lacrimale (17). Agger nasi cells can affect drainage of the frontal sinus and cause frontal sinusitis. They are generally bilateral and their effects vary according to
ANATOMY AND CLINICAL SIGNIFICANCE OF THE NASAL CAVITY 91 the degree of pneumatization. The agger nasi cells, which are in close proximity to the lacrimal fossa, can also cause dacryocystitis and epiphora (12). 4.4.2.HallerCells These are ethmoidal air cells that spread across the medial roof of the maxillary sinus (16). They are located around the ostium of the maxillary sinus, from the bottom of the ethmoid bulla towards the roof of the orbit. They are also known as infraorbital or ethmoido-maxillary cells. They can also be located from the medial wall of the maxillary sinus towards the lower part of the lamina papyracea (7). The lateral deviation of the uncinate process and the haller cells narrow the infundibulum. Due to its narrowing of the maxillary sinus ostium and infundibulum, it is defined as a predisposing factor in the etiology of recurrent maxillary sinusitis (7). 4.4.3.OnodiCell This is the excessive growth of the posterior ethmoidal air cells located on the upper-outer side of the sphenoid sinus. It is quite important due to its close association with the optic nerve. If there is significant pneumatization, it can compress the optic nerve because it affects the drainage of the sphenoid sinus (7). 4.4.4.CristaGalliPneumatization This is the aeration within the crista galli. This pneumatization can cause obstruction in the ostium sinus frontalis and recessus frontalis, leading to chronic sinusitis. To prevent possible complications, it is necessary to clearly distinguish it from the ethmoid air cells (18). 4.5.CongenitalAnomaliesoftheNasalRegion These anomalies are not very common, occurring in 1 in 20,000-40,000 births. The most detailed system for classifying these anomalies was developed in 2004 (18). 4.5.1.HypoplasticandAplasticAnomalies These are the most common class of congenital nasal anomalies. Complete nasal agenesis or total arhinia: Absence of the nasal cavity, olfactory system, and external nose. It is quite rare, and its etiology is still unknown. Cases associated with anomalies of chromosomes 9, 13, and 21 have been reported. It is thought
92 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY to result from a defect occurring during nasal placode invagination (18). Heminasal aplasia or unilateral agenesis: It can be seen with anomalies affecting the same side of the face or in isolation. Radiological studies suggest the loss of the ipsilateral nasal placode during development and show the absence of the cribriform plate (19). 4.5.2.SeptumDeviationorNasalTipDeviationinNewborns It is known as a type of congenital nasal deformity. Although they are not true aplastic or hypoplastic congenital anomalies, these deformities may have potential functional or cosmetic effects. Prolonged labor, primiparous delivery, and intrauterine pressure have been identified as risk factors (20). 4.5.3.DuplicationandHyperplasticAnomalies These anomalies are thought to be embryologically due to olfactory placode duplication or an accessory olfactory pit. Polyrhinia is a duplication of the medial nasal process. A unilateral and milder form of polyrhinia also creates an extra nostril. Among the associated anomalies, choanal atresia and piriform aperture stenosis are significant. Since duplication and hyperplastic anomalies are generally associated with bone anomalies, magnetic resonance imaging and/or computed tomography are recommended to assist in controlling nasal obstruction and for preoperative planning (21). 4.5.4.VascularAnomaliesoftheNasalRegion The most common vascular anomaly in the nose is hemangioma. An infantile hemangioma is described as a tumor originating from endothelial cells, appearing in the first weeks of life, and being benign. It shows rapid proliferation in the first year and is characterized by a stationary period lasting several years. Those causing functional problems such as visual impairment and nasal obstruction or bleeding lesions should be treated (22). 4.6.Epistaxis This refers to vascular pathologies caused by mucosal damage or coagulation disorders and the resulting bleeding in the nasal cavity. Sixty percent of people experience epistaxis at least once in their lives. Treatment is required for 6% of these cases. It peaks in individuals over 50 years of age and under 10 years of age. It is more common in men than in women (23). 90-95% of epistaxis cases are anterior bleeding and generally occur in the Kisselbach plexus region.
ANATOMY AND CLINICAL SIGNIFICANCE OF THE NASAL CAVITY 93 In most patients, the nosebleed is not severe. Bleeding may stop spontaneously or with simple interventions. Treatment options include cauterization, anterior packing, posterior packing, and, very rarely, arterial ligation and septoplasty (24). 4.7.Rhinoplasty “Rhinoplasty” comes from the Greek words “rhis, rhinos” (nose) and “plasticós” (to shape, to change). It refers to the reshaping of the nose (25). Rhinoplasty is performed according to the surgeon’s preference and the patient’s requests. It can be performed under local anesthesia with intravenous sedation or under general anesthesia. With general anesthesia, a throat pack can be used to prevent intragastric blood from causing nausea or vomiting. It also facilitates the protection of airway safety. Rhinoplasty has numerous techniques and applications in clinical practice, including closed submucosal rhinoplasty, letdown rhinoplasty, open rhinoplasty, closed rhinoplasty, filler rhinoplasty, and revision rhinoplasty (26). 5. Conclusion The nasal cavity and paranasal sinuses constitute one of the most critical areas of head and neck anatomy due to both their functional characteristics and their clinical importance. The morphological diversity and neighboring relationships of these structures directly affect physiological functions, the course of pathological processes, and the reliability of surgical interventions. Inflammatory diseases, congenital anomalies, traumatic lesions, and neoplastic formations, in particular, necessitate detailed anatomical knowledge of the nasal cavity and sinuses. Modern diagnostic methods and endoscopic surgical techniques can only be applied effectively and without complications with a thorough understanding of the three-dimensional anatomy of this region. Therefore, knowledge of the anatomicclinical correlation of the cavitas nasi and related structures is indispensable for increasing both diagnostic accuracy and therapeutic success rates. References 1. Grevellec A, Tucker AS. The pharyngeal pouches and clefts: Development, evolution, structure and derivatives. Semin Cell Dev Biol. 2010;21(3):325-332. 2. Som PM, Naidich TP. Illustrated review of the embryology and development of the facial region, Part 2. Neuroradiology. 2013.
94 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY 3. Moore KL, Persaud TVN. Clinically oriented embryology. 8th ed. In: Dalçık H, Yıldırım M, eds. Klinik yönleriyle insan embriyoloji. 2nd ed. İstanbul: Nobel Tıp Kitabevi; 2009:182-187. 4. Som PM, Naidich TP. Illustrated review of the embryology and development of the facial region part 1: early face and lateral nasal cavities. Neuroradiology. 2013;34(12):2233-2240. 5. Moore KL, Dalley AF, Agur AMR. Clinically Oriented Anatomy. 8. Edition:WoltersKluwer;2017.Netter FH. İnsan Anatomisi Atlası. Cumhur M, ed. 4th ed. İstanbul: Nobel Tıp Kitabevleri; 2008. 6. Bloom JD, Antunes MB, Becker DG. Anatomy, physiology, and general concepts in nasal reconstruction. Facial Plast Surg Clin North Am. 2011;19(1):1-11. 7. Drake TL, Vogl WA, Mitcheel AWM. Gray’s Anatomy for Students. 4. Edition:Elsevier; 2014 8. Moore KL, Dalley AF. Kliniğe yönelik anatomi. 4th ed. İstanbul: Nobel Tıp Kitabevi; 2007:743-747. 9. Bolger WE, Butzin CA, Parsons DS. Paranasal sinus bony anatomic variations and mucosal abnormalities: CT analysis for endoscopic sinus surgery. Laryngoscope. 1991;101:56-64. 10. Yiğit Ö, Acıoğlu E, Çakır ZA, Şişman AS, Barut AY. Concha bullosa and septal deviation. Eur Arch Otorhinolaryngol. 2010;267:1397-1401. 11. Snell RS. Clinical anatomy for medical students. 6th ed. In: Yıldırım M, ed. Klinik anatomi 6. Edisyon. 1st ed. İstanbul: Nobel Tıp Kitabevi; 2004:950961. 12. Orhan İ, Soylu E, Altın G, Yılmaz F, Çalım ÖF, Örmeci T. Paranazal sinüs anatomik varyasyonlarının bilgisayarlı tomografi ile analizi. Abant Medical Journal. 2014;3(2):145-149. 13. Şapcı T. Nazal Septum Hastalıkları. In: Koç C, ed. Kulak Burun Boğaz Hastalıkları ve Baş Boyun Cerrahisi. Güneş Kitapevi; 2004:535-545. 14. Turna Ö, Aybar MD, Karagöz Y, Tuzcu G. Anatomic variations of the paranasal sinus region: evaluation with multidetector CT. Istanbul Med J. 2014;15. 15. Kaplan Y, Müderris S, Kunt T. Sinonazal varyasyonların BT analizi ve sinüzit ile ilişkisi. Cumhuriyet Üniversitesi Tıp Fakültesi Dergisi. 2004;26(1):29-36. 16. Talaiepour AR, Sazgar AA, Bagheri A. Anatomic variations of the paranasal sinuses on CT scan images. Journal of Dentistry. 2005;2:142-146.
ANATOMY AND CLINICAL SIGNIFICANCE OF THE NASAL CAVITY 95 17. Ebrahim Z, Lockhat Z. Paranasal sinus variants. SA Journal of Radiology. 2012;301. 18. Losee JE, et al. Congenital nasal anomalies: a classification scheme. Plast Reconstr Surg. 2004;113(2):676-689. 19. Abulezz T. Congenital heminasal aplasia: clinical picture, radiological findings, and follow-up after early surgical intervention. J Craniofac Surg. 2019;30(3):e199-e202. 20. Funamura JL, Tollefson TT. Congenital anomalies of the nose. Facial Plast Surg. 2016;32(02):133-141. 21. Leung M, Krakovitz P, Koltai P. Congenital sinonasal disorders. In: Rhinology: Diseases of the Nose, Sinuses, and Skull Base. New York, NY: Thieme; 2012:381-393. 22. Hogeling M, Adams S, Wargon O. A randomized controlled trial of propranolol for infantile hemangiomas. Pediatrics. 2011;128(2):e259-e266. 23. Pollice PA, Yoder MG. Epistaxis: a retrospective review of hospitalized patients. Otolaryngol Head Neck Surg. 1997;117:49-53. 24. Alvi A, Joyner-Triplett N. Acute epistaxis. How to spot the source and stop the flow. Postgrad Med. 1996;99(5):83-90. 25. Dick MK, Patel BC. Rhinophyma. StatPearls. Treasure Island (FL): StatPearls Publishing; 2024. 26. Rohrich RJ, Ahmad J. Rhinoplasty. Plast Reconstr Surg. 2011;128(2):49-73.
PRESERVATION RHINOPLASTY 103 verification of the achieved contour and cautious, step-by-step removal. In cases of a markedly low radix, a graft may be employed for camouflage. The fourth most common complication is supratip collapse, which may occur in both high and low septal strip resections. Prevention requires gradual resection of the distal septum. In high septal strip resection, supratip collapse typically results from overly aggressive lowering of the W ASA segment, whereas in low septal strip resection, it is usually caused by excessive resection of the septum at the anterior nasal spine (ANS) level. Although largely preventable, supratip collapse can be corrected with the placement of a supratip graft. Therefore, resections in this region should always be performed in a stepwise and conservative manner (14). 7. Conclusion Preservation rhinoplasty offers significant advantages in maintaining natural nasal aesthetics and function, though it requires advanced surgical skills and careful patient selection. With ongoing advancements and increasing clinical experience, this technique is expected to become more widely adopted in rhinoplasty practice. References 1. Daniel RK, Kosins AM. Current trends in preservation rhinoplasty. Aesthet Surg J Open Forum. 2020;2(1):ojaa003. 2. Çakır B, Doğan T, Öreroğlu AR, Daniel RK. Rhinoplasty: surface aesthetics and surgical techniques. Aesthet Surg J. 2013;33(3):363-375. 3. DeSisto NG, Okland TS, Patel PN, Most SP. State of the evidence for preservation rhinoplasty: a systematic review. Facial Plast Surg. 2023;39(4):333361. 4. Lee J, Abdul-Hamed S, Kazei D, Toriumi D, Lin SJ. The first descriptions of dorsal preservation rhinoplasty in the 19th and early-to mid-20th centuries and relevance today. Ear Nose Throat J. 2021;100(10):713-719. 5. Çakır B, Genç B, Finocchi V, Haack S. My approach to preservation rhinoplasty. Facial Plast Surg Clin North Am. 2023;31(1):25-43. 6. Kosins AM. Preservation rhinoplasty: open or closed? Aesthet Surg J. 2022;42(9):990-1008. 7. Sadri A, East C, Badia L, Saban Y. Dorsal preservation rhinoplasty: core beam computed tomography analysis of the nasal vault, septum, and skull base—its role in surgical planning. Facial Plast Surg. 2020;36(3):329-334.
104 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY 8. Neves JC, Zholtikov V, Cakir B, Coşkun E, Arancibia-Tagle D. Rhinoplasty dissection planes (subcutaneous, sub-SMAS, supra-perichondral, and sub-perichondral) and soft tissues management. Facial Plast Surg. 2021;37(1):2-11. 9. Ri C, Ri H, Yu J, Mao J, Zhao M. Update on rhinoplasty research trends: a bibliometric analysis. Aesthet Plast Surg. 2022;46(6):2950-2963. 10. Goksel A, Cason RW, Tran KN, Rohrich RJ. The blocking points: the keys to consistent success in preservation rhinoplasty. Plast Reconstr Surg. 2024;153(5):922e-931e. 11. Lazovic GD, Daniel RK, Janosevic LB, Kosanovic RM, Colic MM, Kosins AM. Rhinoplasty: the nasal bones–anatomy and analysis. Aesthet Surg J. 2015;35(3):255-263. 12. Stubenitsky BM. Prevention and correction of the most common problems in preservation rhinoplasty. In: Clinical Atlas of Preservation Rhinoplasty: Steps for Surgeons in Training. Cham: Springer International Publishing; 2023:183-206. 13. Ishida LC, Ishida J, Ishida LH, Tartare A, Fernandes RK, Gemperli R. Nasal hump treatment with cartilaginous push-down and preservation of the bony cap. Aesthet Surg J. 2020;40(11):1168-1178. 14. Ferraz MB, Sella GC. Indications for preservation rhinoplasty: avoiding complications. Facial Plast Surg. 2021;37(1):45-52.
105 CHAPTER VII ANATOMY AND CLINICAL SIGNIFICANCE OF THE EUSTACHIAN TUBE Zeynep Sena COŞAR¹ & Aynur Emine ÇİÇEKCİBAŞI² ¹(Ph.D. Can.), Necmettin Erbakan University, Faculty of Medicine, Department of Anatomy E-mail: [email protected] ORCID: 0000-0001-9772-3974 ²(Prof. Dr. MD), Necmettin Erbakan University, Faculty of Medicine, Department of Anatomy E-mail: aynurcicekcibası@yahoo.com.tr ORCID: 0000-0002-1373-3065 1. Introduction The Eustachian tube (Latin: tuba auditiva) is a crucial anatomical structure that ventilates the middle ear, equalizes pressure, facilitates drainage of secretions, and provides protection against infections. Its function is maintained through both passive and active mechanisms. However, any dysfunction in this system may lead to degenerative changes within the middle ear cavity. For the diagnosis and management of such pathologies, it is particularly important to understand the tube’s age-related protective features, morphometric parameters such as length and angle, and its structural subdivisions. Indeed, the success of surgical treatment in common ear diseases such as chronic otitis media largely depends on the anatomical integrity and functional competence of the Eustachian tube (1,2). Historically, the Eustachian tube has also attracted considerable scientific interest. In 1562, the Italian anatomist Bartholommeus Eustachius first provided a detailed description of this structure in his work Epistola de Auditus Organis. Subsequently, Antonio Maria Valsalva elaborated on its anatomy and named it the “Tuba Eustachii.” Du Verney made the first observations on its function.
106 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY In the 19th century, Arnold Joseph Toynbee noted that the tube opens during swallowing to regulate middle ear pressure, while Adam Politzer distinguished between its cartilaginous and osseous segments and developed the technique of positive pressure application known as “politzerization.” Some researchers, however, trace the recognition of this structure back to Ancient Greece, attributing its discovery to Alcmaeon of Croton around 500 BC or to the writings of Aristotle (3–5). Eustachian tube dysfunction, nasopharyngeal reflux, and otitis media occur at varying rates across different ages and populations, with the tube playing a central role in their etiopathogenesis. The anatomical and physiological integrity of the Eustachian tube is essential for the proper function of middle ear structures and the maintenance of hearing. In recent years, due to the complex anatomy of the skull base, the Eustachian tube has also gained importance as a surgical corridor in techniques such as trans-Eustachian approaches (6). A comprehensive and clinically oriented understanding of the anatomy of the Eustachian tube is therefore indispensable for elucidating these pathological conditions, identifying surgical landmarks, and achieving successful treatment outcomes. In the literature, this structure is referred to by various names, including Eustachian tube, auditory tube, and pharyngotympanic tube. 2. Embryology of the Eustachian Tube The Eustachian tube begins to develop in the early stages of the embryonic period. This process is shaped by the fusion of the pharyngeal arches and clefts. Along with the tympanic cavity and mastoid cells, it is of endodermal origin. During development, the structure attains integrity first through endodermal epithelial formation, followed by the migration and differentiation of mesenchymal cells. Various growth factors, including transforming growth factor-beta (TGF-β), play an important role in this process (7,8). The distal portion of the first pharyngeal pouch expands to form the tubotympanic recess, which gives rise to the primitive tympanic cavity, while its proximal portion remains tubular and constitutes the basis of the Eustachian tube. By the fourth week of embryonic development, a groove appears on the lateral wall of the pharyngeal floor, representing the primordial form of the tube. By the fifth week, this structure becomes more distinct, and by the sixth week it begins to take on a tubular shape. Around the seventh week, the pharyngeal opening of the tube, initially appearing as a depression in the pharyngeal wall, gradually closes and transforms into a canal.
ANATOMY AND CLINICAL SIGNIFICANCE OF THE EUSTACHIAN TUBE 107 The lumen of the Eustachian tube is lined by endodermal epithelium derived from the first pharyngeal pouch. Throughout development, this epithelium maintains continuity with the mucosa of the middle ear. While the middle ear mucosa remains relatively undifferentiated, the Eustachian tube mucosa differentiates into pseudostratified columnar respiratory epithelium (9,10). Normal development of the Eustachian tube is essential for the proper functioning of the auditory system. Developmental anomalies may predispose to Eustachian tube dysfunction, otitis media, hearing loss, and other otologic disorders. 3. Ear Anatomy in the Context of the Eustachian Tube The ear, located within the temporal bone, is the primary sensory organ responsible for hearing and balance. Anatomically, it is divided into three major regions: the external ear, middle ear, and inner ear. These structures work together to receive environmental stimuli related to hearing and equilibrium, transmit them, and convey the signals to the central nervous system. The external ear collects sound waves from the environment and consists of the auricle and the external acoustic meatus. The sound waves directed by these structures are transmitted to the middle ear via the tympanic membrane. The middle ear comprises the auditory ossicles and their associated muscles—the tensor tympani and the stapedius—as well as neural components such as the chorda tympani and the tympanic plexus. This cavity transmits sound vibrations mechanically to the inner ear. In addition, through its anterior wall, it communicates with the Eustachian tube, which opens into the nasopharynx, thereby ensuring aeration and drainage of secretions. The inner ear consists of specialized, complex canals and labyrinthine systems that mediate the reception and neural transmission of auditory and vestibular stimuli. These structures detect fluid motion, convert mechanical energy into neural impulses, and transmit them to higher centers (11). 3.1.MiddleEarAnatomy The middle ear cavity, located within the petrous part of the temporal bone between the tympanic membrane and the inner ear, is an irregularly shaped, air-filled space lined with mucosal epithelium. In addition to transmitting sound vibrations to the inner ear, it also serves a protective role by limiting the potential damage that excessively loud sounds may cause to inner ear structures. Laterally, it is bounded by the tympanic membrane, and medially by the bony
108 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY wall of the inner ear. Posteriorly, it communicates with the mastoid antrum, and anteriorly, it connects to the nasopharynx via the Eustachian tube, which provides ventilation and drainage of the middle ear. The cavity is divided by an imaginary horizontal plane passing through the upper margin of the tympanic membrane into two parts: the epitympanic recess (attic) superiorly, and the tympanic cavity proper inferiorly. Within the tympanic cavity are the three small, mobile auditory ossicles responsible for sound transmission: the malleus, incus, and stapes. Structurally, the middle ear resembles an irregular cube with six walls: lateral, medial, anterior, posterior, superior, and inferior. The anterior wall, also called the carotid wall, is particularly important due to its relationship with the Eustachian tube. In its upper part, there are two parallel canals separated by a thin bony septum (the septum of the musculotubal canal). The upper canal, known as the semicanal for the tensor tympani muscle, houses the tensor tympani, while the lower canal, the semicanal for the auditory tube, forms the osseous portion of the Eustachian tube. Together, these two structures constitute the musculotubal canal, which contains both the muscle and the tube (11,12). 4. Anatomy of the Eustachian Tube 4.1.GeneralStructureoftheEustachianTube The Eustachian tube is a key structure in the head and neck region that provides a functional connection between the nasal cavity, pharynx, middle ear, and mastoid cells. Measuring approximately 36 mm in length and shaped like a truncated cone, it extends between the tympanic cavity and the nasopharynx. Originating from the carotid wall of the middle ear, it courses anteroinferomedially and is supported by surrounding soft tissues and associated muscles. Structurally, the Eustachian tube is divided into two main segments: the osseous part and the cartilaginous part. 4.1.1.OsseousPart The osseous portion constitutes the proximal one-third of the tube closest to the middle ear and measures approximately 12 mm in length. This segment is located within the petrous part of the temporal bone. 4.1.2.CartilaginousPart The cartilaginous portion forms the distal two-thirds of the tube, with an average length of about 24 mm. It opens into the nasopharyngeal wall
ANATOMY AND CLINICAL SIGNIFICANCE OF THE EUSTACHIAN TUBE 109 approximately 12.5 mm posterior to the inferior nasal concha. The middle ear opening of the tube is termed the tympanic orifice, while the nasopharyngeal opening is known as the pharyngeal orifice. From the pharyngeal view, the elevation created by the underlying cartilage is identified as the torus tubarius. 4.1.3.Isthmus The transitional region between the osseous and cartilaginous segments is referred to as the isthmus of the Eustachian tube. This is the narrowest portion of the tube and functions as a physiological barrier between the middle ear and the external environment. Distal to the isthmus, the cartilaginous canal gradually expands toward the nasopharynx and terminates in a broad structure known as the tubal pavilion. While the cartilaginous portion remains closed at rest and opens during swallowing, chewing, or sneezing, the osseous segment remains constantly open, functioning as a passive transmission channel (13,14). 4.2.MorphologyoftheEustachianTube The length of the Eustachian tube, the morphometric ratios of its osseous and cartilaginous parts, their angular orientations, and the distances of the orifices from the inferior nasal concha are important anatomical determinants in both functional assessment and surgical planning. The position of the tube, the proportion of its osseous and cartilaginous segments, and its structural measurements differ between infants and adults. In addition, age-related changes occur in the mucosal lining and the luminal diameters. In a healthy adult, the Eustachian tube typically measures about 36 mm in length, approximately one-third of which is osseous and the remainder cartilaginous. The lumen of the osseous segment varies among individuals and may appear irregular, triangular, or rectangular in shape. The mean distance between this segment and the tegmen tympani is approximately 3.5 mm. At the level of the isthmus, the cartilaginous portion has an average width of 3 mm and a thickness of 2 mm. This narrowest region of the tube is of particular clinical importance in selecting instruments for endoscopic applications. At its distal end, where the cartilaginous portion reaches the nasopharynx, the width averages 12 mm and the thickness about 7 mm (15,16). The tympanic orifice, which opens into the middle ear cavity, has an average width of 1 mm and a length of about 2 mm. The pharyngeal orifice, which opens into the nasopharynx, measures approximately 2 mm in width and 5 mm in length. The cartilaginous portion courses at an angle of about 30°–40° in
110 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY the transverse plane and approximately 45° in the sagittal plane. At the isthmus, the osseous and cartilaginous segments join at an angle of roughly 160° (17,18). 4.3.MusclesoftheEustachianTube There are four muscles that directly or indirectly contribute to Eustachian tube function: 4.3.1.Tensorvelipalatinimuscle The tensor veli palatini is the principal muscle responsible for actively opening the Eustachian tube. It attaches to the lateral lamina of the cartilaginous portion and to the fibrous membrane. The medial portion of this muscle is sometimes referred to in the literature as the dilatator tubae. When contracted, it pulls the lateral lamina downward, thereby widening the lumen of the tube. It becomes active during swallowing, yawning, and mandibular movements, and is innervated by the mandibular branch of the trigeminal nerve (11,19). 4.3.2.Levatorvelipalatinimuscle The levator veli palatini originates from the skull base adjacent to the osseous portion of the Eustachian tube. Cylindrical in shape, it courses parallel to the base of the cartilaginous tube toward the nasopharynx and inserts into the aponeurosis of the soft palate. Contraction of this muscle elevates the nasopharyngeal orifice and part of the cartilaginous segment, thereby facilitating opening of the tube. Although it cannot achieve full dilation on its own, it augments the action of the tensor veli palatini. Its innervation is provided through the pharyngeal plexus (11,19). 4.3.3.Salpingopharyngeusmuscle The salpingopharyngeus arises from the inferior aspect of the medial cartilaginous portion of the Eustachian tube and descends to merge with the posterior fibers of the palatopharyngeus. This slender muscle is often underdeveloped, and its complete formation is uncommon. Functionally, it is considered to play a minimal role in tube opening (11,19). 4.3.4.Tensortympanimuscle The tensor tympani runs within the upper portion of the musculotubal canal, specifically in the semicanal for the tensor tympani muscle. It originates
ANATOMY AND CLINICAL SIGNIFICANCE OF THE EUSTACHIAN TUBE 111 from the cartilaginous portion of the Eustachian tube and adjacent areas of the greater wing of the sphenoid bone. Its fibers course anteriorly to insert onto the medial surface of the malleus handle, near the neck of the malleus. The muscle is innervated by the medial pterygoid branch of the mandibular nerve (11,19). 4.4.VascularizationandInnervation The arterial supply of the Eustachian tube is provided by branches of the ascending pharyngeal artery (external carotid artery), the middle meningeal artery, and the artery of the pterygoid canal (a branch of the maxillary artery). Venous drainage occurs through the pterygoid venous plexus, while lymphatic drainage is directed to the retropharyngeal and deep cervical lymph nodes. Neural innervation is supplied via the tympanic plexus and the pharyngeal branch originating from the pterygopalatine ganglion (11). 4.5.FunctionoftheEustachianTube The Eustachian tube has three principal functions: 4.5.1.Ventilation(PressureRegulation) The Eustachian tube allows air from the nasopharynx to reach the middle ear, thereby equalizing air pressure on both sides of the tympanic membrane. This mechanism enables the tympanic cavity, which has no direct communication with the external environment, to adapt to atmospheric pressure changes without being adversely affected. Under normal conditions, the tube remains open for approximately 0.4 seconds, permitting the passage of about 1–2 µL of air. This cycle occurs on average 1000 times per day. According to Adam Politzer’s hydrops ex vacuo theory, adequate aeration of the middle ear depends on effective contraction of the paratubal muscles and the preservation of the elastic properties of the cartilage. In a study evaluating the role of the tensor veli palatini in ventilation, botulinum toxin was injected into the muscle, and failure of the Eustachian tube orifice to open was observed. In contrast, another experiment demonstrated that even after removal of the levator veli palatini, the tube continued to open and ventilation was maintained. A further experimental study suggested that muscular activity is the primary factor in tube opening, while the elasticity of the cartilage has a more limited effect. Nevertheless, other reports in the literature have emphasized structural changes in the cartilaginous portion as a major cause of Eustachian tube dysfunction (20,21).
112 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY 4.5.2.Clearance The removal of secretions accumulated in the middle ear is primarily achieved through the mucociliary activity of the Eustachian tube and the action of its associated muscles, which transport secretions toward the nasopharynx. In the literature, observation of methylene blue applied to the middle ear subsequently appearing in the nasopharynx has demonstrated that this clearance occurs via the functional activity of the Eustachian tube. Experimental studies using radioisotopic methods have shown that the mucociliary system provides clearance at an average rate of 0.7–1.1 mm per minute. Low-viscosity but high-volume secretions are typically removed through muscular activity, whereas the clearance of more viscous secretions requires the combined contribution of both ciliary motion and muscular contraction. When a difficult-to-drain exudate accumulates in the middle ear, contraction of the paratubal muscles actively opens the Eustachian tube, allowing fluid to enter the lumen. Once muscular contraction subsides, the tube passively closes, completing the process by emptying the exudate into the nasopharynx (20,21). 4.5.3.Protection The Eustachian tube serves as a crucial barrier by preventing nasopharyngeal secretions from entering the middle ear. In this way, the tympanic cavity is protected both from the invasion of pathogenic microorganisms and from the effects of nasopharyngeal pressure fluctuations. Additional protective functions include preventing retrograde flow of nasopharyngeal reflux, attenuating the individual’s own voice during speech, and defending against sudden changes in ambient air pressure. This mechanism primarily depends on the cartilaginous portion of the tube remaining physiologically closed. When muscular contractions open the tube, the fatty tissue known as Ostmann’s fat pad restricts the lumen, thereby maintaining protection during ventilation. The structural properties and quality of the cartilage also play a decisive role in this function. In cases where the medial lamina is underdeveloped, it has been reported that inflammation from the nasopharynx may more easily spread into the lumen of the Eustachian tube. Conversely, when the medial lamina is well developed, inflammatory processes arising in the Rosenmüller fossa may be restricted. Some studies have also proposed that mastoid cells function as a physiological air buffer, preventing reflux into the middle ear when the tube is open. In addition, the isthmus of the Eustachian tube has been emphasized as a
ANATOMY AND CLINICAL SIGNIFICANCE OF THE EUSTACHIAN TUBE 119 with appropriate case selection, detailed CT-based preoperative planning, and precise understanding of tubal-carotid-pterygoid relationships—offers a safe alternative that provides clear visualization and operative access to the ITF. Early experiences and cadaveric/radiologic data support its feasibility, and it is anticipated that future larger clinical series will better define the indications and functional outcomes of this approach (34). 8. Conclusion The Eustachian tube is of critical importance for the maintenance of hearing function and middle ear health. Understanding its morphological and functional characteristics contributes to clarifying the mechanisms of Eustachian tube dysfunction and developing appropriate treatment strategies. Among minimally invasive methods, balloon tuboplasty has demonstrated its effectiveness in reducing symptoms and improving quality of life in chronic cases, while endoscopic trans-Eustachian approaches provide safe access to the skull base. Current literature emphasizes the reliability of these techniques and their role in reducing complication risks. In conclusion, the integration of Eustachian tube knowledge into clinical practice enhances surgical success and guides future research. References 1) Proctor B. Embryology and anatomy of the eustachian tube. Arch Otolaryngol. 1967;86(5):503-514. 2) Schilder AG, Bhutta MF, Butler CC, et al. Eustachian tube dysfunction: consensus statement on definition, types, and etiology. Lancet Respir Med. 2015;3(8):e34-e45. 3) Mudry A. The history of the eustachian tube. Otol Neurotol. 2000;21(4):439-447. 4) Bluestone CD. Eustachian Tube: Structure, Function, Role in Otitis Media. Hamilton: BC Decker Inc; 2005. 5) Schroder S, Ebmeyer J. Historical concepts of the eustachian tube. Laryngorhinootologie. 2018;97(S 01):S113-S138. 6) Tos M. Manual of Middle Ear Surgery. Vol. 1. Stuttgart: Thieme; 1998. 7) Cummings CW, Flint PW, Haughey BH, et al. Cummings Otolaryngology – Head and Neck Surgery. 3rd ed. Mosby; 1998. 8) Park SN, Back SA, Kim DK, Yeo SG. Development of the Eustachian tube in human embryos: a morphometric study. Ann Otol Rhinol Laryngol. 2000;109(12):1149–1152.
120 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY 9) Sadler TW. Langman’s Medical Embryology. 12th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2011. 10) Moore KL, Persaud TVN, Torchia MG. The Developing Human: Clinically Oriented Embryology. 9th ed. Philadelphia, PA: Elsevier; 2012. 11) Drake RL, Vogl AW, Mitchell AWM. Gray’s Anatomy for Students. 4th ed. Philadelphia, PA: Elsevier; 2014. 12) McCoul ED, Anand VK, Christos PJ. Clinical factors associated with prolonged healing after endoscopic sinus surgery. Laryngoscope. 2012;122(6):1261–1266. 13) Prades JM, Dumollard JM, Calloc’h F, Merzougui N, Martin C. Descriptive anatomy of the human auditory tube. Surg Radiol Anat. 1998;20(5):335-340. 14) Stoikes NF, Dutton JM. The effect of endoscopic sinus surgery on symptoms of eustachian tube dysfunction. Am J Rhinol. 2005;19(2):199-202. 15) Djeric D, Savic D. Anatomical variations and relations in the medial wall of the bony portion of the eustachian tube. Acta Otolaryngol (Stockh). 1985;99(5–6):551–556. 16) Yang L, Gong PG, Zheng MF, Zhao XD, Liu YY, Peng H. Eustachian tube and its dysfunction related diseases’ occurrence and treatments. Lin Chung Er Bi Yan Hou Tou Jing Wai Ke Za Zhi. 2016;30:1001-1005. 17) Leopold DA, Hummel T, Schwob JE, Hong SC, Knecht M, Kobal G. Anterior distribution of human olfactory epithelium. Laryngoscope. 2000;110:417-421. 18) Szymanski A, Agarwal A. Anatomy, head and neck, ear eustachian tube. In: StatPearls. Treasure Island, FL: StatPearls Publishing; 2022. 19) Rosen L. The Morphology of the Salpingopharyngeus Muscle. [master’s thesis]. Pittsburgh, PA: University of Pittsburgh; 1970. 20) Poe D, Pyykko I, Valtonen H, Silvola J. Analysis of Eustachian tube function by video endoscopy. Am J Otol. 2000;21(5):602-607. 21) Tideholm B. Middle ear cleft pressure. In: Ars B, ed. Fibrocartilaginous Eustachian Tube–Middle Ear Cleft. The Hague, Netherlands: Kugler Publications; 2003:97-112. 22) Ars B. Balance of pressure variation in the middle ear cleft. In: Ars B, ed. Fibrocartilaginous Eustachian Tube–Middle Ear Cleft. Amsterdam, Netherlands: Kugler Publications; 2003:57-66. 23) McCoul ED, Anand VK, Christos PJ. Validating the clinical assessment of Eustachian tube dysfunction: the Eustachian Tube Dysfunction Questionnaire (ETDQ-7). Laryngoscope. 2012;122(5):1137-41.
ANATOMY AND CLINICAL SIGNIFICANCE OF THE EUSTACHIAN TUBE . . . 121 24) Smith ME, Tysome JR. Tests of Eustachian tube function: a review. Clin Otolaryngol. 2015;40(4):300-11. 25) Ishijima K, Sando I, Suzuki C, Balaban C, Takasaki K. Length of the eustachian tube and its postnatal development: computer-aided threedimensional reconstruction and measurement study. Ann Otol Rhinol Laryngol. 2000;109(6):542-548. 26) Takasaki K, Takahashi H, Miyamoto I, et al. Functional anatomy of the tensor veli palatini muscle and Ostmann’s fatty tissue. Ann Otol Rhinol Laryngol. 2002;111(11):1045-1049. 27) Llewellyn A, Norman G, Harden M, et al. Interventions for adult Eustachian tube dysfunction: a systematic review. Health Technol Assess. 2014;18(46):1-180. 28) Doyle WJ, Swarts JD, Banks J, Casselbrant ML, Mandel EM, Alper CM. Sensitivity and specificity of Eustachian tube function tests in adults. JAMA Otolaryngol Head Neck Surg. 2013;139(7):719-727. 29) Anastasiadou S, Bountzis P, Gkogkos DE, Karkos P, Constantinidis J, Triaridis S, Psillas G. Eustachian Tube Dysfunction Diagnostic Pathway—What Is the Current State of the Art and How Relevant Is Chronic Nasal Disease? J Clin Med. 2024;13(13):3700. 30) Bal R, Deshmukh P. Management of Eustachian tube dysfunction: a review. Cureus. 2022;14(11):e31432. 31) Khairkar M, Jaju ND, Shingane H, et al. Chronic suppurative otitis media: a comprehensive review. Cureus. 2023;15(8):e174481. 32) Gołota K, Dzieciuchowicz Ł, Szyfter W, et al. Balloon Eustachian tuboplasty: a systematic review of technique, safety, and clinical outcomes in chronic obstructive Eustachian tube dysfunction. Healthcare (Basel). 2025;13(15):1832. 33) Karadag A, Yuncu ME, Middlebrooks EH, Tanriover N. Endoscopic trans-eustachian tube approach: identifying the precise landmarks, a novel radiological and anatomical evaluation. Surg Radiol Anat. 2024;46(5):625-634. 34) Damante MA, Turri-Zanoni M, Guazzoni A, et al. Endoscopic endonasal transpterygoid approach and the eustachian tube: preservation vs resection. Laryngoscope. Published online 2024.
123 CHAPTER VIII THE COCHLEA: ANATOMY, DEVELOPMENT, VARIABILITY AND CLINICAL IMPLICATIONS Rukiye SOYAL (Lecturer), Karabuk University, Vocational School of Health Services, Karabuk/Turkey E-mail: [email protected] ORCID: 0000-0002-1285-7883 1. Introduction The human cochlea, with its complex structure that converts auditory stimuli into neural impulses, lies at the center of auditory physiology and thus serves as a fundamental model for understanding both normal hearing mechanisms and pathological processes. Its distinctive spiral morphology, micromorphology, and biomechanical properties play a decisive role not only in auditory function but also in the success of surgical interventions such as cochlear implantation. However, due to its fragile structure, surrounding bony capsule, and rapid postmortem autolytic changes, this organ remains difficult to investigate. In recent years, macroand microanatomical studies, electron microscopy, and immunohistochemical analyses have provided new insights into the structural and molecular characteristics of the cochlea. These investigations have yielded valuable information across a broad spectrum—from sensory and supporting cells to membranous structures, from the distribution of nerve fibers to the features of the vascular network. This chapter aims to comprehensively examine the fundamental anatomical features and variations of the human cochlea, discuss the surgically critical anatomical landmarks reported in the literature that affect cochlear implant electrode placement, and evaluate the clinical significance of this region.
124 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY 2. Historical Discovery and Anatomical Description of the Human Cochlea The scientific recognition of the human cochlea dates back to the 16th century. The first records of this structure were made by Eustachi in 1564 and published nearly two centuries later by Albini in 1744. In the mid-18th century, the Neapolitan anatomist Cotugno presented a detailed description of the inner ear—particularly the cochlea—in his work De aqueductibus Auris Humana Interna using corrosion cast techniques. In the mid-19th century, Corti made a major contribution to cochlear anatomy by identifying the sensory organ that now bears his name. Toward the end of the century, Retzius advanced histological techniques and introduced detailed cellular-level descriptions and surface preparations of the human cochlea into the literature (1). 3. Development of the Cochlea The development of the cochlea begins in the early stages of pregnancy, progressing in parallel with the morphogenesis of the inner ear, and continues as a gradual process until birth. By the 4th week, the otic placode forms from the ectoderm and invaginates to become the otic vesicle; its dorsal portion differentiates into vestibular structures, while the ventral portion gives rise to the cochlea. By the 5th week, the primitive tubular form of the cochlea and the ductus reuniens develop from the ventral extension of the vesicle. Between the 8th and 9th weeks, the cochlea assumes its spiral shape, and by the 10th week, it forms a structure resembling the adult cochlea with approximately 2.5 turns. By the 12th week, the inner and outer hair cells differentiate and the Reissner’s membrane develops; at the 16th week, the scala vestibuli and scala tympani become continuous via the helicotrema. Between the 10th and 18th weeks, the cochlea grows in size and volume. From the 18th week onward, ossification of the cartilaginous tissue occurs, forming the bony labyrinth. Thus, the foundations of the hearing function are established before birth (2, 3, 4). 4. Anatomy of the Cochlea The inner ear is located within the petrous part of the temporal bone. It consists of two main components: the osseous labyrinth and the membranous labyrinth. The outer osseous labyrinth is divided into three regions — anteriorly the cochlea, centrally the vestibule, and posteriorly the semicircular canals (5, 6).
THE COCHLEA: ANATOMY, DEVELOPMENT, VARIABILITY AND CLINICAL . . . 125 The cochlea is a spiral tube approximately 3.2–4.2 cm in length and filled with endolymph. The cochlear base has a conical structure about 9 mm in diameter and extends medially toward the wall of the middle ear. In general, the human cochlea has about 2.75 spiral turns, although some cases with three complete turns have been reported (7). The entire cochlea is housed within the otic capsule, which forms part of the temporal bone. In rodents, part of the cochlea extends into the middle ear cavity, whereas in humans only a small portion (the promontory) is visible (1, 8). The most characteristic feature of the cochlea is its distinct spiral morphology ascending toward the apex. Its Latin name is derived from its coiled, snail shell– like shape. One of the proposed reasons for this nautilus-like configuration is the spatial constraints within the temporal bone. However, recent studies suggest that the cochlea’s morphological organization cannot be explained solely by anatomical limitations but also provides various functional advantages in terms of auditory processing (9, 10). Several investigations have shown that the cochlea’s gradually curving morphology may play an important role in the transmission of low-frequency sound waves. This structure, through a mechanism similar to the “whispering gallery” phenomenon, may facilitate the propagation of low frequencies and thus contribute to defining the lower limits of hearing sensitivity (11). 4.1.Modiolus In sections from the base of the cochlea to the apex of the cochlea, the inner conical structure is called the modiolus. This bony axis of the cochlea does not extend fully to the apex and terminates at the modiolar plate. Within the modiolus there are two main canals: the longitudinal canal of the modiolus, which runs along the axis, and the spiral canal of the modiolus (also known as Rosenthal’s canal), which spirals around it. The longitudinal canal reaches the base of the modiolus, forming the spiral tract of foramina and carrying the fibers of the cochlear nerve, while the spiral canal of the modiolus provides the site for the spiral ganglion of the cochlea (Corti’s ganglion) (1, 5, 10). Frequency coding in the cochlea is based on the tonotopic organization established by the passive and active properties of the basilar membrane. This arrangement allows low frequencies to be perceived at the apex and high frequencies at the base. The spiral ganglion neurons within Rosenthal’s canal encode this range of approximately 20 Hz to 20 kHz, and cochlear implants mimic this map by directing low frequencies to apical electrodes and high frequencies to basal electrodes (10, 12).
126 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY 4.2.SpiralCanaloftheCochlea The spiral canal of the cochlea begins at the base of the cochlea and extends around the modiolus up to the apex of the cochlea, measuring approximately 3 mm in diameter and 35 mm in length, making about 2.75 turns around the modiolus. Its first bend forms the promontory in the tympanic cavity (5, 6). At its base there are three main openings: the vestibular window (oval window), the cochlear window (round window), and the cochlear canaliculus. The vestibular window connects the tympanic cavity to the scala vestibuli, while the cochlear window connects the tympanic cavity to the scala tympani and is covered by the secondary tympanic membrane. The cochlear canaliculus begins in the scala tympani and opens into the jugular fossa, transmitting the cochlear aqueduct, thereby creating a pathway between the perilymph and the cerebrospinal fluid (5, 6). 4.3.OsseousSpiralLamina The osseous spiral lamina is a bony projection that spirals through the center of the spiral canal of the cochlea, dividing it into two parts. Beginning at the base of the cochlea and extending toward the apex of the cochlea, it makes approximately 2.75 turns and terminates in a hook-shaped structure called the hamulus of the osseous spiral lamina. This structure consists of two plates: the upper vestibular plate and the lower tympanic plate. Between them lie basal plates, which are more densely distributed near the spiral ganglion. This porous architecture provides both pathways for nerve fibers and structural support for the lamina (5, 6, 13). A micro-CT study by Bom et al. (13) showed that the porous structure of the osseous spiral lamina is more prominent in the tympanic plate than in the vestibular plate at the basal and middle turns, whereas the opposite is true at the apical turn. In the same study, the osseous spiral lamina was reported to be about 0.1 mm thick, with its width decreasing from approximately 1.8 mm at the base to 0.2 mm at the apex. This structure does not extend fully to the lateral wall but ends at the limbus of the osseous spiral lamina. The upper portion of the limbus is called the vestibular lip, the lower portion the tympanic lip, and the groove between them is known as the internal spiral sulcus. Through the nervous foramina in this region, nerve fibers emerging from the organ of Corti pass into the spiral canal of the modiolus (5, 6). The opening between the limbus of the osseous spiral lamina and the spiral canal of the cochlea is closed by the basilar membrane, dividing the cochlea into
THE COCHLEA: ANATOMY, DEVELOPMENT, VARIABILITY AND CLINICAL . . . 127 its three main chambers: the scala vestibuli, the scala media (cochlear duct), and the scala tympani. These chambers communicate at the apex through the helicotrema (3, 5, 6). 4.4.ScalaMedia(CochlearDuct) The cochlear duct is a triangular cross-sectional membranous canal located between the scala vestibuli and the scala tympani, containing endolymph unlike the surrounding spaces. Its base is formed by the lateral wall of the cochlea, and its apex by the limbus of the osseous spiral lamina (1, 5). Its walls are named as follows: • Upper wall: Vestibular wall of the cochlear duct (Reissner’s membrane) • Lower wall: Tympanic wall of the cochlear duct (Basilar membrane) • Outer wall: External wall of the cochlear duct This canal ends blindly at both ends of the cochlea: at the apex as the cupular cecum and at the base as the vestibular cecum. In addition, the cochlear duct connects to the saccule via the reuniting duct (ductus reuniens), which is located near the vestibular cecum (1, 5). 4.5.Reissner’sMembrane The Reissner’s membrane is a thin, avascular, bilayered structure that separates the endolymph in the cochlear duct from the perilymph in the scala vestibuli. Its inner surface is lined with simple epithelial cells of the membranous labyrinth, while the outer surface is covered by mesenchymalderived fibroblasts and mesoepithelial cells. These two layers are separated by a thin basement membrane, providing selective permeability between the two fluids of different ionic composition and thereby contributing to the maintenance of the endocochlear potential. Reissner’s membrane also plays a role in fluid homeostasis through its ion-pumping capacity and the presence of cation, chloride, and potassium channels on its apical surface (1, 8, 14). In humans, epithelial cell boundaries display an irregular, puzzlelike pattern, whereas in children they are more regularly polygonal. The discontinuous mesoepithelial layer and the function of melanocytes on the perilymphatic side remain unclear. When the pressure balance between endolymph and perilymph is disrupted, the membrane may bulge; moreover, electrode placement into the scala vestibuli can compromise the integrity
128 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY of Reissner’s membrane, leading to loss of the endocochlear potential and reduction of residual hearing (1, 8, 14). 4.6.BasilarMembrane The basilar membrane is an avascular, elastic band of connective tissue extending between the osseous spiral lamina and the lateral wall of the cochlea, forming the boundary between the scala media and the scala tympani. This trampoline-like structure consists of radial and rectangular fibers embedded in a matrix containing components such as type II, IV, and XI collagen, fibronectin, and proteoglycans. Its medial portion, called the pars tecta (arcuate zone), is partially covered by the osseous spiral lamina and transmits nerve fibers to the organ of Corti via the habenulae perforatae, while its lateral portion, the pars pectinata, is free to vibrate in response to sound. Beneath both regions lies a connective tissue layer rich in blood vessels, including the spiral vessel (1, 5, 8). The basilar membrane is narrow and thick at the basal region (about 0.1 mm) and becomes wider and thinner toward the apex (about 0.5 mm). This morphological gradient underlies the tonotopic organization that spatially encodes auditory frequencies. Hair cells and nerve fibers tuned to specific frequencies are distributed along the membrane according to these properties, enabling the auditory organ to detect and process sound frequencies (1, 5, 8). Because of its thinning in the apical portion, the basilar membrane carries a risk of perforation during surgical procedures such as electrode implantation. In addition, phagocytic tympanic covering cells located along the scala tympani may form a fibroblastic capsule upon contact with the electrode; excessive proliferation of this capsule can increase electrode impedance and negatively affect the implant’s long-term performance. Therefore, maintaining the integrity of the basilar membrane during surgery is of critical importance (1, 5, 8). 4.7.StriaVascularisandSpiralLigament The lateral wall of the cochlea is bounded medially by the stria vascularis and laterally by the spiral ligament, forming the outer margin of the scala media. The stria vascularis displays a three-layered arrangement consisting of marginal, intermediate, and basal cell layers extending from inside to outside. This unique structure is critical for the production and maintenance of the endocochlear potential. Through its rich capillary network, ion pumps, and particularly
THE COCHLEA: ANATOMY, DEVELOPMENT, VARIABILITY AND CLINICAL . . . 135 most commonly damaged structures are the spiral ligament, basilar membrane, and the junctional parts of the osseous spiral lamina at the first turn (30). In developmentally underdeveloped cochleae, an increased angle between the first and second turns and a shortened basal length can make electrode advancement more difficult, thereby increasing the risk of membrane perforation. Sharp bends in this region may further hinder electrode progression and elevate the perforation risk. Additionally, some authors have reported that the orientation of the cochlea can change during the early stages of life (1, 31). 7. Conclusion The human cochlea, as the primary sensory organ of hearing, serves not only as a critical model for understanding auditory physiology but also for surgical applications such as cochlear implantation. As summarized in this review, the anatomical characteristics of the cochlea, along with its developmental and individual variations, have a direct impact on electrode placement and longterm outcomes of implantation. A detailed understanding of these anatomical variations helps minimize intraoperative trauma, preserve residual hearing, and improve implant success. Furthermore, factors such as aging, malformations, and ossification, which affect the cochlea, must be carefully considered during surgical planning and patient selection. Therefore, advances in modern imaging techniques and anatomical research will enable cochlear implantation to be performed more safely and effectively in the future. References 1. Rask-Andersen H, Liu W, Erixon E, et al. Human cochlea: anatomical characteristics and their relevance for cochlear implantation. Anat Rec (Hoboken). 2012;295(11):1791-1811. 2. Lim R, Brichta AM. Anatomical and physiological development of the human inner ear. Hear Res. 2016;338:9-21. 3. Driver EC, Kelley MW. Development of the cochlea. Dev. 2020;147. 4. Feraco P, Piccinini S, Gagliardo C. Imaging of inner ear malformations: a primer for radiologists. Radiol Med. 2021;126(10):1282-1295. 5. Drake TL, Vogl WA, Mitcheel AWM. Gray’s Anatomy for Students. 4. Edition:Elsevier;2014. 6. Moore KL, Dalley AF, Agur AMR. Clinically Oriented Anatomy. 8. Edition:WoltersKluwer;2017. 7. Tian Q, Linthicum FH Jr, Fayad JN. Human cochleae with three turns: an unreported malformation. Laryngoscope. 2006;116(5):800-803.
136 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY 8. Raphael Y, Altschuler RA. Structure and innervation of the cochlea. Brain Res Bull. 2003;60(5-6):397-422. 9. Simoni E, Gentilin E, Candito M, et al. Immune Response After Cochlear Implantation. Front Neurol. 2020;11:341. 10. Hrncirik F, Roberts I, Sevgili I, Swords C, Bance M. Models of Cochlea Used in Cochlear Implant Research: A Review. Ann Biomed Eng. 2023;51(7):1390-1407. 11. Manoussaki D, Chadwick RS, Ketten DR, Arruda J, Dimitriadis EK, O’Malley JT. The influence of cochlear shape on low-frequency hearing. Proc Natl Acad Sci U S A. 2008;105(16):6162-6166. 12. Hallowell D, Silverman R. Hearing and deafness. 4th ed. J. Acoust. Soc. Am. 65(3):867–867, 1979. 13. Bom Braga GO, Parrilli A, Zboray R, Bulatović M, Wagner F. Quantitative Evaluation of the 3D Anatomy of the Human Osseous Spiral Lamina Using MicroCT. J Assoc Res Otolaryngol. 2023;24(4):441-452. 14. Iurato S, Taidelli G. Struttura della membrana di Reissner [Structure of Reissner’s membrane]. Boll Soc Ital Biol Sper. 1967;43(23):1657-1659. 15. Glueckert R, Pfaller K, Kinnefors A, Schrott-Fischer A, Rask-Andersen H. High resolution scanning electron microscopy of the human organ of Corti. A study using freshly fixed surgical specimens. Hear Res. 2005;199(1-2):40-56. 16. Nakashima T, Naganawa S, Sone M, et al. Disorders of cochlear blood flow. Brain Res Brain Res Rev. 2003;43(1):17-28. 17. Würfel W, Lanfermann H, Lenarz T, Majdani O. Cochlear length determination using Cone Beam Computed Tomography in a clinical setting. Hear Res. 2014;316:65-72. 18. Meng J, Li S, Zhang F, Li Q, Qin Z. Cochlear Size and Shape Variability and Implications in Cochlear Implantation Surgery. Otol Neurotol. 2016;37(9):1307-1313. 19. Wever EG. II The Width of the Basilar Membrane in Man. Ann Otol Rhinol Laryngol 1938;47(1):37-47. 20. Liu W, Atturo F, Aldaya R, et al. Macromolecular organization and fine structure of the human basilar membrane - RELEVANCE for cochlear implantation. Cell Tissue Res. 2015;360(2):245-262. 21. Meenderink SWF, Shera CA, Valero MD, Liberman MC, Abdala C. Morphological Immaturity of the Neonatal Organ of Corti and Associated Structures in Humans. J Assoc Res Otolaryngol. 2019;20(5):461-474.
THE COCHLEA: ANATOMY, DEVELOPMENT, VARIABILITY AND CLINICAL . . . 137 22. Raufer S, Idoff C, Zosuls A, et al. Anatomy of the Human Osseous Spiral Lamina and Cochlear Partition Bridge: Relevance for Cochlear Partition Motion. J Assoc Res Otolaryngol. 2020;21(2):171-182. 23. Demarcy T, Vandersteen C, Guevara N, et al. Automated analysis of human cochlea shape variability from segmented μCT images. Comput Med Imaging Graph. 2017;59:1-12. 24. Keithley EM. Pathology and mechanisms of cochlear aging. J Neurosci Res. 2020;98(9):1674-1684. 25. Wu PZ, Liberman LD, Bennett K, de Gruttola V, O’Malley JT, Liberman MC. Primary Neural Degeneration in the Human Cochlea: Evidence for Hidden Hearing Loss in the Aging Ear. Neuroscience. 2019;407:8-20. 26. Sennaroğlu L, Bajin MD. Classification and Current Management of Inner Ear Malformations. Balkan Med J. 2017;34(5):397-411. 27. Vashishth A, Fulcheri A, Prasad SC, et al. Cochlear Implantation in Cochlear Ossification: Retrospective Review of Etiologies, Surgical Considerations, and Auditory Outcomes. Otol Neurotol. 2018;39(1):17-28. 28. Walker N, Pham N, Ledbetter L. Cochlear Implantation: Current and Future Roles of Imaging Before, During, and After Implantation. Curr Radiol Rep. 2023;11:97–107. 29. Tokat T, Catli T, Bozkurt EB, Olgun L. Surgical methods and auditory outcomes of cochlear implantation in cochlear ossification. J Int Adv Otol. 2022;18:51–6. 30. Kennedy DW. Multichannel intracochlear electrodes: mechanism of insertion trauma. Laryngoscope. 1987;97(1):42-49. 31. Martinez-Monedero R, Niparko JK, Aygun N. Cochlear coiling pattern and orientation differences in cochlear implant candidates. Otol Neurotol. 2011;32(7):1086-1093.
139 CHAPTER IX ANATOMICAL AND CLINICAL PERSPECTIVES ON THE EXTERNAL AUDITORY CANAL Sümeyra DOĞMUŞ (PT, PhD. Can.), Necmettin Erbakan University, Faculty of Medicine, Department of Anatomy, Konya/Turkey E-mail: fzt.smyr[email protected] ORCID: 0009-0005-7673-1293 1. Introduction The external auditory canal is one of the peripheral components of the auditory system and plays a critical role in transmitting sound waves from the external environment to the middle ear. The canal functions both as a protective barrier between the external environment and the middle ear and as a modulator of the resonance properties of sound, thereby contributing to the quality of hearing. (1,2) Anatomically, the external auditory canal consists of cartilaginous and osseous components extending from lateral to medial. The length, diameter, inclination, and contour of the canal walls may vary considerably among individuals. (1) Such individual morphological variations must be taken into account in a wide range of clinical contexts, from otoscopic examination to endoscopic surgery, from the fabrication of patient-specific hearing aids to the interpretation of imaging modalities. (3) The external auditory canal is susceptible to a variety of pathological conditions. These include otitis externa, cerumen impaction, traumatic lesions, and both benign and malignant neoplasms. (2) Accurate identification of these pathologies and the implementation of appropriate therapeutic strategies require a comprehensive understanding of both the normal anatomical configuration and developmental variations of the canal. In recent years, advances in high-resolution computed tomography (CT) and cone-beam computed tomography (CBCT) have enabled detailed assessment of the three-dimensional morphological characteristics of
140 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY the external auditory canal. These imaging techniques facilitate the identification of structural variations and stenoses of the canal in clinical evaluations, thereby allowing optimization of surgical planning. (4,5) This chapter will address the embryological development, anatomical characteristics, morphological variations, and clinical significance of the external auditory canal. 2. Embryology of the External Auditory Canal The anatomical structures of the adult human develop from the embryonic branchial arches. The term “branchial arches” may alternatively be referred to as “pharyngeal arches”. The development of the branchial structures occurs between the fourth and sixth weeks of gestation. (6) Disruptions in the developmental processes of the branchial arches, numbered one through six, can result in congenital anomalies. (7) While the majority of the ear originates from the first branchial arch, certain portions are derived from the second branchial arch. (6) Structures arising from the first branchial arch include the auricle, external auditory canal, malleus, incus, the mandibular branch of the trigeminal nerve, the mandible, and the masticatory muscles. In contrast, the second branchial arch gives rise to the stapedius, facial nerve, vestibulocochlear nerve, facial expression muscles, and the body and lesser horn of the hyoid bone. (8) According to the developmental theory proposed by Wilhelm His in 1885, six auricular prominences contribute to the shaping of the human auricle. Three of these prominences (tragus, helix, and cymba concha) are located on the first pharyngeal arch, whereas the remaining three (auricular concha, antihelix, and antitragus) are situated on the second pharyngeal arch. (8) These prominences fuse to form the auricle. During embryonic development, the external ear begins to form in the lower cervical region, subsequently migrating postero-laterally to reach its normal anatomical position. The external auditory canal begins to form as an invagination of the first branchial arch at approximately the sixth week of gestation. During the medial invagination and morphogenesis of the external auditory canal, the annulus tympanicus serves as an anatomical stabilizer in the developmental process. In other words, the annulus tympanicus provides a fundamental structural framework for stabilizing the bony portion of the external auditory canal and determining the final configuration of its medial boundary. (9) By approximately the eighteenth week of gestation, the morphological type of the
ANATOMICAL AND CLINICAL PERSPECTIVES ON THE EXTERNAL AUDITORY . . . 141 external auditory canal becomes distinct. The fetus acquires auditory function around the twenty-sixth week of gestation, whereas the auricle continues to grow until approximately seven to ten years of age. (6) 3. Anatomy of the External Auditory Canal 3.1.GeneralAnatomicalFeatures The ear is a vital organ responsible for the functions of hearing and balance. Anatomically, it is divided into three regions: the external ear, the middle ear, and the inner ear. The external ear, which is responsible for collecting and transmitting sound waves, consists of the auricle (pinna) and the external auditory canal (meatus acusticus externus). (2) The external auditory canal is a tubular structure, typically S-shaped, extending from the conchae of the auricle to the tympanic membrane. The canal measures approximately 2.5-3 cm in length, with the lateral one-third forming the cartilaginous portion and the medial two-thirds comprising the bony portion. (10) In neonates, nearly the entire external auditory canal is cartilaginous, with the bony portion increasing as the temporal bone develops. (11) Two areas of constriction are observed in the external auditory canal: the first at the junction of the cartilaginous and bony portions, and the second, referred to as the “isthmus”, typically located approximately 5 mm lateral to the tympanic membrane, representing the narrowest point. (2) The junction between the cartilaginous and bony portions is termed the “osteocartilaginous junction.” Due to its S-shape, the canal has two bends: the segment up to the second bend corresponds to the cartilaginous portion, whereas the portion beyond the second bend constitutes the bony portion. The angle of the first bend is referred to as the “conchae-meatal angle,” while that of the second bend is called the “cartilage-bone angle”. (12) The cartilaginous portion, referred to as the cartilago meatus acustici, extends postero-superiorly up to the porus acusticus externus. The bony portion, beginning at the porus acusticus externus, extends antero-inferiorly to the annulus tympanicus, where the tympanic membrane attaches. (5,6) The bony portion of the external auditory canal (including the floor, anterior wall, and infero-posterior wall) is primarily formed by the tympanic part of the temporal bone, whereas the roof and supero-posterior wall are composed of the squamous part. The posterior wall of the canal is also contributed to by the mastoid part of the temporal bone. (13) The pars tympanica lies beneath the squamous part of the temporal bone, with the tympanosquamous fissure separating the two structures. The
142 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY pars tympanica is located anterior to the mastoid part of the temporal bone, with the tympanomastoid fissure demarcating the boundary. (14) In addition to contributing to the majority of the bony portion, the pars tympanica serves as a critical structure guiding the trajectory of the external auditory canal (2). The skin covering the auricle continues along the external auditory canal, extending to cover the lateral surface of the tympanic membrane. The portion of skin covering the tympanic membrane consists solely of the epidermal layer. (2) The skin overlying the cartilaginous portion is thick, containing sebaceous glands, ceruminous glands, hair follicles known as tragi, and the Santorini fissures beneath it. In contrast, the skin covering the bony portion is thin, devoid of these structures, and firmly adherent to the underlying periosteum. (6,13) The ceruminous and sebaceous glands secrete cerumen, which, together with the tragi, forms a protective barrier preventing the entry of foreign bodies into the middle ear. (2) The Santorini fissures are small, normal anatomical openings located in the antero-inferior region of the cartilaginous portion, playing a critical role in the potential spread of infections to the temporomandibular joint, parotid gland, and external auditory canal. (6) The external auditory canal is vascularized by branches of the external carotid artery, including the posterior auricular artery and the superficial temporal artery, particularly via its auricular branches. Its venous drainage occurs via the pterygoid plexus, the maxillary vein, and the external jugular vein. Lymphatic drainage is directed to the superficial parotid lymph nodes, mastoid lymph nodes, and superficial cervical lymph nodes. The external auditory canal is innervated by the auriculotemporal nerve and the auricular branch of the vagus nerve. (2) 3.2.MorphologicalShapeTypes Mahboubi et al. (2012) reported six morphological types of the bony portion of the external auditory canal based on coronal CT images, where the maximal supero-inferior diameter was observed. These shape types include conical, cylindrical, ovoid, reverse conical, and hourglass configurations. If the diameter of the bony portion increases from medial to lateral, the canal is classified as a conical external auditory canal; conversely, if the diameter decreases from medial to lateral, it is termed a reverse conical external auditory canal. If the diameter initially decreases and then increases from medial to lateral, it is defined as an hourglass shaped external auditory canal; if it first increases and then decreases, it is classified as ovoid shaped; and if no significant change in diameter is observed, it is defined as cylindrical. (15)
ANATOMICAL AND CLINICAL PERSPECTIVES ON THE EXTERNAL AUDITORY . . . 143 In the study by Mahboubi et al. (2012), the conical external auditory canal was the most prevalent (64%), whereas the cylindrical type was the least common (2%). In contrast, Lee et al. (2020) reported that the cylindrical type was most frequent (36%) and the reverse conical type least frequent (6%), and they did not observe any ovoid-shaped canals. (16) These findings indicate that the prevalence of external auditory canal morphological types varies across studies in the literature. Atlanoğlu and Topuz (2022), in their CT-based evaluation of the external auditory canal, reported three morphological types of the bony portion on sagittal images near the level of the tympanic membrane. These were classified as oval (74.4%), triangular (16.3%), and round (9.4%) external auditory canals. (17) 3.3.Variations Significant variations of the external auditory canal include bony overhangs, the presence of the foramen tympanicum, exostosis (new bone formation), and duplication of the canal. These anatomical variations (particularly the bony overhangs) may hinder both the clinical examination of critical regions such as the tympanic membrane and the tympanic cavity, and surgical access to these structures during otologic procedures. (18) Bony overhangs of the external auditory canal are classified according to their location within the canal as anterior canal overhang, posterior canal overhang, and inferior canal overhang. (19) Some authors have further divided the canal into four quadrants, describing antero-superior, antero-inferior, postero-superior, and postero-inferior canal overhangs. (18) The anterior canal overhang is located laterally, forming a narrow angle with the tympanic membrane, thereby restricting the visual field during otoscopy. (19) Middle ear surgery is particularly more challenging in the presence of an anterior canal overhang. Ohira et al. (2022) reported that in cases with an inferior canal overhang, the sinus tympani was shallower and the vertical segment of the facial nerve coursed more superficially. In such cases, the risk of iatrogenic injury is increased. Preoperative identification of a posterior canal overhang may reduce the risk of facial nerve injury during canal resection. (4) The presence of a secondary, rudimentary external auditory canal is referred to as a duplicated external auditory canal and represents a very rare anomaly of the first branchial arch. Duplicated external auditory canals account for 1-8% of all branchial arch anomalies. In cases of duplication, it may appear as a mass protruding from the external auditory canal or as a
144 OVERVIEW OF HEAD & NECK CLINICAL ANATOMY fistula at the osseocartilaginous junction, and it generally does not affect the middle ear cavity. (6) Another variation observed in the external auditory canal is the foramen tympanicum. The foramen tympanicum was first described in 1844 by the German anatomist and embryologist Emil Huschke, and is therefore also known as “Huschke’s foramen”. (20) The foramen tympanicum is a developmental defect located in the antero-inferior portion of the external auditory canal and posteromedial to the temporomandibular joint. (21) It arises due to abnormal ossification of the tympanic part of the temporal bone during embryogenesis and typically diminishes during childhood, closing completely before the age of five, or may persist into adulthood. If it persists into adulthood, it is considered an anatomical variation. (22) Although the presence of the foramen tympanicum is generally asymptomatic, infections in the external acoustic meatus can potentially spread to adjacent structures such as the temporomandibular joint and the parotid gland, may pose complications during temporomandibular joint arthroscopy, and can result in salivary flow into the external acoustic meatus during mastication. (20,21,23) Less commonly, it has also been reported to cause tinnitus, otalgia, and conductive hearing loss (20). The reported prevalence of the foramen tympanicum ranges between 4.6% and 17.9%. (24) Another variation observed in the external auditory canal is exostosis, commonly referred to as surfer’s ear and it is typically bilateral. (25) Exostoses are irreversible, non-life-threatening bony protrusions in the external auditory canal that may develop in individuals exposed to cold water for prolonged periods. (26) Exostoses are classified into three grades based on the percentage of external auditory canal occlusion: Grade I: 1%-33% occlusion, Grade II: 34%-66% occlusion, Grade III: 67%-100% occlusion. (27) The prevalence of exostoses among cold-water surfers has been reported to range from 61% to 80%. (26) 4. Clinical Significance and Related Pathologies of the External Auditory Canal The external auditory canal represents the initial transmission segment in which the resonance of sounds within the 2–4 kHz frequency range, collected by the auricle, is modulated and amplified. (28) The anatomical structures involved in sound conduction include, in sequence, the auricle, external auditory canal, tympanic membrane, and auditory ossicles (stapes, malleus, and incus).