nuclei of the cranial pair V via the secondary ventral and dorsal routes. The solitary tract nucleus in the dorsal part of the medulla oblongata is reached by afferent general (sensitivity) and special (taste) routes that are guided by the cranial nerves VII and IX. This is followed by afferent path­ways connecting to the base nuclei, such as the thalamus, and then to the cerebral cortex on the postcentral gyrus of both hemispheres. From there, efferent pathways lead to the brainstem motor nuclei (V, VII, IX, XII). Both afferent general (sensitive) and special (taste) and efferent special (motor) and general (parasympathetic) routes connecting both sides of the cortex and brainstem come and depart as direct and cross paths, according to the hemisphere dominance. By combining the cranial nerves that function in the oral phase, this arrangement provides each cerebral hemisphere with access to the entirety of the information gathered in the oral cavity. This allows effective directives from each hemisphere to reach both sides of the brainstem. The peripheral information travels to the motor cortex, where it is regulated and retransmitted to the base nuclei and brainstem after the base nuclei have activated the sensory cortex on both sides. The latter would result in an oral dynamic that would expel its contents into the pharynx through the efferent pathways of the tri­geminal, facial, and hypoglossal nerves. Despite the dominance of one hemisphere, both are fully aware and capable of performing their entire range of duties. There is proof that the non-dominant (non-damaged) hemisphere can be more represented when the dominant hemisphere is wounded, which is linked to apparent function recovery. The corpus callosum has channels that connect the hemispheres by going from side to side. Therefore, in healthy people, a connection that travels through the corpus callosum allows the dominant cortex to inhibit the contralateral one. Excitatory routes from the dominant motor cortex to the base nuclei of the contralateral hemisphere can also be taken into account. Despite the inhibition of the non-dominant hemisphere’s motor and sensory cortex, this architecture would account for both the integrated bilateral stimulus that is observed and the function recovery that has already been demonstrated in cases of dominant hemisphere lesions. The existence of these excitatory routes in both directions might also be assumed. There are also connecting channels that lead to and depart from the cerebellum between the brainstem and the cortex. These pathways are thought to be able to control the sequencing and intensity of muscle contractions. In this manner, the motor nuclei of the cranial nerves V, VII, IX, and XII will form synapses with the cerebellar pathways that link to efferent voluntary (cortex-nuclear) routes. The oral effectors receive efferent impulses from these nuclei, which provide them with signal­ing of appropriate contraction intensity and sequence. The cerebellum and brain coordinate these signals. In order to produce the required oral ejection, the bolus volume and viscosity will inter­fere with the muscle contraction intensity, which is determined by the cortex based on the oral qualication. However, all sequences involving the oral phase will share the effectors’ contraction activation sequence, indicating that the neural organization has a preset sequence. Temperature and taste had no effect on the cortical denition of the intensity of mouth muscle activity. This nding indicates that, within acceptable bounds, chemical, thermal, and most denitely pain perception do not impede oral activity, which is controlled by mechanical reception, specically volume, and viscosity, which will inuence the number of motor units that must be depolarized for an efcient oral phase. Information transmission and maintenance during the reex phase of swallowing will depend on the production of the required and sufcient muscle contraction intensity. The brain regulation of the reex pharyngeal phase will respond to the stimulus of the pressure intensity transmitted by the oral phase. The oral phase should have some inuence on the esophageal phase, which is also reex. The following is a description of the fundamental mechanics of the oral phase of swallowing: by contracting their chewing muscles, the dental arcades make contact with one another (pair V). In order to stop pressure from escaping from the oral cavity during the bolus transference to the pharynx, the arrangement of the dental arcades enables skin-inserted muscles in the orbicularis oris (pair VII) and specic buccinators to create intraoral pressure resistance. The tongue (pair XII) will be able to evacuate the bolus due to the pressured and resistive oral cavity, which will then convey the bolus and pressure to the throat. At the start of the pharyngeal phase, the levator veli palatini muscle will project the soft palate superiorly and posteriorly against the pterygo-pharyngeus fascicle, the rst fascicle of the pharynx superior constrictor muscle, while the tensor veli palatini muscle (pair V) will provide resistance to the soft palate as part of the oral phase actions. Because the suprahyoid muscles reverse the tweezers action between the larynx and vertebral body, they raise the hyoid and larynx, opening the pharyngoesophageal transition. The cranial nerves V and VII, as well as C1 through the ansa cervicalis, are primarily responsible for the elevation of the hyoid and larynx, which serves to reverse the tweezers action caused by the larynx’s apposition against the spine. Beginning at the end of the oral phase, the hyoid elevation continues to be active until the end of the pharyngeal phase. The pharyngeal distal resistance will decrease

properties, and the cranial nerves VII (facial) and IX (glossopharyngeal) mediate this process through parasympathetic bers. Saliva is distributed over the oral, pharyngeal, and even vestibular mucosa during spontaneous swallowing, which humidies these membranes and most likely aids in keeping the mucus uid over the laryngeal ventricles. Continuous airow from inhalation and expiration dries the mucosa, but spontaneous swallowing maintains the mucous membranes’ mois­ture content. Controlling the small volume of liquids adsorbed to the laryngeal vestibule walls and eliminating any overow over this mucosa are two other benets of spontaneous swallowing. The epiglottic tubercle presses on the adducted vestibule folds during swallowing, creating a virtual vestibule lumen and expelling any surplus to the pharynx.

subsequently be connected to the vagus nerve, which would also exhibit this type of ber. Therefore, in conjunction with the vagus nerve, the accessory (XI) nerve is also in charge of motor innervation of the musculature of the palate, pharynx, larynx, and esophagus. The palatoglossal muscle, inner­vated by the motor component of the pharyngeal plexus (X, XI), adjusts over the tongue on both sides during the pharyngeal phase to stop pressure from returning to the oral cavity. The potential pressure escape from the oropharynx to the rhinopharynx is prevented by the tension (V) and ele­vation of the palate (X, XI) against the rst fascicle (pterygopharyngeal) of the upper constrictor muscle of the pharynx, which is innervated by the cranial nerves X and XI. Each of the pharynx’s superior, middle, and inferior constrictor muscles is made up of separate components with unique insertions. Each of these components is placed in the posterior median line of the pharynx (pharyn­geal raphé) on one side and in anterolateral xed places on the other. They are able to contract in sequential mode as a result of their motor units being individually tailored. There are two portions (chondropharyngeal and ceratopharyngeal) in the middle, two parts (thyreopharyngeal and crico­pharyngeal) in the inferior, and four parts (pterygopharyngeal, buccopharyngeal, mylopharyngeal, and glossopharyngeal) in the superior. Two fascicles, the upper oblique and the lower transverse, are present in the cricopharyngeal, and their bers appear to cross in the midline. Muscular absence results in an architecturally less-resistant region between the two cricopharyngeal muscle fascicles. The entire oropharyngeal extension is occupied by the superior constrictor’s four components. In order to isolate and stop pressure escapes from the oropharynx to the rhinopharynx, just the rst segment of its upper (pterygopharyngeal) section must perform apposition against the palate. The pharynx can simultaneously receive oral pressure without encountering any resistance. Since the pharynx wall lacks a circular muscle, pharyngeal peristalsis is not produced by the successive con­traction of the superior, middle, and inferior constrictors. A constrictor muscle contraction causes a pressure sequence to be generated in the cranial-caudal direction when the pharyngeal contiguous cavities close, with the exception of the pharyngoesophageal transition, which opens due to the elevation of the hyoid and larynx. By opening the pharyngoesophageal transition, this pressure series moves the temporary bolus from the pharynx to the permissive, less resistive esophagus. Peristalsis is by denition a sequential expression generated by the circular layer of muscles. Thus, it is not appropriate to classify this cranial-caudal pressure sequence with distal reduced resistance and no muscle circular layer as peristalsis or peristalsis-like, as is commonly dened. The cranial nerves V and VII as well as the (C1) cervical plexus, which is related to the hypoglossal nerve via the ansa cervicalis, innervate the suprahyoid muscles. The mylohyoid and anterior belly of the digastric muscles are innervated by the mylohyoid branch of the mandibular nerve (mixed root of trigemi­nal–V); the facial nerve (VII) innervates the posterior belly of the digastric and the stylohyoid mus­cles. Through the hypoglossa l (XII) nerve, the ansa cervicalis (typically C1) in nervates the geniohyoid and thyrohyoid muscles. The additional infrahyoid muscles are innervated by the cervical plexus (often C2) via the ansa cervicalis. The infrahyoid group modulates the suprahyoid muscle group, which is in charge of the hyoid and larynx’s upward and forward motion. By doing this, the pharyn­goesophageal transition is opened and the larynx is moved away from the vertebral body. Furthermore, depending on the bolus volume and viscosity, the suprahyoid group can maintain this open position while moving the larynx away. The contraction of the longitudinal pharyngeal mus­cles, the palatopharyngeal muscle, innervated by motor bers from cranial nerves X and XI, and the stylopharyngeal muscles, innervated by the glossopharyngeal (IX) nerve, also aids in the opening of the pharyngoesophageal transition. A preventative apnea, also known as swallowing apnea, develops as a nal act while still in the oral phase. It is absorbed by the pharyngeal phase and lasts until its conclusion. Independent vocal fold adduction (X, XI) and vestibular fold closure with the bolus passage through the already open pharyngoesophageal transition are linked to the airways resistance caused by apnea. By elevating the hyoid and larynx, the pre-epiglottic fatty cushion is compressed, causing the vestibular folds to adduct. This compression occurs within the pre­epiglottic brous area. The lateral portions of the tapering end of the epiglottis, which correspond to the protrusion of the vestibular folds on both sides, are the space’s point of least resistance. As a result, the vestibular folds medially move and end up in apposition against the epiglottis tubercle due to the compression created by this fatty cushion on the epiglottis’s sides. When it is its turn, the tongue-everted epiglottis travels posteriorly, adjusting its tubercle against the vestibular folds that have now been adduced. The bolus is forced from the pharynx into the esophagus at the same time by the sequential, cranio-caudal contraction of the constrictor muscles, including the crycopharin­geal one (nerves X and XI). Both the reex pharyngeal and esophageal phases exhibit anatomical and functional relationships. Skeletal striated muscles, such as those of the mouth and throat, form the rst 10 cm of the esophagus. In fresh anatomical specimens, a muscular distinction is visible

macroscopically in the distal extremity of this striated segment by 2 or 3 cm. This muscular distinc­tion is dened microscopically as a mixture of skeletal striated muscle (long and multinucleated bers) and short and mononucleated smooth muscle bers, where the rst ganglion of the myenteric plexus appears. The distal pharynx, where a tweezer action seals the pharynx between the larynx (cricoid cartilage) and the cervical lordosis at the level of the fth to sixth cervical vertebrae, is the high-pressure zone known as the upper esophageal sphincter. The cricopharyngeal muscle, which is a component of the inferior pharyngeal constrictor, is typically thought to be the cause of this elevated pressure. This idea is a serious misinterpretation of the region’s anatomical and functional features. The thyropharyngeal and cricopharyngeal fascicles make up the skeletal striated muscle that serves as the inferior constrictor of the pharynx. The organization of the cricopharyngeal fas­cicle consists of two ber parts: an upper, oblique and a lower, transverse. The top one attaches on the posterior pharyngeal raphé on both sides of the cricoid cartilage, where its bers extend from the bottom upward and from lateral to medial. The lower or transverse portion intercrosses at the mid­line, where the raphé is invisible, and inserts on either side of the cricoid cartilage in a transverse manner. At the level of the transverse cricopharyngeal portion, the pharyngeal lumen is about 17 mm wide. This area lacks a muscular ring, which is more accurately described as a muscular half-curvature. An anatomically less-resistant point, known as the Killian zone, is created by the divergence of the oblique and transverse parts of the cricopharyngeal muscle. It is in this zone that the posterior pharyngeal diverticulum, also referred to as Zenker’s diverticulum, can occur. Because of the tweezer action created by the vertebral body and the larynx, this anatomically less-resistant location also happens to be the point of higher pressure levels. The pharynx and esophagus are intercommunicated by the open pharyngeal-esophageal transition, which enables the ow of con­trast material to ll both cavities nearly simultaneously during the videouoroscopic examination. It is evident that during the pharyngeal phase, there is a relationship between the esophageal and pharyngeal cavities and the contrast medium. As a result, the esophageal and pharyngeal phases almost begin at the same time, indicating a denite functional link between them that is as consis­tent, if not more so, than that between the oral and pharyngeal phases. This fact indicates that the conduction of the contents transferred by the oral phase is the responsibility of the pharyngeal and esophageal phases.

contraction from the retention point on. Occasionally, they halt at the level of the smooth muscle of the esophagus. Secondary peristalsis is the term for this downward contractile wave that ultimately transports the remaining contents of the esophagus to the stomach. The general visceral efferent pathway (parasympathetic bers) has been thought to originate in the posterior motor nucleus of the vagus as preganglionic bers that will connect to the esophageal wall’s intraparietal ganglia. From there, postganglionic bers will connect to visceral effectors that release neurohormones that can affect the smooth portion of the esophagus’s tonus and motility. The distal circular muscula­ture is thought to be involved in the resting tonic contraction of the esophageal distal extremity. In conjunction with intrinsic and extrinsic nerves, hormones would control this resting tonic contrac­tion, producing pressure readings of about 20 mmHg. According to this widely accepted theory, the gastroesophageal transition opens to the necessary muscle relaxation that would accompany primary peristalsis. This relaxation would be brought on by vagus bers, which would prevent the circular musculature from contracting tonically. It may be mediated by vasoactive intestinal polypeptide (VIP) neurotransmitters and nitric oxide (NO). Despite popular belief, a muscular ring with the traditional features of smooth muscle sphincters has not been found in the distal part of the esophagus. Without muscle thickening, the gastroesophageal transition exhibits positive resting pressure, which disappears during the main peristaltic wave that transports the bolus to the stom­ach. This transition, known as the cardia, has been classied as a physiological sphincter because of the lack of understanding of the morphology that causes its high pressure. A total of around 27 potential pathways, either alone or in combination, have been proposed as a result of this circum­stance, including those affecting the regional muscle organization. The esophagus, as we already know, has two layers: an external layer that is longitudinal and an internal layer that is circular. When it contracts, the external layer lowers the esophageal tube’s resistance, while the internal layer forces the bolus to contract sequentially. It is plausible that the arrangement of the esophageal muscle layers is such that the internal layer exhibits short-pitch spiral bers and the external layer long-pitch spiral bers. This morphology, which is linked to the idea of energy preservation, enables us to acknowledge that the external layer’s contraction could extend the esophagus, lowering ow resistance and most likely opening the gastroesophageal transition as well. The meal would then be propelled downward by the internal layer’s successive contractions. Therefore, there would be no energy expenditure during the resting esophagus stage. The myenteric plexus would be activated during the bolus’s passage into the esophagus by the esophageal peristalsis, which would cause the gastroesophageal transition to open. The fact that the esophagus reacts differently to pure pressure distension than it does when the solid bolus is present supports this theory.

superior pharyngeal constrictors, also come together to create a strong circular seal. Aside from the elevation of the soft palate, many other processes take place to provide space for the ingested bolus to enter the oropharynx. In the sagittal plane, the pharynx expands as the posterior tongue, hyoid, and larynx travel upward and forward. Essentially, the bolus descends down the ramp, formed by the attening and forward motion of the posterior tongue, and enters the chute. In addition, the contraction of the pharyngeal levators, such as the stylopharyngeus muscle, helps to widen the width of the pharynx.