I. Overview of swallowing disorders (a) Definition Swallowing disorders refer to the impairment of the physiological function of transferring food through the mouth to the stomach. The term does not cover transfer disorders before food enters the mouth, nor does it cover transfer disorders after food reaches the stomach (e.g., duodenal leak). (b) Why should we be concerned about swallowing disorders? 1. Important function: Healthy people need to swallow about 600 times a day, which is one of the basic components of the ability to perform activities of daily living. 2. High prevalence: 35%-45% of patients in the acute phase of stroke have swallowing disorders. About half of these patients are unable to regain swallowing function within the first week after stroke onset, resulting in swallowing disorders that last for months or even a lifetime after stroke. About 60% of patients with traumatic brain injury also have varying degrees of swallowing disorders after the acute phase. 3. Serious consequences: Aspiration pneumonia, malnutrition and dehydration are the three major medical problems of swallowing disorders. Food invasion of the airway, malnutrition and dehydration are the three major risk factors for the development of pneumonia. Pneumonia is responsible for approximately 34% of deaths due to stroke. In stroke patients who survive the acute phase with persistent dysphagia, about 20% die of asphyxia and 37% develop aspiration pneumonia within the first year. In stroke patients with swallowing disorders, malnutrition begins after one week in 48.3% of patients. Malnutrition can lead to poor physical performance and reduced immunity, making it impossible to implement a functional physical rehabilitation program. Swallowing disorders may lead to a chronic state of dehydration as patients are afraid to drink or cannot drink water. Reduced saliva production predisposes to oral and pulmonary infections; leading to a state of weakness, drowsiness and apathy, which further affects swallowing ability. In addition, there is a risk of infection and dental caries due to food residue in the mouth, damage to tissue or teeth due to improper feeding and oral care, pain due to factors such as TMJ braking and dental caries, and psychosocial problems due to salivation and halitosis. All these complications significantly affect the quality of life of patients and increase their disability and mortality rate. Swallowing therapy is effective: swallowing therapy can effectively reduce complications, improve patients’ quality of life and prolong their survival. Some patients can recover physiological swallowing function through swallowing therapy. The physiological and pathological mechanisms of swallowing If the food swallowed in one swallow is regarded as a food mass of a certain volume, the physiological process of swallowing can be roughly divided into three phases according to the location of the food mass: oral phase, pharyngeal phase and esophageal phase. The oral phase can be subdivided into the oral preparation phase and the oral transit phase. Although the ingestion phase is not included in the definition of dysphagia, it is often referred to as the “ingestion-swallowing” process because ingestion and swallowing are a continuous and active process. If we start from the prior phase of ingestion, the ingestion-swallowing process can be divided into five periods: the prior phase, oral preparation phase, oral transit phase, pharyngeal phase, and esophageal phase. (a) Advance phase 1. Physiology: It includes the perception and cognition of food and tools, the planning of ingestion procedures and the execution of ingestion actions. The cerebral cortex receives food information and analyzes it, recognizes information about the hardness, consistency, temperature, odor, and the amount of bites, and decides on the speed and quantity of food to be eaten, as well as predicts the handling methods in the mouth, and reflexively causes an increase in the secretion of saliva and gastric juice. This stage ends with the entrance of food. 2. Pathology: Theoretically, any neuromuscular system injury that affects food perception and feeding movements can cause impaired feeding during the antecedent phase. (1) frontal lobe injury: mainly executive dysfunction, with one or more of the following effects on feeding: (1) behavioral initiation disorder: either a reduced internal drive to eat, or a “pathological inertia” of inconsistent speech and behavior, i.e., the patient can say how to eat correctly, but cannot actually do it. (ii) Behavioral switching disorder: a persistent phenomenon or stereotyped behavior, such as the patient continues to perform eating actions even after utensils and food are removed, or the patient continues to perform the same set of stereotyped eating actions for different foods and eating environments; (iii) Termination disorder: usually described by the family as loss of control over eating, swallowing, and binge eating. (4) Self-awareness impairment: the patient is not aware of his or her own deficits, behaves without regard for the occasion and social conventions, and even develops a polarized personality. (2) Non-dominant hemisphere cortical damage: especially seen in patients with damage to the inferior parietal lobe. In right-handed patients with right hemisphere damage, left-sided spatial neglect, left-sided feeding neglect, and left-sided food residuals are common. (3) Temporal, parietal, and occipital damage: In particular, the combined cortical areas involved in multiple sensory information processing are damaged, resulting in loss of recognition and use, which affects proper food perception and utensil use. (4) Damage to the vertebral system: typically, damage to the internal capsule vasculopathy of the corticospinal tract. Early limb weakness is followed by spastic hemiparesis and hyperreflexia, and upper extremity casual motor involvement resulting in inability to perform feeding movements. (5) Extravertebral damage: typically basal ganglia lesions, such as Parkinson’s disease or Huntington’s chorea, manifest as coordinated motor deficits that interfere with feeding function due to the inability to grasp food properly. (6) Vestibulocerebellar lesions: Ataxia with nystagmus, balance disorders, walking difficulties, or dysarthria. Inability to accurately deliver food to the mouth during ingestion. (7) Brainstem and polyneurological dysfunction: Clinical manifestations vary from mild impairment of consciousness and limb movements to severe lesions that threaten the stability of vital signs. It can affect not only the feeding function in the anterior phase, but also often affects other phases of swallowing. (B) Oral preparation 1. Physiology: The stage of food entering the mouth to be chewed, the key is to form a food mass of suitable size and consistency for swallowing. The coordinated movement of the muscles of the lips, jaw and tongue, normal taste, temperature, touch and proprioception are necessary to complete this process. The lips close to ensure that food does not spill out of the mouth and the tongue root meets the soft palate to prevent food from falling into the pharynx, thus creating a closed space in the mouth. The temporomandibular joint is an important joint for mastication. During mastication and grinding movements, the jaw alternates between anterior and retracted movements on both sides, and is accompanied by elevation movements. As a result, the lower jaw teeth can be ground diagonally over the upper jaw teeth and the food is fully ground. During this process, all masticatory muscles are mobilized. These muscles contract rhythmically in turn to complete the masticatory movement. The intraparietal muscles are the main muscles that produce the diagonal diagonal movement. The buccal and lingual muscles each play a role in mastication in order to keep food between the teeth and prevent it from falling into the buccal sulcus. The buccal muscle is responsible for extruding the food present in the buccal sulcus. The lingual muscle is responsible for mixing the food into a food mass and pushing the food mass to the anterolateral side to grind it against the hard palate. 2. Pathology: A variety of factors affecting the above physiological aspects can cause dysfunction in the oral preparatory period. Poor anterior oral closure: Poor lip closure causes food to spill out of the mouth. The pursing action of the lips and teeth is one of the elements that trigger swallowing. Even if the patient has a swallowing reflex, there is a risk of choking due to poor siping. Poor closure of the posterior part of the mouth: poor closure between the tongue root and the soft palate, resulting in food falling backward into the airway and causing aspiration. 4. Residual food in the buccal sulcus: Usually caused by paralysis of the buccal muscles, while impaired movement of the lingual muscles causes the patient to be unable to get food out of the buccal sulcus. It is common on the side of the hemiplegic patient with a shallow nasolabial sulcus and is associated with cheek puffing, lip lifting and tooth exposure. Food left in the buccal sulcus is not adequately chewed and tends to leak into the mouth when not eating, causing aspiration. 5. Dietary mass formation disorder: Aqueous, semi-liquid food does not require chewing, but it is not easy to form a suitable food mass. Semi-solid food is easier to form food masses, but requires tongue agitation and squeezing. Solid foods require chewing. The selection of food that is not suitable for the patient’s chewing ability, the disorder of tongue movement and the abnormal function of saliva secretion can cause the disorder of food mass formation. 6. Temporomandibular joint occlusion disorder: It is common for patients to suffer from joint range of motion disorder and pain caused by long-term braking of the temporomandibular joint due to nasal feeding. The masticatory muscles are innervated by the mandibular branch of the trigeminal nerve, so trigeminal nerve injury can also cause occlusal disorders. For example, if the mandibular branch of the trigeminal nerve is injured on one side, the jaw will be tilted to the affected side when opening the mouth and the bite will be weak. In addition, patients with brain injury may also experience weakness or spasticity of the occlusal muscles. 7. Cognitive dysfunction or mental abnormalities: can cause a variety of problems such as misaspiration, food residue, and unfavorable chewing. (3) Oral transit period 1. Physiology: The stage of sending the food mass formed by chewing into the pharynx. This is a random movement process, which is controlled by the cortical medulla oblongata. The beginning of the oral phase is when the tongue starts to push the food mass backward, and the beginning of the pharyngeal phase is when the food mass crosses the palatoglossal arch. First, the food mass formed during the preparatory phase is located in the middle of the lingual surface. Then, the tip of the tongue starts to move above the tongue and the contact between the tongue and the palate expands to the posterior. The tongue is lifted upward in a wavy pattern from anterior to posterior and the food mass is pushed towards the pharynx. 2. Pathology: The same pathological factors as in the oral preparatory phase can be present, in addition to a weakness of the tongue root that may lead to unfavorable pushing of food into the pharynx. (iv) Pharyngeal phase 1. Physiology: The phase of transfer of food mass from the pharynx to the esophagus through the swallowing reflex. The entire phase normally takes less than 1 second and is accompanied by a momentary cessation of respiratory movements. This phase begins when the food mass passes through the palatoglossal arch and ends when the larynx is lifted. After the food mass crosses the palatoglossal arch, the root of the tongue continues to push the food upward and backward, the receptors of the soft palate are stimulated first, triggering the soft palate to lift upward, the posterior pharyngeal wall meets the soft palate forward, closing the gap between the nasopharynx and oropharynx and closing the palatopharynx to prevent the backflow of food into the nasal cavity. The food mass is surrounded by the root of the tongue, the soft palate and the pharyngeal wall. The pharyngeal constrictor muscle contracts and the food is pushed toward the cricopharyngeal muscle, resulting in a downward pharyngeal peristaltic wave. At the same time, the larynx closes the laryngeal cavity by closing the vocal cords and the arytenoid eccrine folds, preventing food from falling into the airway. As the larynx is lifted, the cricopharyngeal muscle (upper esophageal sphincter) is stretched and relaxed, the esophagus opens, and the swallowing process enters the esophageal phase. The afferent nerves of the swallowing reflex are mainly from the soft palate (cranial nerve pairs V and IX), the posterior pharyngeal wall (cranial nerve pair IX) and the ecclesiastis (cranial nerve pair X). The swallowing center is located in the medulla oblongata, where the nucleus tractus solitarius, the nucleus suspensus, and other brainstem reticular structures near the motor nucleus of the cranial nerves are currently considered to be the medulla oblongata pattern generators for swallowing movements. The efferent nerves supporting the muscular movements of the tongue, pharynx, and larynx are located in the V, IX, and XII cranial nerve pairs. Pathology: (1) Soft palate abnormality: weakness of the soft palate elevation leads to inability to close the palatopharynx, so that the oropharynx remains connected to the nasopharynx during swallowing and food flows backwards into the nasal cavity, resulting in aspiration after swallowing. The same situation can occur in patients with cleft palate or in patients who have undergone uvulopalatotomy for snoring or other diseases. (2) Abnormal pharyngeal lift: Dysfunction of the thyrohyoid and palatopharyngeal muscles and hyoid lift can lead to abnormal pharyngeal and laryngeal lift and failure of the airway to close in time during swallowing, leading to aspiration. (3) Pharyngeal constrictor muscle weakness: this can lead to residual food in the epiglottis and pear-shaped crypt, resulting in aspiration at the end of swallowing. (4) Cricopharyngeal muscle dysfunction: impaired relaxation, abnormal tone, fibrosis, or hyperplasia of the cricopharyngeal muscle may lead to impaired swallowing coordination. (5) Medulla oblongata palsy: It can be divided into true medulla oblongata palsy and pseudo medulla oblongata palsy, and the etiology and differentiation of the two are described separately in this chapter. (5) Esophageal phase 1. Physiology: The stage of esophageal to gastric transfer of food mass. This phase is controlled by the brainstem (IX and X cranial nerve pairs) and the intermuscular plexus. The peristaltic wave that starts in the pharynx travels gradually downward, pushing the mass across three physiological narrowings of the esophagus and eventually to the stomach. The first esophageal stricture is located at its origin, approximately 375 px from the central incisor; the second stricture is located at its intersection with the left main bronchus posteriorly, approximately 625 px from the central incisor; and the third stricture is at the esophageal foramen through the diaphragm, approximately 1000 px from the central incisor. This phase begins with the crossing of food over the upper esophageal sphincter and ends with the crossing of food over the lower esophageal sphincter. Unlike the upper esophageal sphincter, the lower esophageal sphincter actively relaxes without the need for pulling by other muscles during the downward movement of the food. Once the food crosses the lower esophageal sphincter, the muscle maintains a certain tension to maintain the closure of the lower esophageal opening and prevent the backflow of food from the stomach into the esophagus. 2. Pathology: esophageal motility disorders: diffuse esophageal spasm, esophageal achalasia, scleroderma, senile esophageal dysfunction, cricopharyngeal muscle dysfunction; esophagitis: gastroesophageal reflux disease, esophageal infections (complications of HIV, Candida or herpes, etc.), radiation esophagitis caused by radiotherapy, drug-induced drug esophagitis (especially when capsules or sugar-coated tablets are ruptured or taken apart in the esophagus, potassium salt solution, quinidine, vitamins and minerals, etc.). (especially if the capsule or sugar-coated tablet is ruptured or taken apart in the esophagus, potassium solutions, quinidine, vitamin and mineral tablets). Structural abnormalities: foreign body impaction, tumor or lymph node enlargement can lead to foreign body sensation and dysphagia, diverticula can lead to dysphagia, and food residues in them may also lead to aspiration at night.