Dysphagia …

Ameeta Karmarkar MD

General Neurology

Updated 03.18.2024
Released 07.12.2000
Expires For CME 03.18.2027

Dysphagia

Author: Ameeta Karmarkar MD

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Editor: Peter J Koehler MD PhD

Dysphagia

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Introduction

Overview

Dysphagia is a disabling symptom of numerous neurologic conditions, including stroke, neurodegenerative disease, and neuromuscular diseases. The resultant impaired ability to tolerate oral intake and inability to protect the airway from aspiration significantly impacts morbidity, mortality, nutritional status, and quality of life. This article describes the pathophysiology, mechanisms, causes, investigations, differential diagnosis, and management of dysphagia, which includes medical treatments, surgical measures, and rehabilitative strategies.

Key points

	• Normal swallowing is a complex patterned response mediated by a vast neural network involving the brainstem, subcortical, and cortical regions. It involves the finely coordinated activation of more than 25 muscle pairs in the oropharynx, larynx, and esophagus.
	• Dysphagia can be caused by impairment at various levels of this process, including mechanical obstruction, impaired oropharyngeal sensation, cranial nerve involvement, bulbar muscle weakness, and central disturbances of higher cortical functions.
	• Nutritional deficiencies, dehydration, weight loss, and aspiration pneumonia are systemic complications of dysphagia that significantly impact morbidity and mortality.
	• Management strategies are disease-dependent and range from supportive care to disease-modifying therapies.
	• Rehabilitation under the supervision of speech therapists is essential for patients with potential for improvement.

Historical note and terminology

Dysphagia (from the Greek dys, meaning disordered, and phagein, to eat) is defined as a difficulty with swallowing, ie, transferring food or liquid from the oral cavity, through the pharynx and esophagus, to the stomach. One classification of dysphagia is based on the distinction between oropharyngeal dysphagia and esophageal dysphagia. Oropharyngeal dysphagia, or transfer dysphagia, is the impaired movement of the food bolus through the oral cavity and pharynx; esophageal dysphagia is the disordered movement of food bolus within the esophagus. The term "swallowing apraxia" is proposed for lingual, labial, and mandibular coordination disorders observed before bolus transfer during the oral stage of swallowing (27).

Dysphagia as a symptom has been well-recognized throughout medical history. Parkinson described dysphagia as a symptom of the disease named after him (80). In his description of amyotrophic lateral sclerosis, Charcot highlighted the difficulty in deglutition associated with "labioglossolaryngeal paralysis" (18). The classic description of the lateral medullary syndrome by Wallenberg contains dysphagia as a prominent symptom (106). Dysphagia associated with neurologic disorders is also referred to as neurogenic dysphagia.

Clinical manifestations

Presentation and course

	• Dysphagia requires a thorough clinical evaluation to identify the underlying cause.
	• Distinguishing oropharyngeal from esophageal dysphagia is important; dysphagia associated with neurologic disorders is usually oropharyngeal.
	• A preliminary step is the exclusion of mechanical or structural obstructions in the oropharynx or esophagus.
	• Dysphagia associated with neurologic conditions can be broadly conceptualized as affecting primarily the peripheral nervous system (neuropathies, muscle disorders, neuromuscular junction disorders) or central nervous system, which often includes the cognitive-linguistic domain (stroke, dementia).
	• An accurate description of swallowing impairment, timeline of symptoms, correlation with the consistency of ingested food, disorders of speech, respiration, cognitive changes, and other key associated symptoms can help localize the area of impairment.

Clinical history

Description of swallowing impairment. Patients with oropharyngeal dysphagia report difficulty initiating a swallow, describing a sensation of "stickiness" and a frequent need to clear the throat. It is important to ask about difficulty in chewing as the oral preparation of foods may be affected by poor dentition, loss of oral bolus control, decreased salivary secretion, weakness, or impaired sensation of the masticatory muscles and tongue. Lingual or buccal weakness may cause oral residue, drooling, food spillage, dysarthria, and pocketing of ingested food. Laryngeal penetration or aspiration will cause coughing, a harsh vocal quality, wet gurgling sounds, or a choking sensation just after initiating a pharyngeal swallow. Patients with associated palatal and velopharyngeal weakness may report nasal regurgitation of liquids and a hypernasal voice.

In esophageal dysphagia, patients may complain of a sensation of food being stuck in the sternal area or chest pain typically occurring several seconds after initiating a swallow. Patients will usually identify the area of discomfort as being below the sternal notch. Ingested food particles may be regurgitated or vomited if the obstruction is severe. Associated symptoms may include heartburn, cough, and hematemesis.

Association with food consistency. Patients may report altering their dietary texture and eating behaviors based on the nature of impairment. It is helpful to ask about avoidance of certain foods and difficulty with pills. Patients with myasthenia gravis may report more difficulty with hot liquids and describe jaw fatigue toward the end of the meal, particularly with tough foods such as steak. Oropharyngeal dysphagia will affect all food consistencies, especially thin liquids. In esophageal dysphagia, difficulty with all food consistencies suggests a motility disorder, whereas dysphagia to solids only is typically seen in fixed obstructive lesions that may progress to include liquids if the obstruction worsens over time.

Speech. Speech articulation is facilitated by adequate respiratory function, vocal cord mobility, intact dentition, and coordinated movements of the face, jaw, tongue, palate, and oropharynx, many of which play an essential role in swallowing. Attention to phonation, speech clarity, volume, rhythm, breath control, prosody, content, and language will help identify associated disorders. Lower motor neuron disorders may cause impaired articulation, strained vocal quality, hypernasality, hypophonia, and hoarseness. Spastic dysarthria observed in upper motor neuron involvement (eg, stroke involving motor or premotor cortex) is characterized by hypernasality, hoarseness, and a breathy vocal quality. A low monotonous speech pattern, hypophonia, hypomimia, voice tremor, and dysarthria may be observed in parkinsonism. Patients with myasthenia gravis may report diurnal fluctuations and fatigability, with dysarthria, dysphonia, hypernasality, and even dyspnea becoming evident after a long conversation.

Respiration. Swallowing, respiration, and phonation are closely interrelated and involve the coordinated contraction of numerous muscles in a narrow anatomical region.

Patients with dysphagia can be at risk for respiratory failure not only due to aspiration but also weakness of the respiratory muscles (diaphragm, intercostals, and accessory) caused by the underlying disease. Some neuromuscular conditions, such as amyotrophic lateral sclerosis and myasthenia gravis, can involve respiratory muscles early in the course of the disease, causing dyspnea and orthopnea. In more acute presentations, Guillain-Barré syndrome and botulism can cause rapidly progressive respiratory failure necessitating mechanical ventilation. Monitoring the pulmonary mechanics with negative inspiratory force and forced vital capacity is important in patients at risk of rapid decline, but measurements may be confounded by poor oral seal if orofacial weakness is present.

Neck flexion weakness is a predictor of respiratory muscle impairment in Guillain-Barré syndrome (05) and correlates well with forced vital capacity in patients with myasthenia gravis (32). Evidence of hypercapnia and acidosis on arterial blood gas sampling may not be apparent until the weakness is severe, and elective intubation should be considered in patients at risk of deterioration. Weak cough, atelectasis, mucous plugging, and aspiration risk due to inability to handle oral secretions further increase the risk of respiratory failure.

Posterior circulation strokes can cause a decreased level of arousal and irregular respiratory patterns due to brainstem involvement. Indicators of impending respiratory compromise on bedside evaluation include short and shallow breaths, decreased single-breath counting, accessory muscle use, a weak cough, and, later, tachypnea and tachycardia. Confusion and decreased responsiveness may result from severe hypercapnia but may also be seen in large intracranial insults and further impair the ability to protect the airway.

Other factors that may contribute to respiratory failure are concomitant interstitial lung disease seen in inflammatory myopathies and cardiomyopathy, which may accompany muscular dystrophies.

Cognitive function. Cognitive and behavioral decline, psychomotor slowing, aphasia, memory impairment, and gait disturbances may help identify an underlying neurodegenerative disorder. Poor coordination and motor apraxia may lead to slowed chewing, piecemeal deglutition, and repetitive swallowing in patients with dementia. Dysarthria, decreased blinking, hypomimia, and slow, hypophonic monotonous speech are known features of parkinsonism, along with rest tremor, postural instability, rigidity, micrographia, and bradykinesia. Dysphagia usually develops in advanced stages of Parkinson disease. Parkinsonism with early bulbar manifestations such as stridor, dysphonia, anterocollis, dysarthria, and dysphagia can be indicative of multiple system atrophy.

Language dysfunction manifesting as anomia, agrammatic speech, impaired repetition, and comprehension may be observed in patients with stroke and early in neurodegenerative disorders such as primary progressive aphasia. Although amyotrophic lateral sclerosis is traditionally considered a disease of motor pathways, its association with frontotemporal dementia is well-described. Cognitive and behavioral changes become more pronounced with disease progression and are closely associated with bulbar dysfunction (21).

On bedside examination, impaired level of arousal, diminished attention span, short-term memory deficits, visuospatial disorientation, hallucinations, apraxia, psychomotor slowing, or agitation may be seen in neurodegenerative disorders and in more acute cognitive impairment due to delirium or medication-adverse effects.

Brainstem syndromes can usually be recognized by a constellation of visual disturbances, incoordination, gait ataxia, sleep disorders, speech, and swallowing difficulties, with impairment of consciousness becoming apparent only in advanced stages.

Onset and timeline of symptoms

Acute onset. Food impaction, typically caused by meat or foreign bodies completely obstructing the esophagus, requires emergency intervention and may need to be relieved with endoscopy. Corrosive upper pharyngeal injuries, severe mucositis, and abscesses may cause oropharyngeal swelling and inflammation. Post-extubation dysphagia is commonly encountered among survivors of acute respiratory failure requiring mechanical ventilation. Risk factors include preexisting neurologic conditions such as stroke and neuromuscular disease (10), prolonged mechanical ventilation, low Glasgow Coma Scale scores (61), cardiac surgery, and advanced age (15).

Acute oropharyngeal dysphagia may be observed after an acute central structural or inflammatory insult, such as stroke, traumatic brain injury, meningoencephalitis, acute demyelination, cranial neuropathies, or cranial or spinal surgery.

The incidence of dysphagia in stroke patients is highly dependent on the method of assessment, ranging from 37% to 45% using water swallow screening tests to 64% to 78% when using instrumental testing (70). Age older than 70 years, higher stroke severity, impaired oral clearance, and palatal weakness are associated with a higher risk of dysphagia (69). The presence of facial palsy, aphasia, or speech impairment is associated with a lower likelihood of early swallowing recovery (66).

In traumatic brain injury, clinically relevant dysphagia is observed in 60% of patients and often is associated with tracheostomy and prolonged ventilatory support (67).

Among infectious causes, rhombencephalitis causes particularly severe brainstem involvement and can be associated with autoimmune disorders, such as Behçet disease, and infections, such as Listeria monocytogenes. Tuberculosis, syphilis, fungal, and bacterial meningitis can cause dense skull base exudates, causing cranial nerve palsies. Infections that can cause cranial neuropathies include Lyme disease, poliomyelitis, syphilis, Varicella Zoster virus, and West Nile virus.

Cranial nerve involvement, most frequently cranial nerve VII, can occur in over 50% of patients with Guillain-Barré syndrome (33). The pharyngeal-cervical-brachial variant of Guillain-Barré syndrome causes particularly severe weakness of the oropharyngeal musculature along with neck and shoulder involvement (105).

Botulism is characterized by rapidly progressive areflexic weakness caused by exposure to a neurotoxin produced by Clostridium botulinum. Cranial nerve involvement is common (93% of cases), and dysphagia is reported in 65% of afflicted patients (19).

In addition to the causes mentioned above, multiple cranial neuropathies may be caused by tumors, leptomeningeal carcinomatosis, trauma, and autoimmune conditions such as neurosarcoidosis (48).

Postoperative dysphagia and dysphonia can occur following anterior cervical spinal surgery. Risk factors include a history of prior cervical spine surgery, multilevel surgery, the upper surgical level at C3/4, and preoperative C2-C7 angle (78). Dysphagia is common after posterior fossa surgery (reported in up to 27% of patients), with improvement occurring in most patients at longitudinal follow-up (104).

Subacute onset. Subacute symptoms, especially with progression over weeks to months, may be observed in progressive neuromuscular disorders such as amyotrophic lateral sclerosis. Up to 30% of patients with amyotrophic lateral sclerosis present with swallowing impairment at diagnosis (53), and as the disease progresses, dysphagia is universally present.

Patients with inflammatory myopathies typically present with a subacute, gradually progressive, symmetric proximal muscle weakness with elevated muscle enzymes. Rashes, weight loss, arthritis, and Raynaud phenomenon may accompany or precede these symptoms. Dysphagia is a frequent complication, with an estimated pooled prevalence of 36% and a peak prevalence of 56% in inclusion body myositis, and is associated with higher mortality and worse functional status. Although the prevalence of dysphagia typically increases with disease progression, it has been described as an early and only presenting symptom in inclusion body myositis (56).

A pattern of fluctuating weakness and fatigue may be observed in neuromuscular junction disorders such as myasthenia gravis. Up to 15% of patients at diagnosis report difficulty swallowing, chewing, slurred speech, or nasal voice, and with progression of the disease, dysphagia may be present in over 50% (37).

In patients with esophageal dysphagia, gradually progressive symptoms may be reported in esophageal strictures, malignancies, and motility disorders such as achalasia. Intermittent dysphagia may be caused by esophageal spasm or lower esophageal rings or webs.

Chronic. Chronic and typically gradually progressive dysphagia may be observed in patients with neurodegenerative conditions, often resulting in silent aspiration, which is often unrecognized until unmasked by an acute illness.

Oropharyngeal dysphagia is widely prevalent in patients with neurodegenerative diseases (80% of Alzheimer disease, 60% of Parkinson disease) (22) and in 37% to 78% of stroke survivors (70). Leukoaraiosis is associated with an increased risk of aspiration after acute stroke, suggesting the role of chronic white matter damage in the pathophysiology of dysphagia (39). Other risk factors for silent aspiration include a history of cranial nerve paresis (IX and X), radiotherapy, and tracheostomy (45).

Chronic, gradually progressive muscle weakness over the course of years may be seen in muscle dystrophies and inclusion body myositis.

Acute on chronic. In hospitalized patients, dysphagia may often be erroneously identified as acute, but a more detailed history and neurologic examination usually reveal an underlying chronic neurodegenerative disorder or other predisposing conditions as mentioned above. Even in healthy older individuals, age-related changes in dentition, taste perception, oropharyngeal muscle mass and contractility, coordination of oropharyngeal musculature, and delayed reflexes (34) can lead to a chronic, gradual multifactorial impairment in the swallowing mechanism in elderly individuals---a condition termed presbyphagia.

Dysphagia may be decompensated or unmasked by acute medical illness, delirium, use of sedating medications, and any superimposed neurologic insult. Myasthenia gravis crisis can be precipitated by acute illnesses, infections, and the use of certain medications.

Medications

Centrally acting medications, such as antipsychotics, sedatives, and hypnotics, can exacerbate pre-existing dysphagia and impair cognition, particularly in the elderly and those with chronic neurodegenerative conditions. Neuroleptics are frequently implicated in dysphagia and are often associated with extrapyramidal symptoms (73). Patients with Lewy body dementia may have particularly severe neuroleptic sensitivity.

A retrospective study of 200 geriatric inpatients, after adjusting for central nervous system diseases, identified a relevant association of oropharyngeal dysphagia with several classes of medications, including antipsychotics, benzodiazepines, anti-Parkinson drugs, antidepressants, antiepileptics, beta-blockers, alpha-blockers, opioids, antihistamines, metoclopramide, domperidone, and anticholinergics among others (113).

In patients with known myasthenia gravis, timing of the last dose of acetylcholinesterase inhibitors relative to the bedside examination can help contextualize the severity of weakness. Myasthenic crisis can be precipitated by the use of high-dose corticosteroids and antimicrobials such as fluoroquinolones and azithromycin.

Immune checkpoint inhibitor therapies are important therapeutic options for patients with advanced malignancy but can rarely cause severe neurotoxicity, usually occurring within 3 months of exposure. Manifestations vary and may include encephalitis, aseptic meningitis, Guillain-Barré syndrome, and myasthenia gravis (30). Immune checkpoint inhibitor-associated myasthenia gravis can also be part of an overlap syndrome with inflammatory myositis and myocarditis, which is associated with high morbidity and mortality (82).

Associated symptoms

Physical examination. Dysphagia can be associated with a variety of neurologic and systemic conditions. Dehydration and malnutrition may cause hypotension and tachycardia. Monitoring body weight and body mass index for unintended weight loss is important to assess the duration of nutritional depletion. A generalized loss of muscle bulk and temporal wasting can be observed in chronic cachexia due to malnutrition and severe systemic comorbidities such as chronic liver or kidney disease and malignancies.

Autonomic dysfunction, with a common manifestation being orthostatic hypotension, can be seen in Guillain-Barré syndrome, multiple system atrophy, advanced Parkinson disease, Lambert Eaton myasthenic syndrome, and paraneoplastic syndromes.

Vitamin deficiencies may cause cheilosis, gingival bleeding, dry skin, and hair loss.

Patients with inflammatory myopathies may have typical cutaneous eruptions, inflammatory arthritis, and Raynaud phenomenon and also show signs of other connective tissue disease in overlap syndromes.

Examination of the oral cavity. Mucosal involvement with infections such as candidiasis and herpes may be apparent with typical lesions and are often associated with immunocompromised status. Halitosis can occur due to xerostomia, retained oral residue, and mechanical obstructive lesions. Poor dentition and impaired salivation can contribute to difficulty with oral preparation. Tongue atrophy and fasciculations may be observed in amyotrophic lateral sclerosis. Older adults may have tongue hypertrophy due to the accumulation of connective tissue and fatty deposits, which can lead to reduced mobility.

Excluding uncommon presentations of muscle-specific kinase (MuSK) antibody-myasthenia gravis and inclusion body myositis, isolated dysphagia without any bulbar or other neurologic involvement may point to a more specific obstructive or mechanical cause. Oropharyngeal malignancies, masses of the parapharyngeal or retropharyngeal space, cervical osteophytes, and Zenker diverticulum are some common causes of upper oropharyngeal obstruction. Oropharyngeal malignancies may be associated with a history of alcohol use, tobacco use, weight loss, mucosal bleeding, pain, cervical lymphadenopathy, and referred otalgia (from hypopharyngeal tumors or lesions).

Further, observing and palpating elevation of the hyoid bone or thyroid notch during swallowing can help assess for contributors to impaired upper esophageal sphincter opening.

Examination of bulbar muscle strength. Assessment of bulbar muscles includes testing extraocular movements, facial muscles (eye closure, cheek puff, labial closure, smile), lingual strength, palatal excursion, jaw closure, sternocleidomastoids, and shoulder shrug.

Corneal irritation, dryness, and tear spillage may occur due to weak eyelid closure. Ptosis and extraocular muscle weakness are features of myasthenia gravis, Lambert Eaton myasthenic syndrome, botulism, oculopharyngeal muscular dystrophy, the Miller-Fisher variant of Guillain-Barré syndrome, and mitochondrial disorders. A weak oral seal, lateral pocketing, and drooling of food and fluids can be indicative of associated facial weakness or impaired facial sensation. Eliciting fatigability on neurologic examination can help identify fluctuating weakness commonly observed in myasthenia gravis. Sustaining cardinal eye positions for 60 seconds to elicit diplopia and ptosis and noting fatigable dysarthria, hypernasality, dyspnea, and hypophonia with prolonged conversation are useful observations. Isolated dysphagia, head drop, or dyspnea without other bulbar weakness may occasionally be encountered in MuSK-myasthenia gravis.

Guillain-Barré syndrome, particularly clinical subtypes such as Miller-Fisher syndrome and bulbar and pharyngeal-cervical-brachial variants, is frequently associated with cranial nerve deficits and associated difficulty chewing and swallowing.

Motor strength examination. Most myopathies present with symmetric proximal weakness predominantly affecting the pelvic and shoulder girdle muscles and neck muscles to a varying degree.

However, asymmetric weakness may be encountered in amyotrophic lateral sclerosis and inclusion body myositis. Distal-predominant weakness may be seen in myotonic dystrophy, inclusion body myositis (characterized by weakness and atrophy of finger flexors and quadriceps), and rare distal myopathies. Muscle atrophy typically occurs in advanced muscle disorders with severe weakness but may be seen early in neuropathies before clinical weakness is apparent. In classic amyotrophic lateral sclerosis, weakness with a combination of upper motor neuron signs (hyperreflexia, spasticity, upgoing toes) and lower motor neuron signs (fasciculations, atrophy) may be present, with sparing of sensation.

“Dropped head syndrome,” or isolated involvement of the neck flexors or extensors, can present as an early manifestation of amyotrophic lateral sclerosis, myasthenia gravis, and some congenital myopathies. The severity of neck flexor weakness is a predictor of survival and respiratory muscle impairment in amyotrophic lateral sclerosis (103). The single breath count is a useful bedside test that shows good correlation with vital capacity and is an indicator of respiratory muscle dysfunction in patients with Guillain-Barré syndrome and myasthenia gravis (47; 32).

The typical presentation of Guillain-Barré syndrome includes a history of preceding viral illness, progressive motor weakness, decreased or absent deep tendon reflexes, nadir of weakness within 4 weeks, dysautonomia, and albuminocytologic dissociation in spinal fluid. Sensory involvement is also present and usually milder than motor weakness, although rarer sensory predominant variants of Guillain-Barré syndrome have been described. Botulism causes symmetric motor weakness, typically progressing from the cranial nerves downward, with blurred vision being the only sensory manifestation.

Lesion dissemination in space and time, a history of prior clinical relapses, and optic neuritis may point to demyelinating diseases such as multiple sclerosis. Dysphagia in patients with multiple sclerosis is usually associated with longer disease duration and significant motor disability (84).

Prognosis

Dysphagia is a commonly encountered syndrome in the geriatric population and has been identified as an independent predictor of mortality. A large cross-sectional study among nursing home residents found that the 6-month mortality of residents with dysphagia was significantly higher than that of those without dysphagia (24.7% vs. 11.9%; P < .001) (112). Dysphagia among inpatients, irrespective of the cause, is independently associated with significantly higher inpatient mortality, longer hospital length of stay, higher inpatient costs, and a higher likelihood of discharge to a post-acute care facility (81). Further, its psychosocial impact on patients and their caregivers cannot be underestimated. A deterioration in swallowing ability is one of the most common complications encountered at the end of life. It may not only cause malnutrition and aspiration pneumonia but also adversely impact the quality of life, socialization, and self-esteem. Patients with dysphagia often report a lack of enjoyment of food as well as increased anxiety, panic, and social avoidance around mealtimes (31).

The prognosis of dysphagia largely depends on the underlying etiology. A benign obstructive lesion amenable to interventions (eg, esophageal balloon dilatation of a stricture) can have a vastly different outcome compared to patients with more advanced neurologic disease.

Dysphagia in stroke is related to the involvement of the hemisphere with the dominant swallowing projection, and clinical recovery can be correlated with compensatory changes in the contralateral, unaffected hemisphere (40). After stroke severity, dysphagia is the second most significant risk factor for death in stroke patients (43).

A 2021 meta-analysis concluded that dysphagia screening in acute stroke care is associated with a lower risk of pneumonia, death, and dependency (91). In most patients, spontaneous improvement in swallowing function usually occurs in the first 2 weeks (92). It is hypothesized that bilateral representation of the swallowing network may facilitate rapid recovery in dysphagia as opposed to other cortical functions that may not show the same trajectory of improvement. However, in a prospective study of 279 stroke patients with severe dysphagia, 30% had insufficient oral intake, and 66% failed to return to their pre-stroke diet after 30 days (35). This indicates a necessity for follow-up assessments in the post-acute setting with close monitoring of nutritional intake. In addition to older age and stroke severity, videofluoroscopic evidence of a delayed or absent swallow reflex, delayed oral transit, and penetration are markers associated with persistent dysphagia 6 months after stroke (68).

A longitudinal follow-up of a cohort of patients with severe traumatic brain injury showed that in most patients, swallowing improved, and the number of aspirations decreased between 3 and 6 months after injury. Prognostic factors for persisting aspiration included severity of cognitive and overall neurologic impairment, alteration in tongue control, and delay in triggering oropharyngeal reflexes (99).

Complications

Complications of dysphagia include dehydration, weight loss, malnutrition, airway obstruction, and aspiration pneumonia. Additionally, post-stroke dysphagia is associated with depression (85) and has a significant negative impact on quality of life.

Aspiration pneumonia. Aspiration is defined as inhalation of either food or oropharyngeal contents below the level of the vocal cords. Sometimes, ingested food is retained in pharyngeal recesses or "pockets" and is aspirated into the pulmonary tree when respiration is resumed after completion of the act of swallowing.

When bolus material enters the laryngeal vestibule but remains above the vocal folds, it is defined as penetration. Both aspiration and penetration may stimulate protective reflexes such as coughing and throat clearing, but in the absence of these reflexes, they may be clinically silent.

Chemical pneumonitis refers to the aspiration of substances, such as gastric fluid, that cause an inflammatory reaction in the lower airways, which may not necessarily be associated with bacterial infection. Aspiration pneumonia is an active infection caused by the inoculation of large amounts of bacteria (aerobic, anaerobic, or mixture) into the lungs via oral or gastric material. Numerous studies demonstrate that aspiration pneumonia is a significant cause of morbidity and mortality in older patients with dysphagia. Certain physiologic abnormalities associated with higher aspiration risk include tongue strength, hyoid movement, and increased pharyngeal bolus transit time (95).

Post-stroke infection, of which pneumonia is the most common, is associated with increased hospital stays, poorer functional outcomes, and increased mortality up to 1 year post-stroke (97). Oral colonization by pathogens, such as Pseudomonas aeruginosa, Klebsiella pneumoniae, and Escherichia coli, has been demonstrated in stroke survivors and is associated with adverse respiratory events (83). Additionally, immunodepression after stroke can increase susceptibility to severe infections (42).

Malnutrition and dehydration. Dysphagia is a significant risk factor for malnutrition, especially in the elderly (90). Associated weight loss should also raise clinical suspicion for an underlying malignancy. Malnutrition, dehydration, weight loss, and sarcopenia can further have a detrimental effect on functional status and rehabilitation potential.

Medication intake. The impaired ability to swallow oral medications, especially large pills, may result in medication noncompliance and, thus, affect the management of other medical comorbidities. Crushing pills, switching formulations, or mixing with thickening agents may affect the bioavailability, palatability, and cost of medications, resulting in inadequate efficacy and adverse events (114). In patients with Parkinson disease, dysphagia for medications is widely prevalent in about 70% of patients and is associated with motor complications, such as fluctuations and dyskinesias (57).

Biological basis

	• Swallowing involves the finely coordinated sequential contraction of numerous muscles in the oral, pharyngeal, laryngeal, and esophageal regions.
	• A normal swallow can be divided into the oral, pharyngeal, and esophageal phases.
	• The upper esophageal sphincter, chiefly composed of the cricopharyngeus muscle, is an important transition point between the pharynx and esophagus.
	• Extensive cortical and subcortical networks play an important role in the central control of swallowing in addition to the brainstem.

Anatomic localization

A normal swallow should ideally provide safety (protecting the airway from aspiration) and efficiency (propelling nutritionally adequate quantities of food into the esophagus without significant residue).

The nuclei of six cranial nerves (trigeminal, facial, glossopharyngeal, vagus, hypoglossal, and accessory cranial nerves) in the brainstem receive afferent sensory input and supply motor innervation to the numerous muscles involved in swallowing.

Somatic stimuli from the oropharynx and larynx, including taste, pressure, temperature, and nociceptive stimuli, are transmitted via cranial nerves V, VII, IX, and X to the medulla oblongata. The central swallow pattern generator near the nucleus of tractus solitarius in the medulla integrates sensory feedback from the cranial nerves as well as supratentorial input from the motor cortex and subcortical regions. It elicits the patterned swallowing response that requires the intricate sequential contraction and relaxation of 25 muscle pairs of the oropharyngeal, laryngeal, and esophageal regions (25).

A normal swallow can be divided into the oral, pharyngeal, and esophageal phases. The oral phase begins with food placement in the mouth, mastication, manipulation, and posterior propulsion by the tongue.

During the pharyngeal phase, the bolus is squeezed through the pharynx by the propagated contraction of the pharyngeal constrictor muscles. Intact oropharyngeal sensation is important to elicit the appropriate motor response to bolus presentation. In addition, the soft palate rises to close the nasopharynx. The hyoid bone rises, pulling the larynx up, while the epiglottis closes the entrance to the larynx. The base of the tongue contacts the pharyngeal wall, concurrently with anterior hyoid movement, coinciding with the opening of the upper esophageal sphincter, also referred to as the pharyngoesophageal segment.

The upper esophageal sphincter is a high-pressure zone extending from the distal pharynx to the proximal esophagus. It is composed of the inferior pharyngeal constrictor, part of the cervical esophagus, and the cricopharyngeus muscle, which is its main component. The cricopharyngeus, composed of striated muscle and abundant connective tissue, is tonically contracted at rest, acting as a C-shaped muscular sling preventing air from entering the esophagus and preventing esophageal regurgitation. It is innervated by the pharyngeal plexus and the recurrent laryngeal nerve, whereas afferent information is carried by cranial nerve IX and cervical sympathetics (52). It relaxes when a bolus is pushed posteriorly by the tongue and pharyngeal constrictor muscles. An additional mechanical component that helps with upper esophageal sphincter opening is provided by anterior traction forces applied (by suprahyoid muscles) to the cricoid cartilage via the laryngohyoid complex. Normal functioning of the upper esophageal sphincter thus requires four key components: cricopharyngeus relaxation, anterosuperior movement of the hyolaryngeal complex, normal upper esophageal sphincter distensibility, and intrapharyngeal propulsive forces by the advancing swallowed bolus (23). Dysfunction at any of these levels can reduce transit and cause pharyngeal residue (111). The pharyngeal stage concludes as the bolus enters the esophagus.

During the esophageal stage, food is involuntarily propelled into the stomach through peristaltic contractions. The upper or cervical esophagus is comprised of striated muscle (therefore, typically involved in myositis) whereas the lower esophagus is primarily smooth muscle.

Data from functional imaging, lesion-symptom mapping, and animal studies indicate that widespread cortical and subcortical neural networks are involved in swallowing function (110). Cortical areas involved include primary and supplemental sensorimotor areas, insula, frontal operculum, inferior frontal gyrus, angular gyrus, and superior temporal gyrus (60; 118). Involvement of the white matter, especially corticobulbar tracts, is also associated with dysphagia as demonstrated in patients with strokes in these regions. Subcortical areas including the thalamus, basal ganglia, cerebellum, and amygdala are also associated with dysphagia post-stroke (64; 41).

Further, the central control of swallowing is partly asymmetrically lateralized rather than uniformly bihemispheric and does not necessarily correlate with language and hand dominance (75). The sensorimotor cortical areas involved in swallowing are interconnected across hemispheres via callosal tracts. The loss of integrity of callosal fibers between swallowing representation sites, indicating a disruption in functional connectivity of the swallowing network, is thought to play a causative role in dysphagia due to strokes (29).

Pathophysiology

Varoius impairments can cause dysphagia at different stages of the process. From a clinical standpoint, it is helpful to first classify the dysphagia as being predominantly oropharyngeal, esophageal, or both. Further, within these two categories, the nature of impairment can be mechanical (or obstructive), functional (affecting sensation, muscle tone, contractility, or coordination), or a combination of both.

Dysphagia associated with neurologic conditions is usually oropharyngeal and can result from lesions in the central nervous system (brainstem, cortical, and subcortical structures), cranial nerves, neuromuscular junction, or muscles.

Beginning with the oral phase, bolus preparation can be affected by dentition, salivation, gustatory function, olfaction, orofacial sensation, and motor strength. Further, as evidenced by the role of extensive cortical and subcortical networks in swallowing function, it is not solely reflexive and requires adequate alertness and attention (76). Cognitive impairment can affect the motor planning and execution of coordinated movements required for mastication. In patients with Parkinson disease, impaired cognitive function, particularly frontal, executive, and memory deficits, are associated with delays in the oral phase of swallowing (50). Impaired cognition, especially in the visual attention and executive domains, is associated with more severe dysphagia in stroke survivors (46).

The pharyngeal phase requires the sequential propulsive movement of the food bolus.

Pharyngeal contractility can be impacted by abnormal tone, sensation, or motor strength. Diminished oropharyngeal sensory input interferes with cortical control of swallowing (98), and hypoesthesia can result in delayed or absent triggering of the swallowing response (55), commonly encountered in post-stroke dysphagia.

After the bolus transits across the posterior pharynx, it reaches the upper esophageal sphincter. Upper esophageal sphincter opening is facilitated, as discussed above, by cricopharyngeus relaxation as well as mechanical factors--chiefly laryngeal elevation and intrapharyngeal bolus pressure.

Cricopharyngeal dysfunction can be a consequence of various neurologic conditions, such as cerebrovascular disease, particularly medullary infarction (117), Parkinson disease, amyotrophic lateral sclerosis, and primary muscle disorders, among others (09). Diminished contractility as well as hypercontractility of the upper esophageal sphincter has been described in patients with myositis (56), which may reflect acute inflammatory disease as opposed to chronic fibrosis. Cricopharyngeal hypercontractility often leads to an opening or relaxation disorder of the upper esophageal sphincter, resulting in pronounced residue or pooling of saliva in the piriform sinus. Pharyngoesophageal manometry may show increased hypopharyngeal intra-bolus pressure with incomplete upper esophageal sphincter relaxation. Patients with post-stroke dysphagia can have reduced pharyngeal propulsive pressures, abnormal upper esophageal sphincter relaxation pressures, or both (58). Anterior excursion of the hyoid and thyroid cartilage is reduced in the elderly and can contribute significantly to presbyphagia (49).

A cricopharyngeal bar is a distinct posterior indentation in the barium column in the cervical esophagus between C3-6 inferior to the vocal cords visualized in videofluoroscopic studies. It can be representative of cricopharyngeal muscle thickening due to spasticity, impaired relaxation, fibrosis, degenerative changes, or decreased connective tissue compliance but is also encountered as an incidental asymptomatic finding in up to 30% of elderly nondysphagic patients (63). Although it may have pathophysiologic significance, patients with this finding need further evaluation with radiography, manometry, endoscopy, and workup for neuromuscular disease to rule out alternative causes (24).

Videofluoroscopic findings of decreased laryngeal excursion and decreased pharyngeal contraction (indicative of decreased propulsive bolus transport) may indicate that the swallowing impairment is multifactorial and not solely related to cricopharyngeal dysfunction. Manometry findings of normal pharyngeal contraction with elevated upper esophageal sphincter residual pressure and elevated hypopharyngeal bolus pressure support cricopharyngeal dysfunction. This delineation is important when considering therapeutic options targeted at cricopharyngeal function, such as myotomy, dilatation, or botulinum toxin injections, discussed later in this article.

Table 1. Oropharyngeal Dysphagia

Mechanical causes
	• Acute
		- Pharyngitis (diphtheria, candidiasis, cytomegalovirus, herpes virus) - Trauma (caustic chemicals, inhalation, head or neck radiation, direct injury, or surgical intervention in the oropharynx) - Post-extubation dysphagia - Retropharyngeal or parapharyngeal abscess
	• Subacute or chronic
		- Oropharyngeal malignancy - Zenker diverticulum - Extrinsic compression by cervical osteophytes - Cervical webs - Congenital (cleft palate, diverticula) - Amyloidosis (macroglossia, intramuscular amyloid deposits)
Neurogenic causes
Although a stark delineation between the various causes of dysphagia can be challenging, for clinical relevance, it is helpful to assess the causes of dysphagia as being primarily peripheral (predominant neuromuscular involvement) as opposed to central (which may overlap with proportionate disturbances of higher cognitive functions and other domains).
Central involvement--often affecting cognitive-communicative or other neurologic domains
	• Ischemic and hemorrhagic stroke
	• Traumatic brain injuries
	• Acute meningoencephalitis: bacterial, fungal, syphilis, Lyme disease, rhombencephalitis (Listeria monocytogenes, herpes, tuberculosis)
	• Primary or secondary neoplasms, especially with brainstem involvement, lymphoma
	• Chronic neurodegenerative conditions: Parkinson disease, Alzheimer disease, Lewy body dementia, vascular dementia, Huntington disease, Frontotemporal dementia, Wilson dsease
	• Anoxic brain injury
	• Demyelinating disease: multiple sclerosis, neuromyelitis optica, especially with brainstem or diencephalic syndromes, myelin oligodendrocyte glycoprotein-associated disease
	• Autoimmune: neurosarcoidosis, Behçet disease, vasculitis, autoimmune encephalitis (Bickerstaff brainstem encephalitis, GAD65), paraneoplastic syndromes (anti-Ri, anti-Yo, Ma2 rhombencephalitis), systemic lupus erythematosus, CLIPPERS
	• Toxic-metabolic encephalopathies (uremia, hepatic encephalopathy, acute systemic infection, acute endocrinologic derangements)
	• Medications: neuroleptics, benzodiazepines, anticholinergics, other sedatives, hypnotics, anxiolytics, antiepileptic drugs
	• Multiple cranial neuropathies (can be caused by a number of the above, including infections, leptomeningeal carcinomatosis, lymphoma, posterior fossa tumors, pachymeningitis, sarcoidosis)
	• Miscellaneous: Cerebral palsy, leukodystrophies, spinocerebellar ataxia, inborn errors of metabolism associated with progressive encephalopathy
Peripheral: predominantly neuromuscular or motor impairment
	• Muscle disorders
		- Inflammatory myopathies: inclusion body myositis, dermatomyositis, polymyositis, overlap syndromes with connective tissue disease - Dystrophies: myotonic dystrophy, oculopharyngeal muscular dystrophy, Duchenne muscular dystrophy - Myopathy: myotubular myopathy, nemaline myopathy - Mitochondrial disorders: Kearns-Sayre syndrome, chronic progressive external ophthalmoplegia
	• Cranial nerve or lower motor neuron involvement
		- Motor neuron disease (amyotrophic lateral sclerosis, spinal muscular atrophy, spinobulbar muscular atrophy) - Poliomyelitis - Botulism - Guillain-Barré syndrome - Multiple cranial neuropathies, as discussed above - Acute infections that can cause polyradiculopathy and cranial nerve involvement include cytomegalovirus, varicella-zoster virus (Ramsay Hunt syndrome), West Nile virus
	• Disorders of neuromuscular junction: myasthenia gravis, Lambert-Eaton myasthenic syndrome, congenital myasthenic syndromes
	• Movement disorders: tardive dyskinesia, oromandibular dystonia

Table 2. Esophageal Dysphagia

Mechanical
Intrinsic
	• Neoplastic (esophageal malignancy, benign tumors) • Trauma (penetrating injuries, chemical or thermal injury, post-surgical) • Inflammatory (infectious, eosinophilic, lymphocytic, radiation, pill esophagitis) • Structural (peptic stricture, esophageal rings or webs, diverticula)
Extrinsic
	• Osteophytes in cervical spondylosis • Thyroid enlargement • Posterior mediastinal masses • Head and neck cancer • Aortic or left atrial enlargement • Aberrant subclavian artery
Motility disorder
	• Achalasia • Systemic sclerosis (scleroderma) • Esophageal spasm

Differential diagnosis

Given the vast range of disorders associated with dysphagia, it is important to discuss terms often used in association with dysphagia, as described below.

Aphagia. The inability to swallow due to complete obstruction of the esophagus.

Presbyphagia. Presbyphagia is the term used to describe difficulty in swallowing in healthy older adults due to multifactorial age-related changes in the anatomy, physiology, and innervation of the structures involved in the swallowing mechanism. Contributors include poor dentition, impaired smell or taste, deceased tissue elasticity, decreased salivation, tongue hypertrophy, weak tongue propulsion, decreased oropharyngeal sensitivity, prolonged and delayed swallow response, and delayed protective reflexes. Decreased muscle mass and contractility affect the strength and function of numerous muscles in the oropharynx (11). Decreased connective tissue elasticity can reduce anterior laryngeal movement and decrease flexibility of the upper esophageal sphincter, impairing its opening. Reduced contractility of the esophagus and delayed emptying are additional factors (38). An acute stressor, such as toxic-metabolic encephalopathy, trauma, stroke, adverse effect of a medication, or hospitalization, can cause a decompensation with the development of dysphagia in the elderly.

Globus pharyngeus. Globus pharyngeus is the sensation of a lump or tightness in the throat. The symptom is considered functional if no organic explanation is detected. The diagnostic criteria include the presence of symptoms for 3 months, with symptom onset at least 6 months before diagnosis and a frequency of at least once per week, the occurrence of sensation between meals, absence of dysphagia or odynophagia (see below), and absence of a motility disorder of the gastrointestinal tract (06).

Phagophobia. Patients present with either acute or chronic dysphagia secondary to fear of swallowing. Routine diagnostic studies, such as a head and neck evaluation and videofluoroscopic swallowing studies, do not reveal any abnormality.

Odynophagia. Odynophagia, or painful swallowing, may be present in isolation or in association with an impairment of the swallowing mechanism. Mucosal inflammation, irritation, and injury due to various causes, including infection, radiation, and malignancy, can cause severe pain typically localized to the oropharynx or esophagus.

Associated or underlying disorders

These are described as causes of dysphagia in previous sections.

Diagnostic workup

Key tests and procedures

• Laboratory studies
• Imaging
• Cerebrospinal fluid sampling
• Muscle biopsy
• Bedside swallow evaluation
• Clinical swallow examination
• Videofluoroscopic swallowing study
• Flexible endoscopic evaluation
• Pharyngoesophageal manometry
• Upper gastrointenstinal endoscopy
• Electrophysiologic studies

All patients with dysphagia should be thoroughly investigated to localize the cause of impairment.

Laboratory studies. Electrolyte disturbances, dehydration, and malnutrition are common complications of dysphagia. A complete blood count, electrolyte panel, and screening for deficiencies (vitamin B12, methylmalonic acid, folic acid, thiamine, iron, ferritin, total iron binding capacity) are routinely performed. Serum albumin and prealbumin levels can be useful indicators of protein-calorie malnutrition. Elevations in serum bicarbonate, although multifactorial, may be seen in patients with chronic hypercapnic respiratory failure, which can be indicative of restrictive physiology from diaphragmatic and other respiratory muscle weakness.

In patients with toxic metabolic encephalopathies, testing ammonia, vitamin levels, TSH, hepatic function panels, toxicology screening, and screening for systemic infections should be considered.

The evaluation should include glycosylated hemoglobin, serum protein electrophoresis, and urine protein electrophoresis in patients with suspected polyneuropathy. If the clinical constellation is consistent with variants of Guillain-Barré syndrome, testing for ganglioside antibody panels (eg, GQ1b for Miller-Fisher syndrome) is useful.

If clinical findings are suspicious for neuromuscular junction disorders, consider antibody panels for acetylcholine receptor binding, blocking and modulating antibodies, MuSK antibodies, and P/Q-type voltage-gated calcium channel antibodies for Lambert Eaton myasthenic syndrome.

In patients suspected of primary muscle disorders, creatine kinase, alanine transaminase, aspartate transaminase, lactate dehydrogenase, aldolase, anti-nuclear antibody, erythrocyte sedimentation rate, and C-reactive protein are usually sent. Inflammatory myopathies can be associated with variable degrees of muscle enzyme elevations, often with creatine kinase elevation more than 10 times the upper limit of normal. For patients suspected of inflammatory myopathies, myositis-specific autoantibody panels should be sent, some of which (NXP2, FHL-1, SAE, HMGCR, NT5c1A, SRP, TIF1y) are associated with an increased risk of dysphagia (56).

For patients suspected of autoimmune overlap syndromes, antibody panels to screen for systemic rheumatologic diseases, such as systemic lupus erythematosus, rheumatoid arthritis, systemic sclerosis, and Sjögren disease, may be considered.

Paraneoplastic autoantibody panels on serum or cerebrospinal fluid are a consideration if there is clinical suspicion for the same. Autoantibodies associated with paraneoplastic rhombencephalitis have included anti-Ri, anti-Ma2, and anti-Yo associated with small cell carcinoma, germinoma, seminoma, and lymphoma (79). Lambert Eaton myasthenic syndrome and myasthenia gravis can also be part of paraneoplastic presentation.

Electrocardiogram and echocardiogram can be considered to screen for cardiac abnormalities that may accompany myopathies.

Imaging. CT scan of the neck can help visualize oropharyngeal mass lesions or cervical lymphadenopathy.

Neuroimaging with head CT and brain MRI can help screen for acute central structural insults, such as stroke, and assess for chronic encephalomalacia, atrophy, and chronic white matter disease in more longstanding conditions. Cervical spine MRI can help assess for osteophytes and spinal cord involvement in demyelinating diseases. In myopathies, muscle MRI can help identify structural changes, such as edema and fatty replacement, and identify biopsy targets.

In patients with suspected myasthenia gravis, CT of the chest to screen for thymoma is recommended. For suspected paraneoplastic syndromes and inflammatory myopathies, such as dermatomyositis, which are frequently associated with systemic malignancies, a malignancy survey with mammography, colonoscopy, whole-body PET scan, or CT of the chest, abdomen, and pelvis may be indicated. The presence of dysphagia is a factor associated with an increased risk of malignancy in patients with dermatomyositis and polymyositis (107).

Cerebrospinal fluid sampling. A lumbar puncture may be indicated in certain clinical scenarios, such as acute meningoencephalitis, multiple cranial neuropathies, Guillain-Barré syndrome, and autoimmune or paraneoplastic syndromes.

Muscle biopsy. Patients with clinical or laboratory evidence of myopathy with uncertain diagnosis should be considered for a muscle biopsy. Examination of motor strength in the extremities and MRI features can help identify an appropriate biopsy site, particularly as changes associated with inflammatory myopathies can be in a patchy distribution. In patients with dermatologic manifestations, a skin biopsy can also be considered.

Bedside swallow evaluation. A typical clinical assessment starts with swallowing sips of water; observations include timing of swallow, laryngeal elevation, and signs of aspiration before, during, or after swallowing. For further testing, 100 ml of water is offered to assess continuous swallowing, and the same observations are made together with the rate and total volume managed and the unswallowed residual. For a water swallow to accurately identify dysphagia, it is critical to administer 10 teaspoons according to the protocol of TOR-BSST (Toronto Bedside Swallowing Screening Test) to make the screening score more accurate and reliable (71). Bedside tests for dysphagia in conditions such as stroke are easy to perform but have variable sensitivity, specificity, and interrater reliability. They are poor at detecting silent aspiration.

Clinical swallowing examination. A detailed clinical swallowing examination by a trained speech and language therapist has a high sensitivity in assessing aspiration risk (62) but has limited specificity, especially in identifying impairments of the pharyngeal phase. In addition to the relevant neurologic examination, the speech pathologist evaluates oral hygiene, dentition, secretions, cough, voice quality, laryngeal motility, oropharyngeal sensitivity, and spontaneous swallowing frequency. Bedside swallowing tests with various food consistencies are performed while monitoring for signs such as coughing, throat clearing, voice change, and decreased laryngeal elevation. Bedside testing, however, cannot detect silent aspiration or pharyngeal residue.

Videofluoroscopic swallowing study, also known as Modified Barium Swallow Study. Dynamic videofluoroscopic swallow studies enable fast and accurate recording of all phases of deglutition and are sensitive for detecting penetration and aspiration. During the study, patients are asked to consume different consistencies of barium contrast, which is then viewed using videofluoroscopy. The patient must be cooperative and maintain an upright position for the test. The various components of swallowing mechanics, including the oral cavity, tongue movement, velar elevation, hyolaryngeal excursion, complete inversion of the epiglottis, pharyngeal contraction, and upper esophageal sphincter opening, can be evaluated (59). The results can help stratify the severity of dysphagia and guide dietary management.

Flexible endoscopic evaluation. Flexible endoscopic evaluation can be an option in uncooperative or bedbound patients and can be performed at the bedside. An endoscope is transnasally inserted into the pharynx, allowing an assessment of pharyngeal and laryngeal structures while liquids and foods colored with dye are swallowed. It does not involve radiation exposure and is cost-effective, but it has the disadvantage of being unable to directly visualize the oral and pharyngeal stages of swallowing. Structural lesions can also be well-visualized by this technique.

Videofluoroscopic swallowing study and flexible endoscopic evaluation may be considered equally as a diagnostic gold standard for oropharyngeal dysphagia regarding penetration, aspiration, and pharyngeal residue (54).

Pharyngoesophageal manometry. Pharyngoesophageal manometry allows endoluminal pressure measurements during swallowing, which helps measure the strength of pharyngeal contraction, upper esophageal sphincter relaxation, and the relative timing of these two events (17). Manometric measurements can, thus, help identify cricopharyngeal dysfunction to select patients for interventions such as myotomy, dilation, or botulinum toxin injections. It can also help diagnose esophageal motility disorders such as achalasia and diffuse esophageal spasm.

Upper gastrointestinal endoscopy. Upper gastrointestinal endoscopy can allow direct visualization of the esophagus to screen for obstructive lesions or malignancies and to perform biopsies if indicated.

Electrophysiological studies. Routine electromyography and nerve conduction studies can help investigate motor neuron disease, neuropathies, and myopathies in the appropriate clinical context. Repetitive nerve stimulation and single-fiber EMG can be used in patients with suspected neuromuscular junction disorders.

EMG can also be used to analyze the activation pattern of muscles involved in swallowing, including masseter, suprahyoid, infrahyoid, and cricopharyngeus. Surface EMG displays a visual or auditory representation of muscle activity and can be employed in biofeedback therapy to enhance compensatory maneuvers but is otherwise largely experimental.

Staging of dysphagia. A functional outcome swallowing scale was devised for patients with oropharyngeal dysphagia to determine the severity of the disorder and the effectiveness of therapy or outcome (88). The following are various stages of this scale:

• Stage 0: normal function and asymptomatic.
• Stage 1: normal function but symptomatic.
• Stage 2: compensated abnormal function manifested.
• Stage 3: decompensated abnormal function with weight loss of up to 10% or aspiration.
• Stage 4: severely decompensated function with weight loss of more than 10% or severe aspiration with bronchopulmonary complications.
• Stage 5: dysphagia severe enough to require nonoral feeding.

Management

	• Management of dysphagia is wide-ranging and disease-specific.
	• Nutritional support may need to be addressed in a time-sensitive manner, but thoughtful discussions are needed for patients with dementia.
	• Supportive strategies include oral care, behavior modification, and compensatory strategies.
	• Specific exercises for rehabilitation under the guidance of a speech therapist can help with strengthening and reduction of aspiration risk.
	• Neurostimulation can be a useful adjunct to rehabilitative measures but requires more research before widespread application.
	• Surgical intervention, most commonly cricopharyngeal myotomy, can be an option in cricopharyngeal dysfunction.
	• Disease-specific therapies are briefly reviewed for the most common neurologic causes of dysphagia.

Dysphagia secondary to mechanical causes is treated by gastroenterologists and surgeons. Management decisions for dysphagia in patients with neurologic disorders are influenced by several factors, including the primary disease condition, age, and other comorbidities.

Alternative routes of nutrition

One of the first priorities in managing dysphagia is addressing dehydration and nutritional deficiencies. Intravenous fluids can help maintain adequate hydration, but enteral nutrition needs to be considered if this is compatible with the patient’s wishes and goals of care. If a modified diet is tolerated, introducing dietary supplements can help boost protein and caloric intake.

It is widely endorsed that artificial nutrition support is needed when oral intake is absent or likely to be absent for longer than 5 to 7 days. Earlier initiation may be needed in malnourished patients and in patients with inadequate oral intake over longer periods (96). In cases where the prognosis is uncertain or the patient’s goals unclear, a planned time-limited trial of enteral feeding may be reasonable.

A nasogastric tube is commonly used for temporary enteral nutrition in hospitalized patients and can typically remain in place for 2 to 4 weeks. Placement is contraindicated in patients with basilar skull or facial fractures due to the risk of intracranial displacement and injury. It is also avoided in patients with esophageal strictures and varices due to the risk of perforation.

The risks of nasogastric tube placement include aspiration due to accidental tracheal intubation, perforation, nasal ulceration, malpositioning, oropharyngeal discomfort, and bleeding from mucosal trauma.

Complications of enteral nutrition may include feed intolerance, diarrhea, and gastric distention. In severely malnourished patients, it is important to monitor for hypophosphatemia, hypokalemia, and hypomagnesemia, which can be manifestations of refeeding syndrome (26).

In patients with severe dysphagia, more durable nutritional support using percutaneous endoscopic gastrostomy may be required if the patient is unable to swallow.

In patients with dysphagia secondary to stroke, a Cochrane review found that compared with nasogastric tube feeding, percutaneous endoscopic gastrostomy tubes reduced treatment failures and gastrointestinal bleeding and were associated with higher feed delivery and albumin concentration (36). Percutaneous endoscopic gastrostomy tubes are not without risk, however, and carry a 10% risk of major complications, including tube dislodgement, infection, bleeding, and perforation (28). Although enteral nutrition will improve caloric intake and nutritional status, its impact on quality of life is uncertain.

In patients suffering from a terminal illness or advanced neurodegenerative conditions, it is important to initiate multidisciplinary discussions with patients and their families regarding their goals pertaining to enteral feeding and the lack of demonstrable benefits in patients with dementia. A 2009 systematic review on enteral nutrition among patients with advanced dementia found no evidence of efficacy in prolonging survival, improving nutrition, or decreasing the risk of pressure sores (89). The American Geriatrics Society and the Choosing Wisely campaign of the American Board of Internal Medicine provide evidence-based recommendations against the use of feeding tubes in patients with advanced dementia, suggesting careful hand feeding as an alternative (02).

Oral care

Oral hygiene plays an important role in aspiration pneumonia. Microbial flora consistent with periodontal pathology has been demonstrated in samples of bronchoalveolar lavages from hospitalized patients with pneumonia (44). In elderly nursing home residents, inadequate oral care (86) and tongue coating or plaque in edentulous patients (01) were independently associated with pneumonia. Impaired cognition impacts oral hygiene and grooming. Decreased fluid intake, gingival inflammation, and decreased salivation in the elderly further contribute to poor dental health.

A systematic review recommended tooth brushing after each meal, cleaning of removable prostheses once a day, and professional oral health care once a week as the most effective regimen to reduce the incidence of aspiration pneumonia in frail elderly patients (102).

Compensatory strategies

Dietary modification. Using texture-modified foods (eg, pureed, chopped, minced, moist) and thickened liquids is a commonly used strategy. Although thickened liquids can reduce the risk of aspiration, they may increase post-swallow residues (93). The changes in taste and texture may be unpalatable to many patients, and close monitoring of weight and caloric intake is important to prevent malnutrition and dehydration.

Eating behaviors. These include precautions such as supervision and cueing by a caregiver and avoiding distractions during meals, especially for patients with cognitive impairment. Sitting upright during meals; taking small, slow bites and sips; alternating solids and liquids; using a cup or straw for liquids; throat clearing after swallowing; and elevating the head of the bed to at least 30 degrees while resting are frequently recommended.

Compensatory and rehabilitative measures. Various exercises and compensatory maneuvers can be implemented under the supervision of speech and language pathologists and tailored to individual patients based on the nature of impairment.

Compensatory positional changes and maneuvers. Head tilt or rotation maneuvers can help compensate for unilateral impairments of oropharyngeal mobility.

The chin tuck maneuver can help with swallowing mechanics in patients with impaired oral bolus control, delayed swallow initiation, or reduced tongue base retraction. A systematic review found that the chin-down maneuver could reduce the risk of aspiration and pharyngeal residue (65) but may be difficult to implement in patients with cervical spine injuries.

The Mendelsohn maneuver involves sustained voluntary elevation of the larynx during swallowing. The technique has been shown to improve hyolaryngeal excursion and upper esophageal sphincter opening in stroke patients (72). It can be combined with EMG biofeedback techniques.

Other frequently used maneuvers include supraglottic swallow (breath holding, double swallowing, and forceful expiration), super-supraglottic swallow, and effortful swallow.

Strengthening exercises. The Shaker head lift is useful in patients who exhibit reduced laryngeal movement with swallowing, impaired upper esophageal sphincter opening, and pharyngeal residue. It consists of isometric and isokinetic head-raising exercises and has been shown to improve the strength and endurance of the suprahyoid muscles and upper esophageal sphincter opening (03).

Lingual exercises, such as resistance training protocols, can help decrease vallecular residue but may not necessarily improve aspiration (94).

Expiratory muscle strength training is intended to strengthen the expiratory and submental muscles. In a meta-analysis, expiratory muscle strength training in patients with neurologic diseases, including stroke, amyotrophic lateral sclerosis, and Parkinson disease, significantly reduced the penetration-aspiration scores (108).

Comprehensive, structured programs such as the McNeill Dysphagia Therapy Program have been found to improve dysphagia severity and oral intake in patients with ischemic stroke (16).

Lee Silverman Voice Treatment (LSVT® LOUD) is a high-effort, intensive speech treatment for hypokinetic dysarthria and has been shown to have modest benefit in patients with Parkinson disease and progressive supranuclear palsy (74; 77).

Medical interventions

Treatment of drug-induced dysphagia. This is usually relieved by discontinuing the offending drug, which can include a variety of centrally-acting medications, such as neuroleptics and anticholinergics. Neuroleptic-induced tardive dyskinesia can improve with discontinuation of the offending drug and, if persistent, by using pharmacological agents such as tetrabenazine or other vesicular monoamine transporter type 2 (VMAT2) inhibitors. Tardive dystonia can be treated with benztropine or botulinum toxin injection.

Disease-specific therapies. In patients with myasthenia gravis or those with a high clinical suspicion for the same, a trial of acetylcholinesterase inhibitors such as pyridostigmine can be considered while awaiting further workup. However, these agents can increase oral secretions and are best avoided in the setting of a severe myasthenic crisis where the risk of acute aspiration is high.

High-dose intravenous corticosteroids can be used to treat acute relapses in demyelinating diseases, such as multiple sclerosis and neuromyelitis optica, inflammatory myopathies, immune checkpoint inhibitor therapy-associated neurotoxicity, and various autoimmune conditions. Acute rescue therapies such as IVIG or therapeutic plasma exchange are frequently used in myasthenia gravis exacerbations, Guillain-Barré syndrome, and inflammatory myopathies.

In patients with inflammatory myopathies, a variety of immunomodulatory agents commonly used in clinical practice, such as methotrexate, IVIG, mycophenolate, and rituximab, have also been shown to be effective in improving dysphagia (56).

Dopaminergic agents are commonly used to treat motor symptoms of Parkinson disease, but it is unclear whether they have any impact on dysphagia. However, levodopa responsiveness leading to clinically relevant improvement of dysphagia in a proportion of advanced Parkinson disease patients has been demonstrated (109), and patients may benefit from medication titration and optimization. It is important to consider alternative routes of administration in patients unable to swallow oral medication.

Riluzole can prolong survival and slow functional decline in patients with amyotrophic lateral sclerosis, with a relatively greater survival advantage demonstrated in bulbar-onset disease (14). Edaravone, a free radical scavenger, has been demonstrated to slow disease progression in a subset of patients with amyotrophic lateral sclerosis and a disease duration of fewer than 2 years, forced vital capacity greater than 80% of predicted, and scores of higher than 2 on a functional rating scale (115). Tofersen, an antisense oligonucleotide, was approved by the United States Food and Drug Association for use in patients with amyotrophic lateral sclerosis associated with superoxide dismutase 1 (SOD1) gene mutation in April 2023. Current therapies for amyotrophic lateral sclerosis may offer a modest survival benefit but are otherwise largely supportive in nature.

Botulinum toxin injections may be useful for cricopharyngeal dysphagia, particularly for patients who are not candidates for myotomy or balloon dilatation.

Classes of pharmacological agents evaluated for their potential to improve disordered swallowing are TRPV1 agonists, ACE inhibitors, dopaminergic agents, and Sigma-1 receptor agonists; however, there is insufficient evidence to support their standardized use in clinical practice.

Surgery. Structural causes of dysphagia, such as pharyngeal or cricopharyngeal strictures, oropharyngeal tumors, posterior pharyngeal diverticulum, and cervical web, can be amenable to surgical intervention and usually require the input of oral and maxillofacial surgeons or gastroenterologists to help guide management. Benign stenoses or webs can be treated with dilatation.

Cricopharyngeal myotomy. Surgical treatment can be considered for cricopharyngeal dysfunction confirmed by FEES or manometry and when conservative measures have failed.

Myotomy requires appropriate patient selection and is most beneficial in patients with structural disorders, such as postcricoid stenosis, webs, and Zenker diverticulum, that limit upper esophageal sphincter opening. Patients with adequate hyolaryngeal excursion and pharyngeal strength can be candidates for targeted cricopharyngeal intervention, such as balloon dilatation, botulinum toxin injection, and myotomy (52). Cricopharyngeal myotomy can be performed by open surgery or endoscopy. A systematic review in 2016 reported a mean success rate for treating cricopharyngeal dysphagia was 76% for botulinum injections, 81% for dilation, and 75% for myotomy. Endoscopic myotomy had a higher success rate (84%) compared with an open surgical approach (71%) and a lower average complication rate (2% for endoscopic myotomy and 11% for open surgery). Surgical complications included retropharyngeal hematoma, fistula, supraglottic edema, mediastinitis, esophageal injuries, laryngospasm, and severe bleeding (51).

Other surgical procedures that have been used to improve swallowing in selected patients with neuromuscular dysphagia include vocal fold augmentation or medialization, laryngeal suspension, intrahyoid myotomy, lateral thyrolaminectomy, and tracheoesophageal separation procedures.

Neurostimulation. Neurostimulation is an evolving area of novel stimulation techniques intended to enhance neuroplasticity through central or peripheral stimulation.

Pharyngeal electrical stimulation involves the passive electrical stimulation of the pharynx using transnasal catheters. As previously discussed, afferent sensory input from the pharynx plays a key role in cortical control of swallowing. It is hypothesized that increasing sensory stimulation of the pharynx may have beneficial effects on cortical reorganization. Although initial pilot studies showed promise, a randomized control trial in patients with subacute post-stroke dysphagia showed no difference in aspiration risk (13).

Neuromuscular electrical stimulation consists of the transcutaneous stimulation of nerve fibers involved in the sensorimotor function of the pharynx and can be used as a supplement to behavioral swallowing therapies. A meta-analysis concluded that swallow therapy combined with neuromuscular electrical stimulation was more effective in improving swallowing function in the short term but was confounded by significant heterogeneity across the studies (20).

The swallowing network has asymmetric bilateral representation. Following a unilateral stroke, dysphagia recovery is associated with functional reorganization in the contralesional hemisphere (40). Central neurostimulation techniques aim to enhance these compensatory changes after an acute structural insult, hoping to facilitate faster recovery. However, more research is needed to study patient selection and further refine stimulation techniques.

Repetitive transcranial magnetic stimulation has been studied at low- and high-frequency settings and can be applied ipsilesionally or contralesionally. It has been demonstrated to induce changes in neuronal excitability, particularly in the motor cortex. A meta-analysis that included 10 studies and 246 patients evaluated the effectiveness and safety of rTMS on post-stroke dysphagia and found that its use was associated with significant improvements in swallowing function. However, there was considerable heterogeneity in the stimulation parameters (116), and further studies are needed to elucidate patient selection and optimal treatment regimens.

Transcranial direct current stimulation applied unilaterally or bilaterally affects neuronal excitability, and further studies are needed to demonstrate effectiveness.

A Cochrane review in 2018 found moderate- to low-quality evidence that swallowing therapy overall and in subgroups by type of intervention (including pharyngeal electrical stimulation, neuromuscular electrical stimulation, acupuncture, transcranial direct current stimulation, transcranial magnetic stimulation) had no significant effect on the outcomes of death or dependency/disability, case fatality at the end of the trial, or penetration aspiration score (12).

Biofeedback. Biofeedback techniques can be combined with EMG in post-stroke dysphagia therapy and have the potential for short-term benefits in dysphagia rehabilitation (04).

Future of dysphagia management. The effective management of dysphagia requires a multidisciplinary approach, with early recognition, appropriate instrumental studies for characterization, implementation of supportive measures, and prioritizing disease-modifying therapies in treatable conditions. Our understanding of the swallowing mechanism continues to evolve, with evidence indicating it is a highly complex patterned response requiring the integrity and interconnectedness of extensive bilateral neural networks. Recovery in swallowing function after stroke correlates with compensatory reorganization in the contralateral hemisphere and interhemispheric white matter tract integrity. Neurostimulation techniques and biofeedback methods are intended to enhance contralesional neuroplasticity, but more research is needed before they can be applied in clinical practice. Initial promising results of experimental studies show potential for using stem cell-based regenerative therapies to treat oropharyngeal dysphagia and warrant further research (101).

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All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

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Ameeta Karmarkar MD

Dr. Karmarkar of Spartanburg Regional Healthcare has no relevant financial relationships to disclose.
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Peter J Koehler MD PhD

Dr. Koehler of Maastricht University has no relevant financial relationships to disclose.
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Former Authors

K K Jain MD†

ICD & OMIM codes

ICD-11: Dysphagia: MD93

Functions related to the digestive system: VV40

Functional swallowing disorder: DD90.1

Other specified iron deficiency anaemia: 3A00.Y

Dysphagia disorder (TM1): SA50

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Dysphagia

Differential Diagnosis

mechanical dysphagia
globus pharyngeus
phagophobia
odynophagia

Also Relevant

Amyotrophic lateral sclerosis
Botulinum toxin treatment of neurologic disorders
Botulism
Chordoma
Chronic progressive external ophthalmoplegia
- Drug-induced myasthenic syndromes
- Inclusion-body myositis
- Neurogastroenterology
- Parkinson disease
- Progressive supranuclear palsy

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General Neurology

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NIH: Dysphagia

	• Dysphagia is a commonly encountered geriatric syndrome.
	• Prevalence of dysphagia increases with advancing age and is frequently encountered in stroke survivors and patients with neurodegenerative disease.

Dysphagia

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Clinical history

Onset and timeline of symptoms

Medications

Associated symptoms

Prognosis

Complications

Biological basis

Anatomic localization

Pathophysiology

Table 1. Oropharyngeal Dysphagia

Table 2. Esophageal Dysphagia

Epidemiology

Differential diagnosis

Associated or underlying disorders

Diagnostic workup

Key tests and procedures

Management

Alternative routes of nutrition

Oral care

Compensatory strategies

Medical interventions

References

Contributors

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Editor

Former Authors

Patient Profile

ICD & OMIM codes

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Also in This Category

Brain death/death by neurologic criteria

Hepatic encephalopathy

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Coma due to primary brainstem and diencephalic lesions

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Sports activities: neurologic complications

Neurotechnology: brain-computer and brain-machine interfaces

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