Post-stroke dysphagia

Abstract

The article presents a global problem in modern neurology: post-stroke dysphagia. The anatomy, physiology, and pathophysiology of swallowing are presented. The prevalence and risk factors of post-stroke dysphagia are shown. The main complications that develop in patients with post-stroke dysphagia are described. The article presents the main diagnostic and therapeutic approaches for ensuring timely prevention and treatment of this serious complication in patients with strokes.

Full Text

Estimates of stroke burden from the Global Burden of Disease 2021 study showed that among non-communicable diseases, stroke remains the second leading cause of death worldwide (approximately 7 million cases) and the third most significant cause of combined death and disability [1]. Globally, from 1990 to 2021, the number of people who had a stroke, died from it, or were living with post-stroke disability increased significantly: stroke incidence rose by 70%, stroke mortality by 44%, and disability-adjusted life years by 32% [1].

One of the most dangerous complications of stroke is dysphagia, defined as any difficulty or discomfort in the passage of food from the mouth to the stomach. Dysphagia often occurs after a stroke, with a prevalence of 50–80% [2]. Post-stroke dysphagia (PSD) is a serious issue for patients, as it can lead to severe complications such as aspiration, pneumonia, and nutritional deficiency, directly affects the patient’s quality of life, and leads to an unfavorable prognosis or even death [3].

Anatomy and Physiology of Swallowing

Swallowing is essential for human survival. It is a complex physiological process that relies on the timely coordination of oropharyngeal and esophageal muscles for the safe and efficient transport of food from the mouth to the stomach. This process is mediated by the central and peripheral nervous systems. Swallowing is a reflex muscular act in which, through the sequential contraction and relaxation of muscles, a bolus is transferred through the pharynx and esophagus into the stomach. More than 25 pairs of muscles of the upper and lower jaw, lips, cheeks, soft palate, larynx, pharynx, and esophagus are involved in swallowing (Table 1) [4]. Throughout the entire swallowing process, these muscles are coordinated in an organized and dynamic manner to ensure processing (if necessary) and the safe and efficient transport of each sip of liquid or food bolus from the oral cavity to the stomach. Some muscles, for example, those that open and close the jaw, work antagonistically to each other. Other muscles, such as the oropharyngeal muscles, can be activated simultaneously to perform complex movements during the swallowing reflex, while muscles involved in the esophageal stage may be engaged sequentially to create peristaltic waves [4].

Table 1. Anatomy of the oropharyngeal and esophageal phases of swallowing

Muscle groups	Individual muscles	Primary function during swallowing
Muscles that close the jaw	Masseter Temporalis Medial pterygoid Digastric	Chewing and food processing
Muscles that open the jaw	Mylohyoid Suprahyoid (muscle group) Lateral pterygoid
Lips and cheeks	Orbicularis oris Risorius Levator labii muscles Depressor labii muscles Buccinator	Retention of the food bolus in the oral cavity during the oral phase
Tongue	Vertical Transverse	Manipulation with the food bolus in the oral cavity to facilitate processing and propulsion during the oral phase
intrinsic muscles	Superior longitudinal Inferior longitudinal
extrinsic muscles	Genioglossus Styloglossus Hyoglossus Palatoglossus
Soft palate	Levator veli palatini Tensor veli palatini Palatoglossus Palatopharyngeus Musculus uvulae	Elevation of the soft palate during the pharyngeal phase of swallowing to close the passage from the oral cavity to the nasal cavity
Larynx — intrinsic muscles of the larynx	Lateral cricoarytenoid Transverse and oblique arytenoids Aryepiglottic Thyroepiglottic	Control of the opening of the laryngeal inlet
Pharynx — external circular muscles of the pharynx	Anterior belly of digastric Geniohyoid Stylohyoid Styloglossus	Constriction of the pharyngeal wall and elevation of the pharynx and larynx during the pharyngeal phase of swallowing
external circular muscles of the pharynx	Superior, middle, and inferior pharyngeal constrictors Palatoglossus
internal longitudinal muscles of the pharynx	Palatopharyngeus Stylopharyngeus Salpingopharyngeus
Esophagus
Upper esophageal sphincter	Cricopharyngeus Thyropharyngeus	Relaxation of the UES allows the food bolus to pass from the pharynx into the esophagus
esophagus	Inner circular muscle layer Outer longitudinal muscle layer	Propulsion of the food bolus toward the stomach via peristaltic waves during the esophageal phase

Swallowing involves a stereotypical motor pattern that can be divided into several main stages depending on the location of the food bolus (Table 2) [5].

Table 2. Main phases of the swallowing process

Swallowing phase	Swallowing process
Oral preparatory phase	Food is broken down and the food bolus is prepared for swallowing. The position (location) of the food bolus is controlled by the base of the tongue, preventing it from entering the pharynx
Oral propulsive phase	The food bolus is moved into the pharynx by the tongue, and the swallowing reflex is triggered
Pharyngeal phase	Coordinated movements of the tongue and pharyngeal structures propel the food bolus from the pharynx into the esophagus. Vocal cord closure and backward movement of the epiglottis prevent food particles or liquid from entering the trachea
Esophageal phase	Coordinated contractions of the esophageal muscles propel the food bolus through the esophagus toward the stomach

Studies have shown that the viscosity, volume, temperature, and chemical properties of a food bolus can alter swallowing physiology. For example, when swallowing thickened liquids, the transit time through the oral cavity and pharynx, as well as the duration of pharyngeal peristaltic waves, increase, and the opening of the upper esophageal sphincter becomes longer and wider [6]. Furthermore, when swallowing thickened liquids, the true vocal folds close earlier and for a longer duration compared to swallowing thin liquids [7]. Increasing the bolus volume leads to an increase in its transit time, earlier closure of the true vocal folds, and opening of the upper esophageal sphincter [8]. Cold liquids, compared to room-temperature and hot liquids, reduce the time required for swallowing. Carbonated beverages promote better swallowing coordination than still water [9]. Moreover, bitter-tasting boluses increase the latency of the swallowing reflex induced by electrical stimulation, while the addition of monosodium glutamate counteracts this delay [10].

Aging is a natural process involving physiological and neurological changes that can affect physical functions. The term presbyphagia is used to describe age-related changes in swallowing physiology that can increase the risk of dysphagia. Sarcopenia, which is the loss of skeletal muscle mass, strength, and function due to aging, can affect the oropharyngeal phase of swallowing and is an independent risk factor for dysphagia in hospitalized older adults [11]. Studies have shown that individuals over 70 years of age, regardless of sex, exhibit significant atrophy of the geniohyoid muscles, which is associated with aspiration [12], reduced tongue strength [13], decreased jaw-opening force [14], reduced pharyngeal wall thickness, and increased pharyngeal lumen area [15]. Other physiological changes, including decreased muscle elasticity, changes in the cervical spine, poor dentition, and reduced saliva production, can also alter swallowing physiology [16]. These physical and physiological changes can lead to increased oral phase onset time, prolonged pharyngeal transit time and upper esophageal sphincter opening time, reduced pharyngeal volume, increased food residue, changes in upper esophageal sphincter pressure, and an elevated risk of aspiration [17].

In summary, the physiology of the normal swallowing process is highly complex and involves dynamic interactions between afferent and efferent pathways in the nervous system. The cerebral cortex, subcortical structures, brainstem, and cerebellum play a vital role in swallowing control [4]. Therefore, it is not surprising that damage to these structures can disrupt the normal swallowing process, leading to dysphagia.

Prevalence of Post-Stroke Dysphagia

PSD is one of the most common complications of stroke, with its frequency estimated at 30–80% across various studies [18–21]. Spontaneous recovery typically occurs within the first few weeks post-stroke, although swallowing impairments are still detected in approximately 50% of survivors 6 months post-stroke [22].

In 2025, results from a large meta-analysis of 58 studies involving 37,404 patients with acute stroke were published [23]. The pooled incidence of PSD in patients with acute stroke was 42%. Subgroup analysis showed the prevalence of PSD was 44% in Europe, 46% in North America, 40% in the Middle East, 46% in Oceania, 47% in South America, 37% in Asia, and 38% in Africa. According to another meta-analysis, also published in 2025, involving 1,059,969 patients, the overall pooled estimated prevalence of PSD was 38.57% [24]. The PSD prevalence showed little variation across different study years, being 37.20% for 2016–2022, 37.54% for 2011–2015, 33.30% for 2005–2010, and 41.76% for studies before 2005 [24].

PSD Risk Factors

Risk factors for PSD in patients with acute stroke may vary depending on study design and continent. It has been noted that male sex was associated with a lower risk of PSD than female sex [23]. Similar data were noted in a Russian study, where men with PSD were 2.75 times more numerous than women [25]. According to X. Wen et al., PSD was observed in 41.17% of women and 37.75% of men [24].

Age is significantly associated with swallowing function. Individuals over 65 years of age demonstrate a higher prevalence of PSD (40.26%) compared to younger patients (37.75%) [24]. Furthermore, it is reported that aging can lead to a gradual weakening of bodily functions, which is closely related to the deterioration of the patient’s oral cavity and maxillofacial apparatus, thereby contributing to dysphagia [26, 27]. Similarly, degeneration of cranial nerves and impairment of the swallowing reflex in elderly patients may be additional risk factors for swallowing disorders [28–30].

A significantly higher risk of PSD was noted in patients with hemorrhagic stroke compared to patients with ischemic stroke (IS) [24, 31]. A recent meta-analysis showed that patients with IS are 2 times less likely to develop PSD compared to patients with hemorrhagic stroke [20]. The exact reason for this is currently unknown. According to a large study from China, among 32,581 patients with hemorrhagic stroke, based on swallowing function assessment, patients were divided into a no-dysphagia group (n = 24,084; 73.9%) and a dysphagia group (n = 8,497; 26.1%). The dysphagia group, compared to the no-dysphagia group, had worse outcomes, including a higher incidence of pneumonia (60.2% vs. 17.3%) and in-hospital mortality (3.5% vs. 0.3%), a longer hospital stay (p < 0.01), and higher hospitalization costs (p < 0.01) [32].

When studying IS subtypes and the risk of PSD, it was found that the risk of PSD in the cardioembolic stroke group was 1.531 times higher than in the atherothrombotic stroke group, and in patients with atherothrombotic stroke, it was 1.044 times higher than in patients with stroke of undetermined etiology. The lowest risk of PSD was noted in patients with small artery occlusion [24].

Severe stroke is considered an important factor in the development of dysphagia [31, 33]. The prevalence of PSD was significantly higher in the group with National Institutes of Health Stroke Scale (NIHSS) scores from 11 to 20 (68.15%) compared to the group with scores from 5 to 10 (42.67%) and with scores below 5 (37.09%) [24]. An NIHSS score of ≥ 12 at admission in stroke patients has been proposed as a threshold for predicting dysphagia 14 days after stroke onset [34, 35].

Arterial hypertension and diabetes have a negative impact on the overall functioning of stroke patients, thereby significantly increasing the risk of PSD [36–38]. Some studies report that atrial fibrillation is significantly associated with cognitive disorders, which play a crucial role in the physiological process of swallowing [39].

Summary data on the main risk factors for PSD based on large meta-analyses published in recent years are presented in Table 3.

Table 3. Risk factors for PSD according to results of large meta-analyses

Risk Factor	K.J. Banda et al., 2022 [20]	W. Song et al., 2024 [36]	H. Gu et al., 2025 [23]	X. Wen et al., 2025 [24]
Number of patients	26,366	25,022	37,404	1,059,969
Female sex	+	+	+	+
Older age	N/A	+	+	+
Hemorrhagic stroke	+	+	+	+
Stroke severity	+	+	N/A	+
History of stroke	+	+	+	N/A
Hypertension	N/A	+	+	N/A
Diabetes	+	-	+	N/A
Atrial fibrillation	N/A	+	+	N/A

Note. N/A — no data available.

Previous studies have shown that the size and location of the lesion, including the internal capsule, primary sensory cortex and insular lobe of the right hemisphere, as well as the brainstem, play an important role in the control of the swallowing process [40].

Consequences of Post-Stroke Dysphagia

Dysphagia is a significant predictor of adverse health outcomes. Consequences associated with PSD include malnutrition, dehydration, reduced quality of life, and aspiration pneumonia [41]. Furthermore, dysphagia increases the length of hospital stay, treatment costs, and more than doubles the in-hospital mortality rate [42]. According to W. Song et al., the mortality rate of patients with PSD upon admission and after discharge at 1, 3 months, and 1 year was 11.8%, 26.5%, 25.7%, and 31.3%, respectively [36].

One of the serious and life- or health-threatening complications in stroke patients is aspiration, which is defined as the entry of any foreign particle into the airways below the level of the true vocal cords. It is the most severe and immediate consequence of PSD [41] and one of the leading factors causing pneumonia [43]. The possibility of aspiration is indicated by the presence in the post-stroke period of any subjective complaints of difficulty swallowing; changes in voice pitch (quiet or hoarse), as well as a “wet”, gurgling voice, especially after drinking water; an increased latency of the swallowing reflex; coughing during or after swallowing; frequent throat clearing during the day, clearing the throat at the beginning of speech; abnormal changes on chest X-rays; chronic or recurrent lower respiratory tract infection; persistent low-grade fever and/or leukocytosis in the blood; auscultatory and other physical signs of focal changes in the lungs [44]. If one or several of the above symptoms are identified during a patient’s examination and interview, this indicates overt aspiration. Silent aspiration means the absence of external signs, such as coughing, within 1 minute after aspiration, and the absence of symptoms of irritating cough or shortness of breath [45]. The frequency of aspiration in PSD ranges from 15% to 54% [43, 46], with approximately 68% being silent aspiration, which is difficult to detect without instrumental examination [47, 48], leading to potential underdiagnosis.

Meta-analysis results showed that patients with PSD were 4.35 times more likely to be at risk of developing pneumonia and 4.07 times more likely to be at risk of a fatal outcome compared to participants without PSD [20]. The results of another study revealed that the relative risk of developing pneumonia in patients with stroke and dysphagia compared to patients with stroke without dysphagia was 9.41 [49]. Similarly, S.A. Eltringham et al. conducted a systematic review of studies and found that stroke patients with dysphagia were at a higher risk of developing stroke-associated pneumonia compared to patients without dysphagia. Stroke-associated pneumonia was detected in 16.2% of patients with dysphagia compared to 5.2% of patients without dysphagia [50].

Stroke-associated pneumonia develops in 14% of patients [51]. It is associated with an increased risk of in-hospital mortality, longer hospital stays, and has a significant economic impact on healthcare resources [50]. The pathophysiology of stroke-associated pneumonia is multifactorial. The combination of stroke-induced immunodepression and aspiration of oropharyngeal secretions and gastric contents into the lungs, associated with impaired consciousness and dysphagia, predisposes patients to stroke-associated pneumonia in the first days after stroke [52]. Patients with dysphagia are more than 3 times more likely to develop pneumonia after stroke, and in patients with confirmed aspiration, this risk increases 11-fold [43]. Early dysphagia screening and specialized swallowing assessment by a speech-language pathologist can reduce the risk of stroke-associated pneumonia [53].

PSD Diagnosis

Accurate PSD diagnosis is crucial and is typically achieved through screening, clinical signs, and instrumental investigations. Currently, there are no standardized assessment tools for PSD [54]. The traditional gold standard for swallowing assessment includes bedside swallowing screening followed by videofluoroscopic swallowing study and endoscopic evaluation of swallowing when dysphagia is suspected [55, 56].

Since videofluoroscopy visualizes movements in the oral cavity and pharynx, it can be used to assess PSD. In a meta-analysis conducted by R. Martino et al. [43], PSD was detected in 37–45% of cases by screening, in 51–55% by clinical signs, and in 64–78% by instrumental investigation [56]. According to a recently published meta-analysis, the PSD prevalence was 64.27% when using fiberoptic endoscopic evaluation of swallowing, 46.93% with videofluoroscopic swallowing study, and 41.36% with assessment by speech-language pathologists [24]. Videofluoroscopy allows for examining all phases of swallowing: oral, oral-transfer, pharyngeal, and partially esophageal, and can detect aspiration before, during, and after swallowing. However, the use of this method is limited due to radioactive isotopes and radiation exposure, cost, and complexity of performance [58].

According to the guidelines of the European Stroke Organisation and the European Society for Swallowing Disorders, screening for dysphagia in stroke patients should be performed as soon as possible after hospital admission and before initiating oral feeding [28]. For screening, water swallow tests or swallowing assessment tests with foods of different consistencies and volumes can be used, such as the Volume-Viscosity Swallow Test (V-VST).

The initial swallowing assessment test includes a three-swallow trial, during which the patient sequentially drinks 3 teaspoons of water. After each swallow, coughing, choking, or a wet/gurgly voice quality is assessed. Finally, if swallowing is successful, the patient is asked to take several sips from a half-filled glass of water. All data are recorded on a testing form [59, 60].

The V-VST is a validated clinical tool that can be used for the clinical assessment of dysphagia and provides precise guidance on the optimal bolus volume (5, 10, and 20 mL) and viscosity (nectar-like, liquid, and extremely thick) for patients with PSD. The test begins with a swallow trial of a medium-viscosity texture (nectar, honey) at a volume of 5 mL; if swallowed successfully, the volume is increased to 10 and then 20 mL. The test is then performed with a low-viscosity bolus texture (liquid), following the same volume progression method (5, 10, and 20 mL), and subsequently with a high-viscosity texture (puree, pudding consistency) at volumes of 5, 10, and 20 mL. The test evaluates clinical signs of impaired swallowing efficiency (impaired lip closure, piecemeal deglutition, oral and pharyngeal residue) and impaired swallowing safety (voice change, cough, and a 3% or greater drop in oxygen saturation as measured by pulse oximetry) [61].

Therapeutic Approaches

The modern approach to treating patients with PSD includes three strategies: compensation, rehabilitation, and artificial feeding. Over recent decades, the arsenal of therapeutic tools has steadily expanded and now allows for dietary and nutritional interventions, behavioral therapy, specialized oral care, various pharmacological treatment options, as well as peripheral or central neurostimulation strategies [28]. Treatment is individualized, and successful dysphagia treatments implemented in one patient population do not necessarily yield the same results in another [62].

The compensation strategy largely involves modifying the texture of foods and liquids [63]. Nutritional support is essential for managing PSD, as up to half of patients with PSD are considered undernourished. Furthermore, dysphagia is also associated with insufficient intake of water and nutrients in stroke patients. Patients with mild to moderate dysphagia can be transitioned to a dysphagia diet, which includes thickened liquids and foods with a smooth texture, while patients with severe dysphagia may require tube feeding [63, 64]. Specifically, regarding liquid thickening, it has been shown that increasing the viscosity level reduces the risk of airway penetration and aspiration [28].

Furthermore, during the rehabilitation phase, patients with PSD require more energy to perform rehabilitation activities [65, 66]. Resting energy expenditure increases in stroke patients [67], and an inability to meet daily energy requirements can lead to a negative energy balance.

Rehabilitation strategies include training patients in exercises or maneuvers to improve swallowing efficiency and safety [68, 69]. Rehabilitation interventions have been shown to lead to significant improvement in the strength and volume of oropharyngeal muscles [70]. They have been used for decades as a means of improving the quality of life for patients with PSD and are currently among the mainstays of treatment for neurogenic dysphagia in clinical settings. Functional imaging studies have shown increased activity in the brain regions responsible for swallowing following rehabilitation exercises [71].

If the above approaches prove ineffective and the patient’s swallowing remains unsafe, artificial nutrition may be considered. It primarily includes nasogastric tube feeding and the placement of a gastrostomy or jejunostomy [72].

Since the mechanisms of neural tissue repair and increased cerebral cortex activity play an important role in the recovery of swallowing after stroke, non-invasive neurostimulation methods are of particular interest for the treatment of PSD. Neurostimulation promotes cerebral cortex reorganization, accelerating the natural recovery after stroke, and is subdivided into peripheral and central stimulation [41]. Peripheral methods include pharyngeal electrical stimulation and neuromuscular electrical stimulation; central methods include repetitive transcranial magnetic stimulation (rTMS), transcranial direct current stimulation, transcranial alternating current stimulation, and transcranial random noise stimulation [4]. The methods with the strongest evidence base for PSD include pharyngeal electrical stimulation — the first neuromodulation technique; rTMS — the technique with the most evidence supporting its use; and transcranial direct current stimulation [73].

Pharyngeal electrical stimulation passively stimulates the pharynx with low-amplitude electrical impulses. It is believed that transnasal catheters with electrodes in the pharyngeal region increase brain activity in areas controlling swallowing and promotes cortical reorganization of the swallowing area in the motor cortex [74].

Another investigated method of peripheral stimulation is neuromuscular electrical stimulation. Percutaneous electrodes pass an electrical current, inducing muscle contractions in the suprahyoid and infrahyoid muscles [75]. Stimulation of the suprahyoid muscles activates the geniohyoid, mylohyoid, and anterior belly of the digastric muscle, leading to elevation of the hyoid bone and larynx. At the same time, stimulation of the infrahyoid muscles activates the omohyoid, sternohyoid, and sternothyroid muscles, causing depression of the hyoid bone and larynx [76].

Meta-analyses by J.M. Pisegna et al. and X. Liao et al. showed that rTMS of the pharyngeal motor cortex combined with traditional dysphagia therapy is an effective method for improving swallowing function in patients with PSD [77, 78].

Thus, significant progress has been made in recent years in attempts to better characterize PSD and predict which stroke variables and patient factors lead to dysphagia and negative outcomes, which is of great importance for enhancing the effectiveness of therapeutic and rehabilitation measures and the quality of life of patients with PSD.