Dysphagia

Role of Mastication and Predisposing Factors

The digestive process begins in the oral cavity, and its disorders often precede deeper pathologies. Key factors here include pain syndromes arising from inflammation (stomatitis, gingivitis, glossitis, periodontitis). Dental arch defects (missing or absent teeth) and disorders of the temporomandibular joint and masticatory muscles, including bone fractures, atrophy, or muscle hypertonus, also play significant roles.

Behavioral habits deserve separate mention: eating on the run or reading at the table leads to insufficient mastication. As a result, poorly chewed food mechanically damages the gastric mucosa, provokes secretory and motor dysfunction, and causes general digestive disorders in the stomach and intestines.

Etiology of Dysphagia and Aphagia

The causes of dysphagia (or its extreme form, aphagia) are diverse. In clinical practice, the following groups of factors are most commonly distinguished:

• Pain syndrome: inflammation, ulceration of the oral mucosa, as well as trauma and skull bone fractures.
• Masticatory apparatus lesions: arthritis and arthrosis of the temporomandibular joints, paresis, paralysis, and hypo- or hypertonus of the masticatory muscles.
• Neurological deficits: damage to the neurons of the swallowing center and conduction pathways (especially secondary to cerebrovascular accidents). This also includes impaired afferent and efferent innervation due to inflammation or damage to branches of the cranial nerves: vagus (n. vagus), trigeminal (n. trigeminus), and glossopharyngeal (n. glossopharyngeus).
• Local structural changes: scars, neoplasms, or ulcers directly in the pharynx and esophagus.
• Psychogenic factors: severe stress or hysterical episodes can provoke the development of aphagia.

Consequences of Swallowing Disorders

The inability to swallow normally triggers a cascade of severe complications:

1. Malnutrition: food does not enter the stomach in sufficient quantities, leading to systemic digestive disorders and cachexia.
2. Food aspiration: entry of food masses into the respiratory tract provokes bronchospasm, bronchitis, aspiration pneumonia, and even lung abscess.
3. Asphyxia: massive entry of food into the respiratory tract (often occurring in unconscious patients or during emergence from anesthesia) results in suffocation.

Esophageal Dysfunction

This is a standard form of digestive pathology characterized by impaired esophageal motility, difficulty passing food into the stomach, and reflux (backward flow of gastric contents). Failures most frequently occur at the level of the upper and lower (cardiac) sphincters.

Main causes of dysfunction include:

• Neurogenic disorders: encephalitis, pathological stress, psychiatric disorders, and dystrophic or destructive changes in the neurons of the vagus nerve and intramural plexuses. Normally, vagal influences enhance peristalsis. Plexus neurons can either activate contraction via cholinergic muscarinic M₂-receptors or inhibit it via nicotinic and muscarinic M₁-receptors.
• Humoral shifts: excessive effects of nitric oxide (NO) or vasoactive intestinal peptide (VIP).
• Sclerotic changes of the wall: scarring following extensive erosions and ulcers, chemical and thermal burns, and systemic diseases (dermatomyositis, systemic sclerosis).
• Spasms: local or diffuse esophageal spasm occurring during neuroses or attempts to swallow an excessively large bolus of solid food.

Main Forms of Esophageal Pathology

The key consequences and forms of dysfunction include:

• Achalasia (from Greek a — absence and chalasis — relaxation) is a condition of prolonged spasm of the smooth muscle wall of the esophageal body and its lower sphincter. Peristalsis ceases, and the sphincter relaxes inadequately, impairing the passage of food into the stomach.
• Diffuse esophageal spasm — contraction of muscle fibers across all segments of the wall. Important distinction from achalasia: in diffuse spasm, the tone of the lower esophageal sphincter remains normal.