Neurologic disorders of the pharynx: causes, symptoms, diagnosis, treatment

The adequate functioning of the pharynx is based on the most complex, mutually consistent neural processes, the slightest disruption of which leads to disorganization of the alimentary and respiratory functions at this level. Situated at the "crossroads" of the respiratory and alimentary tracts, richly supplied with blood and lymphatic vessels, innervated by the V, IX, X and XI cranial nerves and sympathetic fibers, abundant in mucous glands and lymphadenoid tissue, the pharynx is one of the most sensitive organs to various pathogenic factors. Among the numerous diseases to which the pharynx is susceptible, its neurological disorders are not uncommon, arising both from inflammatory and traumatic lesions of its peripheral nerves, and from numerous diseases of the stem and higher centers that provide integral regulation of the physiological (reflex and voluntary) and trophic functions of the pharynx.

Neurogenic disorders of the pharynx cannot be considered in isolation from similar disorders of the esophagus and larynx, since these anatomical structures represent a single functional system that receives nervous regulation from common centers and nerves.

Classification of neurogenic dysfunctions of the pharynx

Dysphagia, aphagia syndrome:

• neurogenic dysphagia;
• painful dysphagia;
• mechanical dysphagia (this form is included in the classification in order to reflect all types of swallowing dysfunction).

Sensory Disorders Syndrome:

• paresthesia of the pharynx;
• hyperesthesia of the pharynx;
• glossopharyngeal neuralgia.

Syndromes of involuntary motor reactions of the pharynx:

• tonic spasm of the pharynx;
• clonic spasm of the pharynx;
• pharyngeal-laryngeal myoclonus.

The above concepts denote symptom complexes based on disorders of the swallowing and alimentary functions of the pharynx and esophagus. According to F. Magendie's concept, the act of swallowing is divided into 3 phases - oral voluntary, pharyngeal involuntary fast and esophageal involuntary slow. The swallowing and alimentary processes normally cannot be arbitrarily interrupted in the second and third phases, but they can be disrupted in any of the above phases by various pathological processes - inflammatory, traumatic (including foreign bodies in the pharynx), tumor, neurogenic, including lesions of the pyramidal, extrapyramidal and bulbar structures. Difficulty swallowing (dysphagia) or its complete impossibility (aphagia) can occur with most diseases of the oral cavity, pharynx and esophagus, and in some cases with diseases of the larynx.

Neurogenic (motor) dysphagia is observed in various processes in the brain (vasculitis, neoplasms, purulent, infectious and parasitic diseases). In this case, both the central supranuclear formations and the peripheral nerve structures that ensure the transmission of regulatory influences of the center to the executive organs of the swallowing act (the nuclei of the IX and X pairs of cranial nerves and their roots - nerves) are affected. In neurogenic dysphagia, not only the motor component of the swallowing act may suffer, but also sensory control over it, which is impaired by hypoesthesia or anesthesia of the pharynx and laryngopharynx. This leads to a violation of the locking function of the pharynx and larynx and the ingress of food and foreign bodies into the respiratory tract. Diphtheritic neuritis of the pharyngeal nerves most often manifests itself as paresis of the soft palate, which is manifested by a swallowing disorder, especially of liquid food that penetrates into the nasopharynx and nasal cavity during the act of swallowing.

Paralysis of the soft palate may be unilateral or bilateral. In unilateral paralysis, functional impairments are insignificant, but visible impairments are clearly revealed, especially during the pronunciation of the sound "A", during which only the healthy half of the soft palate contracts. In a calm state, the uvula is deflected to the healthy side by the pull of the muscles that have retained their function (m. azygos); this phenomenon is sharply enhanced during phonation. In central lesions, unilateral paralysis of the soft palate is rarely isolated; in most cases, it is accompanied by alternating paralysis, in particular, homonymous laryngeal hemiplegia and rarely by paralysis of other cranial nerves.

Unilateral paralysis of the soft palate often occurs with central lesions that occur in the initial stage of hemorrhagic stroke or softening of the brain. However, the most common cause of hemiplegia of the soft palate is damage to the glossopharyngeal nerve by herpes zoster, which is second only to herpes zoster n. facialis and is often associated with it. With this viral disease, unilateral paralysis of the soft palate occurs after herpetic eruptions on the soft palate and lasts for approximately 5 days, then disappears without a trace.

Bilateral paralysis of the soft palate is manifested by open nasal speech, nasal reflux of liquid food, especially in an upright position of the body, and the inability to suck, which is especially detrimental to the nutrition of infants. During mesopharyngoscopy, the soft palate appears to hang sluggishly toward the root of the tongue, float during respiratory movements, and remain motionless when pronouncing the sounds "A" and "E". When the head is tilted backwards, the soft palate passively, under the action of gravity, deviates toward the back wall of the pharynx, and when the head is tilted forward, toward the oral cavity. All types of sensitivity are absent in paralysis of the soft palate.

The cause of bilateral paralysis of the soft palate in most cases is diphtheria toxin, which has high neurotropism (diphtheria polyneuritis), less often these paralyses occur with botulism, rabies and tetany due to calcium metabolism disorders. Diphtheria paralysis of the soft palate usually occurs with insufficient treatment of this disease or with unrecognized diphtheria of the pharynx. As a rule, these paralyses appear from the 8th day to 1 month after the disease. Dysphagia syndrome is sharply increased with damage to the nerve fibers innervating the inferior constrictor of the pharynx. Often after diphtheria of the pharynx, combined paralysis of the soft palate and ciliary muscle of the eye is observed, which allows for a retrospective diagnosis of diphtheria, taken for vulgar pharyngitis or tonsillitis. Treatment of diphtheria paralysis of the soft palate is carried out with antidiphtheria serum for 10-15 days, strychnine preparations, B vitamins, etc.

Central paralysis of the soft palate, caused by damage to the brainstem, is combined with alternating paralysis (bulbar paralysis). The causes of these lesions may be syphilis, cerebral apoplexy, syringobulbia, brainstem tumors, etc. Paralysis of the soft palate is also observed in pseudobulbar paralysis caused by damage to the supranuclear pathways.

Soft palate paralysis may occur during a hysterical attack, which usually manifests itself with other symptoms of hysterical neurosis. Usually, with such paralysis, the voice becomes nasal, but there is no nasal reflux of swallowed liquid. The manifestations of hysterical neurosis are extremely diverse and can externally simulate various diseases, but most often they imitate neurological and mental diseases. Neurological symptoms include paralysis of varying severity and prevalence, cuts, disturbances of pain sensitivity and movement coordination, hyperkinesis, tremors of the limbs and contractions of the facial muscles, various speech disorders, spasms of the pharynx and esophagus. The peculiarity of neurological disorders in hysterical neurosis is that they are not accompanied by other disorders common to neurological disorders of organic origin. Thus, in hysterical paralysis or spasms of the pharynx or larynx there are no changes in reflexes, trophic disorders, dysfunctions of the pelvic organs, spontaneous motor vestibular reactions (spontaneous nystagmus, the symptom of missing the target, etc.). Sensitivity disorders in hysteria do not correspond to the zones of anatomical innervation, but are limited to the zones of "stockings", "gloves", "socks".

Paresis and paralysis in hysteria affect muscle groups involved in performing any voluntary, purposeful motor act, such as chewing, swallowing, sucking, squinting, and movements of the internal muscles of the larynx. Thus, hysterical glossoplegia, which occurs under the influence of negative emotions in people suffering from neurasthenia, leads to a disruption of active movements of the tongue, its participation in the acts of chewing and swallowing. In this case, voluntary slow movements of the tongue are possible, but the patient cannot stick the tongue out of the oral cavity. The resulting decrease in sensitivity of the mucous membrane of the tongue, pharynx, and entrance to the larynx aggravates dysphagia, often leading to aphagia.

Diagnostics of functional dysphagia of hysteroid genesis does not cause difficulties due to its remittent (recurring) nature and rapid disappearance after taking sedatives and tranquilizers. In case of true dysphagia of organic genesis, the diagnosis is based on the signs of the causal (underlying) disease. Such diseases may include banal inflammatory processes with vivid symptoms, specific processes, neoplasms, injuries, developmental anomalies.

Pharyngeal paralysis is characterized by impaired swallowing, especially of solid food. It does not occur in isolation, but is combined with paralysis of the soft palate and esophagus, and in some cases with paralysis of the laryngeal muscles that expand the glottis. In these cases, a gastric tube for feeding is always adjacent to a tracheotomy tube. The most common causes of such paralysis are diphtheritic neuritis of the glossopharyngeal and other nerves involved in the innervation of the pharynx, larynx and esophagus, as well as severe forms of typhus, encephalitis of various etiologies, bulbar poliomyelitis, tetany, barbiturate and narcotic poisoning. Functional disorders are explained by paralysis of the pharyngeal constrictors and muscles that lift it and the larynx during the act of swallowing, which is determined by palpation of the larynx and mesopharyngoscopy (examination of the pharynx during swallowing can be carried out provided that the person being examined clamps a cork or other object between the molars before swallowing, the size of which allows endoscopy). This technique is necessary due to the fact that a person cannot swallow if his jaws are not clenched.

Pharyngeal paralysis may be unilateral in the case of unilateral damage to the glossopharyngeal nerve and motor fibers of the vagus nerve. This type of pharyngeal hemiplegia is usually associated with unilateral paralysis of the soft palate, but does not affect the larynx. This picture can be observed either in case of cerebral circulatory insufficiency or after a viral infection. In herpes zoster, unilateral pharyngeal paralysis is usually associated with the same paralysis of the soft palate and facial muscles of the same etiology. Hypesthesia of the pharyngeal mucosa on the affected side is also noted. Glossopharyngeal nerve paralysis is manifested by the accumulation of saliva in the pyriform sinuses.

X-ray examination with contrast reveals asynchrony of the movements of the epiglottis and pharyngeal constrictors during swallowing and accumulation of contrast agent in the area of the epiglottis fossa and especially in the pyriform sinus on the affected side.

The occurrence of bulbar laryngopharyngeal paralysis is explained by the commonality of their innervation apparatus, the proximity of the nuclei of the glossopharyngeal nerve and the vagus nerve and the efferent fibers of these nuclei. These disorders will be described in more detail in the section on neurogenic functional disorders of the larynx.

Painful dysphagia occurs with inflammatory processes in the oral cavity, pharynx, esophagus, larynx and in the tissues surrounding these organs, with foreign bodies in the pharynx and esophagus, injuries to these organs, inflammatory complications, disintegrating infectious granulomas (except syphilis), tumors, etc. The most painful are tuberculous ulcers, less painful are disintegrating malignant tumors and the least painful are syphilitic lesions of the walls of the esophageal tract. Painful dysphagia with inflammatory processes in the oral cavity, paratonsillar space is often accompanied by contracture of the temporomandibular joint or reflex trismus. Somewhat less frequently, painful dysphagia has a neurogenic nature, for example, in neuralgia of the trigeminal, glossopharyngeal and superior laryngeal nerves, as well as in various hysterical neuroses manifested by prosopalgia, paralysis, paresis and hyperkinesis in the masticatory and swallowing-esophageal complex.

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