Investigation of cranial nerves. XII pair: sublingual nerve (n. Hypoglossus)

The sublingual nerve innervates the muscles of the tongue (except for M. Palatoglossus, supplied with X pair of cranial nerves).

Inspection

The study begins with a survey of the tongue in the oral cavity and when it protrudes. Pay attention to the presence of atrophy and fasciculations. Fasciculations are wormlike, rapid irregular twitching of the muscle. Atrophy of the tongue is manifested by a decrease in its volume, the presence of furrows and folds of its mucosa. Fascicular jerking in the tongue indicates the involvement of the sublingual nerve nucleus in the pathological process . Unilateral atrophy of the muscles of the tongue is usually observed with a tumor, vascular or traumatic lesion of the trunk of the sublingual nerve at or below the level of the base of the skull; it is rarely associated with an intramedullary process. Bilateral atrophy often occurs with motor neuron disease [ amyotrophic lateral sclerosis (ALS) ] and syringobulbia. To assess the function of the muscles of the tongue, the patient is offered to stick out his tongue.

Normally, the patient easily displays the tongue; when protruding it is located on the middle line. Paresis of the muscles of one half of the tongue leads to its deviation to the weak side (that is, the genioglossus of the healthy side pushes the tongue towards the paretic muscles). Language is always rejected in the direction of the weak half, regardless of the consequence of what - supranuclear or nuclear - defeat is the weakness of the muscle language. You should make sure that the deviation of the language is true, not imaginary.

A false impression of the presence of a deflection of the tongue can arise when the face is asymmetric due to the one-sided weakness of the facial muscles. The patient is offered to perform fast movements of the tongue from side to side. If the weakness of the tongue is not entirely obvious, ask the patient to press his tongue against the inner surface of the cheek and assess the strength of the tongue, counteracting this movement. The pressure of the tongue on the inner surface of the right cheek reflects the strength of the left m. Genioglossus, and vice versa. Then the patient is offered to pronounce the syllables with the front-language sounds (for example, "la-la-la"). With weakness of the tongue muscles, he can not clearly pronounce them. To identify a mild dysarthria, the subject is asked to repeat complex phrases, for example: "administrative experiment", "episodic assistant", "on the Mount Ararat, a large red grapes ripen," etc.

Combined damage to the nuclei, rootlets or trunks of IX, X, XI, XII pairs of HF causes the development of bulbar paralysis or paresis. Clinical manifestations of bulbar paralysis are dysphagia (dysfunction and sweating when eating because of the paresis of the muscles of the pharynx and epiglottis ); nasolalia (nasal shade of the voice associated with the paresis of the muscles of the palatine curtain); dysphonia (loss of sonority due to muscle paresis involved in constriction / widening of the glottis and tension / relaxation of the vocal cords); dysarthria (paresis of muscles that provide proper articulation); atrophy and fasciculation of the muscles of the tongue; extinction of the palatine, pharyngeal and cough reflexes; respiratory and cardiovascular disorders; sometimes flaccid paresis of the sternocleidomastoid and trapezius muscles.

IX, X and XI nerves together come out of the cranial cavity through the jugular opening, therefore, unilateral bulbar paralysis is usually observed when the lesion of these cranial nerves is swollen. Two-sided bulbar palsy can be caused by poliomyelitis and other neuroinfections, ALS, Kennedy's bulbospinal amyotrophy, or toxic polyneuropathy (diphtheria, paraneoplastic, with GBS, etc.). The defeat of neuromuscular synapses in myasthenia or the pathology of muscles in certain forms of myopathies are the cause of the same disorders of bulbar motor functions as in bulbar paralysis.

From bulbar paralysis, which affects the lower motoneuron (the nucleus of the cranial nerves or their fibers), it is necessary to distinguish pseudobulbar paralysis, which develops with bilateral damage to the upper motor neuron of the cortical-nuclear pathways. Pseudobulbar paralysis is a combined disturbance of the functions of IX, X, XII pairs of cranial nerves, caused by bilateral damage to the cortical-nuclear tracts going to their nuclei. The clinical picture resembles the manifestations of bulbar syndrome and includes dysphagia, nasolalia, dysphonia and dysarthria. In pseudobulbar syndrome, in contrast to the bulbar syndrome, pharyngeal, palatine, and cough reflexes are preserved; reflexes of oral automatism appear, the mandibular reflex increases; observed violent crying or laughter (uncontrollable emotional reactions), hypotrophy and fasciculation of the muscles of the tongue are absent.