7 pair of cranial. VII pair - facial nerves

Of the twelve pairs of cranial nerves, I, II and V III pairs are sensory nerves, III, IV, VI, VII, XI and XII - motor, V, IX and X - mixed. The motor fibers of the cranial nerves innervate the muscles of the eyeballs, face, soft palate, pharynx, vocal cords and tongue, and sensory neurons provide sensitivity to the skin of the face, mucous membranes of the eye, oral cavity, nasopharynx and larynx.

I PAIR: OLFA NERVE (N. OLFA CTORIUS)

The function of the nerve (smell perception) is provided by several neurons from the nasal mucosa to the hippocampus (Fig. 1-2).

The sense of smell is checked both in the presence of complaints about a violation of the perception of smells, and without them, since often the patient himself does not realize that he has a disorder of smell, but complains of a violation of taste (full taste sensations are possible only if the perception of food aromas is preserved), as well as when suspicion of a pathological process in the area of ​​the bottom of the anterior cranial fossa.

To check the sense of smell, they find out if the patient distinguishes known smells - coffee, tobacco, soup, vanilla: they ask him to close his eyes and determine the smell of a substance that is brought alternately to the right and left nostrils (the second nostril should be clamped with the index finger of the hand). You can not use substances with a pungent odor (for example, ammonia), because they cause irritation of receptors not so much olfactory as trigeminal nerve. The ability to distinguish odors in healthy individuals varies greatly, therefore, when testing, it is more important not whether the patient was able to identify a certain substance by smell, but whether he noticed the presence of a smell at all. special clinical significance acquires a unilateral loss of smell, if it cannot be explained by the pathology of the nasal cavity. Unilateral anosmia is more typical for neurological diseases than bilateral. Unilateral or bilateral anosmia is the classic feature of olfactory fossa meningioma. It is also characteristic of other tumors located in the anterior cranial fossa. Anosmia may be a consequence of TBI. Bilateral anosomia most often occurs in the cold, especially in the elderly.

Rice. 12 . The pathways of the olfactory analyzer: 1 - olfactory cells; 2 - olfactory threads; 3 - olfactory bulb; 4 - olfactory triangle; 5 - corpus callosum; 6 - cells of the cortex of the parahippocampal gyrus.

II PAIR: OPTIC NERVE (N. OPTICUS)

The nerve conducts visual impulses from the retina to the cortex of the occipital lobe (Fig. 1-3).

Rice. 1-3. Scheme of the structure of the visual analyzer: 1 - retinal neurons; 2 - optic nerve; 3 - optic chiasm; 4 - visual tract; 5 - cells of the external geniculate body; 6 - visual radiance; 7 - medial surface of the occipital lobe (spur groove); 8 - the nucleus of the anterior colliculus; 9 - cells of the nucleus of the third pair of CNs; 10 - oculomotor nerve; 11 - ciliary knot.

When collecting an anamnesis, they find out if the patient has any changes in vision. Changes in visual acuity (far or near) are within the competence of the ophthalmologist. With transient episodes of impaired visual clarity, limited visual fields, the presence of photopsies or complex visual hallucinations, a detailed study of the entire visual analyzer is necessary. The most common cause of transient visual impairment is migraine with visual aura. Visual disturbances are more often represented by flashes of light or sparkling zigzags (photopsies), flickering, loss of a site or the entire field of vision. The visual aura of migraine develops 0.5-1 hour (or less) before a headache attack, lasting an average of 10-30 minutes (no more than 1 hour). Headache with migraine occurs no later than 60 minutes after the end of the aura. Visual hallucinations of the photopsy type (flashes, sparks, zigzags) can represent an aura of an epileptic seizure in the presence of a pathological focus that irritates the cortex in the region of the spur groove.

Visual acuity and its study

Visual acuity is determined by ophthalmologists. To assess distance visual acuity, special tables with circles, letters, and numbers are used. The standard table used in Russia contains 10-12 rows of signs (optotypes), the sizes of which decrease in arithmetic progression from top to bottom. Vision is examined from a distance of 5 m, the table should be well lit. For the norm (visual acuity 1) take such visual acuity at which from this distance the subject is able to distinguish the optotypes of the 10th (counting from the top) line.

If the subject is able to distinguish the signs of the 9th line, his visual acuity is 0.9, the 8th line is 0.8, etc. In other words, reading each subsequent line from top to bottom indicates an increase in visual acuity by 0.1. Near visual acuity is checked using other special tables or by offering the patient to read the text from the newspaper (normally small newspaper print is distinguished from a distance of 80 cm). If the visual acuity is so small that the patient cannot read anything from any distance, they are limited to counting fingers (the doctor's hand is at eye level of the subject). If this is also impossible, the patient is asked to determine in which room: in a dark or in a lighted room - he is. Reduced visual acuity (amblyopia) or complete blindness (amaurosis) occurs when the retina or optic nerve is damaged. With such blindness, the pupil's direct reaction to light disappears (due to interruption of the afferent part of the pupillary reflex arc), but the pupil's reaction in response to illumination of the healthy eye remains intact (the efferent part of the pupillary reflex arc, represented by fibers of the third cranial nerve, remains intact). A slowly progressive decrease in vision is observed when the tumor compresses the optic nerve or chiasm.

Signs of violations. Transient short-term loss of vision in one eye (transient monocular blindness, or amaurosis fugax - from Latin "transient") may be due to a transient disturbance of the blood supply to the retina. It is described by patients as a "curtain falling from top to bottom" when it occurs and as a "rising curtain" when it develops back.

Usually vision is restored in a few seconds or minutes. Decreased vision, which is acute and progresses over 3-4 days, then recovers within a few days or weeks and is often accompanied by pain in the eyes, is characteristic of retrobulbar neuritis. Sudden and persistent loss of vision occurs with fractures of the bones of the anterior cranial fossa in the region of the optic canal; with vascular lesions of the optic nerve and temporal arteritis. With blockage of the bifurcation zone of the main artery and the development of bilateral infarction of the occipital lobes with damage to the primary visual centers of both cerebral hemispheres, "tubular" vision or cortical blindness occurs. "Tubular" vision is due to bilateral hemianopia with the preservation of central (macular) vision in both eyes. Preservation of vision in a narrow central field of view is explained by the fact that the projection zone of the macula in the pole of the occipital lobe is supplied with blood from several arterial basins and, in case of infarcts of the occipital lobes, most often remains intact.

Visual acuity in these patients is slightly reduced, but they behave like blind people. "Cortical" blindness occurs in case of insufficiency of anastomoses between the cortical branches of the middle and posterior cerebral arteries in the areas of the occipital cortex responsible for central (macular) vision. Cortical blindness is characterized by the preservation of pupillary reactions to light, since the visual pathways from the retina to the brain stem are not damaged. Cortical blindness in bilateral lesions of the occipital lobes and parietal-occipital regions in some cases can be combined with the denial of this disorder, achromatopsia, apraxia of conjugate eye movements (the patient cannot direct his gaze towards an object located in the peripheral part of the visual field) and inability to visually perceive the object and touch him. The combination of these disorders is referred to as Balint's syndrome.

Fields of view and their and research

The field of view is the portion of space that the fixed eye sees. The safety of the visual fields is determined by the state of the entire visual pathway (optic nerves, optic tract, visual radiation, cortical zone of vision, which is located in the spur groove on the medial surface of the occipital lobe). Due to the refraction and crossing of light rays in the lens and the transition of visual fibers from the same halves of the retina to the chiasm, the right half of the brain is responsible for the preservation of the left half of the visual field of each eye. Visual fields are evaluated separately for each eye. There are several methods for their approximate assessment.

Sequential evaluation of individual visual fields. The doctor sits opposite the patient. The patient closes one of his eyes with his palm, and with the other eye looks at the nose of the doctor. The hammer or moving fingers are moved around the perimeter from behind the head of the subject to the center of his field of vision and the patient is asked to note the moment the hammer or fingers appear. The study is carried out in turn in all four quadrants of the visual fields.

The "threat" technique is used in those cases when it is necessary to examine the visual fields of a patient inaccessible to speech contact (aphasia, mutism, etc.). The doctor with a sharp "threatening" movement (from the periphery to the center) brings the unbent fingers of his hand closer to the patient's pupil, observing his blinking. If the field of view is intact, the patient blinks in response to the approach of the finger. All visual fields of each eye are examined.

The described methods are screening, more precisely, visual field defects are detected using a special device - the perimeter.

Signs of violations. Monocular visual field defects are usually caused by pathology of the eyeball, retina, or optic nerve - in other words, damage to the visual pathways in front of their intersection (chiasm) causes a violation of the visual fields of only one eye located on the side of the lesion.

Binocular visual field defects (hemianopsia) can be bitemporal (the temporal visual fields fall out in both eyes, that is, the right eye has the right, the left has the left) or homonymous (each eye has the same visual fields - either left or right). Bitemporal visual field defects occur with lesions in the region of the optic chiasm (for example, damage to the chiasm with swelling and pituitary gland). Homonymous visual field defects occur when the optic tract, optic radiation or visual cortex is damaged, that is, when the visual pathway above the chiasm is damaged (these defects occur in the visual fields opposite to the lesion: if the lesion is in the left hemisphere, the right visual fields of both eyes fall out, and vice versa) . The defeat of the temporal lobe leads to the appearance of defects in the homonymous upper quadrants of the visual fields (contralateral upper quadrant anopsia), and the defeat of the parietal lobe - to the appearance of defects in the homonymous lower quadrants of the visual fields (contralateral lower quadrant anopsia).

Conduction defects of the visual fields are rarely combined with changes in visual acuity. Even with significant peripheral visual field defects, central vision may be preserved. Patients with visual field defects caused by damage to the visual pathways above the chiasm may not be aware of the presence of these defects, especially in cases of damage to the parietal lobe.

The fundus of the eye and its study

The fundus of the eye is examined using an ophthalmoscope. Assess the condition of the disk (nipple) of the optic nerve (visible during ophthalmoscopy initial, intraocular part of the optic nerve), retina, fundus vessels. The most important characteristics of the condition of the fundus are the color of the optic disc, the clarity of its boundaries, the number of arteries and veins (usually 16-22), the presence of pulsation of the veins, any anomalies or pathological changes: hemorrhages, exudate, changes in the walls of blood vessels in the area of ​​the macula (macula) and on the periphery of the retina.

Signs of violations. Edema of the optic disc is characterized by its bulging (the disc stands above the level of the retina and protrudes into the cavity of the eyeball), redness (the vessels on the disc are sharply dilated and overflowing with blood); the borders of the disk become fuzzy, the number of retinal vessels increases (more than 22), the veins do not pulsate, there are hemorrhages. Bilateral edema of the optic disc (congestive optic nerve papilla) is observed with an increase in intracranial pressure (volumetric process in the cranial cavity, hypertensive encephalopathy, etc.). Visual acuity initially, as a rule, does not suffer. If the increase in intracranial pressure is not eliminated in a timely manner, visual acuity gradually decreases and blindness develops due to secondary atrophy of the optic nerve.

Congestive optic disc must be differentiated from inflammatory changes (papillitis, optic neuritis) and ischemic optic neuropathy. In these cases, disc changes are more often unilateral, pain in the eyeball and decreased visual acuity are typical. Paleness of the optic nerve head in combination with a decrease in visual acuity, narrowing of the visual fields, and a decrease in pupillary reactions are characteristic of optic nerve atrophy, which develops in many diseases that affect this nerve (inflammatory, dysmetabolic, hereditary).

Primary optic nerve atrophy develops when the optic nerve or chiasm is damaged, while the disc is pale, but has clear boundaries. Secondary optic atrophy develops following edema of the optic disc, the boundaries of the disc are initially indistinct. Selective blanching of the temporal half of the optic disc can be observed in multiple sclerosis, but this pathology is easily confused with a variant of the normal state of the optic disc. Pigmentary degeneration of the retina is possible with degenerative or inflammatory diseases nervous system. Other important pathological findings for the neurologist when examining the fundus include arteriovenous angioma of the retina and a cherry-stone symptom, which is possible with many gangliosidoses and is characterized by the presence of a white or gray rounded focus in the macula, in the center of which there is a cherry-red spot. Its origin is associated with atrophy of retinal ganglion cells and translucence of the choroid through it.

III, IV, VI PARbI: OCULAMOTORIUS (N. OCULOMOTORIUS), BLOCKS (N. TROCHLEAR/S) AND EXHAUSTIVE (N. ABOUCENS) NERVE

The oculomotor nerve contains motor fibers that innervate the medial, upper and lower rectus muscles of the eyeball, the inferior oblique muscle and the muscle that lifts the upper eyelid, as well as autonomic fibers, which, interrupted in the ciliary ganglion, innervate the internal smooth muscles of the eye - the pupillary sphincter and the ciliary muscle (Fig. 1-4).

Rice. 1-4. Topography of the nuclei of the oculomotor nerves: 1 - the nucleus of the abducens nerve; 2 - the nucleus of the trochlear nerve; 3 - accessory nucleus of the oculomotor nerve; 4 - middle unpaired nucleus of the oculomotor nerve (pusl. caudal is sen thl is); 5 - the core of the medial longitudinal bundle; 6 - large cell nucleus of the oculomotor nerve.

The trochlear nerve innervates the superior oblique muscle, and the abducens nerve innervates the external rectus muscle of the eyeball.

When collecting an anamnesis, they find out if the patient has diplopia and, if it is present, how doubling objects are located - horizontally (pathology of the VI pair), vertically (pathology of the III pair) or when looking down (lesion of the IV pair). Monocular diplopia is possible with intraocular pathology, leading to dispersion of light rays on the retina (with astigmatism, corneal diseases, with incipient cataracts, vitreous hemorrhage), as well as with hysteria; with paresis of the external (striated) muscles of the eye, monocular diplopia does not occur. The sensation of imaginary trembling of objects (oscillopsia) is possible with vestibular pathology and some forms of nystagmus.

Eyeball movements and their study

There are two forms of friendly movements of the eyeballs - conjugated (gaze), in which the eyeballs simultaneously turn in the same direction; and vergent, or disconjugated, in which the eyeballs simultaneously move in opposite directions (convergence or divergence).

In neurological pathology, four main types of oculomotor disorders are observed.

Mismatch of the movements of the eyeballs due to weakness or paralysis of one or more striated muscles of the eye; as a result, strabismus (strabismus) and a split image occur due to the fact that the object in question is projected in the right and left eyes not onto similar, but onto disparate areas of the retina.

Concomitant violation of the conjugated movements of the eyeballs, or concomitant gaze paralysis: both eyeballs consistently (jointly) cease to move arbitrarily in one direction or another (right, left, down or up); in both eyes, the same deficit of movements is revealed, while double vision and strabismus do not occur.

A combination of paralysis of the muscles of the eye and paralysis of the gaze.

Spontaneous abnormal movements of the eyeballs, occurring mainly in patients in a coma.

Other variants of oculomotor disorders (concomitant strabismus, internuclear ophthalmoplegia) are observed less frequently. The listed neurological disorders should be distinguished from a congenital imbalance in the tone of the eye muscles (non-paralytic strabismus or non-paralytic congenital strabismus, oftophoria), in which the mismatch of the optical axes of the eyeballs is observed both during eye movements in all directions and at rest. Latent non-paralytic strabismus is often observed, in which images cannot fall on identical places on the retina, but this defect is compensated by reflex corrective movements of the covertly squinting eye (fusion movement).

With exhaustion, mental stress, or other reasons, the fusional movement may weaken, and latent strabismus becomes apparent; in this case, double vision occurs in the absence of paresis of the external muscles of the eye.

Evaluation of the parallelism of the optical axes, analysis of strabismus and diplopia

The doctor stands in front of the patient and asks him to look straight ahead and into the distance, fixing his gaze on a distant object. Normally, the pupils of both eyes should be in the center of the palpebral fissure. Deviation of the axis of one of the eyeballs inward (esotropia) or outward (exotropia) when looking straight and far indicates that the axes of the eyeballs are not parallel (strabismus), and this is what causes doubling (diplopia). To identify minor strabismus, you can use the following technique: holding a light source (for example, a light bulb) at a distance of 1 m 01: the patient at the level of his eyes, monitor the symmetry of light reflections from the irises. In that eye, the axis of which is deviated, the reflection will not coincide with the center of the pupil.

Then the patient is asked to fix his gaze on an object that is at the level of his eyes (a pen, his own thumb hands), and in turn close one or the other eye. If, when closing the “normal” eye, the squinting eye makes an additional movement to maintain fixation on the object “alignment movement”), then most likely the patient has congenital strabismus, and not paralysis of the eye muscles. With congenital strabismus, the movements of each of the eyeballs, if test them separately, saved and run in full.

Evaluate the performance of the smooth tracking test. They ask the patient with his eyes (without turning his head) to follow the object, which is held at a distance of 1 m from his face and slowly move it horizontally to the right, then to the left, then on each side up and down (the trajectory of the doctor's movements in the air should correspond to the letter "H ") . They follow the movements of the eyeballs in six directions: to the right, to the left, down and up with the abduction of the eyeballs in turn in both directions. They are interested in whether the patient has double vision when looking in one direction or another. In the presence of diplopia, they find out when moving in which direction the doubling increases. If a colored (red) glass is placed in front of one eye, then it is easier for a patient with diplopia to distinguish between double images, and for the doctor to find out which image belongs to which eye.

Slight paresis of the external muscle of the eye does not give a noticeable strabismus, but at the same time, subjectively, the patient already has diplopia. Sometimes a doctor's report of a patient about the occurrence of double vision during a particular movement is enough to determine which eye muscle is affected. Almost all cases of newly occurring double vision are due to acquired paresis or paralysis of one or more striated (external, extraocular) muscles of the eye. As a rule, any recent paresis of the extraocular muscle causes diplopia. Over time, visual perception on the affected side slows down, and doubling disappears. There are two main rules to consider when analyzing a patient's complaints of diplopia to determine which muscle of which eye is affected: (1) the distance between the two images increases when looking in the direction of action of the paretic muscle; (2) the image produced by an eye with a paralyzed muscle appears more peripheral to the patient, that is, more distant from the neutral position. In particular, you can ask a patient whose diplopia increases when looking to the left, look at an object on the left and ask him which of the images disappears when the doctor's palm covers the patient's right eye. If the image closer to the neutral position disappears, this means that the open left eye is "responsible" for the peripheral image, and therefore its muscle is defective. Since double vision occurs when looking to the left, the lateral rectus muscle of the left eye is paralyzed.

Complete damage to the oculomotor nerve trunk leads to diplopia in the vertical and horizontal plane as a result of weakness of the superior, medial, and inferior rectus muscles of the eyeball. In addition, with complete paralysis of the nerve on the side of the lesion, ptosis occurs (weakness of the muscle that lifts the upper eyelid), deviation of the eyeball outward and slightly downward (due to the action of the preserved lateral rectus muscle, innervated by the abducens nerve, and the superior oblique muscle, innervated by the trochlear nerve) , pupil dilation and loss of its reaction to light (paralysis of the sphincter of the pupil).

The defeat of the abducens nerve causes paralysis of the external rectus muscle and, accordingly, the medial deviation of the eyeball (convergent strabismus). When looking in the direction of the lesion, horizontal double vision occurs. Thus, diplopia in the horizontal plane, not accompanied by ptosis and changes in pupillary reactions, most often indicates a lesion of the VI pair.

If the lesion is located in the brainstem, in addition to paralysis of the external rectus muscle, paralysis of the horizontal gaze also occurs.

Damage to the trochlear nerve causes paralysis of the superior oblique muscle and is manifested by restriction of downward movement of the eyeball and complaints of vertical double vision, which is most pronounced when looking down and in the opposite direction to the focus. Diplopia is corrected by tilting the head to the shoulder on the healthy side.

The combination of paralysis of the eye muscles and gaze paralysis indicates damage to the structures of the brain bridge or midbrain. Double vision that gets worse after physical activity or towards the end of the day, typical of myasthenia gravis. With a significant decrease in visual acuity in one or both eyes, the patient may not notice diplopia even in the presence of paralysis of one or more extraocular muscles.

Evaluation of coordinated movements of the eyeballs, analysis of concomitant disorders of eye movements and gaze paralysis

Gaze paralysis occurs as a result of supranuclear disorders, and not due to damage to III, IV or VI pairs of CN. Glance (gaze) in the norm is a friendly conjugated movements of the eyeballs, that is, their coordinated movements in one direction (Fig. 1-5). There are two types of conjugated movements - saccades and smooth tracking. Saccades are very precise and fast (about 200 ms) phase-tonic movements of the eyeballs, which normally occur either with an arbitrary look at an object (at the command "look to the right", "look to the left and up", etc.), or reflexively when a sudden visual or auditory stimulus causes the eyes (usually the head) to turn in the direction of that stimulus. Cortical control of saccades is exercised by the frontal lobe of the contralateral hemisphere.

Rice. 15. Innervation of friendly movements of the eyeballs along the horizontal plane to the left, the system of the medial longitudinal bundle: 1 - middle gyrus of the right frontal lobe; 2 - anterior leg of the internal capsule (tr. frontopontinus); 3 - large cell nucleus of the oculomotor nerve (cells innervating the medial rectus muscle of the eye); 4 - bridge center of gaze (cells of the reticular formation); 5 - the core of the abducens nerve; 6 - abducens nerve; 7 - vestibular node; 8 - semicircular canals; 9 - lateral vestibular nucleus; 10 - medial longitudinal bundle; 1 1 - oculomotor nerve; 1 2 - interstitial nucleus.

The second type of conjugated movements of the eyeballs is smooth tracking: when an object moves in the field of view, the eyes involuntarily fix on it and follow it, trying to keep the image of the object in the zone of the clearest vision, that is, in the area of ​​yellow spots. These movements of the eyeballs are slower compared to saccades and, in comparison with them, are more involuntary (reflex). Their cortical control is carried out by the parietal lobe of the ipsilateral hemisphere.

Violations of the gaze (if the nuclei 111, IV or V I pairs are not affected) are not accompanied by a violation of the isolated movements of each eyeball separately and do not cause diplopia. When examining the gaze, it is necessary to find out if the patient has nystagmus, which is detected using the smooth tracking test.

Normally, the eyeballs move smoothly and friendly when tracking an object. The appearance of jerky twitching of the eyeballs (involuntary corrective saccades) indicates a violation of the ability to smooth tracking (the object immediately disappears from the area of ​​​​best vision and is found again with the help of corrective eye movements). Check the ability of the patient to keep the eyes in the extreme position when looking in different directions: to the right, to the left, up and down. Attention is paid to whether the patient does not experience gaze-induced nystagmus when the eyes are taken away from the middle position, i.e. nystagmus, which changes direction depending on the direction of gaze. The fast phase of gaze-induced nystagmus is directed towards the gaze (when looking to the left, the fast component of nystagmus is directed to the left, when looking to the right - to the right, when looking up - vertically upwards, when looking down - vertically down). Impairment of smooth tracking ability and the occurrence of gaze-induced nystagmus are signs of damage to the cerebellar connections with brainstem neurons or central vestibular connections, and may also be a consequence of side effects anticonvulsants, tranquilizers and some other drugs.

With a lesion in the occipital-parietal region, regardless of the presence or absence of hemianopia, reflex slow tracking eye movements towards the lesion are limited or impossible, but voluntary movements and movements on command are preserved (that is, the patient can make voluntary eye movements in any direction, but cannot follow an object moving towards the lesion). Slow, fragmented, dysmetric tracking movements are observed in supranuclear palsy and other extrapyramidal disorders.

To check voluntary movements of the eyeballs and saccades, the patient is asked to look to the right, left, up and down. The time required to start performing movements, their accuracy, speed and smoothness are estimated (often a slight sign of dysfunction of friendly movements of the eyeballs in the form of their "stumbling" is detected). Then the patient is asked to alternately fix his gaze on the tips of two index fingers, which are located at a distance of 60 cm from the patient's face and about 30 cm from each other. Evaluate the accuracy and speed of arbitrary movements of the eyeballs.

Saccadic dysmetria, in which voluntary gaze is accompanied by a series of jerky eye movements, is characteristic of damage to the cerebellar connections, although it can also occur with pathology of the occipital or parietal lobe of the brain - in other words, the inability to overtake the target with the gaze (hypometria) or the gaze “jumping” through the target due to excessive range of eyeball movements (hypermetry), corrected with saccades, indicate a lack of coordinating control. Severe slowness of saccades can be observed in diseases such as hepatocerebral dystrophy or Huntington's chorea. Acute damage to the frontal lobe (stroke, head injury, infection) is accompanied by paralysis of the horizontal gaze in the direction opposite to the focus. Both eyeballs and the head are deviated towards the lesion (the patient "looks at the lesion" and turns away from the paralyzed limbs) due to the preserved function of the opposite center of turning the head and eyes to the side. This symptom is temporary and lasts only a few days, as the imbalance of the gaze is soon compensated. The ability to reflex tracking with frontal gaze palsy may be preserved. Horizontal gaze paralysis in frontal lobe lesions (cortex and internal capsule) is usually accompanied by hemiparesis or hemiplegia. With the localization of the pathological focus in the region of the roof of the midbrain (pretectal lesions involving the posterior commissure of the brain, which is part of the epithalamus), vertical gaze paralysis develops, combined with a violation of convergence (Parino's syndrome); the upward gaze usually suffers to a greater extent. When the pons of the brain and the medial longitudinal fasciculus, which provides lateral friendly movements of the eyeballs at this level, are damaged, horizontal gaze paralysis occurs in the direction of the focus (the eyes are turned to the side opposite to the focus, the patient "turns away" from the stem lesion and looks at the paralyzed limbs). Such gaze paralysis usually persists for a long time.

Assessment of disconjugated eyeball movements (convergence, divergence)

Convergence is tested by asking the patient to focus on an object that is moving towards their eyes. For example, the patient is offered to fix his gaze on the tip of the hammer or index finger, which the doctor smoothly brings closer to his bridge of the nose. When an object approaches the bridge of the nose, the axes of both eyeballs normally turn towards the object. At the same time, the pupil constricts, the ciliary (ciliary) muscle relaxes, and the lens becomes convex. Due to this, the image of the object is focused on the retina. Such a reaction in the form of convergence, pupillary constriction and accommodation is sometimes called the accommodative triad. Divergence is the reverse process: when the object is removed, the pupil expands, and the contraction of the ciliary muscle causes the lens to flatten.

If convergence or divergence is broken, horizontal diplopia occurs when looking at nearby or distant objects, respectively. Convergence paralysis occurs when the pretectal region of the roof of the midbrain is damaged at the level of the superior colliculus of the quadrigeminal plate. It can be combined with upward gaze paralysis in Parino's syndrome. Divergence paralysis is usually caused by a bilateral lesion of the sixth pair of CNs.

The isolated reaction of the pupil to accommodation (without convergence) is checked in each eyeball separately: the tip of the neurological hammer or finger is set perpendicular to the pupil (the other eye is closed) at a distance of 1 - 1.5 m, then quickly approach the eye, while pupil constricts. Normal pupils react vividly to light and convergence with accommodation.

Spontaneous abnormal movements of the eyeballs

Syndromes of spontaneous rhythmic gaze disorders include oculogyric crises, periodic alternating gaze, "pingpong" gaze syndrome, ocular bobbing (English), ocular dipping (English), alternating oblique deviation, periodic alternating gaze deviation, etc. Most of these syndromes develop with severe brain damage, they are observed mainly in patients who are in a coma.

Oculogiric crises - suddenly developing and persisting from several minutes to several hours, the deviation of the eyeballs upwards, less often downwards. They are observed during intoxication with neuroleptics, carbamazepine, lithium preparations; with stem encephalitis, glioma of the third ventricle, TBI and some other pathological processes. An oculogiric crisis should be distinguished from tonic upward gaze deviation, sometimes observed in patients in a coma with diffuse hypoxic brain lesions.

The "ping-pong" syndrome is observed in patients who are in a coma, it consists in periodic (every 2-8 s) friendly deviation of the eyes from one extreme position to another.

In patients with gross damage to the bridge of the brain or structures of the posterior cranial fossa, ocular bobbing is sometimes observed - rapid jerky movements of the eyeballs down from the middle position, followed by their slow return to the central position. There are no horizontal eye movements.

"Ocular dipping" is a term that refers to slow downward movements of the eyeballs, followed by a quick return to their original position after a few seconds. The horizontal movements of the eyeballs are preserved. The most common cause is hypoxic encephalopathy.

Pupils and palpebral fissures

The reactions of the pupils and palpebral fissures depend not only on the function of the oculomotor nerve - these parameters are also determined by the state of the retina and optic nerve, which make up the afferent part of the reflex arc of the pupil's reaction to light, as well as by the sympathetic effect on the smooth muscles of the eye (Fig. 1-6). Nevertheless, pupillary reactions are examined when assessing the state of the III pair of CNs.

Rice. 1-6. Scheme of the arc of the pupillary reflex to light: 1 - cells of the retina of the eyeball; 2 - optic nerve; 3 - optic chiasm; 4 - cells of the upper mounds of the roof plate; 5 - accessory nucleus of the oculomotor nerve; 6 - oculomotor nerve; 7 - ciliary knot.

Normal pupils are round, equal in diameter. Under normal room lighting, pupil diameter can vary from 2 to 6 mm. A difference in pupil size (anisocoria) less than 1 mm is considered normal. To check the direct reaction of the pupil to light, the patient is asked to look into the distance, then quickly turn on a flashlight and evaluate the degree and stability of the pupillary constriction of this eye. The switched on light bulb can be brought to the eye from the side, from the temporal side, in order to exclude the accommodative reaction of the pupil (its narrowing in response to the approach of the object). Normally, when illuminated, the pupil constricts, this constriction is stable, that is, it persists all the time while the light source is near the eye. When the light source is removed, the pupil expands.

Then, the friendly reaction of the other pupil, which occurs in response to illumination of the eye under study, is evaluated. Thus, it is necessary to illuminate the pupil of one eye twice: during the first illumination, we look at the reaction to light of the illuminated pupil, and at the second illumination, we observe the reaction of the pupil of the other eye. The pupil of the non-illuminated eye normally constricts exactly at the same speed and to the same extent as the pupil of the illuminated eye, that is, normally both pupils react in the same way and at the same time. The test of alternating illumination of the pupils reveals the defeat of the afferent part of the reflex arc of the pupillary reaction to light. One pupil is illuminated and its reaction to light is noted, then the bulb is quickly moved to the second eye and the reaction of its pupil is re-evaluated. Normally, when the first eye is illuminated, the pupil of the second eye initially constricts, but then, at the moment the light bulb is transferred, it slightly expands (a reaction to the removal of illumination that is friendly with the first eye) and, finally, when a beam of light is directed at it, it narrows again (direct reaction to light) . If at the second stage of this test, with direct illumination of the second eye, its pupil does not narrow, but continues to expand (paradoxical reaction), this indicates damage afferent pathway pupillary reflex of a given eye, that is, damage to its retina or optic nerve. In this case, direct illumination of the second pupil (pupil of the blind eye) does not cause its constriction.

However, at the same time, it continues to expand friendly with the first pupil in response to the cessation of illumination of the latter.

To test the pupillary reflexes of both eyes for convergence and accommodation, the patient is asked to first look into the distance (for example, at the wall behind the doctor's back), and then look at a nearby object (for example, at the tip of a finger, which is held directly in front of the patient's nose). If the pupils are narrow, the room is darkened before the test. Normally, fixation of the gaze on an object close to the eyes is accompanied by a slight constriction of the pupils of both eyes, combined with convergence of the eyeballs and an increase in the bulge of the lens (accommodative triad).

Thus, normally the pupil constricts in response to direct illumination (direct pupillary response to light); in response to illumination of the other eye (friendly reaction to light with the other pupil); when focusing on a nearby object. Sudden fright, fear, pain cause dilation of the pupils, except in those cases when the sympathetic fibers to the eye are interrupted.

Signs of damage. Assessing the width of the palpebral fissures and the protrusion of the eyeballs, one can detect exophthalmos - protrusion (protrusion) of the eyeball from the orbit and from under the eyelid. The easiest way to identify exophthalmos is to stand behind a seated patient and look down at his eyeballs. The causes of unilateral exophthalmos can be a tumor or pseudotumor of the orbit, thrombosis of the cavernous sinus, carotid-cavernous anastomosis.

Bilateral exophthalmos is observed with thyrotoxicosis (unilateral exophthalmos occurs less frequently in this condition).

Assess the position of the eyelids in different directions of gaze. Normally, when viewed directly, the upper eyelid covers the upper edge of the cornea by 1-2 mm. Ptosis (drooping) of the upper eyelid is a common pathology, which is usually accompanied by a constant contraction of the frontalis muscle due to the patient's involuntary attempt to keep the upper eyelid raised.

The drooping of the upper eyelid is most often caused by damage to the oculomotor nerve; congenital ptosis, which can be unilateral or bilateral; Bernard-Horner syndrome; myotonic dystrophy; myasthenia gravis; blepharospasm; eyelid edema due to injection, trauma, venous stasis; age-related tissue changes.

Ptosis (partial or complete) may be the first sign of damage to the oculomotor nerve (develops due to weakness of the muscle that lifts the upper eyelid). It is usually combined with other signs of damage to the third pair of CN (ipsilateral mydriasis, lack of pupillary response to light, impaired eyeball movements up, down and inwards).

In Bernard-Horner syndrome, the narrowing of the palpebral fissure, ptosis of the upper and lower eyelids are caused by functional insufficiency of the smooth muscles of the lower and upper cartilages of the eyelids (tarsal muscles). Ptosis is usually partial, unilateral.

It is combined with miosis due to a lack of pupillary dilator function (due to a defect in sympathetic innervation). Miosis is most pronounced in the dark.

Ptosis in myotonic dystrophy (dystrophic myotonia) is bilateral, symmetrical. The size of the pupils is not changed, their reaction to light is preserved. There are other signs of this disease.

With myasthenia gravis, ptosis is usually partial, asymmetric, and its severity can vary significantly throughout the day. Pupillary reactions are not disturbed.

Blepharospasm (involuntary contraction of the circular muscle of the eye) is accompanied by partial or complete closure of the palpebral fissure. Mild blepharospasm can be confused with ptosis, but at first, the upper eyelid periodically rises actively and there is no contracture of the frontalis muscle.

Irregular attacks of expansion and contraction of the pupils, lasting for several seconds, are denoted by the terms hippus, or undulation.

This symptom can occur with metabolic encephalopathy, meningitis, multiple sclerosis.

Unilateral mydriasis (dilated pupil) in combination with ptosis and paresis of the external muscles is observed with damage to the oculomotor nerve. Pupil dilation is often the first sign of damage to the oculomotor nerve when the nerve trunk is compressed by an aneurysm and when the brain stem is dislocated. On the contrary, with ischemic lesions of the 3rd pair (for example, with diabetes mellitus), the efferent motor fibers going to the pupil usually do not suffer, which is important to consider when differential diagnosis. Unilateral mydriasis, not combined with ptosis and paresis of the external muscles of the eyeball, is not typical for lesions of the oculomotor nerve. Possible causes of this disorder include drug-induced paralytic mydriasis, which occurs when topical application atropine solution and other m-anticholinergics (in this case, the pupil stops narrowing in response to the use of a 1% pilocarpine solution); Adie's pupil; spastic mydriasis, caused by contraction of the dilator of the pupil during irritation of the sympathetic structures innervating it.

Adie's pupil, or pupillotonia, is usually seen on one side. Typical pupil dilation on the affected side (anisocoria) and its abnormally slow and prolonged (myotonic) reaction to light and convergence with accommodation. Because the pupil does eventually respond to light, anisocoria is in the process neurological examination gradually decreases. Typical denervation hypersensitivity of the pupil: after instillation of a 0.1% solution of pilocarpine into the eye, it sharply narrows to point sizes.

Pupillotonia is observed in a benign disease (Holmes-Eidy syndrome), which is often familial, occurs more often in women aged 20-30 years and, in addition to the "tonic pupil", may be accompanied by a decrease or absence of deep reflexes from the legs (less often from the hands) , segmental anhidrosis (local disturbance of sweating) and orthostatic arterial hypotension.

In Argyle Robertson syndrome, the pupil constricts when the gaze is fixed near (the reaction to accommodation is preserved), but does not react to light. Usually Argyle Robertson syndrome is bilateral, combined with an irregular pupil shape and anisocoria. During the day, the pupils have a constant size, do not respond to the instillation of atropine and other mydriatics. This syndrome is observed in lesions of the midbrain tegmentum, for example, in neurosyphilis, diabetes mellitus, multiple sclerosis, epiphyseal tumors, severe TBI, followed by expansion of the Sylvian aqueduct, etc.

A narrow pupil (due to paresis of the pupil dilator), combined with partial ptosis of the upper eyelid (paresis of the muscle of the upper cartilage of the eyelid), anophthalmos, and impaired sweating on the same side of the face indicates Bernard-Horner syndrome. This syndrome is caused by a violation of the sympathetic innervation of the eye. In the dark, the pupil does not dilate. Bernard-Horner syndrome is more often observed with infarctions of the medulla oblongata (Wallenberg-Zakharchenko syndrome) and the brain bridge, tumors of the brain stem (interruption of the central descending sympathetic pathways coming from the hypothalamus); damage to the spinal cord at the level of the ciliospinal center in the lateral horns of the gray matter of the C 8 -t 2 segments; with complete transverse lesions of the spinal cord at the level of these segments (Bernard-Horner syndrome is bilateral, combined with signs of impaired sympathetic innervation of organs located below the level of the lesion, as well as conduction disorders of voluntary movements and sensitivity); diseases of the apex of the lung and pleura (tumor of Pancoast, tuberculosis, etc.); with damage to the first thoracic spinal root and the lower trunk of the brachial plexus; internal aneurysm carotid artery; tumors in the area of ​​the jugular foramen, cavernous sinus; tumors or inflammatory processes in the orbit (interruption of postganglionic fibers from the superior cervical sympathetic ganglion to the smooth muscles of the eye).

When sympathetic fibers are irritated to the eyeball, symptoms occur that are “reverse” to the Bernard-Horner symptom: pupil dilation, palpebral fissure and exophthalmos (Pourfure du Petit syndrome).

With unilateral loss of vision due to interruption of the anterior parts of the visual pathway (retina, optic nerve, chiasm, optic tract), the direct reaction of the pupil of the blind eye to light disappears (since the afferent fibers of the pupillary reflex are interrupted), as well as the consensual reaction to light of the pupil of the second, healthy eye. In this case, the pupil of the blind eye is able to constrict when the pupil of the healthy eye is illuminated (that is, the friendly reaction to light in the blind eye is preserved). Therefore, if the flashlight bulb is moved from a healthy to an affected eye, one can note not a narrowing, but, on the contrary, an expansion of the pupil of the affected eye (as a friendly response to the stopped illumination of the healthy eye) - a symptom of Marcus Gunn.

The study also pays attention to the color and uniformity of the color of the irises. On the side where the sympathetic innervation of the eye is disturbed, the iris is lighter (Fuchs' symptom), there are usually other signs of Bernard Horner's syndrome.

Hyaline degeneration of the pupillary edge of the iris with depigmentation is possible in the elderly as a manifestation of the involutionary process. Axenfeld's symptom is characterized by depigmentation of the iris without the accumulation of hyaline in it; it is observed in disorders of sympathetic innervation and metabolism.

With hepatocerebral dystrophy, copper is deposited along the outer edge of the iris, which is manifested by yellowish-green or greenish-brown pigmentation (Kaiser-Fleischer ring).

V PAIR: TRINITY NERVE (N. TRIGEMINUS)

The motor branches of the nerve innervate the muscles that provide the movements of the lower jaw (chewing, temporal, lateral and medial pterygoid; maxillohyoid; anterior belly digastric); a muscle that strains the eardrum; muscle that tenses the velum of the palate.

Sensitive fibers supply the main part of the skin of the head (skin of the face and the fronto-parietal part of the scalp), the mucous membrane of the nasal and oral cavities, including the frontal and maxillary sinuses; part of the ear canal and eardrum; eyeball and conjunctiva; anterior two-thirds of the tongue, teeth; periosteum of the facial skeleton; the dura mater of the anterior and middle cranial fossae, the cerebellum. The branches of the V nerve are the ophthalmic, maxillary and mandibular nerves (Fig. 1-7).

Rice. 1-7. Conductors of sensitivity from the skin of the face (scheme): 1 - trigeminal ganglion; 2 - the nucleus of the spinal tract of the trigeminal nerve; 3 - bulbotalamic tract; 4 - thalamus cells; 5 - the lower part of the cortex of the postcentral gyrus (face area); 6 - upper sensory nucleus of the trigeminal nerve; 7 - ophthalmic nerve; 8 - maxillary nerve; 9 - mandibular nerve.

Sensitivity on the face is provided by both the trigeminal nerve and the superior cervical spinal nerves (Fig. 1-8).

Pain, tactile and temperature sensitivity is sequentially checked in the innervation zones of all three branches of the V pair on both sides (a pin, a soft hair brush, a cold surface of a metal object - a neurological hammer, a dynamometer are used). Simultaneously touch symmetrical points in the forehead (1 branch), then cheeks (11 branch), chin (III branch).

Rice. eighteen. Innervation of the skin of the face and head (scheme). BUT - peripheral innervation: branches of the trigeminal nerve (1 - n. ophtalmicus, 11 - n. maxill aris, 111 - n. mandibularis): 1 - n. occipital is maj or; 2 - p. auricularis magnus; 3 - n. occipitalis minor; 4 - n. transversus coll i. B - segmental innervation by the sensitive nucleus of the trigeminal nerve (1-5 - Zelder dermatomes) and the upper cervical segments of the spinal cord (c 2 -c 3): 6 - nuclei of the spinal cord of the trigeminal nerve.

A dissociated sensory disturbance on the face, that is, a violation of pain and temperature sensitivity with intact tactile, indicates damage to the nucleus of the spinal cord of the trigeminal nerve (nucl. tractus spinalis n. pontinus n. trigetint). This disorder most often occurs with syringobulbomyelia, ischemia of the posterolateral parts of the medulla oblongata.

Trigeminal neuralgia is characterized by sudden, short, and very intense, repeated attacks of pain so short-lived that they are often described as an electric shock or an arrow. The pain spreads to the zones of innervation of one or more branches of the trigeminal nerve (usually in the region of the 11th and III branches, and only in 5% of cases in the region of the 1st branch). With neuralgia, loss of sensitivity on the face usually does not happen. If trigeminal pain is combined with disorders of superficial sensitivity, trigeminal neuralgia-neuropathy is diagnosed.

The corneal (corneal) reflex is examined using a piece of cotton wool or a strip of newsprint. They ask the patient to look at the ceiling and, without touching the eyelashes, lightly touch the cotton wool to the edge of the cornea (not to the sclera) from the lower outer side (not above the pupil!). Assess the symmetry of the reaction on the right and left. Normally, if the V and V II nerves are not damaged, the patient shudders and blinks.

Preservation of sensitivity of the cornea in the presence of paralysis of mimic muscles is confirmed by the reaction (blinking) of the contralateral eye.

To assess the motor portion of the trigeminal nerve, the symmetry of opening and closing the mouth is assessed, noting whether there is any displacement of the lower jaw to the side (the jaw is displaced towards the weakened pterygoid muscle, while the face seems skewed)

To assess the strength of the masticatory muscle, the patient is asked to clench his teeth strongly and palpate m. masseter on both sides, and then try to unclench the patient's clenched jaws. Normally, the doctor cannot do this. The strength of the pterygoid muscles is assessed with the movements of the lower jaw to the sides. The revealed asymmetry can be caused not only by paresis of the masticatory muscles, but also by malocclusion.

To evoke the mandibular reflex, the patient is asked to relax the muscles of the face and slightly open the mouth. The doctor places the index finger on the patient's chin and applies light blows with a neurological hammer from top to bottom on the distal phalanx of this finger, first on one side of the lower jaw, then on the other. At the same time, the masticatory muscle on the side of impact is reduced and the lower jaw rises upwards (the mouth closes). In healthy people, the reflex is often absent or difficult to elicit. An increase in the mandibular reflex indicates a bilateral lesion of the pyramidal tract (corticonuclear tract) above the middle sections of the bridge.

VII PAIR: FACIAL NERVE (N. FACI ALI S)

The motor fibers innervate the mimic muscles of the face, the subcutaneous muscle of the neck (platysma), the stylohyoid, occipital muscles, the posterior belly of the digastric muscle, and the stirrup muscle (Fig. 1-9). Vegetative parasympathetic fibers innervate the lacrimal gland, sublingual and submandibular salivary glands, as well as glands of the nasal mucosa, hard and soft palate. Sensory fibers conduct taste impulses from the anterior two-thirds of the tongue and from the hard and soft palate.

Rice. 1-9. Topography of the facial nerve and facial muscles: a - the structure of the facial nerve and the muscles innervated by it: 1 - the bottom of the IV ventricle; 2 - the nucleus of the facial nerve; 3 - stylomastoid opening; 4 - back ear muscle; 5 - occipital vein; 6 - posterior belly of the digastric muscle; 7 - stylohyoid muscle; 8 - branches of the facial nerve to the facial muscles and subcutaneous muscle of the neck; 9 - muscle that lowers the corner of the mouth; 10 - chin muscle; 11 - muscle that lowers the upper lip; 12 - buccal muscle; 13 - circular muscle of the mouth; 14 - muscle that raises the upper lip; 15 - canine muscle; 16 - zygomatic muscle; 17 - circular muscle of the eye; 18 - muscle wrinkling the eyebrow; 19 - frontal muscle; 20 - drum string; 21 - lingual nerve; 22 - pterygopalatine node; 23 - node of the trigeminal nerve; 24 - internal carotid artery; 25 - intermediate nerve; 26 - facial nerve; 27 - vestibulocochlear nerve; b - the main muscles of the upper and lower mimic muscles: 1 - the bridge of the brain; 2 - inner knee of the facial nerve; 3 - the nucleus of the facial nerve; 4 - internal auditory opening; 5 - outer knee; 6 - stylomastoid opening.

The study of the functions of the facial nerve begins with an assessment of the symmetry of the patient's face at rest and with spontaneous facial expressions. Particular attention is paid to the symmetry of the nasolabial folds and palpebral fissures. . The strength of facial muscles is examined in turn, inviting the patient to wrinkle his forehead (m.frontalis), close his eyes tightly (m. orbicularis oculi), puff out his cheeks (m. b iscinator), smile, show his teeth (m. risorius, etc. zygomaticus maj or) , squeeze your lips and do not let them open (m. orbicularis oris). The patient is asked to take air into his mouth and puff out his cheeks; Normally, with pressure on the cheeks, the patient retains air without releasing it through the mouth. If weakness of facial muscles is found, it is found out whether it concerns only the lower part of the face or extends to its entire half (both lower and upper).

Taste is checked on the anterior third of the tongue. Ask the patient to stick out his tongue and hold it by the tip with a gauze pad. With the help of a pipette, droplets of sweet, salty, neutral solutions are alternately applied to the tongue. The patient must report the taste of the solution by pointing to the corresponding inscription on a piece of paper. It is noted whether tears are released when taste stimuli are applied (this paradoxical reflex is observed in patients with improper germination of secretory fibers after previous damage to the branches of the facial nerve).

The facial nerve contains a very small number of fibers that conduct impulses of general sensitivity and innervate small areas of the skin, one of which is located on the inner surface of the auricle near the external auditory canal, and the second is located directly behind the ear. Examine pain sensitivity by inflicting injections with a pin directly posterior to the external auditory canal.

Signs of defeat. The defeat of the central motor neuron (for example, with a hemispheric stroke) is the cause of central, or "supranuclear", paralysis of the facial muscles (Fig. 1-10).

Rice. 1-10. The course of the central motor neurons to the nucleus of the facial nerve: 1 - facial nerve (left); 2 - the lower part of the nucleus of the facial nerve; 3 - knee of the inner capsule; 4 - pyramidal cells of the right precentral gyrus (face area); 5 - the upper part of the nucleus of the facial nerve.

It is characterized by contralateral paresis of the facial muscles located only in the lower half of the face (very slight weakness of the orbicular muscle of the eye and slight asymmetry of the palpebral fissures are possible, but the possibility of wrinkling the forehead remains). This is due to the fact that that part of the motor nucleus n. facialis, which innervates the lower mimic muscles, receives impulses only from the opposite hemisphere, while the part that innervates the upper mimic muscles is under the influence of the cortical-nuclear tracts of both hemispheres. Due to damage to the peripheral motor neuron (neurons of the motor nucleus n.facialis and their axons), peripheral paralysis of the facial muscles (prosoplegia) develops, which is characterized by weakness of the facial muscles of the entire ipsilateral half of the face. Closing of the eyelids on the affected side is not possible (lagophthalmos) or is incomplete. in patients with peripheral paralysis of the mimic muscles of the face, Bell's symptom is often observed: when the patient tries to close his eyes, the eyelids on the side of the lesion of the facial nerve do not close, and the eyeball moves upward and outward. The movement of the eyeball in this case is a physiological synkinesis, which consists in moving the eyeballs upward when closing the eyes. To see it in a healthy person, it is necessary to forcibly hold his eyelids up, asking him to close his eyes.

Peripheral paralysis of the facial muscles in some cases may be accompanied by a violation of taste in the anterior two-thirds of the ipsilateral half of the tongue (if the trunk of the facial nerve is damaged above the chorda tympani fibers from its distal part). With central paralysis of the facial muscles, that is, with damage to the cortical-nuclear tracts leading to the motor nucleus of the facial nerve, taste disturbances do not occur.

If the facial nerve is affected above the fibers from it to the stapedius muscle, a perversion of the timbre of perceived sounds occurs - hyperacusis. When the facial nerve is damaged at the level of its exit from the pyramid of the temporal bone through the stylomastoid foramen, the parasympathetic fibers to the lacrimal gland (n. petrosus maj or) and the sensory fibers coming from the taste buds (chorda tympani) do not suffer, so the taste and tearing remain intact.

Lachrymation is characteristic on the side of the lagophthalmos, which is explained by excessive irritation of the mucous membrane of the eye due to the absence of a protective blinking reflex and difficulty in moving the tear into the lower lacrimal canaliculus due to the sagging of the lower eyelid. All this leads to the fact that tears flow freely down the face.

Bilateral acute or subacute lesions of the facial nerve of the peripheral type are observed in Guillain-Barré syndrome (GBS). Acute or subacute unilateral peripheral paralysis of the facial muscles most often occurs with compression-ischemic neuropathy of the facial nerve (with compression-ischemic changes in the part of the nerve that passes through the facial canal in the pyramid of the temporal bone.

In the recovery period after peripheral paralysis, pathological regeneration of the fibers of the facial nerve is possible. At the same time, on the side of paralysis, over time, a contracture of facial muscles develops, due to which the palpebral fissure becomes narrower, and the nasolabial fold becomes deeper than on the healthy side (the face "skews" no longer to the healthy, but to the diseased side).

Contracture of facial muscles usually occurs against the background of residual effects of prosoparesis and is combined with pathological synkinesis of facial muscles. For example, when closing the eyes on the diseased side, the angle of the mouth simultaneously rises involuntarily (ocular synkinesis), or the wing of the nose rises, or the platysma contracts; when the cheeks are puffed up, the palpebral fissure narrows, etc.

VIII PAIR: Vestibulo-cochlear nerve (N. VESTlBULOCOCHLEARIS)

The nerve consists of two parts - auditory (cochlear) and vestibular (vestibular), which conduct, respectively, auditory impulses from cochlear receptors and information about balance from receptors of the semicircular canals and membranous sacs of the vestibule (Fig. 1 - 11).

Rice. 1-11. Structure auditory analyzer: 1 - superior temporal gyrus; 2 - medial geniculate body; 3 - lower mound of the plate of the roof of the midbrain; 4 - lateral loop; 5 - posterior nucleus of the cochlear nerve; 6 - trapezoid body; 7 - anterior nucleus of the cochlear nerve; 8 - cochlear part of the vestibulocochlear nerve; 9 - cells of the spiral node.

With the defeat of this nerve, hearing acuity decreases, tinnitus and dizziness appear. If the patient complains of ringing / noise in the ear, you should ask him to describe in detail the nature of these sensations (ringing, whistling, hissing, buzzing, crackling, pulsing) and their duration, as well as comparing them with natural sounds "" like the sound of the sea surf ", "like wires buzzing in the wind", "like the rustling of leaves", "like the noise of a running steam locomotive", "like the beating of one's own heart", etc.) Constant noise in the ear is characteristic of damage to the eardrum, ossicles of the middle ear or cochlea and cochlear nerve.High-frequency sounds, ringing in the ear are more often observed in the pathology of the cochlea and the cochlear nerve (damage to the neurosensory apparatus).Noise in the ear caused by the pathology of the middle ear (for example, with otosclerosis), usually more constant, low-frequency.

Rumor and its research

The most accurate data on hearing loss is obtained with a special instrumental examination, but a routine clinical examination can also provide important information for determining the diagnosis. First, the external auditory canal and the eardrum are examined. Approximately assess the hearing in each ear, finding out if the patient hears whispered speech, clicks of the thumb and middle fingers at a distance of 5 cm from the patient's ear. If he complains of hearing loss or does not hear clicks, further special instrumental examination of hearing is necessary.

There are three forms of hearing loss: conductive (conductive) deafness is associated with impaired conduction of sound to the cochlear receptors (closing of the external auditory canal with a sulfur plug or a foreign object, pathology of the middle ear); neural (neurosensory) deafness - with damage to the cochlea and auditory nerve; central deafness - with damage to the nuclei of the auditory nerve or their connections with the overlying centers and with the primary auditory fields in the temporal lobes of the cerebral cortex.

For differentiation of conductive and neurosensory hearing loss, tests with a tuning fork are used. Air conduction is preliminarily assessed by comparing the sound perception threshold of the patient (each ear) with its own (normal) perception threshold.

The Rinne test is used to compare bone and air conduction. The leg of a vibrating high-frequency tuning fork (128 Hz) is placed on the mastoid process. After the patient stops hearing the sound, the tuning fork is brought close to his ear (without touching it). In healthy people and in patients with sensorineural hearing loss, air conduction is better than bone conduction, therefore, after bringing the tuning fork to the ear, the subject again begins to hear the sound (positive Rinne symptom). When the middle ear is affected, the bone conduction of sound remains normal, and the air one worsens, as a result, the first turns out to be better than the second, so the patient will not hear the tuning fork if it is brought to the ear (negative Rinne symptom).

Weber test: a vibrating tuning fork (128 Hz) is placed in the middle of the patient's crown and they are interested in which ear he hears the sound better. Normally, the sound is heard equally by the right and left ears (in the center). With sensorineural hearing loss (Ménière's disease, neurinoma of the VIII pair, etc.), the sound is perceived more clearly and for a longer time by the healthy ear (laterization of perception to the unaffected side). With conductive hearing loss, there is a relative improvement in bone conduction and the sound is perceived as louder on the affected side (lateralization of sound perception to the affected side).

With sensorineural hearing loss, the perception of high frequencies suffers to a greater extent, with conductive hearing loss - low frequencies. This is found out with audiometry - an instrumental study, which must be carried out in patients with hearing impairment.

Dizziness

When complaining of dizziness, it is necessary to find out in detail what sensations the patient is experiencing. True dizziness is understood as the illusion of movements of the person himself or surrounding objects, meanwhile, very often patients call dizziness a feeling of "emptiness" in the head, blackout in the eyes, instability and unsteadiness when walking, fainting or general weakness, etc.

True dizziness (vertigo) usually has the character of seizures lasting from a few seconds to several hours. In severe cases, dizziness is accompanied by nausea, vomiting, blanching, perspiration, imbalance. The patient usually feels the rotation or movement of surrounding objects around him. During seizures, horizontal or rotatory nystagmus is often recorded. True dizziness is almost always caused by damage to the vestibular system in any of its departments: in the semicircular canals, the vestibular portion of the VIII pair of CNs, and the vestibular nuclei of the brainstem. A more rare cause is damage to the vestibulocerebellar connections (Fig. 1-12), even less often dizziness is a symptom of an epileptic seizure (with irritation of the temporal lobe).

Rice. 1-12. The structure of the vestibular conductors: 1 - the cortex of the parietal lobe of the brain; 2 - thalamus; 3 - medial nucleus of the vestibular nerve; 4 - the nucleus of the oculomotor nerve; 5 - superior cerebellar peduncle; 6 - upper vestibular nucleus; 7 - dentate nucleus; 8 - the core of the tent; 9 - vestibular part of the vestibulocochlear nerve (VIII); 10 - vestibular node; 11 - pre-door-spinal path (anterior funiculus of the spinal cord); 12 - lower vestibular nucleus; 13 - intermediate and core of the medial longitudinal bundle; 14 - lateral vestibular nucleus; 15 - medial longitudinal bundle; 16 - the core of the abducens nerve; 17 - cells of the reticular formation of the brain stem; 18 - red core; 19 - cortex of the temporal lobe of the brain.

The most common causes of an acute attack of vertigo are benign positional vertigo, Meniere's disease, and vestibular neuronitis.

Most often in clinical practice, benign positional vertigo is observed. An attack of rotational positional vertigo occurs suddenly with a rapid change in the position of the head and in a certain position, mainly provoked by laying and turning in bed or tilting the head back. Vertigo is accompanied by nausea and nystagmus. The attack lasts from a few seconds to 1 minute, passes on its own. Seizures may recur intermittently over several days or weeks. Hearing is not affected.

In Meniere's disease, attacks are characterized by severe dizziness, which is accompanied by a sensation of buzzing and noise in the ear; feeling of fullness in the ear, hearing loss, nausea and vomiting. The attack lasts from several minutes to an hour and forces the patient to lie down all this time. When performing a rotational or caloric test, nystagmus on the affected side is depressed or absent.

Vestibular neuronitis is characterized by an acute isolated prolonged (from several days to several weeks) attack of severe dizziness.

It is accompanied by vomiting, imbalance, fear, nystagmus towards the healthy ear. The symptoms are aggravated by moving the head or by changing the position of the body. Patients hardly tolerate this condition and do not get out of bed for several days.

Noise in the ear and hearing loss does not occur, headache missing. When conducting a caloric test, the reaction on the affected side is reduced.

Constant dizziness, which can vary in its intensity, but does not have the character of seizures, accompanied by hearing loss, cerebellar ataxia, ipsilateral lesions of the U, UN, IX and X pairs of CNs, is characteristic of neurinoma VIII of the CN pair.

nystagmus

Nystagmus - fast repetitive involuntary oppositely directed rhythmic movements of the eyeballs. There are two types of nystagmus: jerky (clonic) nystagmus, in which slow movements of the eyeball (slow phase) alternate with oppositely directed fast movements (fast phase). The direction of such nystagmus is determined by the direction of its fast phase. Pendulum (swinging) nystagmus is a rarer form in which the eyeballs make pendulum-like movements of equal amplitude and speed relative to the middle position (although when looking away, two different phases can be traced, the faster of which is directed towards the gaze).

Nystagmus can be both normal (for example, with extreme aversion of gaze), and a sign of damage to the brainstem, cerebellum, peripheral or central vestibular system. in each of these cases, nystagmus has its own characteristics.

The easiest way to observe nystagmus is during the smooth tracking test, when the patient follows the movement of the doctor's finger or the neurological hammer.

Normally, the eyeballs should follow the object, moving smoothly and in concert. Mild clonic nystagmus (several low-amplitude rhythmic movements) that appears with extreme abduction of the eyeballs is physiological; it disappears when moving the eyes a little closer to the midline and does not indicate pathology. The most common cause of large-scale clonic nystagmus with extreme abduction of the eyeballs is the use of sedatives or anticonvulsants. Optokinetic clonic nystagmus is a variant of physiological reflex nystagmus that occurs when tracking objects of the same type moving past (for example, trees flashing through a train window, fence rails, etc.). It is characterized by slow tracking movements of the eyeballs, which are involuntarily interrupted by fast saccades directed in the opposite direction. In other words, the eyes are fixed on a moving object and slowly follow it, and after it disappears from the field of view, they quickly return to the central position and are fixed on a new object that has fallen into the field of view, starting to pursue it, etc. Thus, the direction of optokinetic nystagmus is opposite to the direction of movement of objects.

Spontaneous clonic peripheral vestibular (labyrinth-vestibular) nystagmus is caused by unilateral irritation or destruction of the peripheral part of the vestibular analyzer (labyrinth, vestibular portion of the VII I pair of CNs). This is spontaneous, usually unidirectional horizontal, less often - rotatory nystagmus, the fast phase of which is directed towards the healthy side, and the slow phase towards the lesion. The direction of nystagmus does not depend on the direction of gaze. Nystagmus is found in any position of the eyeballs, but increases when the eyes are turned towards its fast phase, that is, it is more clearly detected when looking in the healthy direction. Usually such nystagmus is suppressed by fixing the gaze.

Combined with nausea, vomiting, tinnitus, hearing loss; is temporary (no more than 3 weeks).

Spontaneous clonic stem-central vestibular nystagmus occurs when the vestibular nuclei of the brain stem, their connections with the cerebellum or other central parts of the vestibular analyzer are affected. It is often multidirectional, can be combined with dizziness, nausea, vomiting. Nystagmus and vertigo are not relieved by fixing the gaze. Often, other neurological disorders are also detected: cerebellar ataxia, diplopia, motor and sensory disorders.

Spontaneous rocking vestibular nystagmus can be caused by gross damage to the vestibular nuclei and vestibulo-oculomotor connections in the brainstem and occurs with stem stroke, brainstem glioma, and multiple sclerosis. A patient with acquired rocking nystagmus complains of trembling and blurry images (oscillopsia).

Spontaneous pendulum (swinging) optical nystagmus is typical for patients with congenital bilateral visual loss, causing impaired gaze fixation.

vestibular reflexes

The motor reactions of the eyes to stimulation of the vestibular apparatus (oculocephalic reflex, vestibulo-ocular reflex) are mediated by pathways through the brain stem from the vestibular nuclei of the medulla oblongata to the nuclei of the abducens and oculomotor nerves. Normally, the rotation of the head causes the movement of the endolymph in the semicircular canals in the opposite direction to the rotation. In this case, in one labyrinth, an endolymph flow occurs towards the ampulla of the horizontal semicircular canal, and in the other labyrinth - in the direction from the ampulla of the canal, while the irritation of the receptors of one channel increases, and the irritation of the opposite channel decreases, i.e. there is an imbalance of impulses coming to the vestibular nuclei. When the vestibular nuclei are stimulated on one side, the information is immediately transmitted to the contralateral nucleus of the abducens nerve in the brain bridge, from where the impulses through the medial longitudinal bundle reach the nucleus of the oculomotor nerve in the midbrain on the side of the irritated vestibular apparatus. This ensures synchronous contraction of the lateral rectus muscle of the eye opposite to the irritated labyrinth and the medial rectus muscle of the eye of the same name, which ultimately leads to a slow friendly deviation of the eyes in the direction opposite to the direction of head rotation. This reflex allows you to stabilize the position of the eyes and fix the gaze on a stationary object, despite the rotation of the head. In a healthy, awake person, it can be arbitrarily suppressed due to the influence of the cerebral cortex on stem structures. in a patient who is in a clear mind, the integrity of the structures responsible for this reflex is determined as follows. The patient is asked to fix his gaze on a centrally located object and quickly (two cycles per second) turn the patient's head either in one direction or the other. If the vestibulo-ocular reflex is preserved, then the movements of the eyeballs are smooth, they are proportional to the speed of head movements and are directed in the opposite direction. To assess this reflex in a patient in a coma, a puppet eye test is used. It allows you to determine the safety of stem functions. The doctor fixes the patient's head with his hands and turns it left and right, then throws it back and lowers it forward; the patient's eyelids should be raised (the test is absolutely contraindicated in cases of suspected trauma to the cervical spine).

The test is considered positive if the eyeballs involuntarily deviate in the opposite direction to the turn (the phenomenon of "doll eyes"). In case of intoxication and dysmetabolic disorders with bilateral lesions of the cerebral cortex, the "doll eye" test is positive (the patient's eyeballs move in the direction opposite to the direction of head rotation). With lesions of the brain stem, the oculocephalic reflex is absent, that is, the test is negative (the eyeballs, when turned, move simultaneously with the head as if they were frozen in place). This test is also negative in case of poisoning by some medicines(for example, with an overdose of phenytoin, tricyclic antidepressants, barbiturates, sometimes muscle relaxants, diazepam), however, the normal size of the pupils and their reaction to light remain.

Caloric tests are also based on reflex mechanisms. Stimulation of the semicircular canals cold water, which is poured into the outer ear, is accompanied by a slow friendly deviation of the eyeballs towards the irritated labyrinth. Cold caloric test is carried out as follows. First you need to make sure that the eardrums in both ears are not damaged. With the help of a small syringe and a short thin soft plastic tube, 0.2-1 ml of ice-cold water is carefully injected into the external auditory canal. In this case, a healthy awake person will have nystagmus, the slow component of which (slow deviation of the eyeballs) is directed towards the irritated ear, and the fast component is directed in the opposite direction (nystagmus, traditionally determined by the fast component, is directed in the opposite direction). After a few minutes, repeat the procedure on the opposite side. This test can serve as an express method for detecting peripheral vestibular hypofunction.

In a patient in a coma, with the brain stem intact, this test causes a tonic coordinated deviation of the eyeballs towards the cooled labyrinth, however, there are no rapid eye movements in the opposite direction (that is, nystagmus itself is not observed). If the structures of the brainstem are damaged in a patient in a coma, the described test does not cause any movements of the eyeballs at all (there is no tonic deviation of the eyeballs).

vestibular ataxia

Vestibular ataxia is detected using the Romberg test and the study of the patient's gait (they offer him to walk in a straight line with his eyes open and then with his eyes closed). With unilateral peripheral vestibular pathology, instability is observed when standing and walking in a straight line with a deviation towards the affected labyrinth. Vestibular ataxia is characterized by a change in the severity of ataxia with sudden changes in the position of the head and turns of the gaze. An index test is also carried out: the subject is asked to raise his hand above his head, and then lower it, trying to get his index finger into the index finger of the doctor. The doctor's finger can move in different directions.

First, the patient performs the test with his eyes open, then he is asked to perform the test with his eyes closed. A patient with vestibular ataxia misses with both hands towards the slow component of nystagmus.

IX AND X PAIRS. Glossopharyngeal and vagus nerves (M. GLOSSOPHARYNGEUS AND N. VA GUS)

The motor branch of the glossopharyngeal nerve innervates the stylopharyngeal muscle (m. stylopharyngeus). The vegetative pair of sympathetic secretory branches go to the ear ganglion, which in turn sends fibers to the parotid salivary gland. Sensitive fibers of the glossopharyngeal nerve supply the posterior third of the tongue, the soft palate. throat skin of the outer ear. the mucous membrane of the middle ear (including the inner surface of the tympanic membrane) and the Eustachian tube; visceral sensory afferents carry impulses from the carotid sinus; taste fibers conduct the sense of taste from the back third of the tongue (Fig. 1-13).

Rice. 1-13. Conductors of taste sensitivity: 1 - thalamus cells; 2 - node of the trigeminal nerve; 3 - intermediate nerve; 4 - epiglottis; 5 - cells of the lower node vagus nerve; 6 - cells of the lower node of the glossopharyngeal nerve; 7 - cell node of the knee; 8 - taste nucleus (pusl. tractus sol itarii nn. intermedii, gl ossopharingei et vagi); 9 - bulbotalamic tract; 10 - parahippocampal gyrus and hook.

The vagus nerve innervates the striated muscles of the pharynx (except for the stylopharyngeal muscle). soft palate (except for the muscle supplied by the trigeminal nerve that pulls the palatine curtain), tongue (m. palato glossus), larynx, vocal cords and epiglottis. Vegetative branches go to the smooth muscles and glands of the pharynx, larynx, internal organs chest and abdominal cavity. Visceral sensory afferents conduct impulses from the larynx, trachea, esophagus, internal organs of the chest and abdominal cavity, from baroreceptors of the aortic arch and chemoreceptors of the aorta. Sensitive fibers of the vagus nerve innervate the skin of the outer surface of the auricle and external auditory canal, part of the outer surface of the tympanic membrane, pharynx, larynx, dura mater of the posterior cranial fossa. The glossopharyngeal and vagus nerves have several common nuclei in the medulla oblongata and pass close to each other, their functions are difficult to separate (Fig. 1 - 14), so they are examined simultaneously.

Rice. 1-14. The course of the central motor neurons to the nuclei of IX, X and XII pairs of CH N: 1 - pyramidal cells of the lower part of the precentral gyrus (zone of the tongue, larynx); 2 - cortical-nuclear pathway; 3 - stylo-pharyngeal muscle; 4 - double core; 5 - muscles of the epiglottis; 6 - muscles of the soft palate and constrictor muscles of the pharynx; 7 - recurrent laryngeal nerve; 8 - vocal muscles; 9 - muscle of the tongue; 10 - the nucleus of the hypoglossal nerve.

When collecting anamnesis, they find out if the patient has problems with swallowing, speech (voice).

Voice. Pay attention to the clarity of speech, timbre and sonority of the voice. If the function of the vocal cords is impaired, the voice becomes hoarse and weak (up to aphonia). Due to a violation of the function of the soft palate, which does not cover the entrance to the nasopharyngeal cavity during phonation, a nasal shade of voice (nasolalia) occurs. Violation of the function of the muscles of the larynx (damage to the vagus nerve) affects the pronunciation of high sounds (and-and-and), requiring convergence of the vocal cords. In order to exclude weakness of facial muscles (VII pair) and muscles of the tongue (XII pair) as possible cause speech disorders, the patient is asked to pronounce labial (p-p-p, mi-mi-mi) and front-lingual (la-la-la) sounds or syllables that include them. The nasality of the voice is revealed when pronouncing syllables that have guttural sounds in their composition (ha-ha-ha, kai-kai-kai). The patient is also offered to cough forcefully.

A patient with acute unilateral vocal cord paralysis is unable to utter the sound "and-and-and" or forcefully cough.

palatine curtain. The soft palate is examined when the subject pronounces the sounds "a-a-a" and "uh-uh." Assess how fully, strongly and symmetrically the soft palate rises during phonation; whether the tongue of the palatine curtain deviates to the side. With unilateral paresis of the muscles of the soft palate, the palatine curtain during phonation lags behind on the side of the lesion and is pulled by healthy muscles in the opposite direction to the paresis; the tongue deviates to the healthy side.

Palatal and pharyngeal reflexes. With a wooden spatula or a strip (tube) of paper, gently touch the mucous membrane of the soft palate alternately on both sides. The normal response is to pull the veil of the palate up. Then they touch the back wall of the pharynx, also on the right and left. Touch causes swallowing, sometimes vomiting movements. The reflex response is expressed to varying degrees (in the elderly it may be absent), but normally it is always symmetrical. The absence or decrease of reflexes on one side indicates a peripheral lesion of the IX and X pairs of CNs.

XI PAIR: ADDITIONAL NERVE (N. A CCESSORIUS)

This purely motor nerve innervates the sternocleidomastoid and trapezius muscles.

The study of the function of the accessory nerve begins with an assessment of the shape, size and symmetry of the sternocleidomastoid and trapezius muscles. it is usually enough to match the right and left sides. When the nucleus or trunk of the XI nerve is damaged, the shoulder girdle on the side of the paralysis is lowered, the scapula is slightly shifted down and laterally. To assess the strength of the sternocleidomastoid muscle, the patient is asked to forcefully turn his head to the side and slightly up. The doctor counteracts this movement by putting pressure on the patient's lower jaw. With unilateral contraction, the sternocleidomastoid muscle tilts the head and neck to its side and, at the same time, additionally turns the head in the opposite direction. Therefore, when testing the right muscle, they place their hand on the left half of the patient's lower jaw, and vice versa. Look at the contours and palpate the abdomen of this muscle during its contraction. To assess the strength of the trapezius muscle, the patient is asked to "shrug" ("raise the shoulders to the ears"). The doctor resists this movement.

XII PAIR: HYPOGENITAL NERVE (N. HYPOGLOSSUS)

The nerve innervates the muscles of the tongue (with the exception of m. palatoglossus, supplied by X with a pair of CNs). The study begins with an examination of the tongue in the oral cavity and when it protrudes. Pay attention to the presence of atrophy and fasciculations. Fasciculations are worm-like, rapid, irregular muscle twitches. Atrophy of the tongue is manifested by a decrease in its volume, the presence of furrows and folds of its mucous membrane. Fascicular twitches in the tongue indicate the involvement of the nucleus of the hypoglossal nerve in the pathological process. Unilateral atrophy of the muscles of the tongue is usually observed with a tumor, vascular or traumatic lesion of the hypoglossal nerve trunk at or below the level of the base of the skull; it is rarely associated with an intramedullary process. Bilateral atrophy most commonly occurs with motor neuron disease [amyotrophic lateral sclerosis (ALS)] and syringobulbia. To assess the function of the muscles of the tongue, the patient is asked to stick out the tongue. Normally, the patient easily shows the tongue; when protruding, it is located in the midline. Paresis of the muscles of one half of the tongue leads to its deviation to the weak side (m. genioglossus of the healthy side pushes the tongue towards the paretic muscles). The tongue always deviates towards the weaker half, regardless of whether the consequence of any - supranuclear or nuclear - lesion is the weakness of the muscle of the tongue. You should make sure that the language deviation is true and not imaginary. A false impression of the presence of a deviation of the tongue can occur with asymmetry of the face, due to unilateral weakness of the facial muscles. The patient is asked to perform rapid movements of the tongue from side to side. If the weakness of the tongue is not quite obvious, ask the patient to press the tongue against the inner surface of the cheek and evaluate the strength of the tongue, counteracting this movement. The pressure force of the tongue on the inner surface of the right cheek reflects the force of the left m. genioglossus, and vice versa. The patient is then asked to pronounce syllables with anterior lingual sounds (eg "la-la-la"). With weakness of the muscles of the tongue, he cannot clearly pronounce them. To identify mild dysarthria, the subject is asked to repeat complex phrases, for example: "administrative experiment", "episodic assistant", "large red grapes ripen on Mount Ararat", etc.

The combined defeat of the nuclei, roots or trunks IX, X, XI, CP pairs of CN causes the development of bulbar paralysis or paresis. Clinical manifestations bulbar palsy are dysphagia (swallowing disorder and choking when eating due to paresis of the muscles of the pharynx and epiglottis); Nazolalia (a nasal tone of voice associated with paresis of the muscles of the palatine curtain); dysphonia (loss of sonority of the voice due to paresis of the muscles involved in the narrowing / expansion of the glottis and tension / relaxation of the vocal cord); dysarthria (paresis of muscles that provide correct articulation); atrophy and fasciculations 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.

Nerves IX, X, and XI together exit the cranial cavity through the jugular foramen; therefore, unilateral bulbar palsy is usually observed when these CNs are affected by a tumor. Bilateral bulbar palsy can be caused by poliomyelitis and other neuroinfections, ALS, bulbospinal amyotrophy

Kennedy or toxic polyneuropathy (diphtheria, paraneoplastic, with GBS, etc.). The defeat of neuromuscular synapses in myasthenia gravis or muscle pathology in some forms of myopathies are the cause of the same disorders of bulbar motor functions as in bulbar paralysis.

From bulbar palsy, in which the lower motor neuron (CN nuclei or their fibers) suffers, pseudobulbar palsy should be distinguished, which develops with bilateral damage to the upper motor neuron of the cortical-nuclear pathways. Pseudobulbar palsy is a combined dysfunction of IX, X, and CN pairs of CNs, caused by a bilateral lesion of the corticonuclear tracts leading to their nuclei. Clinical picture resembles manifestations of the bulbar syndrome and includes dysphagia, nasalolia, dysphonia and dysarthria. With pseudobulbar syndrome, in contrast to the bulbar syndrome, the pharyngeal, palatine, and cough reflexes are preserved; reflexes of oral automatism appear, the mandibular reflex increases; observe violent crying or laughter (uncontrolled emotional reactions), hypotrophy and fasciculations of the muscles of the tongue are absent.

7. VII pair of cranial nerves - facial nerve

He is mixed. The motor pathway of the nerve is two-neuron. The central neuron is located in the cerebral cortex, in the lower third of the precentral gyrus. The axons of the central neurons are sent to the nucleus of the facial nerve, located on the opposite side in the pons of the brain, where the peripheral neurons of the motor pathway are located. The axons of these neurons make up the facial nerve root. The facial nerve, passing through the internal auditory opening, is sent to the pyramid of the temporal bone, located in the facial canal. Next, the nerve exits the temporal bone through the stylomastoid foramen, entering the parotid salivary gland. In the thickness of the salivary gland, the nerve divides into five branches, forming the parotid plexus.

The motor fibers of the VII pair of cranial nerves innervate the mimic muscles of the face, the stirrup muscle, the muscles of the auricle, the skull, the subcutaneous muscle of the neck, the digastric muscle (its posterior belly). In the facial canal of the pyramid of the temporal bone, three branches depart from the facial nerve: a large stony nerve, a stapedial nerve, and a tympanic string.

The large stony nerve passes through the pterygopalatine canal and ends at the pterygopalatine ganglion. This nerve innervates the lacrimal gland by forming an anastomosis with the lacrimal nerve after interruption in the pterygopalatine ganglion. The large stony nerve contains parasympathetic fibers. The stapedial nerve innervates the stapedial muscle, causing its tension, which creates conditions for the formation of better audibility.

The drum string innervates the anterior 2/3 of the tongue, being responsible for the transmission of impulses with a variety of taste stimuli. In addition, the drum string provides parasympathetic innervation of the sublingual and submandibular salivary glands.

Damage symptoms. If the motor fibers are damaged, peripheral paralysis of the facial muscles develops on the side of the lesion, which is manifested by asymmetry of the face: half of the face on the side of the nerve lesion becomes motionless, mask-like, the frontal and nasolabial folds are smoothed out, the eye on the affected side does not close, the palpebral fissure expands, the corner of the mouth is lowered down .

Bell's phenomenon is noted - an upward turn of the eyeball when trying to close the eye on the side of the lesion. There is paralytic lacrimation due to the absence of blinking. Isolated paralysis of the mimic muscles of the face is characteristic of damage to the motor nucleus of the facial nerve. In the case of attachment of a lesion to the radicular fibers, the Miyar-Gubler syndrome (central paralysis of the extremities on the side opposite to the lesion) is added to the clinical symptoms.

With damage to the facial nerve in the cerebellopontine angle, in addition to paralysis of the facial muscles, there is a decrease in hearing or deafness, the absence of a corneal reflex, which indicates a simultaneous lesion of the auditory and trigeminal nerves. This pathology occurs with inflammation of the cerebellopontine angle (arachnoiditis), acoustic neuroma. The addition of hyperacusis and a violation of taste indicate damage to the nerve before the large stony nerve leaves it in the facial canal of the temporal bone pyramid.

Damage to the nerve above the tympanic string, but below the origin of the stapedial nerve, is characterized by a taste disorder, lacrimation.

Paralysis of the mimic muscles in combination with lacrimation occurs in case of damage to the facial nerve below the discharge of the tympanic string. Only the cortical-nuclear pathway may be affected. Clinically observed paralysis of the muscles of the lower half of the face on the opposite side. Often paralysis is accompanied by hemiplegia or hemiparesis on the side of the lesion.

VII pair - facial nerve (p. Facialis). It is a mixed nerve. It contains motor, parasympathetic and sensory fibers, the last two types of fibers are isolated as an intermediate nerve.

The motor part of the facial nerve provides innervation to all facial muscles, muscles of the auricle, skull, posterior belly of the digastric muscle, stapedius muscle and subcutaneous muscle of the neck.

In the facial canal, a number of branches depart from the facial nerve.

1. The large stony nerve from the geniculate node on the outer base of the skull connects with the deep stony nerve (a branch of the sympathetic plexus of the internal carotid artery) and forms the nerve of the pterygoid canal, which enters the pterygopalatine canal and reaches the pterygopalatine node. The connection of the large stony and deep stony nerves is the so-called vidian nerve. The nerve contains preganglionic parasympathetic fibers to the pterygopalatine ganglion, as well as sensory fibers from the cells of the knee ganglion. When it is damaged, a peculiar symptom complex occurs, known as neuralgia of the vidian nerve (File's syndrome). The large stony nerve innervates the lacrimal gland. After a break in the pterygopalatine node, the fibers go as part of the maxillary and further zygomatic nerves, anastomose with the lacrimal nerve, which approaches the lacrimal gland. With damage to the large stony nerve, dryness of the eye occurs due to a violation of the secretion of the lacrimal gland, with irritation - lacrimation.

2. The stapedial nerve enters the tympanic cavity and innervates the stapedial muscle. With the tension of this muscle, conditions are created for the best audibility. If innervation is disturbed, paralysis of the stapedius muscle occurs, as a result of which the perception of all sounds becomes sharp, causing painful, unpleasant sensations (hyperacusia).

3. The drum string is separated from the facial nerve at the bottom facial channel, enters the tympanic cavity and through the stony-tympanic fissure enters the outer base of the skull and merges with the lingual nerve. At the point of intersection with the lower alveolar nerve, the drum string gives off a connecting branch to the ear node, in which motor fibers pass from the facial nerve to the muscle that lifts the soft palate.

The drum string transmits taste stimuli from the anterior two-thirds of the tongue to the knee node, and then to the nucleus of the solitary pathway, to which the taste fibers of the glossopharyngeal nerve approach. As part of the drum string, secretory salivary fibers also pass from the superior salivary nucleus to the submandibular and sublingual salivary glands, previously interrupted in the submandibular and sublingual parasympathetic nodes.

With damage to the facial nerve, the asymmetry of the face immediately attracts attention. Usually mimic muscles are examined during motor load. The subject is offered to raise his eyebrows, frown them, close his eyes. Pay attention to the severity of the nasolabial folds and the position of the corners of the mouth. They ask you to show your teeth (or gums), puff out your cheeks, blow out a candle, and whistle. A number of tests are used to detect mild muscle paresis.

Blink test: eyes blink asynchronously due to slow blinking on the side of the paresis.

Eyelid vibration test: with closed eyes, eyelid vibration is either reduced or absent on the side of the paresis, as determined by a light touch of the fingers on the closed eyelids at the outer corners of the eye (especially when pulling the eyelids backwards).

Orbicularis oculi muscle test: on the side of the lesion, the strip of paper is held weaker by the corner of the lips.

Eyelash symptom: on the affected side, with the eyes closed as much as possible, the eyelashes are visible better than on the healthy one, due to insufficient closure of the orbicular muscle of the eye.

For the differentiation of central and peripheral paresis, the study of electrical excitability, as well as electromyography, is important.

The loss of taste sensitivity is called ageusia, its decrease is called hypogeusia, the increase in taste sensitivity is called hypergeusia, its perversion is called parageusia.

Damage symptoms. With damage to the motor part of the facial nerve, peripheral paralysis of the facial muscles develops - the so-called prosoplegia. Facial asymmetry occurs. The entire affected half of the face is motionless, mask-like, the folds of the forehead and nasolabial fold are smoothed out, the palpebral fissure expands, the eye does not close (lagophthalmos - hare's eye), the corner of the mouth drops. When wrinkling the forehead, folds do not form. When trying to close the eye, the eyeball turns upward (Bell's phenomenon). There is increased lacrimation. At the heart of paralytic lacrimation is the constant irritation of the mucous membrane of the eye with a stream of air and dust. In addition, as a result of paralysis of the circular muscle of the eye and insufficient fit of the lower eyelid to the eyeball, a capillary gap is not formed between the lower eyelid and the mucous membrane of the eye, which makes it difficult for the tear to move to the lacrimal canal. Due to the displacement of the opening of the lacrimal canal, the absorption of tears through the lacrimal canal is impaired. This is facilitated by paralysis of the circular muscle of the eye and the loss of the blinking reflex. Constant irritation of the conjunctiva and cornea with a stream of air and dust leads to the development of inflammatory phenomena - conjunctivitis and keratitis.

For medical practice, it is important to determine the location of the lesion of the facial nerve. In the event that the motor nucleus of the facial nerve is affected (for example, with the pontine form of poliomyelitis), only paralysis of the facial muscles occurs. If the nucleus and its radicular fibers suffer, the nearby pyramidal path is often involved in the process and, in addition to paralysis of the mimic muscles, central paralysis (paresis) of the limbs of the opposite side (Miyar-Gubler syndrome) occurs. With simultaneous damage to the nucleus of the abducens nerve, convergent strabismus occurs on the side of the lesion or gaze paralysis towards the focus (Fauville's syndrome). If at the same time sensitive pathways at the level of the nucleus suffer, then hemianesthesia develops on the side opposite to the focus. If the facial nerve is affected at the site of its exit from the brain stem in the cerebellopontine angle, which is often the case with inflammatory processes in this area (arachnoiditis of the cerebellopontine angle) or acoustic neuroma, then paralysis of the facial muscles is combined with symptoms of auditory damage (hearing loss or deafness) and trigeminal (lack of corneal reflex) nerves. Since the conduction of impulses along the fibers of the intermediate nerve is disrupted, dryness of the eye (xerophthalmia) occurs, taste is lost in the anterior two-thirds of the tongue on the side of the lesion. In this case, xerostomia should develop, but due to the fact that other salivary glands are functioning, dryness in the oral cavity is not noted. There is also no hyperacusis, which theoretically exists, but due to the combined damage to the auditory nerve, it is not detected.

Damage to the nerve in the facial canal up to its knee above the origin of the large stony nerve leads, along with mimic paralysis, to dry eyes, taste disorder and hyperacusis. If the nerve is affected after the departure of the large stony and stirrup nerves, but above the discharge of the tympanic string, then mimic paralysis, lacrimation and taste disorders are determined. With the defeat of the VII pair in the bone canal below the discharge of the tympanic string or at the exit from the stylomastoid foramen, only mimic paralysis with lacrimation occurs. The most common lesions of the facial nerve at the exit from the facial canal and after exiting the skull. Perhaps bilateral damage to the facial nerve, and even recurrent.

In cases where the cortical-nuclear pathway is affected, paralysis of the facial muscles occurs only in the lower half of the face on the side opposite to the lesion. Hemiplegia (or hemiparesis) often occurs on this side. The peculiarities of paralysis are explained by the fact that the part of the nucleus of the facial nerve, which is related to the innervation of the muscles of the upper half of the face, receives bilateral cortical innervation, and the rest - one-sided.

VIII pair - vestibulocochlear nerve (n. vestibulocochlea-ris). Consists of two roots: lower - cochlear and upper - pre-door Symptoms of the lesion. Hearing loss, increased perception of sounds, ringing, tinnitus, auditory hallucinations. After that, hearing acuity is determined. With a decrease (hypacusia) or loss (anacusia) of hearing, it is necessary to determine whether it depends on the damage to the sound-conducting (external auditory canal, middle ear) or sound-receiving (organ of Corti, cochlear part of the VIII nerve and its nucleus) apparatus. To distinguish between a lesion of the middle ear and a lesion of the cochlear part of the VIII nerve, tuning forks (Rinne and Weber's technique) or audiometry are used. Since the peripheral auditory apparatus turns out to be communicating with both hemispheres of the brain, then the defeat of the auditory conductors above the anterior and posterior auditory nuclei does not cause loss of auditory functions. Unilateral hearing loss or deafness is possible only with damage to the receptor auditory apparatus, the cochlear part of the nerve and its nuclei. In this case, there may be symptoms of irritation (sensation of noise, whistling, buzzing, cod, etc.). When the cortex of the temporal lobe of the brain is irritated (for example, with tumors), auditory hallucinations may occur.

The vestibular part (pars vestibularis).

Damage symptoms. The defeat of the vestibular apparatus - the labyrinth, the vestibular part of the VIII nerve and its nuclei - leads to three characteristic symptoms: dizziness, nystagmus and coordination disorder. Conscious and automatic orientation in space is disturbed: the patient has false sensations of displacement of his own body and surrounding objects. Dizziness often occurs in attacks, reaches a very strong degree, may be accompanied by nausea, vomiting .. Rarely, nystagmus is expressed when looking directly; usually it is better detected when looking to the side. Irritation of the vestibular part of the VIII nerve and its nuclei causes nystagmus in the same direction. Switching off the vestibular apparatus leads to nystagmus in the opposite direction.

The defeat of the vestibular apparatus is accompanied by incorrect jet movements, a violation of the normal tone of the muscles and their antagonists. Movements are deprived of proper regulatory influences, hence the discoordination of movements (vestibular ataxia). A wobbly gait appears, the patient deviates towards the affected labyrinth, and in this direction he often falls.

Dizziness, nystagmus, and ataxia can be observed with damage not only to the vestibular apparatus, but also to the cerebellum; therefore, it is important to differentiate labyrinthine lesions from similar cerebellar symptoms. Diagnosis is based on the following data: 1) dizziness with labyrinthitis is extremely intense; 2) in the Romberg test, the body leans to the side with closed eyes, and there is a dependence on the position of the head and the affected labyrinth; 3) ataxia is always general, that is, it is not limited to only one limb or limbs of one side, it is not accompanied by intentional trembling, as is observed with cerebellar ataxia; 4) nystagmus in labyrinthine lesions is characterized by a clearly defined fast and slow phase and has a horizontal or rotatory direction, but not vertical; 5) labyrinthine lesions are usually associated with symptoms of hearing loss (eg, tinnitus, hearing loss).

2.37 Symptoms of damage to the 9th and 10th pairs of cranial nerves.

Glossopharyngeal and vagus nerves (n. glossopharyngeus et n. vagus). They have common nuclei, which are laid in the medulla oblongata in one place, therefore they are examined simultaneously.

IX pair - glossopharyngeal nerve (p. glossopharyngeus). Contains 4 types of fibers: sensory, motor, gustatory and secretory. Sensory innervation of the posterior third of the tongue soft palate, pharynx, pharynx, anterior surface of the epiglottis, auditory tube and tympanic cavity. The motor fibers innervate the stylo-pharyngeal muscle, which raises the upper part of the pharynx during swallowing.

Parasympathetic fibers innervate the parotid gland.

Damage symptoms. When the glossopharyngeal nerve is affected, taste disorders are observed in the posterior third of the tongue (hypogeusia or ageusia), loss of sensitivity in the upper half of the pharynx; motor function disorders are not clinically expressed due to the insignificant functional role of schiloglo-

precise muscle. Irritation of the cortical projection area in the deep structures of the temporal lobe leads to the appearance of false taste sensations (parageusia). Sometimes they can be harbingers (aura) of an epileptic seizure. Irritation of the IX nerve causes pain in the root of the tongue or tonsil, spreading to the palatine curtain, throat, ear.

X pair - vagus nerve (p. vagus). Contains sensory, motor and autonomic fibers. Provides sensory innervation of the dura mater of the posterior cranial fossa, posterior wall of the external auditory canal and part of the skin of the auricle, mucous membrane of the pharynx, larynx, upper trachea and internal organs Motor fibers innervate the striated muscles of the pharynx, soft palate, larynx, epiglottis and upper esophagus .

Vegetative (parasympathetic) fibers go to the heart muscle, smooth muscle tissue of blood vessels and internal organs. Impulses traveling through these fibers slow down the heartbeat, dilate blood vessels, constrict the bronchi, and increase intestinal motility. Postganglionic sympathetic fibers from the cells of the paravertebral sympathetic nodes also enter the vagus nerve and spread along the branches of the vagus nerve to the heart, blood vessels and internal organs.

Damage symptoms. When the periphery of the vagus neuron is damaged, swallowing is disturbed due to paralysis of the muscles of the pharynx and esophagus. There is a hit of liquid food in the nose as a result of paralysis of the palatine muscles, drooping of the soft palate on the affected side. With paralysis, the voice of the ligaments is weakened by the sonority of the voice, with bilateral damage, up to aphonia and suffocation. The symptoms of vagus damage include a disorder of cardiac activity - tachycardia and bradycardia (with irritation). With a unilateral lesion, the s-we are slightly expressed, with a bilateral lesion, pronounced disorders of swallowing, phonation, respiration and heart activity. When the feelings of the branches of the vagus are affected, the feeling of the mucus of the ob-ki of the larynx, pain in the larynx and ear are disturbed. With the defeat of the 9th pair, the taste for bitter and salty in the back of a third of the tongue is lost, as well as the feeling of mucus from the upper part of the pharynx.

TWELVE PAIRS OF CRANIONERVOUS

Compiled by Academician of the Russian Academy of Medical Sciences, Doctor of Medical Sciences, Professor of the Department of Normal Anatomy of the Moscow State Medical University, Pavlova Margarita Mikhailovna

Twelve pairs of cranial nerves:

I pair of cranial nerves - n. olfactorius - olfactory nerve;

II pair of cranial nerves - n. opticus - optic nerve;

III pair of cranial nerves - n. oculomotorius - oculomotor nerve;

IV pair of cranial nerves - n. trochlearis - trochlear nerve;

V pair of cranial nerves - n. trigeminus - trigeminal nerve;

VI pair of cranial nerves - n. abducens - abducens nerve;

VII pair of cranial nerves - n. facialis - facial nerve;

VIII pair of cranial nerves - n. vestibulocochlearis - static auditory nerve;

IX pair of cranial nerves - n. glossopharyngeus - glossopharyngeal nerve;

X pair of cranial nerves - n. vagus - vagus nerve;

XI pair of cranial nerves - n. accessorius - accessory nerve;

XII pair of cranial nerves - n. hypoglossus - hypoglossal nerve.

I a pair of cranial nerves n . olfactorius - olfactory nerve , sensitive. It develops from the olfactory brain - an outgrowth of the forebrain, therefore there are no nodes. From the nasal cavity (from the receptors) - the posterior sections of the superior and middle turbinates → 18-20 threads (filae olfactoriae) - these are the central processes of the olfactory cells → regio olfactoria (olfactory region) → lamina cribrosa ossis ethmoidalis → bulbus olfactorius (olfactory bulb) → tractus olfactorius (tract) → trigonum olfactorium (olfactory triangle).

In pathology: decrease, increase, absence or perversion (olfactory hallucinations) of smell.

II a pair of cranial nerves n . opticus - optic nerve , by function - sensitive. It is an outgrowth of the diencephalon, connected with the midbrain. Has no nodes. It starts from the rods and cones on the retina → canalis opticus → chiasma optici (optic chiasm), at the level of sella thurcica in the sulcus chiasmatis of the sphenoid bone. Only the medial bundles cross → tractus opticus → corpus geniculatum laterale → pulvinar thalami → superior tubercles of the quadrigemina. It ends in the occipital lobe - sulcus calcarinus.

In case of damage, the fields of view of one's own or someone else's eye fall out:

With damage to the optic nerve: blindness, decreased vision, visual hallucinations.

III a pair of cranial nerves n . oculomotorius - oculomotor nerve . By function - mixed, but mainly motor for the muscles of the eye. It has motor and parasympathetic nuclei - (nucleus accessorius). It leaves the brain along the medial edge of the brain stem → fissura orbitalis superior → into the orbit

Root → to ganglion celiare with parasympathetic fibers - for m. sphincter pupillae and m. ciliaris.

The triad of symptoms in the defeat of n. oculomotorius:

1) Ptos (drooping of the upper eyelid) - the defeat of m. levator palpebrae superior.

2) Divergent strabismus (innervation of the VI pair of cranial nerves prevails) → stropismus divergens.

3) Pupil dilation (damage to m. sphincter pupillae). The dilator (mydrias) prevails.

The superior, inferior, and medial rectus muscles are innervated by the third cranial nerve.

The external rectus muscle of the eye is the VI pair of cranial nerves.

The superior oblique muscle of the eye is the 4th pair of cranial nerves.

The inferior oblique muscle of the eye is the 3rd pair of cranial nerves.

The muscle that lifts the upper eyelid (m. Levator palpebrae superior - III pair of cranial nerves (antagonist of the VII pair of cranial nerves for m. orbicularis oculi).

M. sphincter pupillae (pupil constrictor) - III pair of cranial nerves (parasympathetic branch as part of n. oculomotorius).

M. dilatator pupillae (the muscle that dilates the pupil) is the antagonist of the constrictor. Innervated by the sympathetic nervous system.

IV a pair of cranial nerves n . trochlearis - trochlear nerve. By function - motor. It emerges from the superior medullary velum, goes around the brain stem → fissura orbitalis superior, enters the orbit. Innervates the superior oblique muscle of the eye - m. obliquus oculi superior. With pathology, double vision due to the oblique standing of the eyeballs, as well as a symptom of the impossible descent from the stairs.

V a pair of cranial nerves n . trigeminus - trigeminal nerve. Functionally, it is a mixed nerve. Contains motor, sensory and parasympathetic fibers. Innervates all chewing muscles, skin of the face, teeth, glands of the oral cavity.

1) one motor and three sensory nuclei;

2) sensory and motor roots;

3) trigeminal node on the sensitive root (ganglion trigemenale);

5) three main branches: ophthalmic nerve, maxillary nerve, mandibular nerve.

Cells of the trigeminal node (ganglion trigemenale) have one process, dividing into two branches: central and peripheral.

The central neurites form a sensitive root - radix sensoria, enter the brainstem → sensitive nerve nuclei: the pontine nucleus (nucleus pontis nervi trigemini), the nucleus of the spinal tract (nucleus spinalis nervi trigemini) - the hindbrain, the nucleus of the mesencephalic tract - the nucleus mesencephalicus nervi trigemini - the middle brain.

The peripheral processes are part of the main branches of the trigeminal nerve.

Motor nerve fibers originate in the motor nucleus of the nerve - the nucleus motorius nervi trigemini (hindbrain). Coming out of the brain, they form a motor root - radix motoria.

Autonomic ganglions are connected with the main branches of the trigeminal nerve.

1) Ciliary node - with the optic nerve;

2) Pterygopalatine node - with the maxillary nerve;

3) Ear and submandibular - with the mandibular nerve.

Each branch of the trigeminal nerve (ophthalmic, maxillary, mandibular) gives off:

1) branch to the dura mater;

2) branches to the mucous membrane of the oral cavity, nose, to the paranasal (paranasal, accessory) sinuses;

3) to the organs of the lacrimal gland, salivary glands, teeth, eyeball.

I. N. ophthalmicus- ophthalmic nerve

Functionally sensitive. Innervates the skin of the forehead, the lacrimal gland, part of the temporal and parietal region, the upper eyelid, the back of the nose (upper third of the face). Passes through fissura orbitalis superior.

Branches: lacrimal nerve (n. lacrimalis), frontal nerve (n. frontalis), nasociliary nerve (n. nasociliaris).

N. lacrimalis innervates the lacrimal gland, the skin of the upper eyelid, and the outer canthus of the eye.

n. supraorbitalis (supraorbital nerve) through incisura supraorbitalis - to the skin of the forehead;

n. supratrochlearis (supratrochlearis nerve) - for the skin of the upper eyelid and medial canthus.

N. nasociliaris. Its terminal branch is n. infratrochlearis (for the lacrimal sac, medial angle of the eye, conjunctiva).

nn. ciliares longi (long ciliary branches) - to the eyeball,

n. ethmoidalis posterior (posterior ethmoid nerve) - to paranasal sinuses(wedge-shaped, lattice).

n. ethmoidalis anterior - to the frontal sinus, nasal cavity: rr. nasales medialis et lateralis, r. nasalis externus.

The vegetative node of the first branch of the V pair of cranial nerves is the ciliary node - ganglion ciliare. It lies on the outer surface of the optic nerve (in the orbit) between the posterior and middle thirds. It comes from three sources:

a) sensitive root - radix nasociliaris (from n. nasociliaris);

b) parasympathetic - from n. oculomotorius;

c) sympathetic - radix sympathicus from plexus sympathicus a. ophthalmica.

II. N. maxillaris- maxillary nerve- for the middle third of the face, the mucous membrane of the nasal cavity and mouth, upper lip. Enters through the foramen rotundum.

r. meningeus (to dura mater) in the pterygopalatine fossa;

nodal branches - rr. ganglionares - sensitive branches to ganglion pterygopalatinum;

zygomatic nerve (n. zygomaticus);

infraorbital nerve (n. infraorbitalis).

The vegetative node of the second branch of the V pair of cranial nerves is the pterygopalatine node - ganglion pterygopalatinum. It comes from three sources:

a) sensitive root - nn. pterygopalatini;

b) parasympathetic root - n. petrosus major (7th pair of cranial nerves + n. intermedius);

c) sympathetic root - n. petrosus profundus (from plexus caroticus internus).

Depart from ganglion pterygopalatinum: rr. orbitales (orbital branches), rr. nasales posteriores superiores (posterior superior nasal branches), nn. palatine (palatine branches).

Rr. orbitalis through fissura orbitalis inferior → into the orbit, then from n. ethmoidalis posterior → to the ethmoid labyrinth and sinus sphenoidalis.

Rr. nasales posteriores → through foramen sphenopalatinum → into the nasal cavity and are divided into: rr. nasales posteriores superiores lateralis and rr. nasales posteriores superiores medialis.

Nn. palatini → through canalis palatinus and are divided into: n. palatinus major (through foramen palatinum major), nn. palatini minores (through foramina palatina minora), rr. nasales posteriores inferiores (for the posterior parts of the nasal cavity).

N. zygomaticus (zygomatic nerve) → exits through the foramen zygomaticoorbitale and divides into: r. zygomaticofacialis and r. zigomaticotemporalis (exit through the holes of the same name). It enters the orbit from the pterygopalatine fossa through the fissura orbitalis inferior.

N. infraorbitalis (infraorbital nerve). From the pterygopalatine fossa → fissura orbitalis inferior → sulcus infraorbitalis → foramen infraorbitale.

nn. alveolares superiores posteriores innervate the posterior third of the teeth of the upper jaw. Pass through foramina alveolaria posteriora to tuber maxillae → canalis alveolaris, form a plexus;

nn. alveolares superiores medii (1-2 stems). They depart within the orbit or pterygopalatine fossa. Innervate the middle third of the teeth of the teeth of the upper jaw;

nn. alveolares superiores anteriores (1-3 stems) - for the front upper teeth of the upper jaw.

From n. infraorbitalis depart:

nn. alveolares superiores (for teeth);

rr. palpebrales inferiores (for eyelids);

rr. nasales externi;

rr. nasales interni;

rr. labiales superiores - for the upper lip.

III. N. mandibularis -mandibular nerve. Mixed nerve. Its branches:

a) r. meningeus - with a. meninfea media passes through the foramen spinosum. The nerve is sensitive to the dura mater.

b) n. massetericus - for the muscle of the same name;

c) nn. temporales profundi - for the temporal muscle;

d) n. pterygoideus lateralis - for the muscle of the same name;

e) n. pterygoideus medialis - for the muscle of the same name;

n. pterygoideus medialis: n. tensor tympani, n. tensor veli palatini - for the muscles of the same name.

e) n. buccalis, sensitive (buccal nerve) - for the buccal mucosa.

g) n. auriculotemporalis - ear-temporal nerve, sensitive, passes anterior to the external auditory canal, perforates the glandula parotis, goes to the temple area: rr. auricularis, rr. parotidei, n. meatus acusticus externus, nn. auriculares anteriores.

h) n. lingualis (lingual), sensitive. It is joined by chorda tympani (drum string) → continued n. intermediate. Contains secretory fibers to the submandibular and sublingual nerve nodes + taste - to the papillae of the tongue.

Branches n. lingualis: rr. isthmi faucium, n. sublingualis, rr. linguales.

Ganglion submandibulare (submandibular node) is formed from three sources:

a) nn. linguales (sensitive, from n. trigeminus);

b) chorda tympani - parasympathetic nerve from the VII pair of cranial nerves (n. intermedius);

c) plexus sympaticus a facialis (sympathetic).

Vegetative node of the third branch n. trigeminus innervates the submandibular and sublingual salivary glands.

Ganglion oticum (ear node) - vegetative node n. mandibularis. Lies under the foramen ovale, on the medial surface n. mandibularis. It comes from three sources:

a) n. mandibularis - sensitive branches (n. auriculotemporalis, n. meningeus);

b) n. petrosus minor - parasympathetic nerve - terminal branch of n. tympanicus (IX pair of cranial nerves);

c) plexus sympathicus a. meningea media.

Ganglion oticum innervates the salivary gland through n. auriculotemporalis.

i) n. alveolaris inferior (lower alveolar nerve) - mixed. Predominantly sensitive to the teeth of the lower jaw, forming a plexus. Leaves the channel through the foramen mentale. It enters the canal through the foramen mandibulare of the lower jaw.

n. mylohyoideus (for venter anterior m. digastrici and m. mylohyoideus);

rr. dentales et gingivales - for the gums and teeth of the lower jaw;

n. mentalis - mental nerve - continuation of the trunk n. alveolaris inferior. It leaves the canalis mandibularis through the foramen mentale.

Its branches:

rr. mentales (for the skin of the chin);

rr. labiales inferiores (for the skin and mucous membrane of the lower lip).

VI a pair of cranial nerves n . abducens - abducens nerve. By function - motor. Innervates the external rectus muscle of the eye - m. rectus oculi lateralis. In case of damage, the internal rectus muscle of the eye (III pair of cranial nerves) prevails - there will be convergent strabismus (stropismus convergens). The core is located in the bridge. It enters the orbit through the fissura orbitalis superior together with III, IV pairs of cranial nerves + the first branch of the V pair of cranial nerves.

VII a pair of cranial nerves n . facialis - facial nerve The nerve is mixed, predominantly motor for the mimic muscles of the face.

Has three cores in the bridge:

From linea trigeminofacialis with the VIII pair (n. vestibulocochlearis) passes into porus acusticus internus → canalis facialis.

There are three directions of the nerve in the canal:

Horizontally (in the frontal plane), then sagitally, then vertically. It exits the skull through the foramen stylomastoideum. Between the first and second parts, a bend is formed in the form of a knee - genu n. facialis with the formation of ganglion geniculi (knee) as a result of the addition of n. intermedius, therefore, below the knee - branches with a vegetative function.

In pathology: an open eye on the side of the lesion and a skew of the face to the healthy side, a violation of salivation, a lack of taste for sweets, the nasolabial fold is smoothed, the corner of the mouth is lowered, dryness of the eyeball.

Branches in the pyramid of the temporal bone:

1) n. stapedius - to m.stapedius (“stapes” - stirrup). motor nerve.

2) n. petrosus major, secretory nerve, autonomic. Departs from genu n.facialis. It leaves the pyramid through the hiatus canalis n. petrosi majoris → sulcus n. petrosi majores → canalis pterygoideus together with the sympathetic nerve - n. petrosus profundus from plexus caroticus internus. Both nerves form n. canalis pterygoidei → ganglion pterygopalatinum: rr. nasales posteriores, nn. palatini.

Part of the fibers through n. zygomaticus (from n.maxillaris) through connections with n. lacrimalis reaches the lacrimal gland.

Branches n. facialis, which form in the glandula parotis plexus parotideus and the great crow's foot - pes anserina major.

3) Chorda tympani - from the vertical part of the nerve. The drum string is a vegetative, parasympathetic nerve.

N. intermedius (intermediate nerve), mixed. Contains:

1) taste fibers - to the sensitive nucleus - nucleus tractus solitarii

2) efferent (secretory, parasympathetic) fibers from the autonomic nucleus - nucleus solivatorius superior.

N. intermedius leaves the brain between n. facialis and n. vestibulocochlearis, joins the VII pair of cranial nerves (portio intermedia n. Facialis). Then it goes into chorda tympani and n. petrosus major.

Sensory fibers originate from ganglion geniculi cells. The central fibers of these cells → to the nucleus tractus solitarii.

Chorda tympani conducts taste sensitivity of the anterior sections of the tongue and soft palate.

Secretory parasympathetic fibers from n. intermedius start from the nucleus solivatorius superior → along chorda tympani → sublingual and submandibular salivary glands (through ganglion submandibulare and along n. petrosus major through ganglion pterygopalatinum - to the lacrimal gland, to the glands of the mucous membrane of the nasal cavity and palate).

The lacrimal gland receives secretory fibers from n. intermedius through n. petrosus major, ganglion pterygopalatinum + anastomosis of the second branch of the V pair of cranial nerves (n. maxillaris with n. lacrimalis).

N. intermedius innervates all glands of the face except glandula parotis, which receives secretory fibers from n. glossopharyngeus (IX pairs of cranial nerves).

VIII a pair of cranial nerves n . vestibulocochlearis - vestibulocochlear nerve n . statoacousticus ). The nerve is sensitive. The fibers come from the organ of hearing and balance. It consists of two parts: pars vestibularis (balance) and pars cochlearis (hearing).

The node pars vestibularis - ganglion vestibulare lies at the bottom of the internal auditory meatus. The node pars cochlearis - ganglion spirale lies in the cochlea.

Peripheral processes of cells end in the perceiving devices of the labyrinth. The central processes - porus acusticus internus - into the nuclei: pars vestibularis (4 nuclei) and pars cochlearis (2 nuclei).

With pathology - impaired hearing and balance.

IX a pair of cranial nerves n . glossopharyngeus - Glossopharyngeal nerve. The function is mixed. Contains: a) afferent (sensory) fibers from the pharynx, tympanic cavity, posterior third of the tongue, tonsils, palatine arches;

b) efferent (motor) fibers innervating m. stylopharyngeus;

c) efferent (secretory) parasympathetic fibers for glandula parotis.

It has three cores:

1) nucleus tractus solitarii, which receives the central processes of the ganglion superior et inferior;

2) vegetative nucleus (parasympathetic) - nucleus solivatorius inferior (lower salivary). Has cells scattered in the formatio reticularis;

3) motor nucleus, common with n. vagus - nucleus ambiguus.

It leaves the skull with the X pair of cranial nerves through the foramen jugulare. Within the hole, a node is formed - ganglion superior, and under it - ganglion inferior (the lower surface of the pyramid of the temporal bone).

1) N. tympanicus (from ganglion inferior → cavum tympani → plexus tympanicus with plexus sympaticus a. crotis interna (for the auditory tube and tympanic cavity) → n. petrosus minor (exits through the hole on the upper wall of the tympanic cavity) → sulcus n. petrosi minores → ganglion oticum (parasympathetic fibers for the parotid salivary gland as part of n. auriculotemporalis (from the third branch of the fifth pair of cranial nerves).

2) R. m. stylopharyngei - to the pharyngeal muscle of the same name;

3) Rr. tonsillares - to the arches, palatine tonsils;

4) Rr. pharyngei - to the pharyngeal plexus.

X a pair of cranial nerves n . vagus - nervus vagus. Mixed, predominantly parasympathetic.

1) Sensitive fibers go from the receptors of internal organs and blood vessels, from dura mater, meatus acusticus externus to the sensitive nucleus - nucleus tractus solitarii.

2) Motor (efferent) fibers - for the hepatic-striated muscles of the pharynx, soft palate, larynx - from the motor nucleus - the nucleus ambiguus.

3) Efferent (parasympathetic) fibers - from the autonomic nucleus - nucleus dorsalis n. vagi - to the heart muscle (bradycardia), to the smooth muscles of the vessels (expand).

As part of n. vagus goes n. depressor - regulates blood pressure.

Parasympathetic fibers narrow the bronchi, trachea, innervate the esophagus, stomach, intestines to the colon sigmoideum (increase peristalsis), liver, pancreas, kidneys (secretory fibers).

It emerges from the medulla oblongata. In the foramen jugulare it forms a ganglion inferior.

Peripheral processes of cells are part of the sensitive branches from the receptors of the viscera and blood vessels - meatus acusticus externus. The central processes end in the nucleus tractus solitarii.

A. Head part:

r. memningeus - to the dura mater;

r. auricularis - to the external auditory canal.

B. Neck:

rr. pharyngei → pharyngeal plexus with cranial nerve IX + truncus sympathicus;

n. laryngeus superior: sensory branches for the root of the tongue, motor branches for m. cricothyreoideus anterior (the remaining muscles of the larynx are innervated by n. laryngeus inferior from n. laryngeus recurrens);

rr. cardiaci superiores (for the heart).

B. Chest:

n. laryngeus recurrents;

r. cardiacus inferior (from n. laryngeus recurrens);

rr. bronchiales et trachleares - to the trachea, bronchi;

rr. esophagei - to the esophagus.

D. Abdomen:

truncus vagalis anterior (together with fibers of the sympathetic nervous system);

truncus vagalis posterior;

plexus gastricus anterior;

plexus gastricus posterior → rr. celiaci.

XI a pair of cranial nerves n . accessorius - Accessory nerve. Motor for m. sternocleidomastoideus and m. trapezius. Has two motor nuclei in medulla oblongata and medulla spinalis → nucleus ambiguus + nucleus spinalis.

It has two parts: head (central), spinal.

XI pair - split off part of n. vagus. The head part connects to the spinal portion and exits the skull through the foramen jugulare along with the IX and X pairs of cranial nerves.

The spinal portion is formed between the roots of the spinal nerves (C 2 -C 5) of the upper cervical nerves. It enters the cranial cavity through the foramen occipitale magnum.

With the defeat of the XI pair of cranial nerves - torticollis (torticolis) - head tilt to the healthy side with a turn in the direction of the lesion.

XII a pair of cranial nerves n . hypoglossus - hypoglossal nerve. Motor, mainly for the muscles of the tongue and neck muscles. It contains sympathetic fibers from the superior cervical sympathetic ganglion. There is a connection with n. lingualis and with the lower node n. vagus. Somatic motor nucleus in trigonum nervi hypoglossi of the rhomboid fossa → formation reticularis, descending through the medulla oblongata. On the basis of the brain - between the olive and the pyramid → canalis n. hypoglossy. Forms the upper wall of the Pirogov triangle - arcus n. hypoglossy.

The branch of the XII pair connects to the cervical plexus, forming ansa cervicalis (innervates the muscles below the os hyoideum) - m. sternohyoideus, m. sternothyreoidus, m. thyreohyoideus and m. onohyoideus.

With the defeat of n. hypoglossus protruding tongue deviates towards the lesion.