Cranial nerves - twelve pairs of nerves in the brain; there is also an intermediate nerve, which some authors consider the XIII pair. The cranial nerves are located at the base of the brain (Figure 1). Some of the cranial nerves have predominantly motor functions (III, IV, VI, XI, XII pairs s), others are sensitive (I, II, VIII pairs), the rest are mixed (V, VII, IX, X, XIII pairs). Some cranial nerves contain parasympathetic and sympathetic fibers.

Rice. 1. Base of the brain. Exit sites of cranial nerves:
a - olfactory bulb;
b - optic nerve;
V - olfactory tract;
g - oculomotor nerve;
d - trochlear nerve;
e - trigeminal nerve;
g - abducens nerve;
h - facial and intermediate nerves;
and - vestibulocochlear nerve;
k - glossopharyngeal and vagus nerves;
l - hypoglossal nerve;
m - accessory nerve.

I pair, olfactory nerve(n. olfactorius), originates from the nerve cells of the nasal mucosa. Thin fibers of this nerve pass through the openings of the cribriform plate ethmoid bone, enter the olfactory bulb, which then passes into the olfactory tract. Expanding posteriorly, this tract forms the olfactory triangle. At the level of the olfactory tract and triangle lies the olfactory tubercle, in which the fibers coming from the olfactory bulb end. In the cortex, olfactory fibers are distributed in the hippocampal region. When the olfactory nerve is damaged, it occurs total loss sense of smell - anosmia or its partial impairment - hyposmia.

II pair, optic nerve(n. opticus), starts from the cells of the ganglion layer of the retina. The processes of these cells gather into the optic nerve, which, after entering the cavity, forms a visual chiasm at the base of the brain. But this intersection is not complete; only the fibers coming from the inner halves of the retina of the eyes intersect in it. After the chiasm, the optic nerve is called the optic tract, which ends in the lateral geniculate body. The central visual pathway begins from the lateral geniculate body and ends in the cortex. occipital lobe brain. With any pathological processes in the brain affecting the optic chiasm, optic tract or pathway, various forms of prolapse occur - hemianopsia.

Diseases of the optic nerve can be inflammatory (neuritis), congestive (stagnant nipple) and dystrophic (atrophy) in nature.

The cause of optic neuritis can be various diseases (meningitis, arachnoiditis, influenza, etc.).

It manifests itself as a sudden decrease in visual acuity and a narrowing of the field of vision.

A stagnant nipple is the most important symptom of increased intracranial pressure, which can most often be associated with a brain tumor, occasionally gumma, solitary tubercle, cyst, etc. Congestive nipple long time does not lead to visual impairment and is detected during fundus examination. As the disease progresses, it decreases and may occur.

Optic nerve atrophy can be primary (with syphilis of the brain, multiple sclerosis, with trauma to the optic nerve, etc.) or secondary, as a result of neuritis or congestive nipple. With this disease, there is a sharp decrease in visual acuity up to complete blindness, as well as a narrowing of the field of vision.

Treatment depends on the etiology of the disease.

Rice. 2. Diagram of the visual pathways.

III pair, oculomotor nerve(n. oculomotorius), is formed by fibers coming from the nuclei of the same name, lying in the central gray matter, under the aqueduct of the brain (Sylvian aqueduct). It reaches the base of the brain between its legs through the superior orbital fissure, penetrates the orbit and innervates all the muscles of the eyeball, with the exception of the superior oblique and external rectus muscles. The parasympathetic fibers contained in the oculomotor nerve innervate the smooth muscles of the eye. The lesion of the third pair is characterized by prolapse upper eyelid(), divergent strabismus and mydriasis (pupil dilation).

Second higher education in psychology in MBA format

item:Anatomy and evolution of the human nervous system.
Manual "Anatomy of the central nervous system"

12 pairs of cranial (cranial) nerves arise symmetrically from the human brain. Both morphologically and functionally, these nerves are not homogeneous. The following nerves are distinguished:

1) olfactory (I);
2) visual (II);
3) oculomotor (III);
4) block (IV);
5) trigeminal (U);
6) abducent (VI);
7) facial (VII);
8) vestibulocochlear (VIII);
9) glossopharyngeal (IX);
10) wandering (X);
11) additional (XI);
12) sublingual (XII).

Each of the listed nerves has its own anatomical areas of entry (for sensory nerves) and exit (for motor nerves). In addition, the cranial nerves may also contain autonomic fibers of the parasympathetic part of the central nervous system.

At the base of the brain, on the sides of the longitudinal fissure, lie the bulbs of the olfactory nerve. From the bulb comes the olfactory tract, which expands into the olfactory triangle. Behind the longitudinal target on the lower surface of the hemispheres is the optic chiasm (II). The oculomotor nerve (III) goes around the cerebral peduncle from the inside, and the trochlear nerve (IV) goes around the outside. At the border of the bridge with the middle cerebellar peduncles, the trigeminal nerve (V) emerges. On the border of the bridge and medulla oblongata successively from the central fissure emerge: abducens nerve (VI), facial nerve (VII), vestibulocochlear nerve (VIII). On the border between the olive and the inferior cerebellar peduncle there are the roots of the lingula of the pharyngeal nerve (IX), vagus nerve (X), and accessory nerve (XI). Between the pyramid and the olive, the roots of the hypoglossal nerve (XII) emerge. Based on the function of the nerve fibers entering the nerve, several groups of cranial nerves are distinguished (Fig. 12.1).

Rice. 12.1. Classification of cranial nerves by function

Many cranial nerves are interconnected by connecting branches, in which sensory, motor and autonomic fibers can pass.

The nuclei of most nerves are located throughout the brain stem and enter the spinal cord: they secrete motor, sensory, and autonomic (autonomous) nuclei. The exceptions are the olfactory and optic nerves, which do not have nuclei and are outgrowths of the brain.

Let's take a closer look at each of the nerves.

I pair - olfactory nerves. They start from the mucous membrane of the olfactory region of the nasal cavity, pass through the cranial cavity and approach the olfactory bulb. As the name implies, this nerve carries information to the brain about the chemical composition of odorous molecules, which serves as the basis for the occurrence of olfactory sensations.

II pair - optic nerve contains axons of retinal ganglion cells. Undoubtedly, vision is the most important channel for receiving information about the world around us.

III pair - oculomotor nerve. Innervates the muscle that lifts the superior eyelid, the superior, inferior, medial rectus and inferior oblique muscles of the eyeball. The oculomotor nerve contains parasympathetic fibers that innervate the sphincter of the pupil and the ciliary muscle of the eye.

IV paratrochlear nerve innervates the superior oblique muscle of the eyeball. With the help of the III, IV and VI pairs of nerves, the gaze is focused on an object.

V pair - trigeminal nerve is the main sensory nerve of the head. The trigeminal nerve innervates the skin of the face, the eyeball and conjunctiva, the dura mater, the mucous membrane of the nasal and oral cavity, most of the tongue, teeth and gums. Its motor fibers go to the muscles of mastication and the muscles of the floor of the mouth. The most vivid (and at the same time least pleasant) sensations associated with ternary nerve, is a toothache that almost every person is familiar with.

VI pair - abducens nerve innervates the external rectus muscle of the eye.

VII pair - facial nerve. It is formed mainly by motor fibers, but also includes parasympathetic fibers. Motor fibers facial nerve innervate all facial muscles. Human facial expressions play an important role in communication, helping to establish more complete and mutual understanding on a non-verbal level.

VIII pair - vestibulocochlear nerve , which conducts stimulation from receptors inner ear. Hearing is the second (after vision) channel for receiving information from the outside world.

IX pair - glossopharyngeal nerve . It conducts motor fibers to the pharyngeal constrictors and stylopharyngeal muscle, and sensory fibers from the mucous membrane of the pharynx, tonsils, tympanic cavity, and contains parasympathetic fibers.

X pair - vagus nerve , has the most extensive area of ​​innervation. Is in charge parasympathetic nerve internal organs, and also conducts most of the afferent fibers from the organs in which it branches. With the help of this nerve, many psychosomatic and somatopsychic connections are organized.

XI pair - accessory nerve , has cranial and spinal roots that unite into a nerve trunk. Participates in the motor innervation of the pharynx and larynx, as well as the sternocleidomastoid and part of the trapezius muscle.

XII pair - hypoglossal nerve , is the motor nerve of the tongue. Human speech (his second signal system, but according to Pavlov) is largely ensured by the control of the muscles of the larynx and tongue with the help of the XI and XII pairs of nerves.

A person has 12 pairs of cranial nerves(see diagrams below).
Scheme of localization of cranial nerve nuclei: anteroposterior (a) and lateral (b) projections

Olfactory, visual, vestibulocochlear - nerves of highly organized specific sensitivity, which in their morphological features represent, as it were, peripheral parts of the central nervous system.

The article below will list all 12 pairs of cranial nerves, information about which will be accompanied by tables, diagrams and figures.

For more convenient navigation through the article, there is a picture with clickable links above: just click on the name of the pair of CNs you are interested in and you will immediately be taken to information about it.

12 pairs of cranial nerves

Motor nuclei and nerves are indicated in red, sensory in blue, parasympathetic in yellow, preocochlear nerve in green.

1 pair of cranial nerves - olfactory (nn. olfactorii)

NN. olfactorii (scheme)

2 pair of cranial nerves - optic (n. opticus)

N. opticus (diagram)

When the 2nd pair of cranial nerves is damaged, various types of visual impairment can be observed, shown in the figure below.

amaurosis (1);
hemianopsia - bitemporal (2); binasal (3); eponymous (4); square (5); cortical (6).

Any pathology of the optic nerve requires a mandatory examination of the fundus, the possible results of which are shown in the figure below.

Fundus examination

Primary optic nerve atrophy. The color of the disk is gray, its boundaries are clear.

Secondary optic nerve atrophy. The color of the disc is white, the contours are unclear.

3 pair of cranial nerves - oculomotor (n. oculomotorius)

N. oculomotorius (diagram)

Innervation of the eye muscles

Scheme of innervation of the muscles of the eyeball by the oculomotor nerve

The 3rd pair of cranial nerves is involved in the innervation of the muscles involved in eye movement.

Schematic representation of the path

- this is a complex reflex act in which not only the 3rd pair, but also the 2nd pair of cranial nerves are involved. The diagram of this reflex is shown in the figure above.

4th pair of cranial nerves - trochlea (n. trochlearis)

5th pair of cranial nerves - trigeminal (n. trigeminus)

Nuclei and central pathways n. trigeminus

The dendrites of sensory cells along their course form three nerves (see the figure below for innervation zones):

• orbital— (zone 1 in the figure),
• maxillary— (zone 2 in the figure),
• mandibular— (zone 3 in the figure).

Zones of skin innervation by branches n. trigeminus

From skull n. ophthalmicus exits through fissura orbitalis superior, n. maxillaris - through foramen rotundum, n. mandibularis - through foramen ovale. As part of one of the branches n. mandibularis, which is called n. lingualis, and chorda tympani, taste fibers are suitable for the sublingual and mandibular glands.

When the trigeminal ganglion is involved in the process, all types of sensitivity suffer. This is usually characterized by excruciating pain and the appearance of herpes zoster on the face.

When the nucleus n. is involved in the pathological process. trigeminus, located in spinal tract, the clinic is accompanied by dissociated anesthesia or hypoesthesia. In case of partial damage, segmental annular zones of anesthesia are noted, known in medicine under the name of the scientist who discovered them “ Zelder zones"(see diagram). When the upper parts of the nucleus are affected, sensation around the mouth and nose is impaired; lower - outer areas of the face. Processes in the nucleus are usually not accompanied by pain.

6th pair of cranial nerves - abducens (n. abducens)

Abducens nerve (n. abducens) - motor. The nerve nucleus is located in the inferior part of the pons, under the floor of the fourth ventricle, lateral and dorsal to the dorsal longitudinal fasciculus.

Damage to the 3rd, 4th and 6th pairs of cranial nerves causes total ophthalmoplegia. When all the muscles of the eye are paralyzed, external ophthalmoplegia.

The defeat of the above pairs, as a rule, is peripheral.

Innervation of gaze

Without the cooperative functioning of several components muscular apparatus it would be impossible to move the eyes eyeballs. The main formation, thanks to which the eye can move, is the dorsal longitudinal fasciculus longitudinalis, which is a system that connects the 3rd, 4th and 6th cranial nerves with each other and with other analyzers. Cells of the nucleus of the dorsal longitudinal fasciculus (Darkshevich) are located in the legs big brain lateral to the cerebral aqueduct, on the dorsal surface in the area of ​​the posterior commissure of the brain and frenulum. The fibers are directed down along the cerebral aqueduct to the rhomboid fossa and on their way approach the cells of the nuclei of 3, 4 and 6 pairs, communicating between them and the coordinated function of the eye muscles. The dorsal bundle includes fibers from the cells of the vestibular nucleus (Deiters), which form ascending and descending paths. The first ones contact the cells of the nuclei of 3, 4 and 6 pairs, the descending branches stretch down, pass in the composition, which end at the cells of the anterior horns, forming the tractus vestibulospinalis. The cortical center that regulates voluntary gaze movements is located in the middle frontal gyrus. The exact path of the conductors from the cortex is unknown; apparently, they go to the opposite side to the nuclei of the dorsal longitudinal fasciculus, then along the dorsal fasciculus to the nuclei of the named nerves.

Through the vestibular nuclei, the dorsal longitudinal fasciculus is connected with the vestibular apparatus and the cerebellum, as well as with the extrapyramidal part of the nervous system, and through the tractus vestibulospinalis with the spinal cord.

7th pair of cranial nerves - facial (n. facialis)

N. facialis

A diagram of the topography of the facial nerve is presented above.

Intermediate nerve (n. intermedius)

Paralysis of facial muscles:
a - central;
b - peripheral.

The intermediate nerve is inherently part of the facial nerve.

When the facial nerve, or more precisely its motor roots, is damaged, peripheral paralysis of the facial muscles is noted. The central type of paralysis is a rare phenomenon and is observed when the pathological focus is localized in, in particular in the precentral gyrus. The differences between the two types of facial muscle paralysis are presented in the figure above.

8th pair of cranial nerves - vestibulocochlearis (n. vestibulocochlearis)

The vestibulocochlear nerve anatomically has two roots with completely different functional abilities (this is reflected in the name of the 8th pair):

1. pars cochlearis, performing an auditory function;
2. pars vestibularis, performing the function of a static feeling.

Pars cochlearis

Other names for the root: “inferior cochlear” or “cochlear part”.

Differences between cranial nerves and spinal nerves:

1. Cranial nerves start from the brain.

2. Cranial nerves 12 pairs.

3. The sensory part of the cranial nerves has a sensory ganglion.

4. Cranial nerves are divided by function into: sensory, motor and mixed.

I, II, VIII – sensitive;

IV, VI, XI, XII – motor;

III, V, VII, IX, X – mixed.

I pair of cranial nerves– n.n. olfactorii begin from receptors located in the regio olfactoria of the nasal mucosa with nerve filaments (fila olfactoria). Fila olfactoria pass through the openings of the lamina cribrosa and end in the olfactory bulbs, continuing into the olfactory tracts, which go to the subcortical and cortical olfactory centers.

II pair of cranial nerves– n. opticus. Receptors are located on the retina (rods and cones, bipolar and ganglion cells), fibers from these cells form the optic nerve (n. opticus), the medial fibers of which cross (chiasma opticus) in the sulcus chiasmatis on the body sphenoid bone. After the chiasm, the optic tract (tractus opticus) is formed, which is directed to subcortical centers vision (colliculi superiores of the roof of the midbrain, corpus geniculatum laterale, pulvinar thalami). From the colliculi superiores the tractus tecto-spinalis goes to the motor nuclei of the anterior horns of the spinal cord, providing motor, protective, unconditional reflex responses to strong visual stimuli. From the corpus geniculatum laterale, pulvinar thalami, impulses go to the cortical centers of vision, which are the occipital lobes of the hemispheres around the calcarine sulcus (sulcus calcarinus).

III pair of cranial nerves– oculomotor nerve (n. oculomotorius).

It has 2 nuclei: motor and parasympathetic.

The nuclei are located in the tegmentum of the midbrain. The nerve exits the brain along the medial edge of the cerebral peduncles. The function of the nerve is mixed, as it contains motor and parasympathetic fibers. Through the fissura orbitalis superior it enters the orbit and is divided into 2 branches:

The upper one is ramus superior and the lower one is ramus inferior. Ramus superior innervates: m. rectus superior, m. levator palpebrae superiores. Ramus inferior innervates: m. rectus inferior, m. rectus medialis, m. obliqus inferior.

Parasympathetic fibers as part of the lower branch reach the parasympathetic ciliary ganglion, which is located in the orbit (ganglion ciliare), postganglionic fibers emerge from the ganglion, which innervate m. sphincter pupillae, m. ciliaris.

IV pair – trochlear nerve(n. trochlearis). Has one motor nucleus – n. motorius, which is located in the tegmentum of the midbrain at the level of the inferior colliculi. It leaves the brain going around the lateral side of the cerebral peduncle. Through fissura orbitalis superior it passes into the orbit and innervates m. obliqus superior of the eyeball.

VI pair – abducens nerve (n. abducens). It has one motor nucleus, which is embedded in the thickness of the facial tubercles on the dorsal surface of the pons. Through fissura orbitalis superior it passes into the orbit and innervates m. rectus lateralis of the eyeball.

V pair – trigeminal nerve (n. trigeminus). It has three sensory nuclei and one motor nucleus. The nuclei are located in the pons, and one sensitive one is in the tegmentum of the midbrain. The nerve is mixed in function, as it contains sensory and motor fibers. The fibers of the motor nucleus form the motor root - radix motoria. The sensitive part of the nerve has a ganglion - ganglion trigeminale. This ganglion contains the bodies of sensory cells. The central processes of these cells connect to the sensory nuclei of the nerve and form a sensory root - radix sensoria. And the peripheral processes are part of the branches of the trigeminal nerve.

After the trigeminal ganglion trigeminal nerve gives off three branches:

1. First branch – optic nerve (n. ophthalmicus).

2. Second branch - maxillary nerve (n. maxillaris).

3. Third branch - mandibular nerve (n. mandibularis).

The first two branches are sensitive in function, and the third branch is mixed, as it contains sensory and motor fibers.

Each of the three branches gives off sensory branches to the dura mater.

Optic nerve (n. ophthalmicus) through the fissura orbitalis superior it enters the orbit and gives off branches:

· N. frontalis leaves the orbit through the incisura supraorbitalis and continues into n. supraorbitalis and innervates the skin of the upper eyelid and forehead from the eye section.

· N. lacrimalis – sensitive innervation of the lacrimal gland, skin and conjunctiva of the lateral corner of the eye.

N. nasociliaris gives away branches:

N. ciliaris longi – sensitive innervation of the membranes of the eyeball.

N. ethmoidalis anterior et posterior pass through the canals of the same name into the nasal cavity and innervate the mucous membrane of the nasal cavity.

N. infratrochlearis innervates the skin and conjunctiva of the medial corner of the eye.

Maxillary nerve(n. maxillaris) goes through foramen rotundum into the pterygopalatine fossa, then through the lower orbital fissure into the orbit and passes into the canalis infraorbitalis, Foramen infraorbitale on the anterior surface of the upper jaw. In the orbit n. maxillaris changes its name, it is called the infraorbital nerve (n. infraorbitalis), which innervates the skin of the lower eyelid, external nose and upper lip.

N. maxillaris in the pterygopalatine fossa gives away branches:

· n. zygomaticus enters the orbit through the inferior orbital fissure (fissura orbitalis inferior), exits through the foramen infraorbitalis, zygomaticofacialis et zygomaticotemporalis and innervates the skin of the cheek and temporal region.

· n.n. The alveolares superiores in the thickness of the upper jaw form a plexus (plexus dentalis superior), from which the rami dentalis superior extends to the teeth of the upper jaw and the rami gingivalis superior to the gums of the upper jaw.

· sensitive branches through the foramen sphenopalatinum to the mucous membrane of the nasal cavity.

· sensitive branches through the canalis palatinus major to the mucous membrane of the hard and soft palate.

· r.r. ganglionares - sensitive branches to the pterygopalatine parasympathetic ganglion, which lies in the fossa of the same name.

Mandibular nerve (n. mandibularis) exits the skull through foramen ovale on the outer base of the skull and gives away branches:

1. Motor - r.r. musculares innervate all masticatory muscles, m. mylohyoideus of the neck and venter anterior m. digastricus, as well as m. tensor veli palatini et m. tensoris tympani.

2. Sensitive:

· N. buccalis – innervates the buccal mucosa.

· N. lingualis – innervates the mucous membrane of the anterior 2/3 of the tongue to the sulcus terminalis.

· N. alveolaris inferior passes into the canal lower jaw, forms a plexus (plexus dentalis inferior), from which the rami dentalis inferior to the teeth of the lower jaw and the rami gingivalis inferior to the gums of the lower jaw emerge, as well as the final branch - n. mentalis, which exits through the foramen mentale and innervates the skin of the lower lip and chin from the lip incision.

· N. auriculotemporalis accompanies a. temporalis superficialis and innervates the skin of the temporal region, auricle and external auditory canal.

VII pair - facial nerve (n. facialis). Has three cores:

1. Motor – n. motorius.

2. Sensitive – n. solitarius.

3. Parasympathetic – n. salivatorius superior.

The nuclei are embedded in the bridge. The nerve exits the brain between the pons and the medulla oblongata. The function of the nerve is mixed, as it has motor, sensory and parasympathetic fibers. Sensitive and parasympathetic fibers form n. intermedius, which is part of n. facialis. N. facialis and n. intermedius go into the canal of the facial nerve, exit the canal through the foramen stylomastoideum.

N. facialis in the canal gives off a branch – n. stapedius, which innervates m. stapedius

N. intermedius gives off two branches in the canal:

N. petrosus major (parasympathetic in function) leaves the canal of the facial nerve through the hiatus canalis nervi petrosi majoris, passes in the groove of the same name, then through the foramen lacerum of the skull it exits to the outer base of the skull, then through the canalis pterigoideus it passes into the pterygopalatine fossa and ends in the pterygopalatine parasympathetic ganglia (ganglion pterygopalatinum). Postganglionic parasympathetic fibers emerge from the ganglion, some of which are part of n. zygomaticus (branch of n. maxillaris) into the orbit through the inferior orbital fissure and innervates lacrimal gland. The second part of the fibers is n.n. nasales posteriores through the foramen sphenopalatinum go into the nasal cavity and innervate the glands of the nasal mucosa. Third part n.n. palatini through the canalis palatinus major go into the oral cavity and innervate the glands of the mucous membrane of the hard, soft palate, and cheeks.

Сhorda tympani - the chorda tympani contains sensory and parasympathetic fibers. The chorda tympani leaves the skull through the fissura petrotympanica; sensory fibers innervate the taste buds of the anterior 2/3 of the tongue. Parasympathetic fibers go to the submandibular parasympathetic ganglion (ganglion submandibulare), which are located on the diaphragm of the mouth, ending in it, postganglionic fibers are part of n. lingualis (branch of n. mandibularis from n. trigeminus) to the sublingual and submandibular salivary gland.

After leaving the channel n. facialis gives off only muscular branches:

· N. auricularis posterior – innervates m. auricularis posterior et venter occipitalis m. epicranius.

· Ramus digastricus innervates the posterior abdomen of m. digastricus and m. stylohioideus.

· Branches to facial muscles: rami temporalis; r. zygomatici; r. buccales; r. marginalis mandibulae (marginal mandibular); r. colli innervates m. platysma of the neck.

Sensitive part n. intermedius has a ganglion of the knee (ganglion geniculi) in the canal. N. intermedius forms parasympathetic fibers that emerge from the parasympathetic nucleus and peripheral processes of ganglion geniculi cells. The central processes of this ganglion connect to the sensitive nucleus.

Neurology and neurosurgery Evgeniy Ivanovich Gusev

4.1. Cranial nerves

4.1. Cranial nerves

In formation clinical symptom complex When any cranial nerve is damaged, not only its peripheral structures, which in the anatomical sense represent the cranial nerve, are involved, but also other formations in brain stem, in the subcortical region. cerebral hemispheres, including certain areas of the cerebral cortex.

For medical practice, it is important to determine the area in which the pathological process is located - from the nerve itself to its cortical representation. In this regard, we can talk about a system that ensures the function of the cranial nerve.

Among the 12 pairs of cranial nerves, three pairs are only sensory (I, II, VIII), five pairs are motor (III, IV, VI, XI, XII) and four pairs are mixed (V, VII, IX, X). The III, V, VII, IX, X pairs contain a large number of vegetative fibers. Sensitive fibers are also present in the XII pair.

The sensory nerve system is a homologue of the segmental sensitivity of other parts of the body, providing proprio- and extraceptive sensitivity. The motor nerve system is part of the pyramidal corticomuscular tract. In this regard, the sensory nerve system, like the system that provides sensitivity to any part of the body, consists of a chain of three neurons, and the motor nerve system, like the corticospinal tract, consists of two neurons.

Olfactory nerves – nn. olfactorii (I pair). Structurally, the first pair of cranial nerves is not homologous to the other nerves, since it is formed as a result of protrusion of the wall brain bladder. It is part of the olfactory system, which consists of three neurons. The first neurons are bipolar cells located in the mucous membrane of the upper part of the nasal cavity. The unmyelinated processes of these cells form about 20 branches on each side (olfactory filaments), which pass through the cribriform plate of the ethmoid bone and enter the olfactory bulb. These threads are the actual olfactory nerves. The second neurons are myelinated processes of the cells of the olfactory bulb, forming the olfactory tract and ending in the primary olfactory cortex (periamygdala and prepiriform areas), mainly in the lateral olfactory gyrus and in the amygdala (corpus amygdaloideum). The third neurons are neurons of the primary olfactory cortex, the axons of which end in the anterior part of the parahippocampal gyrus (entorhinal area, area 28). This is the cortical area of ​​the projection fields and the associative zone of the olfactory system. It should be borne in mind that third neurons are connected to the cortical projection fields of both their own and the opposite side; the transition of part of the fibers to the other side occurs through the anterior commissure. This commissure connects both olfactory areas and the temporal lobes of both cerebral hemispheres, and also provides communication with the limbic system.

The olfactory system is connected through the medial fasciculus forebrain and the medullary striae of the thalamus with the hypothalamus, the autonomic zones of the reticular formation, with the salivary nuclei and the dorsal nucleus of the vagus nerve. Connections of the olfactory system with the thalamus, hypothalamus and limbic system provide the accompaniment of olfactory sensations with emotions.

Research methodology The state of smell is characterized by the ability to perceive odors of varying intensity by each half of the nose separately and identify (recognize) different odors. With calm breathing and closed eyes, a finger is pressed against the wing of the nose on one side and the odorous substance is gradually brought closer to the other nostril. It is best to use familiar non-irritating odors (volatile oils): laundry soap, rose water (or cologne), bitter almond water (or valerian drops), camphor. The use of irritating substances such as ammonia or vinegar, since this simultaneously causes irritation of the endings of the trigeminal nerve. It is noted whether odors are correctly identified. In this case, it is necessary to keep in mind whether the nasal passages are clear or whether there is catarrhal discharge from the nose. Although the subject may be unable to name the substance being tested, the mere awareness of the presence of the odor rules out anosmia (lack of smell).

Symptoms of defeat. Impaired perception of smell - anosmia (lack of sense of smell). Bilateral anosmia is usually observed with a viral infection affecting the upper respiratory tract, rhinitis. Unilateral anosmia may be of diagnostic value for brain lesions such as a tumor of the base of the frontal lobe.

Hyperosmia– an increased sense of smell is noted in some forms of hysteria and sometimes in cocaine addicts.

Parosmia– a perverted sense of smell is observed in some cases of schizophrenia, damage to the uncus of the parahippocampal gyrus and in hysteria.

Olfactory hallucinations in the form of odors are observed in some psychoses and in epileptic seizures, which are caused by damage to the uncus of the parahippocampal gyrus.

The olfactory nerve may serve as a portal of entry for cryptogenic infections of the brain and meningeal membranes, such as polio, epidemic meningitis and encephalitis. Impaired sense of smell can be caused by inflammatory and other damage to the nasal cavity, fracture of the bones of the anterior cranial fossa, tumors of the frontal lobes and the pituitary gland, meningitis, hydrocephalus, post-traumatic cerebral syndrome, atherosclerosis, cerebral stroke, certain drug intoxications, psychoses, neuroses and birth defects. Specific syndromes involving the olfactory nerve include Foster-Kennedy syndrome and epileptic aura (an olfactory sensation that is a precursor to a seizure).

Optic nerve – n. opticus (II pair). It is formed from the axons of multipolar retinal cells, which reach the external geniculate body, as well as from central fibers, which are feedback elements.

Myelinated ganglion cell processes form the optic nerve. It enters the cranial cavity through the optic canal, runs along the base of the brain and anterior to the sella turcica forms the optic chiasma (chiasma opticum), where the nerve fibers from the nasal half of the retina of each eye intersect, the nerve fibers from the temporal half of the retina of each eye remain uncrossed. After the chiasm, the visual pathways are called optic tracts. They are formed from nerve fibers from the same halves of the retina of both eyes.

Subsequently, the optic tracts rise upward from the base, bending around the outside of the cerebral peduncles, and approach the external geniculate bodies, the superior colliculi of the roof of the midbrain and the pretectal region.

The main part of the fibers of the optic tract enters the external geniculate body. The axons of its neurons, having formed the optic radiation, end in the cortex of the medial surface of the occipital lobe along the calcarine groove (field 17).

The central connections of the optic nerve are as follows:

– from the pretectal region to the small cell accessory nuclei (Edinger-Westphal) through the posterior commissure;

– from the superior colliculi through the tectobulbar and tectospinal tracts to other cranial and spinal nuclei;

– from the occipital region of the cortex to other cortical and subcortical areas.

Fibers from the pretectal region provide a direct and responsive response to light. Fibers from the superior colliculus are responsible for involuntary oculoskeletal reflexes. The pretectal region is associated with light reflexes, and the superior colliculus is associated with eye and head movements in response to visual stimulation.

Associative and reflex fibers pass from the occipital region of the cortex to other cortical centers (associated with higher functions, such as reading, speech) and to the superior colliculus and, as a result, through the tectobulbar and tectospinal tracts are sent to the cranial and spinal nuclei to provide involuntary reflexes (for example, accommodation ) and to the pontine nuclei via the corticopontine pathway to provide postural reflexes.

The space that is perceived by the retina of the eye is called the visual field. The field of view is divided into 4 parts: external and internal, upper and lower. The optical system of the eye is similar to a camera lens: the image of the objects in question on the retina is reversed. Therefore, the outer (temporal) halves of the visual fields are projected onto the inner (nasal) halves of the retina of both eyes, the inner (nasal) halves of the visual fields are projected onto the outer (temporal) halves of the retina of both eyes , and the right halves of the visual fields are perceived by the left halves of the retina and vice versa. In the optic nerve, optic tract, and optic radiation, the fibers are arranged in a retinotopic order; the same order is maintained in the cortical visual field. Thus, fibers from the upper fields of the retina go to the upper parts of the nerve and tract; fibers from the lower fields of the retina - in the lower sections. As a result of the peculiarities of the optic chiasm, fibers pass through the optic tract not from one eye, as in the optic nerve, but from the same halves of the retina of both eyes: for example, in the left optic tract from both left halves of the retina. Thus, the optic tracts, the external geniculate bodies, the optic radiation, and the cortical territories in the area of ​​the calcarine sulcus (sulcus calcaneus) are connected with the same halves (of their side) of the retina of both eyes, but with the opposite halves of the visual fields, since the refractive media The eyes project the reverse image of what is visible onto the retina.

Research methodology. To judge the state of vision, it is necessary to examine visual acuity, visual field, color perception and fundus.

Determination of visual acuity is carried out using special tables on which there are 10 rows of letters or other signs of decreasing value. The subject is placed at a distance of 5 m from the table and names the symbols on it, starting from the largest and gradually moving to the smallest. Each eye is examined separately. Visual acuity (visus) is equal to one if the smallest letters are distinguished on the table (10th row); in those cases when only the largest ones are distinguished (1st row), visual acuity is 0.1, etc. Near vision is determined using standard text tables or maps. Finger counting, finger movements, and light perception are noted in patients with significant visual impairment.

The field of view is examined using perimeters of different designs (white and red, less often green and blue). Normal boundaries fields of vision for white color: upper – 60°, internal – 60°, lower -70°, external – 90°; for red, 40, 40, 40, 50°, respectively. The result of the research is depicted on special maps.

Often in seriously ill patients it is necessary to resort to an approximate determination of visual fields. The person conducting the examination sits in front of the patient (if possible, the patient is also seated, but always with his back to the light source) and asks him to close his eye with his palm, without pressing on the eyeball. The patient's other eye should be open and his gaze fixed on the bridge of the examiner's nose. The patient is asked to report when he sees a hammer or finger of the examiner's hand, which he draws along an imaginary line of the perimeter of a circle, the center of which is the patient's eye. When examining the external visual field, the examiner's hand movement begins at the level of the patient's ear. Continuing to move his fingers along the perimeter of the circle, the examiner directs his hand to the inner field of vision and asks the patient whether he sees it clearly all the time. The internal field of vision is examined in a similar way, but with the help of the examiner's other hand. To examine the upper boundary of the visual field, the hand is placed above the scalp and guided along the perimeter from top to bottom. Finally, lower limit determined by moving the hand from below forward and upward.

For an indicative study, the patient is asked to indicate with his finger the middle of a towel, rope or stick. If there is no visual field impairment, then the patient correctly divides the entire length of the object approximately in half. If there is a limited field of vision, the patient divides approximately 3/4 of the object in half, due to the fact that about 1/4 of its length falls out of the field of view. Studying the blink reflex helps to identify hemianopsia. If you suddenly bring the hand of the person being examined to the side of the eye with a visual field defect (hemianopia), then blinking will not occur.

The study of color perception is carried out using special polychromatic tables, on which, using spots different color numbers, figures, etc. are depicted. Use colored threads, fibers or fabrics.

Examination of the fundus is carried out with an ophthalmoscope.

Symptoms of the lesion. In case of defeat visual pathway The following disorders are observed.

Decreased visual acuity – amblyopia(amblyopia).

Complete loss of vision - amaurosis(amaurosis).

Limited visual field defect that does not reach its boundaries – scotoma(scotoma). Pathological scotomas occur with lesions of the retina, the choroid itself, visual pathways and centers. There are positive and negative scotomas. Positive (subjective) scotomas are those defects in the visual field that the patient himself sees in the form of a dark spot covering part of the object in question. The presence of a positive scotoma indicates damage to the inner layers of the retina or the vitreous just in front of the retina. Negative scotomas the patient does not notice, they are detected only during visual field examination (perimetry, campimetry). Typically, such scotomas occur when the optic nerve is damaged. In this case, visual perception is absent or weakened. Based on topography, central, paracentral and peripheral scotomas are distinguished. Bilateral scotomas located in the same or opposite halves of the visual field are called hemianopic or hemiscotomas. With small focal lesions of the visual pathways in the area of ​​the optic chiasm, heteronymous (opposite) bitemporal, less often binasal, scotomas are observed. When a small pathological focus is localized above the optic chiasm (optic radiation, subcortical and cortical visual centers), homonymous (unilateral) paracentral or central hemianoptic scotomas develop on the side opposite to the localization of the pathological focus.

Loss of half of the visual field – hemianopsia. When the homonymous (both right or both left) halves of the visual fields of each eye are lost, they speak of homonymous, i.e. the same name hemianopsia. When both internal (nasal) or both external (temporal) halves of the visual fields fall out, then such hemianopsia is called heteronomous, i.e. heteronymous. Loss of the outer (temporal) halves of the visual fields is referred to as bitemporal hemianopsia, and the loss of the inner (nasal) halves of the visual fields as binasal hemianopsia.

Marked color vision disorder, fundus changes, change in pupillary reactions.

Visual hallucinations– simple (photopsies - in the form of spots, colored highlights, stars, stripes, flashes) and complex (in the form of figures, faces, animals, flowers, scenes).

Visual disorders depend on the localization of the process in various areas visual path.

If the optic nerve is damaged, i.e. area from the retina to the chiasm, decreased vision or amaurosis of the corresponding eye develops with the loss of the direct reaction of the pupil to light. The pupil constricts when illuminated healthy eye, i.e. the friendly reaction was preserved. Damage to only part of the nerve fibers manifests as scotomas. Atrophy of the macular (i.e., coming from the macula) fibers causes blanching of the temporal half of the optic nerve head, which can be combined with deterioration of central vision while maintaining peripheral vision. Damage to the peripheral fibers of the optic nerve (periaxial nerve injury) leads to a narrowing of the field of peripheral vision while maintaining visual acuity. Complete damage to the nerve, leading to its atrophy, is accompanied by blanching of the entire optic nerve head.

There are primary and secondary optic atrophy. In this case, the optic disc becomes light pink, white or gray. Primary atrophy of the optic disc is caused by processes that directly involve the optic nerve (tumor, intoxication with methyl alcohol, lead, tabes dorsalis). Secondary optic nerve atrophy is a consequence of papilledema due to glaucoma, increased intracranial pressure due to a brain tumor, abscess, hemorrhage, and arterial hypertension. It should be borne in mind that intraocular diseases (retinitis, cataracts, corneal damage, atherosclerotic changes in the retina, etc.) may also be accompanied by a decrease in visual acuity.

When the chiasm is completely damaged, bilateral amaurosis occurs. If the central part of the chiasm is affected, i.e. that part in which the crossover of visual fibers occurs, for example, with a tumor of the cerebral appendage, craniopharyngioma, meningioma of the tubercle of the sella turcica, the fibers that originate from the inner (nasal) halves of the retina of both eyes will fall out, accordingly the outer (temporal) fields of vision will fall out, i.e. .e. for the right eye the right half is lost, for the left eye the left half of the visual field is lost, and clinically there will be different hemianopsia. Since the temporal fields of vision disappear, such hemianopia is called bitemporal. When the outer parts of the chiasm are damaged (for example, with aneurysm of the carotid arteries), fibers coming from the outer halves of the retina, which correspond to the internal (nasal) fields of vision, fall out and a different name bilateral nasal hemianopsia clinically develops.

If the optic tract is damaged, i.e. area from the chiasm to the subcortical visual centers, the same hemianopsia clinically develops, only half of the visual fields opposite the affected visual tract are lost. Thus, damage to the left optic tract will cause the outer half of the retina of the left eye and the inner half of the retina of the right eye to become unresponsive to light, resulting in loss of the right halves of the visual fields. This disorder is called right-sided hemianopsia. When the optic tract is damaged on the right, the left halves of the visual fields fall out - the same name left-sided hemianopsia.

Hemianopsia of the same name occurs not only with damage to the optic tract, but also with damage to the optic radiance (Graziole radiance) and the cortical visual center (sulcus calcarinus)

To recognize the location of damage to the visual pathway in hemianopia, the reaction of the pupils to light is important. If, with hemianopsia of the same name, there is no reaction to light from the switched-off halves of the retina (the study is carried out using a slit lamp), then damage to the optic tract is located in the area of ​​the optic tract.

If the light reflex of the pupils is not impaired, then the lesion is localized in the area of ​​Graziole radiance, because it no longer contains pupillary fibers, which, before the optic tract enters the external geniculate body, are separated, forming the medial pupillary-sensitive bundle, which is directed to the superior colliculi of the roof of the midbrain and the nuclei of the pretegmental zone. With tractus hemianopsia, significant asymmetry of visual field defects is noted due to the characteristics of the course of crossed and uncrossed fibers and their uneven involvement in the process with partial damage to the optic tract, as well as a positive central scotoma due to macular vision disorders– involvement in the process of the papillomacular bundle passing through the tract.

Lesions of the external geniculate body are characterized by homonymous hemianopia of opposite visual fields.

Damage to the optic radiance causes homonymous hemianopia on the contralateral side of the lesion. Hemianopsia can be complete, but most often it is incomplete due to the widespread distribution of radiant fibers. The optic radiation fibers are located in contact only at the exit from the external geniculate body. After passing the isthmus temporal lobe they fan out, located in the white matter of the temporal lobe near the outer wall of the inferior and posterior horn lateral ventricle. Therefore, with damage to the temporal lobe, there may be quadrant loss of visual fields, in particular, superior quadrant hemianopsia due to the passage of the lower part of the optic radiation fibers through the temporal lobe.

When the cortical visual center is damaged in the occipital lobe, in the area of ​​the calcarine sulcus (sulcus calcarinus), symptoms of both loss (hemianopia or quadrant loss of the visual field) and irritation (photopsia - sensations of luminous dots, lightning, luminous rings, fiery surfaces, the appearance of broken lines, etc.) in opposite fields of view. They can occur when there is a violation cerebral circulation, with ophthalmic migraine, tumors, inflammatory processes. A lesion in the area of ​​the calcarine groove causes homonymous hemianopia on the side opposite to the lesion; the visual field defect forms a characteristic notch corresponding to the preservation of macular vision. Damage to individual parts of the occipital lobe (the wedge or the lingual gyrus) is accompanied by quadrant hemianopia on the opposite side: the lower - when the wedge is damaged and the upper - when the lingual gyrus is damaged.

Oculomotor nerve – n. oculomotoris (III pair). The oculomotor nerve is a mixed nerve.

Cores oculomotor nerves consist of five cell groups: two external motor large cell nuclei, two small cell nuclei and one internal, unpaired, small cell nucleus.

The motor nuclei of the oculomotor nerves are located anterior to the central gray matter surrounding the aqueduct, and the autonomic nuclei are located within the central gray matter. They receive impulses from the cortex of the lower part of the precentral gyrus. These impulses are transmitted through the cortical-nuclear pathways passing in the knee of the internal capsule. All nuclei receive innervation from both hemispheres of the cerebrum.

The motor nuclei innervate the external muscles of the eye: the superior rectus muscle (upward and inward movement of the eyeball); inferior rectus muscle (movement of the eyeball downward and inward); medial rectus muscle (inward movement of the eyeball); inferior oblique muscle (movement of the eyeball upward and outward); muscle that lifts the upper eyelid.

In each nucleus, neurons responsible for specific muscles form columns.

Two small cell accessory nuclei of Yakubovich–Edinger–Westphal give rise to parasympathetic fibers that innervate internal muscles eyes: the muscle that constricts the pupil (m. sphincter pupillae), and the ciliary muscle (m. ciliaris), which regulates accommodation.

The posterior central unpaired nucleus of Perlia is common to both oculomotor nerves and mediates the convergence of the eyes.

Some axons of motor neurons cross at the level of the nuclei. Together with uncrossed axons and parasympathetic fibers, they bypass the red nuclei and are sent to the medial parts of the cerebral peduncle, where they connect to the oculomotor nerve. The nerve passes between the posterior cerebral and superior cerebellar arteries. On the way to the orbit, it passes through the subarachnoid space of the basal cistern, pierces the upper wall of the cavernous sinus and then follows between the leaves of the outer wall of the cavernous sinus to the upper orbital fissure.

Penetrating into the orbit, the oculomotor nerve divides into 2 branches. Upper branch Innervates the superior rectus muscle and the levator palpebral muscle. The inferior branch innervates the medial rectus, inferior rectus, and inferior oblique muscles. A parasympathetic root departs from the lower branch to the ciliary ganglion, the preganglionic fibers of which switch inside the node to short postganglionic fibers that innervate the ciliary muscle and the sphincter of the pupil.

Symptoms of defeat. Complete damage to the oculomotor nerve is accompanied by a characteristic syndrome.

Ptosis(drooping eyelid) is caused by paralysis of the muscle that lifts the upper eyelid.

Exotropia(strabismus divergens) - a fixed position of the eye with the pupil directed outward and slightly downward due to the action of the unresisting lateral rectus (innervated by the VI pair of cranial nerves) and superior oblique (innervated by the IV pair of cranial nerves) muscles.

Diplopia(double vision) is a subjective phenomenon that is noted in cases where the patient looks with both eyes. In this case, the image of the focused object in both eyes is obtained not on the corresponding, but on different zones of the retina. Double vision of the object in question occurs as a result of deviation of the visual axis of one eye due to muscle weakness due to impaired innervation. In this case, the image of the object in question falls in the correctly fixating eye onto the central fovea of ​​the retina, and with a deviation of the axis, onto the non-central part of the retina. In this case, the visual image, in association with habitual spatial relationships, is projected into the place in space where the object should be located in order to cause irritation of this particular part of the retina, given the correct position of the visual axis of this eye. A distinction is made between homonymous diplopia, in which the second (imaginary) image is projected towards the deviated eye, and opposite (crossed) diplopia, when the image is projected towards the opposite side.

Midriaz(pupil dilation) with lack of pupillary response to light and accommodation. Reflex arc pupillary reflex to light: afferent fibers as part of the optic nerve and optic tract, the medial bundle of the latter, heading to the superior colliculi of the midbrain roof and ending in the nucleus of the pretectal region. Interneurons associated with the accessory nucleus of both sides ensure synchrony of pupillary reflexes to light: light falling on one eye also causes constriction of the pupil of the other, unlit eye. Efferent fibers from the accessory nucleus, together with the oculomotor nerve, enter the orbit and are interrupted in the ciliary ganglion, the postganglionic fibers of which innervate the muscle that constricts the pupil (m. sphincter pupillae). This reflex does not involve the cerebral cortex. Therefore, damage to the optic radiation and visual cortex does not affect this reflex. Paralysis of the constrictor pupillary muscle occurs when the oculomotor nerve, preganglionic fibers, or ciliary ganglion are damaged. As a result, the reflex to light disappears and the pupil dilates, as sympathetic innervation is preserved. Damage to the afferent fibers in the optic nerve leads to the disappearance of the pupillary reflex to light both on the affected side and on the opposite side, since the conjugation of this reaction is interrupted. If at the same time light falls on the contralateral, unaffected eye, then the pupil reflex to light occurs on both sides.

Paralysis (paresis) of accommodation causes deterioration of vision at close distances. Accommodation of the eye is a change in the refractive power of the eye to adapt to the perception of objects located at different distances from it. Afferent impulses from the retina reach the visual cortex, from which efferent impulses are sent through the pretectal region to the accessory nucleus of the oculomotor nerve. From this nucleus, through the ciliary ganglion, impulses go to the ciliary muscle. Due to the contraction of the ciliary muscle, the ciliary girdle relaxes and the lens acquires a more convex shape, as a result of which the refractive power of the entire lens changes. optical system eyes, and the image of an approaching object is recorded on the retina. When looking into the distance, relaxation of the ciliary muscle leads to flattening of the lens.

Paralysis (paresis) of convergence of the eyes characterized by the inability to rotate the eyeballs inwards. Eye convergence is the bringing together of the visual axes of both eyes when viewing close objects. It is carried out due to the simultaneous contraction of the medial rectus muscles of both eyes; accompanied by constriction of the pupils (miosis) and strain of accommodation. These three reflexes can be caused by voluntary fixation on a nearby object. They also arise involuntarily when a distant object suddenly approaches. Afferent impulses travel from the retina to the visual cortex. From there, efferent impulses are sent through the pretectal region to the posterior central core Perlia. Impulses from this nucleus propagate to neurons innervating both medial rectus muscles (for convergence of the eyeballs).

Limitation of upward, downward and inward movement of the eyeball.

Thus, when the oculomotor nerve is damaged, paralysis of all external eye muscles occurs, except for the lateral rectus muscle, innervated by the abducens nerve (VI pair) and the superior oblique muscle, which receives innervation from the trochlear nerve (IV pair). Paralysis of the internal eye muscles, their parasympathetic part, also occurs. This manifests itself in the absence of a pupillary reflex to light, pupil dilation and disturbances of convergence and accommodation,

Partial damage to the oculomotor nerve causes only part of these symptoms.

Trochlear nerve – n. trochlearis (IV pair). The nuclei of the trochlear nerves are located at the level of the inferior colliculi of the midbrain roof anterior to the central gray matter, below the nuclei of the oculomotor nerve. The internal nerve roots wrap around the outer part of the central gray matter and intersect at the superior medullary velum, which is a thin plate that forms the roof of the rostral part of the fourth ventricle. After the decussation, the nerves leave the midbrain downward from the inferior colliculi. The trochlear nerve is the only nerve emerging from the dorsal surface of the brain stem. On their way in the central direction to the cavernous sinus, the nerves first pass through the coracoid cerebellopontine fissure, then through the notch of the tentorium of the cerebellum, and then along the outer wall of the cavernous sinus, and from there, together with the oculomotor nerve, they enter the orbit through the superior orbital fissure.

Symptoms of defeat. The trochlear nerve innervates the superior oblique muscle, which rotates the eyeball outward and downward. Paralysis of the muscle causes the affected eyeball to deviate upward and somewhat inward. This deviation is especially noticeable when the affected eye looks down and towards the healthy side. There is double vision when looking down; it clearly appears if the patient looks at his feet, in particular when walking up the stairs.

Abducens nerve – n. abductens (VI pair). The nuclei of the abducens nerves are located on both sides of the midline in the tegmentum of the lower part of the pons near the medulla oblongata and under the bottom of the fourth ventricle. The internal genu of the facial nerve passes between the nucleus of the abducens nerve and the fourth ventricle. The fibers of the abducens nerve are directed from the nucleus to the base of the brain and emerge as a trunk at the border of the pons and medulla oblongata at the level of the pyramids. From here, both nerves travel upward through the subarachnoid space on either side of the basilar artery. Then they pass through the subdural space anterior to the clivus, pierce the membrane and join the other oculomotor nerves in the cavernous sinus. Here they are in close contact with the first and second branches of the trigeminal nerve and with the internal carotid artery, which also pass through the cavernous sinus. The nerves are located near the upper lateral parts of the sphenoid and ethmoid sinuses. Next, the abducens nerve goes forward and enters the orbit through the superior orbital fissure and innervates the lateral muscle of the eye, which rotates the eyeball outward.

Symptoms of defeat. When the abducens nerve is damaged, the outward movement of the eyeball is impaired. This happens because the medial rectus muscle is left without an antagonist and the eyeball deviates towards the nose (convergent strabismus - strabismus convergens). In addition, double vision occurs, especially when looking towards the affected muscle.

Damage to any of the nerves that provide movement of the eyeballs is accompanied by double vision, since the image of an object is projected onto different areas of the retina. Movements of the eyeballs in all directions are achieved through the cooperative action of six eye muscles on each side. These movements are always very precisely coordinated because the image is projected mainly only onto the two central fovea of ​​the retina (the place of best vision). None of the eye muscles is innervated independently of the others.

If all three motor nerves of one eye are damaged, it is deprived of all movements, looks straight, its pupil is wide and does not react to light (total ophthalmoplegia). Bilateral ocular muscle palsy usually results from damage to the nerve nuclei.

The most common causes leading to nuclear damage are encephalitis, neurosyphilis, multiple sclerosis, circulatory disorders, hemorrhages and tumors. The most common causes of nerve damage are also meningitis, sinusitis, aneurysm of the internal carotid artery, thrombosis of the cavernous sinus and communicating artery, fractures and tumors of the base of the skull, diabetes, diphtheria, botulism. It should be borne in mind that transient ptosis and diplopia can develop as a result of myasthenia gravis.

Only with bilateral and extensive supranuclear processes extending to central neurons going from both hemispheres to the nuclei can bilateral ophthalmoplegia occur central type, since, by analogy with most motor nuclei of the cranial nerves, the nuclei of the III, IV and VI nerves have bilateral cortical innervation.

Innervation of gaze. Isolated movements of one eye independently of the other are impossible in a healthy person; both eyes always move simultaneously, i.e. a pair of eye muscles always contracts. For example, when looking to the right, the lateral rectus muscle of the right eye (abducens nerve) and the medial rectus muscle of the left eye (oculomotor nerve) are involved. Combined voluntary eye movements in different directions - the gaze function - are provided by the system of the medial longitudinal fasciculus (fasciculus longitudinalis medialis). The fibers of the medial longitudinal fasciculus begin in the nucleus of Darkshevich and in the intermediate nucleus, located in the tegmentum of the midbrain above the nuclei of the oculomotor nerve. From these nuclei, the medial longitudinal fasciculus runs on both sides parallel to the midline from the tegmentum of the midbrain down to the cervical part of the spinal cord. It connects the nuclei of the motor nerves of the eye muscles and receives impulses from the cervical part of the spinal cord (providing innervation to the posterior and anterior muscles of the neck), from the nuclei vestibular nerves, from the reticular formation, which controls the “vision centers” in the pons and midbrain, from the cerebral cortex and basal ganglia.

Movements of the eyeballs can be either voluntary or reflexive, but only friendly, i.e. conjugate, all the muscles of the eye participate in all movements, either tensing (agonists) or relaxing (antagonists).

The direction of the eyeballs towards the object is carried out arbitrarily. But still, most eye movements occur reflexively. If any object comes into the field of vision, the gaze involuntarily fixes on it. When an object moves, the eyes involuntarily follow it, and the image of the object is focused at the point of best vision on the retina. When we voluntarily look at an object that interests us, our gaze automatically lingers on it, even if we ourselves or the object moves. Thus, voluntary eye movements are based on involuntary reflex movements.

The afferent part of the arc of this reflex is a path from the retina, the visual pathway, to the visual cortex (field 17). From there, impulses enter fields 18 and 19. From these fields, efferent fibers begin, which in the temporal region join the optic radiation, following to the contralateral oculomotor centers of the midbrain and pons. From here the fibers go to the corresponding nuclei of the motor nerves of the eyes, perhaps some of the efferent fibers go directly to the oculomotor centers, the other makes a loop around field 8.

In the anterior part of the midbrain there are special structures of the reticular formation that regulate certain directions of gaze. The interstitial nucleus, located in the posterior wall of the third ventricle, regulates upward movements of the eyeballs, and the nucleus in the posterior commissure regulates downward movements; interstitial nucleus of Cajal and nucleus of Darkshevich – rotational movements.

Horizontal eye movements are provided by the region of the posterior part of the pons, close to the nucleus of the abducens nerve (pontine gaze center).

Innervation of voluntary movements of the eyeballs is carried out mainly by neurons located in the posterior part of the middle frontal gyrus (field 8). From the bark cerebral hemispheres fibers accompany the cortical-nuclear tract on the way to the internal capsule and cerebral peduncles, cross and transmit impulses through the neurons of the reticular formation and the medial longitudinal fasciculus and the nuclei of the III, IV, VI pairs of cranial nerves. Thanks to this congenial innervation, a combined rotation of the eyeballs occurs upward, sideways, and downward.

In case of defeat cortical center gaze (cerebral infarction, hemorrhage) or the frontal oculomotor tract (in the corona radiata, anterior limb of the internal capsule, cerebral peduncle, anterior part of the tegmentum of the bridge), the patient cannot voluntarily move the eyeballs to the side opposite to the lesion, while they are turned to the side pathological focus (the patient “looks” at the focus and “turns away” from the paralyzed limbs). This occurs due to the dominance of the corresponding zone on the opposite side, manifested by friendly movements of the eyeballs towards the lesion.

Irritation of the cortical center of gaze is manifested by a friendly movement of the eyeballs in the opposite direction (the patient “turns away” from the source of irritation). Sometimes the movements of the eyeballs are accompanied by turns of the head in the opposite direction. With bilateral damage to the frontal cortex or frontal oculomotor tract as a result of cerebral atherosclerosis, progressive supranuclear degeneration, corticostriopallidal degeneration, voluntary movements of the eyeballs are lost.

Damage to the pontine center of gaze in the area of ​​the posterior part of the pontine tegmentum, close to the nucleus of the abducens nerve (with thrombosis of the basilar artery, multiple sclerosis, hemorrhagic polioencephalitis, encephalitis, glioma), leads to paresis (or paralysis) of gaze towards the pathological focus. In this case, the eyeballs are reflexively turned in the direction opposite to the lesion (the patient turns away from the lesion, and if the path of voluntary movements is involved in the process, he looks at the paralyzed limbs). So, for example, when the right pontine gaze center is destroyed, the influences of the left pontine gaze center prevail and the patient’s eyeballs turn to the left.

Damage (compression) of the tegmentum of the midbrain at the level of the superior colliculus (tumor, cerebrovascular accident, secondary upper brainstem syndrome with increased intracranial pressure, as well as hemorrhages and infarctions in the cerebral hemispheres, less often - with encephalitis, hemorrhagic polioencephalitis, neurosyphilis, multiple sclerosis) causes upward gaze paralysis. Downward gaze paralysis is less common. When the lesion is located in the cerebral hemisphere, gaze paralysis is not as long-lasting as when the lesion is localized in the brainstem.

When the occipital areas are affected, reflex eye movements disappear. The patient can make voluntary eye movements in any direction, but he cannot follow an object. The object immediately disappears from the field of best vision and is found again using voluntary eye movements.

When the medial longitudinal fasciculus is damaged, internuclear ophthalmoplegia occurs. With unilateral damage to the medial longitudinal fasciculus, the innervation of the ipsilateral (located on the same side) medial rectus muscle is disrupted, and monoocular nystagmus occurs in the contralateral eyeball. At the same time, muscle contraction in response to convergence is maintained. Due to the fact that the medial longitudinal fascicles are located close to each other, the same pathological focus can affect both fascicles. In this case, the eyes cannot be brought inward with horizontal gaze abduction. Monocular nystagmus occurs in the dominant eye. The remaining movements of the eyeballs and the reaction of the pupils are preserved. The cause of unilateral internuclear ophthalmoplegia is usually vascular disease. Bilateral internuclear ophthalmoplegia is commonly seen in multiple sclerosis.

Research methodology. The study of all three pairs (III, IV, VI) of the oculomotor nerves is carried out simultaneously. The patient is asked if there is double vision. The following are determined: the width of the palpebral fissures, the position of the eyeballs, the shape and size of the pupils, pupillary reactions, the range of movements of the upper eyelid and eyeballs.

Double vision (diplopia) is a sign that is sometimes more subtle than an objectively determined deficiency of one or another external eye muscle. When complaining of diplopia, it is necessary to find out which muscle (or nerve) is affected by this disorder. Diplopia occurs or worsens when looking towards the affected muscle. Insufficiency of the lateral and medial rectus muscles causes diplopia in the horizontal plane, and in other muscles - in the vertical or oblique planes.

The width of the palpebral fissures is determined: narrowing with ptosis of the upper eyelid (unilateral, bilateral, symmetrical, asymmetrical); extension palpebral fissure due to elevation of the upper eyelid. Possible changes in the position of the eyeballs are observed: exophthalmos (unilateral, bilateral, symmetrical, asymmetrical), enophthalmos, strabismus (unilateral, bilateral, converging or diverging horizontally, diverging vertically - Hertwig-Magendie symptom), increasing when looking in one of the directions.

Pay attention to the shape of the pupils (regular - round, irregular - oval, unevenly elongated, multifaceted or scalloped - “corroded” contours); on the size of the pupils: 1) miosis - moderate (narrowing up to 2 mm), pronounced (up to 1 mm), 2) mydriasis - slight (dilation up to 4-5 mm), moderate (6-7 mm), pronounced (over 8 mm ), 3) difference in pupil size (anisocoria). Anisocoria and deformation of the pupils, sometimes immediately noticeable, do not always prove the presence of a lesion n. oculomotoris (possible congenital features, consequences of eye injury or inflammation, asymmetry of sympathetic innervation, etc.).

It is important to study the reaction of the pupils to light. Both direct and conjugate reactions of each pupil are checked separately. The patient's face is turned towards the light source, the eyes are open; the examiner, first tightly covering both eyes of the subject with his palms, quickly removes one of his hands, thus observing the direct reaction of a given pupil to light; The other eye is also examined. Normally, the reaction of the pupils to light is lively - with a physiological value of 3-3.5 mm, darkening leads to dilation of the pupil to 4-5 mm, and lighting leads to a narrowing to 1.5-2 mm. To detect a friendly reaction, one eye of the subject is closed with the palm of his hand; in a different open eye pupil dilation is observed; when the hand is removed from the closed eye, a simultaneous concomitant constriction of the pupils occurs in both. The same is done for the other eye. A pocket flashlight is convenient for studying light reactions.

To study convergence, the doctor asks the patient to look at the hammer, which is moved 50 cm away from the patient and located in the middle. When the hammer approaches the patient’s nose, the eyeballs converge and are held in the position of reduction at the fixation point at a distance of 3-5 cm from the nose. The reaction of the pupils to convergence is assessed by the change in their size as the eyeballs come closer together. Normally, there is a constriction of the pupils, reaching a sufficient degree at a distance of 10-15 cm from the fixation point. The study of the reaction of the pupils to accommodation is carried out as follows: one eye of the patient is closed, and the other is asked to alternately fix the gaze on far and close objects, assessing the change in the size of the pupil . Normally, when looking into the distance, the pupil dilates; when looking at a nearby object, it narrows.

To assess the movements of the eyeball, the subject is asked, without moving his head, to follow with his gaze a finger or hammer moving up, down, right and left, and a restriction in the movements of the eyeball inward, outward, up, down, up and out, down and out can be detected. (paralysis or paresis of any external muscle), as well as the absence or limitation of voluntary friendly movements eyeballs left, right, up, down (paralysis or paresis of gaze).

From the book Neurology and Neurosurgery author Evgeniy Ivanovich Gusev

Chapter 4 Cranial nerves. Main lesion syndromes

From the book Speech Pathologist's Handbook author Author unknown - Medicine

4.1. Cranial nerves In the formation of the clinical symptom complex when any cranial nerve is damaged, not only its peripheral structures, which in an anatomical sense represent the cranial nerve, but also other formations in the brain stem, take part.

From the book Computer and Health author Nadezhda Vasilievna Balovsyak

CRANIAL NERVES DIRECTLY PARTICIPATED IN SPEECH FORMATION N. glossopharyngeus is a mixed nerve related to somatic and autonomic innervation. It contains motor, sensory, gustatory and secretory fibers; respectively has 4 cores,

From the book To make life a joy. Wellness tips for those over 50 author Larisa Vladimirovna Alekseeva

From book Nervous diseases: lecture notes author A. A. Drozdov

Take care of your nerves A person’s dependence on the weather is determined, in addition to meteodependence, by such a concept as meteoneurosis. “As soon as I see that it’s raining outside the window, my mood immediately spoils, everything falls out of hand,” is the most common statement in this case.

From the book Dictionary medical terms author author unknown

LECTURE No. 4. Cranial nerves. Symptoms of their damage 1. I pair of cranial nerves - olfactory nerve The pathway of the olfactory nerve consists of three neurons. The first neuron has two types of processes: dendrites and axons. The endings of the dendrites form the olfactory receptors,

From the book Five Steps to Immortality author Boris Vasilievich Bolotov

Nerves (nervi) 880. Abducens (PNA, BNA, JNA), abducens nerve - VI pair of cranial nerves; origin: abducens nerve nucleus; innervates the lateral rectus muscle of the eyeball.881. Accessorius (PNA, BNA, JNA; Willisii), accessory nerve - XI pair of cranial nerves - beginning: nucleus ambiguus and accessory nerve nucleus;

From the book Gymnastics while driving by I. A. Lebedev

Optic nerves Night blindness (weakened vision at dusk), strabismus, head tilt, dilated pupils, hallucinations, negativity of evening vision. Source plant material: celandine, sedum, eyebright, hairy hawksbill, night blindness, galangal,

From the book Metals that are always with you author Efim Davidovich Terletsky

Taste nerves Loss of taste, taste hallucinations. Source plant material: pepper, coriander, cumin, mountain lavender, horseradish, parsley, dill, nutmeg, bay tree (leaf), flax, carrots (seeds), poppy (seeds), hemp (seeds), mustard, rowan, onion,

From the book Knee Pain. How to restore joint mobility author Irina Aleksandrovna Zaitseva

Auditory nerves Stuttering, noise in the head, habit of repeating what was said. The noises of the forest and stream seem to be human speech. Source plant material: hiccup, arnica, cocklebur (not required), peony, mandrake, poppy, hemp, tobacco, shag, ephedra, nightshade, tomatoes,

From the book Healing Spices. Spices. Seasonings. From 100 diseases author Victoria Karpukhina

Olfactory nerves Odors are detected where there are none; numerous sneezes. Source plant material: nightshade, oregano, yarrow, bay tree, dill, fennel, pine, wormwood (emshan), currant (leaves), lilac (flowers), jasmine (flowers), elderberry

From the book Atlas: human anatomy and physiology. Complete practical guide author Elena Yurievna Zigalova

Take care of your nerves from a young age Explain that psychological and nervous load When driving a car, they often exceed the physical load unnecessarily. This, as they say, is understandable to a baby. Remember how you released bile in a traffic jam or wiped cold sweat from the forehead, slowing down at

From the author's book

From the author's book

Nerves The main nerve in the knee area is the popliteal nerve, which is located on the back surface knee joint. It is a component of the sciatic nerve, passes through the lower leg and foot and provides sensitivity and movement of data

From the author's book

Brain and nerves There are spices that reduce nervous excitement and improve brain activity! The nervous system is perfectly calmed medicinal herbs. Who among us does not know about valerian or mint tea? Mint spice, breath freshening, almost

From the author's book

Spinal nerves There are 31 pairs of spinal nerves formed from roots extending from the spinal cord: 8 cervical (C), 12 thoracic (Th), 5 lumbar (L), 5 sacral (S) and 1 coccygeal (Co). Spinal nerves correspond to segments of the spinal cord and are therefore designated