Vestibulocochlear nerve, symptoms of damage. Anatomy of the vestibulocochlear nerve: location and functions of the pharyngeal nerve, its branches, their anatomy, topography, areas of innervation

21.7. Neuralgia of the cranial and spinal nerves Neuralgia is a lesion of the peripheral segment of a nerve (branch or root), manifested by symptoms of irritation. If neuropathies are characterized by symptoms of loss of nerve function, neuralgia is characterized by symptoms of irritation.

50. Damage to the 1st and 2nd pairs of cranial nerves. Pathway olfactory nerve consists of three neurons. The first neuron has two types of processes: dendrites and axons. The endings of the dendrites form olfactory receptors located in the mucous membrane of the nasal cavity.

54. Damage to the VIII pair of cranial nerves When the fibers of the VIII pair of cranial nerves of the auditory cochlear nuclei are damaged, there is no impairment of hearing function. When the nerve is damaged at various levels, auditory hallucinations, symptoms of irritation, hearing loss,

55. Lesions of the IX–X pairs of cranial nerves IX–X pairs of cranial nerves are mixed. The sensitive nerve pathway is three-neural. The bodies of the first neuron are located in the nodes glossopharyngeal nerve. Their dendrites end in receptors in the posterior third of the tongue, the soft

56. Lesions of the XI–XII pair of cranial nerves. It consists of two parts: the vagus and the spinal nerves. The motor pathway is two-neuron. The first neuron is located in the lower part of the precentral gyrus. Its axons enter the cerebral peduncle, pons, oblongata

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 olfactory receptors located in the mucous membrane of the cavity

2. II pair of cranial nerves - optic nerve The first three conductive neurons visual pathway located in the retina of the eye. The first neuron is represented by rods and cones. Second neurons are bipolar cells. Ganglion cells are third neurons.

3. III pair of cranial nerves - oculomotor nerve The nerve pathway is two-neuron. The central neuron is located in the cells of the cortex of the precentral gyrus of the brain. The axons of the first neurons form a cortical-nuclear path leading to the nuclei

4. IV pair of cranial nerves - trochlear nerve The pathway is two-neuron. The central neuron is located in the cortex of the lower part of the precentral gyrus. The axons of the central neurons end in the cells of the nucleus of the trochlear nerve on both sides. The nucleus is located in

5. V pair of cranial nerves – trigeminal nerve It is mixed. The sensory pathway of a nerve consists of neurons. The first neuron is located in the semilunar ganglion of the trigeminal nerve, located between the layers of the dura mater on the anterior surface

6. VI pair of cranial nerves – abducens nerve The pathway is two-neuron. The central neuron is located in lower section precentral gyrus cortex. Their axons end on the cells of the nucleus of the abducens nerve on both sides, which are peripheral

7. VII pair of cranial nerves - facial nerve It 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. Axons of central neurons are directed to the nucleus of the facial

9. IX pair of cranial nerves - glossopharyngeal nerve This nerve is mixed. The sensory nerve pathway is three-neuron. The cell bodies of the first neuron are located in the ganglia of the glossopharyngeal nerve. Their dendrites end in receptors in the posterior third of the tongue, the soft

10. X pair of cranial nerves - vagus nerve It is mixed. The sensitive pathway is three-neuron. The first neurons form the nodes of the vagus nerve. Their dendrites end with receptors on the hard meninges rear cranial fossa,

11. XI pair of cranial nerves - accessory nerve It consists of two parts: the vagus and the spinal nerve. The motor pathway is two-neuron. The first neuron is located in the lower part of the precentral gyrus. Its axons enter the cerebral peduncle, pons,

12. XII pair of cranial nerves - hypoglossal nerve For the most part, the nerve is motor, but it also contains a small part of the sensory fibers of the lingual nerve branch. The motor pathway is two-neuron. The central neuron is located in the inferior cortex

YIII - COHLEO-VESTIBULAR NERVE

This pair combines two functionally different sensory nerves: auditory and vestibular (the organ of hearing and the organ of balance).

Auditory nerve, having the organ of Corti (ganglion) located in the cochlea of ​​the labyrinth. The primary auditory centers are the nuclei of the inferior colliculi and the internal geniculate bodies. The cortical auditory area is middle section superior temporal gyrus (Heschl's gyrus).

Damage options:

• Decreased hearing acuity - hypacusia,
• hearing loss - surditism or anakusia,
• worsening of hearing - hyperacusis.
• Can be auditory hallucinations- with irritation of the temporal lobe, and with irritation of the organ of Corti of the auditory nerve, a sensation of noise, squeaking, grinding in the ear may occur.
• Damage to the “auditory cortex” can lead to auditory agnosia.

Vestibular nerve has a vestibular ganglion located in the semicircular canals. The axons of its cells form fibers of the vestibular nerve, which end in 4 nuclei located in the brain stem: Bekhterev, Schwalbe, Deiters and Roller. From these nuclei, axons are directed to their own and the opposite side, as well as to the cerebellum, nuclei of the vagus nerve, to spinal cord, to the oculomotor nerves (III, IV, VI). The cortical section is the parietotemporal region. The vestibular apparatus regulates the position of the head, torso and limbs in space.

• In case of defeat vestibular apparatus observed: dizziness- it seems to the patient that all objects around him are rotating in a certain direction, clockwise or counterclockwise, and the earth is shaking. This kind of dizziness is called systemic. It intensifies when looking up or sharply turning the head. Against this background, there may be nausea And vomit; nystagmus- rhythmic twitching of the eyeballs; impaired coordination of movements- staggering.

Causes of damage to the facial nerve:

1) Iatrogenic damage (removal of tumors of the cerebellopontine angle, surgery on the hearing organs, interventions on the parotid region and face) 2) Trauma (injuries of the skull and brain, accompanied by fractures of the bones of the base of the skull, wounds of the neck and face) 3) Inflammatory lesions (neuritis and otogenic damage)

Symptoms of facial nerve damage

With complete conduction disorder syndrome, atrophy and paralysis of the facial muscles of the corresponding half of the face develop. There is a pronounced asymmetry of the facial muscles at rest, there is a smoothness of wrinkles on the affected side of the face, and the acts of chewing and swallowing are disturbed. There is no movement of the lower eyelid, tear production is impaired. On the damaged side, when pronouncing consonants and puffing out the cheeks, the cheek oscillates like a sail (“parusitis”), liquid food pours out of the corner of the mouth.

Partial conduction disorder syndrome is manifested by paresis of the facial muscles of the corresponding half of the face. Other signs are present to one degree or another.

Most of the instrumental examination methods actively used in previous decades (rheoencephalography, study of muscle electrical excitability and the intensity-duration curve, skin thermometry, etc.) have now sunk into oblivion. Currently relevant are EMG and MRI.

Treatment of facial nerve lesions

In case of partial conduction disturbance, conservative treatment is carried out, which is prescribed by a doctor specializing in the pathology of peripheral nerves. The set of measures includes injections of corticosteroids, massage, exercise therapy, electrical stimulation of muscles, taking B vitamins, and drugs that improve microcirculation. Personally, I am not a proponent of acupuncture; I believe that as a result of the use of acupuncture, early contracture of the facial muscles develops (I emphasize that this is my value judgment).

The presence of complete conduction disorder syndrome in a patient for 3-4 months is a reason for surgical treatment. The decision to operate here is made purely individually, based on the nature of the pathology and the dynamics of the disease.

Operations can be divided into several groups:

1) operations on the intracranial part of the facial nerve (decompression of the nerve in the fallopian canal). 2) operations on the extracranial part (nerve suture, nerve autoplasty, nerve neurolysis). 3) reinnervation of the facial nerve, if it is impossible to restore the integrity of the trunk. 4)plastic surgery to correct a cosmetic defect.

28 Syndromes of lesions of the vestibulocochlear nerve.

vestibulocochlear nerve- (VIII pair of cranial nerves) a nerve of special sensitivity, responsible for the transmission of auditory impulses, as well as impulses emanating from the vestibular part of the inner ear.

The vestibular-cochlear nerve is a nerve of special sensitivity, consisting of two roots of different functions: the vestibular root, which carries impulses from the static apparatus, represented by the semicircular ducts of the vestibular labyrinth, and the cochlear root, which carries auditory impulses from the spiral organ of the cochlear labyrinth.

When the cochlear part is damaged, there is a decrease in hearing or the occurrence of deafness on the affected side, sometimes an exacerbation of hearing, the appearance of a sensation of extraneous sounds (noise, whistle, hum, crackling, etc.), and when the cortical hearing analyzers are irritated, auditory hallucinations occur.

Damage to the vestibule is accompanied by systemic dizziness, nystagmus (involuntary high-frequency oscillatory eye movements) and ataxia (impaired coordination of movements of various muscles in the absence of muscle weakness). Dizziness depends on the position of the head and body. Sometimes it is paroxysmal in nature. Ataxia is general and often worsens when the eyes are closed. The patient has an unsteady gait, a violation of coordination tests, positive test Romberg (standing position with feet together, with eyes closed and arms extended straight in front of you.)

To whom is dedicated a large number of works IN last years in connection with the development of radiation and other imaging technologies tumor formations pyramid of the temporal bone and the cerebellopontine angle, as well as video and microsurgical methods, the problem of neuroma of the vestibulocochlear nerve became extremely difficult at the beginning of the 20th century. in our time has become solvable.

By the middle of the last century, neuroma of the vestibulocochlear nerve in relation to brain tumors was 9%, in relation to tumors of the posterior cranial fossa - 23%, while tumors of the posterior cranial fossa in relation to all brain tumors were 35%, in At the same time, neuromas of the vestibulocochlear nerve accounted for 94.6% of tumors of the lateral cistern of the brain. The disease is most often diagnosed at the age of 25-50 years, but can occur in children and the elderly. In women, neuroma of the vestibulocochlear nerve is twice as common.

Pathogenesis of neuroma of the vestibulocochlear nerve

Neuroma of the vestibulocochlear nerve is a benign encapsulated tumor that primarily develops in the internal auditory canal from the neurolemma of the vestibular nerve with further growth in the direction of the cerebellopontine angle. During the growth process, the tumor fills the entire space of the lateral cistern of the brain, significantly stretching and thinning the CN of the cerebellopontine angle (vestibular-cochlear, facial, intermediate and trigeminal) located on its surface, which leads to trophic disorders in these nerves and morphological changes, disrupting their conductivity and distorting the functions of the organs they innervate. Filling the entire internal auditory canal, the tumor compresses the internal auditory artery, which supplies the structures of the inner ear, and when it enters the area of ​​the cerebellopontine angle, it puts pressure on the arteries supplying the cerebellum and brainstem. By exerting pressure on the bone walls of the internal auditory canal, the tumor causes their resorption, which leads to an x-ray sign of its expansion, and upon entering the area of ​​the apex of the pyramid, its destruction, after which the tumor rushes into the cerebellopontine angle, without experiencing anything in its free space. mechanical obstacles, no lack of nutrients. This is where its rapid growth begins.

Large tumors are displaced and compressed medulla, pons, cerebellum, causing the corresponding neurological disorders caused by damage to the nuclei of the cranial nerves, vital centers and their pathways. Small tumors (2-3 mm) with a long development cycle can be asymptomatic and discovered incidentally during biopsy. Such cases, according to B.G. Egorov et al. (1960), amounted to up to 1.5% in the last century. In 3% of cases, bilateral tumors are observed; They usually occur with widespread neurofibromatosis (Recklinghausen's disease). Gardner-Turner syndrome, which occurs with hereditary bilateral neuroma of the vestibulocochlear nerve, should be distinguished from this disease.

Symptoms of neuroma of the vestibulocochlear nerve

Classic division clinical forms Neuromas of the vestibulocochlear nerve into four periods do not always correspond to the chronological sequence of the appearing signs characteristic of these periods. And although in most cases clinical manifestations Neuromas of the vestibulocochlear nerve are directly dependent on the growth rate of the tumor and its size; atypical cases may also occur when ear symptoms(noise, hearing loss, dizziness) can be observed with small tumors, and vice versa, when the neurological signs that arise when the tumor enters the cerebellopontine angle appear without otiatric symptoms of neuroma of the vestibulocochlear nerve.

There are four clinical period development of neuroma of the vestibulocochlear nerve.

Otiatric period

During this period, the tumor is located in the internal auditory canal and the symptoms of neuroma of the vestibulocochlear nerve caused by it are determined by the degree of compression of the nerve trunks and vessels. Usually, the first signs of impairment of auditory and gustatory functions appear (tinnitus, perceptual hearing loss without FUNG). At this stage vestibular symptoms less constant, but it is possible that they go unnoticed due to the fact that they are quickly leveled out by the mechanism of central compensation. However, with a bithermal caloric test using videonystagmography at this stage, it is often possible to establish a sign of asymmetry in the labyrinth within 15% or more, indicating depression of the vestibular apparatus on the affected side. At the same stage, in the presence of dizziness, spontaneous nystagmus can be recorded, directed first towards the “sick” ear (irritation due to hypoxia of the labyrinth), then towards the “healthy” ear due to compression of the vestibular portion of the vestibular-cochlear nerve. At this stage, OKN, as a rule, is not disturbed.

Sometimes in the otiatric period, Meniere-like attacks can be observed, which can imitate Meniere's disease or vertebrogenic labyrinthopathy.

Otoneurological period

A characteristic feature of this period, along with a sharp increase in otiatric symptoms caused by damage to the vestibular-cochlear nerve, is the appearance of signs of compression of other cranial nerves located in the cerebellopontine angle due to the release of the tumor into its space. Usually this stage occurs 1-2 years after the otiatric stage; it is characterized by x-ray changes in the internal auditory canal and the apex of the pyramid. Severe hearing loss or deafness in one ear, severe noise in the ear and the corresponding half of the head, ataxia, impaired coordination of movements, deviation of the body towards the affected ear in the Romberg position are also characteristic. Attacks of dizziness, which are accompanied by spontaneous nystagmus, become more frequent and intensified. If the tumor size is significant, gravitational positional nystagmus appears when the head is tilted to the healthy side, due to the displacement of the tumor towards the brain stem.

During this period, dysfunction of other cranial nerves arises and progresses. Thus, the effect of a tumor on the trigeminal nerve causes paresthesia on the corresponding half of the face (Barre's symptom), trismus or paresis of the masticatory muscles on the side of the tumor (Christiansen's symptom). At the same time, there is a symptom of a decrease or disappearance of the corneal reflex on the same side. At this stage, dysfunction of the facial nerve is manifested only by paresis, most pronounced for its lower branch.

Neurological period

During this period, otiatric disorders recede into the background, and they begin to occupy a dominant position. neurological symptoms Neuromas of the vestibulocochlear nerve, caused by damage to the nerves of the cerebellopontine angle and tumor pressure on the trunk, pons and cerebellum. These signs include paralysis of the oculomotor nerves, trigeminal pain, loss of all types of sensitivity and corneal reflex on the corresponding half of the face, decrease or loss of taste sensitivity on the posterior third of the tongue (damage to the glossopharyngeal nerve), paresis of the recurrent nerve (vocal fold) on the side of the tumor (damage vagus nerve), paresis of the sternocleidomastoid and trapezius muscles (damage to the accessory nerve) - all on the side of the tumor. At this stage, the vestibular-cerebellar syndrome is pronounced, manifested by gross ataxia, multidirectional large-scale, often undulating nystagmus, ending with gaze paresis, and pronounced autonomic disturbances. On the fundus - congestion on both sides, signs of increased intracranial pressure.

Terminal period

With further growth of the tumor, cysts filled with yellowish liquid form in it; the tumor enlarges and puts pressure on vital centers - respiratory and vasomotor, compresses the cerebrospinal fluid pathways, which increases intracranial pressure and causes swelling of the brain. Death occurs from blockade of vital centers of the brain stem - cessation of breathing and cardiac activity.

IN modern conditions the third and fourth stages of neuroma of the vestibular-cochlear nerve are practically never encountered; existing methods diagnostics with appropriate oncological alertness of the doctor to whom the patient turns with complaints about the appearance of constant noise in one ear, decreased hearing in it, dizziness, provides for the implementation of appropriate diagnostic techniques to determine the origin of these complaints.

Diagnosis of neuroma of the vestibulocochlear nerve

Diagnosis of neuroma of the vestibulocochlear nerve is difficult only in the otiatric stage, in which in most cases there are no radiological changes in the internal auditory canal, at the same time such a patient may have radiological changes in the cervical spine, especially since, according to A .D Abdelhalima (2004, 2005), every second person, starting from the age of 22, experiences initial radiological signs cervical osteochondrosis and complaints, often similar to subjective feelings arising from neuroma of the vestibulocochlear nerve. Starting from the otoneurological (second) stage, a tumor of the internal auditory canal is practically detected in all cases, especially when using such highly informative methods as CT and MRI.

X-ray projections such as the Stenvers, Highway III, and transorbital projections with visualization of the pyramids of the temporal bone also have a fairly high information content.