Tumors of the lateral cistern of the pons (cerebellopontine angle). Damage to the organs of vision due to brain tumors Features of surgery to remove a tumor of the cerebellopontine angle

The X-ray method of examination is especially important for diagnosing tumors of the cerebellopontine angle, i.e., the space limited by the posterior surface of the pyramids of the temporal bones, the bottom of the posterior cranial fossa, the cerebellar tentorium and the pons. In the area of ​​the cerebellopontine angle, pathological processes of two types can occur: tumors and inflammatory changes in the membranes (arachnoiditis).

Arachnoiditis in the area of ​​the cerebellopontine angle is not detected by X-ray examination methods. When diagnosing tumors of this localization, the x-ray method is the leading one.

Initially, the tumor causes irritation of the auditory nerve; patients note noise in the ear, squeaking, and ringing. Then the hearing in that ear gradually decreases. As the tumor grows in the internal auditory canal, it also compresses the facial nerve, which leads to asymmetry in the innervation of the facial muscles. Subsequently, the tumor emerges from the pyramid at the base of the skull and compresses the cerebellum and brain stem.

Depending on the direction of tumor growth, compression and displacement of the brain stem, one or another neurological symptoms develop. Wedged into the lateral cistern of the bridge, the tumor displaces and stretches the cranial nerves passing here and compresses the vessels. In the late stage, due to compression of the cerebrospinal fluid ducts, general cerebral symptoms occur.

The clinical picture of neuroma of the VIII pair is sometimes very similar to arachnoiditis of the cerebellopontine angle and multiple sclerosis. In such cases, x-ray examination of the pyramids of the temporal bones is crucial. The internal auditory canal is most often evenly expanded, its walls remain parallel to each other, but there may be a spindle-shaped and flask-shaped expansion. Changes in the internal auditory canal can be detected on direct radiographs of the skull with a projection of the pyramids into the orbits.

Upon exiting the internal auditory canal, the tumor can put pressure on the pyramid of the temporal bone, which is manifested by osteoporosis and destruction of its apex. The spread of the tumor posteriorly along the bottom of the posterior cranial fossa can lead to destruction of the edges of the corresponding jugular foramen. Growing forward along the Blumenbach slope can cause destruction of the dorsum sella and its anterior inclination.

In addition to images with the projection of the pyramids into the orbits and Stenvers images, a posterior semi-axial Altschul image and an image of the base of the skull can be used. But changes are especially clearly visible on tomograms. Tomograms are performed in a posterior viewing position at depths of 7, 8 and 9 cm. The tomograms clearly show changes in the petrous part of the pyramid, the bottom of the posterior cranial fossa and the edges of the jugular foramen.

Acoustic neuromas can be bilateral. Bilateral damage is observed in Recklinghausen's neurofibromatosis. Clinical diagnosis of bilateral tumors is difficult. In addition to damage to the auditory nerves, Recklinghausen's disease reveals small tumor-like nodules under the skin, and other cranial nerves and spinal roots are often affected. X-rays reveal bilateral destruction of the pyramids of the temporal bones. In addition to acoustic neuromas, other tumors can occur in the area of ​​the cerebellopontine angle - sarcomas of the skull base, gastrointestinal tumors, cholesteatomas, arachnoidal lotelioma of the Blumenbach clivus, and others. However, they are much less common. All these tumors can cause destructive changes in the pyramids of the temporal bones and adjacent parts of the bones of the base of the skull. Summarizing the section on craniographic changes in brain tumors, it should be emphasized that this method cannot detect tumors of any location or histological structure. The leading methods of X-ray diagnosis of brain tumors are contrast studies of the cerebrospinal fluid tract and blood vessels.

The pontocerebellar angle is the depression between the pons, medulla oblongata, and cerebellum. This area is often affected by neoplasms that compress the nerves, blood vessels and cerebrospinal fluid pathways passing there. The urgency of the issue of removing tumors of the cerebellopontine angle is due to the impossibility of treating them with modern radiosurgical methods, including a gamma knife and a linear accelerator. Thus, the method in this case is surgical treatment, which in turn requires adequate anesthesia and technical equipment.

I, Gavrilov Anton Grigorievich, neurosurgeon at the N. N. Burdenko Research Institute of Neurosurgery, have 20 years of practical experience, including the removal of tumors of the cerebellopontine angle. My clinical base (the aforementioned research institute) allows for complex interventions: high-tech equipment in operating rooms in combination with a well-coordinated team of anesthesiologists and resuscitators is an essential condition for achieving an optimal result.

Types of tumors of the cerebellopontine angle

Approximately every tenth brain tumor develops in the cerebellopontine angle. At the same time, the most common tumor localized in this area is neuroma of the vestibulocochlear nerve - it accounts for 85–95%. Meningiomas and cholesteatomas of the cerebellopontine angle are much less common.

In most cases, neuroma of the vestibulocochlear nerve is benign. Most often it develops in people of working age, usually women. Removal of tumors of the cerebellopontine ganglion can be either unilateral or bilateral.

Clinical picture

Timely removal of tumors of the cerebellopontine angle is complicated by the slow development of the disease without severe clinical manifestations. The patient may experience noise in one ear for several months or even years (so-called cochleovestibular syndrome). Then comes a period when the signs of the disease become more pronounced (deafness, facial nerve paresis). In most cases, diagnosis and then removal of tumors of the cerebellopontine angle are carried out precisely at this stage.

Other consistently occurring symptoms of the disease include:

• headaches;
• loss of corneal and conjunctival reflexes;
• cerebellar phenomena - unilateral hemiataxia and general cerebellar ataxia, adiadochokinesia, unsteady gait, decreased muscle tone, dizziness;
• paralysis of limbs.

Features of surgery to remove a tumor of the cerebellopontine angle

Removal of the tumor of the cerebellopontine angle is carried out surgically. Before surgery, patients of this profile undergo general clinical and neurootological examination, CT and MRI. According to indications, myo- and angiography and neuropsychological testing are prescribed.

Removal of a tumor of the cerebellopontine angle is performed using modern methods of endoscopic microsurgery under conditions of constant neurophysiological monitoring (including stimulation and EMG of the facial nerve). After neuroimaging, the doctor develops a surgical plan, determines its volume and the point of best access. The intervention is carried out using high-speed drills and pneumatic drills, which ensure minimal invasiveness and reduce the extent of damage to nearby tissues.

Removal of a tumor of the cerebellopontine angle is carried out under endotracheal anesthesia in a closed circuit using Propofol and inhalational anesthetics (Sevoflurane, Isoflurane). Necessary conditions for the operation, which is performed in a sitting position, are also Doppler ultrasound of the heart and a special surgical table with supports for the surgeon’s hands. During the removal of a tumor of the cerebellopontine angle, it is possible to perform a rapid analysis of the removed fragment of the tumor with subsequent correction of the course of the operation.

The final result of surgical intervention is determined by the characteristics of tumor growth, the degree of damage to the base of the skull, and its fusion with neurovascular structures. In most cases, I, together with a team of assistants at the N. N. Burdenko Research Institute of Neurosurgery, manage to solve all the problems facing us.

The cerebellopontine angle is the space between the posterior inner edge of the pyramid, the brainstem and the cerebellum (Fig. 8). Several nerves pass through this area: trigeminal, facial, vestibulocochlear and intermediate.

Accordingly, when certain nerves are damaged, their own specific symptoms are observed. When the trigeminal nerve is damaged, corneal reflexes and sensitivity in the nasal cavity and pharynx are lost.

Damage to the facial and intermediate nerves leads to paresis of the facial muscles and impaired taste.

Rice. 8. Cerebellopontine angle:

1 - brain stem; 2 - posterior inner edge of the pyramid: 3 - trigeminal nerve; 4 - cochlear nerve; 5 - facial and intermediate nerves; 6 - vestibular (vestibular) nerve; 7 - cerebellum

howling sensitivity on the anterior -/w tongue. If the vestibular-cochlear nerve is involved, one-sided deafness or a sharp decrease in hearing, nystagmus and loss of excitability of the labyrinth are characteristic. The syndrome is characteristic of tumors of the cerebellopontine angle - acoustic neuroma, meningioma, neurinoma of the facial nerve and other neoplasms of this area.

A computed tomogram (CT) for cerebellopontine angle syndrome is shown in Fig. 125. adj. With. 238. From the CT scan it follows that the size of the opening of the internal auditory canal on the right is more than 7 mm. The right and left channel apertures are not symmetrical. The posterior wall of the right internal auditory canal has a tortuous surface without signs of bone destruction. A contrast-enhanced tomogram revealed a slowly growing intracanal acoustic neuroma. The tumor pushed aside the dura mater of the posterior cranial fossa and the structures of the cerebellopontine angle space.

1. Cerebellopontine angle syndrome. Etiology. Clinical manifestations.

All pons nerves (5-8) and the cerebellum are involved. All symptoms are on the side of the lesion. Reasons:

— acoustic neuroma - adhesive process about the spinal cord of the pontocerebellar angle

Acoustic neuromas are more common, followed by meningiomas and cholesteatomas. Neuromas grow from the sheath of the vestibular branch of the VIII nerve, ^ ^ but its lesion here is detected only during otoneurological examination; dizziness is rare. Usually the first symptom is hearing loss accompanied by noise. The trigeminal nerve root (decreased corneal reflex, pain, paresthesia in the face) and the Wrisberg nerve (taste disorder in the anterior 2/3 of the tongue) are involved early in the process.

In half of the cases, involvement of the facial nerve was noted (severe damage is rare), as well as the abducens nerve. As the tumor grows. 5u cerebellar, brainstem (nystagmus) and cerebral symptoms are detected. Bilateral neuromas of the VIII nerve occur in neurofibromatosis of Recklinghausen (see). Radiologically determined expansion of the internal auditory canal is of great diagnostic importance.

pyramids of the temporal bone. With meningiomas, general cerebral symptoms appear faster than with neuromas. Cholesteatomas occur as a result of chronic otitis media. With them, unlike neuromas, the VIII nerve suffers little. 3 x - Tumors of the IV ventricle. Ependymomas are more common, choroid papillomas are less common. Intracranial hypertension appears early, headaches are paroxysmal in nature, often accompanied by vomiting and dizziness, impaired cardiovascular activity and breathing. Cerebellar disorders (primarily gait disturbances) are common. Typically forced head position. Of the cranial nerves, the VI and VIII nerves are most often affected, less often the V, VII, IX, and X nerves. Focal symptoms include attacks of hiccups, respiratory and cardiovascular disorders. Attacks of tonic spasms of the muscles of the trunk and limbs are also observed.

Tumors of the trunk are rare. Among the intracerebral ones there are astrocytomas, spongioblastoma multiforme, and among the extracerebral ones there are meningiomas.

2. Damage to the nervous system due to AIDS. Clinical manifestations.

Etiology and pathogenesis. HIV infection is a disease caused by the human immunodeficiency virus. This virus belongs to non-oncogenic human retroviruses, the so-called lentiviruses (slow viruses), the main point of application is the immune system. Viruses have a long incubation period and are capable of persistence in the body. When they enter the body, the helper population of T-lymphocytes is primarily affected. In addition, they have a clear tropism for certain groups of cells - macrophages, monocytes, and neuroglial cells, which causes chronic demyelinating damage to the nerve system. Activation of endogenous - opportunistic flora (herpes virus, yeast-like fungi) and sensitivity to exogenous microbes (mycobacteria, cryptococci, cytomegaloviruses, toxoplasma, etc.) causing secondary damage to various organ systems.

Clinic and diagnostics. Neurological disorders were observed in 1/3 of cases of the disease and usually correspond to stages III (stage of secondary diseases - cerebral form) and IV (terminal stage - specific damage to the central nervous system). In rare cases, during the period of infection, acute viral meningoencephalitis may develop, manifested by epileptic seizures and disturbances of consciousness up to coma. Lymphocytic pleocytosis is detected in the cerebrospinal fluid. The most common syndromes of late damage to the nervous system include AIDS dementia complex, sensory polyneuropathy, or a combination of both. The cause of the AIDS-dementia complex is brain damage in the form of multifocal giant cell encephalitis and progressive diffuse leukoencephalopathy. In the initial stage of the disease, the patient complains of drowsiness, impaired concentration, and memory disorders. Then a slight increase in muscle tone, sucking and grasping reflexes, adiadochokinesis, apathy, indifference to one’s condition, bradykinesia, and tremor are added. In the advanced stage of the disease, against the background of severe dementia, mutism, epileptic seizures, paraplegia, ataxia and dysfunction of the pelvic organs occur. The cerebrospinal fluid shows slight pleocytosis. Computed tomography and magnetic resonance imaging reveal cortical atrophy and ventricular enlargement.

The syndrome of sensory popineuropathy is manifested by pain and paresthesia in the arms and legs of the “gloves” and “socks” type in combination with a decrease or loss of knee reflexes, flaccid paresis and autonomic disorders. At different stages of the disease, multiple mononeuropathies (damages of the trigeminal and facial nerves), as well as muscle lesions in the form of polymyositis and myopathy may occur: Treatment. There is currently no pathogenetic treatment. Zidovudine (200 mg 6 times a day) is used, as well as symptomatic therapy. 3. Osteochondrosis g.o.p.

Osteochondrosis of the spine is a degenerative process that has developed in the intervertebral disc and adjacent vertebrae, which together is called the vertebral movement of the segment of the SDS.

Disk functions; Shock absorption, Fixation, Providing movement. OCP is a dystrophic lesion or change that begins with the nucleus pulposus, spreads to the fibrosis ring and then to other elements of the PDS and often forms a conflict with adjacent neurovascular diseases . Theorem about the origin of acute acute respiratory syndrome: involutional, hormone, vessel, genetic, infectious, mechanical, abnormal, etc. According etiology zab-e multiphacotrial. There are 2 main factors: decompensation in trophic systems and local overload of the PDS. Pathogenesis. Stages: Chondrosis is a process only in the disc. Osteochondrosis is a process in the disc and bone. Periods: 1 period of intradiscal movement of the pulpous tissue. Drying of the nucleus pulposus, the appearance of cracks in the inner part of the fibrosis ring.

2P-od of instability of the PDS. The nucleus pulposus was completely cracked. ZP-od formation of a hernia. 4P-od of disc fibrosis and total changes in other structures.

Fibrosis - immobilization by scar.

Clinic OCP is determined by the level of damage. First of all, these are vertebral syndromes. They are characterized by the following manifestations: pain in the area of ​​the affected part (local pain during movement and movement, limitation of movements, vertebral deformity (scoliosis, smoothing of lordosis/kyphosis), tension of the paravertebral muscles, pain in protruding striae p, spinous processes), cervical lumbago, cervicalgia, thoracalgia, lumbar lumbago (lumbago), lumbodynia (subacute pain in the lower back), sacralgia, coccygia.

Extrovert syndromes are also distinguished; they develop as follows: post afferent impulses from the affected SMS along the sinovertebral nerve, through the posterior horn, spreading to the anterior and lateral horns of the corresponding segment of the spinal cord. At the same time, some patients develop muscle-tonic ones, others develop vasomotor ones, and others develop neurodystrophic ones.

Flow OCP m.b. hron (no complete remissions), recurrent (alternating exacerbations and remissions), hron-recurrent (emergence of a new syndrome or increased clinical manifestations against the background of a slowly occurring disease). Each exacerbation has 3 stages: progression, stationary, regression.

Vertebral syndrome - pain in the affected area of ​​the spine 1 .Local pain during active and passive movements. 2.0limited movement.

Z. Vertebral deformation (scoliosis, flattened lordosis, kyphosis, asymmetry of the transverse processes).

4. Direction of paravertebral muscles. b. Pain in protruding structures affected by the SMS Extravertebral syndrome— presence of symptoms at a distance. Radicular syndrome:

Compression of the root can be caused by a herniated disc, bone growth, hypertrophy of the yellow ligament, cicatricial adhesions in the epidural tissue; -deficiency stage: hyporeflexia, hypotrophy, muscle hypotonia, hypo- and anesthesia in the area of ​​the corresponding dermatome; -irritative stage: reflexes are normal or animated, hyperesthesia. Diag. Clinic + X-ray signs:

Local change in vertebral configuration (flattening of physiological lordosis, appearance of kyphosis, scoliosis) - reduction in the height of the m/n disc

The image of marginal bone growths of “osteophytes” (“whiskers”) - subchondral osteosclerosis

Pathological mobility (spondylopisthesis) is displacement of adjacent vertebral bodies. As well as MRI, CG, ultrasound.

Treatment: exhaustive and adequate information about the disease; high-quality, adequate, timely pain relief; orthopedic regimen in the acute period. First-line analgesics are NSAIDs:

Non-select COX-1 and -2 inhibitors: ibuprofen, diclofenac, naproxen, indomethacin, piroxicam, lornoxicam, ketoprofen, ketorolac

Highly selective COX-1 ingers: low doses of acetylsalicylic acid

Selective agents COX-2: nimesulide, meloxicam

Highly selective ing COX-2: coxibs.

They need to be combined with 1 table. Omeprazole (for the stomach)

Muscle relaxants are used: baclofen, tizanidine, topperisone.

Chondroprotectors: stimulate the production of the main components of cartilage in chondrocytes + help slow down the degeneration of cartilage tissue and restore its structure.

Neck fixation with Shants collar pom. Manual therapy, massage, Acupuncture, physiotherapy. For chronic pain syndrome - antidepressants.

At home: rubs, ointments, applications, herbs, cupping massage, self-massage, needle applicators, reflexology with pepper patch, metal and magnetic therapy.

Surgical treatment Absolute indication: acute compression of the spinal column of the brain and cauda equina roots, relative indication: severity and persistence of the root. syndromes in the absence of effect from adequate conservative therapy carried out for more than 3-4 months. 4 .Pseudobulbar syndrome. Research technique for pseudobulbar syndrome.

Central. Develops with damage to the corticonuclear pathways 9, 10 and 12 pairs of h.n. and manifested (with bilateral lesions): dysarthria, dysphonia, dysphagia and pathological pseudobulbar reflexes (oral automatism - Proboscis reflex. Ankylosing spondylitis oral reflex- Lightly tapping with a hammer on the patient’s upper lip or on his finger placed across the lips causes involuntary protrusion of the lips; Sucking reflex. Oppenheim sucking reflex— Streak irritation of the lips leads to the appearance of sucking movements; Wurpe-Toulouse reflex. Wurpa lip reflex- Involuntary stretching of the lips, reminiscent of a sucking movement, occurring in response to line irritation of the upper lip or its percussion; Oppenheim oral reflex- Line irritation of the lips, except sucking reflex, causes chewing and sometimes swallowing movements; Nasolabial reflex. Astvatsaturova nasolabial reflex - Tapping the back or tip of the nose with a hammer causes contraction of the orbicularis oris muscle and protrusion of the lips; Palmochin reflex. Marinescu-Radovic reflex- Caused by streak irritation of the skin of the palm in the thenar area. In this case, contraction of the mental muscle occurs on the same side. Normally caused in children under 4 years of age; grabbed.), violent crying and laughter

Cerebellopontine angle syndrome neurology

Cerebellopontine angle It is a depression in which the middle peduncle plunges into the substance of the cerebellum. Here, at the base of the middle cerebellar peduncle, the VIII, VII, VI and V cranial nerve roots pass through the lateral cistern of the pons.

Cerebellopontine angle syndrome(lateral pontine cistern syndrome) is a combined lesion of the facial (VII), vestibulocochlear (VIII), trigeminal (V) and abducens (VI) nerves with ipsilateral cerebellar symptoms, as well as often contralateral pyramidal insufficiency.

Given syndrome most often observed with neuromas of the VIII nerve, meningiomas, cystic-adhesive arachnoiditis of the lateral cistern of the pons, space-occupying processes in the cerebellopontine angle.

Ipsilateral clinical symptoms:
- hearing impairment at the level of the sound-receiving apparatus;
- vestibular disorders in the form of non-systemic dizziness, often in combination with ipsilateral nystagmus and vestibular ataxia;
- peripheral paresis of the facial muscles;

Paresis of the external rectus muscle of the eye;
- disorders of all types of sensitivity on the face according to the innervation of the trigeminal nerve or predominantly one of its branches;
- cerebellar disorders in the form of dynamic, but with elements of static ataxia.

Contralateral to the lesion pyramidal insufficiency is often determined, which, as a rule, does not reach the degree of pronounced central hemiparesis.

Cerebellopontine angle syndrome

It appears with neuroma of the cochlear root of the vestibulocochlear nerve, cholesteatomas, hemangiomas, cystic arachnoiditis, leptomeningitis of the cerebellopontine angle, aneurysm of the basilar artery.

Symptoms: hearing loss and tinnitus, dizziness, peripheral paralysis of facial muscles, pain and paresthesia in half of the face, unilateral decrease in taste sensitivity in the anterior 2/3 of the tongue, paresis of the rectus lateral muscle of the eye with convergent strabismus and diplopia on the side of the lesion. When the process affects the brain stem, hemiparesis occurs on the side opposite to the lesion, and cerebellar ataxia on the side of the lesion.

Damage to the cerebellopontine angle. The cerebellopontine angle is topographically divided into three sections: anterior, middle and posterior (Fig. 21). Depending on which department the pathological process is located in; the corresponding syndrome is obtained. Pathological foci located in these sections may belong to the processes of a wide variety of pathological categories (arachnoiditis, abscesses, gummas, tumors of the cerebellum, pons, cranial nerves - neuroma of the trigeminal nerve and the 8th pair, meningeomas, cholesteatomas).

Trigeminal neuromas are observed in the anterior section. In the middle section, neuromas of the 8th pair (tumor of the auditory nerve) most often occur. In the posterior sections there are tumors originating from the substance of the cerebellum and heading to the middle section of the cerebellopontine angle. Not only tumors, but also the above-mentioned formations of a different order can originate in these areas. Since the trunks of the facial and auditory nerves pass through the middle section in almost horizontal and frontal positions, it is clear that pathological foci located in this area will manifest themselves primarily from these cranial nerves.

In general, whatever process develops in the cerebellopontine angle, depending on its location in one of its sections, the auditory nerve root is almost always involved to a greater or lesser extent. Early or late development of the cochlear-vestibular-cerebellar syndrome depends on which parts of the cerebellopontine angle the tumor originally came from: 1) from parts of the rocky bone, 2) from the dura mater of the posterior surface of the pyramid, 3) soft meninges of the same area, 4) cerebellum, 5) medulla oblongata and 6) cranial nerves.

Let us examine in sequential order those diseases that usually nest in the cerebellopontine angle, and focus on the oto-neurological syndrome of these diseases, since this area is a selective site for frequently observed pathological processes.

Diagnosis of diseases of the cerebellopontine angle, as a rule, does not present much difficulty, if only the doctor’s attention is paid to the consistent development of both general and cochlear-vestibular cerebellar syndromes. Meanwhile, as a rule, tumor-like diseases of the 8th pair are still not diagnosed by otolaryngologists, which will be discussed below.

Arachnoiditis. Of the acute diseases of the membranes in the cerebellopontine angle, otogenic lepto-meningitis should be noted in the first place. They are usually caused during the development of acute or chronic purulent labyrinthitis by the transfer of infection from the internal auditory canal to the meninges

Tumors of the cerebellopontine angle. As we have already indicated above, a tumor can come from any part that makes up the designated angle. To illustrate, we present a case in which the tumor originated from the bone formations of the jugular foramen and grew into the cerebellopontine angle.

Tumors of the auditory nerve. Tumor-like diseases of the auditory nerve are of great interest to otolaryngologists, because the first complaints resulting from damage to the 8th pair of nerves (tinnitus, decreased hearing, static disturbances) force patients to seek help from an otolaryngologist

Symptoms Diagnostics. The onset of the disease is characterized by noise in the ear; with bilateral processes, which is extremely rare, noise is noted in both ears, followed by a gradual decrease in hearing until it is lost in the corresponding ear. In rare cases, at the beginning of the disease, in the absence of noise, hearing loss is not noticed for a long time and is discovered by the patient by chance (telephone conversation). Sometimes noise and hearing loss are preceded by a headache. Often patients feel pain in the corresponding ear. In this period of the disease, an objective lesion of the cochlear nerve of a radicular nature is established with an akumetric formula typical for this disease. This latter is expressed as follows. The border of low tones is raised, the border of high tones is relatively better preserved; Weber in the healthy direction and bone conduction is shortened.

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Localization of the pathological process in one half of the brain pons can lead to the development of the following alternating syndromes.

Millard-Hübler syndrome- occurs with a unilateral pathological focus in the lower part of the pons and damage to the nucleus of the facial nerve or its root and the corticospinal tract. On the affected side, peripheral paresis or paralysis of the facial muscles occurs, on the opposite side - central hemiparesis or hemiplegia. It was described in 1856 by the French physician A. Millard (1830-1915) and in 1896 by the German physician A. Gubler (1821-1897).

Foville syndrome- occurs with a unilateral pathological focus in the lower part of the pons of the brain, caused by damage to the nuclei or roots of the facial and abducens nerves, as well as the pyramidal tract and sometimes the medial lemniscus. On the affected side it is manifested by peripheral paresis or paralysis of the facial muscles and the external rectus muscle of the eye; on the opposite side - central hemiparesis or hemiplegia and, possibly, a hemitype disorder of pain and temperature sensitivity. Described in 1858 by the French neurologist A. Foville (1799-1879).

Raymond-Sestan syndrome- occurs with a unilateral pathological focus in the pons due to combined damage to the pontine center of gaze, the middle cerebellar peduncle, the medial lemniscus and the pyramidal tract. Paresis of gaze towards the pathological lesion is noted, on the side of the lesion - hemiataxia; on the opposite side - central hemiparesis or hemiplegia, hemitype disorders of pain and temperature sensitivity. It was described in 1903 by French neurologists F. Raymond (1844-1910) and E. Cestan (1873-1932).

Gasperini syndrome- occurs due to a pathological focus in the bridge tire. It manifests itself as signs of dysfunction of the auditory, facial, abducens and trigeminal nerves on the affected side and a disorder of pain and temperature sensitivity according to the hemitype on the opposite side. Described by the Italian neuropathologist M. Gasperini.

With extracerebral localization of the pathological focus in the cranial cavity, the following syndromes are possible.

Lateral pontine cistern syndrome, or cerebellopontine angle, is a combination of signs of damage to the auditory, facial and trigeminal nerves passing through the lateral pontine cistern. It usually develops with the formation of a pathological process in it, more often with an acoustic neuroma.

Gradenigo syndrome- hearing loss caused by combined damage to the sound-conducting and sound-receiving apparatus of the auditory nerve, in combination with dysfunction of the facial, abducens and trigeminal nerves. It manifests itself as paresis of facial and masticatory muscles, convergent strabismus, diplopia and facial pain. Usually it is a consequence of purulent otitis media, in which the infection penetrates through the apex of the temporal bone pyramid into the cranial cavity, which leads to the formation of limited leptomeningitis with the involvement of these cranial nerves in the process. Described in 1904 by the Italian otorhinolaryngologist G. Gradenigo (1859-1925).

With a unilateral lesion of the so-called pontine center of gaze located in the tegmentum, gaze paresis develops in the direction of the pathological process.

With bilateral damage to the pons, the following syndromes are possible.

Pontine myelinolysis syndrome- bilateral demyelination of mainly efferent pathways at the level of the brain pons: corticospinal (pyramidal), frontopontocerebellar and corticonuclear. It manifests itself as central tetraparesis, signs of pseudobulbar syndrome and cerebellar insufficiency. Characterized by ophthalmoparesis, pupillary disorders, tremor, tonic convulsions, decreased activity of mental processes. Over time, stupor and coma may develop. Occurs due to metabolic disorders during fasting, chronic intoxication (alcoholism, infectious diseases, severe somatic pathology). There is an opinion that pontine myelinolysis can be triggered by excess hydration, leading to severe hyponatremia with edema of brain tissue, which more often occurs in patients with alcoholism, since in them abstinence from alcohol leads to an increase in the level of antidiuretic hormone in the blood and the likelihood of developing hyponatremia with intravenous infusion of fluids and treatment with diuretics is especially high. CT and MRI scans reveal foci of low density in the central part of the pons and in the adjacent parts of the brain stem. The selectivity of damage to the base of the bridge is explained by the peculiarities of its myeloarchitecture.

Dancing eyes syndrome (ocular myoclonus)- hyperkinesis of the eyeballs in the form of friendly, fast, irregular, uneven in amplitude of their movements, performed in the horizontal plane and especially pronounced in the initial stage of fixation of the gaze on an object. Possible when the tegmentum of the pons or midbrain is affected.

Roth-Bielschowsky syndrome (Bielschowsky pseudoophthalmoplegia)- loss of the ability to voluntarily move the eyeballs to the sides while maintaining their reactions to stimulation of the labyrinth, while convergence of the eyes is possible and their movements in the vertical plane are preserved. It occurs as a result of tumor growth or circulatory problems in the trunk tire, and may also be a manifestation of multiple sclerosis. Described in 1901 by Russian neuropathologist V.K. Roth (1848-1916), in 1903 the German neuropathologist M. Bielschowsky (1869-1940).

The main nerves of the cerebellopontine angle are n. facialis (VII nerve) with n. intermedius Wrisbergi (XIII nerve) and n. acusticus (VIII nerve). The same group often includes those emerging in close proximity. abducens (VI nerve) and n. trigeminus (V nerve). During processes in the area of ​​the cerebellopontine angle (for example, with tumors), in addition to the VII and VIII nerves, these nerves are often involved in the process. The VI pair will be considered in the group of oculomotor nerves.

VII pair, n. facialis- motor nerve. Core n. facialis is located quite deep in the lower part of the pons, on its border with the medulla oblongata. Fibers emanating from the cells of the nucleus rise dorsally to the bottom of the rhomboid fossa and bend around the nucleus n located here from above. abducentis (VI nerve), forming the so-called knee (internal) of the facial nerve.

Next, the fibers are directed downwards and emerge as a root at the base between the pons and the medulla oblongata, lateral to the olive, in the cerebellopontine angle (together with the n. intermedius Wrisbergi and n. acusticus), following in the direction of the porus acusticus internus. At the base of the meatus acusticus, the facial and Wrisberg nerves depart from the auditory nerve and enter the canalis facialis Fallopii. Here, in the pyramid of the temporal bone, the VII nerve again forms a knee (external) and finally exits the skull through the foramen stylomastoideum, dividing into a number of terminal branches (“crow's foot”, pes anserinus).

N. facialis is the motor nerve of the facial muscles and innervates all facial muscles (except for the m. levator palpebrae superioris - III nerve), m. digastricus (posterior abdomen), m. stylo-hyoideus and, finally, m. stapedius and m. platysma myoides on the neck. For a considerable distance, the companion of the facial nerve is n. intermedius Wrisbergi, also called the XIII cranial nerve.

This- a mixed nerve, having centripetal sensory, more precisely, taste, and centrifugal secretory salivary fibers. In its significance, it is in many ways identical to the glossopharyngeal nerve, with which it has common nuclei.

Sensitive taste fibers begin from the cells of the ganglion geniculi, located in the genu canalis facialis, in the temporal. bones. They go to the periphery along with n. facialis no fallopian canal and leave the latter as part of the chorda tympani, later they enter the trigeminal nerve system and through r. lingualis n.. trigemini reach the tongue, supplying its anterior two thirds with taste endings (the posterior third is innervated by the glossopharyngeal nerve).

Axons of cells n. intermedii from ganglion geniculi together with n. facialis enter the brain stem at the cerebellopontine angle and end in the “taste” nucleus, the nucleus tractus solitarius, in common with the IX nerve.

“Topical diagnosis of diseases of the nervous system”, A.V.Triumfov

Central paralysis (paresis) of the facial muscles is observed, as a rule, in combination with hemiplegia. Isolated lesions of the facial muscles of the central type are rare and are sometimes observed with damage to the frontal lobe or only the lower part of the anterior central gyrus. It is clear that central paresis of the facial muscles is the result of a supranuclear lesion of the tractus cortico-bulbaris in any part of it (cerebral cortex, corona radiata, capsula...

The following neurons transmitting visual stimuli to the cortex begin only from the corpus geniculatum laterale thalami optici. Fibers from its cells pass through the internal capsule in the posterior part of the hind thigh and, as part of the Graciolet bundle, or radiatio optica, end in the cortical visual areas. These pathways are projected onto the inner surface of the occipital lobes, into the area of ​​fissurae calcarinae (cuneus...

A true auditory nerve that has a ganglion spirale Corti, which is located in the cochlea of ​​the labyrinth. The dendrites of the cells of the named sensitive node are directed to the organ of Corti, to its auditory hair cells. Axons exit the temporal bone into the cranial cavity through the porus acusticus internus and as part of the root n. cochlearis with n. vestibularis, n. facialis and n. intermedius Wrisbergi enter…

PONTOCEREBELLAR ANGLE (angulus cerebellopontinus) - the space where the pons (pons), medulla oblongata and cerebellum meet. M. u. open anteriorly, to the base of the skull, in the region of the posterior cranial fossa (Fig. 1). On the ventral side of M. u. covered by the arachnoid membrane, the edges do not go deep into it, but are located superficially, as a result of which a container for cerebrospinal fluid is formed in this area - the lateral cistern of the bridge (cisterna pontis lat.), often identified in the literature with M. at. in the broad sense of the word. In this case, under M. u. understand a narrow space resembling a flattened irregular pyramid in shape, bounded in front and on the side by the posterior surface of the pyramid of the temporal bone, from the inside by the junction of the pons, medulla oblongata and cerebellum, constituting the apex of the cerebellopontine region, behind by the surface of the cerebellar hemisphere, and above by the tentorium of the cerebellum. In the area of ​​M. u. (Fig. 2) the roots of the V-XI pairs of cranial nerves, the anterior inferior cerebellar and labyrinthine arteries and numerous cerebellar veins flowing into the superior petrosal sinus are located, among which the flocculus vein is distinguished by its constancy.

Pathology

In M. u. patol, processes of both inflammatory and tumor nature develop.

Arachnoiditis M. u. usually develop after an infection, in the acute stage there is pleocytosis in the cerebrospinal fluid, in the chronic stage - the cerebrospinal fluid is normal, there are no changes in the internal auditory canal on radiographs, audiometry reveals bilateral hearing loss, and vestibular excitability often increases (symptom of cochleovestibular scissors); dizziness is common. Arachnoiditis (see) often leads to the formation of arachnoid cysts, which cause symptoms of an inflammatory and compression nature.

Of the neoplasms of M. u. the most common are neuromas of the auditory (vestibular-cochlear, T.) nerve (see vestibular-cochlear nerve), less often meningiomas, cholesteatomas and tumors of the cerebellum or brain stem, spreading to the M. at. These tumors manifest themselves initially as focal symptoms, which are caused by damage to the area of ​​the brain or nerve that is the source of tumor growth (auditory nerve, brain stem), and then, as the tumor grows, symptoms of damage to adjacent brain formations and general cerebral symptoms develop (headache, hypertensive changes on craniograms, congestion in the fundus). The latter are associated with secondary occlusion of the cerebrospinal fluid ducts at the level of the posterior cranial fossa (see Occlusion syndrome).

Neuromas give pronounced symptoms of damage to the auditory nerve, edges often appear long before all other symptoms. The disease usually begins with local symptoms - a slow and gradual decrease in hearing in one ear of the sensorineural type. Wedge, the picture with neuromas is initially characterized by damage to the cranial nerves in the cerebellopontine angle. Later, brainstem and cerebellar disorders appear, more pronounced on the side of the tumor. All symptoms have a clear lateralization. The phenomena of increased intracranial pressure develop relatively late. There are 3 stages in the development of neuromas:

1. Early stage - the tumor is small (1.5-2 cm). During this period, only cranial nerves in the mucous membrane are affected: vestibular-cochlear, trigeminal, facial, glossopharyngeal (on the side of the tumor, hearing, vestibular excitability, and taste in the anterior 2/3 of the tongue are reduced or lost; mild dysfunction of the trigeminal and facial nerves is noted ). Hearing loss begins at high frequencies, and the intelligibility of received speech suffers more; sound in Weber's experiment (see Weber's experiment) does not lateralize, despite unilateral deafness. There are no stem and hypertension symptoms. In almost half of the patients, radiographs show that the internal auditory canal is widened, and in almost all patients the protein content in the cerebrospinal fluid is increased. Some of these tumors are clearly detected by computed axial tomography. At this stage, diagnosis is difficult. Surgery is the most effective (the tumor is completely removed). Facial nerve function is often preserved.

2. Stage of pronounced wedge, symptoms - tumor size approx. 4-4.5 cm in diameter. The tumor affects the brain stem, cerebellum, and often causes hypertension. Multiple spontaneous nystagmus is detected (in the direction of the tumor it is larger, tonic, and in the healthy direction it appears even with direct gaze), optokinetic nystagmus is disrupted (see), ataxia appears on the side of the tumor, the trigeminal and facial nerves are more often affected. The clinical picture of the disease at this stage in most patients is clearly expressed. In most cases, the tumor can be completely removed. After surgery, facial paralysis often develops.

3. In the advanced stage, swallowing disorders, damage to the cranial nerves and brain stem on the healthy side, and severe hypertensive-hydrocephalic phenomena occur.

Meningiomas and cholesteatomas M. u. the symptoms are similar to acoustic neuromas, but signs of damage appear later and may not be so pronounced. With cholesteatomas, the cerebrospinal fluid contains an increased content of cellular elements with a normal protein content.

The diagnosis of patol, processes localized in M. u., is based on data from the clinical picture and rentgenol, research methods - craniography (see) and radiopaque studies of the cerebrospinal fluid and vascular systems of the brain (see Vertebral angiography).

A thorough tomographic examination of the skull, in particular the pyramids of the temporal bones (see Tomography), the use of pneumoencephalography (see) and cisternography (see Encephalography) make it possible in most cases to identify even relatively small tumors of M. at. Computed tomography has high diagnostic effectiveness (see Computed tomography), with the help of a cut it is possible to detect space-occupying formations of M. at. diameter, up to 1.5-2 cm (Fig. 3).

Craniographic diagnosis of tumors of M. u. is based on local changes in the bones of the skull caused by the direct influence of the tumor, and long-term changes caused by displacement of brain structures and compression of bones, disruption of the outflow of cerebrospinal fluid and displacement of its reservoirs, compression and displacement of blood vessels in the posterior cranial fossa.

For greater reliability, rentgenol. signs of a tumor are produced by the following paired craniograms of the diseased and healthy sides on one film under identical shooting conditions: transverse radiographs of the temporal bones according to Stenvers; direct radiographs with projection of the pyramids into the orbits; Posterior semiaxial radiographs to identify destruction of the posterior surface of the pyramid. Of primary importance are the Stenvers images, which give an idea of ​​the size of the internal auditory canal on the side of the tumor, the state of its upper and lower walls, the deep ampullary part, the relationship of the tumor bone defect to the cochlear capsule and the vertical semicircular canal of the labyrinth (Fig. 4, i, b ). Sometimes photographs with a projection of the pyramids into the eye sockets are more informative.

According to craniography data, it is sometimes possible to differentiate various tumors of M. u. Thus, meningiomas rarely cause expansion of the internal auditory canal, more often destruction of the apex of the pyramid and its surfaces with uneven outlines, calcareous inclusions are often observed along the periphery of the tumor (Fig. 5); with cholesteatomas, there is a sharp expansion of the internal auditory canal with destruction of the anterior surface of the pyramid and linear arched calcareous marks with smooth outlines of the adjacent bones.

On vertebral angiograms for acoustic neuromas, the tumor vasculature is rarely contrasted, and therefore symptoms of vascular displacement (secondary signs) are of primary importance. When the tumor spreads caudally, the basilar artery is pressed against the clivus (Blumenbach's clivus) and laterally displaced in the opposite direction. As the tumor grows in the oral direction, the basilar artery moves posteriorly from the clivus and in the opposite direction.

The superior posterior cerebellar arteries on the side of the tumor are displaced upward and medially. The inferior cerebellar artery on the side of the tumor is usually displaced downward. With meningiomas, the tumor vasculature is often visible.

Pneumocisternography and pneumoencephalography can reveal different rentgenol signs: lack of filling of the lateral cistern of the bridge due to its closure by a tumor; detection of a tumor in the form of a filling defect in the lateral cistern of the bridge; displacement of the IV ventricle, cerebral aqueduct (Aqueduct of Sylvius) to the opposite side and compression of the lateral inversion of the IV ventricle by the tumor. With oral spread of the tumor, the cerebral aqueduct and the fourth ventricle are displaced posteriorly. Positive ventriculography (see) with mayodil emulsion for M. tumors. reveals a displacement of the cerebral aqueduct and the fourth ventricle in the opposite direction with defects in the filling of the lateral eversion of the fourth ventricle. When the tumor spreads orally, these formations move in an arcuate manner backwards and upwards. Such symptoms can be detected both with occlusion of the fourth ventricle and in the absence of disturbances in the patency of the cerebrospinal fluid pathways, which is important for the early diagnosis of tumors. The severity of the symptoms described above depends more on the direction of tumor growth than on its nature.

Operations in the field of M. at. taken for diseases associated with damage to the nerves passing through the muscle. (Meniere's disease, neuralgia of the trigeminal and glossopharyngeal nerves); arachnoiditis M. u. and its tumors (acoustic neuromas, meningiomas, cholesteatoma, etc.).

During operations, unilateral approaches are used. The most widespread are the accesses proposed by W. Dendy and A. W. Adson (Fig. 6, a, b).

With the Dandy approach, a parabola-shaped incision of soft tissue is made.

The skin, subcutaneous tissue, aponeurosis and muscles covering the occipital bone on the side of the operation are dissected. A skin incision is made at the midline, at the point of intersection of the midline with the lower nuchal line (linea nuchae inf.). From this point, the incision is directed towards the lesion and, rising in an arcuate manner, reaches the junction of the upper nuchal line (linea nuchae sup.) with the lambdoid suture.

Then the incision line goes down along the convexity of the mastoid process, almost to its apex.

Bleeding is stopped by diathermocoagulation (see). Educated thus. the flap is separated from the bone and retracted downwards. If there is bleeding from the emissary veins of the bone, it is stopped by rubbing wax.

Then a milling hole is made in the exposed surface of the occipital bone and expanded with pliers to the required size.

At the midline, the burr hole does not reach the external occipital crest; outward it reaches the mastoid process, from above it reaches the superior nuchal line or the lower edge of the transverse sinus. From below, the edge of the trepanation window ends approximately at the level of the upper edge of the foramen magnum, which corresponds to the place of thickening of the occipital scales. The dura mater of the brain is cut with a cross-shaped incision. During operations on the nerves that take place in the cerebellum, after opening this membrane, good access to its formations is created, for which purpose the cerebellar hemisphere is lifted upward and somewhat medially with a careful movement.

The cerebellopontine angle is exposed after the leakage of cerebrospinal fluid from the lateral pons cistern.

For tumors of M. u. Often, to create good access, it is necessary to resort to resection of the lateral part of the cerebellar hemisphere. For this purpose, the cerebellar cortex is coagulated and after its dissection and aspiration of the white matter, the desired portion of the cerebellum is removed.

When using the Adson approach, a linear skin incision is made approximately halfway between the midline of the occiput and the mastoid process (Fig. 6, a). At the top, the incision begins from a point located 2-3 cm above the upper nuchal line, and then is lowered vertically down to the level of the arch of the atlas. The skin and underlying soft tissue are gradually dissected down to the bone. Bleeding is systematically stopped by coagulation, due to which the operation, as a rule, is almost bloodless. The muscles are separated from the bone using a raspatory and a coagulation knife and spread apart using automatically self-retaining wound retractors. Then a milling hole is made. If, when biting the bone towards the mastoid foramen and damaging the emissary vein passing through this hole, venous bleeding appears from the emissary, it must be covered with wax in order to prevent air embolism. The dura mater of the brain is dissected as described during the Dendy approach, and further manipulations are performed. Some neurosurgeons, in addition to the described trepanation of the occipital bone, additionally bite the edge of the occipital bone and the arch of the atlas on the corresponding side. This is usually done when removing large tumors (neurinomas, meningiomas) of the cerebellopontine angle.

Chemotherapy and radiation therapy combined with surgery are identical to those for other brain tumors - see Brain, tumors.

Bibliography: Egorov B.G. Neuroma of the VIII nerve, p. 80, M., 1949; 3 l about t-n and to E.I. and Sklyut I.A. Neuromas of the auditory nerve, Minsk, 1970; K o p y-l ov M. B. Fundamentals of X-ray diagnostics of brain diseases, p. 211, M., 1968; Fundamentals of practical neurosurgery, ed. A. L. Polenova and I. S. Babchina, p. 233 and others, L., 1954; Ad son A. W. A straight lateral incision for unilateral suboccipital craniotomy, Surg. Gynec. Obstet., v. 72, p. 99, 1941; G u s h i n g H. Acoustic neuromas, Laryngoscope, v. 31, p. 209, 1921; D a n d y W. E. Removal of cerebellopontile (acoustic) tumors through a unilateral approach, Arch. Surg., v. 29, p. 337, 1934; Kleinhirnbriickenwinkel-Tu-moren, Diagnostik und Therapie, hrsg. v. D. Plester u. a., B., 1978; P ertui set B. Les neurinomes de l'acoustique developpes dans 1'angle ponto-cerebelleux, P., 1970; T a v e r a s J. M. a. W o o d E. H. Diagnostic neuroradiology, Baltimore, 1964. I. S. Blagoveshchenskaya (otoneurologist),

E. I. Zlotnik (neurosurgeon), 3. N. Polyanker (rent.), V. V. Turygin (anat.).