Removal of a tumor of the cerebellopontine angle. Cerebellopontine angle: description, possible diseases, diagnosis, treatment Traditional methods of treating neuroma

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 the 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 bone compression, impaired 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. When the tumor spreads orally, 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.).

MRI of the brain. T1-weighted axial MRI (fragment). The cerebellopontine angles are normal. Color processing of the image.

The pontocerebellar angle (MCA) is the junction of the pons, medulla oblongata and cerebellum. The main reason for research in this area is sensorineural hearing loss. ENT methods allow you to narrow the search by determining that hearing loss is associated with nerve damage retrocochlearly (in the MMU, not in the ear), or in the structures of the ear. In the latter case, CT is more often used. MRI St. Petersburg allows you to choose the location of the MRI; we recommend that you be examined with us, where the possibilities for targeted research are greater than in many other MRI centers. When performing MRI in St. Petersburg in our centers for retrocochlear hearing loss, the method of choice is MRI of the brain, since the 8th cranial nerve (vestibular-cochlear) is affected.

Typical tumors of this area are neuromas (schwannomas) and meningiomas. With neuromas, there may be a tumor fragment in the internal auditory canal, which is visible, especially with contrast-enhanced MRI of the brain.

MRI of the brain. T1-dependent MRI with contrast. Schwannoma with compression of the 4th ventricle.

MRI of the brain. Schwannoma with a component inside the tubule.

MRI of the brain. T1-weighted coronal MRI with contrast. Completely intracanalicular neuroma.

Tumors of the endolymphatic sac, cholesteatoma, paraganglioma, lipoma and aneurysm of the internal carotid artery are also found in the area of ​​the apex of the temporal bone.

Tumors of the endolymphatic sac are benign, slow-growing, bilateral and associated with Hippel-Lindau disease, which belongs to the group of phakomatoses. A CT scan shows bone erosion of the apex of the pyramid, and an MRI of the brain with contrast enhances the formation well.

MRI. T1-dependent with contrast. Tumor of the endolymphatic sac.

Cholesteatomas (epidermoid cysts) are often found in the area of ​​the petrous apex. Their display on MRI depends on the amount of cholesterol present.

Target:

Target: to assess the condition of patients and neurological symptoms in the postoperative period in patients operated on for tumors of the cerebellar-pontine angle.

Material and methods. The course of the postoperative period in 109 patients was analyzed, among whom 84 (77.1%) cases were after removal of vestibular schwannoma, 21 (19.3%) - meningiomas of the cerebellar pons angle, 4 (3.6%) - schwannomas of the caudal group of nerves . Among the patients, women predominated (87(79.8%), the average age of the patients was 51 + 1.2 g. Due to continued tumor growth, 17 (15.3%) patients were operated on. The volume of the removed tumor in almost half of the patients (49 (44.1%) cases) was more than 30 mm in diameter. Total tumor removal was performed in 71 (64.5%) cases, subtotal - in 30 (27.3%), partial - in 9 (8.2%). The condition of the patients was assessed in the early postoperative period and up to 6 years (average observation period from 3±1.2 years). Methods: standard diagnostic neurosurgical complex, Karnofsky scale.

Results. The immediate postoperative course was smooth in 85 (76.6%) cases. Among postoperative complications, vascular disorders in the great vessels of the brain were noted in 3 (2.7%) cases; meningitis - in 27 (24.3%) cases, herpetic eruptions in the trigeminal nerve - in 11 (9.9%) cases; neuroparalytic keratitis - in 6 (5.4%) cases, acute cardiopulmonary failure with pulmonary embolism in 1 case, subcutaneous accumulation of cerebrospinal fluid was observed in 6 (5.4%) cases, nasal liquorrhea - in 5 patients. Postoperative neurological status was assessed on average 10-15 days after surgery. Neurological disorders in the immediate postoperative period were represented by unilateral dysfunction of the acoustic-facial group of nerves (up to 77.5%), symptoms of loss of function of the V (51.4%) and VI nerves (24.3%), bulbar syndrome (30.5 %), vestibular-cerebellar disorders (up to 70%). Statistically significant differences in assessing the condition on the Karnofsky scale between preoperative (74.8 + 0.9 points) and the immediate post-operative periods (75.5 + 0.9 points) we did not receive. In the long-term period, the condition of patients on the Karnofsky scale averaged 75.3 + 11.7 points, the condition of the majority of patients in the long-term period corresponded to 80 points (in 39 (35.8%) observations) and was better in patients operated on for the first time (p<0,05), а также в более молодой возрастной группе (p<0,01). Головные боли (оболочечно-сосудистые, напряжения, хронические формы головной боли) в отдаленном периоде беспокоили 68 (62,4%) пациентов и выявлялись чаще у пациентов с наличием синдрома внутричерепной гипертензии на дооперационном уровне (22(32%) набл.,p<0,05). Дисфункция V нерва в отдаленном периоде была выявлена в 42(39%) набл., а ее улучшение относительно ближайшего после-операционного уровня, наблюдалось в 21(19%) случае. Чаще данные нарушения отмечались у больных, оперированных повторно (p<0,05) и при наличии признаков внутричерепной гипертензии в дооперационном периоде (p<0,05). При маленьких размерах удаленной опухоли функция V нерва в отдаленном периоде нарушалась реже (p<0,05). Чувствительные нарушения на языке (V,VII нервы) в отдаленном периоде выявлялись в 37 (33,9%). Нарушение функции VI нерва в отдаленном периоде отмечалась в 31(28%) наблюдении, а регресс нарушений относительно ближайшего послеоперационного периода отмечен в 11 наблюдениях, стойкие нарушения - в 12, ухудшение -в 19. Дисфункция акустико-фациальной группы нервов была стойкой и чаще отмечалось при вестибулярных шванномах (p<0,01). Снижение слуха было во всех случаях с вестибулярными шванномами, у 14 больных с менингиомами ММУ и 2 больных со шванномами каудальной группы нервов. Бульбарные нарушения отмечались в отдаленном периоде в 26 (22%) и в основном были представлены дисфагией с дальнейшей положительной динамикой - в 46,7%. Вестибулярные нарушения в отдаленном периоде были выявлены в 42(39%) с последующим регрессом в отдаленном периоде в 50% наблюдений. Атаксия в отдаленном периоде отмечена в 48(44,0%) наблюдениях, преобладала в случаях резекции полушария мозжечка (p<0,05) и у больных, оперированных по поводу продолженного роста опухоли (p<0,05).

Conclusions. In the long-term postoperative period, clinically significant neurological disorders were noted in 70%, of which the most persistent were dysfunction of the acoustic-facial group of nerves. Bulbar, cerebellar and vestibular disorders partially regressed in the long term. The addition or increase in focal symptoms of prolapse indicated the risk of relapse/continued tumor growth.

In these cases, the chiasma is affected by 2 pathogenetic factors: expansion of the ventricular system of the brain and displacement of the brain (brain dislocation syndrome).

The chiasm can be affected by tumors of the following localization.

• Tumors of the posterior cranial fossa: subtentorial tumors (cerebellum, cerebellopontine angle), tumors of the fourth ventricle.
• Tumors of the lateral and third ventricles.
• Parasagittal tumors of the frontal and parietal lobes.
• Other tumors of the cerebral hemispheres.
• Tumors of the quadrigeminal gland and pineal gland.

With occlusion of the cerebrospinal fluid pathways at the level of the posterior cranial fossa, a symptom complex of an enlarged optic recess of the third ventricle develops.
The development of the syndrome, especially in the initial stage of the process, is based on the pressure of the expanded optic pocket (diverticulum) of the third ventricle on the nearby dorso-caudal section of the chiasm, where the crossed fibers of the papillomacular bundle pass. Pressure leads to disruption of microcirculation in this area and the processes of excitation transmission in the fibers. Further increase in hydrocephalus increases pressure on the chiasm and aggravates the disruption of its function. Optic nerve atrophy gradually develops.
With intracranial tumors, hypertension syndrome is observed, which is manifested by headache with maximum intensity at night or in the morning. The pain has a bursting character and “presses from behind” on the eyeballs. Nausea, vomiting, changes in cardiovascular activity, mental disorders, and depression of consciousness of varying degrees develop. The appearance of meningeal and radicular symptoms and convulsive seizures is possible.
Eye symptoms. During ophthalmoscopy, in the vast majority of cases, congestive optic disc discs and Foster Kennedy syndrome are observed. Congestive discs are combined with changes in the visual field characteristic of chiasmatic syndrome. Changes in the central field of vision occur in the form of central hemianopic scotomas, most often bitemporal, homonymous scotomas appear less frequently, and even more rarely, binasal scotomas. Moreover, among changes in the peripheral visual field, the most common is partial bitemporal hemianopsia with blindness of the second eye. Less commonly observed are pronounced forms of chiasmatic changes in the visual field (complete temporal hemianopsia in one eye combined with blindness in the other eye).
It is observed in intracranial pathological processes (more often with tumors of the lesser wing of the sphenoid bone and the adjacent basal parts of the cerebral hemisphere, less often with aneurysms of the vessels of the base of the skull, arachnoiditis, etc.). Often accompanied by hypo- or anosmia on the side of the pathological focus with symptoms of the patient’s frontal psyche.
Reverse Kennedy syndrome is possible, in which a congestive optic disc develops on the side of the pathological focus, and optic nerve atrophy develops on the opposite side. This is explained by the peculiarity of tumor growth or circulatory disorders in the brain.
With subtentorial tumors, almost every second patient experiences omnubulation - a short-term (usually within 2-10 seconds) blurring of vision in both eyes with increasing intracranial hypertension. More often, blurring covers the entire field of vision, much less often - only the central part; in some cases, blurring of vision of the hemianopic type is observed.
The main cause of omnubulation is considered to be compression of the intracranial part of the optic nerves, or chiasma, caused by a short-term increase in intracranial pressure. Symptoms of omnubulation are observed not only in patients with congestive optic discs, but also before signs of congestion appear in the fundus. These symptoms occur mainly with physical stress and sudden changes in body position.
In children with brain tumors, a symptom complex occurs involving the retina in the pathological process, which is described as opticoretinoneuritis syndrome. There are 3 forms of this syndrome.
The first form is called “optic retinoneuritis without atrophy of retinal neurons and optic nerve.” In this form of the disease, the appearance of hyperemia, significant edema and prominence of the optic disc is ophthalmoscopically noted. Changes in the optic disc are combined with swelling of the peripapillary retina, sudden dilatation of veins, and hemorrhages in the retina. With slowly growing (astrocytomas) or paraventricularly located tumors, the symptoms are less pronounced. Much more pronounced changes are observed in malignant tumors or already in the initial stages of tumor development that block the cerebrospinal fluid pathways.
The second form - opticoretinoneuritis with phenomena of secondary atrophy of retinal neurons and the optic nerve - develops with rapidly growing tumors. Characteristic is pronounced swelling of the optic nerves and retina. Venous congestive hyperemia of the optic disc occurs, plasmorrhea and hemorrhages appear. When hypertension persists for 2-4 months, atrophic changes occur first in the neurons of the retina, and then in the fibers of the optic nerve.
With slowly growing supratentorial tumors, a third form of this syndrome occurs - opticoretinoneuritis with the phenomena of secondary atrophy of retinal neurons and primary atrophy of the optic nerves. This form is characterized by a rapid decrease in visual acuity, which in the fundus does not correspond to the severity of the changes caused by the hypertension syndrome. Primary atrophy of the optic nerves in this form of the disease is due to the fact that the tumor directly affects the visual pathways. Changes in retinal neurons are secondary in nature and are associated with the development of local hypertension.

Cerebellar tentorium syndrome (Burdenko-Kramer syndrome)

Most often, the syndrome occurs with cerebellar tumors, tuberculomas and abscesses of the cerebellar vermis, arachnoidendotheliomas of the posterior cranial fossa, inflammatory processes of various etiologies localized in the posterior cranial fossa, as well as after brain injuries.
Clinical signs and symptoms. Characteristic is the appearance - more often at night - of a headache, localized mainly in the forehead and back of the head. Meningeal symptoms also occur.
Eye symptoms. There is pain in the eyeballs, orbits, pain in the area where the first branch of the trigeminal nerve exits. Hyperesthesia of the skin of the eyelids, increased sensitivity, conjunctiva and cornea are observed, as a result of which photophobia, lacrimation, and blepharospasm develop.
When the brainstem and cerebellum are herniated and pinched between the edge of the tentorium cerebellum and the dorsum of the sella turcica, irritation of the tentorium cerebellum may occur. In these cases, a very severe headache appears, especially in the back of the head, vomiting, involuntary tilting of the head, and dizziness. There is a dysfunction of the vestibulocochlear organ, extinction of tendon reflexes, and sometimes convulsions occur in the limbs. Pre-existing eye symptoms (especially pain in the eyeballs) intensify. New changes in the organ of vision occur - nystagmus, Hertwig-Magendie syndrome, paralysis or paresis of upward gaze (less often downward), sluggish reaction of the pupils to light.

Cerebellopontine angle syndrome

It is observed with tumors (mainly neuromas of the cochlear root of the vestibulocochlear nerve), as well as with inflammatory processes (arachnoiditis) in the area of ​​the cerebellopontine angle.
Clinical signs and symptoms. There are symptoms of unilateral damage to the roots of the facial, vestibulocochlear nerves and the intermediate nerve passing between them. As the size of the pathological lesion increases, depending on the direction of its spread, symptoms of damage to the trigeminal nerve and dysfunction of the cerebellum on the side of the lesion may appear. In this case, hearing loss, noise in the ear, and vestibular disorders occur. Also, in the half of the face corresponding to the side of the localization of the pathological process, peripheral paralysis of the facial muscles, hypoesthesia, pain and paresthesia develop. There is a unilateral decrease in taste sensitivity on the anterior two-thirds of the tongue. If the process affects the brain stem, hemiparesis (on the side opposite to the lesion) and cerebellar ataxia occur.
Peripheral motor neuron dysfunction can occur anywhere between the pons and muscle. Depending on the predominance of symptoms of damage to a particular nerve, a topical diagnosis of the localization of the pathological
hearth. If there is a predominant lesion of the abducens nerve, then the focus is in the bridge.
Eye symptoms. There is a convergent paralytic strabismus with diplopia, which intensifies when looking towards the affected muscle. Strabismus is caused by unilateral damage to the abducens nerve. Due to damage to the facial nerve, lagophthalmos, Bell's synkinetic phenomenon, and eyelash symptom occur. Spontaneous horizontal medium- to large-wide clonicotonic nystagmus may be observed. Symptoms of dry eye occur on the side of the lesion, and sometimes corneal damage occurs.

Lateral ventricle syndrome

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Clinical signs and symptoms. As a result of disruption of the intraventricular outflow of cerebrospinal fluid caused by blockade of the interventricular foramen of Monroe, symptoms of intracranial hypertension occur - headache, vomiting, etc. Lateral ventricle syndrome is characterized by a combination of symptoms of increased intracranial pressure with olfactory and gustatory hallucinations, which arise as a result of irritation of the mediobasal parts of the temporal lobe.
Eye symptoms. Signs of stagnant optic discs appear. As a result of pressure from the cerebrospinal fluid or pathological focus on the central neuron of the visual pathway, which is located in the wall of the inferior horn of the lateral ventricle, visual hallucinations are observed in the superior outer quadrant of the homolateral visual field. The development of transient dysfunction of the oculomotor nerve on the affected side is characteristic.

Third ventricle syndrome

The disease occurs due to tumor and inflammatory processes in the third ventricle of the brain.
Clinical signs and symptoms. There is a combination of hypertension syndrome with hypothalamic and extrapyramidal syndromes. In addition, symptoms characteristic of thalamus syndrome occur - sharp constant or paroxysmal intensifying pain in the half of the body opposite to the lesion, hyperpathy and hemihypesthesia with a decrease in superficial or loss of joint-muscular sensitivity, sensitive hemitaxia, disturbances in facial expressions (“facial facialis”) and characteristic hand position.
Eye symptoms. Ophthalmoscopy reveals a picture of congested optic disc discs.

IV ventricle syndrome

Develops with occlusion of the fourth ventricle of the brain. Among tumors affecting the fourth ventricle, ependymomas are the most common, and choroid papillomas are less common.
Clinical signs and symptoms. Signs of increased intracranial pressure develop, which are combined with cardiovascular disorders and respiratory disorders. Characterized by a forced position of the head (antalgic posture), which is caused by reflex tension of the neck muscles or by consciously placing the head in a position in which the headache weakens or disappears.
In case of damage to the upper corner of the bottom of the fourth ventricle, dysfunction of the vagus and glossopharyngeal nerves occurs.
When the lateral part of the ventricle is damaged, dysfunction of the vestibular-cochlear organ, hearing loss, and sensory impairment in the face of the bulbous type develop.
When the roof of the ventricle is affected, the clinical picture is dominated by hydrocephalic and cerebellar disorders.
Eye symptoms develop in case of damage to the upper corner of the bottom of the fourth ventricle. The appearance of Hertwig-Magendie syndrome is characteristic, which includes deviation of the eyeball downward and inward on the affected side and upward and outward on the opposite side. Paresis of the abducens nerve occurs. In the late stage of the disease, stagnant optic discs are observed. When the pathological focus is localized inside the ventricle (the cause of the pathological process is often a cysticercus, less often a tumor), Bruns syndrome develops - ptosis, strabismus, diplopia, nystagmus, transient amaurosis, decreased sensitivity of the cornea, sometimes swelling of the optic disc and its atrophy. In Bruns syndrome, ocular and general signs of intracranial hypertension occur with physical stress and sudden movements of the head.

Deep Temporal Lobe Syndrome

The syndrome occurs due to damage to the temporopontine tract and the central neuron of the visual pathway, located in the white matter of the temporal lobe.
Clinical signs and symptoms. With this disease, the so-called Schwab triad occurs.
In the case of extensive lesions of the temporal lobe in the prolapse variant, pathological forgetfulness is observed, especially for current events. With the irritation variant, a special mental state arises in which surrounding objects and phenomena seem unreal or were once seen, and/or, conversely, well-known objects and phenomena seem unfamiliar.
Eye symptoms. In the variant of irritation in the upper-outer quadrants of the visual field, opposite to the localization of the focus, metamorphopsia and formalized visual hallucinations occur (bright, vivid images of people, animals, paintings, etc.). In the variant of prolapse, on the side opposite to the lesion, quadrant - usually the upper - and then complete homonymous hemianopsia develops first.
When the altered temporal lobe puts pressure on the brain stem, oculomotor disorders may occur due to damage to the oculomotor nerve.

Inferior frontal lobe syndrome

The disease occurs as a result of tumors, infectious and vascular lesions located in the anterior cranial fossa and frontal lobe.
Clinical signs and symptoms. Mental disorders characterized by apathetic-abulic or disinhibited-euphoric syndromes are observed. Quite often there is a combination of both types of mental disorders. Hypo- or anosmia occurs on the side of the lesion. Characteristic is the appearance of the symptom of “facial facialis” (Vincent’s symptom) - insufficiency of lower facial innervation during crying, laughing, smiling, as well as grasping phenomena. Symptoms of frontal ataxia are observed, which are manifested by a violation of statics and coordination. The appearance of pain upon percussion along the zygomatic process or the frontal region of the head is typical.
Eye symptoms occur when the process spreads posteriorly. The appearance of signs of Foster Kennedy syndrome (Gowers-Paton-Kennedy syndrome) is characteristic. This syndrome includes a combination of primary optic nerve atrophy on the side of the lesion and congestive optic disc of the other eye. When the pathological process is localized near the base of the skull and orbit on the affected side, exophthalmos occurs.

Occipital lobe syndrome

Occurs with tumors (usually gliomas and meningiomas), inflammatory processes and injuries of the occipital lobe.
Clinical signs and symptoms. They are characterized by the appearance of general cerebral symptoms and gnostic disorders - primarily alexia. Clinical signs occur when the pathological process spreads anteriorly.
Eye symptoms. In the irritation variant, both unformed visual hallucinations (photopsia), as well as metamorphopsia, and formalized visual hallucinations (vivid images of people, animals, paintings, etc.) can occur. Unlike hallucinations that occur in mental disorders, in this pathology they are characterized by stereotypy and repetition. Hallucinations are caused by irritation of the cortex of the superior-lateral and inferior surfaces of the occipital lobe (according to Brodmann, fields 18 and 19). It should be noted that the closer the localization of the pathological focus is to the temporal lobes, the more complex the picture of hallucinations becomes.
In the prolapse variant, when the upper part of the calcarine groove is affected, lower quadrant homonymous hemianopsia occurs. In case of damage to the lower part of the calcarine sulcus and the lingual gyrus, superior quadrant homonymous hemianopsia develops. When the inner surface of the occipital lobe and the area of ​​the calcarine sulcus are affected (according to Brodmann, field 17), homonymous hemianopia occurs, often combined with impaired color perception and the appearance of a negative scotoma in the visible halves of the visual fields. Lesions of the superior-lateral surface of the left occipital lobe (according to Brodmann, fields 19 and 39) in right-handers and the right occipital lobe in left-handers cause visual agnosia. If the cerebellum is involved in the process, signs of damage to the tentorium and posterior cranial fossa appear (Burdenko-Kramer syndrome).

Quadrigeminal syndrome

The pathological process occurs when the quadrigeminal area is compressed from the outside (for example, by a tumor of the pineal gland, temporal lobe, cerebellum, etc.) or from the inside (due to occlusion of the Sylvian aqueduct).
Clinical signs and symptoms. Cerebellar ataxia and bilateral hearing loss occur with a predominance of the disorder on the side opposite to the lesion. As the pathological process develops, hyperkinesis, paralysis or paresis of the facial and hypoglossal nerves appear. It should be noted that there is an increase in righting reflexes - a rapid turn of the eyeballs and head during sudden visual and auditory stimulation.
Eye symptoms caused by damage to the anterior tubercles of the quadrigeminal and oculomotor nerve. There are divergent strabismus, floating movements of the eyeballs, paresis of upward gaze, absence or weakening of convergence, mydriasis, ptosis, and sometimes ophthalmoplegia.

Brain dislocation syndrome

Occurs when the brain substance is displaced and deformed under the influence of a tumor, as well as hemorrhage, cerebral edema, hydrocephalus, etc.
Clinical signs and symptoms. With axial displacement of the brain stem, bilateral hearing loss (up to complete deafness), generalized changes in muscle tone, breathing disorders, and pathological foot reflexes appear. If a tentorial hernia develops, a sharp headache and vomiting occurs. Autonomic disorders develop. The tendon gradually fades away and pathological reflexes appear.
Eye symptoms. With axial displacement of the brainstem with its infringement in the notch of the tentorium of the cerebellum, paresis or paralysis of upward gaze, decreased or absent pupillary response, mydriasis, and convergence disorder occur. Similar changes are observed when the hippocampal gyrus is strangulated in the tentorial foramen (tentorial hernia). When the temporal lobe of the brain is displaced and pinched in the lateral parts of the cerebellar tentorium (temporotentorial herniation), Weber-Hübler-Gendrin syndrome occurs. It includes symptoms of complete or partial paralysis of the oculomotor nerve on the side of the lesion - ophthalmoplegia, ptosis, mydriasis or paralysis of only individual extraocular muscles; sometimes contralateral homonymous hemianopsia occurs. When the optic tract is damaged, homonymous hemianopsia is observed.
Other variants of dislocation are possible - diencephalic level syndrome, bulbar level syndrome (cerebellar hernia). However, clear eye symptoms are not observed with such lesions.

Another picture, also quite well outlined, is tumor of the cerebellopntine angle. Here we are talking about a neoplasm, which is located in a depression bounded by the pons, medulla oblongata and cerebellum. Most often, such tumors come from the auditory nerve, less often from other neighboring ones. To make the picture of the disease clearer to you, I will list the formations located here that are functionally important: 1) the auditory nerve; 2) facial nerve - by location, two nerves very close to each other; 3) other bulbar nerves; 4) abducens nerve; 5) trigeminal nerve; 6) pons; 7) medulla oblongata and 8) one hemisphere of the cerebellum. The progression of the disease here is very slow. The beginning is very typical with irritation of the auditory nerve: the patient has been bothered by noise in one ear for many months, sometimes even several years. Then symptoms of loss appear: he becomes deaf in this ear. At the same time, paresis of a close neighbor, the facial nerve on the same side, appears. We can say that this entire stage of the disease is the most important for diagnosis: if the doctor himself can observe it or get an accurate story about it from the patient, then this will be the basis for the diagnosis. At the same time, partly general cerebral phenomena, which are usually expressed very rarely here, partly irritation of the trigeminal nerve is created by headaches, and objectively - loss of corneal and conjunctival reflexes. Then compression of the cerebellum begins and the development of cerebellar phenomena. They can be expressed first by hemiataxia on the side of the tumor, and then by general cerebellar ataxia, adiadochokinesia, unsteady gait, and a tendency to fall towards the tumor. decreased muscle tone and dizziness. Even later comes the turn of the bulbar nerves, as well as the abducens and trigeminal nerves. And finally, compression of the pyramids in the pons or in the medulla oblongata causes paralysis of the limbs.

I repeat once again that general cerebral phenomena here, as in general with tumors of the posterior cranial fossa, are strongly expressed, especially starting from the second stage of the disease, when paralysis develops. From this point on, the disease generally moves forward quickly, in contrast to the first period, which most often lasts for a very long time.

8. course of brain tumors.

To end the clinical picture of brain tumors, it remains for me to say a few words about their course. It is always protracted, chronically progressive, the disease slowly grows over many months or even several years, and according to the rule common to all neoplasms, in the absence of medical intervention inevitably leads to death. Occasionally, during the course of the disease, exacerbations are observed - due to hemorrhages into the tumor substance.

I have given you a quick sketch of the brain tumor clinic. You probably noticed what I warned you about from the very beginning, namely, the vagueness and indistinctness of all these pictures, especially striking if you remember many of the clear, sharply defined clinical descriptions that you have heard before. The reason for this phenomenon does not depend at all on the lack of good will on my part - it lies in the fact that now it is generally impossible to do anything more. And this, in turn, depends on the lack of our diagnostic information. Indeed, when you try to apply everything that I have told you in practice, you will often be seriously disappointed: you will not be able to correctly make a topical diagnosis. I can reassure you, if this can only be called reassurance; the most experienced specialists make the same mistakes in a very large percentage of cases.

Rice. 129 Brain tumor. Bilateral ptosis.

If this is so, then it is quite natural to need some more auxiliary research techniques that could have their say when ordinary neurological research refuses to say more.

Recent years have been rich in attempts to propose such methods. Most of them are clearly temporary in nature: they are technically difficult, burdensome, and sometimes even unsafe for patients. But I will still list them for you so that you can once again see for yourself what difficult and winding paths science takes.

I'll start with a regular x-ray examination. Such images especially facilitate the diagnosis of a tumor of the appendage of the brain if an expansion of the sella turcica has already been created. Tumors: vaults, emanating, for example, from the membranes and giving rise to the bones, are also sometimes suitable for a conventional x-ray. But most of them are still not suitable for conventional radiography. Therefore, there are also attempts at so-called ventriculography: air is blown into the cavity of the cerebral ventricles through a needle, and then a picture is taken. Air creates contrasts, and sometimes you can, for example, consider the following pictures: an undiagnosable tumor sits in the white matter of the hemisphere, it protrudes one of the walls of the ventricle and changes its contours; This contour is used to judge its localization. In addition to air, they are trying to use various contrasting mixtures, for example indigo carmine; the essence of their action is the same as that of air.

Under local anesthesia, a series of test punctures are made: a needle is injected into different parts of the brain to different depths, tissue particles are sucked in with a syringe and examined under a microscope. In this way, it is possible to obtain a tumor particle and find out not only its location, but also its anatomical nature. The smoothly shaved skull is tapped and listened to: sometimes the “sound of a cracked pot” and other shades of percussion sound are heard over the tumor; Sometimes noises are heard during auscultation. A series of punctures are used: ordinary lumbar, so-called suboccipital and finally puncture of the cerebral ventricles. At the same time, the state of fluid pressure in the subarachnoid cavity and in the ventricles is determined. If, for example, the pressure in the ventricles is much greater than in the spinal cavity, then this indicates a complete or partial blockade, that is, narrowing or closing of the foramina of Magendie and Luschka; and in case of tumors this indicates localization in the posterior cranial fossa. By the way, a few words about cerebrospinal fluid. In general, it can present different pictures, ranging from normal to an increased amount of protein, pleocytosis, xanthochromia. But in the mass there is still a tendency to give a kind of dissociation: increased protein content and absence of pleocytosis. Of course, lues cerebri, especially its gummous form, must be excluded by all existing means. But you know that modern research technology cannot always do this, and often the doctor remains suspicious of syphilis, despite negative data. That is why the rule still remains in force: when there is a picture of a compression brain process, always prescribe a so-called explorator, trial course of specific treatment. It should be done for about a month, since shorter periods do not provide complete confidence that there is no syphilis. pathological anatomy. Almost all known types of neoplasms can develop in the brain, some primarily, some metastatically. Cancer can develop primarily in the appendage of the brain, but in other places it occurs only in the form of metastasis. The largest number of tumors, almost half of all cases. constitute gliomas; then about 20% give rise to adenomas; and finally the last third of all cases occur in all other species. The microscopic picture of tumors has already been studied by you in the course of pathological anatomy, and therefore I will not dwell on it (Fig. 130).

As for the changes in the nervous tissue itself, they come down to the well-known degeneration of fibers, cell disintegration, sometimes to a weak inflammatory reaction on the part of the blood vessels and to significant phenomena of edema and stagnation. pathogenesis and etiology. The pathogenesis of clinical phenomena has already been partly discussed by me and partly should be understandable to you based on everything that you already know about vascular processes and syphilis of the brain. Therefore, there is no point in talking about this again. Likewise, it is not difficult to imagine the mechanism of anatomical changes on the part of the nervous system: the reasons that create them are: 1) mechanical compression of the nervous tissue by the tumor; 2) its swelling due to dropsy and stagnation from compression of the vascular system; 3) random hemorrhages and softening; 4) toxic effects from the tumor on nervous tissue and 5) general metabolic disorders: cachexia, anemia, diabetes, etc.

Men get the disease approximately twice as often as women. Neoplasms can develop at any age, from early childhood to old age. But the vast majority of all cases, about 75%, occur in adolescence and middle age, up to 40 years. Before and after this period, tumors are rarely observed. You have probably heard a lot about the causes of tumors in lectures on pathological anatomy, and you know that these causes are currently unknown. The main doctrine, which is still dominant today, sees in neoplasms the result of embryonic anomalies, the development of stray tissue sprouts, which for a long time were in a dormant state, and then, under the influence of some additional conditions, suddenly received the energy of growth.

Rice. 130. Tumor of the occipital lobe of the brain.

In general, as you can see, the main method of treating tumors - surgery - does not promise much for the patient. And therefore, only a small percentage of patients can count on recovery - complete or with a flaw.

In recent years, before our eyes, a new principle of treatment of neoplasms has emerged - already conservative, with the help of so-called radiation therapy: I mean treatment with radium and X-rays. These methods are still in the development stage, and it is too early to talk about them categorically. Scattered observations of individual authors provide both undoubted failures and dubious successes. Here we still have to wait for the accumulation of facts.

In the absence of radical therapy, we are left with the sad and unfruitful task of symptomatic therapy. Unfortunately, there is no need to talk much about it. This is the entire arsenal of painkillers, including the most powerful ones - in the form of morphine. This is followed by specific, mainly mercury, treatment, which helps the resorption of edema and dropsy and thus gives temporary relief to the patient. Finally, the so-called palliative valve-trepanation is sometimes used: part of the bone of the vault is removed in order to reduce intracranial pressure and thus temporarily alleviate the course of the disease.