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, to the posterior region 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 rear surface of the pyramid temporal bone, from the inside - by the junction of the pons, medulla oblongata and cerebellum, constituting the apex of the pontocerebellar 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) roots V-XI pairs are located cranial nerves, anterior inferior cerebellar and labyrinthine arteries and numerous cerebellar veins flowing into the superior petrosal sinus, 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 develops after infection, in acute stage there is pleocytosis in the cerebrospinal fluid, in chronic - 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- slow and gradual hearing loss 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 with high frequencies, 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. Clinical picture The disease at this stage is clearly expressed in most patients. 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 Computer 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 tract, which is important for early diagnosis 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.
They cut the skin, subcutaneous tissue, aponeurosis and muscles covering the occipital bone on the side of the operation. 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.).
The lateral pons cistern is located at the junction of the cerebellum, pons, medulla oblongata and base of the skull. The VII, VIII and intermediate nerves pass in the center of this area, the V nerve is located anterior to them, and the IX, X nerves are located posteriorly. The posterior wall of the pyramid of the temporal bone limits this area anteriorly and laterally. The topography of this area is covered in detail by B. G. Egorov.
Tumors of the lateral cistern of the pons are common, accounting for 13.1 - 12% of all brain tumors and 1/3 of all tumors of the posterior cranial fossa. Among tumors of the lateral pontine cistern, acoustic neuromas are the most common tumors.
In 1889, G. Oppenheim was the first to correctly diagnose intravital tumors of the cerebellopontine angle tumor. Subsequently, a description of individual casuistic observations was given. The development of the clinic, surgery and otoneurological symptoms of this issue is given in the works of many specialists.
Tumors of the VIII nerve arise from its Schwann sheath. Typically, tumors have the appearance of round-oval nodes in the capsule, well demarcated from the surrounding tissue. The size of the tumor varies (from cherry to very large, 8 x 3.5 cm). Tumors are located in a bed formed by the pons, medulla oblongata and cerebellar hemisphere on the affected side, which are usually sharply compressed. As the tumor grows, the peduncles of the brain are compressed upward, and dents form on the lower surface of the temporal lobe of the brain. Tumors often create an enlarged lumen of the internal auditory canal.
The roots of the cranial nerves (VIII, V, VII, and also often IX, X, XI) on the side of the tumor are stretched, thinned or fused with the tumor and are lost in its mass, so that it is sometimes difficult to decide which nerve the tumor comes from.
Tumors of the lateral cistern of the bridge, having a clearly defined lateral location, gave characteristic lateral displacements and compression of the trunk in the posterior cranial fossa, its S-shaped curvatures and twists; the pons and medulla oblongata sharply atrophy and become thinner, especially on the side of the tumor. Often, asymmetric changes are found in the cerebral hemispheres, which are more pronounced on the side of the lesion (compression of the base of the temporal lobe of the brain, greater protrusion of the hippocampal and rectal gyri on the side of the tumor). These morphological data in tumors of the lateral cistern of the pons are confirmed by studies of biocurrents of the cerebral cortex with asymmetry electrical activity in the cerebral hemispheres and more frequent asymmetrical impairment of smell on the side of the tumor.
Neuromas are benign encapsulated tumors. According to Verokay, neuromas have a connective tissue stroma, the spaces of which are filled with tumor tissue originating from elements of the Schwann membrane. According to B. G. Egorov, the main and initial structure of neuromas is fascicular. Neuromas are characterized by large polymorphism, which depends on exogenous and endogenous causes; different structures occur in the same tumor.
Neuromas most often occur between the ages of 30 and 50 years. They are 2 times more common in women, often appearing for the first time during pregnancy. The duration of the disease is on average 2-4 years, sometimes 10-20 years. Symptoms of damage to the VIII nerve often appear long before the development of other symptoms (sometimes 5-7 or even 20 years). The disease usually begins with local symptoms, with a very slow and gradual decrease in hearing in one ear and often noise in it. At this stage of the disease, patients have no other complaints. Patients turn to otiatrists, who usually make a diagnosis of neuritis of the VIII nerve. With neuromas of the VIII nerve, typical vestibular vertigo rarely occurs and tinnitus is quite often absent. Due to the very slow and gradual decrease in hearing, good compensation of auditory function by the healthy ear, and the frequent absence of noise, patients often do not notice the very slowly onset of one-sided deafness. It is often discovered by chance in late stages illness, when other symptoms are already detected.
The most typical for tumors of the lateral cistern of the pons at the stage at which patients are admitted to neurosurgical institutions was complete one-sided deafness on the side of the tumor with preservation of hearing on the healthy side.
In Weber's experiment, the patient more often does not lateralize sound, despite unilateral deafness, less often lateralizes it into the healthy ear, and very rarely into the deaf or worse-hearing ear. The lack of lateralization of sound in Weber’s experience is quite common with central asymmetric hearing loss and may be one of the differential diagnostic signs between radicular and cochlear lesions of the VIII nerve.
When studying bone conduction in Schwabach's experiment, it was usually shortened due to changes in the conducting media of the skull. When studying bone conduction audiometrically from the mastoid processes, bone conduction on the tumor side was preserved significantly better than air conduction. In case of complete one-sided deafness, this can be explained by “overhearing” vibrations from the mastoid process from the affected side to the healthy one.
What frequencies of hearing are most affected by neuromas of the VIII nerve? This question can be studied in patients with incomplete loss hearing on the affected side. There are conflicting statements on this issue in the literature. G.S. Zimmerman, F.M. Ioselevich, Ya.S. Temkin more often observed damage to low sounds. I. S. Babchin, Brown, Lowe, Adams more often encountered damage to high tones. O. G. Ageeva-Maikova, N. S. Blagoveshchenskaya Lundborg, Graf detected hearing damage at the most different frequencies in different patients. This can be explained by the wide variety of topography and direction of tumor growth in relation to the VIII nerve root. During audiometric hearing testing, high-pitched sounds (4000, 8000 Hz) were most often affected.
To establish radicular hearing damage in neuromas of the VIII nerve, it is of great importance to study the phenomenon of loudness equalization or recruitment phenomen. It was noted that when the organ of Corti is damaged, there is a phenomenon of loudness leveling, but when the auditory nerve root is damaged, it is absent. This symptom makes it possible to differentiate hearing damage in the cochlea from hearing loss in the VIII nerve root. This determines whether the sensitivity of the affected ear increases with greater sound intensity. It has been proven that when hearing is damaged in the cochlea, the hearing impairment from the threshold level weakens as the intensity of stimulation increases until it reaches a level at which the sound is heard equally well in both ears. In this case there is positive symptom“loudness leveling”, which happens when there is hearing damage in the cochlea. With a radicular lesion, with any increase in sound intensity in the affected and healthy ear, the patient will still hear the sound worse on the affected side.
Vestibular disorders with neurinomas of the VIII nerve are observed in all patients. Typical dizziness is extremely rare, which is explained by the very slow development of the process and compensation of vestibular disorders by vision, deep muscle-articular sense and a healthy labyrinth of the opposite side.
Spontaneous nystagmus with neuromas of the VIII nerve is one of the most common and early symptoms (occurs in 95%). Spontaneous nystagmus was absent with small tumors of the VIII nerve and with their lateral location. In the initial stages there was only horizontal nystagmus, more pronounced in the healthy direction. The most common occurrence in patients was multiple spontaneous nystagmus when looking to both sides and up. Horizontal spontaneous nystagmus usually had asymmetrical character and clearly prevailed in degree in the healthy direction. This was explained by the loss of vestibular function on the diseased side, as a result of which the vestibular formations on the healthy side predominated in functional terms. The predominance of spontaneous nystagmus in the healthy side was expressed in the appearance of nystagmus in this direction when looking straight or at a smaller angle of eye abduction, in the appearance of diagonal nystagmus when looking up and down (diagonal nystagmus was directed up and to the healthy side, or down and to the healthy side) . More rarely, when looking up and down, horizontal spontaneous nystagmus was detected, directed in the healthy direction.
In the direction of the tumor, the nystagmus was slower, sweeping and tonic, which was explained by a greater effect on the vestibular nuclei on the affected side.
The larger the size of the tumor and its effect on the brainstem, the larger, sweeping and tonic the spontaneous nystagmus became. The nature of spontaneous nystagmus in neuromas of the VIII nerve changed less with changes in position than in tumors of the cerebellum and IV ventricle.
Vestibular excitability on the side of the tumor usually disappears. However, this is almost always not easy to establish due to pronounced multiple spontaneous nystagmus, which can be mistaken for experimental nystagmus. During the caloric test, it is necessary to monitor whether spontaneous nystagmus increases with direct gaze. Post-rotation nystagmus usually does not fall in the direction of the tumor, which is explained by irritation during rotation of the healthy labyrinth. During rotation, both horizontal semicircular canals are always irritated, but normally stronger irritation occurs where the endolymph moves towards the ampulla and post-rotation nystagmus is directed towards this labyrinth. If vestibular excitability is lost on the side of the tumor, then weak irritation of the horizontal canal on the healthy side (the endolymph flow comes from the ampulla) still leads to the appearance of post-rotational nystagmus towards the labyrinth with the lost function. Moreover, usually post-rotational nystagmus on the healthy and painful side is insignificant
differs in character due, obviously, to functional restructuring and compensatory phenomena.
Optokinetic nystagmus is often disturbed more towards the tumor due to its effect on the vestibular nuclei and vestibulo-oculomotor connections. In advanced stages of the disease, with a sharp effect on the brain stem, optokinetic nystagmus occurred in all directions.
Loss of taste on the anterior 2/3 of the tongue on the side of the tumor is an almost constant and early symptom in neuromas of the VIII nerve due to damage portio intermedia Wrisbergi in the internal auditory canal. Much less frequently and in later stages, taste was impaired in the posterior third of the tongue on the affected side due to the influence of the tumor on the nuclei or root of the glossopharyngeal nerve. Taste disturbances are detected especially early with more detailed study taste thresholds according to the method of S. A. Kharitonov and S. D. Rolle.
With a pronounced clinical picture of neuroma of the VIII nerve, a clearly defined clinic with pronounced lateralization of symptoms was given. The clinical picture consisted of unilateral damage to the V, VII, VIII nerves, often with the maximum and earliest damage to the VIII nerve. Usually there was complete deafness, loss of vestibular excitability and taste in the anterior 2/3 of the tongue on the side of the tumor. The function of the V nerve was impaired early, the corneal reflex and sensitivity in the nose on the side of the tumor decreased especially early. Elliott attributes this to damage to the motor portion of the reflex arc in the facial nerve, and not necessarily to damage to the sensory V nerve. More often, the facial nerve is involved relatively little, since it is quite resistant, despite its pronounced changes detected at autopsy.
Later, these main symptoms (damage to the V, VII, VIII nerves) are joined by cerebellar and brainstem symptoms, much more pronounced on the side of the tumor, damage to adjacent cranial nerves on the side of the tumor (VI, IX, X, XII, III), and in later stages and on the opposite.
The majority of patients with tumors of the lateral cistern of the pons at the time of admission to the hospital had symptoms of increased intracranial pressure (hypertensive headaches, congestion in the fundus and, less often, hypertensive changes in the cranial vault and sella turcica), which, however, developed significantly with tumors of the lateral cistern later than with cerebellar tumors.
Forced head posture with tumors of the lateral cistern of the bridge occurs in more advanced stages of the disease. This sign is not as characteristic for tumors of this localization as for tumors of the cerebellum and the fourth ventricle.
Neuromas of the VIII nerve give peculiar local changes in the pyramid of the temporal bone (in 50-60%), causing a uniform and expansive expansion of the internal auditory canal; At first, it retains its tube-like shape, but later the parallelism of the walls of the internal auditory canal disappears, and on Stenvers’ radiographs it approached a parabola and a hyperbola. Atrophy and porosity of areas of the pyramid near destruction increase.
Characteristic of neuromas of the VIII nerve is a sharp increase in protein in cerebrospinal fluid with normal or slightly increased composition of cellular elements.
Depending on the size of the tumor and the severity of symptoms, several stages are distinguished in the development of neuromas of the VIII nerve. Cushing, Christiansen, Genshen distinguish three stages; K. F. List - five stages. We, like O. G. Ageeva-Maikova, L. O. Korst, G. S. Zimmerman, R. L. Babat and F. M. Ioselevich, distinguish four stages in the development of neuromas.
First stage- otiatr and cheska I. At this stage, there are disturbances from the VIII nerve in the form of a unilateral decrease, and then loss of hearing and vestibular function. Spontaneous nystagmus is directed in the healthy direction or is absent. Diagnosis at this stage is difficult, since the clinical picture of the disease is very similar to neuritis of the VIII nerve. At this stage, patients usually do not go to neurosurgical institutions.
Second stage- otoneurological. A unilateral lesion of the VIII nerve is accompanied by damage to neighboring cranial nerves on the side of the tumor: V, VII, intermediate nerve (the corneal reflex and sensitivity in the nose are reduced, taste is reduced on the anterior 2/3 of the tongue on the side of the tumor). Spontaneous nystagmus is absent or expressed in the healthy direction. The fundus is often normal, the internal auditory canal is dilated, and there is slight hyperalbuminosis in the cerebrospinal fluid. Brainstem, cerebellar and hypertensive symptoms are absent in patients at this stage of the disease. The otoneurological stage of neuroma VIII is the most favorable for surgery; at this stage the tumor can be easily removed completely.
Third stage. Most patients have to be operated on at this stage. The tumor reaches a size walnut and more, affects the brain stem, cerebellum and begins to cause disturbances in liquor outflow. The above symptoms are accompanied by cerebellar hemiataxia on the affected side. Brainstem symptoms are detected in the form of multiple very peculiar spontaneous nystagmus when looking to the sides and up, weakening of optokinetic nystagmus, especially towards the focus. Damage to adjacent cranial nerves on the side of the tumor is more clearly identified. Hyperalbuminosis increases in the cerebrospinal fluid. Diagnosis of neurinomas of the VIII nerve at this stage is not difficult. Even incomplete removal of the tumor at this stage of the disease can give a long-term good result.
Fourth stage. Tumors in this period of the disease reach very large sizes. There is a further harsh effect on the brain stem. Spontaneous nystagmus acquires a sharply tonic character, especially towards the tumor, vertical spontaneous nystagmus appears downwards, optokinetic nystagmus completely disappears in all directions. Severe disturbances in speech, swallowing (damage to the X nerve), myoclonus of the pharyngeal muscles appear, and cerebellar disturbances sharply increase. Often pronounced dislocation symptoms appear on the opposite side: hearing loss up to bilateral deafness, damage to the V, VII, VI nerves and pyramidal tracts on the healthy side. At this stage, secondary hypertensive-hydrocephalic symptoms are sharply expressed: vision usually decreases, supratentorial disturbances appear - visual, auditory, olfactory hallucinations, the sense of smell decreases, and the psyche changes. Due to the wide variety of symptoms and severe mental disorders, the difficulty of examining patients, diagnosis at this stage can be difficult.
Depending on the characteristics of the topography and the preferential direction of growth of the tumor of the lateral cistern of the bridge, various clinical variants may develop.
Neuromas of the VIII nerve can be divided into more medial and laterally located ones. With laterally located neuromas of the VIII nerve, growing towards the pyramid of the temporal bone, loss of hearing, vestibular function and taste in the anterior 2/3 of the tongue is detected earlier. This is explained by the fact that such tumors grow early into the internal auditory canal, and the VIII and intermediate nerves are strongly compressed in a stubborn bone ring. With lateral tumors, hypertensive-hydrocephalic symptoms develop later, the fundus remains normal longer, and brainstem disorders occur later. In extreme cases, lateral tumors of the VIII nerve may be similar to tumors of the petrous temporal bone.
With a more medial location of the tumor, the function of the VIII nerve on the affected side may disappear later. Symptoms of increased intracranial pressure and brainstem disorders are detected earlier. There may be no destruction of the internal auditory canal on the side of the tumor. With a medial location of the tumor, dislocation symptoms are more pronounced on the opposite side and damage to the cranial nerves is more pronounced on the healthy side, since the trunk is more sharply pressed in the opposite direction.
When tumors are located medially, the internal auditory canal on the healthy side often expands, which is not a very favorable prognostic sign.
Tumors of the lateral cistern of the pons can grow upward, be located in the middle sections of the lateral cistern of the pons (this is the most common) and grow downward, resulting in damage to the IX, X, XII cranial nerves.
When the tumor of the lateral cistern of the pons grows upward, the V nerve on the affected side is roughly involved in the process (neuralgic pain appears in the face, hypoesthesia on the face is detected early, and sometimes weakness of the masticatory muscles is detected). These tumors usually elevate the cerebellar tentorium, project into the medial-basal-temporal regions of the brain, elevate and narrow posterior horn lateral ventricle. With this arrangement of tumors, the function of the VIII nerve on the affected side can be partially or completely preserved. Such symptoms develop especially often with arachnoidendotheliomas of the lateral cistern of the pons and neuromas of the fifth nerve. With the growth of the tumor of the lateral cistern of the pons downwards, towards the cerebello-bulbar fissure, severe damage to the IX, X, XII cranial nerves on the side of the lesion was detected early, expressed in unilateral paresis soft palate, vocal cord, unilateral decrease in sensitivity on the back wall of the pharynx, palpitations, etc.
Tumors of the lateral pontine cistern sometimes grow predominantly towards the cerebellar hemisphere. In these patients, with relatively mild symptoms of damage to the lateral cistern of the bridge, hemicerebellar disorders clearly appear.
Sometimes tumors of the VIII nerve, despite their significant size, are asymptomatic and are accompanied only by dysfunction of the VIII nerve, which is often observed with cystic neuromas.
Alternative names: magnetic resonance imaging of the brain and cerebellopontine angle.
The cerebellopontine angle is a small area of the brain bounded by the cerebellum, medulla oblongata, and pons. Within this angle, two pairs of cranial nerves leave the brain - VII and VIII (vestibular-cochlear and facial nerves). In the immediate vicinity of the cerebellopontine ganglion, there are two more pairs of cranial nerves - V and VI (trigeminal and abducens nerves).
When various pathological processes, such as tumors or inflammation, are localized in the area of the cerebellopontine ganglion, symptoms of damage to these nerves are noted. The most informative method for diagnosing damage to this area is magnetic resonance imaging of the brain with targeted scanning of the cerebellopontine angle area.
Indications for MRI of the cerebellopontine angles
MRI of the brain, of which MRI of the cerebellopontine angle is part, is done for the following conditions and diseases:
- suspected brain tumor;
- diagnosis of intracerebral and subarachnoid hemorrhages;
- infectious diseases of the central nervous system;
- abscess of the cerebellopontine region;
- abnormalities of brain development;
- thrombosis of the venous sinuses;
- postoperative monitoring of patients undergoing brain surgery;
- preparation for surgical treatment of brain tumors.
The basis for targeted tomography of the cerebellopontine ganglion is signs of damage to the cranial nerves from the V to the VIII pairs.
Such signs are the patient’s complaints about:
- hearing disorders – hearing loss;
- dizziness, which is a sign of damage to the vestibular apparatus;
- paralysis of facial muscles;
- impaired sensitivity of facial skin;
- taste disorders;
- hypersecretion of tears.
Preparation
No special preparation is required. Before the procedure, the patient must remove all metal objects.
For children and emotionally labile patients, MRI of the brain can be performed under sedation.
How is an MRI of the cerebellopontine ganglion performed?
Scanning is carried out in T1 and T2 modes, which improves diagnostic accuracy.
The procedure takes 15-30 minutes. According to indications, tomography with intravenous administration contrast agent.
Interpretation of results
The most common tumor of the cerebellopontine angle is neuroma (schwannoma) of the 8th cranial nerve. On a series of tomograms of a tumor of the cerebellopontine ganglion, these tumors are visualized quite clearly. In difficult cases, intravenous contrast is used to more clearly determine the boundaries of the tumor.
The protocol described by the radiology doctor reflects the state of the brain structures and its symmetry. The presence or absence of pathological space-occupying formations is necessarily described, and if they are tumors, they are measured. Tomograms can be used to determine whether other brain structures are involved in the tumor process - this fact affects the prognosis surgical treatment tumors.
Additional Information
MRI of the cerebellopontine angle is a fairly accurate method for diagnosing tumor processes in this area. The advantages of this method are high accuracy of research, the disadvantage is high price and inaccessibility for certain categories of patients.
Alternative this method research - positron emission tomography, however, it is less accessible, and in terms of diagnostic accuracy it is only slightly superior to MRI.
Literature:
- Rameshvili T.E. Difficulties in X-ray diagnostics of tumors of the brainstem and peri-brain region // 4th All-Union. Congress of Neurosurgeons: Proc. report: - M., 1988.-S.
- Enzmann DR, O"Donohve J. Optimizing MR imaging for detecting small tumors in the cerebellopontine angle and internal auditory canal. Am J Neuroradiol, 1987
Tumors of the cerebellopontine angle. Tumors of the ventricles of the brain.
A special place is occupied tumors of the cerebellopontine angle. Usually these are neuromas of the auditory portion of the vestibulocochlear nerve. The disease debuts with gradually emerging and slowly progressive hearing loss, and sometimes there are mild vestibular disorders. Subsequently, signs of the tumor affecting neighboring structures appear: the root of the facial nerve (paresis of facial muscles), the root of the trigeminal nerve (decrease, and subsequently loss of the corneal reflex, hypalgesia in the face), cerebellum - ataxia, etc. Hypertensive phenomena, As a rule, they arise late. Tumors have a slow, long-term course.
Among the rarer brain tumors, we should highlight brain ventricular tumors.
Primary tumors(ependymomas, plexulopapillomas, etc.) can be asymptomatic for a long time.
Primary ventricular tumors often debut with hormonal disorders. This is obesity of the adiposogenital type or, on the contrary, cachexia, as well as sexual disorders, diabetes insipidus, anorexia, bulimia, etc. Subsequently, symptoms of the tumor’s impact on neighboring structures are revealed: compression of the chiasm (visual impairment), quadrigeminal disorder (pupillary disorders, upward gaze paresis, ptosis, etc.), tegmentum and bases of the midbrain (extrapyramidal and pyramidal disorders, etc.).
With unstable compression of the cerebrospinal fluid circulation pathways, transient occlusal crises- Bruns attacks described in other articles. These attacks are often provoked by movements of the head and can themselves lead to a forced position of the head, which improves conditions for the outflow of cerebrospinal fluid.
Infiltrating tumors neighboring structures gradually grow, including bone ones, for example, pituitary adenomas grow into the formations of the base of the skull, spreading to the cavernous sinuses, sinuses of the sphenoid bone, and nasopharynx. This causes the addition of corresponding symptoms - syndromes of damage to the apex of the orbit, retrosphenoidal space, superior sphenoidal fissure, cavernous sinus.
The result matters fundus examination- identification of congestion, namely: dilation of veins, swelling of the optic nerve head.
Serious information can be provided by special research methods, in particular cerebrospinal fluid examination. Brain tumors are characterized by an increase in protein content with normal cytosis (protein-cell dissociation). However, at present, due to the availability of other informative research methods (CT, MRI, etc.) and taking into account the unsafety of lumbar puncture at high intracranial pressure This research method is used less frequently in patients with suspected tumors.
Significant displacement median signal during echoencephalography gives reason to assume the presence intracranial space-occupying process.
The most informative are neuroimaging methods(neuroimaging) - computer and, in particular, magnetic resonance imaging, which allows you to directly visualize a tumor, identify its location, size, degree and prevalence of perifocal cerebral edema, the presence and severity of displacement of the median structures.
In some cases, it can be highly informative to clarify the nature and details of the pathological process. cerebral angiography with preliminary administration of a contrast agent and obtaining an image of the vascular system. However, angiography is an invasive method that has a certain percentage of complications.
Currently, non-invasive and therefore safe magnetic resonance angiography method.
For primary brain tumors, in cases of their surgical accessibility and the absence of contraindications (severe somatic condition patient, etc.), surgical treatment is applied.
In some cases, previously palliative operations are performed, for example, decompressive craniotomy, or various drainage operations that eliminate acute occlusive-hypertensive-hydrocephalic phenomena and transfer the patient from an inoperable state to an operable one.
For pituitary adenomas, as well as radiosensitive inoperable other tumors (tumors pineal gland, base of the skull, etc.) X-ray and gamma therapy, irradiation with a beam of protons and other heavy particles are used.
Drug treatment is actually only effective with prolactinoma of the pituitary gland- use bromocriptine (Parlodel), which suppresses the secretion of prolactin.
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 - / third 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. Tomogram with contrast enhancement allowed us to identify 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. Causes:
— 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 (pronounced 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. Shows up early intracranial hypertension, 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. TO 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 initial stage illness, 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.
Osteocondritis 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 (alternate 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 roots of cranial nerves 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, and also often contralateral pyramidal insufficiency.
The syndrome most often observed with neurinomas of the VIII nerve, meningiomas, cystic adhesive arachnoiditis of the lateral cistern of the bridge, volumetric 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 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 influences brain stem hemiparesis occurs on the side opposite to the lesion, cerebellar ataxia on the side of the hearth.
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).
IN anterior section trigeminal neuromas are observed. 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 the same area, 4) the cerebellum, 5) the 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 bone formations 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 onset of the disease, in the absence of noise, hearing loss for a long time is not noticed 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. Described in 1856 by the French physician A. Millard (1830-1915) and in 1896. German doctor 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 appears 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 focus 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. Manifested by 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.
Pontine lateral cistern syndrome, or cerebellopontine angle, is a combination of signs of damage to the auditory, facial and trigeminal nerves passing through side tank bridge. 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 detect 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 eyeballs in the form of friendly fast, irregular, uneven in the amplitude of their movements, performed in horizontal plane and especially pronounced in the initial stage of fixing 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. Occurs as a result of tumor growth or circulatory problems in the trunk tire, and may also be a manifestation multiple sclerosis. Described in 1901 by Russian neuropathologist V.K. Roth (1848-1916), in 1903 the German neuropathologist M. Bielschowsky (1869-1940).
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