Ophthalmoplegia - paralysis of the eye muscles. oculomotor nerve (n
20-02-2012, 20:51
Description
Violations of the functions of the extraocular muscles
Data on the frequency of oculomotor disorders in brain tumors are scarce. It is believed that they occur in 10-15% of cases [Tron E. Zh., 1966; Huber D., 1976]. The most frequently occurring signs of impaired innervation of the abducens nerve, paresis and paralysis of the oculomotor nerve are rare and lesions of the trochlear nerve are extremely rare.
Paralysis usually results to a violation of binocular vision, especially if the upper rectus muscles are affected and vertical diplopia develops. In patients with severe paresis, especially with horizontal, binocular vision is absent in all parts of the visual field.
Paresis and paralysis of the III, IV, VI pairs of cranial nerves, resulting from increased intracranial pressure, do not have independent significance in the topical diagnosis of brain tumors.
The largest abducens nerve injury with increased intracranial pressure, it finds an explanation in its anatomical and topographic connections with individual structures of the brain, the vascular system and the bones of the skull base. The fact is that, upon exiting the bridge, the abducens nerve is located between the dura mater and the branches of the basilar artery. Sometimes for a short distance it lies between the branches of the basilar artery and the pons. In these cases, increased intracranial pressure can lead to nerve entrapment between the pons and the posterior cerebellar artery. A partial violation of the conduction of the abducens nerve develops and, as a result, the weakening of the external rectus muscle on the side of the same name. If the paresis is insignificant, a well-defined horizontal diplopia appears with extreme abduction of the eye towards the weakened muscle. Thus, diplopia has a horizontal homonymous character. In the literature there is information about the predominance of bilateral lesions of the abducens nerve in patients with tumors of the brain moeg [Tron E. Zh., 1966; Kirkham T. et al., 1972].
Of interest are daily fluctuations in the severity abducens paresis. In patients with brain tumors, diurnal variations in intracranial pressure were observed, and at the time of its decrease, a sharp relaxation of the abducens nerve paresis was noted. The latter is also observed during degradation therapy.
Second plot the least resistance of the abducens nerve to increased intracranial pressure is the place where it passes over the upper edge of the pyramid of the temporal bone. A growing tumor and increased intracranial pressure can dislocate the brain, and the trunk of the abducens nerve is pressed against the sharp edge of the pyramid.
Abducens nerve paresis observed in patients with tumors subtentorial localization and their supratentorial location. Describing paresis of the abducens nerve with an increase in intracranial pressure, N. Cusching emphasized that this symptom in brain tumors should be regarded as a false localization sign. His opinion was confirmed in later works [Tron E. Zh., 1966; Gassel M., 1961; Nier A., 1976].
The oculomotor nerve, moving away from the legs of the brain, also passes between two vessels (the posterior cerebral and superior cerebellar arteries). Therefore, an increase in intracranial pressure can lead to nerve damage between vessels. In addition, the nerve may be pressed against the Blumenbach's eye. Since the pupillary fibers that run as part of the oculomotor nerve are more vulnerable, an early symptom may be unilateral mydriasis with complete areflexia.
With paresis and paralysis, to clarify the diagnosis, it is important to find out at what level the lesion occurred: 1) in the muscle, 2) in the nerve trunk, or 3) at the level of nuclei or roots.
In recent years, topical diagnosis has been facilitated by the use of electromyography .
The accumulated experience shows that using this method made it possible to differentiate various types of myopathies (myositis, endocrine ophthalmopathy), myasthenia gravis, peripheral and central muscle paralysis.
Abducens nerve injury at the level of the trunk is characterized horizontal diplopia, especially with the maximum removal of the eyes outward. If there is mild paresis, slight convergent movements are possible. As mentioned above, the abducens nerve is most vulnerable to increased intracranial pressure. Evaluation of only one stem palsy has no independent diagnostic value. Its combination with other neurological symptoms is important (damage to III, IV, V, VII, VIII pairs of cranial nerves).
nuclear palsy usually combined with gaze paralysis in the same direction, since the center of gaze for horizontal movements is located near the nucleus of the oculomotor nerve.
Fascicular paralysis characterized by two syndromes. Millard-Gubler syndrome consists of the following features: paresis of the lateral muscle, homolateral peripheral facies paralysis, cross hemiplegia. All signs of damage to the facies bundles of the VI and V pairs of cranial nerves can occur not only with the localization of the pathological process in the bridge, but also as a dislocation sign in the defeat of the quadrigemina or cerebellum.
Fauville syndrome characterized by paresis of the lateral rectus muscle, homolateral peripheral facial palsy, homolateral horizontal gaze palsy. A combination with Horner's syndrome is possible.
stem palsy of the oculomotor nerve is characterized by a violation of the functions of all the eye muscles innervated by this nerve. E. Zh. Tron (1966) notes that progressive stem paralysis of the oculomotor nerve is characterized by the initial appearance of ptosis, followed by damage to all other muscles.
Clinical picture of nuclear paralysis depends on the topography of the nuclei oculomotor nerve (Fig. 80).
Rice. 80. The layout of the nuclei that innervate the eye muscles (according to Hubar A.) I - small cell medial nucleus (the center of innervation of the ciliary muscle); II - small cell lateral nuclei (the center of innervation of the sphincter of the pupil); III - large-celled lateral nuclei: 1 - the nucleus of the levator, 2 - the nucleus of the superior rectus muscle; 3 - the core of the medial rectus muscle; 4 - core of the superior rectus muscle, 5 - core of the inferior rectus muscle; IV - the nucleus of the trochlear nerve; V - the core of the abducens nerve; 6 - cortical center of gaze.
They are represented by paired large-cell lateral nuclei that innervate the rectus muscles of the eye and the levator, paired small-cell Yakubovich-Westphal-Edinger nuclei that innervate the sphincter of the pupil, and a single Perlia nucleus that sends fibers to the ciliary muscle. Large cell nuclei have a large extent under the bottom of the Sylvian aqueduct, as they are represented by five cell formations that send representation to each muscle. At the same time, the superior rectus muscle and the levator receive fibers from the cell formations of the same side, the inferior rectus muscle - from the cell formations of the opposite side, and the fibers innervating the internal rectus and inferior oblique muscles have a bilateral representation. In this regard, nuclear palsy is characterized by dysfunction of single or multiple muscles in both eyes. There may be pupillary disorders (mydriasis, weakening of pupillary reactions, paresis of accommodation).
Fascicular paralysis characterized by the possibility of the appearance of two syndromes.
Weber syndrome- unilateral complete paralysis of the oculomotor nerve with cross hemiplegia, cross paralysis of the face and tongue is possible.
Benedict syndrome- unilateral paresis of the oculomotor nerve with cross hemitremor. Sometimes it is combined with cross hemianesthesia.
Stem paralysis of the trochlear nerve has no independent diagnostic value in brain tumors. Isolated paralysis and paresis are extremely rare.
Nuclear palsies in combination with paresis of the oculomotor nerve and vertical gaze palsy, spasm of convergence or its paralysis are characteristic of pineal gland tumors.
Paresis and paralysis of the gaze in brain tumors, according to the literature, are extremely rare (about 1.5%). In contrast to paresis and paralysis of the extraocular muscles, paresis and paralysis of gaze are characterized by an equal restriction of the mobility of both eyes. They do not have strabismus or diplopia. The functions of the muscles concerned are only partially limited. They develop as a result of the localization of the pathological process in the supranuclear or nuclear centers. Gaze paralysis can be vertical and horizontal.
Vertical gaze paralysis are observed when the center of gaze in the quadrigemina is turned off. Paralysis of the gaze up is more common. With paresis of upward gaze, eye movements in this direction are not limited, but when you try to look upward, vertical nystagmus occurs. E. Zh. Tron (1966) emphasizes that in diseases of the quadrigemina, vertical nystagmus may precede the appearance of upward gaze paralysis.
Horizontal gaze paralysis arise either as a result of turning off the cortical center of gaze in the frontal gyrus, or when turning off the center of gaze in the bridge. There is a certain dependence of the nature of gaze paralysis to the side on the level of the lesion.
Violation of the frontal center and fronto-pontine path leads to turning off voluntary eye movements, vestibular and optical eye movements are preserved.
Defeat in the center zone in the pons varolii leads to the absence of movements, both volitional and vestibular and optical, in the direction of gaze paralysis. Gaze paralysis is pronounced, stable. Friendly deviations of the eyes are rare and mild. R. Bing and R. Brückner (1959) believe that the loss of vestibular excitability of the extraocular muscles in gaze paralysis characterizes the lesion of the trunk. Lack of voluntary movements while maintaining the optical and vestibular, it indicates the defeat of the frontal center or the frontal-pontine path. A. Huber (1976) formulates the possibility of differentiation as follows: bilateral lesions of the frontal-pontine path cause complete bilateral paralysis, often with the appearance of bilateral vertical paralysis. Bilateral involvement in the pons is usually accompanied by only paralysis, horizontal in both directions. At the same time, vertical movements are preserved.
nystagmus- involuntary rhythmic movements of one or both eyes with a certain or any direction of gaze. Nystagmus may be pendulum, when eye movements in both directions are performed at the same speed and in the same volume, and jerky, in which there are two phases of the rhythm: the eye moves quickly in one direction (fast phase of nystagmus), in the opposite direction - slowly (slow phase of nystagmus). The direction of movement of nystagmus is determined by the direction of movement of its fast phase. In the direction of movement, horizontal, vertical, rotatory and mixed nystagmus are also distinguished. The latter is characterized by the presence of several components.
According to the intensity of movements three stages of nystagmus:
Stage I - nystagmus appears only when the eye is turned towards the fast phase, stage II - active nystagmus when the eye is turned towards the fast phase and when the gaze is directed straight, and, finally, stage III - pronounced nystagmus when looking straight, expressed when the gaze is directed to the side fast phase and weak nystagmus when moving the eye towards the slow phase.
By range of motion allocate small nystagmus, in which the amplitude of eye movements does not exceed 3 °; average nystagmus, in which the amplitude of movements ranges from 5 to 10 °, and gross nystagmus, eye oscillations with it are more than 15 °.
Nystagmus may be physiological and pathological. The latter occurs in diseases of the labyrinth or under the action of a pathological process on the nuclei of the vestibular nerve or the paths extending from it to the nuclei of the nerves of the oculomotor apparatus. Vestibular nystagmus is almost always jerky, and in the direction of movement - horizontal, vertical or rotatory. Labyrinthine, or peripheral, nystagmus always has one direction for all directions of gaze and does not depend on the position of the body. In addition, it does not differ in particular duration and tends to decrease as the duration of its existence increases. Often associated with dizziness and deafness.
Nuclear, or central, nystagmus can change its direction with a change in gaze, which is never observed with peripheral nystagmus. It exists for a long time, months and even years, if the cause that caused it is not eliminated. Usually, central nystagmus is not accompanied by hearing loss and tends to increase as the duration of its existence lengthens. Unlike peripheral nystagmus, it disappears when examining the patient in the dark (electronystagmography in the dark).
Central nystagmus usually occurs with tumors of subtentorial localization, especially in the region of the pontocerebellar angle. With tumors of the trunk, central pathological nystagmus is almost always a permanent symptom. Vestibular central nystagmus is also possible with supratentorial tumors (tumors of the frontal, temporal lobes), but in these cases it is due to the displacement of the brain by a growing tumor.
In recent years, researchers have attracted the attention of state of saccadic eye movements in various diseases of the central nervous system. Eye micromovements, or physiological nystagmus, are involuntary eye micromovements that occur when a fixed point is fixed. The function of saccadic eye movements is to move the image of objects to the region of the fovea of the retina. According to the nature of the emerging movements distinguish between drift, tremor and jumps.
Drift is called smooth, slow displacement of the eyes within 5-6 arc. min. Oscillatory movements with an amplitude of 20-40 arc. min and with a high frequency is called a tremor. Microjumps, or microsaccades, are rapid eye movements ranging from 1 arc. min up to 50 arc. min. The jumps of both eyes are normally always synchronous, have the same direction and amplitude.
S. A. Okhotsimskaya and V. A. Filin (1976, 1977) showed that saccadic eye movements with basal paresis and paralysis are directly dependent on the degree of damage to the oculomotor nerve. So, with paresis of a mild degree, microjumps practically do not differ from the norm. As the severity of paralysis increases, the interval between jumps increases, the number of jumps decreases. An increase in the degree of paralysis ultimately leads to a sharp decrease in the amplitude of all types of eye micromovements up to their complete disappearance. These changes correspond to the side of the lesion and do not depend on which eye is the fixer. The authors found that the amplitude of the drift increases with paresis, and decreases with paralysis.
Brain stem injury accompanied by a violation of the central mechanisms of control of fixation movements. The frequency, direction and amplitude of micromovements change, pathological spontaneous nystagmus occurs. As noted earlier, spontaneous nystagmus often precedes paresis and paralysis of the oculomotor nerves. The close topographic relationships of nuclei and supranuclear stem gaze centers in the brainstem usually lead to mixed lesions. Examining 15 patients with stem paralysis, S. A. Okhotsimskaya (1979) found that changes in saccadic eye movements can also be detected in cases where clinical gaze paresis is still absent. Thus, these changes can be regarded as early symptom developing gaze paresis with intra-stem lesions. A characteristic sign of unilateral nuclear paralysis, according to S. A. Okhotsimskaya, can be considered an asymmetry in the distribution of “jumps”, the loss of all types of jumps in the direction of the lesion for both eyes. This symptom was observed more clearly in patients with unilateral pontine tumors. With bilateral lesions of the trunk, jumps were absent even in cases of incomplete ophthalmoplegia.
Pupillary reaction disorders
The literature describes many syndromes associated with a disorder of pupillary reactions in diseases of the central nervous system. Of practical importance are those pupillary disorders that occur with brain tumors. Of these, the most important is pupillary reaction to light.
Before proceeding to a description of changes in the shape of the pupils and their reaction in patients with brain tumors, it is advisable to dwell on the anatomical features. pupillary reflex pathways(Fig. 81).
Figure 81. Scheme of the visual pathway and pupillary reflex. 1 - ciliary node; 2 - optical path; 3 - lateral geniculate body; 4 chiasma; 5 - optical radiation (Graziola beam); 6 - visual cortex, Yakubovich-Westphal-Edinger nuclei; 8 - anterior quadrigemina.
Afferent fibers of the pupillary reflex upon exiting the optic cords form a synapse in the anterior quadrigemina (regio pretectalis), from where they go to the nuclei of the oculomotor nerve (the Yakubovich-Westphal-Edinger nucleus), and some of the fibers go to the nucleus of the homolateral side, some of the fibers form a cross in the posterior commissure, after which they reach the contralateral nucleus of Yakubovich-Westphal- Edinger. Thus, each Yakubovich-Westphal-Edinger nucleus, which innervates the sphincter of the iris, has a representation of the fibers of the afferent pupillary arch of both the same and the opposite side. This explains the mechanism of direct and friendly pupillary reactions to light T.
In normal vision, there is synkinetic pupillary constriction with eyeball convergence or ciliary muscle contraction during accommodation. There is no clear understanding in the literature about mechanism of miosis in connection with convergence and accommodation. O. N. Sokolova (1963), referring to S. Duke Elder, describes this mechanism as follows: proprioceptive impulses arising from the contraction of the internal rectus muscles through the oculomotor nerve, and possibly through the trigeminal, reach the nuclei of the Vth nerve and Yakubovich's nuclei -Westphal-Edinger. Excitation of these nuclei leads to contraction of the pupillary sphinker. Accommodation is stimulated by visual impulses that originate in the retina and go to the cortex of the occipital lobe, and from there to the Yakubovich-Westphal-Edinger nuclei. The efferent path for convergence and accommodation is common and it passes as part of the oculomotor nerve to the ciliary muscle and to the sphincter of the pupil.
It was possible to identify the most subtle and delicate violations of pupillary reactions only with the help of method of local pupillography or local illumination of the investigated.
According to E. Zh. Tron (1966), impaired pupillary reactions are a very rare symptom in brain tumors (it occurs in no more than 1% of cases). Symptom of pupillary disorders appears, as a rule, with tumors of the quadrigemina of the epiphysis, III ventricle and Sylvian aqueduct. Occlusion the latter is accompanied by the appearance of an early symptom of impaired pupillary reactions in response to local illumination of the macular area while maintaining a reaction to accommodation and convergence [Sokolova ON, 1963]. The combination of pupillary disorders with disturbance of acts of accommodation and convergence is a later sign, indicating a significant spread of the tumor process, including the region of the quadrigemina. Tumors of the quadrigemina and pineal gland, in addition, may also be accompanied by paresis and paralysis of the gaze upward.
The shape and size of the pupils importance should also be attached, since a change in the size of the pupils can sometimes be one of the symptoms of the onset of blindness, of which the patient is not aware.
Normal Pupil Width varies in a fairly wide range - from 3 to 8 mm. It should be borne in mind that fluctuations in the diameter of the pupils are normally acceptable: anisocoria can reach. 0.9 mm [Samoilov A. Ya. et al., 1963]. Pupils in children are always wider than in adults. For pupil size influences the color of the iris. It is noticed that blue-eyed and gray-eyed pupils are wider than brown-eyed ones. Ophthalmologists are aware of the fact that pupils dilate in nearsighted people, so the nature of refraction should also be taken into account when assessing pupils. Unilateral myopia may be the cause of anisokeria. The latter is observed in diseases of the gallbladder, damage to the tops of the lungs.
For brain tumors anisocoria occurs in approximately 11% of patients [Tron E. Zh., 1966]. Paralytic mydriasis, especially combined with paresis of accommodation- a typical sign of damage to the oculomotor nucleus in the midbrain. A. Huber (1966) describes unilateral mydriasis in tumors of the temporal lobe. At the same time, anisocoria was combined with mild homolateral ptosis, which appeared before mydriasis and was caused by compression of the peripheral part of the oculomotor nerve near the clivius by a displaced brain or a growing tumor. As the tumor process progresses, paralysis of the external rectus muscles of the eye may join.
Tumors of the orbit, localized paraneurally and squeezing the ciliary node, sometimes cause mydriasis on the side of the lesion with mild exophthalmos or even before it appears [Brovkina A.F., 1974]. It should also be borne in mind that after orbitotomy and removal of the tumor, unilateral mydriasis with the correct form of the pupil, the lack of its reaction to light and convergence as a result of a violation of the efferent pupillary soul. We observed in such patients paresis of accommodation and a slight violation of the sensitivity of the cornea. Given that postoperative mydriasis persists for 8-12 months, this symptom should be taken into account in the differential diagnosis of brain tumors.
Unilateral mydriasis in combination with paresis of the rectus muscles of the eye occurs when the pathological process is located at the top of the orbit, in the region of the superior orbital fissure. Pituitary tumors with their extrasellar spread to the temporal side, causing paresis of the oculomotor nerve, can also lead to the appearance of unilateral mydriasis and ptosis.
In 1909, S. Baer described unilateral mydriasis in patients with tractus hemianopsia. A wide pupil and marked dilation of the palpebral fissure were found on the side of the hemianopia. The syndrome described by S. Baer seems to facilitate the topical diagnosis of a tumor accompanied by hemianopia. However, E. Zh. Tron, analyzing cases of injury to the occipital lobe, found hemianopsia with anisocoria in 1/3 of cases. According to I. I. Merkulov (1971), this does not detract from the advantages of Baer's syndrome in the topical diagnosis of tractus hemianopsia.
Visual field changes
Brain tumors in almost half of the cases are associated with visual field changes. Often these changes make it possible to make a topical diagnosis of a tumor lesion.
The optimal use should be kinetic and static perimetry, both suprathreshold and quantitative. In this case, the boundaries of the field of view from 1 to 3 isopters are examined. However, it should be noted that in most cases in neurological patients it is extremely difficult to investigate isopters as well as to conduct profile static perimetry. This is due to the rapid fatigue of the patient, insufficient attention and often the lack of sufficient contact between the patient and the doctor. In such cases, it may be useful to study the central field of view (up to 25 ° from the fixation point) with multiple objects on the so-called field of view analyzers [Astralenko GG, 1978; Friedman, 1976]. When examining the visual field analyzer, the patient is presented with 2 to 4 suprathreshold objects at the same time, from 50 to 100 objects in total. Examination of one eye takes 2-3 minutes.
In patients with low visual acuity or with the lack of proper attention, it is advisable to use a simple, so-called control method (confrontation test), in which the field of view of the researcher is compared with the field of view of the researcher. The technique of the control method of studying the visual field is described in all manuals. Less well known is the test proposed by A. Kestenbaum (1947). It is unreasonably little used in the control study of neurological patients.
The essence of the Kestenbaum test or "contour" perimetry is that the field of view in the plane of the face approximately coincides with the outlines of the face of the subject. Therefore, the contours of the patient's face can serve as a reference point. The test is carried out as follows. The patient looks straight ahead. The researcher, being behind, moves the object (finger or pencil) from the periphery to the center along 12 meridians in the plane of the patient's face, but no further than 2 cm (!) from him. The patient must report when he begins to distinguish the object. Normally, the field of view should coincide with the contours of the face: the nasal border runs along the line of the nose, the temporal border - along the bony edge of the outer wall of the orbit. A. Kestenbaum believes that the method error in the hands of an experienced researcher does not exceed 10°.
Simplified methods for studying the visual field include the test reflex closure of the eye. A hand is held in front of the patient's eye from four sides, reflexively the eyelids close. With hemianopsia in the zone of lack of vision, closing of the eyelids will not occur. This test can be recommended when examining patients with stupor, aphasia, or with a decrease in visual acuity to the movement of the hand near the face.
Control Study for relative hemianopia carried out with open both eyes of the patient. The doctor moves both hands (or two fingers) symmetrically from the temple to the center along the four meridians. The main condition should be good lighting. The patient must say when he sees one or two hands or when he recognizes their contours (with poor visual acuity). If there is a difference in perception on both sides, one can speak of relative hemianopia, as opposed to absolute hemianopia, which can only be detected with an isolated examination of each eye. However, early topical diagnosis in lesions of the visual-neural pathway requires a qualified study using kinetic perimetry with a sufficient number of objects and campimetry.
A. Huber (1976) believes that at present there is no point in making perimetry on colors. To detect scotoma in red, which is one of the early signs of developing atrophy of the optic nerve or tract, it is quite enough to conduct perimetry with a red object of 5 mm from a distance of 33 cm (5/330).
At the core topical diagnostics damage to the visual-nerve pathway in brain tumors lies a clear idea of the course of its fibers. A schematic representation of the visual pathway is shown in fig. 82.
Rice. 82. Scheme of the location of nerve fibers in the chiasm. 1 - retina; 2 - optic nerve; 3 - chiasma; 4 - optical path; 5 - diagram of the cross section of the chiasm; 6 - pituitary gland; 7 - zone of passage and intersection of the papillomacular bundle.
We think it's worth stopping on some features of the cross nerve fibers in the chiasm. Non-crossing nerve fibers, starting from the outer halves of the retina, pass in the outer part of the optic nerve. They also occupy a lateral position in the chiasm and optic tracts. The fibers from the nasal halves of the retina in the chiasm have a decussation. The level of decussation depends on the location of the nerve fibers in the retina and optic nerve. Fibers starting from the lower nasal sections of the retina are located in the lower sections of the optic nerve. In the chiasm, they pass to the opposite side at its anterior edge closer to the lower surface. After crossing the chiasma, these fibers go for some distance into the opposite optic nerve, where they form the anterior knee of the chiasma. Only after that they, located medially, pass into the optic tract. From the upper nasal sections of the retina, the nerve fibers, located in the upper half of the optic nerve, pass to the other side at the posterior edge of the chiasma closer to its upper surface. Before the intersection, they enter the optic tract of the same side, where they form the posterior knee of the chiasma. The bulk of the crossed fibers is located in the medial parts of the chiasm. It should be remembered that the crossover is also carried out by the fibers of the papillomacular bundle.
The main types of visual field changes, occurring in brain tumors, are the following: 1) concentric narrowing of the visual field (symmetrical or eccentric); 2) unilateral sector-shaped visual field defects; 3) absolute or relative scotomas (central, paracentral, cecocentral); 4) heteronymous bitemporal and binasal hemianopsias; 5) homonymous hemianopsia. The listed defects of the visual field, depending on the level of damage to the visual-nerve path, are shown in Fig. 83.
Rice. 83. Scheme of typical changes in visual fields depending on the level of localization of the pathological focus (according to Duke-Elder S.).
1 - unilateral amaurosis with monolateral damage to the optic nerve; 2 - unilateral amaurosis and contralateral temporal hemianopia in case of damage to the intracranial portion of the optic nerve near the chiasm; 3 - bitemporal over hemianopsia with damage to the medial part of the chiasm; 4 - incongruent homonymous hemianopsia with damage to the optical tract; 5 - homonymous hemianopsia without preservation of the macular zone in case of damage to the posterior part of the optical tract or the anterior part of the optical radiation; 6 - incongruent upper homonymous quadrantopsia with damage to the anterior part of optical radiation (temporal lobe); 7 - mild incongruent homonymous lower quadrantopsia with damage to the inner part of optical radiation (parietal lobe); 8 - incongruent homonymous hemianopia without preservation of the macular zone in case of damage to the middle part of optical radiation; 9 - congruent homonymous hemianopsia with preservation of the macular zone in case of damage to the back of the optical radiation; 10 - congruent homonymous hemianopsic central scotoma with damage to the occipital lobe.
Of primary importance for the topical diagnosis of damage to the visual-nerve path are hemianopic visual field defects[Troya E. Zh., 1968]. They can be unilateral or bilateral, complete, partial, quadrant (quadrantopia) and, finally, can be presented as hemianopic scotomas (central or paracentral).
Unilateral hemianopic changes develop with lesions intracranial portion of the optic nerve. Bilateral hemianopic defects occur when nerve fibers in the chiasm, optic tracts, or central optic neuron are affected. They can be heteronymous when opposite sides of the visual fields fall out (binasal or bitemporal, Fig. 84)
Rice. 87. Incomplete homonymous incongruent left-sided hemianopsia (lesion at the level of the anterior sections of the right optic radiation).
The nervous type of hemianopia occurs with lesions in the posterior part of the radiatio optica or in the cerebral cortex. The second type of hemianopsia is detected in patients with damage to the visual tracts.
Concentric narrowing of the visual field in patients with a brain tumor is usually due to developing secondary postcongestive atrophy of the optic nerve. Bilateral tubular narrowing of the visual field is sometimes the result of bilateral homonymous hemianopsia with preservation of the macular region in patients with a tumor localized in the spur sulcus. Unilateral concentric constriction field of vision is observed in cases of involvement in the pathological process of the intracranial part of the optic nerve between the optic opening and the chiasm. This can be observed with tumors of the optic nerve itself, meningiomas of the tubercle of the Turkish saddle, the crest of the sphenoid bone, or the olfactory fossa. The described changes in the visual field were also observed in craniopharyngiomas, pituitary adenomas with extrasellar distribution.
Without dwelling on other causes that cause unilateral concentric narrowing of the visual field (diseases of the retina, orbital part of the optic nerve), we consider it necessary to emphasize difficulty in differential diagnosis his reasons. In some cases, the true genesis of optic nerve atrophy and perimetric symptoms can only be established by analyzing a whole range of additional research methods, and, perhaps, by dynamic observation over a period of time.
Unilateral visual field defects are more common combined with scotomas. A. Huber (1976) observed quadrant unilateral defects visual fields merging with the area of the blind spot, with compression of the optic nerve by the tumor. We observed similar changes [Brovkina AF, 1974] in the case of eccentric growth of meningioma of the orbital part of the optic nerve. With a sufficiently high visual acuity (0.5 on the side of the lesion), a lower temporal visual field defect was determined in the visual field, merging with the blind spot area (Fig. 88).
Rice. 88. Unilateral inferior temporal quadrantopsia in a patient with a tumor of the right optic nerve.
Of great importance in the early diagnosis of tumor lesions of the visual-nerve pathways is absolute or relative livestock. At the onset of the disease, they can only be determined when examining colored objects or when examining small objects for white (no more than 1 mm on the Foerster perimeter or 0.25 mm on hemispherical perimeters). By location, these scotomas are classified into central, paracentral, caecocentral, and peripheral.
Unilateral central or paracentral scotomas s arise when the optic nerve is involved in the pathological process in its orbital (Brovkina A. F., 1974) or intracranial part [Tron E. Zh., 1968; Huber A., 1976].
Scotomas in chiasm tumors can be unilateral or bilateral, forming typical temporal hemianopic defects.
Homonymous hemianopic central scotomas develop only in cases of damage to the papillomacular bundle above the chiasm. The anatomical justification for the appearance of these symptoms is the isolated position of the papillomacular bundle and its partial decussation in the chiasm. However, homonymous hemianopic scotomas rarely occur with tumors involving the optic tract. More often they are associated with damage to the radiatio optica and are negative, that is, they are not felt by the patient. These scotomas should be regarded as a sign of a slowly progressive lesion of the optic nerve pathway in the postchiasmatic region.
Heteronymous bitemporal defects visual fields are almost pathognomonic for lesions of the central part of the chiasm.
It is known that chiasma from above it borders on the bottom of the third ventricle, from below - with the diaphragm of the Turkish saddle, behind the chiasm adjoins the infundibulum, descending from the gray tubercle to the pituitary gland. In front, the chiasm sometimes closely adjoins the main bone in the region of the chiasmal groove. From the sides, the chiasma is surrounded by the arteries of the circle of Willis. Thus, tumors growing in the region of the chiasm are capable of cause damage to fibers in any part of the chiasma, but mainly in its central section. So, for example, tumors of the sella turcica lead to the appearance of typical bitemporal hemianopsia or hemyapopist bitemporal defects in the field of view. Symmetrical bitemporal quadrantopsia or hemianopsia are most common in pituitary tumors, while asymmetric bitemporal hemianopsia or quadrantopsia are more common in parasellar or suprasellar tumors (Fig. 89).
Rice. 89. Hemianopic bitemporal visual field defects with compression of the chiasm from above.
Often, tumors are asymmetric growth pattern. In such cases, one of the optic nerves (with tumor growth anteriorly) or the optic tract (with tumor growth posteriorly) may be directly involved in the tumor process. As a result, typical symptoms develop, shown in Fig. 82.
Homonymous hemianopia visual field defects indicate damage to the optic tract or the central neuron of the optic pathway on the opposite side. Homonymous hemianopic defects in the form of quadrantopsia indicate an incomplete interruption of the optical path or optical radiation. With classic homonymous hemianopsia, there is no doubt that the visual-nerve path is damaged in some area throughout the entire diameter. It is possible to differentiate tractus hemianopsia from hemianopsia caused by a lesion of radiatio optica and above by signs of congruence. An incongruent onset with a progressive change in visual fields passing through the fixation point (without preserving the macular area), blanching of the temporal half of the optic disc is characteristic of lesions of the optic tract (tumors of the temporal lobe, middle fossa, thalamus, quadrigemina). Tumors of the temporal lobe often accompanied by the appearance of upper quadrant hemianopia; on the contrary, lower quadrant hemianopsia occurs in patients with tumors of the parietal region. With tumors of the occipital lobe, complete homonymous hemianopsia develops. According to A. Huber, congruent homonymous hemianopsias without preservation of the macular region most often indicate a complete lesion of the radiatio optica.
Continued in the next article: Changes in the organ of vision in diseases of the central nervous system | Part 3
Article from the book: .
PARASES AND PARESIS OF THE EYE MUSCLES. Etiology and pathogenesis. They occur when the nuclei or trunks of the oculomotor, trochlear and abducent nerves are damaged, as well as as a result of damage to these nerves in the muscles or the muscles themselves. Nuclear paralysis is observed mainly with hemorrhages and tumors in the nuclear region, with tabes, progressive paralysis, encephalitis, multiple sclerosis, and skull trauma. Stem or basal paralysis develops as a result of meningitis, toxic and infectious neuritis, fractures of the base of the skull, mechanical compression of the nerves (for example, by a tumor), and vascular diseases at the base of the brain. Orbital or muscle lesions occur in diseases of the orbit (tumors, periostitis, subperiosteal abscesses), trichinosis, myositis, after injuries.
Symptoms. With an isolated lesion of one of the muscles, the deviation of the diseased eye in the opposite direction (paralytic strabismus). The angle of strabismus increases as the gaze moves and the direction of action of the affected muscle. When fixing any object with a paralyzed eye, the healthy eye deviates, and at a much larger angle compared to that at which the diseased eye was deviated (the angle of the secondary deviation is greater than the angle of the primary deviation). Eye movements in the direction of the affected muscle are absent or severely limited. There is double vision (usually with fresh lesions) and dizziness that disappears when one eye is closed. The ability to correctly assess the location of an object viewed by a sore eye is often impaired (false monocular projection or localization). There may be a forced position of the head - turning or tilting it in one direction or another.
Diverse and complex clinical picture occurs in cases of simultaneous damage to several muscles in one or both eyes. With paralysis of the oculomotor nerve, the upper eyelid is lowered, the eye is deviated outward and somewhat downward and can only move in these directions, the pupil is dilated, does not respond to light, accommodation is paralyzed. If all three nerves are affected - the oculomotor, block and abducent, then complete ophthalmoplegia is observed: the eye is completely motionless. There are also incomplete external ophthalmoplegia, in which the external muscles of the eye are paralyzed, but the sphincter of the pupil and the ciliary muscle are not affected, and internal ophthalmoplegia, when only these last two muscles are affected.
Flow depends on the underlying disease, but, as a rule, long-term. Sometimes the process remains persistent even after the cause has been eliminated. In some patients, double vision disappears over time due to active suppression (inhibition) of the visual impressions of the deviated eye.
Diagnosis based on characteristic symptoms. It is important to establish which muscle or group of muscles is affected, for which they resort mainly to the study of double images. To clarify the etiology of the process requires a thorough neurological examination.
Treatment. Treatment of the underlying disease. Exercises for the development of eye mobility. Electrical stimulation of the affected muscle. With persistent paralysis - surgery. To eliminate double vision, glasses with prisms or a bandage over one eye are used.
Motor neurons of the oculomotor nerves (n. oculomotorius, third pair of cranial nerves) are located on both sides of the midline in the rostral part of the midbrain. These nuclei of the oculomotor nerve are innervated by five external muscles of the eyeball, including the muscle that lifts the upper eyelid. The nuclei of the oculomotor nerve also contain parasympathetic neurons (Edinger-Westphal nucleus) involved in the processes of pupil constriction and accommodation.
There is a division of the supranuclear groups of motor neurons for each individual muscle of the eye. The fibers of the oculomotor nerve that innervates the medial rectus, inferior oblique and inferior rectus muscles of the eye are located on the same side. The subnucleus of the oculomotor nerve for the superior rectus muscle is located on the contralateral side. The levator levator muscle of the upper eyelid is innervated by the central group of cells of the oculomotor nerve.
Block nerve (n. trochlearis, IV pair of cranial nerves)
Motoneurons of the trochlear nerve (n. trochlearis, IV pair of cranial nerves) are closely adjacent to the main part of the complex of nuclei of the oculomotor nerve. The left nucleus of the trochlear nerve innervates the right superior oblique muscle of the eye, the right nucleus - the left superior oblique muscle of the eye.
Abducens nerve (n. abducens, VI pair of cranial nerves)
Motor neurons of the abducens nerve (n. abducens, VI pair of cranial nerves), which innervates the lateral (external) rectus muscle of the eye on the same side, are located in the nucleus of the abducens nerve in the caudal part of the bridge. All three oculomotor nerves, leaving the brainstem, pass through the cavernous sinus and enter the orbit through the superior orbital fissure.
Clear binocular vision is provided precisely by the joint activity of individual muscles of the eye (oculomotor muscles). Friendly movements of the eyeballs are controlled by the supranuclear gaze centers and their connections. Functionally, there are five distinct supranuclear systems. These systems provide different types of eyeball movements. Among them there are centers controlling:
- saccadic (rapid) eye movements
- purposeful eye movements
- converging eye movements
- keeping the eye in a fixed position
- vestibular centers
Saccadic (rapid) eye movements
Saccadic (fast) movements of the eyeball occur as a command in the opposite visual field of the cortex of the frontal region of the brain (field 8). The exception is fast (saccadic) movements that occur when the fovea fovea is stimulated and originate from the occipital-parietal region of the brain. These frontal and occipital control centers in the brain have projections on both sides to the supranuclear stem centers. The activity of these supranuclear stem vision centers is also influenced by the cerebellum and the complex of vestibular nuclei. The paracentral divisions of the reticular formation of the bridge are the stem center, which provides friendly fast (saccadic) movements of the eyeballs. Simultaneous innervation of the internal (medial) rectus and opposite external (lateral) rectus muscles during horizontal movement of the eyeballs is provided by the medial longitudinal bundle. This medial longitudinal bundle connects the nucleus of the abducens nerve with the subnucleus of the complex of oculomotor nuclei, which are responsible for the innervation of the opposite internal (medial) rectus muscle of the eye. For the onset of vertical rapid (saccadic) eye movements, bilateral stimulation of the paracentral sections of the pontine reticular formation from the side of the cortical structures of the brain is required. The paracentral divisions of the reticular formation of the bridge transmit signals from the brain stem to the supranuclear centers that control the vertical movements of the eyeballs. The rostral interstitial nucleus of the medial longitudinal fasciculus, located in the midbrain, belongs to such a supranuclear eye movement center.
Purposeful eye movements
The cortical center for smooth targeted or tracking movements of the eyeballs is located in the occipito-parietal region of the brain. Control is exercised from the side of the same name, i.e., the right occipital-parietal region of the brain controls smooth, purposeful eye movements to the right.
Converging eye movements
The mechanisms of control of converging movements are less understood, however, as is known, the neurons responsible for converging eye movements are located in the reticular formation of the midbrain surrounding the complex of nuclei of the oculomotor nerve. They give projections to the motor neurons of the internal (medial) rectus muscle of the eye.
Keeping the eye in a certain position
Stem centers of eye movement, called neuronal integrators. They are responsible for keeping the gaze in a certain position. These centers change incoming signals about the speed of movement of the eyeballs into information about their position. Neurons with this property are located in the pons below (caudal to) the nucleus of the abducens nerve.
Eye movement with changes in gravity and acceleration
The coordination of eyeball movements in response to changes in gravity and acceleration is carried out by the vestibular system (vestibulo-ocular reflex). If the coordination of the movements of both eyes is disturbed, double vision develops, since images are projected onto disparate (inappropriate) areas of the retina. In congenital strabismus, or strabismus, an imbalance in the muscles that causes the eyeballs to be misaligned (non-paralytic strabismus) can cause the brain to suppress one of the images. This decrease in visual acuity in the non-fixing eye is called amblyopia without anopsia. In paralytic strabismus, double vision occurs as a result of paralysis of the muscles of the eyeball, usually due to damage to the oculomotor (III), trochlear (IV), or abducens (VI) cranial nerves.
Muscles of the eyeball and gaze paralysis
There are three types of paralysis of the external muscles of the eyeball:
Paralysis of individual muscles of the eye
Characteristic clinical manifestations occur with isolated injuries of the oculomotor (III), trochlear (IV) or abducens (VI) nerve.
Complete damage to the oculomotor (III) nerve leads to ptosis. Ptosis manifests itself in the form of a weakening (paresis) of the muscle that lifts the upper eyelid and a violation of voluntary movements of the eyeball upward, downward and inward, as well as divergent strabismus due to the preservation of the functions of the lateral (lateral) rectus muscle. If the oculomotor (III) nerve is damaged, pupil dilation and the absence of its reaction to light (iridoplegia) and accommodation paralysis (cycloplegia) also occur. Isolated paralysis of the muscles of the iris and ciliary body is called internal ophthalmoplegia.
Damage to the trochlear (IV) nerve causes paralysis of the superior oblique muscle of the eye. Such damage to the trochlear (IV) nerve leads to an outward deviation of the eyeball and difficulty in moving (paresis) downward gaze. Paresis of downward gaze is most clearly manifested when the eyes are turned inwards. Diplopia (doubling) disappears when the head is tilted to the opposite shoulder, at which there is a compensatory deviation of the intact eyeball inwards.
Damage to the abducens (VI) nerve leads to paralysis of the muscles that divert the eyeball to the side. When the abducens (VI) nerve is damaged, convergent strabismus develops due to the predominance of the influence of the tone of the normally working internal (medial) rectus muscle of the eye. With incomplete paralysis of the abducens (VI) nerve, the patient can turn his head towards the affected abducens muscle of the eye in order to eliminate the doubling he has with the help of a compensatory effect on the weakened lateral (lateral) rectus muscle of the eye.
The severity of the above symptoms in case of damage to the oculomotor (III), trochlear (IV) or abducens (VI) nerve will depend on the severity of the lesion and its location in the patient.
Friendly Gaze Paralysis
Friendly gaze is the simultaneous movement of both eyes in the same direction. Acute damage to one of the frontal lobes, for example, in case of cerebral infarction (ischemic stroke), can lead to transient paralysis of voluntary friendly movements of the eyeballs in the horizontal direction. At the same time, independent eye movements in all directions will be completely preserved. Paralysis of voluntary friendly movements of the eyeballs in the horizontal direction is detected with the help of the eye phenomenon of a doll with a passive turn of the head of a horizontally lying person or with the help of caloric stimulation (infusion of cold water into the external auditory meatus).
Unilateral damage to the paracentral part of the reticular formation of the bridge located downwards at the level of the nucleus of the abducens nerve causes persistent gaze paralysis in the direction of the lesion and loss of the oculocephalic reflex. The oculocephalic reflex is a motor reaction of the eyes to stimulation of the vestibular apparatus, as in the phenomenon of the head and eyes of a doll or caloric stimulation of the walls of the external auditory canal with cold water.
Damage to the rostral interstitial nucleus of the medial longitudinal fasciculus in the anterior midbrain and/or injury to the posterior commissure causes upward gaze supranuclear palsy. To this focal neurological symptom is added the dissociated reaction of the patient's pupils to light:
- sluggish pupillary response to light
- quick reaction of the pupils to accommodation (change in the focal length of the eye) and look at closely spaced objects
In some cases, the patient also develops convergence paralysis (the movement of the eyes towards each other, in which the gaze will focus on the bridge of the nose). This symptom complex is called Parino's syndrome. Parino syndrome occurs with tumors in the pineal gland, in some cases with cerebral infarction (ischemic stroke), multiple sclerosis and hydrocephalus.
Isolated downward gaze palsy is rare in patients. When this occurs, obstruction of the lumen (occlusion) of the penetrating midline arteries and bilateral infarcts (ischemic strokes) of the midbrain are the most common causes. Some hereditary extrapyramidal diseases (Huntington's chorea, progressive supranuclear palsy) can cause restrictions on the movement of the eyeballs in all directions, especially upward.
Mixed paralysis of the gaze and individual muscles of the eyeball
The simultaneous combination in a patient of gaze paralysis and paralysis of individual muscles that move the eyeball is usually a sign of damage to the midbrain or pons of the brain. Damage to the lower parts of the pons with destruction of the nuclei of the abducens nerve located there can lead to paralysis of rapid (saccadic) movements of the eyeballs horizontally and paralysis of the lateral (external) rectus muscle of the eye (abducens nerve, VI) on the side of the lesion.
With lesions of the medial longitudinal bundle, various disorders of gaze in the horizontal direction occur (internuclear ophthalmoplegia).
Unilateral damage to the medial longitudinal bundle, caused by a heart attack (ischemic stroke) or demyelination, leads to a violation of bringing the eyeball inward (to the bridge of the nose). This can be clinically manifested as complete paralysis with the inability to abduct the eyeball medially from the midline, or as a mild paresis, which manifests itself in the form of a decrease in the speed of adducting rapid (saccadic) movements of the eye to the bridge of the nose (adductive (adduction) delay). Abduction (abduction) nystagmus is usually observed on the side opposite to the lesion of the medial longitudinal fasciculus: nystagmus that occurs when the eyeballs are retracted outward with a slow phase directed towards the midline and fast horizontal saccadic movements. The asymmetric arrangement of the eyeballs relative to the vertical line often develops with unilateral internuclear ophthalmoplegia. On the side of the lesion, the eye will be located higher (hypertropia).
Bilateral internuclear ophthalmoplegia occurs with demyelinating processes, tumors, infarcts, or arteriovenous malformations. Bilateral internuclear ophthalmoplegia leads to a more complete syndrome of eyeball movement disorders, which are manifested by bilateral paresis of the muscles that bring the eyeball to the bridge of the nose, a violation of vertical movements, tracking purposeful movements and movements due to the influence of the vestibular system. Note the violation of the gaze along the vertical line, nystagmus upward when looking up and nystagmus down when looking down. Lesions of the medial longitudinal fasciculus in the overlying (rostral) parts of the midbrain are accompanied by a violation of convergence (convergent movement of the eyes towards each other, towards the bridge of the nose).
Gaze paralysis is a violation of friendly movements of the eyeballs in one direction OR another (Fig. 30).
The cortical center of gaze is localized in the posterior sections of the 2nd frontal gyrus (fields 8.6) (Fig. 10). In addition, there are additional centers of gaze - in the parietal, temporal and occipital lobes.
Of great importance in the implementation of friendly movements of the eyeballs is the posterior longitudinal bundle, the extrapyramidal system, and the cerebellum. The posterior longitudinal bundle is a system of connections that provides complex reflex reactions, including combined movements of the eyes and head, eyes, vegetative affects, etc. It consists of descending and ascending fibers. Descending fibers originate from the cells of the interstitial nucleus of Cajal and slightly below the nucleus of Darkshevich. Both cores are laid under the bottom of the Sylvian aqueduct. To descending fibers from nuclei
Cahal and Darkshevich are joined by fibers from the vestibular nuclei, mainly from the nucleus of Deiters (vestibulospinal path) (Fig. 31).
Descending fibers of the posterior longitudinal bundle descend under the bottom
II ventricle near the midline, terminate at the nucleus of the XI pair and at the cells of the anterior horns, mainly the cervical part of the spinal cord. From the estibular nuclei - Bechterew's (n. vezblyana air.) and the triangular nucleus (n. linangu1anz, n. s1sha1e zei n. vesibu1anas dorgzanz) - ascending fibers originate. The system of fibers of the posterior longitudinal bundle connects nuclei III and
VI pairs of CN in such a way that the nucleus of the VI pair, which innervates the external rectus muscle, is connected with that part of the nucleus of the III pair, which innervates the internal rectus muscle of the contralateral side. This connection ensures that the eyes turn to the right or to the left (Fig. 20, 32).
Combined eye movements up or down are carried out by a system of connections through fibers coming from the Cajal nuclei. Through the vestibular nuclei, the posterior longitudinal bundle communicates with the cerebellum. The system of the posterior longitudinal bundle also includes fibers from the nuclei IX, X pairs of CN, the reticular formation of the trunk. Thanks to the above connections, tonogenic effects of the extrapyramidal system on the muscles of the neck are carried out through the gamma broom system; the inclusion of muscles of agonists and antagonists is regulated, adequate vegetative reactions are provided.
Differential diagnosis of supranuclear and stem gaze palsies.
With supranuclear palsies, reflex movements of the eyeballs are preserved, which can be detected using special techniques:
1. The phenomenon of "doll eyes". The patient is not able to voluntarily follow a moving object, but if he is asked to fix his gaze on any object and passively tilt his head or turn it to the sides, then the patient seems to follow him.
2. Caloric test - instillation of cold water into the ear causes slow involuntary eye movements.
3. The Bell phenomenon. In supranuclear vertical gaze palsies, if you ask the patient to close the eyelids and then passively lift them, then a reflex upward movement of the eyes can be detected.
Cortical gaze paralysis is short-lived, eye movements are quickly restored due to connections with the other hemisphere and the existence of additional gaze centers. If the restriction of friendly eye movements remains for a long time, then this rather indicates the stem localization of the process.
Nuclear stem gaze palsy, as a rule, is combined with peripheral paralysis of the abducens and facial nerves.
The combined rotation of the eyes and head is always due to the cortical localization of the focus, the spasm of upward gaze occurs exclusively with the focus in the trunk.
Semiotics of gaze paralysis (Fig. 10, 32). Posterior sections of the second frontal gyrus (fields 8.6). With this localization of the process, both symptoms of irritation and loss can be observed. Irritation syndrome occurs in the presence of irritative foci. It is characterized by a turn of the eyes and head towards the healthy hemisphere, due to the transmission of irritation
on the nuclei of the abducens and oculomotor nerves associated with the innervation of the external and internal rectus muscles of the opposite side. Following this, paresis of these muscles develops, the function of opposite muscles begins to prevail, and the eyes "look at the focus" and "turn away" from the paralyzed limbs.
Gaze gaps can also occur when foci are localized in additional centers of gaze. In these cases, patients are not aware of their defect, in contrast * to gaze paresis with lesions in the main center of gaze. When irritated in the occipital center of the gaze, along with turning the eyes, visual hallucinations are observed. When its function falls out, there is a transient deviation of the eyes to the sides of the focus. With the destruction of the frontal center of the gaze, the reflex movements of the eyes are preserved (the positive phenomenon of "doll eyes"); when the occipital center of the gaze is destroyed, the reflex movements of the eyes disappear (negative pshomen of “doll eyes”). The patient voluntarily follows the movement of the object.
In caustic cases, there may be a bilateral shutdown of the cortical-stem oculomotor tracts (Rothe-Bilshovsky syndrome, cited by "Krolk M.B., Fedorova E.A., 1966). It occurs in some cases of pseudobulbar paralysis and is characterized by a persistent violation voluntary lateral eye movements with the preservation of reflex ones. Pseudobullar paralysis in the localization of the process in the trunk is not accompanied by gaze paresis. This is due to the fact that the cortical-nuclear path to the nuclei III, IV, VI pairs of CN passes in the trunk cover separately from pyramidal p / ti, which occupies the base and can be affected independently.
Oval gaze palsy (Fig. 32) occurs when the focus is located in the covering of the pons near the nucleus of the abducens nerve. With bridging gaze paralysis, the eyes are deviated in the direction opposite to the focus, and “look” at the parsed limbs. Due to the fact that hairs descend to the core of the XI pair in the tire, along with gaze paralysis, it is possible to turn the head in a storzha, the opposite deviation of the eyes ( the function of the sternocleidomastoid muscle on the side of the focus falls out, as a result, the function of the muscle of the other side begins to predominate, and the head turns in the direction of gaze paresis). carbamazepine).
Isolated stem gaze palsy is rarely observed, more often it protes with paresis on the side of the focus of the abducens and facial nerves and is included in the category of alternating syndromes.
Raymond-Sestan syndrome is topically associated with the pons. With it, gaze paresis, choreoathetoid hyperkinesis is determined on the side of the focus, 1 on the opposite side - a pyramidal syndrome or impaired sensitivity according to the hemitype, or a combination of these syndromes (Fig. 33.A). Bilateral paralysis of the horizontal gaze has been described in multiple sclerosis, infarction of the pons, hemorrhage in the pons, metastases, cerebellar abscess, and congenital defects of the central nervous system.
Looking up (Fig. 30) is observed in tumors of the quadrigemina, pineal gland, inflammatory processes in the zone of the Sylvian aqueduct, degenerative diseases of the nervous system (olivo-ponto-cerebellar degeneration, primary cerebellar atrophy, progressive infranuclear palsy). In tumors of the pineal gland, it is more often supranuclear in nature; in degenerations, it may be due to damage to the nuclei. Supranuclear palsy of vertical gaze can be differentiated from peripheral gaze using Bell's phenomena, "doll eyes", and a caloric test (see above).
Parino syndrome. The most common cause is a tumor of the pineal gland. Clinically, it manifests itself as paresis of the upward gaze in combination with convergence paralysis, sometimes with a violation of pupillary reactions. Vertical gaze paresis can serve as a formidable sign of the displacement of the cerebral hemispheres into the opening of the cerebellum tenon. It is included in the structure of the so-called mesencephalic syndrome (displacement stage) and is combined with vertical nystagmus, sluggish pupillary reactions.
These symptoms usually characterize the onset of displacement. They are followed by oculomotor disorders - first ptosis, then limitation of the mobility of the eyeballs. Unilateral ptosis with mydriasis and impaired pupillary reflex, as a rule, corresponds to the side of the pathological process.
Oculomotor disorders are due to pressing the III pair of CNs to the Blumenbach clivus, vessels, and hemodynamic disorders. In mesencephalic syndrome, vertical gaze paresis is never combined with impaired convergence and hearing. The last symptoms always indicate the localization of the process in the trunk.
As the displacement progresses, signs of compression of the tegmental pedicle appear. The extrapyramidal, cerebellar-1H.1C pathways are concentrated here, the n. ruber with its afferent and efferent connections is located (Fig. 13). The consequence of compression will be: violations of the tone in the limbs (diffuse muscle hypotension; increased tone in the extrapyramidal muscle; flexor setting of the arms with the extensor - legs; dissociated meningeal syndrome), hyperkinesis, intentional tremor, pyramidal gimptomatics on its own and opposite sides (Dukhin A.L. , 1963).
With an increase in displacement, signs of damage to V, VI, VII, IX, X, XII pairs of CN appear (mesencephalic-pontine and pontine-bulbar syndromes, cerebellar and occlusive-hydrocephalic syndromes). 11 CN lesions often occur on the side of the tumor. Moreover, the early appearance of figeminal pain, a unilateral decrease in the corneal reflex is attributed to the temporal-basal localization, damage to the motor t. Hydrocephalic-occlusive syndrome is caused by the deviation of the Sylvian aqueduct.
With dislocation syndrome, it is very difficult to resolve the issue of the primary "tissue" of the focus - whether it is located in the sub- or supratentorial space. To solve it, it is necessary to take into account the dynamics of the process, including muscle-tonic phenomena, which are more characteristic of the guiratentorial localization of the focus.
T.V. MATVEEVA
In acute occlusive hydrocephalus, the so-called "setting sun" syndrome occurs - the deviation of the eyeballs down with constriction of the pupils.
Gruner-Bertolotti syndrome - paresis of gaze up, impaired pupillary reactions to light, paresis of III and IV pairs of CN on the side of the focus, on the opposite side - capsular syndrome (hemiplegia with central paresis of the facial and hypoglossal nerves, hemianesthesia and homonymous hemianopsia). Occurs when blood circulation is disturbed in the pool of the anterior villous artery.
