To determine the level lesions with such deviation of the eyes in general, the following considerations are relevant. Most of the supranuclear frontopoitin fibers ending in the pontine center of the gaze are crossed and come from the opposite hemisphere of the cerebrum. Only a small part of the fibers comes from the hemisphere on the same side.
Crossed supranuclear pathway for horizontal directions of gaze, passes the centerline at the level of the front edge of the bridge. If this path is interrupted by a pathological process located proximal to the intersection, then when the focus is located on the right, it becomes impossible to look to the left. If the right-sided focus is located in the bridge, that is, distal from the intersection, then the look to the right falls out. Due to the predominance of continuous antagonistic innervation, there is a deviation of the eyes: in the first case to the right and in the second to the left.
When, in this way, when you turn off supranuclear innervation Deviation conjuguee develops, first described by the Geneva physiologist Provost, then when the focus is located above the bridge, the patient looks towards the focus. If there is a break in the bridge, then the patient, in contrast, looks in the direction opposite to the focus.
Deviation conjuguee however, is not a persistent symptom. For the innervation of the lateral directions of gaze, the hemisphere of the opposite side is of predominant importance. Along with this, those ratios that we have stated in relation to bilateral cortical innervation of the eye muscles are also important. So, with cerebral hemorrhage (the most common cause of Deviation conjuguee), the patient looks towards the focus of the disease only during the first quarter of an hour or the first hours after a stroke. This is an excellent criterion for determining on which side the hemiplegia is present even in the stage of general muscle relaxation.
Then this phenomenon, which is often combined with a long turn of the head of the same name, disappears. The latter is due to the fact that instead of the switched off conductors, corticonuclear connections of another hemisphere are switched on.
Thus, temporary Deviation conjuguee indicates the location of the lesion "somewhere" between the cortex and the bridge. For a more accurate localization, it is necessary to take into account other, including non-ocular, symptoms. Clinical experience shows that in cases where the Deviation conjuguee turns into divergence of the eyeballs, death quickly occurs. Deviation conjuguee on the basis of a supranuclear lesion in the bridge itself is rarely observed.
"Deviation conjuguee" of the head and eyes together with a spasm of the left facial nerve at the onset of Jackeon's seizure in a right-sided brain tumor (according to Bing)
Diagnostic rules for supranuclear (supranuclear) eye paralysis
Supranuclear Disorders eye movements are characterized by the fact that they are combined (internuclear paralysis). Persistent gross paralysis of gaze in diseases of the brain - even with lesions of both hemispheres - are relatively rare. Most often they are still observed with meningitis, extending to the entire convex surface of the brain.
If the patient still looks straight ahead, then a positive puppet phenomenon or a slow deviation of the eyes after the introduction of cold water into the external auditory canal indicates an impaired brain stem, that is, a supranuclear lesion (cerebral cortex - white matter or corticobulbar pathways).
If at persistent paralysis it is possible to reveal a real paralysis of the abducens nerve on the same side (it is recognized by the fact that the internal rectus muscle of the other eye functions normally during convergence), this indicates the localization of the lesion at the caudal end of the bridge. Due to the fact that the knee of the facial nerve forms a loop around the nucleus of the abducens nerve, lontine gaze palsy is usually combined with paralysis of the facial nerve (peripheral type) on the same side. Disorders of vertical eye movements are almost always caused by lesions of the quadruple (bilateral oculomotor nerve palsies can simulate gaze palsies; see also Sylvian aqueduct syndrome).
If jackson fit begins with gaze cramps, then this speaks of a focus in the cortex of the frontal lobe of the opposite side. The patient looks to the side opposite to the focus. From time to time, isolated gaze seizures occurring without the spread of seizures to other muscle groups, it makes no difference whether the eyes deviate in the vertical or horizontal direction, in contrast to this, they indicate a lesion of the brain stem due to Encephalitis lethargica. As an exception, they are also observed with skull trauma and tumors.
The same applies to disorders- both paralysis and spasms - symmetrical eye movements, namely, with convergence for near and the necessary divergence in the transition from setting closer to looking into the distance. At the same time, one should not forget about possible ocular causes (weak convergence in myopia, excessive convergence up to spasm in hyperopia, latent strabismus or insufficient binocular vision due to refractive errors or unilateral amblyopia), as well as convulsions with hysteria or insufficient attention of patients. The sometimes observed phenomenon of the so-called predominant gaze movements seems to indicate damage to the brain stem due to trauma. So, for example, a proposal to look down is first followed by a short glance up, followed by a look down.
Only experience in research disorders of eye movements to some extent protects against errors. In particular, one should beware of haste in the diagnosis of gaze palsy in patients with blurred consciousness and in patients who do not understand enough for themselves what is required of them. On the other hand, it should be noted that in patients with multiple focal arteriosclerotic changes (miliary foci of softening and hemorrhage in the capsula interna, thalamus opticus and corpus striatum), in whom paralysis of bilaterally innervated muscles that provide speech, swallowing and chewing, also indicate clinical a picture of pseudobulbar paralysis, yet only in exceptional cases it is possible to reveal the presence of gaze paralysis.
20-02-2012, 20:51
Description
Dysfunctions of extraocular muscles
Information on the frequency of oculomotor disorders in brain tumors is scarce. It is believed that they are found in 10-15% of cases [Tron E. Zh., 1966; Huber D., 1976]. Most often occur signs of violation of the 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 impairment of binocular vision, especially if the upper rectus muscles are affected and vertical diplopia develops. In patients with severe paresis, especially with horizontal paresis, binocular vision is absent in all parts of the visual field.
Paresis and paralysis of the III, IV, VI pairs of cranial nerves, arising as a result of increased intracranial pressure, have no independent significance in the topical diagnosis of brain neoplasms.
The greatest Vulnerability of the abducens nerve 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 at the exit from 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, an increase in intracranial pressure can lead to a pinching of the nerve between the pons and the posterior cerebellar artery. A partial violation of the abducens nerve conduction develops and, as a result, a weakening of the external rectus muscle on the side of the same name. If the paresis is insignificant, a pronounced horizontal diplopia appears with extreme abduction of the eye towards the weakened muscle. Thus, diplopia is horizontal and homonymous. In the literature there is information about the predominance of bilaterial lesions of the abducens nerve in patients with tumors of the head moeg [Tron E. Zh., 1966; Kirkham T. et al., 1972].
Daily fluctuations in severity are of interest. paresis of the abducens nerve... In patients with brain tumors, diurnal variations in intracranial pressure were observed, and at the time of its decrease, a sharp weakening of the abducens nerve paresis was noted. The latter is also observed during degradation therapy.
Second section the least resistance of the abducens nerve to increased intracranial pressure is the place where it passes over the upper edge of the temporal bone pyramid. 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 are observed in patients with tumors subtentorial localization and their supratentorial location. Describing paresis of the abducens nerve with increased 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; Neer A., 1976].
The oculomotor nerve, extending from the cerebral peduncles, also passes between two vessels (posterior cerebral and superior cerebellar arteries). Therefore, an increase in intracranial pressure can lead to a pinched nerve between the vessels. In addition, the nerve can be pressed against the Blumenbach's oculus. Since the pupillary fibers that run as part of the oculomotor nerve are more vulnerable, unilateral mydriasis with complete areflexia may be an early symptom.
In case of paresis and paralysis, in order 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 the nuclei or roots.
In recent years, topical diagnosis has been facilitated by the use of electromyography .
Experience has shown that with this method it was possible to differentiate various types of myopathies (myositis, endocrine ophthalmopathies), myasthenia gravis, peripheral and central muscle paralysis.
Abducens nerve damage at the trunk level is characterized by horizontal diplopia, especially when the eyes are maximally outward. If there is mild paresis, slight converging movements are possible. As mentioned above, the abducens nerve is most vulnerable with an increase in intracranial pressure. Assessment of only one brainstem paralysis has no independent diagnostic value. Its combination with other neurological symptoms is important (lesion of the III, IV, V, VII, VIII pairs of cranial nerves).
Nuclear paralysis usually combined with paralysis of the gaze 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 symptoms: paresis of the lateral muscle, homolateral peripheral facial palsy, cross hemiplegia. All signs of damage to the facial bundles of the VI and V pairs of cranial nerves can occur not only when the pathological process is localized in the bridge, but also as a dislocation sign when the quadruple or cerebellum is affected.
Fauville syndrome characterized by paresis of the lateral rectus muscle, homolateral peripheral facial palsy, and homolateral horizontal gaze palsy. A combination with Horner's syndrome is possible.
Stem paralysis the oculomotor nerve is characterized by dysfunction of all ocular muscles innervated by this nerve. E. Zh. Tron (1966) notes that the initial appearance of ptosis with subsequent damage to all other muscles is characteristic of progressive brainstem paralysis of the oculomotor nerve.
The clinical picture of nuclear paralysis depends on the topography of the nuclei the oculomotor nerve (Fig. 80).
Rice. 80. Diagram of the location 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 (center of innervation of the pupil sphincter); III- large-cell lateral nuclei: 1 - the levator nucleus, 2 - the nucleus of the superior rectus muscle; 3 - the core of the medial rectus muscle; 4 - the core of the superior rectus muscle, 5 - the core of the lower rectus muscle; IV - the nucleus of the block nerve; V - the nucleus of the abducent nerve; 6 - cortical gaze center.
They are represented by paired large-cell lateral nuclei that innervate the rectus muscles of the eye and the levator, paired small-cell nuclei of Yakubovich-Westphal-Edinger, which innervate the sphincter of the pupil, and a single Perlia nucleus, which sends fibers to the ciliary muscle. Large-cell nuclei have a large length under the Sylvian aqueduct, as they are represented by five cell formations that send representation to each muscle. In this case, the upper rectus muscle and the levator receive the fibers of the cell formations of the same side, the lower rectus muscle - from the cell formations of the opposite side, and the fibers innervating the internal rectus and lower oblique muscles are bilaterally represented. In this regard, nuclear paralysis is characterized by dysfunction of single or several 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's Syndrome- unilateral complete paralysis of the oculomotor nerve with cross hemiplegia, cross paralysis of the face and tongue is possible.
Benedict's Syndrome- unilateral paresis of the oculomotor nerve with cross hemitremor. Sometimes it is combined with cross hemianesthesia.
Trunk palsy of the block 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, convergence spasm or its paralysis are characteristic of pineal gland tumors.
Paresis and paralysis of the gaze with brain tumors, according to the literature, are extremely rare (about 1.5%). In contrast to paresis and paralysis of the extraocular muscles, paresis and gaze paralysis are characterized by an equal limitation of the mobility of both eyes. With them, there is neither strabismus nor 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 paralysis of gaze observed when the center of gaze is turned off in the quadruple. Upward gaze paralysis is more common. With paresis of gaze upward, eye movements in this direction are not limited, but when trying to look upward, vertical nystagmus occurs. E. Zh. Tron (1966) emphasizes that in diseases of the quadruple, vertical nystagmus may precede the appearance of paralysis of the gaze upward.
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 definite dependence of the nature of the paralysis of the gaze to the sides on the level of the lesion.
Violation of the frontal center and frontal-pontic path leads to turning off volitional eye movements, vestibular and optical movements of the eyes are preserved.
Defeat in the center zone in the varoliev bridge leads to the absence of movements, both volitional, and vestibular and optical in the direction of gaze paralysis. Paralysis of the gaze is sharply expressed, stable. Concomitant eye deviations are rare and mild. R. Bing and R. Brueckner (1959) believe that the loss of vestibular excitability of extraocular muscles with paralysis of the gaze characterizes the defeat of the trunk. Lack of voluntary movement while maintaining the optical and vestibular, it indicates a lesion of the frontal center or frontal-pontic path. A. Huber (1976) formulates the possibility of differentiation as follows: bilateral lesions of the front-pontic path cause complete bilateral paralysis, often with the appearance of bilateral vertical paralysis. Bilateral damage in the bridge is usually accompanied only by paralysis, horizontal in both directions. At the same time, vertical movements are preserved.
Nystagmus- involuntary rhythmic movements of one or both eyes in a certain or any direction of gaze. Nystagmus may be pendulum-like, 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 rhythm: in one direction the eye moves quickly (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, there are three stages of nystagmus:
Stage I - nystagmus appears only when the eye is turned towards the fast phase, stage II is active nystagmus when the eye is turned towards the fast phase and when the gaze is directed directly and, finally, stage III is pronounced nystagmus when looking directly, expressed when the gaze is directed to the side fast phase and weak nystagmus when moving the eye towards the slow phase.
By the range of motion emit small nystagmus, in which the amplitude of eye movements does not exceed 3 °; middle nystagmus, in which the range of motion ranges from 5 to 10 °, and gross nystagmus, eye fluctuations with it are more than 15 °.
Nystagmus may be physiological and pathological... The latter occurs in diseases of the labyrinth or when a pathological process acts on the nuclei of the vestibular nerve or the pathways departing 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. Labyrinth, or peripheral, nystagmus always has one direction in 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 its duration increases. It is often combined with dizziness and deafness.
Nuclear, or central, nystagmus can change its direction with a change in gaze, which is never observed in 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 a decrease in hearing and, as the period of its existence lengthens, it tends to increase. Unlike peripheral nystagmus, it disappears when the patient is examined in the dark (electronystagmography in the dark).
Central nystagmus usually occurs with tumors of subtentorial localization, especially in the area of the cerebellar pontine angle. With tumors of the trunk, central pathological nystagmus is almost always a constant symptom. Vestibular central nystagmus is also possible with supratentorial tumors (tumors of the frontal, temporal lobes), but in these cases it is caused by the displacement of the brain by a growing tumor.
In recent years, the attention of researchers has been attracted by state of saccadic eye movements for various diseases, the central nervous system. Micro-movements of the eyes, or physiological nystagmus, are involuntary micro-movements of the eyes that occur when fixing a fixed point. The function of saccadic eye movements is to move the image of objects to the region of the fovea of the retina. By the nature of the emerging movements distinguish between drift, tremor and jumps.
Drift is called smooth, slow displacement of the eyes in the range of 5-6 angles. min. Oscillatory movements with an amplitude of 20-40 angles. min and with a high frequency is called tremor. Micro-jumps, or microsaccades, are rapid eye movements ranging from 1 arcsec. min up to 50 ang. min. The leaps 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 in direct proportion to the degree of damage to the oculomotor nerve. So, with mild paresis, the microshoes practically do not differ from the norm. As the severity of the 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 micromovements of the eyes, up to their complete disappearance. These changes correspond to the side of the lesion and do not depend on which eye is fixing. The authors found that with paresis, the amplitude of the drift increases, and with paralysis, it decreases.
Brainstem involvement accompanied by a violation of the central mechanisms of control of fixation movements. The frequency, direction and amplitude of micromovements changes, pathological spontaneous nystagmus occurs. As noted earlier, spontaneous nystagmus often precedes paresis and paralysis of the oculomotor nerves. The close topographic relationship of the nuclei and the supranuclear stem gaze centers in the brain stem, as a rule, leads to mixed lesions. Examining 15 patients with stem paralysis, S.A. Thus, these changes can be regarded as early symptom developing paresis of the gaze with intra-stem lesions. A characteristic sign of unilateral nuclear paralysis, according to SA Okhotsimskaya, is asymmetry in the distribution of jumps, the loss of all types of jumps in the direction of injury for both eyes. This symptom was observed more clearly in patients with unilateral pontine tumors. With bilateral lesion of the trunk, there were no jumps even in cases of incomplete ophthalmoplegia.
Disorders of pupillary reactions
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. The most important of them is pupil response to light.
Before proceeding to the description of changes in the shape of the pupils and their reactions in patients with brain tumors, it is advisable to dwell on the anatomical features pupillary reflex pathways(fig. 81).
Fig 81. Diagram of the visual pathway and pupillary reflex. 1 - ciliary node; 2 - optical path; 3 - lateral geniculate body; 4 chiasma; 5 - optical radiation (Graziole beam); 6 - visual cortex, nuclei of Yakubovich-Westphal-Edinger; 8 - anterior quadruple.
Afferent fibers of the pupillary reflex at the exit from the optical cords form a synapse in the anterior quadruple (regio pretectalis), from where they go to the nuclei of the oculomotor nerve (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 name and the opposite side. This explains the mechanism of direct and friendly pupil response to light T.
With normal vision, synkinetic constriction of the pupil with convergence of the eyeballs or contraction of the ciliary muscle during accommodation. In the literature, there is no clear understanding of the mechanism of miosis in connection with convergence and accommodation. ON 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 nerve, reach the nuclei of the V nerve and Yakubovich nuclei -Westfall-Edinger. Excitation of these nuclei also leads to a contraction of the sphinker of the pupil. Accommodation is stimulated by visual impulses arising in the retina and heading to the occipital cortex, and from there to the Yakubovich-Westphal-Edinger nuclei. The efferent pathway for convergence and accommodation is common and it runs as part of the oculomotor nerve to the ciliary muscle and to the sphincter of the pupil.
The most subtle and delicate violations of pupillary reactions were possible to identify only with the help local pupillography method or local illumination of the investigated.
According to E. Zh. Tron (1966), violation of pupillary reactions is a very rare symptom in brain tumors (it occurs in no more than 1% of cases). Pupillary disorders symptom appears, as a rule, with tumors of the quadruple of the pineal gland, 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 region while maintaining the reaction to accommodation and convergence [Sokolova ON, 1963]. The combination of pupillary disorders with impaired acts of accommodation and convergence is a later sign indicating a significant spread of the tumor process, including the quadruple region. Tumors of the quadruple and pineal gland, in addition, can also be accompanied by paresis and paralysis of the gaze upward.
The shape and size of the pupils also should be given importance, since a change in the size of the pupils can sometimes be one of the symptoms of the onset of blindness, which the patient does not know about.
Normal pupil width varies in a fairly wide range - from 3 to 8 mm. It should be borne in mind that normally fluctuations in the diameter of the pupils are permissible: anisocoria can reach. 0.9 mm [Samoilov A. Ya. Et al., 1963]. In children, the pupils are always wider than in adults. By the size of the pupils the color of the iris is also influenced. It has been noticed that blue-eyed and gray-eyed pupils are wider than brown-eyed ones. Ophthalmologists are aware of the fact that the pupils are dilated in myopic people, so the nature of refraction should be taken into account when assessing the pupils. Unilateral myopia can be the cause of anisokeria. The latter is observed in diseases of the gallbladder, lesions of the tops of the lungs.
With brain tumors anisocoria occurs in approximately 11% of patients [Tron E. Zh., 1966]. Paralytic mydriasis especially when 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 in the cleivus by a displaced brain or a growing tumor. As the tumor progresses, paralysis of the external rectus muscles of the eye may join.
Orbital tumors localized perineurally and compressing the ciliary node, sometimes cause mydriasis on the side of the lesion with a weakly expressed exophthalmos or even before its appearance [Brovkina AF, 1974]. It should also be borne in mind that after an orbitotomy and removal of the tumor, unilateral mydriasis with the correct shape of the pupil, its lack of reaction to light and convergence as a result of a violation of the efferent pupillary shower. We observed in such patients paresis of accommodation and a slight violation of the sensitivity of the cornea. Considering 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 apex of the orbit, in the region of the superior orbital fissure. Tumors of the pituitary gland 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 a noticeable dilatation of the palpebral fissure were found on the hemianopsia side. The syndrome described by S. Baer seems to facilitate the topical diagnosis of a tumor accompanied by hemianopsia. However, E. Zh. Tron, analyzing cases of injury to the occipital lobe, found hemianopsia with anisocoria in 1/3 of cases. According to II Merkulov (1971), this does not detract from the merits of Beer's syndrome in the topical diagnosis of tractus hemianopsia.
Visual field changes
Brain tumors in almost half of cases are combined with changes in visual field... Often, these changes make it possible to make a topical diagnosis of a tumor lesion.
The optimal application should be kinetic and static perimetry, both above-threshold and quantitative. In this case, the boundaries of the field of view from 1 to 3 isopter 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 carry out profile static perimetry. This is due to the patient's rapid fatigue, 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 point of fixation) by multiple objects on the so-called analyzers of the field of view [Astralenko GG, 1978; Friedman, 1976]. When examining the visual field analyzer, the patient is presented with 2 to 4 suprathreshold objects simultaneously, a total of 50 to 100 objects. Examination of one eye takes 2-3 minutes.
In patients with low visual acuity or in the absence of proper attention, it is advisable to use a simple, so-called control method (confrontation test), in which the field of view of the subject is compared with the field of view of the investigator. The visual field control technique 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 subject's face. 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, from 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 it. The patient must report when he begins to distinguish the object. Normally, the field of vision should coincide with the outlines 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 error of the method in the hands of an experienced researcher does not exceed 10 °.
The simplified methods for examining the visual field include the test reflex closure of the palpebral fissure... A hand is held in front of the patient's eye from four sides, reflexively the eyelids close. With hemianopsia in the area of absence of vision, the eyelids will not close. This test can be recommended when examining patients with stupor, aphasia, or with a decrease in visual acuity to the movement of the hand in the face.
Control study for relative hemianopsia carried out with both eyes of the patient open. The doctor moves both hands (or two fingers) symmetrically from the temple to the center along the four meridians. The main condition should be considered good lighting... The patient should 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, we can talk about relative hemianopsia, as opposed to absolute hemianopsia, which can be detected only with an isolated study of each eye. However, early topical diagnosis in case of damage to the optic-nerve pathway requires a qualified study using kinetic perimetry with a sufficient number of objects and campimetry.
A. Huber (1976) believes that at the present time it makes no sense to produce perimetry for colors. To detect scotoma for red, which is one of the earliest signs of developing optic nerve or tract atrophy, it is quite sufficient to conduct perimetry with a red object 5 mm from a distance of 33 cm (5/330).
At the heart of topical diagnosis damage to the optic-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. Diagram of the arrangement of nerve fibers in the chiasm. 1 - retina; 2 - optic nerve; 3 - chiasm; 4 - optical path; 5 is a cross-sectional diagram of the chiasm; 6 - pituitary gland; 7 - the zone of passage and intersection of the papillomacular bundle.
We consider it advisable to stop on some crosshair features nerve fibers in the chiasm. Noncrossing nerve fibers, starting from the outer halves of the retina, pass in the outer part of the optic nerve. In the chiasm and the optic tracts, they also occupy a lateral position. Fibers from the nasal halves of the retina in the chiasm have a cross. The level of intersection depends on the level of nerve fibers in the retina and optic nerve. Fibers originating from the lower nasal retina are located in the lower optic nerve. In chiasm, they pass to the opposite side at its front edge closer to the lower surface. After crossing the chiasm, these fibers enter the opposite optic nerve for some extent, where they form the anterior knee of the chiasm. Only after that, they, located medially, pass into the optic tract. From the upper nasal parts of the retina, nerve fibers, located in the upper half of the optic nerve, pass to the other side at the posterior edge of the chiasm closer to its upper surface. Before the intersection, they enter the optic tract of the side of the same name, where they form the back knee of the chiasm. The bulk of the crossed fibers are located in the medial sections of the chiasm. It should be remembered that the cross is also carried out by the papillo-macular bundle.
The main types of changes in the field of vision, found in brain tumors, are as follows: 1) concentric narrowing of the visual field (symmetric or eccentric); 2) unilateral sector-shaped defects of the visual field; 3) absolute or relative scotomas (central, paracentral, cecocentral); 4) heteronymous bitemporal and binasal hemianopsia; 5) homonymous hemianopsia. The listed defects of the visual field, depending on the level of damage to the optic-nerve pathway, 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 lesion of the optic nerve; 2- unilateral amaurosis and contralateral temporal hemianopsia with damage to the intracranial portion of the optic nerve near the chiasm; 3 - bitemporalnad hemianopsia with damage to the medial part of the chiasm; 4 - incongruent homonymous hemianopsia with damage to the optic tract; 5 - homonymous hemianopsia without preserving the macular zone with 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 hemianopsia without preserving the macular zone with damage to the middle part of optical radiation; 9 - congruent homonymous hemianopsia with preservation of the macular zone in case of damage to the posterior part of optical radiation; 10 - congruent homonymous hemianopsic central scotoma with lesions of the occipital lobe.
Of primary importance for topical diagnosis of lesions of the optic-nerve pathway are hemianopic visual field defects[Troy E. Zh., 1968]. They can be unilateral or bilateral, complete, partial, quadrant (quadrantopias) and, finally, can be presented as hemianopic scotomas (central or paracentral).
Unilateral hemianopic changes develop with damage intracranial optic nerve... Bilateral hemianopic defects occur when nerve fibers in the chiasm, optical tracts, or the central optic neuron are damaged. 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 optical radiation).
The nervous type of hemianopsia occurs with lesions in the posterior region of the radiatio optica or in the cerebral cortex. The second type of hemianopsia is detected in patients with lesions of the optic tract.
Concentric narrowing of the visual field in patients with a brain tumor is usually due to a developing secondary post-congestive optic atrophy... 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 region of the groove. One-sided concentric taper the visual field is observed in cases of involvement in the pathological process of the intracranial part of the optic nerve between the optical opening and the chiasma. This can be observed with tumors of the optic nerve itself, meningiomas of the sella turcica tubercle, spinal ridge or olfactory fossa. The described changes in the visual field were also observed in craniopharyngiomas, pituitary adenomas with extrasellar spread.
Without dwelling on other reasons causing unilateral concentric narrowing of the visual field (diseases of the retina, orbital area of the optic nerve), we consider it necessary to emphasize Difficulty in differential diagnosis its reasons. In a number of 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, dynamic observation over a period of time.
Unilateral visual field defects are more common in combination with cattle... A. Huber (1976) observed quadrant unilateral defects visual fields that merge with the area of the blind spot, when the optic nerve is compressed by a 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), an inferior temporal defect of the visual field was determined in the field of view, merging with the area of the blind spot (Fig. 88).
Rice. 88. Unilateral inferior temporal quadrantopsia in a patient with a tumor of the right optic nerve.
The identification of absolute or relative livestock... At the onset of the disease, they can be determined only when examining for colored objects or when examining small objects for white (no more than 1 mm on the Förster perimeter or 0.25 mm on hemispherical perimeters). By location, these scotomas are classified into central, paracentral, cecocentral, and peripheral.
Unilateral central or paracentral cattle y arise when the optic nerve is involved in the pathological process in its orbital (Brovkina AF, 1974] or the 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 papillo-macular bundle above the chiasm. The anatomical rationale for the appearance of these symptoms is the isolated position of the papillo-macular bundle and its partial intersection in the chiasm. However, homonymous hemianopic scotomas rarely occur with tumors that involve the optical tract in the process. More often they are associated with a lesion of the radiatio optica and have a negative character, that is, they are not felt by the patient. These scotomas should be regarded as a sign of a slow progressive lesion of the optic nerve pathway in the postchiasmal region.
Heteronymous bitemporal defects the visual fields are almost pathognomonic for the lesion 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 - on the diaphragm of the sella turcica, behind the chiasm adjoins the infundibulum, descending from the gray tubercle to the pituitary gland. In front, the chiasm is sometimes closely adjacent to the main bone in the region of the chiasmatic groove. From the sides, the chiasm is surrounded by the arteries of the circle of Willis. Thus, tumors growing in the area of the chiasm are capable of cause fiber damage in any part of the chiasm, but mainly in its central section. So, for example, tumors of the sella turcica lead to the appearance of typical bitemporal hemianopsia or hemiapopic bitemporal defects in the visual field. Symmetrical bitemporal quadrantopsia or hemianopsias are most common in pituitary tumors, while asymmetric bitemporal hemianopsias or quadrantopsias are more common in parasellar or suprasellar tumors (Fig. 89).
Rice. 89. Hemyanopic bitemporal defects of the visual field when the chiasm is compressed from above.
Often, tumors have asymmetric growth pattern... In such cases, one of the optic nerves (with the growth of the tumor anteriorly) or the optic tract (with the growth of the tumor posteriorly) may be directly involved in the tumor process. As a result, the typical symptomatology develops, shown in Fig. 82.
Homonymous hemianopic defects in the visual field 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 a quadrantopsia indicate an incomplete break in the optical path or optical radiation. With classical homonymous hemianopsia, there is no doubt about the lesion of the optic-nerve pathway in some area along the entire diameter. It is possible to differentiate tractus hemianopsia from hemianopsia caused by lesions of radiatio optica and higher by signs of congruence. An incongruent onset with a progressive change in visual fields passing through the fixation point (without preserving the macular region), blanching of the temporal half of the optic nerve head is characteristic of lesions of the optic tract (tumors of the temporal lobe, middle fossa, thalamus, quadruple). Tumors of the temporal lobe often accompanied by the appearance of the upper quadrant hemianopsia; on the contrary, the lower quadrant hemianopsia occurs in patients with tumors of the parietal region. With tumors of the occipital lobe, complete homonymous hemianopsia develops. Congruent homonymous hemianopsias without preserving the macular region, according to A. Huber, most often indicate a complete defeat of the radiatio optica.
Continued in the next article: Changes in the organ of vision in diseases of the central nervous system | Part 3.
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Anatomy
The actions of the external muscles of the eye are shown in Fig. 1. The superior oblique muscle of the eye is controlled by the trochlear cranial nerve, the external rectus muscle - by the abductor. All other muscles are innervated by the oculomotor nerve, which also carries parasympathetic fibers to the sphincter of the pupil and approaches the muscle that lifts the upper eyelid.
Rice. 1. Motor effects and innervation of the outer muscles of the eye (left eyeball)
Survey
Examination of a conscious patient includes an assessment of tracking an object (doctor's finger, hammer, pen) moving in vertical and horizontal directions. The subject should move along an H-shaped path (not a cruciform) in order to more accurately assess the movement of the eyeballs. This makes it possible to study the functions of the external muscles of the eye relatively independently of each other (Fig. 1).
Eye tracking the object is the best way to detect existing violations, since normal tracking is ensured by the integrity of all pathways involved in the friendly movements of the eyeballs. Elements of this complex system can be examined separately using other clinical methods:
- Saccades- fast movement of the gaze; achieved when the doctor asks the patient to look quickly to the right, left, up, or down
- Convergence- the ability of the eyeballs to adapt to near vision by friendly insight, while tracking and saccades use movement at a constant distance from the eyes
- Optokinetic movements observed when the cylinder rotates with alternating white and black stripes in front of the patient's eyes. In the normal state, noticeably slow tracking alternating with fast corrective saccades ( optokinetic nystagmus). These movements are absent in the patient, with depression of consciousness. The study of optokinetic nystagmus is valuable for identifying simulated disorders of consciousness.
- Vestibulo-ocular reflex... Unlike all the above methods, which require a preserved level of wakefulness, this test can be used in a patient with depression of consciousness. The pathways of the brain stem, in particular those that connect the vestibular nuclei (receive a signal from the vestibular apparatus in the inner ear; see below) with the nuclei of the III, IV and VI nerves, can be investigated in the following ways:
Rice. 2. The study of the vestibulo-ocular reflex, and - an intact trunk - turning the head causes a transient movement of the eyeballs in the opposite direction - an oculocephalic reflex, or a symptom of a doll's head. This reflex is also applicable to vertical movements of the eyeballs when tilting back and lowering the head. Caloric test - the introduction of 50 ml of cold water into the external auditory canal causes friendly abduction of the eyeballs in the direction of irritation; b - death of the brain stem: absence of oculocephalic and caloric reactions
These tests are important for diagnosing a brain stem lesion in an unconscious patient.
Disorders of movement of the eyeballs and eyelids
Symptoms
The patient may complain of drooping of the upper eyelid (partial or complete ptosis).
Diplopia, or double vision, in neurological practice occurs due to misalignment of the eyeballs, as a result of which the light falls on different parts of the two retinas and the brain cannot combine the two images. This is the case binocular diplopia that occurs with both eyes open, it should be distinguished from monocular diplopia that occurs when looking with one eye. The disorder is not a symptom of a neurological disease and may be due to an ophthalmic disorder (eg, lens opacity) or, more commonly, a functional defect.
The cause of binocular diplopia is the imbalance in the work of the external muscles of the eye and the violation of their innervation. Diplopia is always clearly detected (either there is double vision, or it is not), however, its severity may vary. The patient can tell in which direction the image bifurcates - horizontal, vertical or oblique.
Syndromes of defeat
The main disorders of the oculomotor innervation are quite easily detected in a conscious patient by identifying classic syndromes using a tracking test.
Oculomotor nerve palsy (III nerve)
Ptosis in its full form is caused by paralysis of the muscle that lifts the upper eyelid. When the doctor lifts the patient's eyelid, the eye is in a position lowered down and turned outward - the result of an action that does not meet resistance of the superior oblique and external rectus muscles. Palsy of the oculomotor nerve can also include a dysfunction of parasympathetic fibers, as a result of which the pupil does not respond to changes in lighting and is dilated ( "surgical" paralysis of the third nerve) or pupillary reflexes are weakened ( "Medicinal" paralysis). The reasons are given in table. 1.
Table 1. Causes of damage to the oculomotor nerve
Block nerve palsy (IV nerve)
Isolated unilateral anterior oblique palsy may result from mild head trauma. The patient usually experiences double vision when walking down stairs and tries to keep his head bowed to compensate for the diplopia. Paralysis of the superior oblique muscle is detected with an appropriate test (see below).
Abducens nerve paralysis (VI nerve)
The patient cannot move the affected eyeball outward due to the uncontrolled action of the medial rectus muscle, in extreme cases this leads to the appearance of converging strabismus. Diplopia appears when looking to the affected side with the appearance of horizontal bifurcation of the image. Isolated paralysis of the VI nerve is usually associated with impaired blood supply to the nerve (damage vasa nervorum) due to diabetes or hypertension. Restoration of nerve functions after such microvascular diseases occur over several months. VI nerve palsy can also be false sign of localization with increased intracranial pressure, since the nerve has a large length and a complex path of passage through the bones of the skull. As a result, there is a high risk of damage due to increased intracranial pressure or volumetric impact.
Horner's Syndrome
Some of the muscles responsible for lifting the upper eyelid are innervated by sympathetic nerve fibers. As a result, damage to the oral part of the sympathetic nervous system can manifest itself as partial ptosis along with miosis(constriction of the pupils as a result of paralysis of the sympathetic fibers that innervate the muscle that expands the pupil). Other signs of Horner's syndrome - a deep standing of the eyeball in the orbit (enophthalmos), reduced or absent sweating on the affected side of the face (anhidrosis) - are less common. The source of the sympathetic innervation of the pupil is the hypothalamus. Horner's syndrome can be caused by damage to sympathetic fibers at various levels (Fig. 3).
Rice. 3. Causes of Horner's syndrome, classified according to the level of damage to the sympathetic nervous system - from the hypothalamus to the eyeball
Nystagmus
Nystagmus is an involuntary rhythmic swaying movement of the eyeballs that occurs when trying to fix the gaze in the extreme vertical or horizontal directions, less often observed when looking in front of you. Nystagmus can occur with the same speed of movement of the eyeballs in both directions ( pendulum nystagmus), however, more often the slow phase (return to the initial position from the direction of gaze) alternates with a corrective fast phase - movement in the opposite direction ( jerky nystagmus). Such nystagmus is defined as a push in accordance with the direction of the fast phase, although these are almost normal saccades, the purpose of which is to compensate for the pathological process represented by the slow component.
Classification of jerky nystagmus:
- It manifests itself only when looking towards the fast component.
- It appears in the normal direction of the gaze (gaze is directed straight ahead).
- It manifests itself when looking towards the slow component.
Nystagmus can be congenital, in which case it is usually pendulum-shaped. Acquired nystagmus can be a sign of a disorder of the inner ear (labyrinth) (see below), brainstem, or cerebellum, and it can also result from side effects of medications (such as anticonvulsants). Rotational (rotatory) nystagmus is observed with damage to either the peripheral (labyrinth) or central (brain stem) parts of the vestibular analyzer. Vertical nystagmus, not associated with drug use, usually indicates a lesion of the brain stem and is of some importance for topical diagnosis of the lesion (in the area of the large foramen) in the event that the fast phase of nystagmus is directed downward when looking down. Patients usually do not experience nystagmus, although it may be associated with vertigo (vertigo) (see below). Sometimes the rhythmic movements of the eyeballs with nystagmus are perceived subjectively ( oscillopsia), especially often with vertical nystagmus. At the same time, the patient realizes that the world around him is unpleasantly moving up and down.
Internuclear ophthalmoplegia
A normal friendly look with both eyes to the right or left is due to the coordinated action of the external rectus muscle of one eyeball together with the reverse action of the internal rectus muscle of the other. The anatomical basis of friendly movements of the eyeballs is medial longitudinal fasciculus- a strip of fast-conducting myelinated nerve fibers connecting the nuclei of the abducens nerves of the pons with the contralateral nuclei, which provide innervation to the internal rectus muscles. As a result of the defeat of this pathway, the possibility of friendly movements of the eyeballs is lost - the conditions for the normal abduction of one eye outward are preserved when it is impossible to move the other eye inward. It is also possible the appearance of nystagmus when looking to the sides, more pronounced in the outwardly diverging eye. This combination of symptoms is known as internuclear ophthalmoplegia and is commonly found in multiple sclerosis. The defeat of the medial longitudinal bundle can also cause different vertical position eyeballs, in which one eyeball is higher than the other in all positions.
The complete or partial loss of the ability to move in a certain direction by both eyeballs is caused by supranuclear lesion pathways responsible for the movement of the eyeballs ( supranuclear gaze palsy). In this case, the connections of the nuclei of the III, IV and VI nerves with the overlying structures suffer. Typically, there is no diplopia as the optical axes can remain aligned with each other.
The defeat can be caused by both compression and destruction of the corresponding structures (for example, hemorrhage or heart attack). Supranuclear gaze palsy can be chronic and progressive, such as in extrapyramidal disorders. If in a patient with gaze paralysis, when examining the oculocephalic reflex, the movements of the eyeballs are preserved, there is most likely a supranuclear lesion. Extensive damage to the brain stem or cerebral hemispheres significantly affects the level of consciousness, as well as the state of the systems responsible for the movement of the eyeballs, and can be the cause converging paresis of gaze(fig. 4). The center that controls eye movements in the horizontal direction is located in the pons varoli (higher centers in the cerebral hemispheres); the centers of vertical vision are not well understood, but are presumably located in the upper midbrain.
Rice. 4. Friendly gaze palsy. The direction of deviation is diagnostically valuable in determining the lesion focus in patients with hemiparesis and impaired consciousness, and - partial epilepsy with a focus of pathological activity in one frontal lobe; the eyeballs deviate towards the affected limbs, which does not correspond to the hemisphere in which the epileptic focus is located; b - destruction of one of the frontal lobes; the eyeballs deviate from the paralyzed limbs, since the centers that control eye movements (frontal gaze center) in the unaffected hemisphere do not send signals to resist; c - unilateral lesion of the brain stem (in the area of the parolium bridge); the eyeballs deviate to the affected side. The lesion is located above the intersection of the pyramids, therefore hemiparesis is detected on the side opposite to the lesion focus. However, the focus is located below the intersection of the fibers from the cortical center of the gaze, heading towards the nuclei of the pons varoli and controlling the horizontal movements of the eyeballs. In this situation, an action that does not meet the resistance of the oculomotor center of the unaffected half of the bridge leads to a deviation of the eyeballs in the direction of the same name.
Complex oculomotor disorders
Combinations of paralysis of several nerves that provide innervation to the eyeballs can be different (for example, damage to the III, IV and VI nerves caused by a pathological process in the cavernous sinus or a fracture of the upper edge of the orbit), the causes of which are not established (for example, a lesion, the brain stem is unclear nature). It should be borne in mind the curable cause of the disease - myasthenia gravis or damage to the muscles of the eyeball due to thyroid disease.
Diplopia
In many patients with binocular diplopia, its mechanism is revealed by observing eye movements when certain muscles are weak. In some cases, the defect is not so pronounced and the movements of the eyeballs seem normal on examination, although the patient still notes double vision. In such cases, it is necessary to determine the direction in which the diplopia is most pronounced, and also establish in which direction the image bifurcates - horizontal, oblique or vertical. The eyes are closed in turn and marked which of the images disappears. Usually false image(for the affected eye) more distant from the center. So, in the case of assessing diplopia with one closed eyeball in a patient with mild paralysis of the right external rectus muscle, the diplopia is maximal when looking to the right, while the image is bifurcated horizontally. When the right eyeball is closed, the image far from the center disappears, while when the left eye is closed, the near one disappears.
Neurology for general practitioners. L. Ginsberg
Paralytic strabismus is caused by paralysis or paresis of one or more oculomotor muscles caused by various reasons: trauma, infections, neoplasms, etc. It is characterized primarily by the limitation or lack of mobility of the squinting eye towards the action of the paralyzed muscle. When looking in this direction, double vision, or diplopia, occurs.
If, with a friendly strabismus, a functional scotoma relieves of double vision, then with paralytic strabismus another adaptive mechanism arises: the patient turns his head towards the action of the affected muscle, which compensates for its functional insufficiency. Thus, a third symptom characteristic of paralytic strabismus arises - a forced turn of the head. So, with paralysis of the abducens nerve (dysfunction of the external rectus muscle), for example, the right eye, the head will be turned to the right. Forced turn of the head and tilt to the right or left shoulder during cyclotropy (shifting the eye to the right or left of the vertical meridian) is called torticollis.
Ocular torticollis should be differentiated from neurogenic, orthopedic (torticollis), labyrinthine (with otogenic pathology). Forced turn of the head allows passively transferring the image of the object of fixation to the central retinal fossa, which eliminates double vision and provides binocular vision, although not quite perfect.
As a result of deviation, as with concomitant strabismus, there is a disorder of binocular vision. However, it should be noted that in children, the topical diagnosis of paralytic strabismus, and sometimes the differential diagnosis with concomitant strabismus, is very difficult.
Causes
Paralytic strabismus can be caused by damage to the corresponding nerves or by dysfunction and morphology of the muscles themselves. Paralysis can be central and peripheral. The former arise as a result of volumetric, inflammatory, vascular or dystrophic disorders and injuries in the brain, and the latter - in the presence of similar processes and consequences of injuries in the orbit and in the nerve branches themselves.
Changes in muscles and nerves can be congenital or occur as a result of infectious diseases (diphtheria), poisoning (botulism), phlegmon of the orbit, and often as a result of direct injury (rupture) of the muscle itself. Congenital paralysis is uncommon and is usually combined. With the simultaneous paralysis of all the optic nerves, complete ophthalmoplegia occurs, which is characterized by immobility of the eye, ptosis and dilated pupil.
Complete damage to the oculomotor (III cranial) nerve causes paralysis or paresis of the upper, medial and lower rectus muscles of the eye, the muscle that lifts the upper eyelid, and, as a rule, the loss of the pupil's response to light and accommodation. With complete damage, ptosis (drooping of the upper eyelid), deviation of the eye outward and slightly downward (due to the predominance of the activity of the abducens nerve and superior oblique muscle) and pupil dilation are also detected.
Compression lesion of the oculomotor nerve (aneurysm, swelling, wedging) usually causes the pupil to dilate on the affected side; ischemic damage (for example, in diabetes mellitus) covers the central part of the nerve and is usually not accompanied by pupil dilation.
Damage to the abducens (VI cranial) nerve causes paralysis of the lateral rectus muscle in combination with abduction of the eye inward; when looking towards the affected muscle, non-crossed diplopia occurs (the image that occurs in the abducted eye is projected lateral to the image in the abducted eye).
Defeat at the level of the Varoliev bridge often accompanied by horizontal gaze paresis or internuclear ophthalmoplegia.
Damage to the block (IV cranial) nerve leads to paralysis of the superior oblique muscle of the eye and is manifested by a violation of the downward movement of the eyeball; diplopia is most pronounced when looking down and inward and disappears when the head is turned to the "healthy" side.
Diagnostics
A sign of paralytic strabismus is also the inequality of the primary angle of strabismus (squinting eye) to the secondary angle of deviation (healthy eye). If you ask the patient to fix the point (for example, look at the center of the ophthalmoscope) with a squinting eye, then the healthy eye will deviate to a much greater angle.
With paralytic strabismus, it is necessary to identify the affected oculomotor muscles. In preschool children, this is judged by the degree of eye mobility in different directions (determining the field of view). At an older age, special methods are used - coordimetry and provoked diplopia .
A simplified way of determining the field of view is as follows. The patient sits opposite the doctor at a distance of 50-60 cm, the doctor fixes the subject's head with his left hand and invites him to alternately follow each eye (the other eye is covered at this time) for the movement of the object (pencil, manual ophthalmoscope, etc.) in 8 directions. Muscle insufficiency is judged by limiting the mobility of the eye in one direction or another. In this case, special tables are used. With this method, only pronounced restrictions on eye mobility can be detected.
With a visible deviation of one eye vertically, a simple adduction method - abduction can be used to identify the paretic muscle. The patient is offered to look at any object, move it to the right and left and observe whether the vertical deviation increases or decreases at extreme gaze abductions. The definition of the affected muscle in this way is also carried out according to special tables.
Chess coordinateimetry is based on the separation of the visual fields of the right and left eyes using red and green filters.
For the study, a coordimetric set is used, which includes a graded screen, red and green flashlights, red-green glasses. The study is carried out in a semi-dark room, on one of the walls of which a screen is fixed, divided into small squares. Each square has a side equal to three angular degrees. In the central part of the screen, nine marks are highlighted, placed in the form of a square, the position of which corresponds to the isolated physiological action of oculomotor mice.
A patient wearing red-green glasses sits at a distance of 1 m from the screen. To examine his right eye, he is given a red flashlight (red glass in front of the right eye) in his hand. The researcher is holding a green flashlight, the beam of light from which he alternately directs to all nine points and invites the patient to combine the light spot from the red flashlight with the green light spot. When trying to combine both light spots, the subject is usually mistaken by some amount. The doctor registers the position of the fixed green and trimmed red spots on the diagram (a sheet of graph paper), which is a reduced copy of the screen. At the time of examination, the patient's head should be motionless.
Based on the results of the coordimetric study of one eye, it is impossible to judge the state of the oculomotor apparatus; it is necessary to compare the coordimetry results of both eyes.
The field of gaze in the diagram drawn up according to the results of the study is shortened in the direction of the weakened muscle, at the same time there is a compensatory increase in the field of gaze in the healthy eye in the direction of the synergist of the affected muscle of the squinting eye.
The method of studying the oculomotor apparatus in conditions of provoked diplopia according to Haab-Lancaster is based on the assessment of the position in space of images belonging to the fixing and deflected eye. Diplopia is caused by putting red glass to the squinting eye, which allows you to simultaneously determine which of the double images belongs to the right and which to the left eye.
The nine point study design is similar to that used for coordimetry, but it is one (not two). The study is carried out in a semi-dark room. There is a light source at a distance of 1–2 m from the patient. The patient's head should be motionless.
As with coordimetry, the distance between the red and white images is recorded in nine gaze positions. When interpreting the results, it is necessary to use the rule according to which the distance between double images increases when looking towards the action of the affected muscle. If during coordinateimetry the field of gaze is recorded (decreases with paresis), then with "provoked diplopia" - the distance between double images, which decreases with paresis.
Diplopia with paralysis of individual muscles of the eye
- Paralysis lateral rectus muscle right eye - inability to divert the right eye to the right. Fields of vision: horizontal homonymous diplopia, aggravated when looking to the right;
- Paralysis medial rectus muscle right eye - inability to move the right eye to the left. Fields of view: horizontal cross diplopia, aggravated when looking to the left;
- Paralysis lower rectus muscle right eye - the inability to move the right eye downward when turning the eyeballs to the right. Fields of vision: vertical diplopia (the image in the right eye is located below), which increases when looking to the right and down;
- Paralysis upper rectus muscle right eye - the inability to move the right eye up when turning the eyeballs to the right. Fields of vision: vertical diplopia (the image in the right eye is located higher), which increases when looking to the right and up;
- Paralysis superior oblique muscle right eye - the inability to move the right eye downward when turning the eyeballs to the left. Fields of vision: vertical diplopia (the image in the right eye is located below), which increases when looking to the left and down;
- Paralysis lower oblique muscle right eye - the inability to move the right eye up when turning the eyeballs to the left. Fields of vision: vertical diplopia (the image in the right eye is located on top), which increases when looking to the left and up.
Treatment
Treatment of paralytic strabismus consists primarily in the elimination of the underlying disease, the consequence of which it was (infections, tumors, trauma, etc.). If, as a result of the general measures taken, paralytic strabismus does not disappear, the question of surgical intervention may arise.
The question of the indications and time of the operation can be resolved positively only in conjunction with the relevant specialists (neuropathologists, oncologists, infectious disease specialists, etc.).
Post-traumatic strabismus, as a rule, is corrected by surgery after at least 6 months. from the moment of damage, since in this case, regeneration of both muscle and nerve is possible, and, consequently, partial or complete restoration of function.
There are several classifications of paralysis, each type has its own characteristics.
The causes of the disease are primarily associated with pathologies of the nervous tissue, such pathologies can be congenital, and can occur as a result of nerve damage in the area of the cranial nerve nuclei, in the area of large nerve trunks, roots and branches.
Reasons for acquired ophthalmoplegia;
Classification
In this case, the eye is displaced into the zone of action of a healthy or less affected muscle. The patient has difficulty moving the eyes in the direction of the paralyzed muscles, which leads to double vision.
With complete external ophthalmoplegia, the eyeball is constantly in a static position, which leads to the development of ptosis. Partial internal ophthalmoplegia occurs due to the expansion of the pupil that does not respond to light.
The symptoms of the disease are as follows:
When the first signs of the disease appear, it is recommended to immediately consult an ophthalmologist.
Diagnostics
Despite the presence of pronounced external signs, the following instrumental studies are prescribed;
Therapy consists in eliminating the causes of the disease, relieving pain and restoring, if possible, nervous and muscular activity.
Physiotherapy methods
Surgical intervention
Surgical treatment is prescribed when it is necessary to eliminate the tumor that caused the disease, the procedure allows you to restore the integrity of the nerve and restore muscle function.
Ophthalmoplegia
Ophthalmoplegia is called paralysis of the muscles of the eye, which occurs when the oculomotor nerves are damaged.
The main causes of ophthalmoplegia
Ophthalmoplegia can occur with congenital or acquired lesions of the nervous system in the area of the nerve roots or trunks, in the area of the nuclei of the cranial nerves. For example, congenital ophthalmoplegia occurs as a result of aplasia of the nuclei of the oculomotor nerves, and in some cases can be combined with changes in the eye muscles and aplasia of the nerve trunks. This pathology is often combined with malformations of the eyeball, it can be observed in several members of the same family.
Acquired ophthalmoplegia can be caused by:
Ophthalmoplegia can also be a symptom of a rare condition such as ophthalmoplegic migraine. It is manifested by attacks of severe headaches, accompanied by unilateral ophthalmoplegia (complete or partial). Headaches can last for a long time, while the function of the oculomotor nerves is gradually restored.
Types of ophthalmoplegia
Ophthalmoplegia can be unilateral or bilateral. External ophthalmoplegia occurs with paralysis of the muscles that are outside the eyeball, and with paralysis of the intraocular muscles, internal ophthalmoplegia occurs. With various degrees of muscle weakening with paralysis, partial internal or external ophthalmoplegia develops. If both the external and internal muscles of the eye are paralyzed at the same time, then complete ophthalmoplegia occurs. Complete external and complete internal ophthalmoplegia can also occur.
With external partial ophthalmoplegia, the eyeball will lean towards the healthy or less paralyzed muscle, and its movements towards the action of the paralyzed muscles will be absent or significantly limited. In this case, doubling of objects will appear. The eyeball with external complete ophthalmoplegia will acquire immobility and ptosis will develop. Internal partial ophthalmoplegia is characterized only by dilatation of the pupil in the absence of a response to light, a decrease in convergence and accommodation.
Ophthalmoplegia is the name for a symptom of many neurological diseases, in which the motor function of the eyeballs is limited due to the decreased muscle tone of the eyes. Simply - paralysis of the eye muscles due to a disease of the optic nerves.
Causes
Ophthalmoplegia is congenital (due to congenital pathologies of the nervous system), or acquired. The reasons for the onset of the disease can be:
In addition, ophthalmoplegia can be a symptom of a rare ophthalmoplegic migraine. After the end of the attack, the eyes slowly return to normal.
Symptoms
The disease immobilizes the eyeball, and voluntary eye movements become impossible. Sometimes the eye is deviated to the side. A person begins to see double. drooping of the upper eyelid (ptosis), headache and soreness in the eyeball may appear. Or the mobility of the eyeball is preserved, but the pupil does not narrow in bright light. Convergence and accommodation are disturbed - due to the wrong position of the eyes and the impossibility of their synchronous work, the patient cannot focus his gaze on the object, regardless of its distance or approach. Bulging of the eyeball, redness of the eye, and swelling around the orbit are also external signs.
Ophthalmoplegia differs depending on which muscles and nerves of the eye are affected, to what extent and what is the nature of the lesion.
Diagnostics
Ophthalmoplegia has pronounced external signs. But to identify its causes, in addition to consultations with an ophthalmologist and a neuropathologist, the patient is assigned hardware studies:
Find out more about such a symptom as a veil in front of the eyes.
Treatment
Treatment for ophthalmoplegia consists of eliminating the causes of the disease, relieving pain and restoring as much as possible muscle and nervous activity.
- anti-inflammatory drugs;
- drugs that prevent dehydration of the body in case of poisoning and intoxication;
- vitamins B6, B12, C, as a general tonic;
- vasodilators for vascular diseases of the brain;
- nootropic to improve nervous activity;
- anticholinesterase drugs that eliminate muscle weakness;
- corticosteroid hormones to normalize metabolism and restore muscle function.
The sooner a disease is discovered, the more likely it is to get rid of it successfully. Do not ignore doctor visits and try to heal yourself.
Ophthalmoplegia is a disease accompanied by paralysis of some or all of the eye muscles, which are set in motion by the abducens, block and oculomotor nerves.
Congenital ophthalmoplegia is a consequence of aplasia of the nuclei of the nerves of the eye, anomalies in the intrauterine development of a child with no abnormalities in the structure of muscles or nerves.
Most often, congenital pathology is accompanied by other defects in the structure of the eye.
Other causes of congenital pathology:
Ophthalmoplegia is unilateral and bilateral, external and internal. External develops as a result of paralysis of the muscles located outside the eye. Internal occurs due to paralysis of the intraocular muscles, with varying degrees of muscle damage, we can talk about partial ophthalmoplegia.
In medicine, a distinction is also made between complete external and internal ophthalmoplegia, in this case we are talking about the simultaneous paralysis of internal and external muscles.
As a result of complete internal oophthalmoplegia, the pupil expands, it ceases to respond to light and convergence, and the ability to distinguish objects at different distances from the eye decreases.
Symptoms
Drug treatment
Depending on the causes of the disease, the following drugs may be prescribed:
In order to reduce pain, relieve spasm and strengthen muscles, acupuncture, electrophoresis and phonophoresis with drugs are prescribed.
What is ophthalmoplegia, its types and methods of treatment
Ophthalmoplegia is a disease that occurs as a result of damage to the optic nerves and is accompanied by paralysis of the ocular muscles. This is a neurological pathology that limits the motor function of the eyeballs.
It can be due to many reasons: infectious diseases. head or eye injuries and poisoning.
Provoking pathologies
The key reasons for the development of ophthalmoplegia are pathologies of nerve tissues. The disease can be congenital or acquired.
The congenital form in most cases occurs with other pathologies in the structure of the eye, is included in the complex of symptoms of various genetic abnormalities. There is a hereditary condition for the disease.
Acquired ophthalmoplegia develops as a result of the following reasons:
The disease can develop against the background of other infectious diseases - tuberculosis or syphilis, as well as tetanus, botulism and diphtheria.
Ophthalmoplegia can be a concomitant symptom of ophthalmoplegic migraine, a rare condition that causes severe headache attacks.
Clinical picture
The symptoms of the disease manifest themselves in different ways, the degree of their severity depends on the type of ophthalmoplegia. The main signs for the diagnosis of pathology are:
In severe forms of the disease, there may be a lack of activity and mobility of the eyeball, a deterioration in the reaction of the pupil to light and its immobility. If ophthalmoplegia develops against the background of other diseases, the clinical picture also includes additional symptoms.
Disease types
The types of ophthalmoplegia are distinguished according to the following criteria:
Depending on the location of the damaged muscles, ophthalmoplegia is of two types:
According to the degree of damage to the optic nerves, partial and complete ophthalmoplegia are distinguished. Partial can be external, in which the work of the oculomotor muscle of the eyelid and the internal muscle is disrupted, if only the nerve columns are paralyzed.
With the full form of the disorder, there is an immobility of the eyeball and a drooping of the upper eyelid, the inability of the pupil to respond to light.
For the nature of the lesions, ophthalmoplegia is:
Diagnostics and treatment
Diagnosis of the type of disease and the causes that cause it is necessary for choosing a treatment method.
The disease is diagnosed by initial examination. It has pronounced external manifestations. To establish the nature of the disease and the causes, it is necessary to consult a neurologist and an ophthalmologist.
The following additional studies may be assigned:
If neoplasms are detected, additional consultation with an oncologist may be needed.
After receiving all the necessary data about the disease and determining the causes, treatment is prescribed. It is aimed at eliminating the factors that resulted in the development of ophthalmoplegia, relieving pain and maximizing the restoration of nervous and muscular activity.
There are three main types of treatment, which are prescribed depending on the severity of the disease and the nature of the damage:
- Drug treatment assigned taking into account background diseases. Anti-inflammatory, vasodilator, nootropic drugs can be prescribed. Part of the therapy is the intake of fortifying agents: vitamins and minerals. Corticosteroid hormones are prescribed to normalize metabolism and regenerate muscle function.
- Physiotherapy treatment consists in carrying out a number of procedures that strengthen muscles, relieve spasms and reduce pain. For this purpose, the patient is prescribed electrophoresis, phonophoresis and acupuncture.
- If the cause of the disease is neoplasms of different types, then it is prescribed surgery to remove them. This type of treatment is also used to repair damaged muscles and remove aneurysms.
- avoid injury to the head and eyes;
- support the body's immune forces, periodically taking vitamin complexes;
- if there are cases of ophthalmoplegia in the family, it is necessary to undergo a routine examination by an ophthalmologist more often;
- treat infectious diseases in time, prevent the development of complications;
- do not abuse alcohol, minimize contact with substances that can cause intoxication of the body: lead, barbiturates;
- for any alarming symptoms, you need to see a doctor in order to timely detect deviations from the norm;
- do not self-medicate.
The first two types of therapy are acceptable in the initial stages of the disease in the absence of serious concomitant diagnoses. With their help, you can get rid of ophthalmoplegia if the disease is detected in a timely manner and the development of complications is prevented.
Preventive measures
There are no specific preventive measures to prevent ophthalmoplegia. The recommendations are general in nature, and their observance helps to protect the eyes not only from the development of this disorder, but also from other eye diseases. To reduce the risk of developing pathology, you must:
Ophthalmoplegia can develop against the background of other neurological diseases. A full preventive examination must be carried out 2 times a year in order to identify them in time and begin treatment.
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