To determine the level lesions with such eye deviation The following considerations are mainly relevant. A larger number of supranuclear frontopoitin fibers ending in the pontine center of vision are crossed and come from the opposite hemisphere of the cerebrum. Only a small part of the fibers comes from the hemisphere of the same side.
Crossed supranuclear tract for horizontal viewing directions, it crosses the midline 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 lesion is located on the right, it becomes impossible to look to the left. If the right-sided focus is located in the bridge, i.e., distal from the point of crossover, then the gaze to the right falls out. Due to the predominance of continuous antagonistic innervation, eye deviation occurs: in the first case to the right and in the second to the left.
When, therefore, when turning off supranuclear innervation Deviation conjuguee develops, first described by the Genevan physiologist Prevost, then when the focus is localized 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, the relationships that we have outlined in relation to the bilateral cortical innervation of the eye muscles are also important. Thus, with cerebral hemorrhage (the most common cause of Deviation conjuguee), the patient only looks towards the source of the disease during the first quarter of an hour or the first hours after a stroke. This is an excellent criterion for establishing on which side there is hemiplegia even at the stage of general muscle relaxation.
Then this one 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, the corticonuclear connections of the other hemisphere are switched on.
Thus, temporary Deviation conjuguee indicates that the lesion is located “somewhere” between the cortex and the pons. For more accurate localization, it is necessary to take into account other, including non-ocular, symptoms. Clinical experience shows that in cases where Deviation conjuguee turns into divergence of the eyeballs, death quickly occurs. Deviation conjuguee due to a supranuclear lesion in the pons itself is rarely observed.
“Deviation conjuguee” of the head and eyes together with a spasm of the left facial nerve at the beginning of a Jackeon’s seizure with a right-sided brain tumor (according to Bing)
Diagnostic rules for supranuclear (supranuclear) eye palsies
Supranuclear disorders eye movements are characterized by the fact that their combination is preserved (internuclear palsy). Persistent gross gaze paralysis in diseases of the cerebrum - even with lesions of both hemispheres - is relatively rare. Most often they are still observed in meningitis, spreading to the entire convex surface of the brain.
If sick still looks straight ahead, then a positive puppet phenomenon or a slow deviation of the eyes after introducing cold water into the external auditory canal indicates an iptactic brain stem, i.e., a supranuclear lesion (cerebral cortex - white matter or corticobulbar tracts).
If at persistent gaze paralysis If it is possible to identify a true abducens nerve palsy on the same side (recognized by the fact that the internal rectus muscle of the other eye functions normally during convergence), this indicates that the lesion is localized at the caudal end of the pons. Because the genu facial nerve forms a loop around the abducens nerve nucleus, longitudinal gaze palsy is usually associated with facial palsy (peripheral type) on the same side. Vertical eye movement disorders are almost always caused by lesions of the quadrigeminal region (bilateral oculomotor nerve palsies may simulate gaze palsies; see also aqueduct of Sylvius syndrome).
If Jacksonian seizure begins with convulsions of the gaze, this indicates a lesion in the cortex of the frontal lobe of the opposite side. The patient looks in the direction opposite to the lesion. Occasional isolated convulsions of the gaze without spreading the convulsions to other muscle groups, regardless of whether the eyes deviate in the vertical or horizontal direction, in contrast, indicate damage to 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 movements of the eye, namely during convergence for near and the necessary divergence when moving from close to distance viewing. In this case, we should not forget about possible ocular causes (weakness of convergence in myopia, excessive convergence up to spasm in hypermetropia, hidden strabismus or insufficient binocular vision due to refractive errors or unilateral amblyopia), as well as convulsions due to hysteria or insufficient attention of patients. Sometimes the observed phenomenon of so-called predominant gaze movements seems to indicate damage to the brain stem due to trauma. So, for example, when asked to look down, there is first a short look up, followed by a look down.
Research experience only eye movement disorders protects against errors to some extent. In particular, one should beware of haste in diagnosing gaze paralysis in patients with clouded consciousness and in patients who have not sufficiently understood 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 hemorrhages 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 picture of pseudobulbar palsy, however, only in exceptional cases is it possible to identify the presence of gaze paralysis.
20-02-2012, 20:51
Description
Dysfunction of extraocular muscles
Information on the frequency of oculomotor disorders in brain tumors is scarce. It is believed that they occur in 10-15% of cases [Tron E. Zh., 1966; Huber D., 1976]. Most often occur signs of disruption 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 impaired binocular vision, especially if the superior rectus muscles are affected and vertical diplopia develops. In patients with severe paresis, especially 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, do not have independent significance in the topical diagnosis of brain tumors.
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 base of the skull. The fact is that upon exiting the pons, 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 pinching of the nerve between the pons and the posterior cerebellar artery. A partial disruption of the conduction of the abducens nerve develops and, as a result, weakening of the external rectus muscle on the side of the same name. If the paresis is minor, clearly defined horizontal diplopia appears with extreme abduction of the eye towards the weakened muscle. Thus, diplopia is horizontal and homonymous in nature. There is information in the literature about the predominance of bilateral lesions of the abducens nerve in patients with brain tumors [Tron E. Zh., 1966; Kirkham T. et al., 1972].
Of interest are the daily fluctuations in severity abducens nerve palsy. In patients with brain tumors, diurnal variations in intracranial pressure were observed, and at the moment of its decrease, a sharp relaxation of abducens nerve paresis was noted. The latter is also observed during dehydration therapy.
Second section The abducens nerve has the least resistance to increased intracranial pressure 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.
Paresis of the abducens nerve is 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; Nieber A., 1976].
The oculomotor nerve, departing from the cerebral peduncles, also passes between two vessels (posterior cerebral and superior cerebellar arteries). Therefore, increased intracranial pressure may cause nerve damage between vessels. In addition, the nerve may become pressed against Blumenbach's ring. Since the pupillary fibers running as part of the oculomotor nerve are more vulnerable, an early symptom may be unilateral mydriasis with complete areflexia.
In case of 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 the nuclei or roots.
In recent years, topical diagnosis has become easier thanks to the use of electromyography .
Experience has shown that using this method it turned out to be possible to differentiate various types of myopathies (myositis, endocrine ophthalmopathies), myasthenia gravis, peripheral and central muscle paralysis.
Damage to the abducens nerve at the trunk level is characterized horizontal diplopia, especially with maximum eye abduction outward. If there is mild paresis, slight converging movements are possible. As mentioned above, the abducens nerve is most vulnerable when intracranial pressure increases. Assessment of only one brainstem palsy does not have independent diagnostic value. Its combination with other neurological symptoms (damage to III, IV, V, VII, VIII pairs of cranial nerves) is important.
Nuclear paralysis 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 palsy characterized by two syndromes. Millard-Gubler syndrome consists of the following features: paresis of the lateralis muscle, homolateral peripheral facial palsy, crossed 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 pons, but also as a dislocation sign when the quadrigeminal or cerebellum is damaged.
Fauville syndrome characterized by paresis of the lateral rectus muscle, homolateral peripheral facial palsy, homolateral horizontal gaze palsy. Possible combination with Horner's syndrome.
Brainstem paralysis oculomotor nerve is characterized by dysfunction of all eye muscles innervated by this nerve. E. Zh. Tron (1966) notes that progressive truncal 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. Scheme of the location of the nuclei innervating the eye muscles (according to Hubar A.) I - parvocellular medial nucleus (center of innervation of the ciliary muscle); II - small cell lateral nuclei (the center of innervation of the sphincter of the pupil); III - magnocellular lateral nuclei: 1 - levator nucleus, 2 - nucleus of the superior rectus muscle; 3 - nucleus of the medial rectus muscle; 4 - nucleus of the superior rectus muscle, 5 - nucleus of the inferior rectus muscle; IV - trochlear nerve nucleus; V - nucleus of the abducens nerve; 6 - cortical center of gaze.
They are represented by paired large-cell lateral nuclei that innervate the rectus oculi and levator muscles, paired small-celled Yakubovich-Westphal-Edinger nuclei that innervate the sphincter of the pupil, and a single nucleus of Perlia that sends fibers to the ciliary muscle. The large cell nuclei have a large extent under the bottom of the Sylvian aqueduct, as they are represented by five cellular formations that send a representative to each muscle. In this case, the superior rectus muscle and the levator receive fibers from the cellular formations of the same side, the inferior rectus muscle - from the cellular formations of the opposite side, and the fibers innervating the internal rectus and inferior oblique muscles have a bilateral representation. In this regard, nuclear palsies are characterized by dysfunction of single or several muscles in both eyes. There may be pupillary disorders (mydriasis, weakened pupillary reactions, accommodation paresis).
Fascicular palsies 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's syndrome- unilateral paresis of the oculomotor nerve with crossed hemitremor. Sometimes it is combined with cross-hemianesthesia.
truncal trochlear nerve palsy has no independent diagnostic value for brain tumors. Isolated paralysis and paresis are extremely rare.
Nuclear palsies in combination with oculomotor nerve palsy and vertical gaze palsy, convergence spasm or its paralysis are characteristic of pineal tumors.
Paresis and paralysis of 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. There is no strabismus or diplopia with them. The functions of the muscles concerned are only partially limited. They develop as a result of localization of the pathological process in supranuclear or nuclear centers. Gaze palsies can be vertical or horizontal.
Vertical gaze palsies observed when the center of gaze in the quadrigeminal region is turned off. Upward gaze paralysis is more common. With paresis of upward gaze, 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 quadrigeminal region, vertical nystagmus may precede the appearance of upward gaze paralysis.
Horizontal gaze palsies arise either as a result of turning off the cortical gaze center in the frontal gyrus, or when turning off the gaze center in the pons. There is a certain dependence of the nature of gaze paralysis on the level of the lesion.
Violation of the frontal center and frontopontine pathway leads to turning off voluntary eye movements, vestibular and optical eye movements are preserved.
Defeat in the center area in the pons leads to the absence of movements, both volitional, vestibular and optical, in the direction of gaze paralysis. Gaze paralysis is pronounced and stable. Concomitant eye deviations 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 damage to the trunk. Lack of voluntary movements if the optical and vestibular ones are preserved, it indicates damage to the frontal center or frontopontine tract. A. Huber (1976) formulates the possibility of differentiation as follows: bilateral lesions of the frontopontine tract cause complete bilateral paralysis, often with the appearance of bilateral vertical paralysis. Bilateral lesions in the pons are 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 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 jerk-like, in which there are two phases of the 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. Based on the direction of movement, horizontal, vertical, rotatory and mixed nystagmus are also distinguished. The latter is characterized by the presence of several components.
Based on the intensity of movements, they are distinguished 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 ahead, 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 movements They distinguish 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 rough nystagmus, in which the eye oscillates more than 15°.
Nystagmus may be physiological and pathological. The latter occurs with diseases of the labyrinth or with 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 jerk-like, and in the direction of movement - horizontal, vertical or rotatory. Labyrinthine, or peripheral, nystagmus always has one direction in all directions of gaze and does not depend on body position. In addition, it is not particularly durable and tends to decrease as its duration increases. Often combined 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 reason that caused it is not eliminated. Typically, central nystagmus is not accompanied by hearing loss and tends to increase as the period of its existence lengthens. Unlike peripheral nystagmus, it disappears when examining the patient in the dark (electronystagmography in the dark).
Central nystagmus usually occurs for tumors of subtentorial localization, especially in the area of the cerebellopontine 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 displacement of the brain by the growing tumor.
In recent years, the attention of researchers has attracted state of saccadic eye movements for various diseases of the central nervous system. Micromovements of the eyes, or physiological nystagmus, are involuntary micromovements 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 area of the central fovea of the retina. By the nature of the movements that appear distinguish between drift, tremor and jumps.
Drift is a smooth, slow movement of the eyes within 5-6 arcs. min. Oscillatory movements with an amplitude of 20-40 arc. min and with high frequency are called tremor. Microjumps, or microsaccades, are rapid eye movements ranging from 1 arc. min up to 50 arc. min. Normally, the saccades of both eyes are synchronous and 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. Thus, with mild paresis, micro-jumps practically do not differ from the norm. As the severity of paralysis increases, the interval between jumps increases and 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 until their complete disappearance. These changes correspond to the side of the lesion and do not depend on which eye is the fixing eye. The authors found that with paresis the drift amplitude increases, and with paralysis it decreases.
Brainstem lesion accompanied by a violation of the central mechanisms of control of fixation movements. The frequency, direction and amplitude of micromovements change, and pathological spontaneous nystagmus occurs. As noted earlier, spontaneous nystagmus often precedes paresis and paralysis of the oculomotor nerves. The close topographic relationships of the nuclei and supranuclear stem gaze centers in the brainstem lead, as a rule, to mixed lesions. Examining 15 patients with brain stem paralysis, S. A. Okhotsimskaya (1979) found that changes in saccadic eye movements can be detected in cases where clinical gaze paresis is still absent. Thus, these changes can be regarded as early symptom developing gaze paresis with intrastem lesions. A characteristic sign of unilateral nuclear palsy, 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, there were no surges even in cases of incomplete ophthalmoplegia.
Disorders of pupillary reactions
The literature describes many syndromes associated with disorders 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 pupil reaction to light.
Before moving on 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).
Fig 81. Diagram of the visual pathway and pupillary reflex. 1 - ciliary node; 2 - optical path; 3 - lateral geniculate body; 4 chiasmus; 5 - optical radiation (Graziole beam); 6 - visual cortex, Yakubovich-Westphal-Edinger nuclei; 8 - anterior quadrigeminal.
Afferent fibers of the pupillary reflex as they exit the optic cords form a synapse in the anterior quadrigemale (regio pretectalis), from where they are directed to the nuclei of the oculomotor nerve (Yakubovich-Westphal-Edinger nucleus), and some of the fibers are directed to the nucleus of the homolateral side, some of the fibers form a decussation in the posterior commissure, after which they reach the contralateral Yakubovich-Westphal nucleus. Edinger. Thus, each Yakubovich-Westphal-Edinger nucleus innervating the sphincter of the iris has a representation of 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.
With normal vision there is synkinetic constriction of the pupil with convergence of the eyeballs or contraction of the ciliary muscle during accommodation. There is no clear idea 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 nerve, reach the nuclei of the V nerve and the Yakubovich nuclei -Westphal-Edinger. Excitation of these nuclei leads to contraction of the sphincer of the pupil. Accommodation is stimulated by visual impulses arising in the retina and directed to the occipital lobe cortex, 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.
The most subtle and delicate disorders of pupillary reactions were possible to identify only with the help of local pupillography method or local exposure to the subject being examined.
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 quadrigeminal epiphysis, third 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 the reaction to accommodation and convergence [Sokolova O. N., 1963]. The combination of pupillary disorders with disturbances in the acts of accommodation and convergence is a later sign, indicating a significant spread of the tumor process, including the quadrigeminal area. Tumors of the quadrigeminal gland and pineal gland may also be accompanied by paresis and upward gaze paralysis.
Shape and size of pupils should also be given importance, since a change in the size of the pupils can sometimes be one of the symptoms of blindness that the patient is not aware of.
Normal pupil width varies within a fairly wide range - from 3 to 8 mm. It should be taken into account that fluctuations in the diameter of the pupils are normally acceptable: anisocoria can reach. 0.9 mm [Samoilov A. Ya. et al., 1963]. Children's pupils are always wider than adults'. By pupil size The color of the iris also influences it. It has been noticed that blue-eyed and gray-eyed people have wider pupils than brown-eyed people. Ophthalmologists know the fact that pupils are dilated in nearsighted people, so the nature of refraction should be taken into account when assessing the pupils. Unilateral myopia can cause anisokeria. The latter is observed in diseases of the gallbladder and damage to the apexes 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. In this case, anisocoria was combined with mild homolateral ptosis, which appeared earlier than mydriasis and was caused by compression of the peripheral part of the oculomotor nerve at the clivus by a displaced brain or a growing tumor. As the tumor process progresses, paralysis of the external rectus muscles of the eye may occur.
Orbital tumors, localized paraneurally and compressing the ciliary ganglion, sometimes cause mydriasis on the affected side with mild exophthalmos or even before its appearance [Brovkina A.F., 1974]. It should also be taken into account that after orbitotomy and tumor removal, 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 soul. We observed in such patients paresis of accommodation and slight impairment of corneal sensitivity. 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 oculi muscles, it occurs when the pathological process is located at the apex of the orbit, in the area of the superior orbital fissure. Pituitary tumors, when they spread extrasellar 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 widening of the palpebral fissure were found on the side of the hemianopsia. 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 hemianopia with anisocoria in 1/3 of cases. According to I. I. Merkulov (1971), this does not detract from the advantages of Baer syndrome in the topical diagnosis of tractus hemianopsia.
Changes in field of view
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.
It should be considered optimal to use 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. It should be noted, however, that in most cases in neurological patients it is extremely difficult to study isopters as well as performing profile static perimetry. This is due to the patient’s rapid fatigue, insufficient attention, and often to the lack of sufficient contact between the patient and the doctor. In such cases, it may be useful to study the central visual field (up to 25° from the point of fixation) with multiple objects on the so-called visual field analyzers [Astralenko G. G., 1978; Friedman, 1976]. When examining a 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 examiner. The technique of the control method for studying the visual field is described in all manuals. Less known is the test proposed by A. Kestenbaum (1947). It is unjustifiably little used in control studies 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, standing behind him, 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 vision should coincide with the contours of the face: the nasal border runs along the line of the nose, the temporal border runs 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°.
Simplified methods for studying the visual field include the test reflex closure of the palpebral fissure. A hand is passed in front of the patient's eye on four sides, and the eyelids reflexively close. For hemianopsia in the zone of lack of vision, the eyelids will not close. This test can be recommended when examining patients with stupor, aphasia, or when visual acuity decreases before hand movements near 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 must say when he sees one or two hands or when he recognizes their contours (if visual acuity is poor). If there is a difference in perception on both sides, we can talk about relative hemianopsia, as opposed to absolute hemianopsia, which can only be detected with an isolated study of each eye. However, early topical diagnosis of lesions of the optic-nervous pathway requires qualified research using kinetic perimetry with a sufficient number of objects and campimetry.
A. Huber (1976) believes that at present there is no point in performing color perimetry. To detect scotoma in red, which is one of the early signs of developing atrophy of the optic nerve or tract, it is quite sufficient to conduct perimetry with a red object 5 mm from a distance of 33 cm (5/330).
At the core topical diagnostics damage to the optic nerve tract due to 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 location of nerve fibers in the chiasm. 1 - retina; 2 - optic nerve; 3 - chiasm; 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 consider it advisable to stop 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. In the chiasm and optic tracts they also occupy a lateral position. The fibers from the nasal halves of the retina in the chiasm are decussated. The level of chiasm depends on the level of nerve fibers in the retina and optic nerve. Fibers starting from the inferior 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 chiasm, these fibers extend for some distance into the opposite optic nerve, where they form the anterior limb of the chiasm. Only after this they, located medially, pass into the optic tract. From the upper nasal parts 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 chiasm closer to its upper surface. Before the chiasm, they enter the optic tract of the same side, where they form the posterior knee of the chiasm. The bulk of the crossed fibers are located in the medial parts of the chiasm. It should be remembered that the fibers of the papillo-macular bundle are also crossed.
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 hemianopsia; 5) homonymous hemianopsia. The listed visual field defects depending on the level of damage to the visual-nervous pathway are presented 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 hemianopsia with damage to the intracranial portion of the optic nerve near the chiasm; 3 - bitemporal hemianopsia with damage to the medial part of the chiasm; 4 - incongruent homonymous hemianopsia with damage to the optic tract; 5 - homonymous hemianopsia without preservation of the macular zone with damage to the posterior part of the optical tract or the anterior part of the optical radiation; 6 - incongruent superior homonymous quadrantopsia with damage to the anterior part of the optical radiation (temporal lobe); 7 - weakly expressed incongruent homonymous inferior quadrantopsia with damage to the internal part of the optical radiation (parietal lobe); 8 - incongruent homonymous hemianopsia without preservation of the macular zone with damage to the middle part of the optical radiation; 9 - congruent homonymous hemianopsia with preservation of the macular zone with damage to the posterior part of the optical radiation; 10 - congruent homonymous hemianoptic central scotoma with damage to the occipital lobe.
Of primary importance for the topical diagnosis of damage to the visual-nervous tract are hemianopic visual field defects[Troy 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 tract, or 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 parts of the right optical radiation).
The nervous type of hemianopsia 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 optic tracts.
Concentric narrowing of the visual field in patients with a brain tumor is usually due to developing secondary post-congestive optic atrophy. Bilateral tubular narrowing of the visual field is sometimes the result of bilateral homonymous hemianopia with preservation of the macular region in patients with a tumor localized in the calcarine sulcus. Unilateral concentric narrowing visual field is observed in cases where the intracranial part of the optic nerve between the optic foramen and the chiasm is involved in the pathological process. This can be observed with tumors of the optic nerve itself, meningiomas of the tubercle of the sella turcica, crest of the sphenoid bone or olfactory fossa. The described changes in the visual field were also observed in craniopharyngiomas and pituitary adenomas with extrasellar distribution.
Without dwelling on other reasons that cause unilateral concentric narrowing of the visual field (diseases of the retina, orbital portion of the optic nerve), we consider it necessary to emphasize difficulty in differential diagnosis its 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 in combination with scotomas. A. Huber (1976) observed quadrant unilateral defects visual fields merging with the blind spot area when the optic nerve is compressed by a tumor. We observed similar changes [Brovkina A.F., 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 affected side), an inferotemporal visual field defect was detected in the visual field, merging with the area of the blind spot (Fig. 88).
Rice. 88. Unilateral inferotemporal 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-nervous tract is the identification absolute or relative scotomas. At the onset of the disease, they can only be determined when examining colored objects or when examining small objects for white color (no more than 1 mm on the Förster perimeter or 0.25 mm on hemispherical perimeters). Based on their location, these scotomas are classified into central, paracentral, cecocentral and peripheral.
Unilateral central or paracentral scotomas They 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 with chiasmal 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 basis for the appearance of these symptoms is the isolated position of the papillo-macular 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 in nature, that is, they are not felt by the patient. These scotomas should be regarded as a sign of slow progressive damage to the optic nerve tract 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 with the bottom of the third ventricle, below - with the diaphragm of the sella turcica, behind the chiasm is adjacent 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 area of the chiasmal groove. The chiasm is surrounded on the sides 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. Thus, for example, tumors of the sella turcica region lead to the appearance of typical bitemporal hemianopsia or hemiapopic bitemporal defects in the visual field. Symmetrical bitemporal quadrantopsia or hemianopsia are most common in pituitary tumors, while asymmetrical bitemporal hemianopsia or quadrantopsia are more common in parasellar or suprasellar tumors (Fig. 89).
Rice. 89. Hemianopic bitemporal visual field defects due to compression of the chiasm from above.
Often tumors have asymmetrical growth pattern. In such cases, one of the optic nerves (if the tumor grows anteriorly) or the optic tract (if the tumor grows posteriorly) may be directly involved in the tumor process. As a result, typical symptoms develop, shown in Fig. 82.
Homonymous hemianopic visual field defects indicate damage to the optic tract or central neuron of the visual 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 about damage to the visual-nervous pathway in some area along its entire diameter. It is possible to differentiate tractus hemianopsia from hemianopsia caused by damage to the radiatio optica and higher by signs of congruence. An incongruent onset with a progressive change in the visual fields passing through the point of fixation (without preserving the macular area), blanching of the temporal half of the optic nerve head is characteristic of damage to the optic tract (tumors of the temporal lobe, middle fossa, thalamus, quadrigeminal). Temporal lobe tumors often accompanied by the appearance of upper quadrant hemianopsia; 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. Congruent homonymous hemianopsia without preservation of the macular area, according to A. Huber, most often indicates complete damage to 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 eye muscles are shown in Fig. 1. The superior oblique muscle of the eye is controlled by the trochlear cranial nerve, the external rectus muscle is controlled by the abducens nerve. 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 extrinsic muscles of the eye (left eyeball)
Survey
The examination of a conscious patient includes an assessment of tracking an object (doctor's finger, hammer, pen) moving in vertical and horizontal directions. The object should move in an H-shaped path (rather than a cross-shaped path) to more accurately estimate the movements of the eyeballs. This makes it possible to study the functions of the extrinsic muscles of the eye relatively independently of each other (Fig. 1).
Eye tracking following an object is the best way to detect existing disturbances, since normal tracking is ensured by the integrity of all pathways involved in the conjugate movements of the eyeballs. Elements of this complex system can be examined separately using other clinical methods:
- Saccades- rapid gaze movements; achieved if the doctor asks the patient to quickly look to the right, left, up or down
- Convergence- the ability of the eyeballs to adapt to near vision by friendly reduction inwards, 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, slow tracking is noticeable, 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 feigned disorders of consciousness.
- Vestibulo-ocular reflex. Unlike all the methods described above, which require a preserved level of wakefulness, this test can be used in a patient with depressed consciousness. Brainstem pathways, particularly those that connect the vestibular nuclei (receive input from the vestibular apparatus in the inner ear; see below) with the nuclei of the third, fourth, and sixth nerves, can be examined in the following ways:
Rice. 2. Study of the vestibulo-ocular reflex, and - intact trunk - turning the head causes a transient movement of the eyeballs in the opposite direction - oculocephalic reflex, or the doll's head symptom. This reflex also applies to the vertical movements of the eyeballs when throwing back and lowering the head. Caloric test - the introduction of 50 ml of cold water into the external auditory canal causes a 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 brainstem lesions in an unconscious patient.
Movement disorders of the eyeballs and eyelids
Symptoms
The patient may complain of drooping 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 light hits 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. This disorder is not a symptom of a neurological disease and may be due to an ophthalmic disease (eg, lens opacity) or, more commonly, a functional defect.
The cause of binocular diplopia is an imbalance in the work of the external muscles of the eye and disruption of their innervation. Diplopia is always clearly visible (either double vision is present or not), but its severity can vary. The patient can indicate in which direction the image is bifurcated - horizontal, vertical or oblique.
Lesion syndromes
The main disorders of oculomotor innervation are quite easily identified 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 levator palpebral muscle. When the doctor lifts the patient's eyelid, the eye is in a downward and outward position - the result of an action that does not meet the resistance of the superior oblique and external rectus muscles. Oculomotor nerve palsy may also involve dysfunction of the parasympathetic fibers, causing the pupil to become unresponsive to changes in light and dilated ( "surgical" third nerve palsy) or weakened pupillary reflexes ( "medicated" paralysis). The reasons are given in table. 1.
Table 1. Causes of damage to the oculomotor nerve
Trochlear 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 tilted to compensate for the diplopia. Paralysis of the superior oblique muscle is detected by performing an appropriate test (see below).
Abducens nerve palsy (VI nerve)
The patient is unable to abduct the affected eyeball outward due to the uncontrolled action of the medial rectus muscle, in extreme cases this leads to the appearance of convergent strabismus. Diplopia appears when looking in the affected direction with the appearance of horizontal splitting of the image. Isolated sixth nerve palsy is usually associated with a disruption of the blood supply to the nerve (damage vasa nerve) due to diabetes or hypertension. Restoration of nerve functions after such microvascular diseases occur over several months. VI nerve palsy may also be false sign of localization with increased intracranial pressure, since the nerve is long and has a complex path through the bones of the skull. As a result, there is a high risk of damage due to increased intracranial pressure or volumetric effects.
Horner's syndrome
Some of the muscles responsible for raising the upper eyelid are innervated by sympathetic nerve fibers. As a result, damage to the oral part of the sympathetic nervous system may manifest itself as partial ptosis along with miosis(constriction of the pupils as a result of paralysis of the sympathetic fibers innervating the muscle that expands the pupil). Other signs of Horner's syndrome - deep standing of the eyeball in the orbit (enophthalmos), decreased or absent sweating on the affected side of the face (anhidrosis) - are less common. The source of 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 depending on 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 extreme vertical or horizontal directions, less often observed when looking in front of oneself. Nystagmus can occur with the same speed of movement of the eyeballs in both directions ( pendular nystagmus), however, more often the slow phase (return to the starting 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 practically normal saccades, the purpose of which is to compensate for the pathological process represented by the slow component.
Classification of jerky nystagmus:
- Appears only when looking towards the fast component.
- Appears in the normal direction of gaze (gaze directed straight ahead).
- Appears when looking towards the slow component.
Nystagmus can be congenital, in which case it is usually pendular. Acquired nystagmus may be a sign of a disorder of the inner ear (labyrinth) (see below), brain stem or cerebellum, or may also occur as a side effect of medications (eg, anticonvulsants). Rotational (rotatory) nystagmus is observed with damage to either the peripheral (labyrinth) or central (brain stem) parts of the vestibular analyzer. Non-drug-related vertical nystagmus usually indicates a brainstem lesion and is of some value for topical diagnosis of the lesion (at the foramen magnum) if the fast phase of the nystagmus is downward in downward gaze. Patients usually do not experience nystagmus, although it may be associated with systemic dizziness (vertigo) (see below). Sometimes the rhythmic movements of the eyeballs during nystagmus are perceived subjectively ( oscillopsia), especially often with vertical nystagmus. At the same time, the patient realizes that the world around him is moving up and down unpleasantly.
Internuclear ophthalmoplegia
A normal friendly gaze 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 conjugal 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, providing innervation to the internal rectus muscles. As a result of damage to this pathway, the possibility of conjugal movements of the eyeballs is lost - the conditions for the normal abduction of one eye outward are preserved, while movements of the other eye inward are impossible. It is also possible that nystagmus may appear when looking to the side, which is more pronounced in the outwardly abducted eye. This combination of symptoms is known as internuclear ophthalmoplegia and is commonly found in multiple sclerosis. Damage to the medial longitudinal fasciculus can also cause different vertical positions eyeballs, in which one eyeball stands higher relative to the other in all positions.
Complete or partial loss of the ability of both eyeballs to move in a certain direction is caused by supranuclear lesion pathways responsible for the movements 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 are affected. Typically, there is no diplopia because the optical axes can remain aligned with each other.
The lesion can be caused by both compression and destruction of the corresponding structures (for example, hemorrhage or infarction). Supranuclear gaze palsy can be chronic and progressive, such as in extrapyramidal disorders. If in a patient with gaze paralysis, eye movements are preserved during the examination of the oculocephalic reflex, 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 may cause convergent gaze paresis(Fig. 4). The center that controls horizontal eye movements is located in the pons (higher centers in the cerebral hemispheres); The centers of vertical vision are not as well studied, but are believed to be located in the upper parts of the midbrain.
Rice. 4. Concomitant gaze palsy. The direction of the deviation is diagnostically valuable in determining the lesion 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 because 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 pons); the eyeballs deviate to the affected side. The lesion is located above the decussation of the pyramids, so hemiparesis is detected on the side opposite to the lesion. However, the focus is located below the intersection of fibers from the cortical center of gaze, directed to the nuclei of the pons and controlling the horizontal movements of the eyeballs. In this situation, an action that does not meet resistance from the oculomotor center of the unaffected half of the pons leads to deviation of the eyeballs in the same direction
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, damage to the brain stem of an unclear nature). One should keep 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 monitoring eye movements, when weakness of certain muscles is detected. In some cases, the defect is not so pronounced and the movements of the eyeballs seem normal upon examination, although the patient still notices double vision. In such cases, it is necessary to determine the direction in which diplopia is most pronounced, and also determine in which direction the image bifurcates - horizontal, oblique or vertical. The eyes are closed in turn and note which of the images disappears. Usually false image(for the affected eye) more distant from the center. Thus, in the case of assessing diplopia with one eyeball covered in a patient with mild paralysis of the right external rectus muscle, diplopia is maximum when looking to the right, while the image bifurcates horizontally. When the right eyeball is closed, the image distant from the center disappears, while when the left eyeball is closed, the image closest to it disappears.
Neurology for general practitioners. L. Ginsberg
Paralytic strabismus is caused by paralysis or paresis of one or more extraocular muscles, caused by various reasons: trauma, infections, neoplasms, etc. It is characterized primarily by the limitation or lack of mobility of the squinting eye in the direction of the action of the paralyzed muscle. When looking in this direction, double vision or diplopia occurs.
If with concomitant strabismus a functional scotoma relieves double vision, then with paralytic strabismus another adaptation mechanism arises: the patient turns his head in the direction of the action of the affected muscle, which compensates for its functional insufficiency. Thus, the third symptom characteristic of paralytic strabismus arises - forced rotation of the head. So, with abducens nerve palsy (impaired function of the external rectus muscle), for example the right eye, the head will be turned to the right. Forced rotation of the head and tilt towards the right or left shoulder with cyclotropia (displacement of the eye to the right or left of the vertical meridian) is called torticollis.
Ocular torticollis should be differentiated from neurogenic, orthopedic (torticollis), and labyrinthine (with otogenic pathology). Forced rotation of the head allows you to passively transfer the image of the object of fixation to the central fovea of the retina, which eliminates double vision and provides binocular vision, although not quite perfect.
As a result of deviation, as with concomitant strabismus, a disorder of binocular vision occurs. It should, however, be noted that in children, topical diagnosis of paralytic strabismus, and sometimes differential diagnosis with concomitant strabismus, is very difficult.
Causes
Paralytic strabismus may be caused by damage to the corresponding nerves or a violation of the function and morphology of the muscles themselves. Paralysis can be central or peripheral. The first arise as a result of volumetric, inflammatory, vascular or dystrophic disorders and injuries in the brain, and the second - 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), orbital phlegmon, and often as a result of direct injury (rupture) of the muscle itself. Congenital paralysis is not a common occurrence and is usually combined. With simultaneous paralysis of all optic nerves, complete ophthalmoplegia occurs, which is characterized by eye immobility, ptosis and pupil dilation.
Complete damage to the oculomotor (III cranial) nerve causes paralysis or paresis of the superior, medial and inferior rectus muscles of the eye, the muscle that lifts the upper eyelid, and, as a rule, loss of pupillary 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 dilation of the pupil are also detected.
Compression lesion of the oculomotor nerve (aneurysm, tumor, herniation) usually causes dilation of the pupil 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 inward abduction of the eye; when looking towards the affected muscle, non-crossed diplopia occurs (the image appearing in the abducted eye is projected laterally than the image in the adducted eye).
Lesion at the level of the pons often accompanied by horizontal gaze paresis or internuclear ophthalmoplegia.
Damage to the trochlear (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 turning the head 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 a point (for example, look at the center of the ophthalmoscope) with a squinting eye, the healthy eye will deviate to a much larger angle.
In paralytic strabismus, it is necessary to determine the affected extraocular muscles. In preschool children, this is judged by the degree of eye mobility in different directions (determination of the visual field). At older ages, special methods are used - coordimetry And provoked diplopia .
A simplified way to determine the field of view is as follows. The patient sits opposite the doctor at a distance of 50-60 cm, the doctor fixes the patient’s head with his left hand and asks him to alternately watch with each eye (the second eye is covered at this time) the movement of an object (pencil, hand ophthalmoscope, etc.) in 8 directions. Muscle deficiency is judged by the limitation of eye mobility in one direction or another. In this case, special tables are used. Using this method, only severe limitations in eye mobility can be identified.
If there is a visible vertical deviation of one eye, a simple adduction-abduction method can be used to identify the paretic muscle. The patient is asked to look at an object, move it to the right and left and observe whether the vertical deviation increases or decreases with extreme gaze aversions. Determination of the affected muscle in this way is also carried out using special tables.
Chess coordimetry is based on dividing the visual fields of the right and left eyes using red and green filters.
To conduct the study, a coordimetric set is used, which includes a graphed screen, red and green flashlights, and red-green glasses. The study is performed in a darkened room, on one of the walls of which there is a screen divided into small squares. The side of each square is equal to three angular degrees. In the central part of the screen there are nine marks placed in the form of a square, the position of which corresponds to the isolated physiological action of the oculomotor movements of the mouse.
A patient wearing red-green glasses sits at a distance of 1 m from the screen. To examine the right eye, a red flashlight is placed in his hand (red glass in front of the right eye). The researcher holds a green flashlight in his hands, the beam of light from which he directs one by one to all nine points and asks the patient to combine the light spot from the red flashlight with the green light spot. When trying to combine both light spots, the examinee usually makes a mistake by some amount. The doctor records the position of the green spot to be fixed and the red spot to be trimmed on a diagram (sheet of graph paper), which is a small copy of the screen. During the examination, the patient's head should be motionless.
Based on the results of a coordimetric study of one eye, it is impossible to judge the state of the oculomotor system; it is necessary to compare the results of coordimetry of both eyes.
The field of view in the diagram drawn up based on the results of the study is shortened in the direction of action of the weakened muscle, while at the same time there is a compensatory increase in the field of view in the healthy eye in the direction of the action of the synergist of the affected muscle of the squinting eye.
The Haab-Lancaster method for studying the oculomotor system in conditions of provoked diplopia is based on assessing the position in space of images belonging to the fixating and deviated eye. Diplopia is caused by placing a red glass on the squinting eye, which makes it possible 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 there is one (rather than two). The study is carried out in a dimly lit 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 in nine gaze positions is recorded. When interpreting the results, it is necessary to use the rule according to which the distance between double images increases when looking in the direction of the action of the affected muscle. If during coordimetry the field of view is recorded (decreases with paresis), then with “provoked diplopia” - the distance between double images, which decreases with paresis.
Diplopia due to paralysis of individual eye muscles
- Paralysis lateral rectus muscle right eye - inability to move the right eye to the right. Visual fields: horizontal homonymous diplopia, increasing when looking to the right;
- Paralysis medial rectus muscle right eye - inability to move the right eye to the left. Visual fields: horizontal crossed diplopia, increasing when looking to the left;
- Paralysis inferior rectus muscle right eye - inability to move the right eye down when turning the eyeballs to the right. Visual fields: vertical diplopia (the image in the right eye is located lower), increasing when looking to the right and down;
- Paralysis superior rectus muscle right eye - inability to move the right eye upward when turning the eyeballs to the right. Visual fields: vertical diplopia (the image in the right eye is located higher), increasing when looking to the right and up;
- Paralysis superior oblique muscle right eye - the inability to move the right eye down when turning the eyeballs to the left. Visual fields: vertical diplopia (the image in the right eye is located lower), increasing when looking to the left and down;
- Paralysis inferior oblique muscle right eye - inability to move the right eye upward when turning the eyeballs to the left. Visual fields: vertical diplopia (the image in the right eye is located above), increasing when looking to the left and up.
Treatment
Treatment of paralytic strabismus consists primarily of eliminating the underlying disease that caused it (infections, tumors, injuries, etc.). If, as a result of the general measures taken, paralytic strabismus does not disappear, the question of surgical intervention may arise.
The issue of indications and timing of surgery can be resolved positively only together with the relevant specialists (neurologists, oncologists, infectious disease specialists, etc.).
Post-traumatic strabismus, as a rule, is corrected surgically after at least 6 months. from the moment of damage, since in this case regeneration of both the muscle and the 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, or can arise as a result of damage to the nerves in the area of the cranial nerve nuclei, in the area of large nerve trunks, roots and branches.
Causes of acquired ophthalmoplegia;
Classification
In this case, the eye shifts to the zone of action of a healthy or less affected muscle. The patient has difficulty moving the eyes towards the paralyzed muscles, resulting in 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 dilation of a 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 hardware tests are prescribed;
Therapy consists of eliminating the causes of the disease, alleviating pain and restoring, if possible, nervous and muscle activity.
Physiotherapeutic methods
Surgical intervention
Surgical treatment is prescribed if 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 a paralysis of the eye muscles that occurs when the oculomotor nerves are damaged.
Main causes of ophthalmoplegia
Ophthalmoplegia can occur with congenital or acquired lesions of the nervous system in the area of nerve roots or trunks, in the area of the cranial nerve nuclei. 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 and can be observed in several members of the same family.
The causes of acquired ophthalmoplegia may be:
Ophthalmoplegia can also be a symptom of a rare condition called ophthalmoplegic migraine. It manifests itself as attacks of severe headaches, accompanied by unilateral ophthalmoplegia (complete or partial). Headaches can continue 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 when the muscles that are located outside the eyeball are paralyzed, and when the intraocular muscles are paralyzed, internal ophthalmoplegia occurs. With varying degrees of muscle weakening during paralysis, partial internal or external ophthalmoplegia develops. If both the external and internal muscles of the eye are paralyzed at the same time, complete ophthalmoplegia occurs. Complete external and complete internal ophthalmoplegia may also occur.
The eyeball with external partial ophthalmoplegia will tilt 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. With external complete ophthalmoplegia, the eyeball will become immobile and ptosis will develop. Internal partial ophthalmoplegia is characterized only by pupil dilation in the absence of reaction to light, decreased convergence and accommodation.
Ophthalmoplegia is the name given to a symptom of many neurological diseases in which the motor function of the eyeballs is limited due to decreased tone of the eye muscles. Simply - paralysis of the eye muscles due to disease of the optic nerves.
Causes
Ophthalmoplegia can be congenital (due to congenital pathologies of the nervous system) or acquired. The causes of the disease may be:
In addition, ophthalmoplegia may be a symptom of the rare ophthalmoplegic migraine. After the attack ends, the eye slowly returns to normal.
Symptoms
The disease immobilizes the eyeball, and voluntary eye movements become impossible. Sometimes the eye is tilted to the side. A person begins to see double. Drooping of the upper eyelid (ptosis), headache and pain 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 impaired - due to the incorrect position of the eyes and the impossibility of their synchronous work, the patient cannot focus his gaze on an object, regardless of its distance or approach. External signs also include bulging of the eyeball, redness of the eye and swelling around the orbit.
Ophthalmoplegia varies depending on which muscles and nerves of the eye are affected, to what extent, and what the nature of the damage is.
Diagnostics
Ophthalmoplegia has pronounced external signs. But to identify its causes, in addition to consultations with an ophthalmologist and neurologist, the patient is prescribed hardware tests:
Find out more about the symptom of blurred vision.
Treatment
Treatment of ophthalmoplegia consists of eliminating the causes of the disease, relieving pain and restoring, as far as possible, muscle and nervous activity.
- anti-inflammatory drugs;
- medications that prevent dehydration of the body during 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 earlier the disease is detected, the more likely it is to successfully get rid of it. Do not ignore visits to the doctor and try to cure yourself.
Ophthalmoplegia is a disease accompanied by paralysis of individual or all eye muscles, which are driven by the abducens, trochlear and oculomotor nerves.
Congenital ophthalmoplegia is a consequence of aplasia of the nerve nuclei 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 structural defects of the eye.
Other causes of congenital pathology:
Ophthalmoplegia can be 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 simultaneous paralysis of the internal and external muscles.
As a result of complete internal oophthalmoplegia, the pupil dilates, it stops responding 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 spasms and strengthen muscles, acupuncture, electrophoresis and phonophoresis with medications are prescribed.
What is ophthalmoplegia, its types and treatment methods
Ophthalmoplegia is a disease that occurs as a result of damage to the optic nerves and is accompanied by paralysis of the eye 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 tissue. The disease can be congenital or acquired.
The congenital form in most cases occurs with other pathologies in the structure of the eye and is part of a complex of symptoms of various genetic anomalies. There is a hereditary cause of 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 may be an accompanying symptom of ophthalmoplegic migraine, a rare disorder that causes severe headache attacks.
Clinical picture
Symptoms of the disease manifest themselves in different ways, the degree of their severity depends on the type of ophthalmoplegia. The main signs for diagnosing 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.
Types of disease
Types of ophthalmoplegia are distinguished according to the following criteria:
Depending on the location of the damaged muscles, ophthalmoplegia is of two types:
Based on the degree of damage to the optic nerves, partial and complete ophthalmoplegia are distinguished. Partial can be external, in which the work of the extraocular muscle of the eyelid is disrupted, and internal, if only the nerve columns are affected by paralysis.
In the full form of the disorder, there is immobility of the eyeball and drooping of the upper eyelid, and the inability of the pupil to respond to light.
Depending on the nature of the lesions, ophthalmoplegia occurs:
Diagnosis and treatment
Diagnosis of the type of disease and the causes that cause it is necessary to select a treatment method.
The disease is diagnosed by initial examination. It has pronounced external manifestations. To establish the nature of the disease and its causes, consultation with a neurologist and ophthalmologist is necessary.
The following additional studies may be prescribed:
If neoplasms are detected, additional consultation with an oncologist may be required.
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 prescribed taking into account underlying diseases. Anti-inflammatory, vasodilating, and nootropic drugs may be prescribed. Part of the therapy is taking general strengthening agents: vitamins and minerals. Corticosteroid hormones are prescribed to normalize metabolism and regenerate muscle functions.
- Physiotherapeutic treatment consists of carrying out a series 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;
- maintain the body’s immune strength by periodically taking vitamin complexes;
- if there are cases of ophthalmoplegia in your family, it is necessary to undergo preventive examinations by an ophthalmologist more often;
- treat infectious diseases in a timely manner and prevent the development of complications;
- do not abuse alcohol, minimize contact with substances that can cause intoxication of the body: lead, barbiturates;
- If you have any alarming symptoms, you should consult a doctor in order to promptly 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 you detect the disease in a timely manner and prevent the development of complications.
Preventive measures
There are no specific preventive measures to prevent ophthalmoplegia. The recommendations are general in nature, and following them helps 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 complete preventive examination should be completed 2 times a year in order to identify them in time and begin treatment.
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