Investigation of cranial nerves. III, IV, VI pairs: oculomotor, block and distracting nerves

The oculomotor nerve contains motor fibers that innervate the medial, upper and lower rectus muscles of the eyeball, the lower oblique muscle and the muscle lifting the upper eyelid, as well as the vegetative fibers that, interrupted in the ciliary ganglion, innervate the inner smooth muscles of the eye-the pupil sphincter and the ciliary muscle . The nerve block innervates the upper oblique muscle, and the abducent nerve - the outer rectus muscle of the eyeball.

Causes of Diplomacy

When collecting an anamnesis, it is determined whether the patient has  diplopia  and, if present, how the doubling objects are located - horizontally (pathology of the sixth pair), vertically (pathology of the third pair) or when looking down (defeat IV pair). Monocular diplopia is possible with intraocular pathology, resulting in the dispersion of light rays on the retina (with  astigmatism, corneal diseases, with cataracts beginning  , hemorrhage into the vitreous humor), and also with  hysteria; with paresis of the external (striated) muscles of the eye monocular diplopia does not happen. The feeling of imaginary jitter of objects (oscilloscopy) is possible with vestibular pathology and some forms of  nystagmus.

[1], [2]

The movements of the eyeballs and their research

There are two forms of friendly movements of the eyeballs-conjugated (eye), in which the eyeballs rotate simultaneously in the same direction; and vergiant, or disconjugated, in which the eyeballs simultaneously move in opposite directions (convergence or divergence).

With neurological pathology, there are four main types of oculomotor disorders.

• Mismatch of eyeball movements due to weakness or paralysis of one or more striated muscles of the eye; as a result, strabismus (strabismus) and bifurcation occur because the object in question is projected into the right and the left eye, not in analogous, but in the disparity areas of the retina.
• Friendly violation of conjugated movements of eyeballs, or friendly paralysis of the eye: both eyeballs co-ordinate (together) cease to arbitrarily move in one direction or another (right, left, down or up); in both eyes, the same deficiency of movements is detected, while dithering and strabismus does not occur.
• The combination of paralysis of the muscles of the eye and paralysis of the eye.
• Spontaneous pathological movements of the eyeballs that occur mainly in patients in a coma.

Other variants of oculomotor disorders ( friendly strabismus, internuclear ophthalmoplegia ) are observed less often. These neurological disorders should be distinguished from a congenital imbalance in the tone of the eye muscles (nonparalytic strabismus or nonparalytic congenital strabismus, oftophoria) in which the misalignment of the optic axes of the eyeballs is observed both in eye movements in all directions and in rest. Often observed latent nonparalytic strabismus, in which images can not reach the identical places of the retina, but this defect is compensated by the reflex corrective movements of the hidden mowing eye (fusional motion). With exhaustion, mental stress, or for other reasons, fusional motion can weaken, and the latent squint becomes apparent; in this case there is a double vision in the absence of a paresis of the external muscles of the eye.

Evaluation of optical axis parallelism, strabismus and diplopia analysis

The doctor is in front of the patient and asks him to look straight and into the distance, fixing his eyes on the remote object. Normally, the pupils of both eyes should be in the center of the eye gap. The deviation of the axis of one of the eyeballs to the inside (esotropia) or outward (exotropy) when viewed directly and into the distance indicates that the axes of the eyeballs are not parallel (strabismus), and this is the cause of double vision (diplopia). To identify minor strabismus, you can use the following method: keeping a light source (for example, a light bulb) at a distance of 1 m from the patient at the level of his eyes, follow the symmetry of the reflections of the light from the iris. In that eye, whose axis is deflected, the reflection does not coincide with the center of the pupil.

Then the patient is offered to fix a sight on the subject, which is at the level of his eyes (the pen, his own thumb), and in turn close one or the other eye. If, at the closing of the "normal" eye, the mowing eye makes an additional movement to preserve the fixation on the object ("alignment movement"), then, most likely, the patient has a congenital strabismus, not a paralysis of the eye muscles. With congenital strabismus movements of each of the eyeballs, if they are tested individually, are preserved and performed in full.

Evaluate the performance of the smooth tracking test. Ask the patient's eyes (without turning his head) to follow the object, which is kept at a distance of 1 m from his face and slowly move it horizontally to the right, then to the left, then from each side up and down (the trajectory of the doctor's movements in the air should correspond to the letter "H "). Follow the movements of the eyeballs in six directions: to the right, to the left, down and up with the leads of the eyeballs in turn in both directions. They are interested in whether the patient has a double vision when looking in one direction or another. In the presence of diplopia find out when moving in which direction doubling intensifies. If you place a colored (red) glass in front of one eye, it is easier for a patient with a diploma to delimit double images, and to the doctor to find out which image belongs to which eye.

The light paresis of the external muscle of the eye does not give noticeable strabismus, but at the same time subjectively, the patient already experiences diplopia. Sometimes a doctor may have enough of the patient's report of the occurrence of double vision with a particular movement to determine which eye muscle is affected. Almost all cases of newly emerging double vision in the eyes are due to the acquired paresis or paralysis of one or more striated (external, extraocular) muscles of the eye. As a rule, any newly arising paresis of the extraocular muscle causes diplopia. Over time, visual perception on the affected side slows down, and doubling at the same time passes. There are two basic rules that must be taken into account when analyzing a patient's complaints about diplopia in order to determine which of the muscles of which the eye suffers:

• The distance between the two images increases when viewed in the direction of the action of the paretic muscle;
• the image created by the eye with the paralyzed muscle seems to the patient located more peripherally, that is, more distant from the neutral position.

In particular, you can ask a patient whose diplopia is magnified when looking to the left, look at an object on the left and ask him which image disappears when the doctor's palm covers the patient's right eye. If the image closer to the neutral position disappears, this means that the open left eye is responsible for the peripheral image, and therefore its muscle is defective. Since double vision occurs when viewed to the left, the lateral rectus muscle of the left eye is paralyzed.

Complete defeat of the trunk of the oculomotor nerve leads to diplopia in the vertical and horizontal plane as a result of weakness of the upper, medial and lower rectus muscles of the eyeball. In addition, with complete paralysis of the nerve, ptosis occurs on the side of the lesion (weakness of the muscle lifting the upper eyelid), deviation of the eyeball from the outside and slightly downwards (due to the action of the retained lateral rectus innervated by the outgoing nerve and the upper oblique muscle innervated by the block nerve) , the dilatation of the pupil and loss of its reaction to light (paralysis of the sphincter of the pupil).

Defeat of the nerve leads to paralysis of the external rectus muscle and, accordingly, the medial deflection of the eyeball ( convergent strabismus ). When you look in the direction of defeat, horizontally doubling appears. Thus, diplopia in the horizontal plane, not accompanied by ptosis and changes in pupillary reactions, most often indicates a lesion of the VI pair. If the lesion is located in the brainstem, in addition to the paralysis of the external rectus muscle, horizontal paralysis also occurs.

The defeat of the nerve block causes paralysis of the upper oblique muscle and is manifested by limiting the movement of the eyeball downwards and complaining of vertical double vision, which is most pronounced when looking down and at the opposite side of the focus. Diplopia is adjusted by tilting the head to the shoulder on the healthy side.

The combination of paralysis of the eye muscles and paralysis of the eye indicates the damage to the structures of the bridge of the brain or midbrain. Doubling in the eyes, intensifying after physical exertion or by the end of the day, is typical of myasthenia gravis.

With a significant reduction in visual acuity in one or both eyes, the patient may not notice diplopia, even if there is a paralysis of one or more extraocular muscles.

[3], [4], [5],

Evaluation of coordinated movements of eyeballs

Paralysis of the eyes arises as a result of supranuclear disorders, and not because of the defeat of 3, 4 or 6 pairs of NN. The gaze (gaze) in norm is a friendly conjugated movement of the eyeballs, that is, their coordinated movements in one direction. There are two types of conjugated movements - saccades and smooth tracking. The saccades are very precise and fast (about 200 ms) phase-tonic movements of the eyeballs, normally arising or with an arbitrary glance at the subject (on the command "look to the right", "look left and up", etc.), or reflexively , when a sudden visual or auditory stimulus causes the eye (usually head) to turn in the direction of this stimulus. Cortex control of saccades is carried out by the frontal lobe of the contralateral hemisphere.

The second type of conjugated movements of eyeballs is a smooth tracking: when the object moves in the field of vision, the eyes involuntarily fix on it and follow it, trying to keep the image of the object in the zone of the most clear vision, that is, in the field of yellow spots. These movements of the eyeballs are slower in comparison with saccades and in comparison with them are more involuntary (reflex). Their cortical control is carried out by the parietal lobe of the ipsilateral hemisphere.

Vision disorders (if the nuclei of 3, 4 or 6 pairs are not affected) are not accompanied by a violation of the isolated movements of each eyeball separately and do not cause diplopia. When examining the gaze, it is necessary to find out whether the patient has a nystagmus, which is detected using a smooth-tracking test. Normally eyeballs, when tracking an object, move smoothly and friendly. The appearance of jerky jerks of eyeballs (involuntary corrective saccades) indicates a violation of the ability to smooth tracking (the object immediately disappears from the area of the best vision and is retrieved again with the help of corrective eye movements). Check the patient's ability to keep his eyes in the extreme position when looking in different directions: to the right, to the left, up and down. Pay attention to whether the patient does not arise from the middle position of the eye-induced nystagmus when he withdraws his eyes; nystagmus, which changes direction depending on the direction of the gaze. The rapid phase of the induced nystagmus is directed toward the eye (when viewed to the left, the fast component of the nystagmus is directed to the left, when viewed from the right to the right, when viewed upward - vertically upward, when viewed downward - vertically downwards). The impairment of the ability to smooth tracking and the appearance of the nystagmus induced by the eye are signs of damage to the cerebellar connections with brainstem neurons or central vestibular bonds, and may be a consequence of side effects of anticonvulsants, tranquilizers and some other medications. With a lesion in the occipital parietal region, regardless of the presence or absence of hemianopsia, reflex slow tracking movements of the eyes towards the lesion focus are limited or impossible, but arbitrary movements and movements are preserved by command (that is, the patient can make arbitrary movements with his eyes in any directions, but can not follow the object moving to the side of the lesion). Delayed, fragmented, dis- metrical follow-up movements are observed in supranuclear palsy and other extrapyramidal disorders.

To test arbitrary movements of eyeballs and saccades, ask the patient to look to the right, left, up and down. Estimates the time required to begin the execution of movements, their accuracy, speed and smoothness (often reveals a slight sign of dysfunction of friendly eyeball movements in the form of their "stumbling"). Then, the patient is asked to alternately fix the sight on the tips of two index fingers, which are located at a distance of 60 cm from the patient's face and approximately 30 cm from each other. Assess the accuracy and speed of arbitrary movements of eyeballs.

Succadic dysmetry, in which an arbitrary gaze is accompanied by a series of abrupt jerky eye movements, is characteristic of the involvement of the cerebellar connections, although it can also occur in the pathology of the occipital or parietal lobe of the brain - in other words, the impossibility of catching sight (hypometry) or "slipping" because of the excessive amplitude of movements of the eyeballs (hypermetry), corrected with the help of saccades, indicate a lack of coordination control. The pronounced deceleration of saccades can be observed in diseases such as hepatocerebral dystrophy or Huntington's chorea. The acute lesion of the frontal lobe (stroke, craniocerebral trauma, infection) is accompanied by a paralysis of the horizontal gaze to the opposite side. Both the eyeballs and the head are deflected towards the lesion (the patient "looks at the hearth" and turns away from the paralyzed limbs) due to the preserved function of the opposite center of the head and eye rotation to the side. This symptom is temporary and lasts only a few days, as imbalance of the eyes is soon compensated. The ability to reflex tracking in the frontal paralysis of the eye can persist. Paralysis of the gaze horizontally with lesion of the frontal lobe (cortex and inner capsule) is usually accompanied by hemiparesis or hemiplegia. With localization of the pathological focus in the midbrain roof (prefectural lesions involving the posterior spinal cord of the epithelamus), vertical paralysis develops, accompanied by a violation of convergence ( Parino syndrome ); in the greater degree, the eye is usually upside down. When the bridge of the brain and the medial longitudinal fascicle, providing lateral friendly movements of eyeballs at this level, occur, horizontal paralysis appears in the direction of the focus (the eyes are diverted to the opposite side of the focus, the patient "turns away" from the stem lesion and looks at the paralyzed limbs). This paralysis of the eye usually lasts a long time.

[6], [7], [8]

Evaluation of disconjugated movements of eyeballs (convergence, divergence)

Convergence is checked by asking the patient to focus on the subject that is moving toward his eyes. For example, the patient is offered to fix a look at the tip of the malleus or index finger, which the doctor smoothly brings closer to his nose. When the object approaches the bridge of the nose, the axes of both eyeballs rotate toward the object. At the same time, the pupil narrows, the ciliary (ciliary) muscle relaxes, and the lens becomes convex. Thanks to this, the image of the subject is focused on the retina. Such a reaction in the form of convergence, narrowing of the pupil and accommodation is sometimes called an accommodation triad. Divergence is the reverse process: when the object is removed the pupil expands, and the contraction of the ciliary muscle causes a flattening of the lens.

If convergence or divergence is violated, horizontal diplopia arises when looking at nearby or deleted objects, respectively.

Paralysis of convergence occurs when the prefectural region of the midbrain roof is damaged at the level of the upper hills of the plate of the quadruple. It can be combined with a paralysis of the eye up in the Parino syndrome. Paralysis of divergence is usually caused by bilateral lesions of 6 pairs of cranial nerves.

Isolated reaction of the pupil to accommodation (without convergence) is checked in each eyeball separately: the tip of the neurological malleus or finger is set perpendicular to the pupil (the other eye is closed) at a distance of 1-1.5 m, then quickly approach the eye, while the pupil tapers. The rate of pupils vividly react to light and convergence with accommodation.

[9], [10]

Spontaneous pathological movements of eyeballs

Syndromes of spontaneous rhythmic disorders of the eye include oculogic crises, periodic alternating gaze, ping-pong visual syndrome, ocular bobbing, ocular dipping, alternating oblique deviation, periodic alternating deviation of the eyes, etc. Most of these syndromes develops with severe brain damage, they are observed mainly in patients who are in a coma.

• Oculogic crises - suddenly developing and lasting from several minutes to several hours deviation of eyeballs up, less often - down. They are observed with intoxication with neuroleptics, carbamazepine, lithium preparations; with stem encephalitis, glioma of the third ventricle, craniocerebral trauma and some other pathological processes. The oculogic crisis should be distinguished from the tonic deviation of the gaze upward, sometimes observed in patients in a coma with diffuse hypoxic brain lesions.
• The syndrome of "ping-pong" is observed in patients who are in a coma, it consists in a periodic (every 2-8 seconds) friendly eye deviation from one extreme position to another.
• In patients with gross damage to the bridge of the brain or structures of the posterior cranial fossa, ocular bobbing is sometimes observed - rapid jerky movements of the eyeballs down from the middle position, followed by their slow return to the central position. Horizontal eye movements are absent.
• "Ocular dipping" is a term for slow movements of the eyeballs, which are replaced after a few seconds by their rapid return to their original position. The horizontal movements of the eyeballs are preserved. The most common cause is hypoxic encephalopathy.

Pupils and eye slits

The reactions of the pupils and the eye slits depend not only on the function of the oculomotor nerve - these parameters are also determined by the state of the retina of the eye and optic nerve, which form the afferent part of the reflex arc of the pupil's reaction to light, and also the sympathetic effect on the smooth muscles of the eye. Nevertheless, pupillary reactions are examined when assessing the state of 3 pairs of cranial nerves.

Normally the pupils are round, equal in diameter. In ordinary room lighting, the diameter of the pupils can vary from 2 to 6 mm. The difference in pupil size (anisocoria), not exceeding 1 mm, is considered a variant of the norm. To test the direct reaction of the pupil to the light, the patient is asked to look into the distance, then quickly turn on the flashlight and assess the degree and stability of the pupillary narrowing of the eye. The included light bulb can be brought to the side of the side, from the temporal side, to exclude the accommodation reaction of the pupil (its narrowing in response to the approach of the object). Normally, when illuminated, the pupil narrows, this constriction is stable, that is, it persists all the time while the light source is near the eye. When the light source is eliminated, the pupil expands. Then, the friendly reaction of the other pupil is evaluated, which occurs in response to the illumination of the eye being examined. Thus, it is necessary to illuminate the pupil of one eye twice: during the first illumination we look at the reaction to the light of the illuminated pupil, and in the second illumination we observe the reaction of the pupil of the other eye. The pupil of the unenlighted eye normally tapers at exactly the same speed and to the same extent as the pupil of the illuminated eye, that is, both pupils normally respond in the same way at the same time. The test of alternating illumination of the pupils makes it possible to reveal the affection of the afferent part of the reflex arc of the pupillary response to light. One pupil is illuminated and his reaction to light is noted, then the light bulb is quickly moved to the second eye and the reaction of his pupil is again evaluated. Normally, when the first eye is illuminated, the pupil of the second eye first narrows, but then, at the time of transfer of the bulb, slightly widens (friendly to the first eye reaction to the elimination of illumination), and finally, when it is directed toward it, the light beam again narrows (direct reaction to light) . If in the second stage of this test, when the second eye is directly illuminated, its pupil does not taper, but continues to expand (a paradoxical reaction), this indicates a damage to the afferent path of the pupillary reflex of this eye, that is, the damage to its retina or optic nerve. In this case, direct illumination of the second pupil (pupil of the blind eye) does not cause its narrowing. However, in doing so, he continues to expand friendly with the first pupil in response to the cessation of illumination of the latter.

To check the pupillary reflexes of both eyes on convergence and accommodation, the patient is asked to first look at the distance (for example, on the wall behind the doctor's back) and then look at the closely located object (for example, on the tip of the finger that is held directly in front of the patient's nose). If the pupils are narrow, the room is darkened before the test. Normally, fixing the gaze on a subject close to the eyes is accompanied by a slight narrowing of the pupils of both eyes, combined with the convergence of eyeballs and an increase in the convexity of the lens (accommodative triad).

Thus, in norm the pupil narrows in response to direct light (direct reaction of the pupil to light); in response to the lighting of another eye (friendly with another pupil's reaction to light); when focusing on a closely located object. Sudden fright, fear, pain cause the pupils to dilate, except when the sympathetic fibers are cut off to the eye.

Symptoms of lesions

Estimating the width of the eye slits and the protrusion of the eyeballs, one can detect exophthalmos - protrusion of the eyeball from the orbit and from under the eyelid. The easiest way to exophthalmos can be identified if you stand behind a seated patient and look down on his eyeballs. The causes of unilateral exophthalmos may be a tumor or pseudotumor of orbit, thrombosis of the cavernous sinus, carotid-cavernous anastomosis. Bilateral exophthalmos observed with thyrotoxicosis (unilateral exophthalmos in this state occurs less often).

Assess the position of eyelids for different directions of view. Normally, when viewed directly, the upper eyelid covers the upper edge of the cornea 1-2 mm. Ptosis (descent) of the upper eyelid is a frequent pathology, which is usually accompanied by a constant contraction of the frontal muscle due to an involuntary attempt of the patient to keep the upper eyelid raised.

Omission of the upper eyelid is most often due to oculomotor nerve damage; congenital ptosis, which can be one- or two-sided; the Bernard-Horner syndrome; myotonic dystrophy; myasthenia gravis; blepharospasm; edema of the century due to injection, trauma, venous stasis; age-related changes in tissues.

• Ptosis (partial or complete) may be the first sign of oculomotor nerve damage (it develops due to weakness of the muscle lifting the upper eyelid). Usually it is combined with other signs of lesion of 3 pairs of cranial nerves (ipsilateral mydriasis, absence of pupillary reaction to light, disturbance of eyeball movements up, down and inside).
• In Bernard-Horner's syndrome, narrowing of the eye gap, ptosis of the upper and lower eyelids is caused by functional deficiency of the smooth muscles of the lower and upper cartilage of the eyelids (tarsal muscles). Ptosis usually partial, one-sided. It is combined with a myosis caused by a deficiency of the dilator function of the pupil (in connection with the defect of sympathetic innervation). Myosis is maximal in the dark.
• Ptosis with myotonic dystrophy (dystrophic myotonia) bilateral, symmetrical. The size of the pupils is not changed, their reaction to light is preserved. There are other signs of this disease.
• When myasthenia gravis ptosis is usually partial, asymmetric, the degree of its severity can vary significantly throughout the day. Pupillary reactions are not disturbed.
• Blepharospasm (involuntary contraction of the circular eye muscle) is accompanied by a partial or complete closure of the eye gap. Light blepharospasm can be confused with ptosis, but with the first upper eyelid periodically actively rises and there is no frontal muscle contracture.

Irregular attacks of enlargement and contraction of the pupils, lasting for several seconds, are denoted by the terms "hippus", or "undulation". This symptom can occur with metabolic encephalopathy, meningitis, multiple sclerosis.

Unilateral mydriasis (dilated pupil) in combination with ptosis and paresis of the external muscles is observed in the defeat of the oculomotor nerve. The dilatation of the pupil is often the first sign of the lesion of the oculomotor nerve when the trunk of the nerve is compressed by an aneurysm and when the brainstem is dislocated. Conversely, with ischemic lesions of 3 couples (for example, in diabetes mellitus), the efferent motor fibers that go to the pupil usually do not suffer, which is important for differential diagnosis. Unilateral mydriasis, which does not combine with ptosis and paresis of the external muscles of the eyeball, is not characteristic for the defeat of the oculomotor nerve. Possible causes of this disorder include drug paralytic mydriasis, which occurs when topical application of atropine solution and other M-anticholinergics (the pupil ceases to taper in response to application of 1% pilocarpine solution); pupil of Adi; spastic mydriasis caused by contraction of the dilator of the pupil with irritation of innervating sympathetic structures.

The pupil of Adi, or puchillotonia, is usually observed from one side. Typically, the pupil dilated on the affected side ( anisocoria ) and its abnormally slow and prolonged (myotonic) reaction to light and convergence with accommodation. As the pupil finally reacts to the illumination, the anisocoria in the process of neurological examination gradually decreases. Typical denervation hypersensitivity of the pupil: after instillation of 0.1% pilocarpine solution into the eye, it sharply narrows to a point size.

Pupillotonia is observed in benign disease (Holmes-Eidi syndrome), which is often of a family nature, occurs more often in women aged 20-30 years and, in addition to the "tonic pupil", can be accompanied by a decrease or lack of deep reflexes from the legs (less often from the hands) , segmental anhidrosis (local sweating) and orthostatic arterial hypotension.

With Argyle Robertson's syndrome, the pupil narrows when fixing the gaze near (the reaction to accommodation remains), but does not respond to light. Typically, Argyle Robertson's syndrome is bilateral, combined with an irregular pupil shape and anisocoria. During the day the pupils are of constant size, do not respond to instillation of atropine and other mydriatic. This syndrome is observed when the middle brain is afflicted, for example, with neurosyphilis, diabetes mellitus, multiple sclerosis, epiphysis tumor, severe craniocerebral trauma, followed by dilatation of the Sylvia aqueduct, etc.

A narrow pupil (due to the paresis of the dilator pupil), combined with partial ptosis of the upper eyelid (paresis of the upper cartilage of the eyelid), anophthalmos and sweating on the same side of the face indicates the Bernard-Horner syndrome. This syndrome is caused by a violation of the sympathetic innervation of the eye. In the dark, the pupil does not expand. Bernard-Horner syndrome is more often observed in cases of medullar oblongata (Wallenberg-Zakharchenko syndrome) and the brain bridge, brainstem tumors (interruption of the central descending sympathetic pathways from the hypothalamus); damage to the spinal cord at the level of the ciliospinal center in the lateral horns of the gray matter of C ₈ -Th ₂ segments ; with a full transverse lesion of the spinal cord at the level of these segments (Bernard-Horner syndrome bilateral, combined with signs of disturbance of sympathetic innervation of organs located below the level of lesion, as well as with conductive disorders of voluntary movements and sensitivity); diseases of the apex of the lung and pleura (Pancost tumor, tuberculosis, etc.); with lesions of the first thoracic spine and the lower trunk of the brachial plexus; aneurysm of the internal carotid artery; tumors in the jugular orifice, cavernous sinus; tumor or inflammatory processes in the orbit (interruption of postganglionic fibers from the upper cervical sympathetic node to the smooth muscles of the eye).

When irritating sympathetic fibers to the eyeball, symptoms arise, the "inverse" Bernard-Horner symptom: the dilatation of the pupil, the widening of the optic cleft and exophthalmos (the Purfur du Petit syndrome).

In the case of a one-sided loss of vision due to the interruption of the anterior sections of the optic path (retina, optic nerve, chiasmus, visual path), the direct reaction of the pupil of the blind eye to light disappears (as the afferent fibers of the pupillary reflex are interrupted), and also a friendly reaction to the pupil's light, healthy eyes. The pupil of the blind eye thus is capable to narrow at illumination of a pupil of a healthy eye (that is the friendly reaction to light at the blind eye is kept). Therefore, if the bulb of the flashlight is moved from the healthy to the affected eye, it is possible to note not the constriction, but, on the contrary, the dilatation of the pupil of the affected eye (as a friendly response to the stopped illumination of a healthy eye) - a symptom of Marcus Hunn.

In the study also pay attention to the color and uniformity of the color of the iris. On the side where the sympathetic innervation of the eye is broken, the iris is lighter (Fuchs symptom), there are usually other signs of the Bernard-Horner syndrome. Hyaline degeneration of the iris pupillary margin with depigmentation is possible in the elderly as a manifestation of the involution process. The symptom of Axenfeld is characterized by depigmentation of the iris without the accumulation of hyaline in it, it is observed in disorders of sympathetic innervation and metabolism. In hepatocerebral dystrophy, copper is deposited along the outer edge of the iris, which is manifested by a yellowish-green or greenish-brown pigmentation (Kaiser-Fleischer ring).