The importance of fundus examination in neurology. Fundus examination - retinal examination

The fundus of the eye is often examined for various diseases. This, in fact, is the only “window” that allows you to look inside the body without surgical intervention and identify many pathologies in the initial stages. Therefore, this topic will be of interest to many people.

The concept of the fundus and how it is examined

The fundus is the inner one, which is visible under ophthalmoscopy. This technique makes it possible to examine in detail, with magnification, the inner surface, with the optic nerve head and blood vessels located on it. In this study, the fundus of the eye is red; against this background, the optic nerve (pink circle or oval), blood vessels and the macula stand out. The following indicators are most informative:

• optic disc color;
• clarity of its boundaries;
• number of veins and arteries (normal – from 16 to 22);
• presence of pulsation.

Any deviations from the norm and the slightest changes can tell an experienced ophthalmologist a lot. And very often, after the diagnosis, he gives referrals to other specialists. As for the ophthalmoscopy procedure itself, it is completely harmless to humans, and no deterioration in vision after such a diagnosis, contrary to various opinions, is observed.

It is a standard procedure when visiting an ophthalmologist and, perhaps, the most informative method of identifying eye diseases.

How and with what is ophthalmoscopy performed?

Before the procedure, a special drug is instilled into the... This is done in order to better examine the bottom of the eye. This procedure has virtually no contraindications. And the most common indications for this are visual impairment, or simply when the eye hurts.

What can changes in the fundus tell us? By the type of vessels located in it, one can to some extent judge the state of the blood vessels of the brain. And the optic disc will also tell you about diseases of the central nervous system. Sometimes such diagnostics can reveal a disease, the symptoms of which are expressed only in changes in the retina. These are very serious illnesses, such as brain tumors.

That is why doctors regularly refer patients for such examinations who have disturbances in the functioning of the following organs and systems:

• cardiovascular;
• endocrine;
• nervous system;
• metabolic disorders.

This manipulation is carried out using an ophthalmoscope - a round concave mirror with a small hole in the center. However, now this procedure is performed using electronic devices, which, if necessary, can even photograph the fundus of the eye.

What ailments do pathological changes indicate?

Ophthalmoscopy provides doctors with a lot of information. What ailments can this type of diagnosis identify? They are as follows:

1. diabetes mellitus One of the very first signs of this disease, when nothing hurts yet and the person feels normal, may be slight bleeding in the retina. With early detection of this phenomenon, the chances that the disease will not progress to a stage when changes in the body become irreversible increase significantly.
2. arterial hypertension. In case of hypertension, the doctor may detect a number of symptoms in the fundus, for example, narrowing of the fundus vessels. This phenomenon, otherwise called angiopathy, indicates problems in the human cardiovascular system. And very often these transformations are the first sign that appears in hypertension.
3. cancer An experienced eye doctor can detect not only signs of cancer of the brain, but also other organs. Moreover, at an early stage, when the patient is not in pain yet. Therefore, we can safely say that timely ophthalmoscopy can save a person’s life.
4. multiple sclerosis. Inflammation of the optic nerve may be a harbinger of this serious disease. According to some studies, this symptom appears first in 75% of cases.
5. rheumatoid arthritis. This insidious disease may not manifest itself for a long time, but will appear when changes affect the cardiovascular system and become irreversible. It is by examining the fundus that this disease can be detected at a very early stage. This diagnosis will reveal inflammation of the choroid, which will be a characteristic symptom of arthritis.

To sum it up

A person who has no pain should still visit an ophthalmologist once a year and undergo an examination.

For people with vision problems, hypertension or other chronic diseases, this procedure should be done even more often - at least once every six months.

The fundus of the eye is a mirror of many ailments. It gives the very first information about them. Early diagnosis of such diseases is very important, because it will contribute to their rapid cure or reduction of symptoms.

Author of the article: Anna Golubeva

Altunbaev Rashid Askhatovich - chief neurologist of the Health Department in Kazan of the Ministry of Health of the Republic of Tatarstan, professor of the Department of Neurology and Rehabilitation of the State Budgetary Educational Institution of Higher Professional Education "Kazan State Medical University" of the Ministry of Health of the Russian Federation

Deterioration of vision requires consultation not only with an ophthalmologist, but also with a neurologist. Often one of the causes of vision problems is neurological pathology.

We talk about the neurological aspects of diagnosing ophthalmological diseases with a professor of the Department of Neurology and Rehabilitation of the Kazan State Medical University of the Ministry of Health of the Russian Federation Rashid Askhatovich Altunbaev.

— TO Visual disorders can result from lesions of the central and peripheral nervous system. What neurological diseases can lead to vision impairment? Please tell us more about this.

— Neurology deals with vision disorders that are localized behind the eyeball. Everything that is behind the eye: the optic nerve, the optic tract, the visual centers in the brain - these are, in the strict sense, not ophthalmological, but neurological clinical problems. But, since the central structures of the visual analyzer are closely connected with the retina, it is sometimes difficult to figure out what is a purely ophthalmological pathology and what is neurological. This applies to diseases such as ischemic optic neuropathy, optic neuritis, hereditary optic neuropathy and some others. In such cases, consultation with both an ophthalmologist and a neurologist is necessary. Often, pathological processes in the brain are reflected in the condition of the fundus of the eye and its vessels, and the neurologist, referring the patient for a consultation with an ophthalmologist to examine the fundus of the eye, expects to receive the necessary signs for making a diagnosis.

Of course, a patient complaining of vision problems first consults an ophthalmologist, and the doctor, not finding changes in the eyeball, refers the patient to a neurologist to decide whether a neurological problem related to the optic nerve, tract or brain could be the cause visual impairment.

It should be noted that the pathology of the visual system has a diverse and complex relationship with cerebral disorders, which led to the formation of an independent scientific and practical direction - neuro-ophthalmology, which is very actively developing in countries with developed medicine, with a cohort of specialists who are deeply immersed in this interdisciplinary problem. In our country, this area of ​​knowledge has not yet formed into an independent branch and is under the jurisdiction of neurologists and ophthalmologists.

Quite often, diseases of the nervous system lead to vision impairment. The visual function has a complex organization, and the visual analyzer itself is a multicomponent structure of the peripheral and central nervous system. A wide variety of diseases of the nervous system can lead to vision impairment. In this case, for example, debuting with isolated optic neuritis, progressive demyelination leads to the expression of multiple sclerosis.

The chiasma of the optic nerves and optic tracts are in close interaction with the pituitary gland, with tumors of which patients begin to complain of visual disturbances, with disturbances in the central or peripheral fields of vision, depending on the nature of tumor growth. Modern neurosurgical technologies, including low-traumatic transnasal ones, have become available for patients with this pathology in Kazan.

Inflammatory diseases of the brain - encephalitis, and more often - acute and chronic disorders of cerebral circulation, can damage the intermediate and terminal parts of the visual analyzer - the thalamus, deep parts of the hemispheres, occipital lobes. The cross principle of functional organization is also valid for vision: the right hemisphere of the brain is responsible for vision in the left visual field, and the left hemisphere, on the contrary, in the right field. During a stroke, unilateral damage often occurs, and a symptom such as hemianopia appears - blindness in both eyes in the same halves of the visual fields. In rehabilitation, neuropsychological computer techniques are used to compensate for hemianopsia.

— Please indicate the common points of contact between a neurologist and an ophthalmologist in terms of diagnosis and patient management.

— Common points of contact between neurology and ophthalmology relate mainly to differential diagnosis: specialists determine what was the cause of the visual disorder: the structures of the eyeball or the conducting neural system.

In the fundus you can see signs of various diseases. It is noteworthy that among our Western colleagues, fundus examination is the prerogative of neurologists themselves. In our country, this is traditionally done by ophthalmologists, although the interpretation of fundus imaging results is part of the training of neurologists.

— Patient N has had pain in his left eye for a month. The pain is pressing, dull, sometimes goes away, but then returns again. The pain is localized, as a rule, in the upper part of the eye, often combined with pain in the left temple, sometimes there is also pain in the area of ​​the left eyebrow. Sometimes, when working with a computer, there may be a cutting pain, but mainly the eyeball hurts. The patient was checked by several ophthalmologists - the eye was healthy, the only thing that was discovered was narrowed blood vessels. The patient also complains of osteochondrosis. Can osteochondrosis cause pain in the eye?

— Pain in the eye and orbit is a symptom of many ophthalmological and neurological diseases. With glaucoma, for example, pain in the eye often occurs, and this is perhaps the first thing that is important to think about. Migraines and cluster cephalgia are often accompanied by pain in the eye area or behind the eye. Of course, prolonged work at the computer and visual fatigue can provoke headaches, including orbital headaches. More rare causes of painful phenomena are associated with inflammatory, vascular, and tumor pathology of orbital formations.

Pain caused by spinal osteochondrosis or spondyloarthrosis can radiate from the neck, head and anterior parts of the brain to the eye area. Such cases are rare. With osteochondrosis, the pain is diffuse, it can involve the back of the head and radiate to the temple. Pain may be associated with pathology of the vertebral artery, namely, the sympathetic plexus of the vertebral artery.

— Can stress and depression become a source of development of eye diseases?

— Any overload, stress, anxiety, depression affect various functions of the human body, including visual ones. Fatigue can also affect visual acuity and the ability to distinguish colors. But the connection between stress and organic disease of the visual system is indirect, not direct.

— Currently, what tasks are facing the city’s neurological service?

— The city’s neurological service faces challenges related to improving the quality of medical neurological care. Nowadays, the staffing problem is getting a little worse; there is a shortage of personnel in the neurological service, which is associated with the development of a system for providing qualified care to patients with stroke, which is very intensive in terms of personnel. Many medical institutions are on duty around the clock, they need more specialists to carry out large volumes of work.

And if we talk about promising aspects, we should note the further specialization of types of neurological care. Currently, there is a center for demyelinating diseases, a center for extrapyramidal pathology, a center for epileptology, we need centers for neuromuscular diseases, headaches, neuropsychology, and somnology, where patients could receive advisory and therapeutic assistance within the framework of compulsory health insurance. It should be noted that in parallel with the existing service, private centers are being developed that offer qualified specialized assistance.

Gulnara Abdukaeva

Of the twelve pairs of cranial nerves I, II and V, pairs III are sensory nerves, III, IV, VI, VII, XI and XII are motor nerves, V, IX and X are mixed. Motor fibers of the cranial nerves innervate the muscles of the eyeballs, face, soft palate, pharynx, vocal cords and tongue, and sensory neurons provide sensitivity to the skin of the face, mucous membranes of the eye, oral cavity, nasopharynx and larynx.

I PAIR: OLFATOR NERVE (N. OLFA CTORIUS)

The nerve function (smell perception) is provided by several neurons from the nasal mucosa to the hippocampus (Fig. 1-2).

The sense of smell is checked both in the presence of complaints about impaired perception of odors, and without them, since often the patient himself does not realize that he has a disorder of smell, but complains about a violation of taste (full taste sensations are possible only if the perception of food aromas is preserved), as well as when suspected pathological process in the area of ​​the bottom of the anterior cranial fossa.

To test the sense of smell, they find out whether the patient distinguishes known smells - coffee, tobacco, soup, vanilla: they ask him to close his eyes and identify the smell of a substance that is brought alternately to the right and left nostril (the second nostril should be closed with the index finger of the hand). You should not use substances with a strong odor (for example, ammonia), since they irritate the receptors of the trigeminal nerve rather than the olfactory one. The ability to distinguish odors varies greatly among healthy individuals, so when testing, what is more important in testing is not whether the patient was able to identify a particular substance by smell, but whether he noticed the presence of the smell at all. Unilateral loss of smell is of particular clinical significance if it cannot be explained by pathology of the nasal cavity. Unilateral anosmia is more typical of neurological diseases than bilateral anosmia. Unilateral or bilateral anosmia is a classic sign of olfactory fossa meningioma. It is also typical for other tumors located in the anterior cranial fossa. Anosmia can be a consequence of TBI. Bilateral anosomia most often occurs in the cold, this is especially typical for older people.

Rice. 1 -2. Conducting pathways of the olfactory analyzer: 1 - olfactory cells; 2 - olfactory threads; 3 - olfactory bulb; 4 - olfactory triangle; 5 - corpus callosum; 6 - cells of the parahippocampal gyrus cortex.

II PAIR: OPTIC NERVE (N. OPTICUS)

The nerve conducts visual impulses from the retina to the occipital lobe cortex (Fig. 1-3).

Rice. 1-3. Diagram of the structure of the visual analyzer: 1 - retinal neurons; 2 - optic nerve; 3 - visual crosshair; 4 - visual tract; 5 - cells of the external geniculate body; 6 - visual radiance; 7 - medial surface of the occipital lobe (calcarine groove); 8 - nucleus of the anterior colliculus; 9- cells of the nucleus of the third pair of CNs; 10 - oculomotor nerve; 11 - ciliary node.

When collecting anamnesis, they find out whether the patient has any changes in vision. Changes in visual acuity (distance or near) are the responsibility of the ophthalmologist. In case of transient episodes of impaired visual clarity, limited visual fields, the presence of photopsia or complex visual hallucinations, a detailed examination of the entire visual analyzer is necessary. The most common cause of transient visual impairment is migraine with visual aura. Visual disturbances are most often represented by flashes of light or sparkling zigzags (photopsia), flickering, loss of an area or the entire field of vision. The visual aura of migraine develops 0.5-1 hour (or less) before a headache attack and lasts on average 10-30 minutes (no more than 1 hour). A migraine headache occurs no later than 60 minutes after the end of the aura. Visual hallucinations of the photopsia type (flashes, sparks, zigzags) can represent an aura of an epileptic seizure in the presence of a pathological focus that irritates the cortex in the area of ​​the calcarine sulcus.

Visual acuity and its examination

Visual acuity is determined by ophthalmologists. To assess distance visual acuity, special tables with circles, letters, and numbers are used. The standard table used in Russia contains 10-12 rows of characters (optotypes), the sizes of which decrease from top to bottom in arithmetic progression. Vision is examined from a distance of 5 m, the table should be well lit. The norm (visual acuity 1) is taken to be such visual acuity at which, from this distance, the subject is able to distinguish the optotypes of the 10th (counting from the top) line.

If the subject is able to distinguish the signs of the 9th line, his visual acuity is 0.9, the 8th line - 0.8, etc. In other words, reading each subsequent line from top to bottom indicates an increase in visual acuity by 0.1. Near visual acuity is checked using other special tables or by asking the patient to read text from a newspaper (normally, small newspaper print is visible from a distance of 80 cm). If visual acuity is so low that the patient cannot read anything from any distance, they are limited to counting fingers (the doctor’s hand is located at the eye level of the subject). If this is not possible, the patient is asked to determine in which room: dark or illuminated, he is located. Reduced visual acuity (amblyopia) or complete blindness (amaurosis) occurs when the retina or optic nerve is damaged. With such blindness, the direct reaction of the pupil to light disappears (due to the interruption of the afferent part of the arc of the pupillary reflex), but the reaction of the pupil in response to illumination of the healthy eye remains intact (the efferent part of the arc of the pupillary reflex, represented by the fibers of the third cranial nerve, remains intact). A slowly progressive decrease in vision is observed when the optic nerve or chiasm is compressed by a tumor.

Signs of violations. Transient short-term loss of vision in one eye (transient monocular blindness, or amaurosis fugax - from the Latin "fleeting") can be caused by a transient disruption of the blood supply to the retina. It is described by the patient as a “curtain falling from top to bottom” when it occurs and as a “rising curtain” when it develops backwards.

Vision is usually restored within a few seconds or minutes. An acute decrease in vision that occurs and progresses over 3-4 days, then recovering within a few days or weeks and often accompanied by pain in the eyes, is characteristic of retrobulbar neuritis. Sudden and persistent loss of vision occurs when the bones of the anterior cranial fossa are fractured in the area of ​​the optic canal; with vascular lesions of the optic nerve and temporal arteritis. When the bifurcation zone of the main artery is blocked and a bilateral infarction of the occipital lobes develops with damage to the primary visual centers of both cerebral hemispheres, “tubular” vision or cortical blindness occurs. “Tubular” vision is caused by bilateral hemianopia with preservation of central (macular) vision in both eyes. The preservation of vision in a narrow central field of view is explained by the fact that the projection zone of the macula at the pole of the occipital lobe is supplied with blood from several arterial basins and, during infarctions of the occipital lobes, most often remains intact.

The visual acuity of these patients is slightly reduced, but they behave as if they were blind. “Cortical” blindness occurs when there is insufficient anastomosis between the cortical branches of the middle and posterior cerebral arteries in the areas of the occipital cortex responsible for central (macular) vision. Cortical blindness is characterized by the preservation of the pupils' reactions to light, since the visual pathways from the retina to the brain stem are not damaged. Cortical blindness with bilateral damage to the occipital lobes and parieto-occipital regions in some cases can be combined with denial of this disorder, achromatopsia, apraxia of conjugate eye movements (the patient cannot direct his gaze towards an object located in the peripheral part of the visual field) and the inability to visually perceive an object and touch it. The combination of these disorders is referred to as Balint syndrome.

Fields of view and their examination

Field of view is the area of ​​space that the fixed eye sees. The preservation of the visual fields is determined by the state of the entire visual pathway (optic nerves, optic tract, optic radiation, cortical visual zone, which is located in the calcarine groove on the medial surface of the occipital lobe). Due to the refraction and crossover of light rays in the lens and the transition of visual fibers from the same halves of the retina in the chiasm, the right half of the brain is responsible for the preservation of the left half of the visual field of each eye. Visual fields are assessed separately for each eye. There are several methods for their approximate assessment.

Sequential assessment of individual visual fields. The doctor sits opposite the patient. The patient covers one of his eyes with his palm, and with the other eye looks at the bridge of the doctor’s nose. The hammer or moving fingers are moved around the perimeter from behind the subject’s head to the center of his field of vision and the patient is asked to note the moment the hammer or fingers appear. The study is carried out alternately in all four quadrants of the visual fields.

The “threat” technique is used in cases where it is necessary to examine the visual fields of a patient who is inaccessible to speech contact (aphasia, mutism, etc.). The doctor, with a sharp “threatening” movement (from the periphery to the center), brings the extended fingers of his hand closer to the patient’s pupil, observing its blinking. If the visual field is intact, the patient blinks in response to the approach of the finger. All visual fields of each eye are examined.

The described methods relate to screening; more accurately, visual field defects are detected using a special device - a perimeter.

Signs of violations. Monocular visual field defects are usually caused by pathology of the eyeball, retina or optic nerve - in other words, damage to the visual pathways in front of their chiasm causes a violation of the visual fields of only one eye on the affected side.

Binocular visual field defects (hemianopsia) can be bitemporal (both eyes lose temporal fields of vision, that is, the right eye has the right, the left has the left) or homonymous (each eye loses the visual fields of the same name - either left or right). Bitemporal visual field defects occur with lesions in the area of ​​the optic chiasm (for example, damage to the chiasm due to a tumor and the pituitary gland). Homonymous visual field defects occur when the optic tract, optic radiation or visual cortex is damaged, that is, when the visual tract above the chiasm is damaged (these defects occur in the visual fields opposite to the lesion: if the lesion is in the left hemisphere, the right visual fields of both eyes are lost, and vice versa) . Damage to the temporal lobe leads to the appearance of defects in the homonymous upper quadrants of the visual fields (contralateral upper quadrant anopsia), and damage to the parietal lobe leads to the appearance of defects in the homonymous lower quadrants of the visual fields (contralateral lower quadrant anopsia).

Conductive visual field defects are rarely combined with changes in visual acuity. Even with significant peripheral visual field defects, central vision can be preserved. Patients with visual field defects caused by damage to the visual pathways above the chiasm may not be aware of the presence of these defects, especially in cases of damage to the parietal lobe.

Fundus and its examination

The fundus of the eye is examined using an ophthalmoscope. The condition of the optic nerve disc (nipple) (the initial, intraocular part of the optic nerve visible during ophthalmoscopy), retina, and fundus vessels is assessed. The most important characteristics of the condition of the fundus are the color of the optic disc, the clarity of its boundaries, the number of arteries and veins (usually 16-22), the presence of pulsation of the veins, any anomalies or pathological changes: hemorrhages, exudate, changes in the walls of blood vessels in the area of ​​the macula (macula ) and on the periphery of the retina.

Signs of violations. Edema of the optic disc is characterized by its bulging (the disc stands above the level of the retina and protrudes into the cavity of the eyeball), redness (the vessels on the disc are sharply dilated and filled with blood); the boundaries of the disc become unclear, the number of retinal vessels increases (more than 22), the veins do not pulsate, and hemorrhages are present. Bilateral papilledema (congestive papilledema) is observed with increased intracranial pressure (volumetric process in the cranial cavity, hypertensive encephalopathy, etc.). Visual acuity initially, as a rule, does not suffer. If the increase in intracranial pressure is not promptly eliminated, visual acuity gradually decreases and blindness develops due to secondary atrophy of the optic nerve.

A congestive optic disc must be differentiated from inflammatory changes (papillitis, optic neuritis) and ischemic optic neuropathy. In these cases, disc changes are often unilateral, pain in the eyeball area and decreased visual acuity are typical. Paleness of the optic nerve head in combination with decreased visual acuity, narrowing of visual fields, decreased pupillary reactions are characteristic of optic nerve atrophy, which develops in many diseases that affect this nerve (inflammatory, dysmetabolic, hereditary).

Primary optic atrophy develops when the optic nerve or chiasm is damaged, and the disc is pale, but has clear boundaries. Secondary optic atrophy develops following swelling of the optic disc; the boundaries of the disc are initially unclear. Selective blanching of the temporal half of the optic nerve head can be observed in multiple sclerosis, but this pathology is easily confused with a variant of the normal state of the optic nerve head. Retinal pigmentary degeneration is possible with degenerative or inflammatory diseases of the nervous system. Other pathological findings that are important for a neurologist when examining the fundus include retinal arteriovenous angioma and the cherry pit symptom, which is possible in many gangliosidoses and is characterized by the presence of a white or gray rounded lesion in the macula, in the center of which there is a cherry-red spot. Its origin is associated with atrophy of retinal ganglion cells and transillumination of the choroid through it.

III, IV, VI PARBI: Oculomotor (N. OCULOMOTORIUS), BLOCK (N. TROCHLEAR/S) AND ABUNDER (N. ABOUCENS) NERVES

The oculomotor nerve contains motor fibers that innervate the medial, superior and inferior rectus muscles of the eyeball, the inferior oblique muscle and the muscle that lifts the upper eyelid, as well as autonomic fibers, which, interrupted in the ciliary ganglion, innervate the internal smooth muscles of the eye - the sphincter of the pupil and the ciliary muscle (Fig. 1-4).

Rice. 1-4. Topography of the nuclei of the oculomotor nerves: 1 - nucleus of the abducens nerve; 2 - nucleus of the trochlear nerve; 3 - accessory nucleus of the oculomotor nerve; 4 - middle unpaired nucleus of the oculomotor nerve (pusl. caudal is sen tgl is); 5 - nucleus of the medial longitudinal fasciculus; 6 - magnocellular nucleus of the oculomotor nerve.

The trochlear nerve innervates the superior oblique muscle, and the abducens nerve innervates the external rectus muscle of the eyeball.

When collecting an anamnesis, they find out whether the patient has diplopia and, if it is present, how the double objects are located - horizontally (pathology of the VI pair), vertically (pathology of the III pair) or when looking down (damage to the IV pair). Monocular diplopia is possible with intraocular pathology leading to dispersion of light rays on the retina (with astigmatism, diseases of the cornea, incipient cataracts, hemorrhage into the vitreous body), as well as with hysteria; With paresis of the external (striated) muscles of the eye, monocular diplopia does not occur. The sensation of imaginary trembling of objects (oscillopsia) is possible with vestibular pathology and some forms of nystagmus.

Eyeball movements and their study

There are two forms of conjugal movements of the eyeballs - conjugated (gaze), in which the eyeballs simultaneously turn in the same direction; and vergent, or disconjugated, in which the eyeballs simultaneously move in opposite directions (convergence or divergence).

In neurological pathology, four main types of oculomotor disorders are observed.

Mismatch of movements of the eyeballs due to weakness or paralysis of one or more striated muscles of the eye; as a result, strabismus (strabismus) and double image occur due to the fact that the object in question is projected in the right and left eyes not onto similar, but onto disparate areas of the retina.

Concomitant violation of conjugated movements of the eyeballs, or concomitant gaze paralysis: both eyeballs in concert (jointly) stop voluntarily moving in one direction or another (right, left, down or up); In both eyes, the same deficit of movements is revealed, while double vision and strabismus do not occur.

A combination of eye muscle paralysis and gaze paralysis.

Spontaneous pathological movements of the eyeballs, occurring mainly in patients in a coma.

Other types of oculomotor disorders (concomitant strabismus, internuclear ophthalmoplegia) are observed less frequently. The listed neurological disorders should be distinguished from congenital imbalance of the tone of the eye muscles (non-paralytic strabismus or non-paralytic congenital strabismus, ophtophoria), in which misalignment of the optical axes of the eyeballs is observed both during eye movements in all directions and at rest. Latent non-paralytic strabismus is often observed, in which images cannot get to identical places in the retina, but this defect is compensated by reflex corrective movements of the hidden squinting eye (fusion movement).

With exhaustion, mental stress or other reasons, the fusional movement may weaken, and hidden strabismus becomes obvious; in this case, double vision occurs in the absence of paresis of the external muscles of the eye.

Assessment of parallelism of optical axes, analysis of strabismus and diplopia

The doctor is in front of the patient and asks him to look straight and into the distance, fixing his gaze on a distant object. Normally, the pupils of both eyes should be in the center of the palpebral fissure. Deviation of the axis of one of the eyeballs inward (esotropia) or outward (exotropia) when looking straight ahead and into the distance indicates that the axes of the eyeballs are not parallel (strabismus), and this is what causes double vision (diplopia). To identify minor strabismus, you can use the following technique: holding a light source (for example, a light bulb) at a distance of 1 m 01: the patient at the level of his eyes, monitor the symmetry of light reflections from the irises. In the eye whose axis is deviated, the reflection will not coincide with the center of the pupil.

Then the patient is asked to fix his gaze on an object that is at the level of his eyes (a pen, his own thumb), and alternately close one or the other eye. If, when closing a “normal” eye, the squinting eye makes an additional movement to maintain fixation on the object ("alignment movement"), then, most likely, the patient has congenital strabismus, and not paralysis of the eye muscles. With congenital strabismus, movements of each of the eyeballs, if they are tested separately, saved and executed in full.

The performance of the smooth tracking test is assessed. They ask the patient with his eyes (without turning his head) to follow the object, which is held at a distance of 1 m from his face and slowly move it horizontally to the right, then to the left, then up and down on each side (the trajectory of the doctor’s movements in the air should correspond to the letter “H” "). Monitor the movements of the eyeballs in six directions: right, left, down and up while abducting the eyeballs in turn in both directions. They are interested in whether the patient has experienced double vision when looking in one direction or another. If there is diplopia, find out which direction the double vision increases when moving. If you place colored (red) glass in front of one eye, it is easier for a patient with diplopia to differentiate between double images, and for the doctor to find out which image belongs to which eye.

Mild paresis of the external eye muscle does not cause noticeable strabismus, but subjectively the patient already experiences diplopia. Sometimes the patient’s report about the occurrence of double vision during a particular movement is enough for the doctor to determine which eye muscle is affected. Almost all cases of new double vision are caused by acquired paresis or paralysis of one or more striated (external, extra-ocular) muscles of the eye. As a rule, any recent paresis of the extraocular muscle causes diplopia. Over time, visual perception on the affected side is inhibited, and the double vision disappears. There are two basic rules that must be taken into account when analyzing a patient's complaints of diplopia in order to determine which muscle of which eye is affected: (1) the distance between the two images increases when looking in the direction of action of the paretic muscle; (2) the image created by the eye with the muscle paralyzed appears to the patient to be located more peripherally, that is, more distant from the neutral position. In particular, you can ask a patient whose diplopia increases when looking to the left to look at an object on the left and ask him which of the images disappears when the doctor's palm covers the patient's right eye. If the image located 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. Because double vision occurs when looking to the left, the lateral rectus muscle of the left eye is paralyzed.

Complete damage to the trunk of the oculomotor nerve leads to diplopia in the vertical and horizontal plane as a result of weakness of the superior, medial and inferior rectus muscles of the eyeball. In addition, with complete paralysis of the nerve on the affected side, ptosis occurs (weakness of the muscle that lifts the upper eyelid), deviation of the eyeball outward and slightly downward (due to the action of the intact lateral rectus muscle, innervated by the abducens nerve, and the superior oblique muscle, innervated by the trochlear nerve) , dilation of the pupil and loss of its reaction to light (pupillary sphincter paralysis).

Damage to the abducens nerve causes paralysis of the external rectus muscle and, accordingly, medial deviation of the eyeball (convergent strabismus). When looking in the direction of the lesion, double vision occurs horizontally. Thus, diplopia in the horizontal plane, not accompanied by ptosis and changes in pupillary reactions, most often indicates damage to the VI pair.

If the lesion is located in the brain stem, in addition to paralysis of the external rectus muscle, horizontal gaze palsy also occurs.

Damage to the trochlear nerve causes paralysis of the superior oblique muscle and is manifested by limited downward movement of the eyeball and complaints of vertical double vision, which is most pronounced when looking down and in the direction opposite to the lesion. Diplopia is corrected by tilting the head to the shoulder on the healthy side.

The combination of ocular muscle paralysis and gaze paralysis indicates damage to the structures of the pons or midbrain. Double vision, worse after exercise or towards the end of the day, is typical of myasthenia gravis. With a significant decrease in visual acuity in one or both eyes, the patient may not notice diplopia even in the presence of paralysis of one or more extraocular muscles.

Assessment of coordinated movements of the eyeballs, analysis of concomitant eye movement disorders and gaze paralysis

Gaze palsy occurs as a result of supranuclear disorders, and not as a result of damage to the III, IV, or VI pairs of the CN. Gaze (gaze) normally represents friendly conjugated movements of the eyeballs, that is, their coordinated movements in one direction (Fig. 1-5). There are two types of conjugated movements - saccades and smooth pursuit. Saccades are very accurate and fast (about 200 ms) phase-tonic movements of the eyeballs, normally occurring either when voluntarily looking at an object (on the command “look to the right”, “look to the left and up”, etc.), or reflexively , when a sudden visual or auditory stimulus causes the eyes (usually the head) to turn towards that stimulus. Cortical control of saccades is carried out by the frontal lobe of the contralateral hemisphere.

Rice. 1 -5. Innervation of conjugal movements of the eyeballs along the horizontal plane to the left, system of the medial longitudinal fasciculus: 1 - middle gyrus of the right frontal lobe; 2 - anterior leg of the internal capsule (tr. frontopontinus); 3 - magnocellular nucleus of the oculomotor nerve (cells innervating the medial rectus muscle of the eye); 4 - pontine center of gaze (cells of the reticular formation); 5 - nucleus of the abducens nerve; 6 - abducens nerve; 7 - vestibular node; 8 - semicircular canals; 9 - lateral vestibular nucleus; 10 - medial longitudinal fasciculus; 1 1 - oculomotor nerve; 1 2 - interstitial nucleus.

The second type of conjugated movements of the eyeballs is smooth tracking: when an object moves into the field of view, the eyes involuntarily fixate on it and follow it, trying to maintain the image of the object in the zone of clearest vision, that is, in the area of ​​the yellow spots. These movements of the eyeballs are slower than saccades and, compared to them, are more involuntary (reflex). Their cortical control is carried out by the parietal lobe of the ipsilateral hemisphere.

Gaze disturbances (if nuclei 111, IV or V I pairs are not affected) are not accompanied by a violation of the isolated movements of each eyeball individually and do not cause diplopia. When examining gaze, it is necessary to find out whether the patient has nystagmus, which is detected using the smooth pursuit test.

Normally, the eyeballs move smoothly and cooperatively when tracking an object. The occurrence of jerky twitching of the eyeballs (involuntary corrective saccades) indicates a violation of the ability to smooth tracking (the object immediately disappears from the area of ​​​​best vision and is found again with the help of corrective eye movements). They check the patient’s ability to keep his eyes in the extreme position when looking in different directions: right, left, up and down. Pay attention to whether the patient experiences gaze-induced nystagmus when moving his eyes away from the average position, i.e. nystagmus, which changes direction depending on the direction of gaze. The fast phase of gaze-induced nystagmus is directed towards the gaze (when looking to the left, the fast component of nystagmus is directed to the left, when looking to the right - to the right, when looking up - vertically up, when looking down - vertically down). Impaired smooth tracking ability and the occurrence of gaze-induced nystagmus are signs of damage to the cerebellar connections with brainstem neurons or central vestibular connections, and may also be a consequence of the side effects of anticonvulsants, tranquilizers and some other drugs.

With a lesion in the occipital-parietal region, regardless of the presence or absence of hemianopia, reflexive slow tracking eye movements towards the lesion are limited or impossible, but voluntary movements and movements on command are preserved (that is, the patient can make voluntary eye movements in any direction, but cannot follow an object moving towards the lesion). Slow, fragmented, dismetric pursuit movements are observed in supranuclear palsy and other extrapyramidal disorders.

To test voluntary movements of the eyeballs and saccades, ask the patient to look to the right, left, up and down. The time required to begin performing the movements, their accuracy, speed and smoothness are assessed (a slight sign of dysfunction of the conjugate movements of the eyeballs in the form of their “stumbling” is often detected). Then the patient is asked to alternately fix his gaze 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. The accuracy and speed of voluntary movements of the eyeballs are assessed.

Saccadic dysmetria, in which voluntary gaze is accompanied by a series of jerky, jerky eye movements, is characteristic of damage to the cerebellar connections, although it can also occur with pathology of the occipital or parietal lobe of the brain - in other words, the inability to catch the target with the gaze (hypometry) or the gaze “skipping” over the target due to excessive amplitude of movements of the eyeballs (hypermetry), corrected by saccades, indicate a deficit in coordination control. Severe slowness of saccades can be observed in diseases such as hepatocerebral dystrophy or Huntington's chorea. An acute lesion of the frontal lobe (stroke, head injury, infection) is accompanied by paralysis of horizontal gaze in the direction opposite to the lesion. Both eyeballs and the head are deviated towards the lesion (the patient “looks at the lesion” and turns away from the paralyzed limbs) due to the preserved function of the opposite center of rotation of the head and eyes to the side. This symptom is temporary and lasts only a few days as the gaze imbalance is soon corrected. The ability to reflexively track may be preserved in frontal gaze palsy. Horizontal gaze paralysis with damage to the frontal lobe (cortex and internal capsule) is usually accompanied by hemiparesis or hemiplegia. When the pathological focus is localized in the area of ​​the roof of the midbrain (pretectal damage involving the posterior commissure of the brain, which is part of the epithalamus), vertical gaze paralysis develops, combined with a convergence disorder (Parinaud's syndrome); The upward gaze is usually affected to a greater extent. When the pons of the brain and the medial longitudinal fasciculus, which provides lateral conjugate movements of the eyeballs at this level, are damaged, paralysis of gaze occurs horizontally towards the lesion (the eyes are diverted in the direction opposite to the lesion, the patient “turns away” from the stem lesion and looks at the paralyzed limbs). This type of gaze paralysis usually lasts for a long time.

Assessment of disconjugated movements of the eyeballs (convergence, divergence)

Convergence is tested by asking the patient to focus on an object that is moving towards his eyes. For example, the patient is asked to fix his gaze on the tip of the hammer or index finger, which the doctor smoothly moves towards the bridge of his nose. When an object approaches the bridge of the nose, the axes of both eyeballs normally rotate towards the object. At the same time, the pupil narrows, the ciliary (eyelash) muscle relaxes, and the lens becomes convex. Thanks to this, the image of the object is focused on the retina. This reaction in the form of convergence, constriction of the pupil and accommodation is sometimes called the accommodative triad. Divergence is the reverse process: when an object is removed, the pupil dilates, and contraction of the ciliary muscle causes flattening of the lens.

If convergence or divergence is impaired, horizontal diplopia occurs when looking at nearby or distant objects, respectively. Convergence palsy occurs when the pretectal region of the midbrain roof is affected at the level of the superior colliculi of the quadrigeminal plate. It can be combined with upward gaze palsy in Parinaud's syndrome. Divergence palsy is usually caused by bilateral involvement of the VI pair of CNs.

The isolated reaction of the pupil to accommodation (without convergence) is checked in each eyeball separately: the tip of a neurological hammer or finger is placed perpendicular to the pupil (the other eye is closed) at a distance of 1 - 1.5 m, then quickly brought closer to the eye, while the pupil narrows. Normally, the pupils react quickly to light and convergence with accommodation.

Spontaneous pathological movements of the eyeballs

Syndromes of spontaneous rhythmic gaze disorders include oculogyric crises, periodic alternating gaze, “ping pong” gaze syndrome, ocular bobbing, ocular dipping, alternating oblique deviation, periodic alternating gaze deviation, etc. Most of these syndromes develop with severe brain damage, they are observed mainly in patients in a coma.

Oculogyric crises are sudden deviations of the eyeballs that suddenly develop and persist from several minutes to several hours, or, less commonly, downwards. They are observed during intoxication with neuroleptics, carbamazepine, and lithium preparations; for brainstem encephalitis, third ventricle glioma, head injury and some other pathological processes. Oculogyric crisis should be distinguished from tonic upward gaze deviation, sometimes observed in comatose patients with diffuse hypoxic brain lesions.

The "ping-pong" syndrome is observed in patients in a comatose state; it consists of periodic (every 2-8 s) friendly deviation of the eyes from one extreme position to another.

In patients with severe damage to the pons 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. There are no horizontal eye movements.

“Ocular dipping” is a term that refers to slow downward movements of the eyeballs, followed after a few seconds by a rapid return to their original position. Horizontal movements of the eyeballs are preserved. The most common cause is hypoxic encephalopathy.

Pupils and palpebral fissures

The reactions of the pupils and palpebral fissures depend not only on the function of the oculomotor nerve - these parameters are also determined by the state of the retina and optic nerve, which constitute the afferent part of the reflex arc of the pupil's reaction to light, as well as the sympathetic influence on the smooth muscles of the eye (Fig. 1-6). Nevertheless, pupillary reactions are examined when assessing the state of the third pair of CNs.

Rice. 1-6. Diagram of the arc of the pupillary reflex to light: 1 - retinal cells of the eyeball; 2 - optic nerve; 3 - visual crosshair; 4 - cells of the upper hillocks of the roof plate; 5 - accessory nucleus of the oculomotor nerve; 6 - oculomotor nerve; 7 - ciliary node.

Normally, the pupils are round and equal in diameter. Under normal room lighting, the diameter of the pupils can vary from 2 to 6 mm. A difference in pupil size (anisocoria) not exceeding 1 mm is considered normal. To test direct pupillary response to light, the patient is asked to look into the distance, then quickly turn on a flashlight and assess the degree and persistence of pupil constriction in that eye. The switched-on light bulb can be brought to the eye from the side, from the temporal side, to eliminate the accommodative reaction of the pupil (its narrowing in response to an approaching object). Normally, when illuminated, the pupil narrows; this narrowing is stable, that is, it persists as long as the light source is near the eye. When the light source is removed, the pupil dilates.

Then the friendly reaction of the other pupil, which occurs in response to the illumination of the eye under study, is assessed. Thus, it is necessary to illuminate the pupil of one eye twice: during the first illumination, we observe the reaction to the light of the illuminated pupil, and during the second illumination, we observe the reaction of the pupil of the other eye. The pupil of an unilluminated eye normally narrows at exactly the same speed and to the same extent as the pupil of an illuminated eye, that is, normally both pupils react equally and simultaneously. The alternating pupillary illumination test allows you to identify damage to the afferent part of the reflex arc of the pupillary reaction to light. They illuminate one pupil and note its reaction to the light, then quickly move the light bulb to the second eye and again evaluate the reaction of its pupil. Normally, when the first eye is illuminated, the pupil of the second eye initially narrows, but then, at the moment the light bulb is transferred, it dilates slightly (a reaction to the removal of illumination that is friendly to the first eye) and, finally, when a beam of light is directed at it, it narrows again (a direct reaction to light) . If at the second stage of this test, when the second eye is directly illuminated, its pupil does not narrow, but continues to expand (paradoxical reaction), this indicates damage to the afferent pathway of the pupillary reflex of this eye, that is, damage to its retina or optic nerve. In this case, direct illumination of the second pupil (the pupil of the blind eye) does not cause its narrowing.

However, at the same time, it continues to expand in concert with the first pupil in response to the cessation of illumination of the latter.

To test the pupillary reflexes of both eyes for convergence and accommodation, the patient is asked to first look into the distance (for example, at the wall behind the doctor), and then to look at a nearby object (for example, at the tip of a finger held directly in front of the bridge of the patient's nose). If your pupils are narrow, darken the room before performing the test. Normally, fixation of gaze on an object close to the eyes is accompanied by a slight constriction of the pupils of both eyes, combined with convergence of the eyeballs and an increase in the convexity of the lens (accommodative triad).

Thus, normally the pupil constricts in response to direct light (direct pupillary response to light); in response to illumination of the other eye (reaction to light friendly with the other pupil); when focusing your gaze on a nearby object. Sudden fear, fear, pain cause dilation of the pupils, except in cases where the sympathetic fibers to the eye are interrupted.

Signs of lesions. By assessing the width of the palpebral fissures and the protrusion of the eyeballs, one can detect exophthalmos - protrusion (protrusion) of the eyeball from the orbit and from under the eyelid. The easiest way to identify exophthalmos is to stand behind a seated patient and look down at his eyeballs. The causes of unilateral exophthalmos may be a tumor or pseudotumor of the orbit, thrombosis of the cavernous sinus, or carotid-cavernous anastomosis.

Bilateral exophthalmos is observed with thyrotoxicosis (unilateral exophthalmos occurs less frequently in this condition).

The position of the eyelids is assessed in different directions of gaze. Normally, when looking straight, the upper eyelid covers the upper edge of the cornea by 1-2 mm. Ptosis (drooping) of the upper eyelid is a common pathology, which is usually accompanied by constant contraction of the frontal muscle due to the patient’s involuntary attempt to keep the upper eyelid raised.

Drooping of the upper eyelid is most often caused by damage to the oculomotor nerve; congenital ptosis, which can be unilateral or bilateral; Bernard-Horner syndrome; myotonic dystrophy; myasthenia; blepharospasm; swelling of the eyelid due to injection, trauma, venous stasis; age-related tissue changes.

Ptosis (partial or complete) may be the first sign of damage to the oculomotor nerve (develops due to weakness of the muscle that lifts the upper eyelid). It is usually combined with other signs of damage to the third pair of CN (ipsilateral mydriasis, lack of pupillary response to light, impaired upward, downward and inward movements of the eyeball).

In Bernard-Horner syndrome, narrowing of the palpebral fissure, ptosis of the upper and lower eyelids are caused by functional deficiency of the smooth muscles of the lower and upper eyelid cartilages (tarsal muscles). Ptosis is usually partial, unilateral.

It is combined with miosis caused by insufficiency of the pupillary dilator function (due to a defect in sympathetic innervation). Miosis is most pronounced in the dark.

Ptosis in myotonic dystrophy (dystrophic myotonia) is bilateral, symmetrical. The size of the pupils is not changed, their reaction to light is preserved. There are other signs of this disease.

With myasthenia gravis, ptosis is usually partial, asymmetrical, and its severity can vary significantly throughout the day. Pupillary reactions are not impaired.

Blepharospasm (involuntary contraction of the orbicularis oculi muscle) is accompanied by partial or complete closure of the palpebral fissure. Mild blepharospasm can be confused with ptosis, but with the former, the upper eyelid periodically actively rises and there is no contracture of the frontal muscle.

Irregular attacks of dilation and contraction of the pupils that last for several seconds are referred to as “hippus” or “undulation”.

This symptom can occur with metabolic encephalopathy, meningitis, and multiple sclerosis.

Unilateral mydriasis (dilation of the pupil) in combination with ptosis and paresis of the external muscles is observed with damage to the oculomotor nerve. Pupil dilation is often the first sign of damage to the oculomotor nerve when the nerve trunk is compressed by an aneurysm and when the brain stem is dislocated. On the contrary, with ischemic lesions of the 3rd pair (for example, with diabetes mellitus), the efferent motor fibers going to the pupil are usually not affected, which is important to consider in differential diagnosis. Unilateral mydriasis, not combined with ptosis and paresis of the external muscles of the eyeball, is not typical for damage to the oculomotor nerve. Possible causes of this disorder include drug-induced paralytic mydriasis, which occurs with topical use of a solution of atropine and other m-anticholinergics (in this case, the pupil stops constricting in response to the use of a 1% solution of pilocarpine); Eidy's pupil; spastic mydriasis, caused by contraction of the pupillary dilator due to irritation of the sympathetic structures innervating it.

Adie's pupil, or pupillotonia, is usually observed on one side. The pupil is typically dilated on the affected side (anisocoria) and has an abnormally slow and prolonged (myotonic) reaction to light and convergence with accommodation. Since the pupil does eventually respond to light, the anisocoria gradually decreases during the neurological examination. Denervation hypersensitivity of the pupil is typical: after instillation of a 0.1% solution of pilocarpine into the eye, it sharply narrows to a pinpoint size.

Pupillotonia is observed in a benign disease (Holmes-Eydie syndrome), which is often familial in nature, occurs more often in women aged 20-30 years and, in addition to the “tonic pupil”, can be accompanied by a decrease or absence of deep reflexes in the legs (less often in the arms) , segmental anhidrosis (local sweating disorder) and orthostatic arterial hypotension.

In Argyll Robertson syndrome, the pupil constricts when the gaze is fixed near (the reaction to accommodation is preserved), but does not respond to light. Argyll Robertson syndrome is usually bilateral and is associated with irregular pupil shape and anisocoria. During the day, the pupils have a constant size and do not respond to instillation of atropine and other mydriatics. This syndrome is observed in cases of damage to the tegmentum of the midbrain, for example, in neurosyphilis, diabetes mellitus, multiple sclerosis, tumor of the pineal gland, severe head injury with subsequent expansion of the aqueduct of Sylvius, etc.

A narrow pupil (due to paresis of the pupillary dilator), combined with partial ptosis of the upper eyelid (paresis of the muscle of the upper eyelid cartilage), anophthalmos and impaired sweating on the same side of the face indicates Bernard-Horner syndrome. This syndrome is caused by a violation of the sympathetic innervation of the eye. In the dark the pupil does not dilate. Bernard-Horner syndrome is more often observed with infarctions of the medulla oblongata (Wallenberg-Zakharchenko syndrome) and pons, brain stem tumors (interruption of the central descending sympathetic pathways coming from the hypothalamus); damage to the spinal cord at the level of the ciliospinal center in the lateral horns of the gray matter of segments C 8 - m 2; with a complete transverse lesion of the spinal cord at the level of these segments (Bernard-Horner syndrome is bilateral, combined with signs of impaired sympathetic innervation of organs located below the level of the lesion, as well as with conduction disorders of voluntary movements and sensitivity); diseases of the apex of the lung and pleura (Pancoast tumor, tuberculosis, etc.); with damage to the first thoracic spinal root and the lower trunk of the brachial plexus; aneurysm of the internal carotid artery; tumors in the area of ​​the jugular foramen, cavernous sinus; tumors or inflammatory processes in the orbit (interruption of postganglionic fibers running from the superior cervical sympathetic ganglion to the smooth muscles of the eye).

When sympathetic fibers to the eyeball are irritated, symptoms “reverse” to the Bernard-Horner symptom occur: pupil dilation, widening of the palpebral fissure and exophthalmos (Pourfur du Petit syndrome).

With unilateral vision loss caused by interruption of the anterior parts of the visual pathway (retina, optic nerve, chiasm, optic tract), the direct reaction of the pupil of the blind eye to light disappears (since the afferent fibers of the pupillary reflex are interrupted), as well as the friendly reaction to light of the pupil of the second, healthy eye. The pupil of the blind eye is able to narrow when the pupil of the healthy eye is illuminated (that is, the friendly reaction to light in the blind eye is preserved). Therefore, if the flashlight bulb is moved from the healthy eye to the affected eye, you can notice not a narrowing, but, on the contrary, a dilation of the pupil of the affected eye (as a friendly response to the cessation of illumination of the healthy eye) - a symptom of Marcus Hun.

During the study, attention is also paid to the color and uniformity of coloring of the irises. On the side where the sympathetic innervation of the eye is impaired, the iris is lighter (Fuchs' sign), and there are usually other signs of Bernard Horner syndrome.

Hyaline degeneration of the pupillary edge of the iris with depigmentation is possible in older people as a manifestation of the involutional process. Axenfeld's symptom 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 yellowish-green or greenish-brown pigmentation (Kayser-Fleischer ring).

V PAIR: TRIGEMINAL NERVE (N. TRIGEMINUS)

The motor branches of the nerve innervate the muscles that provide movements of the lower jaw (masticatory, temporal, lateral and medial pterygoid; mylohyoid; anterior belly of the digastric); tensor tympani muscle; muscle that strains the velum palatine.

Sensitive fibers supply the main part of the skin of the head (facial skin and the frontoparietal part of the scalp), the mucous membrane of the nasal and oral cavities, including the frontal and maxillary sinuses; part of the ear canal and eardrum; eyeball and conjunctiva; anterior two-thirds of the tongue, teeth; periosteum of the facial skeleton; dura mater of the anterior and middle cranial fossae, tentorium of the cerebellum. The branches of the V nerve are the orbital, maxillary and mandibular nerves (Fig. 1-7).

Rice. 1 -7. Conductors of sensitivity from the skin of the face (diagram): 1 - trigeminal nerve ganglion; 2 - nucleus of the spinal tract of the trigeminal nerve; 3 - bulbothalamic tract; 4 - thalamic cells; 5 - lower part of the cortex of the postcentral gyrus (face area); 6 - superior sensory nucleus of the trigeminal nerve; 7 - optic nerve; 8 - maxillary nerve; 9 - mandibular nerve.

Sensation to the face is provided by both the trigeminal nerve and the upper cervical spinal nerves (Fig. 1-8).

Pain, tactile and temperature sensitivity are sequentially checked in the innervation zones of all three branches of the V pair on both sides (use a pin, a soft hair brush, the cold surface of a metal object - a neurological hammer, a dynamometer). Synchronously touch symmetrical points in the forehead (1st branch), then the cheeks (11th branch), chin (III branch).

Rice. 1 -8. Innervation of the skin of the face and head (diagram). A - peripheral innervation: branches of the trigeminal nerve (1 - n. ophtalmicus, 11 - n. maxill aris, 111 - n. mandibularis): 1 - n. occipital is maj or; 2 - n. auricularis magnus; 3 - n. occipitalis minor; 4 - p. transversus coll i. B - segmental innervation by the sensory nucleus of the trigeminal nerve (1-5 - Zelder dermatomes) and the upper cervical segments of the spinal cord (from 2-c 3): 6 - nuclei of the spinal tract of the trigeminal nerve.

A dissociated disturbance of sensitivity on the face, that is, a violation of pain and temperature sensitivity while maintaining tactile sensitivity, indicates damage to the nucleus of the spinal tract of the trigeminal nerve (nucl. tractus spinalis n. trigetint) with the preservation of the main sensory nucleus of the trigeminal nerve, located in the dorsolateral part of the tegmentum of the bridge (nucl . pontinus n. trigetint). This disorder most often occurs with syringobulbomyelia, ischemia of the posterolateral parts of the medulla oblongata.

Trigeminal neuralgia is characterized by sudden, short, very intense, repeated attacks of pain that are so short-lived that they are often described as feeling like a gunshot or an electric shock. The pain spreads to the innervation zones of one or more branches of the trigeminal nerve (usually in the area of ​​the 11th and 3rd branches and only in 5% of cases in the area of ​​the 1st branch). With neuralgia, loss of sensitivity on the face usually does not occur. If trigeminal pain is combined with disorders of surface sensitivity, trigeminal neuralgia-neuropathy is diagnosed.

The corneal (corneal) reflex is examined using a piece of cotton wool or a strip of newsprint. The patient is asked to look at the ceiling and, without touching the eyelashes, lightly touch the edge of the cornea (not the sclera) from the lower outer side (not above the pupil!) with a cotton swab. The symmetry of the reaction on the right and left is assessed. Normally, if the V and V II nerves are not damaged, the patient shudders and blinks.

The preservation of corneal sensitivity in the presence of paralysis of the facial muscles is confirmed by the reaction (blinking) of the contralateral eye.

To assess the motor portion of the trigeminal nerve, the symmetry of the opening and closing of the mouth is assessed, noting whether there is a displacement of the lower jaw to the side (the jaw moves towards the weakened pterygoid muscle, the face appears skewed)

To assess the strength of the masticatory muscle, ask the patient to clench his teeth tightly and palpate m. masseter on both sides, and then try to open the patient’s clenched jaws. Normally, the doctor cannot do this. The strength of the pterygoid muscles is assessed by moving the lower jaw to the sides. The identified asymmetry can be caused not only by paresis of the masticatory muscles, but also by malocclusion.

To induce the mandibular reflex, the patient is asked to relax the facial muscles and open the mouth slightly. The doctor places the index finger on the patient's chin and applies light blows with a neurological hammer from top to bottom along the distal phalanx of this finger, first on one side of the lower jaw, then on the other. In this case, the masticatory muscle on the side of the blow contracts and the lower jaw rises upward (the mouth closes). In healthy people, the reflex is often absent or difficult to evoke. An increase in the mandibular reflex indicates bilateral damage to the pyramidal tract (corticonuclear tracts) above the middle sections of the pons.

VII PAIR: FACIAL NERVE (N. FACI ALI S)

Motor fibers innervate the facial muscles, subcutaneous neck muscle (platysma), stylohyoid, occipital muscles, posterior belly of the digastric muscle, stapedius muscle (Fig. 1-9). Autonomic parasympathetic fibers innervate the lacrimal gland, sublingual and submandibular salivary glands, as well as glands of the nasal mucosa, hard and soft palate. Sensory fibers conduct taste impulses from the anterior two-thirds of the tongue and from the hard and soft palate.

Rice. 1-9. Topography of the facial nerve and facial muscles: a - the structure of the facial nerve and the muscles innervated by it: 1 - the bottom of the IV ventricle; 2 - nucleus of the facial nerve; 3 - stylomastoid foramen; 4 - posterior ear muscle; 5 - occipital vein; 6 - posterior belly of the digastric muscle; 7 - stylohyoid muscle; 8 - branches of the facial nerve to the facial muscles and subcutaneous muscle of the neck; 9 - muscle that lowers the angle of the mouth; 10 - mental muscle; 11 - muscle that lowers the upper lip; 12 - buccal muscle; 13 - orbicularis oris muscle; 14 - muscle that lifts the upper lip; 15 - canine muscle; 16 - zygomatic muscle; 17 - circular muscle of the eye; 18 - muscle that wrinkles the eyebrow; 19 - frontal muscle; 20 - drum string; 21 - lingual nerve; 22 - pterygopalatine node; 23 - trigeminal nerve node; 24 - internal carotid artery; 25 - intermediate nerve; 26 - facial nerve; 27 - vestibulocochlear nerve; b - main muscles of the upper and lower facial muscles: 1 - cerebral bridge; 2 - internal knee of the facial nerve; 3 - nucleus of the facial nerve; 4 - internal auditory opening; 5 - outer elbow; 6 - stylomastoid foramen.

The study of the functions of the facial nerve begins with assessing the symmetry of the patient’s face at rest and during spontaneous facial expressions. Particular attention is paid to the symmetry of the nasolabial folds and palpebral fissures. . The strength of the facial muscles is examined one by one, asking the patient to wrinkle his forehead (m. frontalis), close his eyes tightly (m. orbicularis oculi), puff out his cheeks (m. b iscinator), smile, show his teeth (m. risorius, etc. zygomaticus maj or) , compress your lips and do not let them unclench (m. orbicularis oris). The patient is asked to take air into his mouth and puff out his cheeks; Normally, with pressure on the cheeks, the patient holds the air without releasing it through the mouth. If weakness of the facial muscles is detected, find out whether it concerns only the lower part of the face or extends to its entire half (both lower and upper).

Taste is tested on the front third of the tongue. The patient is asked to stick out his tongue and hold it by the tip with a gauze pad. Using a pipette, droplets of sweet, salty, and neutral solutions are alternately applied to the tongue. The patient must report the taste of the solution by pointing to the corresponding inscription on a piece of paper. It is noted whether tears are released when taste stimuli are applied (this paradoxical reflex is observed in patients with improper germination of secretory fibers after previous damage to the branches of the facial nerve).

The facial nerve contains a very small number of fibers that conduct impulses of general sensitivity and innervate small areas of the skin, one of which is located on the inner surface of the auricle near the external auditory canal, and the second is located directly behind the ear. Pain sensitivity is examined by making injections with a pin directly posterior to the external auditory canal.

Signs of lesions. Damage to the central motor neuron (for example, with a hemispheric stroke) can cause central, or “supranuclear”, paralysis of the facial muscles (Fig. 1-10).

Rice. 1-10. The course of central motor neurons to the nucleus of the facial nerve: 1 - facial nerve (left); 2 - lower part of the nucleus of the facial nerve; 3 - elbow of the internal capsule; 4 - pyramidal cells of the right precentral gyrus (face area); 5 - upper part of the nucleus of the facial nerve.

It is characterized by contralateral paresis of the facial muscles located only in the lower half of the face (very slight weakness of the orbicularis oculi muscle and slight asymmetry of the palpebral fissures are possible, but the possibility of wrinkling of the forehead remains). This is explained by the fact that that part of the motor nucleus n. facialis, which innervates the lower facial muscles, receives impulses only from the opposite hemisphere, while the part innervating the upper facial muscles is influenced by the corticonuclear tracts of both hemispheres. Due to damage to the peripheral motor neuron (neurons of the motor nucleus n.facialis and their axons), peripheral paralysis of the facial muscles (prosoplegia) develops, which is characterized by weakness of the facial muscles of the entire ipsilateral half of the face. Closing of the eyelids on the affected side is impossible (lagophthalmos) or is incomplete. In patients with peripheral paralysis of the facial muscles, Bell's symptom is often observed: when the patient tries to close his eyes, the eyelids on the side of the lesion of the facial nerve do not close, and the eyeball moves upward and outward. The movement of the eyeball in this case represents physiological synkinesis, which consists in moving the eyeballs upward when closing the eyes. To see it in a healthy person, it is necessary to forcibly hold his eyelids raised, asking him to close his eyes.

Peripheral paralysis of the facial muscles in some cases may be accompanied by a taste disturbance in the anterior two-thirds of the ipsilateral half of the tongue (if the trunk of the facial nerve is affected above the origin of the chorda tympani fibers from its distal part). With central paralysis of the facial muscles, that is, with damage to the corticonuclear tracts going to the motor nucleus of the facial nerve, taste disturbances do not occur.

If the facial nerve is affected above the fibers from it to the stapedius muscle, a distortion of the timbre of perceived sounds occurs - hyperacusis. When the facial nerve is damaged at the level of its exit from the pyramid of the temporal bone through the stylomastoid foramen, the parasympathetic fibers to the lacrimal gland (n. petrosus maj or) and the sensory fibers coming from the taste buds (chorda tympani) are not affected, so taste and lacrimation remain intact.

Lagophthalmos is characterized by lacrimation, which is explained by excessive irritation of the mucous membrane of the eye due to the lack of a protective blink reflex and the difficulty of moving tears into the lower lacrimal canaliculus due to sagging of the lower eyelid. All this leads to the fact that tears flow freely down the face.

Bilateral acute or subacute peripheral lesions of the facial nerve are observed in Guillain-Barré syndrome (GBS). Acute or subacute unilateral peripheral paralysis of the facial muscles most often occurs with compression-ischemic neuropathy of the facial nerve (with compression-ischemic changes in the part of the nerve that passes through the facial canal in the pyramid of the temporal bone.

In the recovery period after peripheral paralysis, pathological regeneration of facial nerve fibers is possible. At the same time, on the side of paralysis, contracture of the facial muscles develops over time, due to which the palpebral fissure becomes narrower and the nasolabial fold deeper than on the healthy side (the face “warps” no longer to the healthy side, but to the diseased side).

Contracture of the facial muscles usually occurs against the background of residual effects of prosoparesis and is combined with pathological synkinesis of the facial muscles. For example, when you close your eyes on the painful side, the corner of your mouth simultaneously involuntarily rises (veculobial synkinesis), or the wing of the nose rises, or the platysma contracts; when the cheeks are puffed out, the palpebral fissure narrows, etc.

VIII PAIR: VESTIBULOCOCHLEARIS NERVE (N. VESTIBULOCOCHLEARIS)

The nerve consists of two parts - auditory (cochlear) and vestibular (vestibular), which respectively conduct auditory impulses from the cochlear receptors and information about balance from the receptors of the semicircular canals and membranous sacs of the vestibule (Fig. 1 - 11).

Rice. 1-11. The structure of the auditory analyzer: 1 - superior temporal gyrus; 2 - medial geniculate body; 3 - lower colliculus of the midbrain roof plate; 4 - lateral loop; 5 - posterior nucleus of the cochlear nerve; 6 - trapezoidal body; 7 - anterior nucleus of the cochlear nerve; 8 - cochlear part of the vestibulocochlear nerve; 9 - cells of the spiral node.

When this nerve is damaged, hearing acuity decreases, tinnitus and dizziness appear. If the patient complains of ringing/noise in the ear, you should ask him to describe in detail the nature of these sensations (ringing, whistling, hissing, buzzing, crackling, pulsating) and their duration, and also compare them with natural sounds “like the sound of the sea surf.” “like wires humming in the wind”, “like the rustling of leaves”, “like the noise of a working steam locomotive”, “like the beating of your own heart”, etc.) Constant noise in the ear is characteristic of damage to the eardrum, the bones of the middle ear or the cochlea, etc. cochlear nerve. High-frequency sounds, ringing in the ear are more often observed with pathology of the cochlea and cochlear nerve (damage to the neurosensory apparatus). Noise in the ear caused by pathology of the middle ear (for example, with otosclerosis), is usually more constant, low-frequency.

Hearing and its research

The most accurate data on hearing impairment is obtained through a special instrumental examination, but a routine clinical examination can also provide important information for determining the diagnosis. First, the external auditory canal and eardrum are examined. Hearing in each ear is roughly assessed, determining whether the patient hears whispered speech, clicks of the thumb and middle finger at a distance of 5 cm from the patient’s ear. If he complains of hearing loss or does not hear clicks, further special instrumental hearing testing is necessary.

There are three forms of hearing loss: conductive deafness is associated with a violation of sound transmission to the receptors of the cochlea (closing of the external auditory canal with a cerumen plug or foreign object, pathology of the middle ear); neural (sensorineural) deafness - with damage to the cochlea and auditory nerve; central deafness - with damage to the nuclei of the auditory nerve or their connections with overlying centers and with the primary auditory fields in the temporal lobes of the cerebral cortex.

Tuning fork tests are used to differentiate between conductive and sensorineural hearing loss. Air conduction is preliminarily assessed by comparing the patient's (each ear's) sound perception threshold with its own (normal) perception threshold.

The Rinne test is used to compare bone and air conduction. The stem of a vibrating high-frequency tuning fork (128 Hz) is placed on the mastoid process. After the patient stops hearing the sound, the tuning fork is brought close to his ear (without touching it). In healthy people and in patients with sensorineural hearing loss, air conduction is better than bone conduction, therefore, after bringing a tuning fork to the ear, the subject begins to hear sound again (positive Rinne sign). When the middle ear is damaged, bone conduction of sound remains normal, but air conduction deteriorates, as a result, the first one turns out to be better than the second one, so the patient will not hear a tuning fork if it is brought to the ear (negative Rinne sign).

Weber test: a vibrating tuning fork (128 Hz) is placed in the middle of the patient's crown and they are asked which ear hears sound better. Normally, sound is heard equally by the right and left ears (in the center). In case of sensorineural hearing loss (Meniere's disease, neuroma of the VIII pair, etc.), the sound is perceived more clearly and for a longer time by the healthy ear (lateralization of perception to the unaffected side). With conductive hearing loss, there is a relative improvement in bone conduction and the sound is perceived as louder on the affected side (lateralization of sound perception to the affected side).

With sensorineural hearing loss, the perception of high frequencies suffers to a greater extent, with conductive hearing loss - low frequencies. This is determined by audiometry - an instrumental study that must be carried out in patients with hearing impairment.

Dizziness

When complaining of dizziness, it is necessary to find out in detail what sensations the patient is experiencing. True dizziness is understood as the illusion of movements of the person himself or surrounding objects, while very often patients call dizziness a feeling of “emptiness” in the head, darkening in the eyes, instability and unsteadiness when walking, lightheadedness or general weakness, etc.

True dizziness (vertigo) usually occurs in attacks lasting from a few seconds to several hours. In severe cases, dizziness is accompanied by nausea, vomiting, paleness, sweating, and imbalance. The patient usually feels rotation or movement of surrounding objects around him. During attacks, horizontal or rotatory nystagmus is often recorded. True dizziness is almost always caused by damage to the vestibular system in any of its parts: in the semicircular canals, the vestibular portion of the VIII pair of the CN, the vestibular nuclei of the brain stem. A more rare cause is damage to the vestibulocerebellar connections (Fig. 1-12), and even less often, dizziness is a symptom of an epileptic seizure (with irritation of the temporal lobe).

Rice. 1-12. The structure of vestibular conductors: 1 - cortex of the parietal lobe of the brain; 2 - thalamus; 3 - medial nucleus of the vestibular nerve; 4 - nucleus of the oculomotor nerve; 5 - superior cerebellar peduncle; 6 - superior vestibular nucleus; 7 - dentate core; 8 - tent core; 9 - vestibular part of the vestibulocochlear nerve (VIII); 10 - vestibular node; 11 - vestibulospinal tract (anterior cord of the spinal cord); 12 - inferior vestibular nucleus; 13 - intermediate and nucleus of the medial longitudinal fasciculus; 14 - lateral vestibular nucleus; 15 - medial longitudinal fascicle; 16 - nucleus of the abducens nerve; 17 - cells of the reticular formation of the brain stem; 18 - red core; 19 - cortex of the temporal lobe of the brain.

The most common causes of an acute attack of vertigo are benign positional vertigo, Meniere's disease, and vestibular neuronitis.

Benign positional vertigo is most often observed in clinical practice. An attack of rotational positional vertigo occurs suddenly with a rapid change in the position of the head and in a certain position, mainly provoked by lying down and turning in bed or throwing the head back. Dizziness is accompanied by nausea and nystagmus. The attack lasts from a few seconds to 1 minute and goes away on its own. Attacks may recur periodically over several days or weeks. Hearing is not affected.

In Meniere's disease, attacks are characterized by severe dizziness, which is accompanied by a sensation of buzzing and noise in the ear; a feeling of fullness in the ear, decreased hearing, nausea and vomiting. The attack lasts from several minutes to an hour and forces the patient to remain in a lying position the entire time. When performing a rotational or caloric test, nystagmus on the affected side is suppressed or absent.

Vestibular neuronitis is characterized by an acute isolated long-term (from several days to several weeks) attack of severe dizziness.

It is accompanied by vomiting, imbalance, a feeling of fear, and nystagmus towards the healthy ear. Symptoms worsen when moving the head or changing body position. Patients have a hard time with this condition and do not get out of bed for several days.

There is no noise in the ear or hearing loss, and there is no headache. When performing a caloric test, the reaction on the affected side is reduced.

Constant dizziness, which can vary in intensity, but does not have the character of attacks, accompanied by hearing impairment, cerebellar ataxia, ipsilateral lesions of the U, UN, IX and X pairs of CN, is characteristic of neuroma of the UIII pair of CN.

Nystagmus

Nystagmus is rapid, repetitive, involuntary, oppositely directed, rhythmic movements of the eyeballs. There are two types of nystagmus: jerky (clonic) nystagmus, in which slow movements of the eyeball (slow phase) alternate with oppositely directed fast movements (fast phase). The direction of such nystagmus is determined by the direction of its fast phase. Pendulum-like (swinging) nystagmus is a rarer form in which the eyeballs perform pendulum-like movements of equal amplitude and speed in relation to the average position (although when looking away to the side, two different phases can be observed, the faster of which is directed towards the gaze).

Nystagmus can be either a normal phenomenon (for example, with extreme abduction of gaze) or a sign of damage to the brain stem, cerebellum, peripheral or central part of the vestibular system. in each of these cases, nystagmus has its own characteristic features.

The easiest way to observe nystagmus is during a smooth pursuit test, in which the patient follows the movement of the examiner's finger or hammer.

Normally, the eyeballs should follow an object, moving smoothly and consistently. Mild clonic nystagmus (several low-amplitude rhythmic movements), appearing with extreme abduction of the eyeballs, is physiological; it disappears when the eyes move a little closer to the midline and does not indicate pathology. The most common reason for the appearance of large-scale clonic nystagmus with extreme abduction of the eyeballs is the use of sedatives or anticonvulsants. Optokinetic clonic nystagmus is a variant of physiological reflex nystagmus that occurs when tracking similar objects moving past (for example, trees flashing in a train window, fence slats, etc.). It is characterized by slow tracking movements of the eyeballs, which are involuntarily interrupted by fast saccades directed in the opposite direction. In other words, the eyes fixate on a moving object and slowly follow it, and after it disappears from the field of view, they quickly return to the central position and fixate on a new object that comes into the field of view, beginning to pursue it, etc. Thus, the direction of optokinetic nystagmus is opposite to the direction of movement of objects.

Spontaneous clonic peripheral vestibular (labyrinthine-vestibular) nystagmus is caused by unilateral irritation or destruction of the peripheral part of the vestibular analyzer (labyrinth, vestibular portion of the VIII pair of CN). This is a spontaneous, usually unidirectional horizontal, less often rotatory nystagmus, the fast phase of which is directed towards the healthy side, and the slow phase towards the lesion. The direction of nystagmus does not depend on the direction of gaze. Nystagmus is detected in any position of the eyeballs, but intensifies when the eyes are moved away towards its fast phase, that is, it is more clearly detected when looking in the healthy direction. Typically, such nystagmus is suppressed by gaze fixation.

Combined with nausea, vomiting, noise in the ear, hearing loss; is temporary (no more than 3 weeks).

Spontaneous clonic brain stem-central vestibular nystagmus occurs when the vestibular nuclei of the brain stem, their connections with the cerebellum or other central parts of the vestibular analyzer are damaged. It is often multidirectional and can be combined with dizziness, nausea, and vomiting. Nystagmus and dizziness do not decrease with gaze fixation. Other neurological disorders are often detected: cerebellar ataxia, diplopia, motor and sensory disorders.

Spontaneous rocking vestibular nystagmus can be caused by gross damage to the vestibular nuclei and vestibuloculomotor connections in the brainstem and occurs with brainstem stroke, brainstem glioma, and multiple sclerosis. A patient with acquired rocking nystagmus complains of shaking and blurred images (oscillopsia).

Spontaneous pendulum-like (swinging) optical nystagmus is typical for patients with congenital bilateral vision loss, causing disturbances in gaze fixation.

Vestibular reflexes

Motor reactions of the eyes to irritation of the vestibular apparatus (oculocephalic reflex, vestibulo-ocular reflex) are mediated by pathways running through the brain stem from the vestibular nuclei of the medulla oblongata to the nuclei of the abducens and oculomotor nerves. Normally, rotation of the head causes endolymph to move in the semicircular canals in the direction opposite to rotation. In this case, in one labyrinth a flow of endolymph occurs towards the ampulla of the horizontal semicircular canal, and in the other labyrinth - in the direction from the ampulla of the canal, while the irritation of the receptors of one channel increases, and the irritation of the opposite one decreases, i.e. an imbalance of impulses arriving to the vestibular nuclei occurs. When the vestibular nuclei on one side are stimulated, information is immediately transmitted to the contralateral nucleus of the abducens nerve in the pons, from where impulses through the medial longitudinal fasciculus reach the nucleus of the oculomotor nerve in the midbrain on the side of the irritated vestibular apparatus. This ensures synchronous contraction of the lateral rectus muscle of the eye opposite to the irritated labyrinth and the medial rectus muscle of the eye of the same name, which ultimately leads to a slow friendly deviation of the eyes in the direction opposite to the direction of head rotation. This reflex allows you to stabilize the position of the eyes and fix your gaze on a stationary object, despite the rotation of the head. In a healthy, awake person, it can be voluntarily suppressed due to the influence of the cerebral cortex on the brainstem structures. in a patient who is in clear consciousness, the integrity of the structures responsible for this reflex is determined as follows. They ask the patient to fix their gaze on a centrally located object and quickly (two cycles per second) turn the patient’s head in one direction or the other. If the vestibulo-ocular reflex is preserved, then the movements of the eyeballs are smooth, they are proportional to the speed of head movements and are directed in the opposite direction. To assess this reflex in a comatose patient, the doll eye test is used. It allows you to determine the safety of stem functions. The doctor fixes the patient’s head with his hands and turns it left and right, then tilts it back and lowers it forward; The patient's eyelids should be raised (the test is absolutely contraindicated if a cervical spine injury is suspected).

The test is considered positive if the eyeballs involuntarily deviate in the direction opposite to the rotation (the "doll's eyes" phenomenon). In case of intoxication and dysmetabolic disorders with bilateral damage to the cerebral cortex, the "doll's eyes" test is positive (the patient's eyeballs move in the direction opposite to the direction of head rotation). With lesions of the brain stem, the oculocephalic reflex is absent, that is, the test is negative (when turning, the eyeballs move simultaneously with the head as if they were frozen in place). This test is also negative in case of poisoning with certain drugs (for example, in case of an overdose of phenytoin, tricyclic antidepressants, barbiturates, sometimes muscle relaxants, diazepam), however, the normal size of the pupils and their reaction to light are preserved.

Caloric tests are also based on reflex mechanisms. Stimulation of the semicircular canals with cold water, which is poured into the outer ear, is accompanied by a slow friendly deviation of the eyeballs towards the irritated labyrinth. A cold caloric test is carried out as follows. First, you need to make sure that the eardrums in both ears are intact. Using a small syringe and a short thin soft plastic tube, 0.2-1 ml of ice water is carefully injected into the external auditory canal. In a healthy, awake person, nystagmus will appear, the slow component of which (slow deviation of the eyeballs) is directed towards the irritated ear, and the fast component - in the opposite direction (nystagmus, traditionally determined by the fast component, is directed in the opposite direction). After a few minutes, repeat the procedure on the opposite side. This test can serve as an express method for identifying peripheral vestibular hypofunction.

In a comatose patient with the brain stem intact, this test causes a tonic coordinated deviation of the eyeballs towards the cooled labyrinth, but there are no rapid eye movements in the opposite direction (that is, nystagmus itself is not observed). If the structures of the brain stem are damaged in a patient in a coma, the described test does not cause any movements of the eyeballs at all (there is no tonic deviation of the eyeballs).

Vestibular ataxia

Vestibular ataxia is detected using the Romberg test and examining the patient's gait (the patient is asked to walk in a straight line with his eyes open and then with his eyes closed). With unilateral peripheral vestibular pathology, instability is observed when standing and walking in a straight line with a deviation towards the affected labyrinth. Vestibular ataxia is characterized by changes in the severity of ataxia with sudden changes in head position and gaze turns. A pointing test is also carried out: the subject is asked to raise his hand above his head and then lower it, trying to get his index finger into the doctor’s index finger. The doctor's finger can move in different directions.

First, the patient performs the test with his eyes open, then he is asked to perform the test with his eyes closed. A patient with vestibular ataxia misses both hands toward the slow component of nystagmus.

IX AND X PAIRS. Glossopharyngeal and Vagus Nerves (M. GLOSSOPHARYNGEUS AND N. VA GUS)

The motor branch of the glossopharyngeus innervates the stylopharyngeus muscle. The autonomic pair of sympathetic secretory branches go to the ear ganglion, which in turn sends fibers to the parotid salivary gland. Sensitive fibers of the glossopharyngeal nerve supply the posterior third of the tongue, the soft palate. throat. skin of the outer ear. mucous membrane of the middle ear (including the inner surface of the eardrum) and the Eustachian tube; visceral sensory afferents carry impulses from the carotid sinus; taste fibers conduct the sense of taste from the posterior third of the tongue (Fig. 1-13).

Rice. 1-13. Conductors of taste sensitivity: 1 - thalamic cells; 2 - trigeminal nerve node; 3 - intermediate nerve; 4 - epiglottis; 5 - cells of the inferior ganglion of the vagus nerve; 6 - cells of the lower ganglion of the glossopharyngeal nerve; 7 - cell of the elbow assembly; 8 - taste kernel (letter: tractus sol itarii nn. intermedii, gl ossopharingei et vagi); 9 - bulbothalamic tract; 10 - parahippocampal gyrus and hook.

The vagus nerve innervates the striated muscles of the pharynx (except the stylopharyngeal muscle). soft palate (except for the muscle supplied by the trigeminal nerve, which stretches the velum palatine), tongue (m. palato glossus), larynx, vocal cords and epiglottis. Autonomic branches go to the smooth muscles and glands of the pharynx, larynx, and internal organs of the thoracic and abdominal cavities. Visceral sensory afferents conduct impulses from the larynx, trachea, esophagus, internal organs of the chest and abdominal cavity, from baroreceptors of the aortic arch and chemoreceptors of the aorta. Sensitive fibers of the vagus nerve innervate the skin of the outer surface of the auricle and external auditory canal, part of the outer surface of the eardrum, pharynx, larynx, and dura mater of the posterior cranial fossa. The glossopharyngeal and vagus nerves have several common nuclei in the medulla oblongata and pass close to each other; their functions are difficult to separate (Fig. 1 - 14), so they are examined simultaneously.

Rice. 1-14. The course of central motor neurons to the nuclei IX, X and XII of pairs ChN: 1 - pyramidal cells of the lower part of the precentral gyrus (tongue area, larynx); 2 - cortical-nuclear pathway; 3 - stylopharyngeal muscle; 4 - double core; 5 - muscles of the epiglottis; 6 - muscles of the soft palate and constrictor muscles of the pharynx; 7 - recurrent laryngeal nerve; 8 - vocal muscles; 9 - tongue muscle; 10 - nucleus of the hypoglossal nerve.

When collecting anamnesis, they find out whether the patient has problems with swallowing and speech (voice).

Voice. Pay attention to the clarity of speech, timbre and sonority of the voice. If the function of the vocal cords is impaired, the voice becomes hoarse and weak (up to aphonia). Due to dysfunction of the soft palate, which does not sufficiently cover the entrance to the nasopharyngeal cavity during phonation, a nasal tone of voice occurs (nasolalia). Impaired function of the laryngeal muscles (damage to the vagus nerve) affects the pronunciation of high-pitched sounds (i-i-i), which requires the vocal cords to be brought closer together. In order to exclude weakness of the facial muscles (VII pair) and the muscles of the tongue (XII pair) as a possible cause of speech impairment, the patient is asked to pronounce labial (p-p-p, mi-mi-mi) and front-lingual (la-la-la) sounds or syllables that include them. The nasality of the voice is revealed when pronouncing syllables containing guttural sounds (ga-ga-ga, kai-kai-kai). The patient is also asked to cough forcefully.

A patient with acute unilateral vocal cord paralysis is unable to produce the sound “ee-ee” or forcefully cough.

Curtain of the palate. The soft palate is examined when the examinee pronounces the sounds “a-a-a” and “uh-uh”. Assess how fully, strongly and symmetrically the soft palate rises during phonation; does the uvula of the palatine deviate to the side? With unilateral paresis of the soft palate muscles, the velum palatine lags behind on the affected side during phonation and is pulled by healthy muscles in the direction opposite to the paresis; the tongue deviates in the healthy direction.

Palatal and pharyngeal reflexes. Using a wooden spatula or a strip (tube) of paper, carefully touch the mucous membrane of the soft palate on both sides alternately. The normal response is to pull the velum upward. Then they touch the back wall of the throat, also on the right and left. Touching causes swallowing and sometimes gagging movements. The reflex response is expressed to varying degrees (in older people it may be absent), but normally it is always symmetrical. The absence or reduction of reflexes on one side indicates peripheral damage to the IX and X pairs of the CN.

PAIR XI: ACCESSORY NERVE (N. A CCESSORIUS)

This purely motor nerve innervates the sternocleidomastoid and trapezius muscles.

The study of the function of the accessory nerve begins with an assessment of the outline, size and symmetry of the sternocleidomastoid and trapezius muscles. Usually it is enough to match the right and left sides. When the nucleus or trunk of the XI nerve is damaged, the shoulder girdle on the side of paralysis is lowered, the scapula is slightly displaced downward and laterally. To assess the strength of the sternocleidomastoid muscle, the patient is asked to forcefully turn his head to the side and slightly upward. The doctor counters this movement by applying pressure to the patient's lower jaw. With unilateral contraction, the sternocleidomastoid muscle tilts the head and neck in its direction and at the same time additionally turns the head in the opposite direction. Therefore, when testing the right muscle, place the hand on the left half of the patient’s lower jaw, and vice versa. They look at the contours and palpate the belly of this muscle during its contraction. To assess the strength of the trapezius muscle, ask the patient to “shrug” (“raise the shoulders towards the ears”). The doctor resists this movement.

XII PAIR: HYPOGLOSSAL NERVE (N. HYPOGLOSSSUS)

The nerve innervates the muscles of the tongue (with the exception of the m. palatoglossus, supplied by the X pair of the CN). The examination begins with examination of the tongue in the oral cavity and when it protrudes. Pay attention to the presence of atrophy and fasciculations. Fasciculations are worm-like, rapid, irregular muscle twitches. Atrophy of the tongue is manifested by a decrease in its volume, the presence of grooves and folds of its mucous membrane. Fascicular twitching in the tongue indicates involvement of the hypoglossal nerve nucleus in the pathological process. Unilateral atrophy of the tongue muscles is usually observed with tumor, vascular or traumatic damage to the trunk of the hypoglossal nerve at or below the level of the base of the skull; it is rarely associated with an intramedullary process. Bilateral atrophy most often occurs in motor neuron disease [amyotrophic lateral sclerosis (ALS)] and syringobulbia. To assess the function of the tongue muscles, the patient is asked to stick out his tongue. Normally, the patient easily sticks out his tongue; when protruding, it is located along the midline. Paresis of the muscles of one half of the tongue leads to its deviation to the weaker side (m. genioglossus of the healthy side pushes the tongue towards the paretic muscles). The tongue always deviates towards the weak half, regardless of whether the consequence of any supranuclear or nuclear lesion is weakness of the tongue muscle. You should make sure that the deviation of the language is true and not imaginary. A false impression of the presence of tongue deviation can arise from facial asymmetry caused by unilateral weakness of the facial muscles. The patient is asked to perform quick movements of the tongue from side to side. If the weakness of the tongue is not completely obvious, ask the patient to press the tongue on the inner surface of the cheek and evaluate the strength of the tongue, counteracting this movement. The force of tongue pressure on the inner surface of the right cheek reflects the force of the left m. genioglossus, and vice versa. The patient is then asked to pronounce syllables with frontal sounds (for example, “la-la-la”). If the tongue muscle is weak, he cannot pronounce them clearly. To identify mild dysarthria, the subject is asked to repeat complex phrases, for example: “administrative experiment”, “episodic assistant”, “large red grapes are ripening on Mount Ararat”, etc.

Combined damage to the nuclei, roots or trunks of the IX, X, XI, HP pairs of the CN causes the development of bulbar palsy or paresis. Clinical manifestations of bulbar palsy are dysphagia (swallowing disorder and choking when eating due to paresis of the muscles of the pharynx and epiglottis); nasolalia (a nasal tone of voice associated with paresis of the muscles of the velum palatine); dysphonia (loss of voice sonority due to paresis of the muscles involved in the narrowing/expansion of the glottis and tension/relaxation of the vocal cord); dysarthria (paresis of muscles that ensure correct articulation); atrophy and fasciculations of the tongue muscles; extinction of the palatine, pharyngeal and cough reflexes; respiratory and cardiovascular disorders; sometimes flaccid paresis of the sternocleidomastoid and trapezius muscles.

The IX, X and XI nerves together exit the cranial cavity through the jugular foramen, so unilateral bulbar palsy is usually observed when these CNs are affected by a tumor. Bilateral bulbar palsy can be caused by poliomyelitis and other neuroinfections, ALS, bulbospinal amyotrophy

Kennedy or toxic polyneuropathy (diphtheria, paraneoplastic, GBS, etc.). Damage to neuromuscular synapses in myasthenia gravis or muscle pathology in some forms of myopathies cause the same disturbances in bulbar motor functions as in bulbar palsy.

From bulbar palsy, in which the lower motor neuron (CN nuclei or their fibers) suffers, one should distinguish pseudobulbar palsy, which develops with bilateral damage to the upper motor neuron of the corticonuclear pathways. Pseudobulbar palsy is a combined dysfunction of the IX, X, CN pairs of the CN, caused by bilateral damage to the corticonuclear tracts going to their nuclei. The clinical picture resembles that of bulbar syndrome and includes dysphagia, nasolalia, dysphonia and dysarthria. In pseudobulbar syndrome, unlike bulbar syndrome, the pharyngeal, palatal, and cough reflexes are preserved; reflexes of oral automatism appear, the mandibular reflex increases; violent crying or laughter is observed (uncontrolled emotional reactions), hypotrophy and fasciculations of the tongue muscles are absent.

Fundus examination is one of the objective methods used in the early childhood neurology clinic. Examination of the fundus in young children is difficult. To dilate the pupil, 1% homatropine is instilled into the conjunctival sac. In newborns and infants, the head is fixed by the mother or nurse. If the child is very restless and closes his eyes, the doctor may use an eyelid lifter. With good contact with a 2-3 year old child, you can force him to fix his gaze on an interesting object. The fundus is examined using a mirror or electric ophthalmoscope.

fundus a newborn is distinguished by a number of features. It is colored light yellow. The optic disc is pale pink with a grayish tint, the boundaries are clear, there is no macular reflex. In adults, such a fundus occurs with optic nerve atrophy. The grayish color of the macular area and depigmentation of the remaining parts of the fundus persist until 2 years of age. The retinal arteries of newborns are of normal caliber, and the veins are wider than usual.

U newborns, born with asphyxia, in the fundus of the eye one can detect pinpoint hemorrhages along the arterioles in the form of flames, blots, streaks, spots, puddles. These hemorrhages resolve on the 6-7th day of life. Macular hemorrhages and periretinal hemorrhages persist longer. Sometimes they appear again on the 12-14th day of life.

In premature babies who were in an atmosphere with a high oxygen content, retrolental fibroplasia is found in the fundus - proliferation of capillary endothelium, hemorrhages, swelling of nerve fibers. Subsequently, the nerve fibers thicken, and the newly formed capillaries grow into the vitreous body. Starting in the periphery, the process involves the entire retina and vitreous body.

When increasing intracranial pressure, decompensated hydrocephalus, volumetric processes in the fundus, dilation of veins, narrowing of arteries, blurring of the optic disc due to retinal edema are noted. The swelling also spreads along the vessels. With increasing hypertension, the disc increases in size and protrudes into the vitreous body, the vessels drown in the edematous retina, and hemorrhages from dilated veins appear. Long-term intracranial hyperthesia leads to subatrophy, and then to secondary atrophy of the optic nerve head. The disc becomes pale gray with unclear boundaries. The vessels are narrowed, especially the arteries.

Congenital optic atrophy characterized by a sharp pallor of the optic nerve head, especially the temporal halves. The disc boundaries are clear, in contrast to secondary optic nerve atrophy. The arteries are narrowed.

For cerebral lipoidoses(gangliosidoses, sphingolipidoses) and some mucolipidoses are characterized by the presence of a cherry-red spot in the macular area, which does not change throughout the course of the disease. These changes in the fundus are associated with retinal atrophy and transillumination of the choroid. They can be detected already in the first months of life, which is important for differential diagnosis. Chorioretinitis and microphthalmos are observed in congenital toxoplasmosis.

Video of reverse ophthalmoscopy technique for fundus examination

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Symptoms revealed during a neuro-ophthalmological examination of patients with TBI, along with other neurological symptoms and the results of additional research methods, indicate, first of all, the topic of the lesion, and also allow monitoring of patients in the acute and long-term period of TBI.

Neuroophthalmological examination for TBI has one peculiarity - patients often must be examined in the ward, which presents certain difficulties.

VISUAL FUNCTIONS: RESEARCH METHODS AND SEMIOTICS

Examination of a patient with TBI, like any neurological patient, should, if possible, begin with a study of visual functions, including determination of visual acuity and visual field boundaries.

The nature of visual disturbances depends on the level of damage to the visual analyzer and, therefore, indicates the localization of the source of damage. Moreover, it is believed that the correlation of visual field defects with neuropsychological tests largely provides clues to the outcome of TBI.

Visual acuity is examined using a distance table with corrective glasses and/or a diaphragm (for mydriasis) for each eye separately. It should be borne in mind that in children, visual acuity normally reaches 1.0 by the fifth year of life.
In bedridden patients, visual acuity is determined using a manual table. If, due to the severity of the patient’s condition, it is not possible to examine visual acuity, an approximate assessment is made by how the patient fixes his gaze on presented objects or a light source, by the pupillary reaction to light (it must be remembered that the pupillary constriction reaction depends not only on the visual acuity vision, but also an indicator of the condition of the oculomotor nerve and brain stem structures).

Visual functions are also assessed using visual evoked potentials.

The visual field is examined using static and dynamic (white, red and green colors) perimetry or approximately using objects or the hand.

A decrease in visual acuity from 0.7-0.8 to blindness and visual field defects: sectoral, hemianopic, concentric narrowing, often in combination with scotomas (Fig. 9-1), occurs with traumatic damage to the optic nerve, which occurs from 0.5 to 5% of TBI cases.

Rice. 9-1. Static perimetry performed on a Humphrey visual field analyzer in a patient with TBI and damage to the left optic nerve.

It should be noted that when the optic nerve is damaged, there is no direct relationship between the degree of loss of visual function and the severity of TBI. The development of blindness is possible even with mild TBI.

Bitemporal hemianopsia clinically manifests itself as damage to the chiasm, which, according to B. Hughes, occurs in 3.9% of cases and, as a rule, occurs with moderate and severe head injury, accompanied by a fracture of the bones of the base of the skull. Hemianopsia can be complete or incomplete, often asymmetrical, combined with decreased visual acuity, since damage to the chiasm is often accompanied by damage to the optic nerves (Fig. 9-2a, b, c).

Rice. 9 - 2a. Dynamic perimetry in a patient with TBI and damage to the right optic nerve and chiasm.

Rice. 9 - 26. Static perimetry performed on a Humphrey visual field analyzer in a patient with TBI and damage to the chiasm, revealing bitemporal hemianopsia.

Rice. 9-2c. Dynamic perimetry in a patient with TBI and damage to the chiasm, revealing bitemporal hemianopia.

Rice. 9 - 3. Static perimetry performed on a Humphrey visual field analyzer in a patient with TBI, which revealed complete right-sided homonymous hemianopsia.

Damage to the optic tract, and especially to the lateral geniculate body, is extremely rare in TBI. Clinically, this is manifested by visual field defects such as homonymous hemianopia. Much more often, homonymous hemianopsia (with preservation of high visual acuity) occurs as a result of damage to the visual analyzer in the cerebral hemispheres.

The reason for this may be either direct traumatic damage to the optic fibers or compression of them due to brain dislocation caused by various factors (cerebral edema, hematoma, etc.).

Inferior altitudinal (horizontal) homonymous hemianopsia is a characteristic sign of damage to the visual pathway at the level of the visual cortex of both occipital lobes, occurring more often with a gunshot wound passing above the protuberantia occipitalis externa (Fig. 9-4).

Rice. 9 - 4. Static perimetry performed on a Humphrey visual field analyzer in a patient with a gunshot wound to the occipital lobe. Inferior altitudinal homonymous hemianopsia and incomplete left-sided homonymous hemianopsia were revealed.

Cortical blindness develops when both occipital lobes are injured. In children, according to J.A. McCrary (17), Digre K., it is possible with minimal trauma to the occipital region. It is also noteworthy that, as Digre K. believes (12), damage to the occipital lobe occurs with forehead trauma. Clinically, cortical blindness is manifested by bilateral homonymous hemianopsia, bilateral blindness with preserved pupillary reaction to light (!), visual hallucinations and can be denied by the patient (Anton'a syndrome). The fundus is normal.

Depending on the nature of the injury, cortical blindness may develop in reverse. The pathophysiology of transient cortical blindness has several alternative options: circulatory disorders, contusion, accompanied by swelling of brain tissue. S.H. Greenblatt (cited by J.S. Glasser divided transient cortical blindness in TBI into three clinical variants: blindness for several hours, combined with somnolence, resulting in complete restoration of vision; blindness with a delayed onset from the moment of injury, lasting for several minutes - several hours with subsequent restoration of vision; blindness after severe TBI, combined with pronounced neurological defects, with variability in terms of restoration of visual functions. The first two clinical options are more typical for pediatric patients, the latter - for adults. Restoration of vision begins with the appearance of light perception, then the perception of movement. , later - shapes; color perception is restored last.

In case of circulatory disorder as a result of injury to the occipital lobe, scotomas in the field of view are more typical. The closer the lesion is located to the pole of the occipital lobe, the closer the location of the scotoma is to the center.

EXTERNAL INSPECTION

As noted earlier, the study of patients with TBI has its own characteristics, therefore, in some cases, an ophthalmological examination begins not with a study of visual functions, but with an external examination, which can provide significant information.

Swelling of the eyelids and subcutaneous hemorrhage are a symptom of retrobulbar hematoma (Fig. 9-5). However, swelling of the eyelids can also be a sign of CCS, so it is imperative to auscultate to exclude the presence of a vascular murmur over the eyeball.

With a fracture of the outer, lower and especially medial walls of the orbit, subcutaneous emphysema of the eyelids can develop, a characteristic sign of which is crepitus on palpation.

It must be remembered that the existing swelling of the eyelids in the acute period of injury can veil lagophthalmos or ptosis.
Lagophthalmos - incomplete closure of the eyelids, is a sign of damage to the VII pair of cranial nerves, which usually occurs with a fracture in the area of ​​the pyramid of the temporal bone.

Ptosis and semiptosis are a symptom of dysfunction of the oculomotor nerve (III pair of cranial nerves), more often found when the oculomotor nerve is damaged at the base of the brain or in the orbit and is accompanied by other signs of damage to this nerve.

Claude Bernard-Horner syndrome - narrowing of the palpebral fissure in combination with miosis with preserved reaction of the pupil to light, small enophthalmos of 1-2 mm - is a sign of inhibition or loss of sympathetic innervation of the eye and its appendages. This symptom complex is observed with damage to the cervical sympathetic nodes and accompanies injury to the cervical spine and spinal cord. It also occurs with a fracture of the base of the skull.

Signs of irritation of the sympathetic system consist of a slight dilation of the palpebral fissure and pupil, while a slight exophthalmos of 1 mm is possible.

Often, damage to the facial nerve in the area of ​​the pyramid of the temporal bone is combined with damage to the trigeminal nerve (V pair of cranial nerves), which is clinically manifested by a decrease in the sensitivity of the cornea, which is examined by touching a hair to the cornea. Unilateral or bilateral asymmetrical decrease in sensitivity indicates inhibition of the function of the trigeminal nerve at the base of the brain, in the area of ​​the superior orbital fissure or orbit.
Bilateral symmetrical decrease in the corneal reflex indicates damage to the brain stem: the pons-midbrain level. It should be noted that decreased sensitivity may be a consequence of previous corneal diseases or surgical interventions on the eyeball.

Exophthalmos of 2-3 mm or enophthalmos is possible with a fracture of the orbital bones. In these cases, not only protrusion or retraction of the eyeball is possible, but also its displacement vertically or horizontally, which is usually accompanied by a complaint of double vision.

The presence of pulsating exophthalmos in combination with a vascular noise heard above the eyeball, congestive injection of the eyeball, conjunctival edema, impaired oculomotor function, mydriasis with impaired pupillary reaction to light are signs of a carotid-cavernous anastomosis.

Mixed injection of the eyeball (conjunctival and pericorneal), pain in the eye, lacrimation, photophobia make it necessary to exclude traumatic injury to the eyeball (contusion or injury, including penetrating). Absolute signs indicating that the injury to the eyeball is penetrating include: a wound passing through all layers of the cornea, sclera or corneo-scleral zone; infringement of the inner membranes of the eye and vitreous body in the wound; traumatic coloboma of the iris. Both penetrating wounds and contusions of the eyeball are accompanied by hypotony of the eye.

MOTOR-PUPILARIAL FUNCTIONS: RESEARCH METHODS AND SEMIOTICS

Oculomotor disorders, as well as pupillary disorders, in addition to evidence of damage to the oculomotor nerves, are also an important indicator of the functional activity of the brain stem and reticular formation.
It should be emphasized that assessing the size of the pupils and their reaction to light is of great importance during the initial examination of patients with TBI. K. Digre attaches great importance to pupillary disorders in the prognosis of TBI.

It is necessary to assess the condition of the pupils in both eyes simultaneously under diffuse lighting, directing the light parallel to the patient’s face. In this case, the patient should look into the distance. Pupil size is measured using a pupillometric or millimeter ruler. It is on average 3.5-4.5 mm. A difference in pupil size of one eye and the other eye of more than 0.9 mm is regarded as pathological anisocoria.

To study the pupillary reaction to light, which is best done in a dark or darkened room, each eye is alternately illuminated separately with a light source (flashlight, hand-held ophthalmoscope). The speed and amplitude of the direct (on the illuminated eye) and conjugate (on the other eye) reaction of the pupil is determined. Normally, the direct reaction to light is the same or slightly more vivid than the friendly one in the other eye.

Bilateral miosis with intact response to light indicates damage to the brainstem and may be the result of structural or physiological inactivation of the sympathetic pathway descending from the hypothalamus through the reticular formation. In addition, bilateral miosis may suggest metabolic encephalopathy or drug use.

Bilateral mydriasis without pupillary response to light in patients with TBI occurs when the parasympathetic system is inactivated as a result, for example, of inadequate cerebrovascular perfusion, which is possible due to secondary hypotension due to blood loss.

Violation of voluntary gaze occurs when the cortical centers of eye movement, localized in the frontal lobe (2nd and 3rd gyri), are damaged or when the connection of these centers with the brain stem is disconnected.

Violation of reflex gaze indicates damage to the supranuclear centers of gaze up and down - (level of the posterior commissure of the brain and quadrigeminal) and to the sides - (level of the pons of the brain). In this case, as a rule, there is no strabismus and patients are not bothered by double vision.

Often, a violation of upward gaze is combined with a weakening or absence of a direct and friendly pupillary reaction to light in both eyes. These symptoms, combined with convergence disorder, form quadrigeminal syndrome.
To assess gaze, the patient is asked to follow an object moving horizontally and vertically. Normally, when looking to the sides, the limbus area should come into contact with the internal or external commissure of the eyelids. Although the norm is considered to be slight undersight of the eyeballs, when you can see 1-2 mm of the sclera (this depends on the structure of the eyeballs). Vertical gaze is more difficult to assess. The deviation of the eyes downward should be about 45°, upward from 45 to 20°, depending on age.

In unconscious patients, reflex gaze is examined, which is achieved either by irritating the cornea or by passively tilting the head down, causing the “doll phenomenon” (vestibular reflex movements). In the case of intact reflex gaze upward, when the cornea is irritated or when the head is tilted down, the eyeballs make friendly upward movements.

Another symptom indicating damage to the brain stem is uneven alignment of the eyeballs. The Hertwig-Magendie sign indicates damage to the posterior longitudinal fasciculus. The uneven alignment of the eyeballs persists when looking up and down.

Unilateral mydriasis with areflexia of the pupil to light (clivus edge symptom) is a sign of damage to the oculomotor nerve, its pupillomotor fibers at the level of the nerve trunk, and may indicate the formation of a hematoma on the affected side or increasing cerebral edema or be a sign of brain dislocation of another etiology.

Mydriasis with a violation of the direct and friendly reaction to light in combination with limited or absent mobility of the eyeball up, down, inward, indicates damage to the root or trunk of the oculomotor nerve (III pair of cranial nerves). Due to the restriction of the mobility of the eyeball inwards, paralytic divergent strabismus develops.

However, you should always remember that mydriasis and impaired pupillary photoreactions can be caused by traumatic damage to the sphincter of the pupil during contusion of the eyeball.

Damage to the optic nerve with the development of amorosis or low visual acuity can also be the cause of unilateral mydriasis and be a manifestation of the Marcus Gunna symptom. In such cases, it is especially important to assess the friendly reaction to light of the pupil both on the side of mydriasis and the pupil of the other eye. Thus, with mydriasis caused by damage to the sphincter of the pupil, the direct and friendly reaction of the pupil of the other eye will be preserved. While in a victim with damage to the optic nerve, the friendly reaction of the pupil on the side of mydriasis will be preserved if the friendly reaction of the other eye is disrupted.

It should be noted that trauma is the most common cause leading to isolated damage to the trochlear nerve (IV pair of cranial nerves). Diplopia when looking down and a slight tilt of the head to the side opposite the affected eye are characteristic signs of damage to n. trochlearis.

Damage to the abducens nerve (VI pair of cranial nerves) is clinically expressed by limitation or absence of outward mobility of the eye, leading to convergent paralytic strabismus.

Patients with paralytic strabismus complain of double vision, which intensifies when the eye moves towards the affected muscle. However, it should be borne in mind that double vision is only possible with sufficiently high visual acuity in both eyes.

FUNDUS EXAMINATION

A neuro-ophthalmological examination usually ends with a fundus examination. Direct and reverse ophthalmoscopy is performed. It is advisable to start with reverse ophthalmoscopy, in which the fundus is reviewed, and the necessary details are clarified using direct ophthalmoscopy.

The most common changes detected in patients with TBI is retinal angiopathy, a characteristic sign of which is arterial spasm and dilation, plethora, and tortuosity of the veins. According to a number of authors, the weakening or disappearance of the venous pulse (normally, ophthalmoscopy detects the pulsation of the central retinal vein at its entry into the vascular funnel of the optic nerve head) is one of the early signs of increased intracranial pressure.

In 20-30% of cases after severe TBI, congestive optic disc may develop - a symptom of intracranial hypertension (Fig. 9-6). The reasons that led to the development of congestive optic discs at different stages of the development of traumatic disease are different. In the first few days after injury, congestive discs are usually the result of diffuse cerebral edema, leading to increased intracranial pressure. Congested optic discs that appear several weeks after TBI may be the result of developed hydrocephalus.

Rice. 9-5. A victim with acute TBI. Right: semiptosis, eyelid edema, exophthalmos, chemosis and congestive injection, conjunctivitis of the eyeball.

Rice. 9-6. Fundus of the eye in acute head injury. Swelling of the optic disc, hemorrhages near it, the veins are tortuous and full of blood - congestive optic disc.

Rice. 9-7. Fundus of the eye in the aftermath of head injury. The optic disc is pale, the boundaries are clear, the vessels are narrowed - primary descending optic nerve atrophy.

In the acute period of TBI, congestive optic discs or retinal angiopathy may be accompanied by hemorrhages on the disc and near it in the peripapillary retina. Hemorrhages indicate a rapid increase in intracranial hypertension and, as a rule, are a poor prognostic sign.

Asymmetry in the severity of both papilledema and the hemorrhagic component is possible. For example, they may be more pronounced on the side of the hematoma.

However, it must be remembered that papilledema during TBI is not always a sign of intracranial hypertension. It may be a manifestation of optic neuropathy as a result of an acute circulatory disorder in the vessels supplying the optic nerve, in case of traumatic damage to it, or in a violation of the venous outflow, which occurs with CCS.

Pallor of the optic disc is a sign of descending atrophy of the optic nerves (Fig. 9-7), which occurs at different times from the moment of injury to the optic pathway, depending on the distance of the site of damage to the optic fibers from the posterior pole of the eye. Thus, if the optic nerve is damaged in the orbit or optic canal, blanching of the optic disc is detected after 4-7 days, and if the fibers are damaged at the level of the chiasm, the period extends to several weeks or even months.