Investigation of cranial nerves. II pair: optic nerve (n. Opticus)

The optic nerve conducts visual impulses from the retina of the eye to the cortex of the occipital lobe.

When collecting anamnesis, it is determined whether the patient has a change in vision. Changes in visual acuity (far or near) are within the competence of the ophthalmologist. With transient episodes of impaired vision, limiting visual fields, the presence of photopsy 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 a visual aura. Visual disorders are more often represented by flashes of light or sparkling zigzags (photopsies), flickering, fallout of the site or the entire field of view. The visual aura of migraine develops 0.5-1 hours (or less) before the onset of headache, lasts an average of 10-30 minutes (not more than 1 hour). Headache with migraine occurs no later than 60 minutes after the end of the aura. Visual hallucinations by type of photopsy (flares, sparks, zigzags) can represent an aura of epileptic seizure in the presence of a pathological focus that irritates the cortex in the region of the furrow groove.

Visual acuity and study

Visual acuity is determined by ophthalmologists. To assess visual acuity in the distance use special tables with circles, letters, numbers. The standard table, used in Ukraine, contains 10-12 rows of signs (optotypes), the sizes of which are reduced from top to bottom by arithmetic progression. Vision is examined from a distance of 5 m, the table should be well lit. For the norm (visual acuity 1) take such a visual acuity, at which from this distance the examinee is able to distinguish the optotypes of the 10th (counting from above) lines. If the subject is able to distinguish the signs of the 9th line, his visual acuity is 0.9, the 8th line is 0.8, and so on. In other words, reading each successive line from top to bottom indicates an increase in visual acuity by 0.1. Visual acuity is checked by using other special tables or by offering the patient to read the text from the newspaper (normally a small newspaper font is distinguished from a distance of 80 cm). If the visual acuity is so small that the patient can not read anything at any distance, they limit themselves to the counting of the fingers (the doctor's hand is located at eye level of the subject). If this is not possible, ask the patient to determine in which room: in the dark or in the lighted - it is located. Reducing visual acuity ( amblyopia ) or complete blindness (amaurosis) occurs with damage to the retina or optic nerve. With this blindness, the direct reaction of the pupil to light disappears (due to the interruption of the afferent part of the pupil reflex arc), but the pupillary response remains in response to the illumination of the healthy eye (the efferent part of the pupil reflex arc, represented by the fibers of the III cranial nerve, remains intact). Slowly progressive decline in vision is observed when the optic nerve or chiasma is compressed by the tumor.

Signs of violations

Transient short-term loss of vision for one eye (transient monocular blindness, or amaurosis fugax - from 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 that dropped from the top down" when it emerges and as a "rising curtain" when it is reversed. Usually vision is restored in a few seconds or minutes. The sharp decrease in vision that has arisen and progresses during 3-4 days, then recovered within a few days-weeks and is often accompanied by pain in the eyes, is characteristic of retrobulbar neuritis. A sudden and persistent loss of vision occurs when fractures of the bones of the anterior cranial fossa in the visual channel area; with vascular lesions of the optic nerve and temporal arteritis. When clogging the zone of bifurcation of the main artery and the development of a bilateral infarct of the occipital lobes with damage to the primary visual centers of both large cerebral hemispheres, there is a "tubular" vision or cortical blindness. "Tubular" vision is due to bilateral hemianopsia with the preservation of the central (macular) vision on both eyes. Preservation of vision in a narrow central field of vision is explained by the fact that the zone of the projection of the macula at the pole of the occipital lobe is supplied from several arterial basins and, in cases of infarctions of the occipital lobes, remains intact. Visual acuity in these patients is reduced slightly, but they behave like a blind person. "Cortical" blindness occurs in the case of inadequate anastomoses 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 marked by the preservation of pupillary responses to light, since the visual pathways from the retina to the brain stem are not damaged. Cortical blindness in cases of bilateral damage to the occipital lobes and parieto-occipital areas can in some cases be combined with the negation of this disorder, achromatopsy, apraxia of friendly eye movements (the patient can not look toward the object in the peripheral part of the field of vision) and the inability to visually perceive the object and touch it. The combination of these disorders is referred to as Balint's syndrome.

Fields of vision and their research

The field of vision is a piece of space that a fixed eye can see. The preservation of visual fields is determined by the state of the entire visual pathway (optic nerves, visual tract, visual radiance, cortical zone of vision, which is located in the spurs on the medial surface of the occipital lobe). Because of the refraction and cross-beam of light in the lens and the transition of visual fibers from the half-retina halves of the same name in chiasm, the right half of the brain is responsible for the preservation of the left half of the field of view of each eye. Fields of vision are assessed separately for each eye. There are several methods for their approximate evaluation.

• A gradual evaluation of individual fields of vision. The doctor is sitting opposite the patient. The patient closes one of his eyes with his palm, and looks at the nose of the doctor with another eye. The malleus or moving fingers are moved around the perimeter from behind the head of the subject to the center of his field of vision and ask the patient to note the moment of the appearance of the malleus or fingers. The study is carried out alternately in all four quadrants of the fields of vision.
• The method of "threat" is used in those cases when it is necessary to investigate the field of vision in a patient inaccessible to verbal contact (aphasia, mutism, etc.). The doctor with a sharp "menacing" movement (from the periphery to the center) brings the fingers of his hand to the patient's pupil's open fingers, watching his flashing. If the field of vision is preserved, the patient flashes in response to the approach of the finger. All fields of vision of each eye are examined.

The described methods refer to screening, more precisely defects of visual fields are detected using a special device - the perimeter.

Signs of violations

Monocular defects of the visual fields are usually caused by the pathology of the eyeball, retina or optic nerve - in other words, the damage to the visual pathways before their crossing (chiasma) causes a violation of the visual fields of only one eye located on the side of the lesion. Binocular defects in the fields of vision (hemianopsia) can be bitemporal (in both eyes, temporal fields of vision fall, that is, the right eye has a right eye, the left eye has a left one) or homonymous (each eye has the same field of vision, either left or right). Bitemporal defects of the visual fields occur when lesions occur in the area of the intersection of visual fibers (eg, damage to the chiasma in the onyxoj and pituitary gland). Homogenous defects in the visual fields occur when the visual tract, visual radiance or visual cortex is affected, that is, when the optic path is damaged above the chiasma (these defects appear in the opposite foci of the lesion of the visual fields: if the focus is in the left hemisphere, the right fields of vision of both eyes fall out, and on the contrary). The defeat of the temporal lobe leads to the appearance of defects in the homonymous upper quadrants of the visual fields (contralateral upper quadrant anopia), and parietal lobe damage to the appearance of defects in the homonymous lower quadrants of the visual fields (contralateral lower quadrant anopia).

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

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The ocellus and its study

The ocular fundus is examined with an ophthalmoscope. Assess the condition of the disc (nipple) of the optic nerve (visible in ophthalmoscopy initial, intraocular part of the optic nerve), retina, vessels of the fundus. The most important characteristics of the status of the fundus are the color of the optic nerve disc, the sharpness of its borders, the number of arteries and veins (usually 16-22), the presence of pulsations of the veins, any abnormalities or pathological changes: hemorrhages, exudate, changes in the walls of blood vessels in the 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 extends into the cavity of the eyeball), redness (the vessels on the disc are sharply enlarged and full of blood); the boundaries of the disc become fuzzy, the number of retinal vessels increases (more than 22), the veins do not pulsate, hemorrhages are present. Two-sided edema of the optic disc ( stagnant nipple of the optic nerve ) 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 eliminated in a timely manner, visual acuity gradually decreases and blindness develops as a result of secondary optic nerve atrophy.

The congestive optic nerve disk must be differentiated from inflammatory changes (papillitis, optic neuritis ) and ischemic neuropathy of the optic nerve. In these cases, changes in the disc are more often one-sided, typical pain in the eyeball area and reduced visual acuity. Pallor of the optic nerve disc in combination with a decrease in visual acuity, narrowing of the visual fields, a decrease in pupillary reactions are characteristic for optic nerve atrophy, which develops in many diseases that affect this nerve (inflammatory, dysmetabolic, hereditary). Primary atrophy of the optic nerve develops with damage to the optic nerve or chiasma, while the disc is pale, but has clear boundaries. Secondary atrophy of the optic nerve develops after the edema of the optic disc, the border of the disc is initially fuzzy. Selective pallor of the temporal half of the optic disc can be observed with multiple sclerosis, but this pathology is easily confused with the variant of the normal state of the optic disc. Pigmented degeneration of the retina is possible with degenerative or inflammatory diseases of the nervous system. Other important for the neurologist pathological findings when examining the fundus are arteriovenous retinal angioma and a symptom of the cherry bones, which is possible with many gangliosidoses and is characterized by the presence of a white or gray rounded focus in the macula area, in the center of which is a cherry-red spot. Its origin is associated with the atrophy of ganglion cells of the retina and the transmission through it of the choroid.