Pupillary reflex: its meaning and structure. Pupillary reflex

1. Simultaneous disturbance of the pupillary response to light, convergence and accommodation is clinically manifested by mydriasis. With a unilateral lesion, the reaction to light (direct and friendly) is not evoked on the affected side. This immobility of the pupils is called internal ophthalmoplegia. This reaction is caused by damage to the parasympathetic pupillary innervation from the Yakubovich-Edinger-Westphal nucleus to its peripheral fibers in the eyeball. This type of pupillary reaction disorder can be observed with meningitis, multiple sclerosis, alcoholism, neurosyphilis, vascular diseases of the brain, and traumatic brain injury.
2. Violation of the friendly reaction to light is manifested by anisocoria, mydriasis on the affected side. In the intact eye, the direct reaction is preserved and the friendly reaction is weakened. In the diseased eye there is no direct reaction, but the friendly reaction remains. The reason for this dissociation between the direct and conjugate reaction of the pupil is damage to the retina or optic nerve before the optic chiasm.
3. Amaurotic immobility of the pupils to light is found in bilateral blindness. In this case, both direct and cooperative reactions of the pupils to light are absent, but to convergence and accommodation are preserved. Amaurotic pupillary areflexia is caused by bilateral damage to the visual pathways from the retina to the primary visual centers inclusive. In cases of cortical blindness or in case of damage on both sides of the central visual pathways running from the external crankshaft and from the cushion of the visual thalamus to the occipital visual center, the reaction to light, direct and friendly, is completely preserved, since the afferent visual fibers end in the area of ​​the anterior colliculus. Thus, this phenomenon (amaurotic immobility of the pupils) indicates a bilateral localization of the process in the visual pathways up to the primary visual centers, while bilateral blindness with preservation of the direct and conjugate reaction of the pupils always indicates damage to the visual pathways above these centers.
4. The hemiopic reaction of the pupils is that both pupils contract only when the functioning half of the retina is illuminated; When illuminating the missing half of the retina, the pupils do not contract. This reaction of the pupils, both direct and concomitant, is caused by damage to the optic tract or subcortical visual centers with the anterior colliculus, as well as crossed and uncrossed fibers in the chiasm area. Clinically, it is almost always combined with hemianopia.
5. The asthenic reaction of the pupils is expressed in rapid fatigue and even in the complete cessation of constriction with repeated light exposure. This reaction occurs in infectious, somatic, neurological diseases and intoxications.
6. The paradoxical reaction of the pupils is that when exposed to light, the pupils dilate, but in the dark they constrict. It occurs extremely rarely, mainly with hysteria, even severe with tabes dorsalis, strokes.
7. With an increased reaction of the pupils to light, the reaction to light is more vivid than normal. It is sometimes observed with mild concussions, psychoses, allergic diseases (Quincke's edema, bronchial asthma, urticaria).
8. The tonic reaction of the pupils consists of an extremely slow dilation of the pupils after their constriction upon exposure to light. This reaction is caused by increased excitability of parasympathetic pupillary efferent fibers and is observed mainly in alcoholism.
9. Myotonic reaction of the pupils (pupillotonia), pupillary disorders of the Eydie type can occur with diabetes mellitus, alcoholism, vitamin deficiencies, Guillain-Barré syndrome, peripheral autonomic disorder, rheumatoid arthritis.
10. Pupillary disorders of the Argyll Robertson type. The clinical picture of Argyll Robertson syndrome, which is specific for syphilitic damage to the nervous system, includes such signs as miosis, slight anisocoria, lack of reaction to light, deformation of the pupils, bilateral disorders, constant pupil sizes during the day, lack of effect from atropine, pilocarpine and cocaine . A similar picture of pupillary disorders can be observed in a number of diseases: diabetes mellitus, multiple sclerosis, alcoholism, cerebral hemorrhage, meningitis, Huntington's chorea, pineal adenoma, pathological regeneration after paralysis of the extraocular muscles, myotonic dystrophy, amyloidosis, Parinaud's syndrome, Munchmeyer's syndrome (vasculitis, which underlies interstitial muscle swelling and subsequent proliferation of connective tissue and calcification), Denny-Brown sensory neuropathy (congenital lack of pain sensitivity, lack of pupillary response to light, sweating, increased blood pressure and increased heart rate with severe painful stimuli), pandysautonomia, familial dysautonomia Riley-Day, Fisher syndrome (acute development of complete ophthalmoplegia and ataxia with decreased proprioceptive reflexes), Charcot-Marie-Tooth disease. In these situations, Argyll Robertson syndrome is called nonspecific.
11. Premortal pupillary reactions. The study of pupils in comatose states acquires great diagnostic and prognostic significance. In case of deep loss of consciousness, severe shock, coma, the reaction of the pupils is absent or sharply reduced. Immediately before death, the pupils in most cases become very constricted. If, in a comatose state, miosis is gradually replaced by progressive mydriasis, and there is no pupillary reaction to light, then these changes indicate the imminence of death.

The following are pupillary disorders associated with impaired parasympathetic function.

1. Reaction to light and pupil size under normal conditions depend on adequate light reception in at least one eye. In a completely blind eye there is no direct reaction to light, but the size of the pupil remains the same as on the side of the intact eye. In case of complete blindness in both eyes with lesions in the area anterior to the lateral geniculate bodies, the pupils remain dilated and do not react to light. If bilateral blindness is caused by destruction of the occipital lobe cortex, then the light pupillary reflex is preserved. Thus, it is possible to meet completely blind patients with normal pupillary reaction to light.

Lesions of the retina, optic nerve, chiasma, optic tract, retrobulbar neuritis in multiple sclerosis cause certain changes in the functions of the afferent system of the light pupillary reflex, which leads to a violation of the pupillary reaction, known as the Marcus Hun pupil. Normally, the pupil reacts to bright light by rapidly constricting. Here the reaction is slower, incomplete and so short that the pupil may immediately begin to dilate. The reason for the pathological reaction of the pupil is a decrease in the number of fibers providing the light reflex on the affected side.

1. Damage to one optic tract does not lead to a change in pupil size due to the preserved light reflex on the opposite side. In this situation, illumination of the intact areas of the retina will give a more pronounced reaction of the pupil to light. This is called Wernicke's pupillary reaction. It is very difficult to cause such a reaction due to the dispersion of light in the eye.
2. Pathological processes in the midbrain (zone of the anterior colliculus) can affect the fibers of the reflex arc of the pupil's reaction to light that intersect in the area of ​​the brain aqueduct. The pupils are dilated and do not react to light. This is often combined with the absence or limitation of upward movements of the eyeballs (vertical gaze paresis) and is called Parinaud's syndrome.
3. Argyll Robertson syndrome.
4. With complete damage to the third pair of cranial nerves, pupil dilation is observed due to the absence of parasympathetic influences and ongoing sympathetic activity. In this case, signs of damage to the motor system of the eye, ptosis, and deviation of the eyeball in the inferolateral direction are detected. The causes of severe damage to the III pair may be a carotid artery aneurysm, tentorial hernias, progressive processes, Tolosa-Hunt syndrome. In 5% of cases with diabetes mellitus, an isolated lesion of the third cranial nerve occurs, while the pupil often remains intact.
5. Eydie syndrome (pupillotonia) is a degeneration of nerve cells of the ciliary ganglion. There is a loss or weakening of the pupil's reaction to light while the reaction to close gaze is intact. Characteristic features include one-sidedness of the lesion, dilation of the pupil, and its deformation. The phenomenon of pupillotonia is that the pupil narrows very slowly during convergence and especially slowly (sometimes only within 2-3 minutes) returns to its original size after the convergence stops. The size of the pupil is not constant and changes throughout the day. In addition, pupil dilation can be achieved by keeping the patient in the dark for a long time. There is an increase in the sensitivity of the pupil to vegetotropic substances (sharp dilation from atropine, sharp constriction from pilocarpine).

Such hypersensitivity of the sphincter to cholinergic drugs is detected in 60-80% of cases. In 90% of patients with tonic Eidi pupils, tendon reflexes are weakened or absent. This weakening of reflexes is widespread, affecting the upper and lower extremities. In 50% of cases, bilateral symmetrical lesions are observed. Why tendon reflexes are weakened in Eydie syndrome is unclear. Hypotheses are proposed about widespread polyneuropathy without sensory impairment, degeneration of spinal ganglion fibers, a peculiar form of myopathy, and a neurotransmission defect at the level of spinal synapses. The average age of illness is 32 years. More often observed in women. The most common complaint, besides anisocoria, is blurred vision when looking at nearby objects. In approximately 65% ​​of cases, residual accommodation paresis is observed in the affected eye. After several months, there is a pronounced tendency towards normalization of the force of accommodation. In 35% of patients, any attempt to look at close range can provoke astigmatism in the affected eye. This is presumably due to segmental paralysis of the ciliary muscle. When examined under slit lamp light, some difference in the pupillary sphincter can be noted in 90% of the affected eyes. This residual reaction is always a segmental contraction of the ciliary muscle.

Over the years, a narrowing of the pupil appears in the affected eye. There is a pronounced tendency for a similar process to occur in the other eye after a few years, so that anisocoria becomes less noticeable. Eventually both pupils become small and do not respond well to light.

It has recently been established that the dissociation of pupillary response to light and accommodation, often observed in Eydie syndrome, can only be explained by the diffusion of acetylcholine from the ciliary muscle into the posterior chamber towards the denervated pupillary sphincter. It is likely that the diffusion of acetylcholine into the aqueous humor contributes to the tension of iris movements in Adie syndrome, but it is also quite clear that the mentioned dissociation cannot be explained so unambiguously.

The pronounced reaction of the pupil to accommodation is most likely due to pathological regeneration of accommodative fibers in the sphincter of the pupil. The nerves of the iris have an amazing ability to regenerate and reinnervate: a fetal rat heart transplanted into the anterior chamber of an adult eye will grow and contract in a normal rhythm, which can vary depending on the rhythmic stimulation of the retina. The nerves of the iris can grow into the transplanted heart and set the heart rate.

In most cases, Eydie syndrome is an idiopathic disease, and the cause of its occurrence cannot be found. Secondarily, Eydie syndrome can occur in various diseases (see above). Familial cases are extremely rare. Cases of a combination of Agey syndrome with autonomic disorders, orthostatic hypotension, segmental hypohidrosis and hyperhidrosis, diarrhea, constipation, impotence, and local vascular disorders have been described. Thus, Eydie syndrome can act as a symptom at a certain stage in the development of a peripheral autonomic disorder, and sometimes it can be its first manifestation.

Blunt trauma to the iris can lead to rupture of short ciliary branches in the sclera, which is clinically manifested by deformation of the pupils, their dilation and impaired (weakened) reaction to light. This is called post-traumatic iridoplegia.

The ciliary nerves can be affected by diphtheria, causing dilated pupils. This usually occurs in the 2-3rd week of the disease and is often combined with paresis of the soft palate. Impaired pupillary function is usually completely restored.

Pupillary disorders associated with impaired sympathetic function

Damage to the sympathetic pathways at any level is manifested by Horner's syndrome. Depending on the level of damage, the clinical picture of the syndrome may be complete or incomplete. The complete Horner's syndrome looks like this:

1. narrowing of the palpebral fissure. Cause: paralysis or paresis of the superior and inferior tarsal muscles, which receive sympathetic innervation;
2. miosis with normal pupil reaction to light. Cause: paralysis or paresis of the muscle that dilates the pupil (dilator); intact parasympathetic pathways to the constrictor pupillary muscle;
3. enophthalmos. Cause: paralysis or paresis of the orbital muscle of the eye, which receives sympathetic innervation;
4. homolateral facial anhidrosis. Cause: disruption of the sympathetic innervation of the sweat glands of the face;
5. conjunctival hyperemia, vasodilation of skin vessels of the corresponding half of the face. Cause: paralysis of the smooth muscles of the blood vessels of the eye and face, loss or insufficiency of sympathetic vasoconstrictor influences;
6. heterochromia of the iris. Cause: sympathetic insufficiency, as a result of which the migration of melanophores into the iris and choroid is disrupted, which leads to disruption of normal pigmentation at an early age (up to 2 years) or depigmentation in adults.

Symptoms of incomplete Horner's syndrome depend on the level of damage and the degree of involvement of sympathetic structures.

Horner's syndrome can be of central origin (damage to the first neuron) or peripheral (damage to the second and third neurons). Large studies of patients hospitalized in neurological departments with this syndrome revealed its central origin in 63% of cases. Its connection with a stroke was established. In contrast, researchers observing outpatients in eye clinics found the central nature of Horner's syndrome in only 3% of cases. In Russian neurology, it is generally accepted that Horner's syndrome occurs most regularly with peripheral damage to sympathetic fibers.

Congenital Horner's syndrome. Its most common cause is birth trauma. The immediate cause is damage to the cervical sympathetic chain, which can be combined with damage to the brachial plexus (most often its lower roots - Dejerine-Klumpke palsy). Congenital Horner's syndrome is sometimes combined with facial hemiatrophy, with developmental anomalies of the intestine and cervical spine. Congenital Horner's syndrome can be suspected by ptosis or heterochromia of the iris. It also occurs in patients with cervical and mediastinal neuroblastoma. To diagnose this disease, all newborns with Horner's syndrome are offered a chest radiography and a screening method to determine the level of mandelic acid excretion, which can be elevated.

The most characteristic feature of congenital Horner's syndrome is heterochromia of the iris. Melanophores move into the iris and choroid during embryonic development under the influence of the sympathetic nervous system, which is one of the factors influencing the formation of the melanin pigment, and thus determines the color of the iris. In the absence of sympathetic influences, the pigmentation of the iris may remain insufficient, its color will become light blue. Eye color is established several months after birth, and the final pigmentation of the iris ends by the age of two. Therefore, the phenomenon of heterochromia is observed mainly in congenital Horner syndrome. Depigmentation following disruption of the sympathetic innervation of the eye in adults is extremely rare, although isolated well-documented cases have been described. These cases of depigmentation indicate that some kind of sympathetic influence on melanocytes continues in adults.

Horner's syndrome of central origin. Hemispherectomy or extensive infarction of one hemisphere can cause Horner's syndrome on that side. The sympathetic pathways in the brainstem run adjacent to the spinothalamic tract throughout its entire length. As a result, Horner's syndrome of stem origin will be observed simultaneously with a violation of pain and temperature sensitivity on the opposite side. The causes of such damage can be multiple sclerosis, pontine glioma, brainstem encephalitis, hemorrhagic stroke, thrombosis of the posterior inferior cerebellar artery. In the last two cases, at the onset of vascular disorders, Horner's syndrome is observed along with severe dizziness and vomiting.

When involved in the pathological process, in addition to the sympathetic pathway, nuclei V or IX, X pairs of cranial nerves, analgesia, thermaneesthesia of the face on the ipsilateral side or dysphagia with paresis of the soft palate, pharyngeal muscles, and vocal cords will be observed, respectively.

Due to the more central location of the sympathetic pathway in the lateral columns of the spinal cord, the most common causes of damage are cervical syringomyelia and intramedullary spinal tumors (glioma, ependymoma). Clinically, this is manifested by a decrease in pain sensitivity in the hands, a decrease or loss of tendon and periosteal reflexes in the hands, and bilateral Horner's syndrome. In such cases, the first thing that attracts attention is ptosis on both sides. The pupils are narrow, symmetrical, and have a normal reaction to light.

Horner's syndrome of peripheral origin. Damage to the first thoracic root is the most common cause of Horner's syndrome. It should, however, immediately be noted that pathology of the intervertebral discs (hernia, osteochondrosis) rarely manifests itself as Horner's syndrome. The passage of the first thoracic root directly above the pleura of the apex of the lung causes its damage in malignant diseases. Classic Pancoast syndrome (cancer of the apex of the lung) presents with pain in the armpit, atrophy of the (small) muscles of the arm, and Horner's syndrome on the same side. Other causes are root neurofibroma, accessory cervical ribs, Dejerine-Klumpke palsy, spontaneous pneumothorax, and other diseases of the apex of the lung and pleura.

The sympathetic chain at the cervical level can be damaged due to surgical interventions on the larynx, thyroid gland, injuries in the neck, tumors, especially metastases. Malignant diseases in the area of ​​the jugular foramen at the base of the brain cause various combinations of Horner's syndrome with damage to the IX, X, XI and CP pairs of cranial nerves.

If the fibers running as part of the plexus of the internal carotid artery are damaged above the superior cervical ganglion, Horner's syndrome will be observed, but only without sweating disorders, since the sudomotor pathways to the face run as part of the plexus of the external carotid artery. Conversely, sweating disorders without pupillary disorders will occur when fibers of the external carotid plexus are involved. It should be noted that a similar picture (anhidrosis without pupillary disturbances) can be observed when the sympathetic chain is damaged caudal to the stellate ganglion. This is explained by the fact that the sympathetic pathways to the pupil, passing through the sympathetic trunk, do not descend below the stellate ganglion, while the sudomotor fibers going to the sweat glands of the face leave the sympathetic trunk, starting from the superior cervical ganglion and ending with the superior thoracic sympathetic ganglia.

Injuries, inflammatory or blastomatous processes in the immediate vicinity of the trigeminal (Gasserian) ganglion, as well as syphilitic osteitis, carotid artery aneurysm, alcoholization of the trigeminal ganglion, herpes ophthalmicus are the most common causes of Roeder syndrome: damage to the first branch of the trigeminal nerve in combination with Horner's syndrome. Sometimes damage to the cranial nerves IV and VI pairs occurs.

Pourfur du Petit syndrome is the reverse of Horner's syndrome. In this case, mydriasis, exophthalmos and lagophthalmos are observed. Additional symptoms: increased intraocular pressure, changes in the vessels of the conjunctiva and retina. This syndrome occurs with local action of sympathomimetic drugs, rarely with pathological processes in the neck area, when the sympathetic trunk is involved, as well as with irritation of the hypothalamus.

Argyle-Robertson pupils

Argyle-Robertson pupils are small, unequally sized and irregularly shaped pupils with poor response to light in darkness and good response to accommodation with convergence (dissociated pupillary response). It is necessary to differentiate between Argyll-Robertson's sign (a relatively rare sign) and Edie's bilateral tonic pupils, which are more common.

Pupillary reflex

The pupil is an opening in the iris of the eye. Normally, its diameter ranges from 1.5 mm in bright light and up to 8 mm in the dark.

Pupillary reflex - a change in the diameter of the pupil under the influence of various stimuli. By increasing its diameter, the flow of light rays to the retina can increase 30 times.

Pupil dilation (mydriasis) - observed in the dark, when examining distant objects, when the sympathetic system is excited, in pain, fear, asphyxia, blockade of the parasympathetic system, under the influence of chemicals, for example, atropine, which blocks M-cholinergic receptors; the latter is used in the eye clinic to dilate the pupil for the purpose of thorough examination of the fundus.

Constriction of the pupil (miosis) - observed when exposed to bright light, when examining close objects (when reading), when the parasympathetic system is excited, when the sympathetic system is blocked.

The pupillary reflex mechanism is reflexive and has a different reflex arc depending on the lighting. When exposed to bright light, stimulation occurs in the retina of the eye. Impulses from it arrive as part of the optic nerve to the midbrain (superior colliculi). From here to the paired autonomic nucleus of the oculomotor nerve (III pair) (Yakubovich - Edinger - Westphal). As part of its branches, impulses are sent to the ciliary ganglion, and postganglionic fibers are sent to the muscle that constricts the pupil (m. Sphincter pupillae)(See Fig. 12.8).

In the dark, on the contrary, the sympathetic centers located in the lateral horns of the CB and T1.2 segments of the spinal cord are excited. From here the impulses are sent to the superior cervical sympathetic ganglion. Postganglionic fibers as part of the sympathetic nerves enter the muscles, dilating the pupil (t. Dilatator pupillae). It should be emphasized that the work of the muscles that constrict or dilate the pupil of both eyes is coordinated; When the pupil of one eye dilates or contracts, a friendly reaction occurs in the other.

The meaning of the pupillary reflex:

Provides elimination of spherical aberration. When the pupil constricts, peripheral rays are cut off.

The pupil is involved in adapting the visual system to changes in lighting.

In the dark the pupil dilates and when exposed to light it contracts.

Participates in ensuring clear vision of objects located at various distances. When viewing close objects (when reading), the pupil narrows, and when viewing distant objects, it expands.

Protective function. By constricting when exposed to bright light, the pupil ensures the preservation of retinal pigments from excessive destruction.

Clinical significance. The state of the pupils indicates the level of excitability of the brain stem centers.

In this regard, the pupillary reflex is used to control the depth of anesthesia. It allows you to diagnose damage to the centers in which the nuclei are located, regulating pupil width, pain effects, etc.

Rice. 12.9. The structure of the retina

Physiology of the retina

Histologically, ten layers are distinguished in the retina, but there are fewer functional layers involved in the perception of light stimuli and their processing. The layer of pigment epithelium farthest from light is the layer of pigment epithelium. The next layer, closer to the light, is the layer of photoreceptors - cones and rods. Even closer to the light is a layer of bipolar, horizontal and amacrine cells. Closest to the light is the layer of ganglion cells, the axons of which form the optic nerve.

A healthy nerve extends beyond the eyeball 3 mm medially and slightly above its posterior pole. This area does not contain photosensitive receptors and is therefore called the blind spot.

The pigment layer is the outer layer of the retina (Fig. 12.9). Its name comes from the fact that it contains the black pigment melanin.

Due to the presence of melanin, light rays are not reflected but absorbed. The significance of the pigment layer is also associated with the presence of vitamin A in it, which comes from it to the outer segments of the photoreceptors. There, vitamin A is used for the resynthesis of visual pigments. In case of insufficient amount of vitamin A, the disease “night blindness” develops - hemeralopia (or nyctalopia). The vision of such people decreases sharply at dusk.

The importance of the pigment layer also lies in the fact that it provides (due to its close connection with the choroid) the transfer of O2 and nutrients to receptor cells.

Functional layers of the retina

There are 3 functional layers in the retina:

Layer of photoreceptor cells;

Layer of bipolar, horizontal and amacrine cells;

Layer of ganglion cells.

The role of photoreceptor cells There are 2 types of photoreceptor cells: cones and rods. They have a general structure plan. Both cones and rods consist of the following parts: an outer segment, a connecting stalk, an inner segment and a nuclear part of the synaptic terminal (Fig. 12.10).

The outer segments of the rods contain rhodopsin, and the cones contain iodopsin.

There are up to 123 million rods, and only 6-7 million cones. In the area of ​​the central fovea there are only cones, there are few of them at the periphery and they are absent in the extreme parts of the retina. The rods are mostly located on the periphery, especially in areas distant from the central fovea.

The pupil (lat. pupilla, pupula) is a circle in the very center of the iris. It has a distinctive feature: thanks to the work of the muscles (sphincter and dilator), it becomes possible to regulate the flow of light directed at the retina. In bright sunlight or electric lighting, the sphincter becomes tense and the pupil narrows, blinding rays are cut off, the image becomes clear, without blur.

In twilight lighting, on the contrary, the pupil dilates (thanks to the dilator). All this is called the “diaphragmatic function”, which is provided by the pupillary reflex.

Pupillary reflex, symptoms of damage

Pupillary reflex: how it occurs

Any reflex has two directions:

• Sensitive - it transmits information to the nerve centers;
• Motor - transmits information from nerve centers directly to tissues. It is precisely this that is the response to an irritating impulse.

Pupil response(lat. pupilla, pupula) the irritating effects of light can be:

• Direct - in which the light has a direct effect directly on the eye being examined;
• Friendly - when the result of the influence of light is observed in the eye, which was not affected.

In addition to the reaction to lighting, pupula (Latin) reacts to the work of convergence (tension of the internal rectus muscles of the eyes) and accommodation - tension of the ciliary muscle, it occurs when a person moves his eyes from an object located in the distance to an object located nearby.

In addition, pupilla expansion can cause:

Pupula narrowing occurs:

• With irritation of the trigeminal nerve;
• With apathy, decreased excitability;
• When taking medications that target the muscle receptors in the eyes directly.

The pupil is affected: symptoms

When the pupilla (Latin) is affected, its constant narrowing or expansion is monitored, regardless of exposure to light on the eyes.

Symptoms:

• Change of form pupilla (Latin);
• Hippus - the shape of the pupil changes in attacks that last several seconds;
• Fixed (amaurotic) - a direct reaction occurs in the blind eye, which is exposed to light, and a friendly reaction in the sighted eye;
• Nystagmus is involuntary rapid repetitive eye movements;
• "Jumping pupils" - periodic dilation of the pupilla (Latin) in both eyes, while the reaction to light is normal;
• Anisocoria - pupils of different sizes in the right and left eyes.

Diagnosis of the lesion

• Visual inspection, determination of pupil equidistance;
• Studying the reaction to exposure to a light source;
• Studying the reaction of the pupula when studying the work of other muscles of the organs of vision;
• Pupillometry (in case of pathology) - study the size of the pupil and the dynamics of its change.

Diseases that affect the pupillary reflex

Diseases that may cause a change in the reaction of the pupula (Latin) to a light source, as well as

The physiology of sensory systems is based on reflex activity. The pupillary reflex is a friendly reaction of both pupils to light. Its adequacy is determined by the coordinated activity of all components of the neural arch, consisting of 4 neurons and the brain center. The eyes do not immediately react to flash or darkness. It takes a fraction of a second for the impulse to reach the brain areas. Too sluggish a reaction indicates pathology at some stage of the reflex chain.

Normally, the direct reaction of constriction and dilation of the pupillary fissure in response to fluctuations in lighting around the human head depends on the adequate activity of afferent and efferent nerve fibers. It is also influenced by the functioning of the center in the optical cortex of the occipital hemispheres of the brain.

Anatomy of the eyeball and nerves

The arc of the pupillary reflex begins on the retina and passes through several nerve regions. In order to better navigate the sequence of movement of impulses to the target point, below is a diagram of the anatomical structure of the eye analyzer:

• Cornea. It is the first obstacle in the path of the light beam. This transparent structure consists of a dense row of cells, the structure of which is dominated by cytoplasm.
• Front camera. It does not contain liquid. This cavity limits the pupillary opening in front.
• Pupil. It is a hole surrounded on all sides by the iris. It is the pigmentation of the latter that gives the eyes their color.
• Lens. It is considered the second refractive structure after the cornea. According to its anatomy, the lens is a biconvex lens, capable of changing curvature due to the contraction and relaxation of the accommodative muscles and the ciliary body.
• Rear camera. It is filled with vitreous humor, which is a gel-like mass that conducts light rays.
• Retina. This is a collection of nerve cells - rods and cones. The former capture light, the latter determine the color of objects around.
• Optic nerve. It conducts light impulses accumulated by rods and cones to the optic tract.
• Bactrian bodies. They are structures of the central nervous system.
• Axons heading to the Jakubovich or Edinger-Westphal nuclei. These fibers represent the afferent site of the unconditioned reflex.
• Axons of parasympathetic oculomotor nerves to the ciliary ganglion.
• Short fibers of neurons of the ciliary ganglion to the muscles that constrict the pupil. They close the reflex arc.

What is he?

Depending on the lighting, a person’s pupil changes: in weak light it expands, in strong light it narrows.

The normal reaction of the pupil to light or photoreaction is a narrowing of the pupillary slit when there is an abundant supply of light photons and its widening in low light. The pupillary reflex pathways begin on the light-refracting structures of the eyeball. Captured by the light-sensitive cells of the retina - rods and cones - photons of light are recorded by specific pigments and arrive in the form of nerve impulses to the optic nerve. From there, through neurotransmitters along myelinated fibers, the impulse passes into the afferent part of the nerve pathway. Afferentation ends at the level of the midbrain nuclei of Yakubovich or Edinger-Westphal. They are also called accessory nuclear structures of the oculomotor nerve. From the tegmentum of the brain stem, impulses through the conductive area enter the muscle fibers, causing the pupillary fissure to expand and contract.

How does the verification take place?

Pupillary response to light is studied in ophthalmology clinics or physical therapy offices. Its demonstration is made possible with the help of a special lamp that supplies pulsating light with different frequencies and strengths. Under the influence of light rays, the nerves that conduct impulses are excited and the doctor registers reflex movements. Using the same technique, convergence and divergence are studied. Their adequacy indicates full binocular vision. Before starting the study, it is necessary to take into account the concomitant medical history. If the diagnosis is carried out in a person who abuses psychoactive substances, is intoxicated, or has a complicated neurological history, adjustments should be made in advance for these characteristics. Physiology studies the mechanics of testing and the boundaries of normal and pathological results.

Normal limits

The change in diameter with normal vision occurs synchronously; in another case, pathology is diagnosed.

The reaction of the pupils to an increase or decrease in the intensity of the glow should be bilateral and synchronous. A slight difference in diameter is allowed if a person has previously been diagnosed with unilateral myopia or hypermetropia. These medical terms refer to nearsightedness or farsightedness in one eye. In such patients, the affected eyeball must capture slightly less or more light, thereby regulating the number of photons reaching the retina. In healthy people, the pupillary diameter varies between 1.2-7.8 mm. In a brown-eyed person, this value will always be higher, since the dark pigment melanin additionally protects the retina from excessive insolation.

IX-XII PAIRS OF CN: STRUCTURE, RESEARCH, SYMPTOMS AND SYNDROMES OF LESION

Obstetric ultrasound examination for diagnosing pregnancy

Pupillary reflexes are examined using a number of tests: pupillary reaction to light, pupillary reaction to convergence, accommodation, pain. The pupil of a healthy person has a regular round shape with a diameter of 3-3.5 mm. Normally, the pupils are the same in diameter. Pathological changes in the pupils include miosis - narrowing of the pupils, mydriasis - their dilation, anisocoria (pupillary inequality), deformation, disorder of the pupils' reaction to light, convergence and accommodation. The study of pupillary reflexes is indicated when selecting for classes in sports sections, when conducting an in-depth medical examination (IME) of athletes, as well as for head injuries in boxers, hockey players, wrestlers, bobsledders, acrobats and in other sports where frequent head injuries occur.

Pupillary reactions are examined in bright diffuse lighting. The lack of reaction of the pupils to light is confirmed by examining them through a magnifying glass. When the pupil diameter is less than 2 mm, the reaction to light is difficult to assess, so too bright lighting makes diagnosis difficult. Pupils with a diameter of 2.5-5 mm that react equally to light usually indicate the preservation of the midbrain. Unilateral dilatation of the pupil (more than 5 mm) with the absence or decrease in its reaction to light occurs with damage to the midbrain on the same side or, more often, with secondary compression or tension of the oculomotor nerve as a result of herniation.

Usually the pupil dilates on the same side where the space-occupying lesion is located in the hemisphere, less often on the opposite side due to compression of the midbrain or compression of the oculomotor nerve by the opposite edge of the tentorium cerebellum. Oval and eccentrically located pupils are observed in the early stages of compression of the midbrain and oculomotor nerve. Equally dilated pupils that do not respond to light indicate severe damage to the midbrain (usually as a result of compression during temporotentorial herniation) or poisoning with M-anticholinergic drugs.

Unilateral constriction of the pupil in Horner's syndrome is accompanied by a lack of pupil dilation in the dark. This coma syndrome is rare and indicates extensive hemorrhage into the ipsilateral thalamus. The tone of the eyelid, assessed by raising the upper eyelid and the speed of closing the eye, decreases as the coma deepens.

Methodology for studying the reaction of pupils to light. The doctor tightly covers both eyes of the patient with his palms, which should be wide open at all times. Then, one by one, the doctor quickly moves his palm away from each eye, noting the reaction of each pupil.

Another option for studying this reaction is to turn on and off an electric lamp or a portable flashlight, brought to the patient’s eye, the patient tightly covers the other eye with his palm.

The study of pupillary reactions should be carried out with the utmost care using a sufficiently intense light source (poor illumination of the pupil may either not constrict at all or cause a sluggish reaction).

Methodology for studying the reaction to accommodation with convergence. The doctor asks the patient to look into the distance for a while, and then quickly move his gaze to fixate an object (finger or hammer) brought close to the eyes. The study is carried out separately for each eye. In some patients, this method of studying convergence is difficult and the doctor may have a false opinion about convergence paresis. For such cases, there is a “testing” version of the study. After looking into the distance, the patient is asked to read a small written phrase (for example, a label on a matchbox) held close to the eyes.

Most often, changes in pupillary reactions are symptoms of syphilitic damage to the nervous system, epidemic encephalitis, less often - alcoholism and organic pathologies such as damage to the stem region, cracks in the base of the skull.

Study of the position and movements of the eyeballs. With pathology of the oculomotor nerves (III, IV and VI pairs), convergent or divergent strabismus, diplopia, limited movements of the eyeball to the sides, up or down, and drooping of the upper eyelid (ptosis) are observed.

It should be remembered that strabismus can be a congenital or acquired visual defect, but the patient does not experience double vision. When one of the oculomotor nerves is paralyzed, the patient experiences diplopia when looking towards the affected muscle.

More valuable for diagnosis is the fact that when clarifying complaints, the patient himself declared double vision when looking in any direction. During the survey, the doctor should avoid leading questions about double vision, because a certain contingent of patients will answer in the affirmative even in the absence of data for diplopia.

To find out the causes of diplopia, it is necessary to determine the visual or oculomotor disorders present in a given patient.

The method used for the differential diagnosis of true diplopia is extremely simple. If there are complaints of double vision in a certain direction of gaze, the patient should close one eye with the palm of his hand - true diplopia disappears, but in the case of hysterical diplopia, the complaints remain.

The technique for studying eye movements is also quite simple. The doctor asks the patient to follow an object moving in different directions (up, down, to the sides). This technique allows you to detect damage to any eye muscle, gaze paresis, or the presence of nystagmus.

The most common horizontal nystagmus is detected when looking to the sides (the abduction of the eyeballs should be maximum). If nystagmus is a single identified symptom, then it cannot be called a clear sign of organic damage to the nervous system. In completely healthy people, examination may also reveal “nystagmoid” eye movements. Persistent nystagmus is often found in smokers, miners, and divers. There is also congenital nystagmus, characterized by rough (usually rotatory) twitching of the eyeballs that persists with a “static position” of the eyes.

The diagnostic technique for determining the type of nystagmus is simple. The doctor asks the patient to look up. With congenital nystagmus, its intensity and character (horizontal or rotatory) are preserved. If nystagmus is caused by an organic disease of the central nervous system, then it either weakens, becoming vertical, or completely disappears.

If the nature of the nystagmus is unclear, it is necessary to examine it by moving the patient to a horizontal position, alternately on the left and right side.

If nystagmus persists, abdominal reflexes should be examined. The presence of nystagmus and extinction of abdominal reflexes together are early signs of multiple sclerosis. The symptoms that confirm the presumptive diagnosis of multiple sclerosis should be listed:

1) complaints of periodic double vision, fatigue of the legs, urination disorders, paresthesia of the extremities;

2) detection during examination of an increase in the unevenness of tendon reflexes, the appearance of pathological reflexes, and intentional trembling.