Cough

Slow pupil reaction to light. Pupillary reflex and signs of its damage

If patients do not have an eye reaction to a light stimulus, a number of questions arise. First of all, you should understand the causes of the manifestation, which may relate to congenital diseases or traumatic injury. Doctors note that symptoms can be confused with serious diseases. A diagnosis of the optic nerves is prescribed, and then complex treatment is used to eliminate the causes.

The pupil dilates due to injuries, in particular cranial injuries, as a result of taking drugs, alcohol, as well as due to eye diseases, chronic pathologies of other organs and systems.

Causes of pathology

When patients are faced with the problem of lack of reaction of the pupils to changes in ambient light, this is a reason to urgently contact a specialist. Such manifestations may occur primarily due to the following reasons:

injured nerve, which is responsible for the movement of the visual organs;
disruption of the structure of the ciliary ganglion, which is visualized as different pupils;
injuries to the sphincter of the eye pupil;
influence of long-term course of medications.

Constriction of the pupils can be caused by an attack of fear.

The pupil does not narrow sufficiently due to age-related characteristics. This is due in part to loss of sensation. Doctors also say that narrow pupils of the eye do not always signal the development of the disease. This happens when exposed to the following factors:

low lighting, in which the visual organs do not need protection from excess light;
when a person experiences strong emotions: fear, panic or anger;
when the patient looks with love or strong sympathy, during which the sympathetic nervous system is activated and provokes mydriasis.

How to distinguish from a disease: manifestations

Pay attention to the fact that when exposed to bright light, the pupil quickly becomes narrow and small from a wide one. The absence of the disease is indicated by the correct symmetry of the face when emotions appear. Usually in such cases, against the background of pathologies, when smiling, it feels like the person is baring his teeth, puffing out his cheeks, or spreading his lips too wide. With physiological mydriasis, no pain should be felt, and there should be no mucus or pus discharge from the eyes. Body temperature is normal, normal sensitivity in the extremities, absence of nausea and vomiting - this indicates that there is no pathology.

Patients in a coma have dilated pupils.

An unnaturally wide pupil and the absence of other signs of life may indicate clinical or biological death. But there are a number of differences that are presented in the table:

When the pupils are dilated unevenly, they speak of anisocoria, which manifests itself as a result of diseases of the nervous system, osteochondrosis of the cervicothoracic zone, pulmonary tuberculosis, pleurisy, and aortic pathologies. It can occur in healthy people, then the characteristic difference is that the left eye is narrower than the right.

The eyes are a fairly important organ for the normal functioning of the body and a full life. The main function is the perception of light stimuli, which is why the picture appears.

Structural features

This peripheral one is located in a special cavity of the skull called the orbit. The eye is surrounded on the sides by muscles with which it is held and moved. The eye consists of several parts:

Directly the eyeball, which has the shape of a ball measuring about 24 mm. It consists of the lens and aqueous humor. All this is surrounded by three membranes: protein, vascular and reticular, arranged in reverse order. The elements that make up the picture are located on the mesh shell. These elements are receptors that are sensitive to light;
The protective apparatus, which consists of the upper and lower eyelids, the orbit;
Adnexal apparatus. The main components are the lacrimal gland and its ducts;
The oculomotor system, which is responsible for the movements of the eyeball and consists of muscles;

Basic functions

The main function that vision performs is to distinguish between various physical characteristics of objects, such as brightness, color, shape, size. In combination with the action of other analyzers (hearing, smell and others), it allows you to regulate the position of the body in space, as well as determine the distance to an object. That is why prevention of eye diseases must be carried out with enviable regularity.

Presence of pupillary reflex

With the normal functioning of the organs of vision, with certain external reactions, so-called pupillary reflexes occur, in which the pupil narrows or dilates. The pupil of which is the anatomical substrate of the pupil's reaction to light, indicates the health of the eyes and the whole organism as a whole. That is why, in some diseases, the doctor first checks for the presence of this reflex.

What is the reaction?

The reaction of the pupil or the so-called pupillary reflex (other names are iris reflex, iritic reflex) is some change in the linear dimensions of the pupil of the eye. Constriction is usually caused by contraction of the muscles of the iris, and the reverse process - relaxation - leads to dilation of the pupil.

Possible reasons

This reflex is caused by a combination of certain stimuli, the main one of which is considered to be a change in the level of illumination of the surrounding space. In addition, changes in pupil size can occur for the following reasons:

the effect of a number of medications. That is why they are used as a way to diagnose drug overdose or excessive depth of anesthesia;
changing a person's point of focus;
emotional outbursts, both negative and positive in equal measure.

If there is no reaction

The absence of a pupil's reaction to light may indicate various human conditions that pose a danger to life and require immediate intervention from specialists.

Diagram of the pupillary reflex

The muscles that control the functioning of the pupil can easily influence its size if they receive a certain stimulus from the outside. This allows you to regulate the flow of light that enters directly into the eye. If the eye is covered from the incoming sunlight and then opened, the pupil, which previously expanded in the dark, immediately decreases in size when light appears. The pupillary arc of which begins on the retina indicates the normal functioning of the organ.

The iris has two types of muscles. One group is the circular muscle fibers. They are innervated by parasympathetic fibers of the optic nerve. If these muscles contract, then this process causes Another group to dilate the pupil. It includes radial muscle fibers that are innervated by sympathetic nerves.

The pupillary reflex, the pattern of which is quite typical, occurs in the following order. Light that passes through and is refracted through the layers of the eye hits the retina directly. The photoreceptors that are located here are in this case the beginning of the reflex. In other words, this is where the path of the pupillary reflex begins. The innervation of the parasympathetic nerves affects the functioning of the sphincter of the eye, and the arc of the pupillary reflex contains it in its composition. The process itself is called the efferent arm. The so-called center of the pupillary reflex is located here, after which various nerves change their direction: some of them go through the cerebral peduncles and enter the orbit through the upper fissure, others - to the sphincter of the pupil. This is where the path ends. That is, the pupillary reflex closes. The absence of such a reaction may indicate some kind of disorder in the human body, which is why such great importance is attached to this.

Pupillary reflex and signs of its damage

When examining this reflex, several characteristics of the reaction itself are taken into account:

the amount of pupil constriction;
form;
uniformity of reaction;
pupil mobility.

There are several most popular pathologies indicating that the pupillary and accommodative reflexes are impaired, which indicates malfunctions in the body:

Amaurotic immobility of the pupils. This phenomenon represents the loss of a direct reaction when illuminating a blind eye and a friendly reaction if there are no problems with vision. The causes are most often a variety of diseases of the retina itself and the visual pathway. If the immobility is one-sided, is a consequence of amaurosis (retinal damage) and is combined with pupil dilation, albeit slight, then there is a possibility of developing anisocoria (the pupils become different sizes). With this disorder, other pupillary reactions are not affected in any way. If amaurosis develops on both sides (that is, both eyes are affected at the same time), then the pupils do not react in any way and even when exposed to sunlight remain dilated, that is, the pupillary reflex is completely absent.
Another type of amaurotic pupillary immobility is hemianopic pupillary immobility. Perhaps there is damage to the optic tract itself, which is accompanied by hemianopia, that is, blindness of half of the visual field, which is expressed by the absence of the pupillary reflex in both eyes.

Reflex immobility or Robertson's syndrome. It consists in the complete absence of both direct and friendly reactions of the pupils. However, unlike the previous type of lesion, the reaction to convergence (constriction of the pupils if the gaze is focused on a certain point) and accommodation (changes in the external conditions in which the person is located) is not impaired. This symptom is due to the fact that changes occur in the parasympathetic innervation of the eye when there is damage to the parasympathetic nucleus and its fibers. This syndrome may indicate the presence of a severe stage of syphilis of the nervous system; less often, the syndrome reports encephalitis, a brain tumor (namely in the region of the legs), as well as traumatic brain injury.

The causes may be inflammatory processes in the nucleus, root or trunk of the nerve responsible for eye movements, a lesion in the ciliary body, tumors, abscesses of the posterior ciliary nerves.

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.
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.
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.
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 chiasma area. Clinically, it is almost always combined with hemianopsia.
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.
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.
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).
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.
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.
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.
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.

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.

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.
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.
Argyll Robertson syndrome.
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.
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. The lesion is characterized by one-sidedness, 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 Eydie 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 pupillary sphincter. 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 combination of Eydi 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:

narrowing of the palpebral fissure. Cause: paralysis or paresis of the superior and inferior tarsal muscles, which receive sympathetic innervation;
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;
enophthalmos. Cause: paralysis or paresis of the orbital muscle of the eye, which receives sympathetic innervation;
homolateral facial anhidrosis. Cause: disruption of the sympathetic innervation of the sweat glands of the face;
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;
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 with this syndrome hospitalized in neurological departments 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 asked to undergo chest radiography and a screening method to determine the level of excretion of mandelic acid, 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 a lesion 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 the local action of sympathomimetic drugs, rarely with pathological processes in the neck, 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.

Parasympathetic nerve stimulation also stimulates the orbicularis iris muscle (pupillary sphincter). When it contracts, the pupil narrows, i.e. its diameter decreases. This phenomenon is called miosis. Conversely, stimulation of the sympathetic nerves excites the radial fibers of the iris, causing pupil dilation, called mydriasis.

Pupillary reflex to light. When light hits the eyes, the diameter of the pupil decreases. This reaction is called the pupillary light reflex. The neural pathway of this reflex is shown in the upper part of the figure with black arrows. When light hits the retina, a small number of impulses generated travel along the optic nerve to the pretectal nuclei. From here, secondary impulses go to the Westphal-Edinger nucleus and ultimately back through the parasympathetic nerves to the iris sphincter, causing its contraction. In the dark, the reflex is inhibited, which leads to pupil dilation.

Light reflex function- help the eye adapt extremely quickly to changes in light. The pupil diameter varies from approximately 1.5 mm at maximum constriction to 8 mm at maximum dilation. Since the brightness of light on the retina increases in proportion to the square of the pupil diameter, the range of light and dark adaptation that can be achieved by the pupillary reflex is about 30:1, i.e. The amount of light entering the eye due to the pupil can change 30 times.

Reflexes(or reactions) of the pupil with lesions of the nervous system. With some lesions of the central nervous system, the transmission of visual signals from the retina to the Westphal-Edinger nucleus is disrupted, which blocks pupillary reflexes. Such a blockade often occurs as a result of syphilis of the central nervous system, alcoholism, encephalitis and other lesions. The block usually occurs in the pretectal region of the brainstem, although it may result from destruction of some of the thin fibers of the optic nerves.

Fibers coming from the pretectal kernels to Westphal-Edinger kernels, mainly brake ones. Without their inhibitory influence, the nucleus becomes chronically active, causing, along with the loss of the pupil's reaction to light, a constant constriction of the pupil.

Besides, pupils may narrow more than normal when the Westphal-Edinger nucleus is stimulated by another route. For example, when the eyes fixate on a near object, the signals that cause accommodation of the lens and convergence of the two eyes at the same time lead to a slight constriction of the pupil. This is called the pupillary accommodation response. A pupil that does not respond to light, but responds to accommodation and at the same time is strongly constricted (Argill Robertson's pupil), is an important diagnostic symptom of damage to the central nervous system (often syphilitic in nature).

Horner's syndrome. Sometimes there is a violation of the sympathetic innervation of the eye, which is often localized in the cervical sympathetic chain. This causes a clinical condition called Horner's syndrome, the main manifestations of which are: (1) the pupil remains permanently constricted due to interruption of the sympathetic innervation of the dilator muscle compared to the pupil of the opposite eye; (2) the upper eyelid droops (it is normally kept open during waking hours partly by contraction of smooth muscle fibers embedded in the upper eyelid and innervated by the sympathetic nervous system).

Thus, destruction of sympathetic nerves makes it impossible to open the upper eyelid as wide as normal; (3) on the affected side, the blood vessels of the face and head are constantly dilated; (4) absence of sweating (which requires sympathetic nerve signals) in the face and head on the side affected by Horner's syndrome.

15-10-2012, 14:25

Description

The size of the pupil is determined by the balance between the sphincter and the dictator of the iris, the balance between the sympathetic and parasympathetic nervous system. Fibers of the sympathetic nervous system innervate the iris dilator. From the sympathetic plexus of the internal carotid artery, fibers penetrate into the orbit through the superior orbital fissure and, as part of the long ciliary arteries, innervate the iris dilator. To a greater extent, the size of the pupil is maintained by the parasympathetic nervous system, which innervates the iris sphincter. It is the parasympathetic innervation that supports the pupillary response to light. Efferent pupillary fibers as part of the oculomotor nerve enter the orbit and approach the ciliary ganglion. Postsynaptic parasympathetic fibers as part of the short ciliary nerves approach the sphincter of the pupil.

The normal pupil size, according to various authors, ranges from 2.5-5.0 mm, 3.5-6.0 mm. Perhaps such fluctuations are due not only to the age of the subjects, but also to the research methodology. Newborns and older people have a narrower pupil. With myopia, eyes with light irises have wider pupils. In 25% of cases in the general population, anisocoria is detected - a difference in the diameter of the pupils of one and the other eye; however, the difference in diameter should not exceed 1 mm. Anisocoria over 1 mm is regarded as pathological. Since the parasympathetic innervation of the pupils from the Edinger Westphal nucleus is bilateral, the direct and conjugate response to light is assessed.

The direct reaction of the pupil to light is on the side of the illuminated eye, the friendly reaction to light is the reaction on the other eye. In addition to the pupil's reaction to light, the reaction to convergence is assessed.

JUSTIFICATION

The size of the pupil, its reaction to light and convergence reflect the state of its sympathetic and parasympathetic innervation, the state of the oculomotor nerve and serve as an important indicator of the functional activity of the brain stem and reticular formation.

INDICATIONS

For the diagnosis of a brain tumor, hydrocephalus, traumatic brain injury, cerebral aneurysm, inflammatory processes of the brain and its membranes, syphilis of the central nervous system, trauma and space-occupying formations of the orbit, neck injury and the consequences of previous carotid angiography, tumors of the apex of the lung.

METHODOLOGY

The condition of the pupils must be assessed 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. Such lighting helps not only to assess the pupil, its diameter, shape, but also to identify anisocoria. Pupil size is measured using a pupillometric or millimeter ruler. On average it is 2.5-4.5 mm. A difference in the size of the pupil of one eye and the other eye of more than 0.9-1.0 mm is regarded as pathological anisocoria. To study the pupillary reaction to light, which is best done in a dark or darkened room, alternately illuminate each eye 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 lively than the friendly one. To assess the pupillary reaction to light, four gradations are usually used: lively, satisfactory, sluggish and no reaction.

In addition to the reaction to light, the reaction of the pupil to the act of convergence (or, as they say in foreign literature, to close distance) is assessed. Normally, the pupils constrict when the eyeballs converge.

When assessing the pupils, pupillary reaction to light and convergence, it is necessary to exclude pathology from the iris and pupillary edge. For this purpose, biomicroscopy of the anterior segment of the eye is indicated.

INTERPRETATION

Unilateral mydriasis with areflexia of the pupil to light (clivus edge symptom) is a sign of damage to the oculomotor nerve. In the absence of oculomotor disorders, the pupillomotor fibers are predominantly affected at the level of the brain stem (nerve root) or the nerve trunk at the point where it exits the brain stem. These symptoms 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 impaired 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 (n. oculomotorius - III cranial nerve). Due to the restriction of the mobility of the eyeball inwards, paralytic divergent strabismus develops. In addition to oculomotor disorders, partial (semiptosis) or complete ptosis of the upper eyelid is observed.

Optic nerve damage any etiology with the development of visual impairment from a slight decrease in visual acuity to amaurosis can also be the cause of unilateral mydriasis with the manifestation of the Markus Gunn symptom (afferent pupillary defect). In this case, anisocoria, in contrast to cases of damage to the oculomotor nerve, is mildly expressed, mydriasis on the affected side is small to moderate. In such cases, it is important to assess not only the direct reaction of the pupil to light on the side of mydriasis, which, depending on the degree of damage to the optic nerve, is reduced from satisfactory to absent, but also the friendly reaction of the pupil to light both on the side of mydriasis and on 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 patient with an afferent pupillary defect (Markus-Gunn symptom), the friendly reaction of the pupil on the side of mydriasis will be preserved if the friendly reaction of the other eye is impaired .

Tonic pupil (Adie's pupil)- wide pupil in one eye with a sluggish sectoral or practically absent reaction to light and a more preserved reaction to convergence. It is believed that the tonic pupil develops as a result of damage to the ciliary ganglion and/or postganglionic parasympathetic fibers.

Eydie syndrome- areflexia of the pupil against the background of its mydriasis. It develops in healthy people and is more common in women aged 20-50 years. In 80% of cases it is unilateral and may be accompanied by complaints of photophobia. The patient sees well both far and near, but the act of accommodation is slow. Over time, the pupil spontaneously contracts and accommodation improves.

Bilateral mydriasis without pupillary reaction to light occurs with damage to both optic nerves and bilateral amaurosis, with bilateral damage to the oculomotor nerves (at the level of the brain stem - damage to the nucleus, root or trunk of the oculomotor nerve at the base of the brain).

Impaired reaction (direct and friendly) of the pupil to light in both eyes, up to its absence with a normal pupil diameter, occurs with damage to the pretectal zone, which is observed with hydrocephalus, tumor of the third ventricle, midbrain. Inactivation of the parasympathetic system as a result, for example, of inadequate cerebrovascular perfusion, which is possible due to secondary hypotension from blood loss, can also lead to bilateral mydriasis.

Unilateral miosis indicates the prevalence of parasympathetic innervation over sympathetic. Usually unilateral miosis comes from Horner's syndrome. In addition to miosis, this syndrome develops ptosis and enophthalmos (as a result of decreased innervation of the Müller muscle) and slight conjunctival irritation. The pupil's reaction to light remains virtually unchanged.

Bilateral miosis, which practically does not expand during instillation of mydriatics with a sluggish reaction to light and normal to convergence - a manifestation of Argyle Robertson syndrome, is recognized as pathognomonic for syphilitic damage to the central nervous system.

Bilateral miosis with intact reaction to light indicates damage to the brainstem and may result from 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.

DIFFERENTIAL DIAGNOSTICS

Afferent pupillary defect(Marcus-Gunn pupil) is characterized by unilateral mydriasis, impaired direct reaction to light on the affected side and impaired conjugate reaction to light on the other eye. Mydriasis, as a manifestation of damage to the oculomotor nerve, is usually combined with impaired upward, downward and inward mobility of the eye, as well as varying degrees of hemiptosis or ptosis of the upper eyelid. Damage to only the pupillomotor fibers of the oculomotor nerve is manifested by unilateral mydriasis with an impaired direct and friendly reaction to light in the affected eye and a normal photoreaction in the other eye. When the midbrain structures are damaged, the pupillary reaction to light is impaired symmetrically in both eyes. In this case, most often the diameter of the pupils is not changed and the pupillary-constricting reaction to convergence (light-near dissociation) remains.

Tonic pupil(Adie"spupil), in addition to unilateral mydriasis, is distinguished by a sluggish sectoral reaction to light (direct and friendly), which is better determined by slit-lamp examination, and a relatively preserved pupil reaction to convergence. However, it must be remembered that mydriasis and disorder pupillary photoreaction may be caused by damage to the sphincter of the pupil and pathology in the iris.

A distinctive feature of unilateral miosis in Horner's syndrome compared with miosis in iritis is the preservation of the photoreaction and the combination of miosis with partial ptosis and enophthalmos.

Pharmacological tests (for pilocarpine, cocaine) play a certain role in differential diagnosis.

Article from the book: .