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Symptoms, treatment of Horner's syndrome. Bernard Horner syndrome - causes of development, characteristic symptoms and treatment The most common cause of Horner syndrome is

– a symptom complex caused by damage to the sympathetic nervous system, manifested by ophthalmological disorders, disorders of sweating and vascular tone on the affected side. The clinical picture is represented by ptosis, miosis, endophthalmos in combination with hyperemia and dyshidrosis of half the face. To make a diagnosis, an oxamphetamine test, eye biomicroscopy, CT scan of the orbits, and a test to study the reaction of the pupils are used. Therapeutic tactics boil down to the administration of electrical neurostimulation. It is possible to correct cosmetic defects using plastic surgery.

ICD-10

G90.2

General information

Horner syndrome (Bernard-Horner syndrome, oculosympathetic syndrome) is a secondary pathology that develops against the background of other diseases. In 75% of cases, the occurrence of the acquired form is associated with blockade of the brachial plexus using a supraclavicular approach using a large volume of anesthetic. Sometimes the appearance of the syndrome indicates severe damage to the neck or chest (malignant neoplasms of the lungs, mediastinitis). The disease was first described by the Swiss ophthalmologist Johann Friedrich Horner in 1869. Pathology occurs with equal frequency among males and females.

Causes of Horner's syndrome

There are congenital or acquired forms of the disease. The congenital variant occurs due to birth trauma. Cases of inheritance of oculosympathetic syndrome according to an autosomal dominant type have been described, while signs of involvement of the autonomic nervous system in the pathological process may be absent. The main reasons for the development of the acquired variant:

Iatrogenic intervention. Horner's syndrome is a common complication of improper placement of Bulau drainage. Symptoms also appear after cutting nerve fibers, blocking the cervical plexus or stellate ganglion in the chest or neck.
Traumatic injuries. The disease is often caused by blunt trauma to the base of the neck with damage to the thoracic or cervical sympathetic nervous chain. Clinical manifestations are observed on the side opposite to the damaged area.
Otogenic pathologies. The disease can occur as a result of the spread of infection from the middle ear cavity during otitis media. This is facilitated by perforation of the eardrum and a history of labyrinthitis.
Malignant neoplasms. Compression of nerve fibers by the tumor leads to the appearance of clinical symptoms of Horner's syndrome. The most common causes are Pancoast tumor or bronchogenic carcinoma of the lung apex.
Neurological diseases. The development of pathology may be associated with lateral medullary syndrome, Dejerine-Klumpke palsy or multiple sclerosis. Less commonly, syringomyelia becomes an etiological factor.
Vascular pathologies. A common cause of Horner's syndrome is aortic aneurysm. Local changes at the level of the arteries supplying blood to the affected area can also act as a trigger.
Thyroid diseases. Oculosympathetic syndrome may occur due to thyroid-cervical venous dilatation or goiter. There is often a relationship between the manifestations of the disease and hyperplasia of the thyroid gland.

Pathogenesis

The development of the disease is based on central, pre- or postganglionic damage to sympathetic nerve fibers. Due to disruption of the innervation of the superior tarsal or Müller muscles, classic drooping of the upper eyelids or inverted ptosis occurs. The severity of the ciliospinal reflex decreases. Pathological pigmentation of melanocytes that form the basis of the iris leads to heterochromia. The conjunctiva appears hyperemic, which is due to vasodilatation due to smooth muscle paralysis or pathology of the sympathetic vasoconstrictor response. Paralysis or paresis of the orbital muscle of the eye leads to enophthalmos. Symptoms of the disease develop on the opposite side of the affected area.

Symptoms of Horner's syndrome

The pathology is characterized by a one-sided course. Patients complain of drooping upper eyelid or slight raising of the lower eyelid. Anisocoria, caused by a narrowing of one of the pupils, is visually determined. On the affected side of the face there is impaired sweating and hyperemia. The eye looks set deep into the orbit, the severity of endophthalmos is insignificant. Clinical symptoms are aggravated by narrowing of the palpebral fissure. The secretion of tears is severely difficult; in rare cases, the eye appears “wet.” Due to persistent miosis, dark adaptation worsens; patients note that they have become worse able to see in the twilight, although visual acuity is preserved. The development of the disease in childhood often leads to the fact that on the affected side the iris has a lighter shade.

Complications

Disruption of innervation is a predisposing factor to the development of inflammatory diseases of the anterior segment of the eye (conjunctivitis, keratitis, blepharitis). Due to the altered topography of the eyeball in relation to the lacrimal gland, its dysfunction occurs, this potentiates the development of xerophthalmia. Recession of the eye facilitates the penetration of infectious agents into the orbit. In severe cases, the formation of phlegmon or subperiosteal abscess of the orbit is possible. Most patients develop secondary hemeralopia, which is not amenable to classical treatment methods.

Diagnostics

The diagnosis is based on the results of a physical examination and special research methods. Upon examination, miosis, heterochromia and retraction of the eyeball on the affected side are revealed. The reaction of the pupils to light is sluggish or undetectable. Basic diagnostic methods:

Oxamphetamine test. Used to determine the cause of miosis. If the third neuron is not involved, amphetamine use leads to persistent mydriasis. In conclusion, they indicate at what interval the nerve pathway is damaged.
Biomicroscopy of the eye. Injection of conjunctival vessels is noted. The transparency of the optical media of the eye is not reduced, the structure of the iris is heterogeneous. Uneven pigment distribution may occur.
Pupil dilatation test. In Horner's disease, ptosis is combined with a narrowed pupillary opening. If the oculomotor nerve is damaged, the study reveals a combination of drooping eyelid with mydriasis.
CT orbits. The study is carried out to determine the etiology of the disease. Computed tomography makes it possible to visualize space-occupying formations of the orbit and traumatic injuries to the organ of vision.

Differential diagnosis is carried out with anisocoria of various origins and Petit syndrome. If anisocoria is detected, patients are subject to further examination, since this symptom can also be observed in cases of cerebral circulation disorders and eye development abnormalities. Petit disease is often called inverse oculosympathetic syndrome. With this pathology, mydriasis, exophthalmos, widened eyelid folds, and ophthalmic hypertension, which are not characteristic of the classic oculosympathetic syndrome, are determined.

Treatment of Horner's syndrome

The disease is difficult to treat. The use of neurostimulation has been proven to be somewhat effective. Thanks to low-amplitude electrical impulses, the affected muscles are stimulated, this helps to improve trophism and complete or partial restoration of lost functions. If the disease occurs due to a hormonal imbalance, hormonal replacement therapy is indicated. If the effectiveness of the method is low, prompt elimination of the cosmetic defect is recommended. The use of plastic surgery techniques allows for the correction of ptosis and enophthalmos. The possibility of using kinesiotherapy in the treatment of the disease is being studied. The essence of the technique is to perform a massage to stimulate the affected areas.

Prognosis and prevention

The outcome of Horner's syndrome may be unfavorable in terms of prognosis if it is impossible to eliminate the cause of damage to the nerve fibers. If the etiological factor is hormonal dysfunction, the appointment of replacement therapy can stop all manifestations of the disease. Specific preventive measures have not been developed. Nonspecific prevention comes down to timely diagnosis and treatment of diseases of the ENT organs and thyroid gland, and correction of hormonal levels. If the clinical picture of the disease is associated with space-occupying formations of the orbit, patients should be registered with an ophthalmologist. Dynamic CT of the orbits is recommended.

Horner's syndrome is a complex symptom complex associated with damage to the human sympathetic nervous system. The disease leads to disruption of the visual apparatus and vascular system. In some cases, the appearance of the syndrome may be a sign of malignant lung tumors or neck lesions.

Horner's syndrome - what is it?

Few people have heard about Horner's syndrome: what the disease causes in humans, what changes it is accompanied by, is known only to patients who have encountered the disease. This set of symptoms is caused by damage to the sympathetic nervous system. As a result of the disorder, patients experience eye damage and impaired vascular tone on the affected side.

The pathology is secondary in nature - it often develops against the background of other diseases. The syndrome was first described in 1869 by an ophthalmologist from Switzerland, Friedrich Horner, and was later named after its discoverer. Since that time, many studies and observations of patients with pathology have been carried out, which has made it possible to develop effective treatment methods.

Horner's syndrome - causes

Scientists who have studied Horner-Bernard syndrome for a long time associated the causes of the development of pathology with damage to the sympathetic pathway of the nervous system in the cervical region. This innervation pathway runs directly from the hypothalamus to the organ of vision. Horner's syndrome can be either acquired or congenital. It is customary to distinguish the following two levels of damage:

central - develops with brain tumors;
peripheral - provoked by head and neck injuries, dissection of the carotid arteries or aorta, thoracic aneurysm.

Congenital Horner's syndrome

Congenital Horner's syndrome is a consequence of damage to the medulla oblongata. The nuclei of neurons that run along the optic canal to the eye are located directly here. Damage to any part of the nerve process causes a failure in the transmission of nerve impulses. As a result, pathological innervation of the eye muscles develops, which is the cause of symptoms characteristic of Horner's syndrome. occurs gradually, but at a rapid pace.

Acquired Horner's syndrome

Often in medical practice the following synonymous name is used - Claude Bernard Horner syndrome. This form of pathology is acquired. The direct cause of the disease can only be determined after a comprehensive examination. In most cases, the patient’s medical history indicates one of the following pathologies that provoke the development of Horner’s syndrome:

complex head injury with damage to a large number of internal structures;
, often with delamination;
thyroid diseases;
malignant brain tumors.

Claude Bernard Horner syndrome - symptoms

Horner's syndrome with cervical osteochondrosis, which often occurs, can be diagnosed by three characteristic signs. In medicine they are called the Bernard-Horner triad. Horner's syndrome includes the following pathological conditions:

ptosis – drooping of the upper eyelid;
miosis – strong, abnormal constriction of the pupil;
enophthalmos – retraction of the eyeball.

The simultaneous presence of these three symptoms almost 100% indicates Horner's syndrome. A characteristic sign is damage to one half of the face. In addition, there is a disturbance in the process of sweating, lacrimation, expansion and redness of the small blood vessels of the eye. The constricted pupil does not respond to light stimuli or administered medications.

Children often experience heterochromia - insufficient pigmentation of the iris due to impaired innervation of the visual apparatus. As a result, both of the child's eyes have different colors. Such pathological changes can lead to visual impairment. What Horner's syndrome looks like, photos of patients are shown below.

Horner's syndrome - diagnosis

To make a diagnosis of Bernard-Horner syndrome, doctors perform a series of examinations and functional tests. Among the main diagnostic methods:

Oxamphetamine test– helps to identify the cause of pupil constriction and the location of damage to the nerve pathway.
Biomicroscopy of the eyes– an uneven distribution of pigment is detected, the iris has a heterogeneous structure, and the transparency of the optical medium of the eye is reduced.
CT scan of the eye orbits– helps to establish the etiology of the disease, visually assess the volumetric formations of the orbit, the nature of traumatic injuries to the eye.

Horner's syndrome - treatment

Before treating Horner's syndrome, doctors perform a comprehensive examination to determine the cause. Depending on the factor that provoked the development of the pathology, doctors draw up an individual treatment plan. Neurostimulation has proven effectiveness. The use of low amplitude electrical impulses helps stimulate affected muscles, improve trophism, and restore lost functions.

Restoration of facial muscle tone occurs gradually, so you have to undergo more than one course of physiotherapeutic procedures. When Horner's syndrome occurs due to hormonal imbalance, hormone replacement therapy is prescribed. If the therapy is not effective, cosmetic removal of the defect is prescribed.

Horner's syndrome - which doctor should I see?

Oculosympathetic syndrome, as Horner's disease is often called, requires complex correction. Taking this into account, a group of specialists simultaneously treats the disorder. A neurologist is involved in excluding disorders affecting the nervous system. Damage to the visual apparatus is corrected by ophthalmologists. If surgery is necessary, an eye surgeon is involved in the treatment of the disease. In practice, patients with pathology initially turn to a pediatrician or therapist, who refers them to the necessary specialist.

Horner's syndrome (or oculosympathetic syndrome) is a pathology of the autonomic nervous system caused by a violation of the sympathetic innervation and accompanied by damage to the oculomotor nerve, which is responsible for the movements of the eyeball, the reaction of the pupils to light and the raising of the eyelid.

The disease itself is not dangerous. But if it indicates a serious pathology, it requires careful diagnosis and adequate treatment.

Forms of Horner's syndrome

Oculosympathetic syndrome can be idiopathic and secondary. In the first case, it develops as an independent disease and is not a consequence of another pathology. Its clinical signs regress on their own. Horner's syndrome of the secondary type, on the contrary, is a complication of some other disease.

Symptoms of damage to the oculomotor nerve

The following signs indicate the development of Horner's syndrome:

The appearance of a sensation of drooping of the upper eyelid (ptosis), which is caused by paralysis of the muscle responsible for raising it (superior tarsal muscle), and narrowing of the palpebral fissure;
Diplopia is an ophthalmological pathology that is manifested by double images and objects falling into a person’s field of vision, and intensifies when looking towards the paralyzed internal rectus muscle or when trying to fix the gaze on nearby objects;
Difficulty moving the eye upward and inward, as well as limited motor activity when trying to look down. When you want to focus your gaze on nearby objects, the eyeball does not converge (does not deviate towards the middle);
Pathological constriction of the pupil on the affected side (miosis);
Weak expression of the direct and friendly reaction of the pupil to light, due to pathology of the sphincter of the pupil;
Heterochromia is a different color of the iris or uneven coloration. This symptom develops in children with the congenital form of Horner's syndrome. Its cause is the lack of sympathetic innervation and, as a consequence, the lack of melanin pigmentation of melanocytes located in the stroma of the iris;
Reduced tearing of the eye on the affected side;
Deterioration of near vision on the affected side due to paralysis of accommodation;
Loss of external muscle tone and, as a result, exophthalmos (protrusion of the eye);
A large number of dilated vessels in the eyeball, which is revealed during examination by an ophthalmologist;
Impaired sweating on the affected side of the face (dyshidrosis);
Delayed dilation or constriction of the pupil;
Redness of the face on the affected side.

It should be noted that a patient with Horner's syndrome may not experience all of the above symptoms. But to make a diagnosis, at least two must be identified and confirmed by special tests.

The most common symptoms of oculosympathetic syndrome are drooping of the upper eyelid (rarely raising of the lower eyelid), narrowing of the pupil and its weak reaction to light stimulation.

Causes of Horner's syndrome

The syndrome most often develops as a result of some pathological process in the body; it can also be congenital or acquired as a result of surgical intervention. The most common causes of Horner's syndrome include:

Inflammatory processes affecting the central nervous system;
Neoplasms in the spinal cord or brain;
Tumor of the superior sulcus of the lung (Pancoast tumor);
Inflammatory processes, as a result of which the first ribs and/or upper parts of the spine are affected;
Trigeminal neuralgia;
Stroke;
Traumatic brain injuries;
Spinal cord injuries;
Multiple sclerosis;
Inflammatory processes in the middle ear;
Aortic aneurysm;
Migraine;
Klumpke's palsy;
Alternating syndromes;
Thrombosis of the cavernous sinus, etc.

The main causes of Horner's syndrome in newborns are:

Use of forceps for obstetrics;
Shoulder birth difficulties;
Delayed birth;
Vacuum extraction of the fruit;
Birth injuries.

The works of some authors describe cases of association of Horner's syndrome in newborns with congenital chickenpox syndrome. An explanation for this may be that the smallpox virus provokes radiculopathy, and this, in turn, leads to impaired development of the upper limb.

Also, trauma, neoplasms in the nasopharynx and in the central nervous system, heredity, agenesis of the internal carotid artery and cytomegalovirus infection can lead to the development of Horner's syndrome in newborns.

How to treat Horner's syndrome

Before choosing the optimal treatment regimen for this disease, the patient is recommended to undergo a series of diagnostic tests.

To begin with, he may be prescribed drops of cocaine hydrochloride. If we are talking about Horner's syndrome, the eye reacts to the injection of the solution with anisocoria (the pupils become different sizes). This is due to the fact that the production of norepinephrine provokes dilation of the pupil of the healthy eye, but a similar effect does not develop in the diseased eye.

The next diagnostic method is instillation of an M-anticholinergic solution into both eyes. The test result for oculosympathetic syndrome is the same as in the first case.

For diagnostic purposes, a test using oxamphetamine may be prescribed, which can detect damage to the third neuron of the sympathetic pathway. A study of the delay in pupillary response to light is often prescribed (in this case, a beam of light is directed into the eye using an ophthalmoscope).

In cases where Horner's syndrome is an independent disease and not a complication of another pathological process, it does not pose a risk to the patient's health and does not require treatment.

How to treat Horner's syndrome when it is acquired depends entirely on the underlying disease. First, the cause is accurately diagnosed, and then the optimal treatment regimen is selected.

Horner (Claude Bernard-Horner) syndrome manifested by miosis - constriction of the pupil (paresis of the muscle that dilates the pupil due to damage to the nuclei or the nerve itself); ptosis of the upper eyelid (paresis of the muscle that lifts the upper eyelid); retraction of the eyeball (enophthalmos) due to damage to part of the fibers of the muscle that lifts the upper eyelid, which receive sympathetic innervation. Lehnert considers enophthalmos to be only apparent due to drooping of the eyelid. The pupil on the affected side, which is in a state of miosis, reacts faster to light than the pupil of the healthy eye. Vasomotor disorders are usually observed on the same side of the face, and in a later period there is often a decrease in sweating. Long-term results, especially in young people, include different colors of the irises (lighter on the affected side).

The syndrome can be of central or peripheral origin and is observed when the medulla oblongata or spinal cord is affected. It is often observed with syringomyelia, cervical ribs, aortic aneurysm, enlarged lymph nodes, with circulatory disorders in the main cerebral vessels, pathological processes of the esophagus or thyroid gland, after operations on it and with pleuropulmonary processes at the apex of the lung, as well as with some alternating syndromes. The syndrome is most strongly expressed when sympathetic fibers are damaged from the orbit to the ciliary ganglion, less strongly when there is damage between the ciliary ganglion and the diencephalon, and most weakly when the process is localized between the diencephalon and the cerebral cortex (V. A. Smirnov). Described by the French pathophysiologist S. Bernard in 1852 and the Swiss ophthalmologist J. Horner in 1869. Bernard wrote a description of the lesion of the sympathetic nerve.

In neurology, there are many symptom complexes called syndromes. As a rule, they are a consequence of some disease. Syndromic diagnosis is extremely important in diagnosing pathologies of the central and peripheral nervous system, as it allows one to determine the topic and level of the lesion. Quite often in the practice of doctors, Claude-Bernard-Horner syndrome occurs.

Claude-Bernard-Horner syndrome

Claude-Bernard-Horner syndrome is the result of impaired functioning of the sympathetic nervous system, or more precisely, the part of it that is responsible for the innervation of the eye.

In order for the eyelids to move, the pupil to contract and dilate, and the palpebral fissure to remain open, the coordinated work of muscles and nerve fibers is necessary. In Horner's syndrome, the functions of the eye muscles are seriously affected.

Fibers of three orders of neurons take part in the formation of the sympathetic nerve pathways of the eye. They form a rather complex path, but understanding its individual segments will help to imagine the causes and consequences of various lesions at this level.

Sympathetic innervation of the eye muscles

First order nerve fibers are the path from the hypothalamus to the Budje-Weller center, which is located in the spinal cord at the level of the cervical and thoracic vertebrae. It is called the “ciliospinal center”. First order neurons pass through the brainstem.

Next, the nerve fibers in the nerve roots leave the spine and spread further to the stellate and middle sympathetic cervical nodes. They end in the superior cervical sympathetic node, and this pathway is called preganglionic.

From there, third-order nerve fibers, as the choroid plexus of the internal and common carotid arteries, reach the cavernous sinus, and together with the ophthalmic artery, the orbit. In this segment they are called postganglionic.

Nerve fibers regulate the functioning of the following muscles:

The muscle that dilates the pupil.
Muscles of the cartilage of the upper eyelid.
Smooth muscle tissue of the orbit.

If the flow of nerve impulses is turned off at any level, a number of characteristic symptoms arise, which are combined into this syndrome.

Symptoms

The symptoms of this pathology are quite striking, and often a neurological diagnosis is made during the first examination of the patient.

But the following triad of signs is most characteristic of Horner’s syndrome:

Drooping eyelid, or ptosis.
Constriction of the pupil, or miosis.
Flattening, retraction of the eyeball, which is called enophthalmos.

Anhidrosis is also an important diagnostic sign. – lack of sweating on one side of the face.

Ptosis

With Horner's syndrome, ptosis of the upper and lower eyelids is observed. With a pronounced form, the edge of the eyelid can even reach the pupil. But more often there are milder variants of pathology, with minor omission. They may be invisible to other people and even the doctor.

Sometimes with this syndrome, ptosis of only the lower eyelid is observed. In this case, it is called “inverted ptosis.”

The drooping of the upper eyelid and some lifting of the lower eyelid due to muscle paresis leads to the narrowing of the palpebral fissure. This makes it difficult to see and impairs vision.

Thus, eyelid ptosis in Horner's syndrome is not only a cosmetic defect.

Miosis

With this pathology, you can notice that the pupil on the affected side is narrower than on the healthy side. This sign - different pupil diameters - is called anisocoria.

However, the difference is not always clearly expressed. In daylight, this symptom may not be noticed. But in a dark room, when the pupils are dilated, the difference in their diameter is more clearly visible.

In mild cases of pathology, pharmacological tests are used to reliably determine pupil constriction.

The most famous is the sample with 4% cocaine. After instilling the medicine into the palpebral fissure, the pupil should dilate. But with Horner's syndrome this does not happen, or it expands slightly.

If the response to pharmacological testing is positive, it means that the drooping of the upper eyelid and the constricted pupil are not related to each other; they are based on other pathological processes.

Enophthalmos

In practical neurology, exophthalmos – protrusion of the eyeball – is much more common. This pathology is quite easy to identify. In contrast, enophthalmos is not always noticeable.

Violation of the sympathetic innervation of the eye leads to the fact that the eyeball flattens, as if sinking inward. The depth of flattening, as a rule, does not exceed 1–2 mm. This is what causes difficulties in diagnosing enophthalmos.

Anhidrosis

Anhidrosis is a decrease or complete cessation of sweating on the corresponding half of the face. This sign is observed in five percent of cases if the preganglionic fibers are damaged. In this case, sweating will be disrupted on the entire half of the face.

There are also less severe options. In such a situation, anhidrosis occurs only on the side of the nose and the inner part of the forehead. This is characteristic of a postganglionic lesion.

Anhidrosis is often accompanied by dilation of the capillaries on the corresponding half of the face. This occurs due to loss of vasoconstrictive ability of the blood vessels. The consequence of this process is redness of the skin in a certain area.

Other symptoms

Also, with this neurological pathology, other eye symptoms may be observed. The most common are the following:

A transient disturbance of accommodation in the form of its intensification.
Changes in the properties of tear fluid and its viscosity.
A change in the color of the iris on one side is heterochromia.

Heterochromia occurs in congenital Horner's syndrome and is most often observed in children. Their iris has a gray-bluish tint.

Causes of pathology

Horner's syndrome occurs for various reasons. Based on their origin, there are three main types of pathology:

Congenital.
Acquired.
Iatrogenic.

In addition, the syndrome can be classified according to the level of damage. Depending on the order of neurons that are damaged, the clinical manifestations will vary. However, such a division is of practical importance only for neuropathologists and neurosurgeons.

Congenital variant

Of all cases of Horner's syndrome in children, about 50% are congenital. Such patients are subject to mandatory examination - CT or MRI of the chest and neck, ultrasound examination of blood vessels.

The most common causes of congenital pathology are:

Birth trauma, especially damage to the brachial plexus.
Neoplasms of the nasopharynx.
Tumors of the central nervous system.
Neuroblastoma.
Congenital form of cytomegalovirus infection.
Intrauterine infection with chickenpox.
Idiopathic Horner's syndrome, in which the underlying disease cannot be identified.
Underdevelopment of the internal carotid artery. This pathology is difficult to diagnose due to the developed collateral cerebral circulation.

Purchased option

The group of diseases leading to the occurrence of this symptom complex is quite extensive. Most often it develops due to the following pathologies:

Cerebral infarction.
Demyelinating diseases (multiple sclerosis).
Amyotrophic lateral sclerosis.
Injuries.
Tumors of various localizations.
Cervical rib syndrome.
Herpetic encephalitis.

Occasionally, intervertebral hernias of the cervical spine lead to its appearance. However, they account for only about two percent of all cases.

Previously, this pathology occurred in the bulbar form of polio. This variant is not currently observed due to vaccination against this disease.

A malignant lung lesion – Pancoast tumor – deserves special attention.

Pancoast tumor

Pancoast tumor is an apical lung cancer. It is characterized by rapid growth and, when spreading, affects all nearby structures. The tumor also affects the stellate nerve ganglion, which causes the appearance of Horner's syndrome.

The development of ptosis, miosis and enophthalmos in middle-aged and elderly patients without other neurological symptoms is always suspicious for Pancoast disease. The diagnosis becomes especially likely if bronchopulmonary symptoms are added - cough, shortness of breath, bloody sputum.

The patient may also notice marked weight loss, weakness, and fatigue. In such a situation, examination of the chest organs is mandatory.

Iatrogenic option

Iatrogenic Horner's syndrome occurs during surgical operations on the chest and neck organs. In this case, nerve pathways and ganglia may be affected, which leads to the appearance of a characteristic symptom complex.

Most often this occurs after operations on the following organs:

Thyroid gland.
Pharynx and larynx.
Lungs with tumor process and tuberculosis.
Cervical vertebrae during their anterior decompression and stabilization.

Treatment

It is impossible to cure Horner's syndrome without eliminating the underlying disease. It is not life-threatening, but causes significant cosmetic inconvenience to patients.

Sometimes neurologists provide symptomatic therapy. For these purposes, the eye muscles are stimulated with weak currents. This procedure is quite painful.

If this pathology leads to a serious cosmetic defect, then only a plastic surgeon can help.

Horner's syndrome is not an independent pathology and does not always require treatment. But it can be a sign of dangerous diseases and necessarily requires a thorough diagnostic search.