Tear production disorder

Phenomenologically, lacrimation disorders can be divided into two types: lacrimation (epiphora) and dry eyes (xerophthalmia, alacrimia - a more accurate term for decreased production or absence of tears).

Lacrimation is not always associated with hyperfunction of the lacrimal glands, more often it is observed when the outflow of lacrimal fluid is impaired. Lacrimation can be paroxysmal or constant, it also depends on the functional state of the brain in the sleep-wake cycle: during sleep, the secretion of tears is sharply suppressed, during wakefulness, approximately 1.22 g of lacrimal fluid is produced, which partially evaporates, the other part is excreted through the nasolacrimal canal.

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Forms of lacrimation

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Cold Epiphora

Lacrimation is observed in cold and windy weather, more often in elderly people. Some authors consider it a form of cold allergy.

Epiphora in allergic rhinitis

It usually occurs in spring and summer. Along with lacrimation, patients report nasal congestion. Swelling of the mucous membrane may be limited to the area of the nasolacrimal canal outlet under the lower concha, where there is a dense venous plexus; this makes it difficult for tears to flow into the nasal cavity.

Epiphora in migraine and cluster headaches

It is paroxysmal in nature, usually combined with nasal congestion and is observed on the side of the headache.

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Senile Epiphora

Often observed in elderly people, associated with age-related changes that impair the outflow of tear fluid.

Epiphora in diseases accompanied by a decrease in vitamin A content The specified hypovitaminosis is possible in diseases of the gastrointestinal tract, liver diseases, helminthic invasion, monotonous diet. Patients complain of lacrimation, photophobia, a feeling of dryness and burning in the eyes; in bright light and in the wind, the eyes turn red. The skin is dry, flaky, the level of vitamin A in the blood is reduced. Alimentary hypovitaminosis A is a serious problem for a number of developing countries.

Epiphora in viral eye infections

It is observed when the eye is affected by herpes zoster, herpes simplex, chickenpox virus, and can be a complication of vaccination. In these cases, lacrimation is associated with obstruction of the lacrimal ducts.

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Epiphora in diseases of the ENT organs

Otolaryngologists were the first to notice this type of lacrimation. Lacrimation appears on the side of irritation of the mucous membrane of the nose or inner ear (rhinitis, otitis, neoplasms) and passes when the inflammatory phenomena are eliminated. Ipsilateral lacrimation can also be caused by severe toothache.

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Crocodile tears syndrome

Lacrimation during eating has been known for a long time. However, more attention was paid to this phenomenon after it was described in 1928 by F. A. Bogorad under the name of "crocodile tears" syndrome. The syndrome can be congenital (in this case, it is combined with damage to the abducens nerve) and acquired (usually after traumatic or inflammatory damage to the facial nerve proximal to the geniculate ganglion). A more pronounced manifestation of the syndrome is observed when eating hard and spicy food. It has been noted that lacrimation during eating often occurs against the background of incomplete restoration of the facial nerve in the presence of synkinesis. To date, more than 100 cases have been described. However, with a targeted survey and consideration of mild forms, the phenomenon of "crocodile tears" can be considered more common. According to the literature, with incomplete restoration of the facial nerve, the "crocodile tears" syndrome occurs in 10-100% of patients, i.e. in 6-30% of all patients with damage to the facial nerve.

The pathogenesis of the "crocodile tears" syndrome deserves special attention. The main mechanism of alimentary lacrimation after traumatic or inflammatory damage to the facial nerve is considered to be the mechanism of incorrect, aberrant regeneration, when the efferent and afferent salivary fibers fuse with the efferent lacrimal fibers. This theory is confirmed by the presence of a latent period after damage to the facial nerve (necessary for regeneration) and the connection with pathological synkinesias with incomplete restoration of the facial nerve, which are also explained by incorrect regeneration of motor fibers.

However, an experiment on animals has established that the appearance of the "crocodile tears" syndrome is possible immediately after damage to the facial nerve, i.e. even before the regeneration of nerve fibers. In this case, lacrimation was caused in dogs not only by food irritants, but also by stroking and scratching the fur, which allows us to explain the "crocodile tears" syndrome by a summation reflex, but in pathological conditions. In the parasympathetic nuclei that innervate the lacrimal glands, summation phenomena easily occur even under normal conditions (for example, increased moistening of the eyeball during eating). The lacrimal and salivary glands appear simultaneously in the phylogenetic series, have a single embryonic origin, which probably explains the anatomical proximity of the stem centers of lacrimation and salivation. With incomplete damage to the facial nerve, partial denervation of the lacrimation center occurs, in which the processes of excitation summation proceed more easily.

The congenital symptom of "crocodile tears" combined with ipsilateral damage to the abducens nerve has been described as a consequence of the teratogenic effect of thalidomide. The most logical explanation for the combination of oculomotor and lacrimal disorders is damage by the type of dysgenesis of brain tissue in the immediate vicinity of the nucleus of the abducens nerve.

Epiphora in Parkinsonism

Often combined with other autonomic disorders characteristic of Parkinsonism (sialorrhea, seborrhea, constipation, etc.). In lateralized forms of Parkinsonism, it is usually observed on the affected side.

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Forced crying

Occurs with pseudobulbar syndrome due to damage to the corticonuclear pathways or subcortical nature.

Xerophthalmia can be observed both with damage to the lacrimal glands and with neurogenic disorder of lacrimal secretion. The following forms of xerophthalmia are known.

Xerophthalmia in Sjogren's syndrome

Dry keratoconjunctivitis is one of the main manifestations of Sjogren's syndrome - an exocrinopathy of autoimmune origin. It is characterized by a gradual onset, slow progression, combination with xerotomy, dryness of the mucous membrane of the nose, pharynx, stomach, and articular syndrome.

Xerophthalmia in Mikulicz syndrome

Characterized by gradual symmetrical enlargement of the lacrimal and salivary glands and decreased secretion. The disease was first described in 1892 by J. F. Mikulicz-Radecki. The nature of the disease is not exactly known, many consider it to be lymphoepithelioma. Enlargement of the bronchopulmonary lymph nodes is also characteristic.

Alacrimia syndrome in combination with achalasia of the esophagus and adrenal insufficiency

Symptoms develop at the age of 1-5 years. The first sign may be the appearance of crying without tears. The disease progresses, later peripheral autonomic neuropathy may develop in combination with pyramidal, cerebellar signs, features of Parkinsonism, mild mental retardation. It is assumed that the disease has an autosomal recessive transmission route.

Congenital alacrimia in Riley-Day syndrome

The syndrome is caused by congenital disorders of predominantly the vegetative apparatus of the peripheral nervous system and is manifested by decreased lacrimation, impaired thermoregulation, orthostatic hypotension, and episodes of severe vomiting. The disease has an autosomal recessive type of inheritance.

Xerophthalmia in acute transient total dysautonomia

The decrease in tear secretion along with other sympathetic and parasympathetic disorders is reversible. The nature of the disease is probably infectious-allergic.

Xerophthalmia due to facial nerve damage

It is observed with damage to the facial nerve in the bone canal before the large petrosal nerve departs. Dryness of the eye is noted on the side of the facial nerve paralysis, combined with taste and salivation disorders. Reduced secretion of tears is also possible with other forms of damage to the nerve fibers going to the lacrimal gland: with herpetic damage to the geniculate ganglion, fractures of the base of the skull, when the large petrosal nerve is damaged, after operations for trigeminal neuralgia and acoustic neuroma.

Brief physiology of lacrimation and pathogenesis of its disorders. Like most organs, the lacrimal glands have dual innervation. Segmental parasympathetic innervation is carried out by cells located in the brainstem in the pons region near the nucleus of the abducens nerve. These neurons are excited by impulses from the hypothalamic or limbic system, as well as signals from a neuron of the sensory trigeminal nucleus. Preganglionic fibers in the greater petrosal nerve approach the pterygopalatine ganglion, posttanglionic fibers in the lacrimal nerve directly innervate the secretory cells. Sympathetic stimulation is carried out by neurons of the lateral horns of the upper thoracic segments of the spinal cord; preganglionic fibers end in neurons of the superior cervical ganglion (SCG), postganglionic fibers in the perivascular plexus of the carotid artery reach the salivary gland. Sympathetic fibers innervate mainly the vessels of the glands and cause vasoconstriction, but can also stimulate tear production to a lesser extent.

There are two main mechanisms of lacrimation: impaired lacrimal fluid outflow and reflex enhancement; a combination of these mechanisms is also possible. An example of increased lacrimation caused by obstructed tear outflow is lacrimation in allergic rhinitis, viral eye infections, post-traumatic or congenital narrowing of the nasolacrimal canal. Paroxysmal epiphora in migraine and cluster headache, combined with nasal congestion, is also associated with temporary obstruction of the lacrimal canal, but the role of sympathetic activation is not excluded. Senile epiphora is explained by age-related changes in the protective apparatus of the eyes: a decrease in the tone of the eyelid tissues, which leads to a lag of the lower eyelid from the eyeball, as well as dislocation of the inferior lacrimal punctum, which impairs tear outflow. In Parkinsonism, lacrimation can develop according to two mechanisms. On the one hand, rare blinking and hypomimia, which weakens the suction action of the nasolacrimal canal, lead to difficulty in tear outflow; on the other hand, activation of central cholinergic mechanisms may be important.

Reflex lacrimation accounts for approximately 10% of all cases of epiphora. Most reflexes that cause increased secretion of tears are triggered by the receptors of the eye, afferent impulses go along the first branch of the trigeminal nerve. A similar mechanism of lacrimation occurs in cold epiphora, lacrimation with pronounced exophthalmos and vitamin A deficiency. In the latter case, the more vulnerable conjunctiva and cornea perceive natural irritants (air, light) as excessive, which leads to a reflex increase in the secretion of tears.

However, reflex lacrimation is also possible with irritation of the receptor fields of the second branch of the trigeminal gland (epiphora in ENT diseases - rhinitis, otitis, neoplasms).

Dry eye sensation (xerophthalmia)

It can be caused by both pathology of the lacrimal glands and neurogenic secretion disorders. Pathology of the lacrimal glands causes decreased tear production in Sjogren's and Mikulicz syndromes. Damage to the peripheral autonomic tear-secreting fibers explains alacrimia in Reilly-Day syndrome, acute transient total dysautonomia, alacrimia syndrome combined with esophageal achalasia and adrenal insufficiency, facial nerve neuropathies with damage levels below the geniculate ganglion, and herpetic damage to the geniculate ganglion.

Treatment of lacrimation disorders

Treatment of epiphora depends on the correctly established cause of lacrimation. In case of epiphora associated with allergic mechanisms, a complex of antiallergic therapy is carried out. Attempts to treat reflex lacrimation with novocaine blockade of the lacrimal gland are known. Lacrimation associated with impaired lacrimal fluid outflow due to various causes (chronic karatoconjunctivitis, congenital narrowing or pathology of the development of the lacrimal ducts) accounts for about 80% of cases of epiphora. In these cases, treatment is mainly surgical. Drugs used for conservative correction of lacrimation act on the basis of anticholinergic direct or side effects (anticholinergic and antihistamines, lithium, diazepam, imipramine). In case of vitamin A deficiency, vitamin A is prescribed at 50,000-100,000 IU.

In various forms of xerophthalmia (alacrimia) not associated with systemic damage to the glands (as in Sjogren's and Mikulicz syndromes), the most successful is the operation of transplanting the parotid (Stenon's) duct into the conjunctival sac with subsequent radiation therapy of the salivary glands to reduce "lacrimation". In Sjogren's syndrome, the underlying disease is treated, various lacrogenic substances (kinins and direct agonists of postsynaptic receptors) are used: pilocarpine, bromhexine (effective in a daily dose of 48 mg), as well as various compositions of artificial tears.