Disturbance of pupillary reactions: causes, symptoms, manifestations

Normally, the pupil necessarily reacts to light, showing a direct and friendly reaction, as well as convergence.

The causes of impaired pupillary reactions

Affection of the optic nerve

These reactions can be disrupted, due, for example, to the lesion of the optic nerve.

On direct light, the blind eye does not respond to its isolated illumination, there is no friendly reduction of the sphincter of the other eye.

However, the blind eye, if its third nerve is intact, responds with a friendly reaction, if the other eye and its optic nerve are not damaged.

Lesion of the oculomotor nerve

Another cause may be lesions of the oculomotor nerve. When the third nerve is damaged, both direct and friendly reactions to light on the affected side do not occur, due to paralysis of the pupil's sphincter, but at the same time both direct and friendly reactions are maintained on the opposite side.

The Eddy Syndrome

Eddie's syndrome also belongs to the number of causes of impaired pupillary reactions.

Symptoms and manifestations of impaired pupillary reactions

There is a type of pupillary disorders in which the paralysis of pupillary reflexes and the absence of reactions to light takes place, but the reaction to convergence persists. A similar pathology occurs in Edie syndrome, neurosyphilis, diabetes mellitus, pathological regeneration due to oculomotor nerve injury, pinealoma, encephalitis, ophthalmic herpes, multiple sclerosis, eye trauma, Fisher syndrome, pandisavtonomy, dystrophic myotonia, the first type of Charcot-Marie-Toot disease.

Synchronous impairment of pupillary reactions to light, accommodation and convergence is manifested in mydriasis. With unilateral defeat, neither direct nor friendly reaction to light on the affected side is manifested. Such immobility of pupils is called internal ophthalmoplegia, and it is explained by the defeat of pupillary parasympathetic innervation from the nucleus of Jakubowicz-Edinger-Westfal to the peripheral fibers of the eyeball. This impaired reaction of the pupil is characteristic of meningitis, alcoholism, multiple sclerosis, neurosyphilis, craniocerebral trauma and cerebrovascular diseases.

With two-sided blindness, there is amaurotic immobility of the pupils to light. There are no both types of reactions to light, but accommodation and convergence are preserved. This is the case with bilateral damage to the visual pathways from the retina to the primary visual centers. With the defeat of the central visual pathways or with cortical blindness, reactions to light are preserved completely.

The hemiophic reaction of the pupils is manifested in the contraction of both pupils only when the working half of the retina is illuminated, but the illumination of the non-functioning half of the retina of pupil contraction does not occur. The direct and friendly response of the pupils here is explained by the defeat of the visual tract or visual subcortical centers, not crossed and crossed fibers in the chiasma zone.

The asthenic reaction of the pupils is manifested in accelerated fatigue and complete absence of constriction with repeated light loads. A similar reaction is observed with intoxication, as well as somatic, infectious and neurological diseases.

With the paradoxical reaction of the pupils, pupils expand under light, and narrowing in the dark. Similar things happen, with hysteria, strokes and dorsal air.

Tonic reaction of pupils consists in very delayed dilatation of pupils after their narrowing by light. This is explained by the excessive excitability of pupillary parasympathetic efferent fibers, which occurs mainly with alcoholism.

Myotonic reaction of the pupils is observed mainly with alcoholism, diabetes, Guillain-Barre syndrome, avitaminosis, rheumatoid arthritis and peripheral vegetative disturbance.

With Argyle Robertson syndrome, characteristic of syphilitic damage to the nervous system, there is a miosis, a lack of response to light, some anisocoria, two-sidedness of the disorders, pupillary deformation, constant pupil sizes throughout the day, no response to atropine, cocaine and pilocarpine. Such pupillary disorders are characteristic of diabetes mellitus, alcoholism, multiple sclerosis, cerebral hemorrhage and, Huntington's chorea, meningitis, pineal gland adenoma, amyloidosis, Munchmeyer and Parino syndromes, Denny-Brown sensory neuropathy, increased blood pressure and pulse rate, excessive pain stimuli, pandisavtonomy, Fisher syndrome, Charcot - Marie - Toot disease.