Ocular migraine is a migraine with an aura in the form of transient visual disturbances that may occur against the background of a headache or in its absence. It is clinically manifested by a feeling of flickering, loss of areas of the field of vision, the appearance of phosphenes, photopsies and scintillating cattle. Diagnosis is based on anamnesis, objective examination, ophthalmoscopy, perimetry, MRI and angiography of cerebral vessels. Symptomatic treatment consists in prescribing analgesics and NSAIDs, conducting periosteal and intraosseous blockades at trigger points. Preventive therapy in the inter-access period includes the appointment of nootropics, muscle relaxants and antidepressants.
Ocular migraine, or atrial fibrillation, is a disease manifested by image loss in certain areas of the visual field and a specific visual aura in the absence of organic changes in the eyes. The first descriptions of ocular migraine were presented by Hubert Airy in the nineteenth century. The disease develops more often at a young age against the background of lability of the autonomic nervous system. Atrial fibrillation is more widespread among female representatives and people whose work is associated with prolonged visual stress. The disease is characterized by a genetic predisposition. There is a tendency to spontaneous short-term remission. The development of complications is not typical, at the height of seizures, loss of vision is possible.
The basis of ocular migraine is neurological dysfunction caused by a malfunction of the visual analyzer. The main etiological factor of the retinal form of the disease is a regional decrease in the tone of the posterior cerebral artery, leading to temporary retinal ischemia. Ophthalmoplegic migraine occurs when the III pair of cranial nerves is squeezed by the dilated venous cavernous sinus or carotid artery. There is a hereditary tendency to develop ocular migraine, the mechanism of inheritance has not been established.
The paroxysmal nature of the disease is associated with vasomotor dysfunction. Sleep and wakefulness disorders, climate change, emotional overstrain, hormonal imbalance, prolonged hypoxia or staying in a room with a flickering light source contribute to the appearance of seizures. Specific predictors are abnormalities of the structure of cerebral vessels (arterial aneurysms and malformations), leading to a violation of the blood supply to the thalamus and occipital region. In the puberty period, clinical manifestations of this pathology are associated with increased stress on the nervous system, a high rate of growth and development of the body.
The retinal form of the disease is characterized by central or paracentral scotomas of different sizes and configurations, as well as loss of certain areas of the visual field. There is a tendency to combine visual field defects with a subsequent total decrease in visual acuity. A specific symptom is the appearance of phosphenes in the peripheral parts of the blind area. Flickering in front of the eyes indicates temporary retinal vascular ischemia, after which a headache develops in the frontal lobe with a transition to the orbit. The nature of the pain syndrome is pulsating. The pain appears from the opposite side in relation to the zone of insufficient blood circulation. Retinal migraine lasts on average from 30 minutes to 2 hours, the duration of the visual aura is 10-20 minutes. At the height of the attack, nausea may develop, followed by vomiting, a subjective feeling of increased intraocular pressure and increased sensitivity to external stimuli. All vision functions are restored within 1 hour.
Specific manifestations of ophthalmoplegic migraine (Mobius disease) are temporary ptosis of the upper eyelid, anisocoria and mydriasis. The development of exotropia of paralytic genesis is possible. When the eyeballs move, diplopia occurs. This form of the disease is more often diagnosed in children. Seizures can last for 1-2 or more weeks. In addition, visual symptoms can also occur with associated basilar migraine. The characteristic features of the pathology are bilateral lesion and ophthalmoparesis, combined with the clinical picture of the brain stem lesion.
The visual aura in migraine with aura is represented by photopsias and scintillating scotomas, prone to progression up to homonymous hemianopia. Patients describe the aura as the appearance of zigzags, flashes of lightning or sparks. The visual edge of the elements is shimmering, spiral-shaped. The first symptoms of pathology are small spots with paracentral localization, which later spread to the peripheral parts of the visual field. Areas of sparkling are replaced by the loss of parts of the visual field. Visual disturbances develop within 4 minutes and are completely leveled within 1 hour. Immediately before the attack, a period of imaginary well-being is possible, the average duration of which is about 60 minutes. Severe course of the disease can lead to ophthalmic hallucinatory disorders, paresthesia of the hands, face or tongue. This form is characterized by diffuse depression of the cortex in combination with local oligemia.
Visual disturbances in basilar migraine occur more often in the puberty period. Clinically, the disease is manifested by flashes of bright light, which lead to the development of temporary blindness and are accompanied by vegetative disorders. For girls, phonophobia and photophobia are more characteristic. In childhood, the “Alice syndrome” may occur, in which a visual aura appears in the form of ophthalmic illusions. Patients note lengthening, shortening or discoloration of objects. Vegetative, or “panic”, migraine is characterized by lacrimation and darkening in front of the eyes. In most cases, the symptoms are preceded by a visual aura.
For the diagnosis of “ocular migraine”, anamnesis data, examination of the anterior parts of the eyes, assessment of the volume of movements and the reaction of the pupils are used. Instrumental diagnostic techniques include ophthalmoscopy, perimetry, MRI of the brain and angiography. The listed studies are uninformative, but their conduct is necessary to exclude organic pathology of the organ of vision and to establish the etiology of the disease.
When interviewing patients with ocular migraine, it is often possible to identify a hereditary predisposition, a connection with certain triggers and a history of recurrent seizures. On examination, conjunctival hyperemia, pupil dilation and anisocoria may be observed. In some cases, the volume of eye movements is somewhat limited, the manifestations of nystagmus are not characteristic. The difference in pupil diameter of more than 0.9 mm indicates pathological anisocoria. The reaction to light is often sluggish. It is not recommended to conduct a study during a migraine attack because of the possible increase in clinical manifestations.
The method of ophthalmoscopy at the height of the attack determines the spasm of the retinal arteries, which is subsequently replaced by the expansion of the fundus veins. Perimetry data indicate a narrowing of the visual fields on the affected side. MRI of the brain and angiography can reveal anomalies of the posterior cerebral artery (aneurysm, malformation, pathological branching) and ischemia of the cortex in the area of its blood supply. In the prodromal period, cerebral edema is possible. A prolonged course of the disease can lead to the formation of small areas of infarction and atrophy of the brain substance, expansion of the ventricles and subarachnoid space. It is possible to establish the form of migraine only on the basis of specific clinical manifestations in the presence of 5 or more seizures in the anamnesis. Differential diagnosis of ophthalmoplegic migraine is performed with an incomplete form of the upper orbital fissure syndrome.
The tactic of treating ocular migraine is to stop seizures and migraine status. The therapy is carried out both in acute and in the intercrime periods. It is recommended to stop acute headache with the help of analgesics and nonsteroidal anti-inflammatory drugs (NSAIDs). Aspirin injections are advisable no later than 2 hours after the development of the first manifestations. Tablet forms (paracetamol, indomethacin) are indicated for mild course of the disease. Combined analgesics are recommended for severe seizures. In case of migraine status, the patient should be hospitalized immediately for intensive therapy. It is necessary to introduce systemic glucocorticosteroids (prednisone) and begin dehydration therapy with diuretics (mannitol). The administration of neuroleptics and metoclopramide is shown. A highly effective method of eliminating pain syndrome is to perform periosteal and intraosseous blockades at trigger points.
Treatment in the intercrime period is indicated with the development of more than 2 attacks of ocular migraine for one month and low effectiveness of conservative therapy. Drug therapy should be selected individually, taking into account the provoking factors of the disease. The most common prescription of nootropics (piracetam), muscle relaxants (tolperisone hydrochloride), antidepressants (fluoxetine). It is necessary to draw the attention of patients to the need for regular intake of basic medications for diseases of the cardiovascular (hypertension) and respiratory system (bronchial asthma, COPD).
Prognosis and prevention
Prevention of ocular migraine is reduced to normalization of sleep and wakefulness, thoughtful distribution of workload. Patients should exclude foods with a high tyramine content from the diet (tomatoes, milk, red wine, chocolate, celery, cocoa). Physical therapy, exercise, swimming are shown. It is necessary to avoid stressful situations, to minimize emotional overstrain. Non-drug prevention consists of massage, hydrotherapy and acupuncture. An alternative option is self-training and rational psychotherapy. The prognosis for ocular migraine is favorable for life and work capacity. Timely examination by an ophthalmologist and neurologist is recommended.