Optochiasmal arachnoiditis is basal meningoencephalitis of the middle cranial fossa, in which the optic nerves and chiasm are affected. The main manifestations of pathology are pain in the eye socket, visual impairment, general weakness, increased visual fatigue. Diagnosis is based on ophthalmoscopy, perimetry, visometry, examination of the reaction of pupils to light and craniography. Conservative therapy of optochiasmal arachnoiditis includes the appointment of antibiotics, glucocorticosteroids, antihistamines, B and C vitamins. If the effectiveness of drug treatment is low, surgical intervention is carried out.
General information
Optochiasmal arachnoiditis is the most common form of inflammation of the arachnoid membrane, in which the pathological process is localized in the region of the base of the brain. According to statistics, in 60-80% of cases, the cause of the disease is the presence of chronic foci of infection in the area of the paranasal sinuses of the nose. In 10-15%, it is not possible to establish the etiology of the disease, such options are considered as idiopathic. Scientists are studying the role of autoimmune mechanisms in the occurrence of arachnoiditis. Pathology occurs with the same frequency among men and women. Basal meningoencephalitis is widespread everywhere.
Causes
The leading role in the development of this pathology is assigned to inflammation of the paranasal sinuses. Infectious agents (viruses, microorganisms) enter the cranial box through the natural openings of the sinuses. Less often, the appearance of symptoms of optochiasmal arachnoiditis is associated with an acute course of otitis media, mastoiditis. The main etiological factors of the disease:
- Traumatic brain injury. Intracranial lesions potentiate the formation of fibrous adhesions in the arachnoid region. Due to the appearance of the first symptoms some time after TBI, the relationship between trauma and arachnoiditis is not always traced.
- Neuroinfections. Inflammation of the arachnoid membrane of the brain is caused by intracranial complications developing against the background of influenza, sore throat, tuberculosis. Symptoms of the disease are often diagnosed in patients with neurosyphilis. The reason for the fibrosing form is the long–term persistence of the influenza virus in the cerebrospinal fluid.
- Multiple sclerosis. This is an autoimmune pathology in which the myelin sheath of nerve fibers is affected not only in the brain, but also in the spinal cord. Pathological changes are most pronounced in the area of the visual intersection and the periventricular space of the large hemispheres.
- Congenital defects. Anomalies of the structure of the optic canal and the bone walls of the orbit contribute to the penetration of infection into the intracranial cavity. This leads to the development of focal symptoms and a recurrent course of the disease.
Pathogenesis
The mechanism of development is based on the effect of an infectious agent (more often of a viral nature) on the meninges. First of all, the spider shell is affected, and then the soft one. Changes in the structure of nervous tissue are more pronounced in the chiasmal zone and adjacent optic nerves. Due to local inflammation, the vessels expand, their permeability increases. There is increased exudation and the formation of cellular infiltrates in the area of the membranes of the brain. Then there are circulatory disorders that provoke an increase in hypoxic manifestations and the development of allergic reactions.
Over time, the inflammatory process leads to fibroplastic changes in the arachnoid in the area of the optic junction and optic nerves. The proliferation of connective tissue causes the formation of extensive synechiae between the dura and arachnoid membranes. In addition to fibrous strands, cysts are formed, the cavities of which are filled with serous contents. There are multiple small or single large cystic formations. Cysts can surround the chiasm from all sides, leading to compression of the optic nerves. Compression of nerves is the main cause of their degenerative-dystrophic changes, and subsequently atrophy.
Classification
There are acute and chronic course of the disease. The chronic variant includes hereditary familial atrophy of the optic nerves (Leber’s amaurosis). There is a clear genetic predisposition to the development of this form of the disease. According to the clinical classification, it is customary to consider 3 types of optochiasmal arachnoiditis, the symptoms of which are dominated by the following signs:
- Retrobulbar nerve syndrome. The most common variant of the flow. Unilateral or asymmetric vision loss is possible. Pathology is accompanied by fascicular narrowing of the visual fields.
- Cystic formations. Clinical manifestations mimic the symptoms of a tumor of the optic chiasmal zone. An increase in the volume of cysts contributes to the compression of brain structures. If the size of the pathological formations is small, there are no symptoms.
- Complicated stagnation of the optic disc. This form of the disease is extremely rare. There are no signs of inflammation, an increase in edema indicates an increase in intracranial pressure. For the second time, the inner shell of the eyeball is involved in the pathological process.
Symptoms
Pathology is characterized by an acute onset. Patients complain of bilateral visual impairment, severe headache, which is not stopped by taking analgesics. There is increased fatigue when performing visual loads (reading books, working at the computer, watching movies). The progression of the disease leads to severe pain in the ocular region, radiating to the forehead, bridge of the nose, brow areas, temples. Pain syndrome can be localized directly in the orbit.
Patients note that visual acuity decreases very quickly. In severe cases, visual dysfunction reaches a maximum after a few hours, but more often this process takes 2-3 days. Gradually, individual sections fall out of the visual field. Pupils can be of different sizes. Patients suffer from color perception, especially the perception of red and green. During this time period, dyspeptic disorders (nausea, vomiting) may occur. In the future, the acute process is replaced by a chronic one. With concomitant damage to the cranial nerves, the sense of smell decreases. Due to a violation of the innervation of the facial nerve, the omission of the lateral corner of the eye or mouth is visualized.
When the affected area spreads to the hypothalamic region, patients suffer from frequent vegetative-vascular crises, thermoregulation is disrupted, convulsive muscle twitching is observed. There is increased sweating, thirst, subfebrility, sleep disorders. In contrast to the acute process, with the chronic course of pathology, the symptoms increase gradually. Some patients note that after diagnostic cisternography, vision is restored for a short period of time.
Complications
A common complication of pathology is optic nerve atrophy. Patients have a high probability of dislocation of brain structures. With an increase in cystic formations, compression of brain tissue and focal symptoms are observed. The spread of the pathological process to other membranes of the brain causes meningitis, meningoencephalitis. With a complicated course, the formation of intracranial abscesses is possible. With secondary damage to the ventricles of the brain, ventriculitis occurs. Patients are at risk of developing acute cerebrovascular accident.
Diagnostics
In the early stages, diagnosis is difficult. Since the most common cause of pathology is the lesion of the paranasal sinuses, radiography is performed at the stage of primary diagnosis. For more information, an MRI of the sinuses is performed. At the same time, it is possible to identify a small parietal swelling of the mucous membrane of the wedge-shaped sinus and a lesion of the posterior cells of the lattice labyrinth. Instrumental diagnostic methods include:
- Perimetry. Segmental or concentric narrowing of the visual field is detected in combination with bilateral limitations or hemianopsias in the temporal regions. If the disease proceeds according to the type of retrobulbar neuritis, central scotomas are observed in patients.
- Visometry. Progressive decrease in visual acuity is diagnosed. The nature of the lesion is symmetrical on both sides. The exception is the retrobulbar form, in which one or both eyes are affected, but asymmetrically.
- Ophthalmoscopy. Edema and hyperemia of the optic nerve disc are visualized. With increased intracranial pressure, OND has a stagnant appearance. The edema zone extends to the peripapillary region of the retina and the macular area.
- The study of pupillary reaction. At the beginning of the development of meningoencephalitis, the reaction of the pupils is sluggish. The progression of the disease leads to the fact that there is no pupillary reaction. Visually, mydriasis or anisocoria can be determined.
- Craniography. In the chronic form of the disease, there is a thickening of the wall of the Turkish saddle. The pineal body becomes calcified. Signs of intracranial hypertension are increasing. In young children, there is a slight divergence of cranial sutures.
- Pneumocysternography. The technique allows us to study the nature of changes in the chiasmal cistern. Adhesions, single or multiple cysts are detected. To improve visualization, air is injected into the tank cavity.
With a unilateral form of pathology, the examination of the patient must be repeated after 1-2 weeks due to the high risk of delayed damage to the second eye. The disease is also characterized by the phenomenon of “migrating defects”, in which hotel changes in the field of vision are determined in other areas.
Treatment
In the acute course of the disease, medication is prescribed. The duration of conservative therapy is 3-6 months. After the acute process is stopped, physiotherapy is indicated. With the help of electrophoresis, calcium preparations, vitamin PP are introduced. Effective use of acupuncture therapy lasting 10 sessions. To eliminate the symptoms of optochiasmal arachnoiditis, prescribe:
- Antibiotics. Antibacterial agents of the cephalosporin series are used. Additionally, sulfonamides can be used. The duration of antibiotic therapy should not exceed 5-7 days.
- Hormonal agents. Glucocorticosteroids (prednisone) are indicated in the acute process or severe course of the disease. Over time, hormones are replaced by nonsteroidal anti-inflammatory drugs.
- Multivitamin complexes. With optochiasmal arachnoiditis, the use of vitamins of group C, B. The introduction of glucose with ascorbic acid should be alternated with nicotinic acid.
- Antihistamines. H2-histamine blockers are used for allergic or toxic-infectious origin of meningoencephalitis. Additionally, calcium preparations are prescribed for hyposensitizing purposes.
- Detoxification therapy. It is indicated in the case of inflammation against the background of intracranial infection. Solutions of glucose, rheopolyglucine, hemodesis are used. The route of administration is intravenous drip.
- Hypotensive therapy. In order to reduce intracranial pressure with signs of hypertension, osmoactive substances are administered.
In the absence of the effect of drug therapy, lumbar puncture with the introduction of oxygen into the opto-chiasmal cistern is indicated. The purpose of this manipulation is to destroy connective tissue junctions. Surgical treatment of arachnoiditis is reduced to dissection of adhesions and removal of cysts in the chiasmal cistern and at the base of the brain. Surgical intervention is contraindicated in meningeal symptoms, pleocytosis or signs of OND edema. In order to prevent relapse of the disease in the postoperative period, anti-inflammatory therapy is prescribed. To control the effectiveness of treatment, a spinal puncture is performed. The treatment is carried out jointly by an ophthalmologist and a neurologist. A consultation with a neurosurgeon is required.
Prognosis and prevention
The outcome of optochiasmal arachnoiditis is determined by the severity and nature of the course of the disease. With a mild course of the disease, the prognosis is favorable, since visual disturbances are little pronounced. The progression of pathology can lead to permanent loss of vision. Specific preventive measures have not been developed. Nonspecific prevention is aimed at timely treatment of brain infections and inflammation of the paranasal sinuses. If symptoms occur in the long-term period after TBI, the patient should be registered with a neurologist at the dispensary.
