Cerebral arachnoiditis , opto - chiasmatic , spinal - Causes, Symptoms and Treatment .MF .
Arachnoiditis - an inflammation of the arachnoid membrane of the brain.However, only one isolated lesion arachnoid practically does not take place, since it is devoid of its own blood vessels, usually, the process proceeds with mild (vascular) shell.Therefore correct to speak of meningitis.
Causes of arachnoiditis
Arachnoiditis caused most infections, including neuroinfections.The cause of arachnoiditis may also be poisoning and injuries.The arachnoid and surrounding membranes marked their opacity and thickening.Arachnoiditis often leads to the adhesion process, resulting in between the shells appear connective adhesions;the welds visible haze and growth of blood vessels, and sometimes form cysts.Depending on the location of the main process distinguish arachnoiditis convex surface of the brain (convexital), opto-chiasmatic, posterior fossa and spinal .
symptoms of arachnoiditis
of the symptoms of cerebral arachnoiditis in the first place are headaches diffuse, less local character.
convexital arachnoiditis, usually located in the front of the brain, and therefore there are focal symptoms of motor and sensory character.There may be a focal and general seizures.
Optical chiasmatic arachnoiditis occurs after injury, common infections and inflammation in the transition from the nearby frontal, ethmoid and sphenoid sinuses.The disease begins with a gradual reduction of vision in both eyes.In the fundus sometimes it marked optic neuritis.There may be symptoms of increased intracranial pressure, and then the disease may resemble tumoroznuyu picture.In the diagnosis of optic-chiasmal arachnoiditis must constantly bear in mind the possibility of optic neuritis, which is half the debut of multiple sclerosis.
arachnoiditis posterior fossa occur after trauma, common infections and the transition of the inflammatory process in the shell.otogennyh from nearby fires.Previously, and most often affected.VIII pair of cranial nerves: there are tinnitus, dizziness, staggering;later joined by hearing loss and falls caloric test;sometimes involved VII and V pairs of nerves.There may be a nystagmus.In severe cases of focal symptoms accompanied by a pronounced gipergenzionno-hydrocephalic syndrome, including stagnant nipples.With such Pseudotumor during indistinguishable from arachnoiditis posterior fossa tumor.
Spinal arachnoiditis often localized in the lumbosacral or thoracic;sometimes there is a diffuse lesion of the arachnoid membrane.
Spinal arachnoiditis is characterized by radicular pain type, which could join the symptoms of spinal cord compression.
crucial in the diagnosis of spinal arachnoiditis are the results of myelography with matsodilom.In some cases the final diagnosis of the inflammatory nature of the compression of the roots or the spinal cord is only set during the surgical revision.
should point to an unreasonable tendency to expansion diagnosis of arachnoiditis in all unclear cases of cerebral and spinal pathology.This trend is particularly evident in the observed cohort of patients with chronic headaches.Meanwhile, not less than 90% of cases are caused by vasomotor headaches factors.It should be constantly aware of the frequency tsefalgicheskogo syndrome with nervousness.
in recent years has become apparent significant rare so-called fiber-chiasmal arachnoiditis and accordingly reduced the number of surgical interventions regarding this form.
highly controversial and differential diagnostic faces of those forms of arachnoiditis posterior fossa, which appear isolated lesion of the nerve VIII at a moderate headache.
important role in the prevalence of the diagnosis of cerebral arachnoiditis plays misinterpretation pnevmoentsefalogramm in such cases.As a rule, the traditional pattern of "cystic arachnoiditis" actually reflects rezidualyaye atrophic processes and expansion podobolochechnyh spaces is a suffragan of the character.And underestimates the wide variability of normal pnevmoentsefalograficheskoy picture.
the presence of bacterial infectious foci - antibiotics, sulfonamides.In all cases shown in preparations of iodine, biostimulants, diuretics, analgesics.
Indications for surgery arise when optical-chiasmatic arachnoiditis and inflammatory lesions of the posterior fossa membranes, occurring with a picture of occlusion.Surgical treatment is also to be inflammation of the spinal cord compression, and arachnoiditis caused by persistent radicular pain.
characterized primarily by progressive decrease of visual acuity in one or both eyes.At the same time it revealed concentric narrowing of visual fields, central scotoma often bitemporal hemianopsia.Usually observed stagnation of the optic nerve atrophy or neuritic changes.Some patients revealed Kennedy syndrome - a combination of a central scotoma and primary atrophy of the optic nerve in one eye with stagnant changes in the other.Along with damage to the optic nerve often have lesions of the olfactory nerves and oculomotor, pyramidal signs light.It is also possible hypothalamic violations -. Diabetes insipidus, the pathology of various types of exchange, premature sexual development, etc.
A. fiber-chiasmatic with acute development in most cases has a favorable prognosis.With the gradual fall in visual acuity and its recovery has been slow and is usually incomplete.A. When diagnostics are important additional research methods: Echo-EG, EEG, computed tomography, angiography.A long-term flow, often with repeated exacerbations, who is usually called infectious diseases and traumatic brain injury.
A. When convexital most often the process is localized in the central convolutions that usually manifests clinically focal (dzheksonovskimi) seizures.They are typical of clonic convulsions of a certain group of muscles, or paresthesia (the localization of A at the rear of the central gyrus and the superior parietal region) with subsequent dissemination in accordance with the topography of motility or sensitivity centers.Consciousness is thus preserved.The process can be extended to the opposite direction, which leads to disruption of consciousness.The most characteristic is their focal component.After a seizure may experience short-term weakness of the limbs on the side of seizures, and is fit - easy hemiparesis or failure cortico-spinal tract.The EEG detect epileptic activity center.
A. posterior fossa usually runs hard, with severe hypertensive sidromom.Headache (persistent or paroxysmal) is accompanied by repeated vomiting, dizziness, and sometimes bradycardia.Sooner appear stagnant changes in the fundus.Because the symptoms of focal brain lesions are usually marked static and locomotor ataxia, nystagmus, intention tremor, muscular hypotonia, and others., Often on one side.When the localization process in the cerebellopontine angle affects the roots of VII and VIII pairs, while the more common process and VI pairs of cranial nerves.A posterior fossa has a lot of common manifestations of the same tumor localization, but is milder symptoms without a clear rise.
divided into disseminated, diffuse and limited in the distribution process.Clinical manifestations depend on the nature, prevalence and localization process.Characteristic of radicular pain syndrome in combination with mild pronounced conduction and segmental impairments.There have peripheral paresis of individual muscles, lungs, central paresis or symptoms of cortico-spinal disease, sensory disorders and segmental conductor type.The cerebrospinal fluid is often determined by protein-cell dissociation.The children are rare.
has many similar manifestations with extramedullary spinal tumor;It can lead to compression syndrome with the presence of the block of subarachnoid space, which is a direct indication for surgical intervention.
treatment.Combined therapy should be carried out taking into account the possible etiology of the disease, clinical manifestations, and the stage of its development.A. In all forms administered broad spectrum antibiotics - ampicillin or carbenicillin at 200-300 mg / kg per day for 12-14 days, sulfonamides (0.25 mg sulfadimethoxine / kg 1 time a day for 5-7 dayset al.), salicylates.In severe cases, it shows the use of steroid hormones.It is advisable the appointment of antihistamines -. Suprastin, fenkorola, Tavegilum, etc., and every 5-7 days should be replaced by medication.Hypertensive syndrome is eliminated by dehydration therapy.Assign glycerol (0.5-1.0 g / kg per day), furosemide (0.02-0.04 g per day) and other widely used drugs that improve cerebral circulation -.. Cinnarizine, cavinton, teonikol and othersremission spend regenerative therapy using vitamins, anticholinesterase agents (oksazil, Neostigmine, galantamine), amino acids, nootropics (piriditol, Pantogamum, nootropil et al.).During this period also shows the absorbable biostimulants therapy - l and so on for 32-64 units (depending on age), aloe extract, etc. When rumolon Jacksonian seizures need long-term treatment with anticonvulsants (better benzonal, phenobarbital pure or in glyuferal. -paglyuferal).With fiber-chiasmal A. the fall in visual acuity spend long (for 4-6 weeks or more) of hormone therapy.In these cases shows retrobulbar administration of hydrocortisone (5-10 mg), and sometimes - surgery.When the optic nerve atrophy spend iodi-Office on Bourguignon or elektoforez lidazy.Surgical treatment - removal (or emptying) cysts, scarring, adhesions.
Arachnoiditis (meningitis) - a chronic autoimmune diffuse proliferative mainly arachnoid adhesions and soft meninges.
With clinical and expert positions is important to distinguish between the two pathogenic variants of cerebral arachnoiditis:
- true (actual) arachnoiditis: active adhesions autoimmune nature, flowing from the formation of antibodies to the lining of the brain, productive changes in the form of hyperplasia arahnoendoteliya leading to the meshes of death andobliteration likvoronosnyh channels in the subarachnoid space.Characterized by diffuse lesions shells involving molecular layer of bark, sometimes ependymal ventricular horeoidnogo plexus.A progressive course of chronic and intermittent.
- Residual condition after neuroinfections or traumatic brain injury with the outcome of obliteration, shells fibrosis (usually restricted), with the formation of adhesions and cysts at the site necrosis.There is a complete or partial regression of symptoms of acute period (exception - epileptic seizures).A progressive, as a rule, lacking.
This chapter examines the questions of clinic, and the ITU concerning only the patients with the true (actual) arachnoiditis.
clinical evolution of the disease concept (emphasis true clinically current arachnoiditis) forced to revise previous ideas about its prevalence.Apparently, arachnoiditis is about 3-5% among organic diseases of the nervous system (VS Lobzin, 1983).At two times more common in men.Clearly dominated by young persons (under 40 years).Over-diagnosis is a major cause unreasonably large number of patients with cerebral arachnoiditis, surveyed in BMSE.True data on disability due to arachnoiditis for the same reason no.
Etiology and pathogenesis
polyetiology disease.Main causes: influenza and other viral infections, chronic tonsillitis, rhinosinusitis, otitis, traumatic brain injury.In general, the infection is the cause of the disease in 55-60% of patients with closed craniocerebral trauma - 30%, 10-15% is definitely judge the etiological factor is difficult (Peel BN 1977; Lobzin VS 1983).
most common cause of infectious arachnoiditis - the flu.Arachnoiditis developed in a period of 3-5 months to a year or more after suffering flu, due to the time required for implementation of the autoimmune process.
Rinosinusogennaya etiology reliably installed in 13% of all cerebral arachnoiditis (Gushchin, AN, 1995).The disease develops slowly, usually in the background of acute rhinosinusitis.After a closed craniocerebral injury lucid interval as long (usually between 6 months and 1.5-2 years).The severity of the injury is not critical, although often adhesive envelope process is formed after brain injury, traumatic subarachnoid hemorrhage.The main pathogenic factor - the production of antibodies to the antigens of damaged membranes and brain tissue.
Depending on the preferential localization of isolated arachnoiditis: 1) convexital;2) the basilar (in particular, optical chiasmatic, interpedunkulyarny);3) posterior fossa (in particular, the cerebellopontine angle, large tanks).However, such rubrification is not always possible due to the diffuse nature of adhesions.
Given the pathological features useful to distinguish between adhesive and adhesive-cystic arachnoiditis.
Risk factors, progression
- Transferred acute infection (usually viral meningitis, meningoencephalitis).
- Chronic focal suppurative infections of the cranial localization (tonsillitis, sinusitis, otitis media, mastoiditis, periodontitis and others.).
- closed craniocerebral injury, especially re.
- predisposing and contributing to the aggravation of factors: heavy physical work in unfavorable microclimate, fatigue, alcohol or other intoxication, trauma of various localization, recurrent flu, SARS.
clinic and diagnostic criteria
1. A history information: 1) the etiological risk factors;2) the development of slowly and gradually.Initially often asthenic-neurotic symptoms, irritative (seizures), followed by hypertensive (headache, etc.).The gradual deterioration, sometimes temporary improvement.
2. Neurological Research, and local cerebral symptoms in different ratios depending on the predominant localization process.
1) cerebral symptoms.The basis - a violation liquorodynamics (liquor circulation), most pronounced when obliteration holes Lyushka Magendie and, much less frequently - due horioependimatita.Clinical symptoms are caused by intracranial hypertension (96%) or hypotension liquor (4%).Hypertensive syndrome more and more pronounced in the posterior fossa arachnoiditis, when 50% of patients on the background of focal symptoms observed stagnation of the optic nerve.Headache (80% of cases), usually morning, arching, pain during movement of the eyeballs, physical exertion, straining, coughing, nausea and 'vomiting.Also include: dizziness, non-systemic nature, tinnitus, hearing loss, autonomic dysfunction, increased sensory excitability (intolerance to bright lights, loud noises, etc.), Meteozavisimost.Frequent neurasthenic symptoms (general weakness, fatigue, irritability, sleep disturbance).
liquorodynamic crises (acute disorders arising dyscirculatory), manifesting increased cerebral symptoms.Accepted provide light (short gain headache, mild dizziness, nausea);moderate severity (more severe headache, poor general health, vomiting) and severe crises.