Arachnoiditis cerebral, optic-chiasmatic, spinal - Causes, symptoms and treatment. MF.
Jun 16, 2018
Arachnoiditis is an inflammation of the arachnoid of the brain. However, an isolated lesion of only one arachnoid membrane practically does not take place, since it lacks its own blood vessels, as a rule, the process passes from a soft( vascular) membrane. Therefore, it is more correct to talk about leptomeningitis.
Causes of arachnoiditis
Arachnoiditis is caused most often by infections, including neuroinfections. The cause of arachnoiditis can also be intoxication and trauma. In the arachnoid and adjacent shells, their turbidity and thickening are noted. Arachnoiditis often leads to adhesive processes, as a result of which connective tissue adhesions appear between the membranes;in places of adhesions, turbidity and growth of vessels are visible, and sometimes cysts are formed. Depending on the localization of the main process, is distinguished by arachnoiditis of the convex surface of the brain( convectional), optic-chiasmatic, posterior cranial fossa and spinal .
Symptoms of arachnoiditis
Symptoms of cerebral arachnoiditis are first of all headaches of diffuse, rarely local character.
Convexity arachnoiditis, as a rule, is located in the anterior parts of the brain, and accordingly there are focal symptoms of an impellent and sensitive nature. There may be both focal and general convulsive seizures.
Optic-chiasmal arachnoiditis occurs after injuries, common infections and in the transition of inflammation from nearby frontal, ethmoidal and sphenoidal sinuses. The disease begins with a gradual decrease in vision in both eyes. On the fundus, optic neuritis is sometimes noted. There may be symptoms of increased intracranial pressure, and then the course of the disease may resemble a tumor-like picture. When diagnosing optic-chiasmal arachnoiditis, one must always keep in mind the possibility of retrobulbar neuritis, which in half the cases is the onset of multiple sclerosis.
Arachnoiditis of the posterior cranial fossa occurs after injuries, common infections and the transition of the inflammatory process to the membranes.from nearby foci of foci. Previously and most often amazed. VIII pair of cranial nerves: there is noise in the ears, dizziness, swaying;Later, a decrease in hearing is added and a caloric test drops out;sometimes VII and V pairs of nerves are involved. Nystagmus may occur. In severe cases, focal symptomatology is accompanied by a pronounced hypergenic-hydrocephalic syndrome, including stagnant nipples. With such a pseudotumorous course, arachnoiditis is indistinguishable from a tumor in the posterior cranial fossa.
Spinal arachnoiditis is more often localized in the lumbosacral or thoracic region;sometimes there is a diffuse lesion of the arachnoid shell.
Spinal arachnoiditis is characterized by pain of the radicular type, to which the symptoms of compression of the spinal cord may join.
Diagnosis of arachnoiditis
The results of myodogy with mazodil are crucial in the diagnosis of spinal arachnoiditis. In some cases, the final diagnosis of the inflammatory nature of compression of roots or spinal cord is established only during surgical revision.
It should be pointed out that there is an unjustified tendency to an extensive diagnostic of arachnoiditis in all cases of cerebral and spinal pathology. This tendency is especially evident in the contingent of patients with chronic headaches. Meanwhile, at least 90% of the cases of headaches are caused by vasomotor factors. You should always remember the frequency of the celiac syndrome with neuroses.
In recent years, a significant rarity of the so-called optic-chiasmal arachnoiditis has become evident and the number of surgical interventions for this form has accordingly decreased.
Very controversial and differential diagnostic faces of those forms of arachnoiditis of the posterior cranial fossa, which are manifested by isolated defeat of the VIII nerve with moderate headache.
A significant role in the prevalence of the diagnosis of cerebral arachnoiditis is played by an incorrect interpretation of pneumoencephalograms in such cases. As a rule, the traditional picture of "cystic arachnoiditis" in fact reflects residual atrophic processes, and the expansion of the subshell spaces is only vicarious. The wide variability of the normal pneumoencephalographic picture is also underestimated.
Treatment of arachnoiditis
In the presence of bacterial infectious foci - antibiotics, sulfonamides. In all cases, iodine preparations, biostimulants, diuretics, analgesics are shown.
Indications for surgical intervention arise with optic-chiasmatic arachnoiditis and inflammatory lesions of the membranes of the posterior cranial fossa occurring with the picture of occlusion. Surgical treatment also includes inflammatory compression of the spinal cord and persistent radicular pain caused by arachnoiditis.
Is characterized primarily by a progressive decrease in visual acuity to one or both eyes. In this case, a concentric narrowing of the visual fields, a central scotoma, and often a bitemporal hemianopia are found. Usually there is a stagnant disk of optic nerves, their atrophy or neuritic changes. Some patients have Kennedy syndrome-a combination of central scotoma and primary optic atrophy on one eye with stagnant changes on the other. Along with the defeat of the optic nerve, lesions of the olfactory and oculomotor nerves, light pyramidal signs are often observed. There are also hypothalamic disorders - diabetes insipidus, pathology of various types of metabolism, premature sexual development, etc.
A. Optical-chiasmatic with acute development in most cases has a favorable prognosis. With a gradual fall in visual acuity, its recovery also passes slowly and is usually incomplete. In the diagnosis of angina, additional methods of investigation are of great importance: Echo-EG, EEG, computed tomography, angiography. Prolonged A. long, often with repeated exacerbations, which are usually caused by infectious diseases and traumatic brain injury.
In A. convectal, the process is most often localized in the area of the central convolutions, which is usually clinically manifested by focal( Jackson) seizures. Typical for them are the clonic convulsions of a certain muscle group or paresthesia( when the A. is localized in the posterior central gyrus or upper parietal region), followed by propagation in accordance with the topography of the centers of motility or sensitivity. Consciousness is preserved. The process can spread to the opposite side, which leads to a violation of consciousness. The most characteristic remains their focal component. After a fit, there may be a short-term weakness of the limbs on the side of the convulsions, and outside the fit - mild hemiparesis or insufficiency of the cortical and spinal tracts. On the EEG, a focus of epileptic activity is detected.
A. The posterior cranial fossa usually flows heavily, with a marked hypertensive sidromus. Headache( constant or paroxysmal) is accompanied by repeated vomiting, dizziness, sometimes bradycardia. Early stagnant changes of the fundus appear. Of the symptoms of focal brain lesion, there are usually static and locomotor ataxia, nystagmus, intentional tremor, muscle hypotension, and others, often on the one hand. When the process is localized in the region of the cerebellar angle, the roots of VII and VIII pairs are affected, and in the more common process and the VI pair of cranial nerves. A. posterior cranial fossa has many common manifestations with a tumor of the same localization, but it proceeds milder, without a clear increase in symptoms.
The prevalence of the process is divided into disseminated, diffuse and limited. Clinical manifestations depend on the nature, prevalence and localization of the process. Characterized by radicular pain syndrome in conjunction with the poorly expressed conductor and segmental disorders. Peripheral paresis of individual muscles, light central paresis or symptoms of cortico-spinal failure, sensory disorders of segmental and conductor type are noted. In cerebrospinal fluid, protein-cell dissociation is often determined. Children are rare.
Has many similar manifestations with extramedullary spinal tumor;can lead to the development of compression syndrome with the presence of a block of subarachnoid space, which becomes a direct indication for surgical intervention.
Treatment. Complex therapy should be carried out taking into account the possible etiology of the disease, clinical manifestations and the stage of its development. For all forms of A. prescribe antibiotics of a wide spectrum of action - ampicillin or carbenicillin at 200-300 mg / kg per day for 12-14 days, sulfonamides( sulfadimethoxin at 0.25 mg / kg once a day for 5-7 daysand others), salicylates. In severe cases, the use of steroid hormones is indicated. It is advisable to prescribe antihistamines - suprastin, fenkrola, tavegil, etc., and every 5-7 days should be changed drug. Hypertensive syndrome is eliminated by dehydrating therapy. Assign glycerol( 0.5-1.0 g / kg per day), furosemide( 0.02-0.04 g per day), etc. Widely used drugs that improve cerebral circulation - cinnarizine, cavinton, theonikol, etc. InRemission therapy is carried out with the use of vitamins, anticholinesterase drugs( oxazil, proserine, galantamine), amino acids, nootropic drugs( pyriditol, pantogam, nootropil, etc.).In this period, resorption therapy with biostimulants is also shown - l and then for 32-64 units( depending on the age), aloe extract, rumolon, etc. In Jacksonian seizures, prolonged treatment with anticonvulsants is necessary( benzonale is better, phenobarbital is pure or in the composition of gluferal -paplouferal).With optico-chiasmatic A. with a drop in visual acuity, a long-term( for 4-6 weeks or more) hormonal therapy is performed. In these cases, retrobulbar injection of hydrocortisone( 5-10 mg) is indicated, and sometimes - surgical intervention. At an atrophy of the optic nerve iodination is carried out according to Bourguignon or electophoresis of lidase. Operative treatment - removal( or emptying) of cysts, scars, adhesions.
Arachnoiditis( leptomeningitis) is a chronic diffuse autoimmune proliferative adhesive process mainly of the arachnoid and soft membranes of the brain.
It is important to distinguish between two pathogenetic variants of cerebral arachnoiditis from clinical and expert positions:
- True( actual) arachnoiditis: active adhesion process of autoimmune nature, which proceeds with the formation of antibodies to the brain envelopes, productive changes in the form of hyperplasia of arachnoendothelium, leading to cell death and obliteration of the liquor-bearing channelsin the subarachnoid space. The diffuse nature of the lesion of the membranes with the involvement of the molecular layer of the cortex, sometimes the ependyma of the ventricles, the choreoid plexus, is characteristic. The course is chronically progressive and intermittent.
- Residual state after neuroinfection or craniocerebral trauma with outcome in the obliteration, fibrosis of the membranes( usually of limited prevalence), with the formation of fusions and cysts at the site of necrosis. There is a complete or partial regression of symptoms of an acute period( except for epileptic seizures).The latter, as a rule, is absent.
This chapter discusses clinic and ITU issues related only to patients with true( actual) arachnoiditis.
The evolution of the clinical concept of the disease( the isolation of a true clinically relevant arachnoiditis) made it necessary to revise the previous notions of its prevalence. Apparently, arachnoiditis is about 3-5% among organic diseases of the nervous system( Lobzin VS, 1983).Twice more common in men. Clearly, young people( up to 40 years) predominate. Hyperdiagnostics is the main reason for an unjustifiably large number of patients with cerebral arachnoiditis, who were examined at the BMSE.True data on disability due to arachnoiditis for the same reason are absent.
Etiology and pathogenesis
Disease is polyethiologically. The 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, closed craniocerebral trauma - in 30%, in 10-15% it is definitely difficult to judge the etiological factor( Bil 'BN, 1977; Lobzin VS, 1983).
The most common cause of infectious arachnoiditis is influenza. Arachnoiditis develops within a period of 3-5 months to a year or more after the flu has been transferred, which is explained by the time needed to carry out an autoimmune process.
Rhinosinusogenic aetiology is reliably established in 13% of all cerebral arachnoiditis( Gushchin AN, 1995).The disease develops slowly, usually against the background of exacerbation of rhinosinusitis. After a closed craniocerebral injury, the light interval is also long( more often from 6 months to 1.5-2 years).The severity of the injury does not play a decisive role, although more often the adhesion process is formed after a brain injury, traumatic subarachnoid hemorrhage. The main pathogenetic factor is the formation of antibodies to antigens of damaged membranes and brain tissue.
Depending on the primary localization, arachnoiditis is distinguished: 1) convective;2) basilar( in particular, optico-chiasmatic, interpeduncular);3) posterior cranial fossa( in particular, bridge-cerebellar angle, large cistern).However, such a classification is not always possible due to the diffusion of the adhesive process.
Given the pathomorphological features, it is advisable to distinguish between adhesive and adhesive-cystic arachnoiditis.
Risk factors for the onset, progression of
- Acute acute infections( more often viral meningitis, meningoencephalitis).
- Chronic focal purulent infections of cranial localization( tonsillitis, sinusitis, otitis, mastoiditis, periodontitis and DR.).
- Closed craniocerebral injury, especially repeated.
- Predisposing and exacerbating factors: heavy physical work in conditions of unfavorable microclimate, overwork, alcohol and other intoxications, traumas of different localization, repeated influenza, SARS.
Clinic and diagnostic criteria for
1. Anamnestic information: 1) etiological risk factors;2) development gradually, gradually. Initially, often astheno-neurotic symptoms, irritative( epileptic seizures), then hypertensive( headache, etc.).Gradual deterioration of the condition, sometimes temporary improvement.
2. Neurological examination: cerebral and local symptoms in different proportions depending on the preferential localization of the process.
1) General cerebral symptoms. At the heart of it is a disturbance of liquorodynamics( liquor circulation), most pronounced with obliteration of the openings of Magendi and Lushka, much less often - due to chorioependimatitis. Clinical symptoms are caused by intracranial hypertension( 96%) or by liquor hypotension( 4%).Hypertensive syndrome is more often and most pronounced in the arachnoiditis of the posterior cranial fossa, when 50% of patients on a background of focal symptomatology observe stagnant disks of optic nerves. Headache( in 80% of cases), usually morning, bursting, tenderness with movement of eyeballs, physical strain, straining, coughing, nausea, vomiting. Also referred to: dizziness non-systemic nature, noise in the ears, hearing loss, autonomic dysfunction, increased sensory excitability( intolerance of bright light, loud sounds, etc.), meteorological dependence. Neurasthenic manifestations are frequent( general weakness, fatigue, irritability, sleep disturbance).
Liquorodynamic crises( acute dyscirculatory disorders), manifested by increased cerebral symptoms. It is customary to isolate the lungs( short-term headache, mild dizziness, nausea);moderate severity( more severe headache, poor overall health, vomiting) and severe crises. The latter last from several hours to 1-2 days, manifested by severe headache, vomiting, general weakness, a violation of adaptation to external influences. Often and vegetative-visceral disorders. Depending on the frequency, rare( 1-2 times a month and less often), medium frequency( 3-4 times a month) and frequent( more than 4 times a month) crises are distinguished.
2) Local or focal symptoms. Determined by the primary localization of organic changes in the shells of the brain and adjacent structures. In general, focal symptoms are characterized by a predominance of the phenomena of stimulation, and not loss. An exception is optic-chiasmal arachnoiditis.
- convective arachnoiditis ( in 25% of patients, more often traumatic etiology).Characteristically, the prevalence of local symptoms( depending on the lesion of the region of the central gyri, parietal, temporal).In the cystic form of arachnoiditis, usually mild or moderately expressed motor and sensory disorders( pyramidal insufficiency, light hemi or monoparesis, hemihypesthesia).Typical epileptic seizures( in 35% of patients), often the first manifestation of the disease. Secondarily, generalized partial seizures( Jacksonian), sometimes with a transient post-paroxysmal neurologic deficit( Todd's paralysis) are common. Characteristic polymorphism of seizures in connection with the often temporal localization of the process: simple and complex( psychomotor), partial with secondary generalization, primarily generalized, their combination. On EEG in 40-80% of patients( according to different data) epileptic activity is detected, including complexes of peak-slow wave. Cerebral symptoms moderate, severe headaches, crisis conditions more often during an exacerbation;
- basilar arachnoiditis ( in 27% of patients) may be prevalent or localized predominantly in the anterior, middle cranial fossa, in the intercostal or optico-chiasmatic cistern. With a significant spread in the adhesive process, many cranial nerves are involved on the basis of the brain( I, III-VI pairs), which determines the clinic of the disease. Pyramidal insufficiency is also possible. The cerebral symptoms are easily and moderately expressed. Mental disturbances( fatigue, loss of memory, attention, mental performance) are more often observed with arachnoiditis of the anterior cranial fossa.
The most distinctive symptomatology in the case of optic-chiasmal arachnoiditis. Currently, it is rarely diagnosed, since in the overwhelming majority of cases the chiasmatic syndrome is caused by other causes( see "Differential diagnosis").It develops more often after a viral infection( influenza), trauma, against a background of sinusitis. General cerebral symptoms are weak or absent. The initial symptoms are the appearance of the net before the eyes, progressive reduction in visual acuity, more often at once bilateral, for 3-6 months. On the fundus - first neuritis, then atrophy of the discs of the optic nerves. The field of vision is concentric, less often a bi-temporal narrowing, single or bilateral central scotoma. Possible endocrine metabolic disorders due to involvement in the process of the hypothalamus;
- arachnoiditis of the posterior cranial fossa of ( in 23% of patients), usually post-infectious, otogenic. Often there is a severe, pseudotemorous flow in connection with pronounced disturbances of liquorodynamics, damage to the cranial nerves of the caudal group, cerebellar symptoms. With the predominant localization in the area of the bridge-cerebellar angle, an earlier appearance of the VIII pair of cranial nerves( tinnitus, hearing loss, dizziness) occurs. In the future, the facial nerve suffers, cerebellar insufficiency, pyramidal symptoms are revealed. The first symptom of the disease may be facial pain as a consequence of trigeminal neuropathy. Arachnoiditis of a large cistern and adjacent formations is characterized by the greatest severity of hypertensive syndrome due to obliteration of the liquor-bearing pathways and disturbance of the outflow of the liquor. Frequent severe crises, expressed cerebellar symptoms. Complication is the development of the syringomyelitic cyst. In view of the severe condition of patients, it is sometimes necessary to resort to surgical intervention.
3. Additional research data. The need for an adequate assessment due to the difficulties and frequent errors in the diagnosis of arachnoiditis. It is wrong to judge the true( actual) arachnoid only on the basis of the morphological changes detected on PEG, in CT, MRI, without taking into account the features of the clinical picture, the course of the disease( the progression of the first symptoms, the appearance of a new symptomatology).Therefore, it is necessary to objectify complaints that testify to hypertensive syndrome, visual impairment, frequency and severity of crises, epileptic seizures.
Only a comparison of the clinical data and the results of additional studies gives grounds to diagnose the true current arachnoiditis and distinguish it from residual stable states:
- craniogram. Symptoms sometimes detected( finger impressions, porosity of the back of the Turkish saddle usually indicate the increase in intracranial pressure in the past( old craniocerebral trauma, infection) and can not in themselves testify in favor of the actual arachnoiditis,
- echoes can provide information about the presenceand the severity of hydrocephalus, but it does not allow to judge its nature( normotensive, hypertensive) and the cause,
- lumbar puncture. The pressure of CSF is increased in different degrees in half of the patientsx When exacerbating the arachnoiditis of the posterior cranial fossa, the basal can reach up to 250-400 mm of water lying down. The decrease in pressure occurs in chorioependimatites. The number of cells( up to several tens of 1 μl) and protein( up to 0.6 g / l) increasesin the case of the activity of the process, the remaining patients are normal, and the protein content is even lower than 0.2 g / l
- PEG has an important diagnostic value. The signs of adhesive arachnoiditis, scar changes, internal or external hydrocephalus, atrophic process are revealed. At the same time, PEG data can be the basis for the diagnosis of true arachnoiditis only when taking into account the features of the clinic and the course of the disease. They are often evidence of residual changes in the subarachnoid space and brain substance after trauma, neuroinfection, occur in epileptic patients without clinical signs of arachnoiditis;
- CT, MRI allow us to objectify the adhesive and atrophic process, the presence of hydrocephalus and its nature( areosorbic, occlusive), cystic cavities, exclude volume formation. CT-cisternography makes it possible to identify direct signs of changes in the configuration of the sub-paternal spaces and cisterns. However, the information obtained is of diagnostic significance only when the lumbar puncture data are adequately assessed( especially the state of liquor pressure), the clinic of the disease as a whole;
- EEG reveals foci of irrigation with convective arachnoiditis, epileptic activity( in 78% of patients with epileptic seizures).These data only indirectly indicate the possibility of an adhesive process and in themselves are not the basis for a diagnosis;
- immunological studies, determination of serotonin and other neurotransmitters in blood and CSF are important for judging the activity of the inflammatory shell process, the degree of involvement of brain substance in it;
- ophthalmic examination is used with a diagnostic purpose not only for optico-chiasmatic, but diffuse arachnoiditis in connection with the frequent involvement of visual pathways in the pathological process;
- otolaryngology diagnosis is important primarily for determining the etiology of arachnoiditis;
- experimental psychological study allows you to objectively assess the state of mental functions, the degree of asthenization of the patient.
1. With volumetric process( especially important and most responsible).It is based on the features of the clinical picture, its dynamics. Difficulties are more common with benign tumors of the posterior cranial fossa, pituitary gland and selar region( see Section 7.2.).
2. Optic-chiasmal arachnoiditis: a) with retrobulbar neuritis, mainly with multiple sclerosis, especially if observed in the onset of the disease. Some clinical features of retrobulbar neuritis: remitting flow;usually unilateral defeat;clinical dissociation between visual acuity and severity of changes on the fundus;rapid( within 1-2 days) reduction in visual acuity, its fluctuations during the day and spontaneous( within a few hours, days, weeks) recovery to tenths or 1.0;instability of the central livestock( see also Chapter 3);b) with hereditary atrophy of the optic nerves of Leber: inheritance associated with sex, a progressive drop in visual acuity in both eyes without remission. Despite the available information about the presence of adhesions in the chiasmatic region, it can not be considered a chiasmatic arachnoiditis;c) with a tumor of the chiasmatic-selar region( see Section 7.2.).
3. With neurosarcoidosis. The defeat of the membranes of the brain is a frequent and clinically most vivid manifestation of the sarcoidosis granulomatous process( Makarov A. Yu. Et al., 1995).It develops in 22% of patients with sarcoidosis organic lesion of the nervous system against the background of lung granulomatosis or peripheral lymph nodes. Sarcoid granulomas are localized in the soft and arachnoid shells, mainly on the basis of the brain. The process can be diffuse and limited, most often optico-chiasmal localization, much less often in the region of the posterior cranial fossa. Granulomas occupy the hypo-thalamo-pituitary area, which sometimes manifests itself as severe diabetes insipidus, other endocrine disorders. Based on the brain, multiple granulomas are well identified by MRI.The clinical picture corresponds to the predominant location of the granulomas. Likvorodinamichesky disturbances, a hydrocephalus are most expressed at the widespread arachnoiditis. During the exacerbation in the cerebrospinal fluid there may be a small lymphocytic pleocytosis. Sarcoidosis is actually one of the etiological factors of arachnoiditis. However, features, pathogenesis( productive process against specific granulomas), good kurabilnost( corticosteroids, presocil, plakvenil, antioxidants), damage to the membranes along with sarcoidosis of the lungs and other internal organs make it an independent disease.
4. With the consequences of a closed or open craniocerebral trauma( usually severe), neuroinfections( meningitis, meningoencephalitis) with residual adhesive, fibrous, cystic changes in the membranes are usually limited, without a progressive course of the disease. Epileptic seizures in this situation are not grounds for diagnosing the true current arachnoiditis. The same should be borne in mind in the case of idiopathic epilepsy, when PEG or visualization methods reveal local shell changes.
5. With neurosis( often neurasthenia) or neurasthenic syndrome with organic diseases and traumas of the nervous system( due to frequent mental disorders in the clinical picture of the actual arachnoiditis).
The course and prognosis of
To a large extent are determined by etiology, the primary localization of the adhesive process. The basis for the diagnosis of true arachnoiditis is a chronic course with exacerbations. A certain regression is possible, a state of relative( sometimes long-term) compensation, which often occurs with age in connection with the atrophic process and, as a consequence, a decrease in the severity of disorders of liquorodynamics. Clinically, the prognosis is usually favorable. It is worse with optic-chiasmal form, better with convecital. Danger represents arachnoiditis of the posterior cranial fossa with occlusive hydrocephalus. The course of the disease is aggravated, and sometimes the prognosis is the other consequences of trauma, neuroinfections acting as the etiological factor of arachnoiditis. The labor forecast is worse in patients with frequent relapses, crises, epileptic seizures, progressive deterioration of vision.
Principles of treatment
- Should be performed in a hospital after diagnosis using additional methods and conclusions about true( actual) arachnoiditis.
- It is determined by the etiology( the presence of the focus of infection), the predominant localization and activity of the adhesive process.
- Repeat rates and duration of drug therapy:
- glucocorticoids( prednisolone) at a dose of 60 mg per day for 2 weeks;
- absorbable( bioquinol, pyrogenal, rumalone, lidase, etc.);
- dehydration( with increased intracranial pressure);
- antihistamine, antiallergic( fenkarol, tavegil, dimedrol, etc.);
- stimulating metabolic processes in the brain( nootropics, cerebrolysin, etc.);
- corrective accompanying mental disorders( tranquilizers, sedatives, antidepressants);
- antiepileptic drugs( taking into account the nature of epileptic seizures).
- Surgical treatment. Indications taking into account the nature of the course and severity of clinical manifestations in arachnoiditis of the optic-chiasmal, posterior cranial fossa. Stimulation of the optic nerves through implanted electrodes with a significant decrease in visual acuity. In addition, the sanation of foci of infection( sinusitis, otitis, etc.).
Medical and Social Expertise VUT Criteria
- During the period of primary diagnosis, treatment. Depending on the severity of HF disease from 1 to 3 months. The continuation of treatment on the hospital sheet, taking into account the nature of the course of the process, the degree of recovery( compensation) of impaired functions is an average of 1-2 months( if possible later return to work in the specialty or lower skills with a decrease in earnings).
- With exacerbations of VL for 3-4 weeks or more, depending on their severity and the effectiveness of therapy( for the period of inpatient or outpatient treatment).The profession and working conditions are taken into account: long periods of work associated with physical stress, performed under the influence of other unfavorable factors in the process of labor( psychoemotional, visual, vestibular, etc.).
- After a severe crisis - a sick leave for 3-4 days.
- After surgery for arachnoiditis of the posterior cranial fossa, optic-chiasmatic( usually not less than 3-4 months with subsequent direction to BMSE).
The main causes of disability
- Visual impairment: progressive reduction in severity and narrowing of the field of vision. Social insufficiency arises with the limitation or loss of the possibility of orientation, the ability of detailed vision. In connection with this, work capacity is limited or lost in many professions, or patients need constant external help.
- Disorders of liquorodynamics, manifested, as a rule, by hypertensive syndrome with repeated crisis conditions. Confirmed during a stationary examination, in particular the results of a lumbar puncture, hypertensive crises limit the vital activity of patients. During the crisis of moderate severity, and especially severe, orientation disorder is possible, the ability to make decisions decreases, which leads to a temporary inability to continue working. Repeated crises, especially accompanied by dizziness, vegetative disorders, can significantly limit the vital activity and ability to work of patients.
- Epileptic seizures lead to the limitation of life and disability due to the periodic loss of control over their behavior to patients, in connection with which it is impossible to work in a number of professions.
- Astheno-neurasthenic syndrome, concomitant vegetative dystonia lead to disadaptation( reduction of endurance to climatic factors, to noise, bright lighting, industrial stresses).This limits the life activity of patients, depending on the nature and conditions of work.
- The combination of these syndromes with cerebellar, vestibular disorders( mainly in the arachnoiditis of the posterior cranial fossa) aggravates the degree of limitation of vital activity due to disruption of locomotor capacity, reduction of manual activity. This can be the reason for the restriction, and sometimes the loss of ability to work.
Examples of diagnosis
- cerebral arachnoiditis of the posterior cranial fossa( otogenic) with severe hypertensive syndrome, frequent severe crises, moderate vestibular and cerebellar disorders in the acute stage;
- arachnoiditis of the brain( posttraumatic) of convective localization with rare secondary generalized epileptic seizures, mild rare hypertensive crises in remission;
- consequences of closed craniocerebral trauma in the form of mild trunk organic symptoms, optic-chiasmal arachnoiditis with partial atrophy of optic nerves of both eyes, moderate decrease in visual acuity and concentric narrowing of the visual field, pronounced asthenic syndrome, with slowly progressing course.
Contraindicated types and working conditions
- General contraindications: significant physical and neuropsychic stress, the impact of unfavorable factors in the labor process( meteorological, vibration, noise, contact with toxic substances, etc.).
- Individual - depending on the main syndrome or a combination of several clinically significant disorders: visual, liquorodynamic, epileptic seizures, vestibular dysfunction, etc. For example, in cases of significant visual disturbances, patients who do not require a constant eye strain or a clear distinction of colors( corrector, engraver,operator COMPUTER, artist, colorimeter and DR.).
- With rare exacerbations( long-term remission) with mild disorders of liquorodynamics, rare epileptic seizures or their absence, moderation of other disorders that do not affect the ability to continue working in the specialty( sometimes with minor limitations on the recommendation of the KEK), without social insufficiency.
- In the stage of compensation after successful therapy, rationally employed( often recognized previously limitedly able-bodied).
Indication for referral to BMSE
- Persistent, severe impairment of function( despite treatment).Primarily hypertensive syndrome, epileptic seizures, visual defect.
- Progressive course with repeated exacerbations, an increase in neurological symptoms, which necessitates the transition to work with a decline in skills or a significant reduction in the volume of production activities.
Necessary minimum of the survey for referral to BMSE
- The results of the liquorological study( pressure, CSF composition), preferably in dynamics.
- Data of PEG, CT, MRI.
- Results of ophthalmologic examination( mandatory eye fundus, acuity and field of vision in dynamics) and otorhinolaryngological examination.
- The data of experimental psychological research.
- Clinical tests of blood, urine.
III group: social insufficiency caused by the need to change working conditions depending on the nature of the impairment of functions( epileptic seizures, hypertensive syndrome, visual impairment, etc.).Patients need a significant reduction in the amount of work or retraining in connection with the loss of the profession( by the criteria for limiting the ability to orientate, first-degree work).At the next re-examination it is necessary to take into account that successful rehabilitation( favorable course of the disease, rational employment) is the basis for recognizing the patient as able-bodied.
II group: severe limitation of vital functions due to progressive course of the disease, frequent exacerbations, persistent severe visual impairment( decrease in visual acuity from 0.04 to 0.08 in the best seeing eye, narrowing of the field of vision to 15-20 °), liquorodynamicdisorders with frequent severe crises, frequent epileptic seizures, vestibular, cerebellar dysfunction, or a combination of these disorders( according to the criteria for limiting the ability to work in the second or third degree,entatsii, to control the behavior of the second degree).Favorable results of treatment, relative stabilization in the course of the disease, make possible the positive dynamics of disability.
group I: rarely, usually with opticchiosmal arachnoiditis( complete blindness, reduced visual acuity up to 0.03 for both or better seeing eye, and sharp narrowing of the field of vision to 10 ° and less in all radians) - according to the criteria of restrictionability to orientation and self-service of the third degree.
In case of persistent and irreversible visual impairment, after 5 years of observation, the disability group is established without specifying the time for reassessment.
After surgical treatment for arachnoiditis of the posterior cranial fossa or optic-chiasmatic at the first examination, the II group of disability is usually determined, in the future the expert decision depends on the results of the operation.
Causes of Disability: 1) a common disease;2) labor injury( with post-traumatic arachnoiditis);3) disability due to illness received during military service and other military reasons.
Prevention of disability
- Prevention of viral diseases( influenza, etc.), which are the cause of arachnoiditis;
- timely treatment of inflammatory processes of cranial localization( rhinosinusitis, otitis, tonsillitis, etc.);
- adequate treatment of victims with traumatic brain injury( including mild).
- timely diagnosis and optimal therapy of a patient with diagnosed arachnoiditis;
- compliance with the terms of VN taking into account the severity of the exacerbation, nature and working conditions;
- dispensary observation( 2 times a year), repeated courses of anti-relapse therapy, including in the dispensary, sanatoriums.
- relapse prevention by excluding risk factors for disease progression, including during labor activity( taking into account contraindications depending on the main clinical syndrome);
- if necessary timely surgical treatment;
- a well-founded definition of disability, retraining and training of disabled people of the III group with subsequent employment.
An individual rehabilitation program should be designed taking into account the severity of clinical manifestations, the primary localization of the adhesion process and the features of the course of the disease. Rehabilitation potential in patients with actual arachnoiditis is usually quite high( except for the severe form of optic-chiasmal arachnoiditis).It is possible to achieve a level of full or partial rehabilitation.
In the program of full rehabilitation( in patients with mild or moderate restriction of vital activity, relatively favorable course of the disease), dispensary observation, anti-relapse treatment, in particular, psychotherapy, in a hospital, a polyclinic, dispensaries;measures for rational employment by creating lightened working conditions for the conclusion of the KEK.
The partial rehabilitation program( for patients with moderate or significant limitation of vital activity) should provide for more active therapeutic measures, if necessary, prompt treatment;rational employment by providing a reduced volume of productive activity or transfer to another job, which may be due to the loss of the profession. In this regard, III group of disability is determined and retraining is necessary. The latter is carried out taking into account the clinical features of the disease, age, general education through training in the technical school, the vocational school of the social protection system, individual apprenticeships. Examples of available professions: repairman for household appliances, television and radio equipment, technologist-technologist, livestock specialist, administrator, manager, etc.
Positive dynamics of disability and return to work without restrictions, provided effective treatment, use of adequate measures of professional and social rehabilitation is achieved in70-80% of patients with cerebral arachnoiditis.