HORIOEPENDIMATYT (chorioepen-dymitis; lat. chorioidea choroid + Greek ependyma, ependy-mat[os] ependyma +-itis; synonym: vent-rikulit, ventrikulyarny meningitis, periventrikulyarny encephalitis) — the inflammatory disease of a brain with preferential defeat of a vystilka (ependyma) and vascular (choroidal) textures of ventricles of a brain which is characterized by disturbance of products, a resorption and circulation of cerebrospinal liquid.
The term «horioependimatit» H is offered in 1972. M. Madzhidov. Horioependimatit as the independent disease meets seldom, considerably more often there is a syndrome of a horioependimatit in combination with a pia-arachnitis of various etiology and localization. Depending on an etiology distinguish rheumatic, postgrippo zny, tonzillo-gene, posttraumatic and other horioependimatita. On a current horioependimatit it is subdivided on acute, subacute and chronic. On a state likvorodina-Mikey horioependimatit can be okklyuziruyushchy (a syndrome of occlusion of a silviyev of a water supply system, Marangdi's opening, Monroe opening) and not ok-klyuziruyushchim in hyper secretory (with a syndrome of open hydrocephaly or a syndrome of intracranial hypertensia without hydrocephaly) and giposekreto to a rny phase (a fibrous and sclerous form with a hypotensive syndrome). Allocate primary and secondary, or reactive, horioependimatita (at tumors, abscesses of a brain).
X about rioependy and Tit occurs equally often at men and women of preferential young age.
The etiology is various. Most often horioependimatit develops after flu, quinsy, at hron. tonsillitis, sinusitis, otitis, abscess of a brain, the rheumatism closed skull-but-hmozgovykh injuries, etc. Horioependimatit complicates encephalitis, meningitis of various etiology less often (meningococcal, tubercular, brucellous, syphilitic), parasitic damages of a brain (cysticercosis, current nozzles and zmoz).
Pathogeny. Inflammatory changes in ventricles of a brain (see) at a horioependimatita can be result of distribution of contagiums in the hematogenous way, and also but to iyerivaskulyar-iy spaces, likvorny ways and kontaktno (in the presence in the neighbourhood with cerebral cavities of the inflammatory center). Aseptic inflammatory reaction in an ependyma, a subependimarny layer, and also in vascular textures (see) cerebral cavities is the cornerstone of development of a posttraumatic horioependimatit. Character etiol. a factor to a certain extent predetermines the course of a disease. Horioependimatit a virus etiology develops sharply, sinusogenny and otogenic — it is subacute, and tonzil-logenny and rheumatic — more slowly. In the mechanism of development of a horioependimatit the large role is played by allergic states and autoimmune reactions.
Patol. the changes similar to changes at a horioependimatita were reproduced in experiments on animals by mechanical obstruction of likvorny ways, introduction to the big tank (the cerebellar and brain tank, T.) a brain of a suspension of talc or a kaolin, intraperitoneal introduction of a reovirus (see).
Pathological anatomy. Acute horioependimatita have exudative character more often. On character of exudate distinguish serous, purulent, fibrinous horioeiyen-dimatit. For hron. a horioependimatita productive processes are characteristic (specific and nonspecific — so-called granulematozny ependimatit). Inflammatory process at horioependimatita is characterized diffuznostyo, at the same time in each case it is possible to find preferential defeat of certain sites of ventricles of a brain and likvoroprovodya-Russian cabbage soup of system. Most often side ventricles are surprised, III and IV cerebral cavities are more rare. At hron. you horioependimatit, often proceeding with occlusion of likvoroprovodya-shchy ways, III, IV cerebral cavities and a silviyeva of a water supply system note preferential defeat.
At an acute serous horioependimatit the brain is macroscopically increased in sizes, its crinkles are flattened, furrows are maleficiated, ventricles, especially side, sharply stretched and filled with exudate. The ependyma and vascular textures are hyperemic, edematous, dimmy; single or multiple hemorrhages are visible. Gisto-
logically reveal desquamation of an ependimarny epithelium, infiltration of an ependyma and loops of a vascular texture lymphocytes, macrophages, plasmocytes with small impurity of neutrophilic leukocytes. Subependimarny departments of a brain note sharp hypostasis, a plethora of vessels with development of perivascular hemorrhages and moderately expressed proliferation of astrocytes.
At an acute purulent horioependi-matit vascular textures and an ependyma are impregnated with the muddy zheltovatozelenovaty viscous liquid filling cavities of ventricles and causing obturation of likvorny ways, the cut is a consequence acute expansion of cerebral cavities and build-up of pressure of cerebrospinal liquid. Microscopically find the expressed leukocytic infiltration of vascular textures, an ependyma and walls of vessels of a subependimarny layer.
At hron. the course of process exudate becomes fibrinous or fibrinopurulent. By the end 3 —
the 4th week of a disease the quantity of cells of a limfogistiotsitar-ny row increases by surfaces of an ependyma, further a part of exudate can undergo the organization with development of commissural process in cerebral cavities.
Hron. productive horioepen-dimatit has a peculiar patomorfologiya: in vascular textures of cerebral cavities inflammatory process leads to fibrosis of a stroma horioidny vorsin, to-ry is quite often combined with an atrophy of a horio-idny epithelium. At the same time the amount of collagenic and argyrophil fibers in a stroma of vascular textures increases; collagenic fibers quite often are exposed to a hyalinosis. There are an expressed sclerosis and an obliteration of a gleam of vessels horioidny vorsin in this connection products of cerebrospinal liquid decrease. In a wall of ventricles proliferation of cells of an ependyma with formation of ledges or immersions in a sub-ependimarny layer, diffusion proliferation of glial elements and collagenic fibers is observed. On the course of subependimarny vessels often find moderate iyerivasku-lyarny lymphoid infiltrates. At hron. horioependimatita almost always observe along with disturbance of a resorption of cerebrospinal liquid (see) formation of the unions and cysts interfering its current and leading to development not only arezorbtivny, but also occlusal hydrocephaly (see).
At specific productive (a tuba rkulezny) ho rioependimati-
those the ependyma is sharply thickened, has grayish-yellow color, a surface its coarse-grained, in it find the miliary or larger tubercular hillocks consisting from lymphoid, epithelial cells and colossal cells like Pirogov's cells — Langkhan-sa. In the center of many granulomas the necrosis is noted. In a subependimarny layer of tissue of brain along with hypostasis and perivascular lymphoid infiltration observe proliferation of a glia and formation of tubercular hillocks, to-rye have more compact structure in comparison with the hillocks which are located on a surface of an ependyma. Outcome hron. a tubercular horioependi-matit growth of granulyatsionny fabric in walls of cerebral cavities with formation of rough commissures and unions in their cavities is.
Productive horioependimatit the nonspecific nature (granulematozny ependimatit) on a gross appearance differs from specific a little and is observed, as a rule, upon transition of a horioependimatit of any etiology in hron. form. Microscopically in such cases along with proliferation of ependimarny cells and formation of nipples diffusion or limited proliferation of elements of a glia and mesenchymal elements around vessels is expressed.
The clinical picture of a horioepen-dimatit is caused first of all by disturbance of products, a resorption and circulation of cerebrospinal liquid. The symptomatology at the same time develops from all-brain and scattered focal nevrol. symptoms, expressiveness to-rykh depends on character and extent of changes of intracranial pressure. Feature a wedge, pictures — emergence nevrol., including and all-brain, symptoms in the remote terms; at the same time emergence of symptoms is not connected with an acute or subacute infection (flu, tonsillitis, etc.).
Gipertenzionno - a gidrotsefalny syndrome at a horioependimatita is shown by diffusion headaches, nausea or vomiting, the high pressure of cerebrospinal liquid revealed at a lumbar puncture, sometimes by congestive disks of optic nerves on an eyeground and also «flickering» symptoms of disturbance of functions of cranial nerves, symptoms of defeat of pyramidal system, disturbances of sensitivity and vestibular and cerebellar functions.
At development the occlusal guide - rotsefalnogo a syndrome (see. An occlusal syndrome) are also observed unstable focal nevrol. symptoms. The last depend both on extent of increase in intracranial pressure, and on preferential localization of periventriku-lyarny inflammatory changes. So, at defeat of basal departments of the III ventricle dysfunctions of diencephalic structures about a wedge, a picture of a hypothalamic syndrome develop (see). Quite often arise an atrophy of an optic nerve (see) and mental disorders in the form of a psychoorganic syndrome (see). On kraniogramma (see Kraniografiya) at these two syndromes signs of increase in intracranial pressure are defined. At children discrepancy of seams and increase in a skull is observed (see Hydrocephaly). At a computer tomography (see the Tomography computer) and a pneumoencephalography (see) reveal considerable expansion of the ventricles which are quite often deformed owing to commissural process. These ekhoentsefalografiya (see) also indicate expansion of ventricles of a brain and a face-voroprovodyashchey of system.
Neokklyuziruyushchy horioependimatit can proceed with giiyersek-retorny hydrocephaly (an acute stage), arezorbtivny hydrocephaly, and sometimes with an intracranial hypotensive syndrome (a fibrous stage). The headaches of the stupid or pressing character decreasing in a prone position are characteristic of the horioependimatit proceeding with pressure decrease of cerebrospinal liquid or sitting, becoming aggravated or amplifying in a standing position or during the walking. Sometimes there are short-term unconscious states, dizzinesses. Asthenoneurotic symptoms, an adynamia, an adynamy develop. Pressure of cerebrospinal liquid can decrease to 10 mm w.g. and even to 0. At this syndrome discrepancy between pressure of cerebrospinal liquid and data of rents-genokrapiografii (in an acute stage, in the presence of all-brain symptoms and high likvorny pressure, gipertenzionny signs on a kraniogramma can not come to light) quite often comes to light. At the same time in hron. stages gipertenzionny changes on kranio-gram can be shown against the background of normal or even low дав^ the line of cerebrospinal liquid.
The current of a horioependimatit can be acute, subacute, hron. recurrent, and each exacerbation of a disease can be caused by nonspecific influence (other infections, an injury, overcooling).
Complications. At hron. recurrent forms persistent hydrocephaly with a gradual diffusion atrophy of a brain develops. At occlusal forms Bruns's syndrome can develop (emergence at changes of position of the head of the attacks of severe headache with dizziness and vomiting which are followed by disturbances of cardiovascular activity and breath). Sometimes there are spontaneous breaks of cerebrospinal liquid from ventricles of a brain in a subarachnoid space on the appearing shunts (artificial messages) between ventricles and other likvorny spaces of a brain. In some cases the decompensation of cerebral circulation develops.
The diagnosis is based on a combination of all-brain symptoms and «flickering» focal symptoms (usually lacks of coordination and a statics). Horioependimatit develops at young age more often, it is usually connected with the postponed infection or an injury, begins sharply or subacutely and is followed by subfebrile temperature. Horioependimatit difficult to differentiate with tumors of a brain (see), that ER of a kulemama (see), a pia-arachnitis (see Meningitis), etc. However long overseeing by the patient, comparison of these repeated objective researches allow to make the correct diagnosis.
Treatment. At horioependimati-those inf. etiologies carry out anti-infectious, giposensibiliziru-shchy and, according to indications, dehydrational therapy. In the presence of the local centers of an infection (hron. tonsillitis, antritis, carious teeth, otitis, etc.) make their sanitation, at an exacerbation of rheumatism appoint antirheumatic treatment. Carry out also resorptional therapy (a lidaz, biyokhinol), use biogenic stimulators (Gumisolum, a vitreous, an aloe, etc.), vitamins of group B, an injection nicotinic to - you. At an asthenoneurotic syndrome small tranquilizers and fortifying treatment are shown. Sometimes at deep fibroziruyushchy process with heavy liquorodynamic disturbances make an operative measure — an adhesiotomy with recovery of passability of likvorny ways. For the purpose of rehabilitation the balneofizioterapiya — Sochi (Matsesta), Chimion, etc. can be recommended.
The forecast at timely begun and systematic treatment favorable. In cases of long intracranial hypertensia, especially at development of hydrocephaly of occlusal character, emergence of psychoorganic disturbances is possible.
Prevention consists in timely treatment hron. infectious processes, and at development of an acute or subacute horioependima-tit in active and long treatment for the prevention of transition to chronic and recurrent forms.
Bibliography: Diseases of a nervous system, under the editorship of P. V. Melnichuk, t. 1, page 200, M., 1982; Ivanovskaya of T. E. Ependima-tita at tubercular meningitis, treated streptomycin, Arkh. patol., t. 14, No. 1, page 73, 1952; Linchenko H. M. Chronic periventrikulyarny encephalitis and arachnoidites, M., 1961; Maggi-d about in H. M. Current state of a question of cerebral pia-arachnites and horioependimatit (arachnoidites), Klin, medical, t. 52, No. 9, page 19, 1974; The Multivolume guide to pathological anatomy, under the editorship of A. I. Strukov, t. 2, page 267, M., 1962; The Pokrovsk V. I., the Favor about in and L. A. and Kostyukov H. H. Meningococcal infection, M., 1976;
Sorkini. AA. Tubercular meningitis, M., 1959; X about r N e c of T.
A meninx, an ependyma, vascular textures of cerebral cavities and their diseases, in book: Patomorfol. nervn. sist., under the editorship of, I. T. Niculescu, the lane from Romanians., page 206, Bucharest, 1963; In a k e of A. V. of Chronic lymphocytic choriomeningitis, J. Neuropath. exp. Neurol., v. 6, p. 253, 1947; DohrmannG. J. The choroid plexus in experimental hydrocephalus, J. Neuro-surg., v. 34, p. 56, 1971; W e 1 1 e r R. O. a. o. Experimental hydrocephalus in young dogs, histological and ultrastructural study of the brain tissue damage, J. Neuropath. exp. Neurol., v. 30, p. 613, 1971.
H. M. Madzhidov; T. S. Gulevskaya (stalemate. An.).