MENINGITIS

From Big Medical Encyclopedia

MENINGITIS (meningitis; grech, meninx, meningos a meninx + - itis) — an inflammation of covers of a head and spinal cord. Distinguish a pia-arachnitis — an inflammation of a soft and web meninx, arachnoiditis (see) — an inflammation of an arachnoid membrane and pachymeningitis (see) — an inflammation of a firm meninx. However in practice mean by the term «meningitis» first of all a pia-arachnitis. At intoxications there can be an irritation of a meninx which is not caused by true inflammatory changes in them. Such state, unlike M., is called meningism (see).

The m is widespread worldwide and various climatic zones. However only meningococcal M. is registered everywhere (see. Meningococcal infection ). The m can arise at persons of any age, but it is most often noted at children of early age.

Systematic registration of incidence and a lethality at other forms of purulent M. it is not carried out, but, according to all authors, the lethality at them makes 25 — 30%.

Various pathogenic microorganisms, various viruses, bacteria and protozoa can be activators M.

HISTORY

Klin, a picture M. is described in Pavel Eginsky's works in 7 century, Ibn-Sina in 11 century and in works of the ital. doctor of G. F. Ingrassia in 16 century; Waite (Whait, 1767) and Vyesse (G. Vieusseux, 1805) for the first time described epidemiology purulent (epidemic cerebrospinal) M.

Podrobno a wedge, a picture M. is described by P. A. Charukovsky in 1836, Linissen (Lienissen, 1887) for the first time offered classification of an inflammation of covers of a brain and allocated purulent M.'s form — Leptomeningitis purulenta. Opening by Veykselbaum (A. Weichselbaum, 1887) epidemic cerebrospinal M.'s activator allowed to begin a broad research of this disease.

The foundation for serous M.'s studying was laid by G. Quincke by method of an intravital research of cerebrospinal liquid (1893). Soon Beningkhaus (S. of Boninghaus, 1897) established existence of a special form of a disease — acute serous M. Nek-rye authors, including and G. Quincke, identified serous M. with «a head edema» and any increase in cerebrospinal liquid, even without change of its structure, treated as serous M. Further fr. authors began to distinguish the true serous M. which is followed by inflammatory changes of a meninx from their irritation because of intoxication of an organism or under the influence of other factors and entered the term «meningism».

The majority it is mute. clinical physicians spoke against differentiation of these concepts, considering that the toxic irritation of a meninx causes the phenomena of a meningism in the beginning, and at sharper irritation — a serous inflammation. T. Vidal (1910), Netter (E. Netter, 1912), etc. acknowledged the possibility of further transition of serous M. in purulent aseptic in connection with penetration into liquid of leukocytes from hyperemic covers.

At the beginning of 20 century the view of serous M. changed. L. O. Darkshevich (1909) allocated in serous M. primary, being independent inf. a disease, and secondary, to-ry can arise at any infection, intoxication or an injury.

A. J. Wallgren in work «A new infectious disease of the central nervous system» described in 1925 epid, flash of the acute serous M. called by it «aseptic serous meningitis». Armstrong and Lilly (Ch. J. Armstrong, V. of D. Lillie, 1934) allocated the special virus which is the activator of one of serous M.'s forms — a choriomeningitis. Later the role of enteroviruses of Koksaki and ECHO in serous M.'s etiologies, and also existence of the serous M. caused by a virus of poliomyelitis was proved.

CLASSIFICATION

Exists several classifications of M. On the nature of inflammatory process in covers and changes of cerebrospinal liquid distinguish serous and purulent M. Primary M. develops without the previous systemic infection or a disease of any body, secondary — is a complication of others inf. diseases, inflammatory and noninflammatory defeats of bodies and systems. The secondary M. arising at tumors of a brain, collagenoses always proceeds as serous. On an etiology distinguish: I. Bacterial meningitis. A. Purulent forms: a) meningococcal (epidemic cerebrospinal); b) pneumococcal; c) caused by Afanasyev's stick — Pfeyffera; d) streptococcal; e) stafilokokkokovy; e) gonococcal; g) caused by a pyocyanic stick; h) salmonellezny; i) typroid (paratyphoid); j) collibacillary; k) listeriozny. B. Serous forms: a) tubercular; b) syphilitic; c) mycoplasmal; d) leptospirozny. II. Viral meningitis (serous): a) acute high-quality lymphocytic choriomeningitis; b) caused by a virus of epidemic parotitis; c) caused by enteroviruses (ECHO and Koksaki); d) herpetic; e) influenzal. III. The meningitis caused by fungi and protozoa (serous or purulent): a) blastomikozny; b) koktsidioidozny; c) toksoplazmenny; d) candidosis; e) mukorozny; e) amoebic.

Depending on development and a current allocate fulminant, acute, subacute and chronic M.

On preferential localization of inflammatory process of M. happens basal, konveksitalny, mesodiencephalic, spinal.

The AETIOLOGY AND EPIDEMIOLOGY

Purulent M. is described almost at all bacterial infections and at the infections caused by protozoa and fungi, but in most cases he is called by rather small group of microbes: meningokokka (30 — 74%), pneumococci (14 — 55%) and a hemophilic stick of an influenza of Afanasyev — Pfeyffera (8 — 13%). The staphylococcal M. and M.'s cases caused by a pyocyanic stick became frequent. According to Smith (H. V. Smith, 1954), on the American continent the stick of an influenza is the most frequent activator of purulent M. at children that connect with broad use of the antibiotics operating preferential on cocci.

According to S. L. Kipnis (1971), meningococcal M. occurs among purulent M. in 59,4%, pneumococcal — in 16,4%, M. caused by a stick of an influenza — in 5,9%, staphylococcal — in 2,5%, M. caused by Esherichia coli — in 2,3%, streptococcal — in 0,4%, fungal — in 0,5%, paratyphoid — in 0,1% of cases; in 12,5% of cases purulent M.'s etiology is not found out. Noted growth of number of cases of purulent M. with the obscure etiology, apparently, is connected with broad use of antibiotics in out-patient conditions.

Are observed epid. serous M.'s flashes enteroviral etiology. The enteroviral infection gained distribution practically in all parts of the globe. The first data on epidemics enteroviral) M. having virusol confirmation, are received in 1954 in the USA. In Europe (Sweden) since 1954 increase of cases of epidemic serous M. Osobenno big distribution is officially registered the enteroviral infection gained in aestivo-autumnal months in the 50th in England, Belgium, the Netherlands, Sweden, Norway, America. So, serous M.'s flash in Belgium in 1956 captured 10% of the population of the country. In the USA in 1957 in the State of Minnesota ached apprx. 400 000 people, in Miluoke — apprx. 280 000 people, i.e. 4% of the population.

The PATHOGENY

the High frequency of M. at children's age is caused by insufficiency of immunity to infections and imperfection of a blood-brain barrier. At babies also direct access of the activator to a meninx through openings of a sievebone is possible, in to-rykh there pass shoots of a soft meninx. Entrance infection atriums at M. are the mucous membrane of a nasopharynx, bronchial tubes, went. - kish. path. Transmission of infection vnutriutrobno through a placenta is possible. The activator, having got on a mucous membrane, causes local inflammatory changes of various degree of manifestation: a nasopharyngitis, quinsy, bronchitis, went. - kish. frustration. Extending in the lymphogenous or hematogenous way, the infection gets further to a meninx. Circulation of the activator in blood can clinically be shown by symptoms of the general intoxication. Sometimes this period happens so short that matches on time with the advent of signs of defeat of a meninx. Distribution of activators M. in an organism can come also from any inflammatory center [pneumonia, a furuncle, an ugly face, intestinal infection, infections bilious and a bladder, an inflammation of adnexal bosoms of a nose (okolonosovy, T.), middle ear, eyeglobe, orbit etc.]. In this case it is about development of secondary metastatic purulent M.

Along with hematogenous and generalized also the segmented and vascular way of distribution of the activator is possible. In these cases the infection extends on the regional vessels having communication with brain vessels, passing the general blood channel.

The contact way of transition of an infection to covers, napr is frequent, at purulent otitises, mastoidites, attic diseases, cerebral abscesses, thrombophlebitis of veins and sine of a firm meninx.

The m can also develop at an open craniocereberal and vertebral and spinal injury, at the changes and cracks of a base of skull which are followed by a liquorrhea. Traumatic M. happens, as a rule, purulent.

PATHOLOGICAL ANATOMY

Pathoanatomical changes at a pia-arachnitis are observed not only in a soft meninx of a head and spinal cord, but also in an ependyma and vascular textures of ventricles.

The form of an inflammation of soft covers is, as a rule, caused by properties of the activator. So, serous M. is caused by viruses, purulent more often — bacterial, generally coccal, flora, and hron, a productive inflammation — fungi and protozoa (Toxoplasmosis). However this pattern has relative value because at purulent M. in the first two days exudate serous, and at the sluggish course of purulent or serofibrinous process the inflammation gains properties of chronic productive.

The inflammatory exudate in soft covers is always more noticeable on the basis of a brain where he crowds in a zone of an optic chiasm, on the inferiolateral surface of the bridge (a varoliyev of the bridge), a cerebellum and a medulla, i.e. in the field of an arrangement of the largest subarachnoidal likvoronosny receptacles — tanks. Cavities or more extensive accumulations of exudate can be observed also in the territory of a frontal temennovisochnykh of shares of hemispheres on the course lateral (silviyevy) and other deep furrows where it shrouds the vessels passing here subarakhnoidalno, stratifying leaves of a soft meninx. It is possible to see exudate also in spinal covers where inflammatory changes usually appear on 1 — 2 day later. More often covers of a back surface of a spinal cord in the field of cervical and lumbar thickenings are surprised.

Fig. 1. Microdrug of a soft cover of a brain of the patient who died from acute serous meningitis: in cellular infiltrate lymphocytes (1) and plasmocytes prevail (2); x 200.
Color rice. And. Fig. 1. A brain of the patient (lower surface) who died from a purulent basilar pia-arachnitis: it is visible zheltovato - the green purulent exudate impregnating a soft cover of the basis of big hemispheres, hemispheres of a cerebellum and a trunk of a brain. Fig. 2. A brain of the patient (a verkhnebokovy surface) who died from purulent meningitis: accumulation of purulent exudate in soft covers of parietofrontal area of hemispheres is visible ("cap"). Fig. 3. A horizontal section of a brain of the patient who died from purulent meningitis: expanded side ventricles are visible. Fig. 4. A brain of the patient (a verkhnebokovy surface) who died from a hemorrhagic pia-arachnitis, a soft cover of hemispheres it is impregnated with hemorrhagic exudate. In left temenno - temporal area hemorrhage (it is specified by an arrow). Fig. 5. A brain of the patient (lower surface) who died from an acute tubercular basilar pia-arachnitis: on the basis of a brain the yellowish exudate impregnating a soft cover is visible. Fig. 6. A brain of the patient (lower surface) who died from an acute tubercular basilar pia-arachnitis: on the basis of a brain miliary hillocks (are specified by shooters) and the yellowish exudate impregnating a soft cover are visible. Fig. 7. A horizontal section of a brain of the patient who died from a tubercular encephalomeningitis: in the left hemisphere, and also in a zone of an interstitial brain the merging centers of a caseous necrosis are visible (are specified by shooters).
Color fig. B. Fig. 1. A brain of the patient who died from a serous pia-arachnitis: a hyperemia of covers of a brain with availability of exudate in furrows of a side surface of a hemisphere. Fig. 2. A brain of the patient who died from a hemorrhagic pia-arachnitis: extensive hemorrhage of dark red color in a soft cover of the basis of a brain is visible. Fig. 3 — 4. Microdrugs of a soft meninx of a brain at a pneumococcal pia-arachnitis. Fig. 3. The soft meninx is impregnated with exudate in which lymphocytes, macrophages and plasmocytes prevail. Fig. 4. In edematous, infiltrirovanny lymphocytes and leukocytes the thrombosed vessel is visible to a soft meninx (it is specified by an arrow). Fig. 5. Microdrug of a brain at a tubercular pia-arachnitis: shooters specified the site of a tubercular epithelioid and cellular granuloma. Fig. 6. Microdrug of a brain at a tubercular encephalomeningitis: in tissue of a brain the centers of a caseous necrosis are visible (are specified by shooters).

At an acute serous pia-arachnitis grayish-yellowish gelatinous exudate accumulates in subarachnoid space head (tsvetn fig. B. 1) and a spinal cord, enveloping the large vessels and nervous trunks passing here, fills cerebral cavities. Soft covers, an ependyma and vascular textures at the same time are hyperemic, edematous, dimmy, with single or multiple hemorrhages. Histologically find a picture of an acute serous or serofibrinous pia-arachnitis, an ependimatit and a choroiditis (see. Horioependimatit ). In infiltrate lymphocytes, macrophages and plasmocytes prevail (fig. 1; see also tsvetn. fig. B 3 and 4). The inflammation has focal or diffusion character with the expressed perifocal hypostasis. Due to the hyperproduction of cerebrospinal liquid there can be acute hydrocephaly (see), swelled also swelling of a brain (see) with a vklineniye of its substance in a big occipital opening. As a rule, the inflammatory exudate is exposed to a resorption with complete elimination patol, process. However sometimes exudate will be organized that is followed by education between leaves of a leptomenings of the commissures cutting subarachnoid space on separate the cavities closed, overflowed with cerebrospinal liquid — cysts. Microscopically at the same time proliferation a meningoteliya and ependimarny cells and focal infiltration of covers and textures lymphocytes, macrophages and plasmocytes, and also a new growth of connecting fabric is found. Such form of a disease carries the name hron, a serous or cystous pia-arachnitis.

At purulent M. the inflammatory exudate has at first serous character, and on 2 — the 3rd day of a disease it takes a form of purulent exudate. At the same time soft covers of parencephalons (tsvetn. rice. And 1), vascular textures and an ependyma are impregnated with a muddy yellowish-greenish viscous liquid. At plentiful accumulation gnoynofibrinozny exudate forms «cap» in frontal and parietal shares of hemispheres (tsvetn. rice. And 2) or shrouds all brain in continuous weight. It fills also medullary cavities, covering with a yellowish film of a texture and a wall of ventricles. The developing obturation of likvorny ways an exudate leads to acute expansion of cerebral cavities (tsvetn. rice. And 3) and cerebral hypertensia. The subshell departments of marrow, but especially often the areas surrounding ventricles can be involved in inflammatory process.

At timely begun treatment purulent exudate is exposed to enzymatic disintegration and a resorption, but in nek-ry cases it will be organized, causing commissural process in covers and cerebral cavities. The productive (adhesive) pia-arachnitis which is characterized by a partial obliteration of subarachnoid space with education between leaves of a soft cover of the closed purulent or serous cavities develops hron, purulent or hron. Commissures can cut as well cerebral cavities, creating separate filled with pus or cerebrospinal liquid of the camera. The gross appearance hron, productive M. is supplemented by a sclerosis of covers, textures and an ependyma with a full or partial obliteration of the vessels which are here. Circulation of cerebrospinal liquid and a brain hemodynamics are sharply broken that leads to development of hydrocephaly. Histologically in covers, an ependyma and textures the picture hron, a purulent inflammation with the expressed sclerous changes is found. In the neighboring sites of brain fabric it is possible to observe zero cellular devastation with dystrophy and death of neurons and accumulation in them of lipofuscin, demyelination) nerve fibrils and a focal gliosis.

The described changes can come to light also without the previous acute M.'s clinic, in several years after an injury, an infectious disease or an operative measure.

If the shell exudate contains erythrocytes and, therefore, a soft meninx is painted in various shades of red color, then such inflammation of these covers carries the name hemorrhagic (tsvetn. fig. B 2). Hemorrhagic pia-arachnitis (tsvetn. rice. And 4) can complicate inf. the disease which is followed by the general trombogemorragichesky syndrome or local giperergichesky reaction of immediate type. Because of impurity of blood the reactive inflammation in a zone of subarachnoidal hemorrhage has a similar gross appearance. Can help differential diagnosis with these cases gistol, a research of material — at infectious hemorrhagic M. fibrinoid necroses of vessels find (see. Fibrinoid transformation ), their thrombosis and preferential granulotsitarny infiltration of the center of an inflammation.

A tubercular pia-arachnitis — result of hematogenous generalization or lymphogenous spread of an infection from pulmonary, limfozhelezisty (or another extra pulmonary) the center. Modern methods of treatment changed morfol, a picture of a disease. To replace the acute serofibrinous inflammation of covers of a brain giving a lethality before nearly 100% limited forms of defeat came with considerably best forecast hron. At

acute tubercular M. the gelatinous grayish-yellowish exudate is found in subarachnoid space head (tsvetn. rice. And 5) and a spinal cord in typical places, and also in cavities of a brain. In a soft cover and in an ependyma miliary or larger grayish hillocks are noticeable (tsvetn. rice. And 6). The fabric impregnated with a serofibrinous exudate can be exposed to a caseous necrosis (tsvetn. rice. And 7). Microscopically in infiltrate from the very first days diseases prevail lymphocytes.

Fig. 2. Microdrug of a brain of the patient who died from a tubercular encephalomeningitis: the merging epithelioid and cellular granulomas in a wall of the III cerebral cavity are specified by shooters; x 100.
Fig. 3. Microdrug of a spinal cord of the patient who died from a tubercular cerebrospinal leptopakhimeningit: 1 — white matter; 2 — the soldered and reinforced covers of a spinal cord; 3 — the obliterated vessels; x 10.
Fig. 4. Microdrug of a brain of the patient who died from tubercular meningitis (the average brain artery is obliterated): 1 — a gleam of an artery, 2 — a reinforced fibrozirovanny internal cover of an artery, 3 — a muscular coat of an artery; x 200.

The most characteristic gistol, line subacute and hron, forms of a tubercular inflammation is formation of preferential epithelioid and cellular granulomas (tsvetn. fig. B 5), it is frequent with a caseous necrosis of their center. Similar granulomas are found also in a wall of vessels, in to-rykh it is possible to see as well other changes — from serous treatment to a fibrinoid and caseous necrosis with thrombosis and development of heart attacks of a brain. At tubercular M. related departments of brain fabric in which the picture caseous develops (tsvetn are often involved in inflammatory process. fig. B 6) or granulematozny (fig. 2) encephalitis. In the outcome of a tubercular inflammation in subarachnoidal (and even subdural) space of a head and spinal cord there can be commissures. The gleam of the vessels passing here is obliterated (fig. 3 and 4) that leads to heavy disturbances of circulation of cerebrospinal liquid and to frustration of a hemodynamics.

At amoebic M. (encephalomeningitis) caused by negleriya the purulent pia-arachnitis, a hemorrhagic necrotizing encephalomeningitis, wet brain, perivascular accumulations of amoebas pathoanatomical comes to light. Morfol, a picture at an encephalomeningitis of an akantamebny origin is shown by granulematozny encephalitis with focal necroses.

The CLINICAL PICTURE

the Meningeal syndrome and changes of cerebrospinal liquid

existence of the symptoms combined in Meningeal, or the shell, a syndrome is characteristic Of all forms M. The full Meningeal symptom complex is observed not always even at purulent M. Neredko, especially at children of early age, persons of senile age, only a part of meningeal symptoms comes to light.

The headache, vomiting, the general hyperesthesia, specific meningeal pose, stiff neck, Kernig's signs, Brudzinsky, a symptom of suspension of Le Sage, a malar symptom of Bekhterev, etc. belong to a meningeal syndrome.

The headache — a constant symptom, is observed practically at all patients at various forms M. It can be diffusion or localized (it is preferential in a forehead and a nape). Developing of a headache is connected with irritation of the sensitive terminations of a trifacial, and also parasympathetic (vagus nerve) and the sympathetic fibers innervating covers of a brain.

Vomiting usually accompanies a headache, arises without communication with meal, has «fontanovidny» character. Vomiting at M. — the central origin is also connected with irritation of receptors of a vagus nerve or its kernels located at the bottom of IT of a ventricle, or the emetic center in a reticular formation of a myelencephalon.

An important symptom is the general skin hyperesthesia and hypersensitivity to sound and light irritants (a hyperacusia, a photophobia). Identification of this symptom at early children's age is complicated since children usually are negative to survey, are irritated at hiting at with it, are capricious, turn away at bright light. The irritation of back roots is the cornerstone of the general hyperesthesia, and it is possible also cells of spinal nodes.

The pose of the patient is characteristic: the thrown-back head, the curved trunk, the «carinate» pulled-in stomach, hands are pressed to a breast, legs are tightened to a stomach (a meningeal pose, a pose of «a lyagavy dog», «cocked»). Meningeal pose — the investigation of reflex tonic contraction of muscles. The thrown-back head of the patient is caused by a stiff neck — increase in a tone of extensor muscles of a neck. In attempt to incline forward the head of the patient who is in a prone position the muscle tension of a nape comes to light, at the same time the chin of the patient does not manage to be given to a thorax. Any attempt to bring the head of the patient out of its fixed situation is followed by sharp morbidity.

Fig. 5. Definition of a Kernig's sign: the doctor cannot unbend the leg of the patient which is previously bent at right angle in knee and coxofemoral joints.
Fig. 6. Definition of an upper symptom of Brudzinsky: in a dorsal decubitus in attempt to lead the head of the patient to a breast there is an involuntary bending of legs in knee joints.

Kernig's sign (see. Kerniga symptom ) — very early and characteristic symptom of defeat of a meninx. It is expressed in impossibility to unbend the leg which is previously bent at right angle in knee and coxofemoral joints (fig. 5) in a knee joint. It is necessary to distinguish a Kernig's sign from antalgichesky (muscular) resistance at a symptom of Lasega (see. Radiculitis ). At children of early age the Kernig's sign can not come to light. Newborns and children of the first two months have lives, and also at patients with parkinsonism, a myatonia the Kernig's sign can be a consequence fiziol. or patol, increases in the general tone of muscles.

The upper symptom of Brudzinsky is expressed in involuntary bending of legs in knee joints in response to attempt to lead the head to a breast in a dorsal decubitus (fig. 6). Malar symptom of Brudzinsky — the same reaction at percussion of a zygoma. The pubic symptom of Brudzinsky is expressed in bending of legs in knee joints during the pressing on a pubic joint. The lower symptom of Brudzinsky is investigated along with a Kernig's sign: in attempt to unbend a leg in a knee joint the second leg is bent in a knee and given to a stomach.

Giyen's symptom is similar to the lower symptom of Brudzinsky — during the squeezing by the four-head of a muscle of one leg other leg is bent in a knee and given to a stomach.

Tension of long muscles of a back is also frequent and typical sign of a meningeal syndrome and comes to light in the form of the following symptoms.

Meytus's symptom: to the patient lying on spin fix the legs unbent in knees the right hand, and support by the left hand a back, helping it to sit down. At a meningeal syndrome of spin of the patient and the unbent legs in a sitting position form an obtuse angle: the patient cannot directly sit at the unbent legs. Fankoni's symptom — impossibility to sit down independently in beds at the unbent and fixed knees. The symptom of «tripod» — the patient can sit in a bed, only leaning hands behind a back. The symptom of «a kiss of a knee» — the patient is not able even to touch at the lower extremities bent in hip joints with lips a knee.

At sick all age the malar symptom of Bekhterev is quite constant: at percussion of a zygoma the headache amplifies and involuntarily there is a painful grimace on the corresponding half of the face.

At children of early age the symptom of suspension of Le Sage is defined: the child lifted under mice tightens legs to a stomach and keeps them in this situation, at the same time the head is thrown slightly back back (the healthy child at this test freely bends and unbends legs).

Great diagnostic value at children of early age has Flatau's symptom — expansion of pupils at a bystry ducking forward.

At babies at M. also permanent and long protrusion of a big fontanel owing to increase is observed intracranial pressure (see) and accumulations of a significant amount of cerebrospinal liquid in cerebral cavities. So-called gidrotsefalichesky shout is characteristic of sharp increase in intracranial pressure — the patient in unconsciousness suddenly screams and clutches hands at the head.

At children of early age of nek-ry meningeal symptoms can not be, and into the forefront in clinic of a disease symptoms of toxicosis act: spasms, high temperature, vomiting, vomiting, dehydration, phenomena of parenteral dyspepsia. Therefore at early children's age the indication to spinal puncture (see), in addition to meningeal symptoms, high temperature, vomiting the fountain, spasms, squint, narrowing of pupils, paresis of extremities, change of nature of shout of the child, resistant tension of a big fontanel are.

Indications to a spinal puncture shall those be wider, than less child. It is also necessary to remember that at early stages of purulent M. liquid can have serous character and a neutrophylic pleocytosis quite often is absent.

Symptoms of local defeat of a nervous system at M. are non-constant and demonstrate transition of inflammatory process to substance of a brain or roots of cranial and spinal nerves.

Paralyzes and paresis can arise at M. owing to damage of a brain, is more rare at damage of a spinal cord (see. Paralyses, paresis ).

At localization of process preferential on the basis of a brain the wedge, a picture M. is characterized by early damage of cranial nerves. So, at syphilitic, tubercular M. function of third cranial nerves is especially often broken — squint, a ptosis, and sometimes full is observed ophthalmoplegia (see). Also damage of facial, visual, acoustical nerves can be noted.

Tendon jerks at the beginning of a disease often raise to clonuses, but further they decrease and can disappear completely. Belly reflexes are almost always reduced or are not caused. Patol, Babinski's reflexes, Oppengeyma and clonuses of feet at uncomplicated forms M. usually are absent. They appear during the involvement in process of substance of a brain.

Vegetative disturbances at M. are shown by arrhythmia, dissociation between pulse and temperature (delay of pulse at an elevated temperature and its acceleration at a standard temperature), weak filling of pulse, disturbance of a rhythm and depth of breath, signs of the increased lability of the vasculomotor device — at a touch or pressing on skin there are red and white spots, Trusso's spots are characteristic (the patient reddens, turns pale).

At localization of inflammatory process on covers of a convex surface of cerebral hemispheres in a wedge, a picture the phenomena of irritation of bark with psychomotor excitement, epileptiform attacks prevail; further paresis and paralyzes, disturbances of sensitivity can join.

At defeat of covers of a spinal cord the radicular phenomena are possible, and at distribution of an inflammation on substance of a spinal cord the central or peripheral paresis, dysfunctions of pelvic bodies, Broun-Sekar's syndrome (see. Broun-Sekara syndrome ).

At distribution of inflammatory process from a soft meninx on an ependyma of cerebral cavities purulent develops ependimatit. At the same time the aggravation of symptoms, strengthening of a headache, muscle tension of a nape, emergence of muscular contractures is characteristic, cerebrate rigidity (see), stupefaction, drowsiness, increase of symptoms of intracranial hypertensia. Muscle tension of the lower extremities is especially expressed. The patient lies with the extended and crossed legs, clonic and tonic spasms can be observed. Weakening of sphincters, sharp emaciation develops up to cachexias (see). Temperature at the same time more often happens normal or subfebrile.

The research is of great importance for establishment of the diagnosis of M. cerebrospinal liquid (see).

Pressure of cerebrospinal liquid, as a rule, happens raised, especially at purulent meningitis.

Low pressure of liquid shall suggest an idea of existence of the block of likvorny ways. The progressing pressure drop of liquid can be observed at an ependimatita.

At purulent M. liquid happens muddy, sometimes greenish color. Muddy, milky-white color of liquid is defined at meningococcal M., a greenish shade more often — at purulent M. of other etiology. At serous M. cerebrospinal liquid is usually completely transparent, colourless, but in nek-ry cases its opalescence comes to light.

The major diagnostic and predictive importance at M. has a pleocytosis. Kletochnobelkovy dissociation — a high pleocytosis is characteristic at the normal or slightly increased protein content. At purulent M. the neutrophylic pleocytosis accrues quickly enough and reaches big figures (1000 — 15 000 and above in 1 mkl). The maintenance of neutrophils makes from 40 to 100%. At serous M. a pleocytosis lymphocytic — within several honeycombs, up to 1000 less often and more elements in 1 mkl.

In nek-ry cases along with a high pleocytosis protein content can also increase: at purulent M. from 0,66 to 16 per milles, at serous M. to 1,0 — 3,3 per milles. High content of protein in cerebrospinal liquid in an acute stage of purulent M. indicates the heavy current.

The sugar content in cerebrospinal liquid at purulent M. is often reduced about 0,4 — 0,2 g/l that is characteristic of a heavy current purulent, and also of tubercular M.; increase in reduced amount of sugar predictively is favorable, and the progressing decrease it testifies to the adverse forecast.

At serous M. the sugar content in cerebrospinal liquid, as a rule, happens normal, seldom raised.

Content of chlorides in cerebrospinal liquid in all cases of purulent M. decreases to 6 — 5 g/l and below (norm of 7,2 — 7,5 g/l).

Great diagnostic value has detection in cerebrospinal liquid of bacteria, viruses, fungi, the elementary etc.

In blood at purulent M. the neutrophylic leukocytosis decides on shift to the left, acceleration of ROE. At serous M., as a rule, specific changes from blood do not come to light or the lymphopenia is expressed.

Separate forms of meningitis

Purulent meningitis

Purulent process in a soft meninx can cause under certain conditions various pathogenic microbes. However generally purulent M. is caused by rather small group of activators: meningokokka, pneumococci, gemoglobinofilny stick of an influenza, stafilokokkama, streptococci, colibacilli, salmonellas, fungi, etc. It is not possible to find the activator in a part of patients with purulent M.

Meningococcal (epidemic cerebrospinal) meningitis — one of forms meningococcal infection (see).

Pneumococcal meningitis — one of the most severe forms of purulent M. differing in a rapid current and a high lethality (in the past apprx. 100%). On the frequency of distribution among purulent M. he takes the second place after meningococcal, making to 1/3 from their total number. Is caused by various pneumococci (see). Pneumococcal M. meets in chest more often (39%) and less often at early children's age (15%), is more often in the spring and in the fall. Quite often M. precede otitises, sinusitis, pneumonia. The contributing factor at adults are the fractures of base of the skull noted in the anamnesis at 17% of patients. Acute and hron, inflammatory diseases of upper respiratory tracts at such patients even in the remote terms after an injury can lead to M.'s development (or through their hernial protrusion per contactum passes inflammatory process through a fistula of a meninx to covers). At 40% of children and 60% of adults primary center does not manage to be established even pathoanatomical. Such, primary, pneumococcal M.'s forms proceed especially violently and hard. Almost at 40% of the patients who died from pneumococcal M. for sections acute swelling and wet brain are noted.

M.'s beginning almost always acute, sometimes apoplektiformny, especially at the persons who transferred a fracture of base of the skull. There is a fever, very sharp headache, vomiting, a photophobia, a sharp hyperesthesia and a hyperacusia, the expressed intoxication. Body temperature usually quickly reaches high figures, but in the hardest cases can remain normal (2% of patients) or subfebrile (11% of patients).

Meningeal symptoms appear quickly, but at the patients with very heavy disease who are in coma can be absent.

Pneumococcal M. proceeds as an encephalomeningitis more often. Consciousness at most of patients (about 60%) is broken already with 1 — the 2nd day of a disease, the psychomotor excitement which is quickly passing into a stupor is often noted, spasms (at 25% of patients), especially at children of early age are observed. Unlike patients with meningococcal M., focal symptoms of defeat of a nervous system appear already on 1 — the 2nd day of a disease. Damages of cranial nerves are noted at 60% of patients (more often at adults), and at 17% — mono - and a hemiparesis of extremities. From cranial nerves generally is surprised front, oculomotor and taking away. Development of a picture of acute swelling and wet brain with its vklineniye is possible.

On 3 — honor the 4th day of a disease at all adults and children years on lips, a mucous membrane of a mouth, auricles, a face, and occasionally are more senior and on skin of hands and trunks are noted herpetic rashes, to-rye occur at babies extremely seldom. Occasionally there is small hemorrhagic rash. On character rash differs from rash at a meningococcemia; it more small, but is more plentiful. Rash is always observed at patients with septic disease.

Pulse in an onset of the illness is speeded usually up, further, especially at increase of symptoms of brain swelling, relative bradycardia is noted. In these cases also arterial hypertension can be observed. Usually normal or is moderately lowered by the ABP. Cardiac sounds are muffled, on an ECG changes of a myocardium come to light. Are possible perikardita (see), often develops pneumonia (see). At adults locks are usual, at babies long ponosa are possible. The liver and a spleen at septic disease increase.

Pneumococcal M. usually proceeds with a leukocytosis and sharp shift of a neutrophylic formula to the left.

ROE accelerates with 3 — the 4th day of a disease to 30 — 60 mm/hour.

Cerebrospinal liquid muddy, purulent, quite often greenish-grayish. During the standing, as a rule, the deposit quickly drops out. At pneumococcal M. disturbance is almost always noted liquorodynamic tests (see) that testifies to the partial block of the likvorny ways and consolidation of pus in subarachnoid space developing with 2 — the 3rd day of a disease.

The neutrophylic pleocytosis with a large number of cells in various stages of disintegration reaches 1000 and more in 1 mkl, protein 1 — 10 per milles and more. The sugar content and chlorides in hard cases decreases.

Most hard and predictively it is unsuccessful pneumococcal M. with a low cytosis (200 — 700 cells in 1 mkl) and sharply increased protein content (6 - 25 per milles) proceed.

The pneumococcal etiology of M. is confirmed by detection of the activator in cerebrospinal liquid or blood, positive serol, reactions.

Treatment to similarly meningococcal M. (see. Meningococcal infection ).

Without treatment in most cases on 5 — the 6th day of a disease comes a lethal outcome. The disease can accept a long current even at timely begun therapy. The residual phenomena meet more often and more expressed, than patients have meningococcal M.

Meningit called by a gemoglobinofilny stick of Afanasyev — Pfeyffera (see. Gemoglobinofilny bacteria ). The Gemoglobinofilny stick is the activator of bacterial purulent M.'s distribution, the third on frequency, the Crimea children of early age, seldom more senior children and adults are ill preferential. Influenzas meningitis develops against the background of already available bronchitis, bronchial pneumonia of a pla of otitis more often, less often it arises along with the listed pathology or precedes it. Almost at all children in the anamnesis symptoms of rickets, a hypotrophy, frequent pneumonia, otitises, etc. are noted. At those children, to-rye to M. had bronchial pneumonia or any other form of influenzas infections, M.'s development is followed by sharp deterioration in the general state, high temperature, vomiting, accession of the dispeptic phenomena and other symptoms. The confused consciousness is occasionally observed. Diagnosis of M. as a rule, is established late.

At persons without previous M.'s diseases develops sharply, but even in these cases further gets a long sluggish current with the periods of improvement and deterioration. Temperature is up to 38 — 41% wavy.

The meningeal syndrome comes to light more often not in the first days of a disease. Focal damages of a brain and infiltrative neuritis of cranial nerves appear late, on 5 — the 12th day of a disease. Is surprised the facial, oculomotor and taking-away nerves more often. A hemiparesis, spasms are possible. Symptoms of acute swelling and wet brain usually are not observed. Often pneumonia, purulent otitises develop. The m without treatment proceeds 3 — 4 weeks, coming to an end, as a rule, with death.

In early terms of a disease (till 10th day) in blood the neutrophylic leukocytosis (12 000 — 37 000 cells in 1 mkl), in later terms easy neutrophylic shift is more often noted at normal quantity of leukocytes. ROE is sharply increased.

Cerebrospinal liquid usually muddy. Pleocytosis from 800 to 13 000 cells in 1 mkl. Dissociation between extent of opacification of cerebrospinal liquid and rather small amount of cells is quite often noted (200 — 600). Opacification of liquid in these cases is connected with a large number of activators. Protein raises to 1 — 3 per mille. At the long course of a disease the sugar content gradually decreases.

The diagnosis is confirmed by detection of the activator in cerebrospinal liquid.

Treatment is carried out by levomycetinum at the rate of 80 — 100 mg on 1 kg of body weight a day, tetracycline on 30 — 50 mg on 1 kg of body weight a day, ampicillin, streptomycin or a combination of several antibiotics; streptomycin in connection with low passability of drug through a blood-brain barrier is entered intramusculary by l endolyumbalno. Fortifying therapy is obligatory. Prolonged treatment, to 7 — the 10th day of standard temperature and decrease in a cytosis to 20 — 50 cells in 1 mkl cerebrospinal liquid.

The forecast at timely and correct treatment favorable, the residual phenomena are rare. Without treatment death comes on 3 — the 4th week of a disease.

Streptococcal meningitis meets seldom and is preferential one of displays of sepsis, can arise at patients with endocarditises as a result of a septic vascular embolism of covers of a brain.

Streptococcal M.'s current rough, a wedge, his picture it is similar a wedge, to a picture at meningococcal M., only focal defeats of a nervous system meet less often. The exception is made by patients with a septic endocarditis, at to-rykh M. begins suddenly and is followed by early emergence of focal symptoms. Other feature of purulent M. at a septic endocarditis is the frequent defeat of a vascular wall leading to subarachnoidal hemorrhages.

The pleocytosis at the same time usually does not reach high figures. The streptococcal etiology of M. is confirmed by detection of the activator in cerebrospinal liquid or blood, positive serol, reactions.

Treatment is same, as well as meningococcal M. (see. Meningococcal infection ). Forecast serious.

Staphylococcal meningitis makes 3 — 5% among: purulent M.

Patogeneticheski is allocated by contact and hematogenous forms of staphylococcal M. Contact forms result from contact transition of inflammatory process to a meninx at osteomyelitis of bones of a skull of a pla of a backbone, suppuration of epidural cysts, suppuration of subdural hematomas or purulent otitises, abscesses of a brain. Hematogenous forms are observed at patients with an aggravation of a bronchoectatic disease, abscess of a lung, at septic abortions, felons and paronychias, hypodermic phlegmons, furuncles and an anthrax. They proceed especially hard since are always manifestation of septicopyemic process (see. Sepsis ).

For staphylococcal sepsis (see. Staphylococcal infection ) tendency to abscessing is characteristic. In 7 — 10 days from the beginning of sepsis in all bodies, including in a meninx and a brain, there are accurately delimited purulent cavities, usually multiple, quite often reported among themselves.

Klien, a picture is extremely various, but the Meningeal phenomena are, as a rule, accurately expressed. Temperature more often high, in blood — a neutrophylic leukocytosis with sharp shift to the left, ROE is accelerated. Focal defeats of a nervous system depend on localization of suppurative focuses. In the cases proceeding with epidurity and abscess of a spinal cord, the wedge, a picture is characterized by loss of functions according to the struck area of a spinal cord, the block of likvorny ways. In the presence of abscesses of a brain focal symptoms are defined by localization of abscess. Pathology from internals is characterized by generally septicopyemic process and localization micro or macroabscesses in these or those bodies.

The diagnosis is made on the basis of the features a wedge, currents (a septicopyemia with primary suppurative focus) allowing to suspect the staphylococcal nature of M. Podtverzhdayetsya the diagnosis bacteriological.

Treatment prior to a research an antibiotic grams of the activator it is reasonable to carry out by a combination from 2 — 3 antibiotics (Oxacillinum + - f-levomycetinum, tseporin + ampicillin, etc.) in the maximum therapeutic doses. Antibiotics should be combined with immunotherapy (see) — anti-staphylococcal plasma, serumal polyglobulins, specific gamma-globulin and anti-staphylococcal phages. Pathogenetic therapy — as well as at M. of a meningococcal etiology. In the presence of suppurative focuses an operative measure is obligatory.

Staphylococcal M.' forecast the heaviest. The lethality reaches 20 — 60%.

Gonococcal meningitis. Isolated cases of gonococcal M. at the weakened patients in the started cases are described gonorrhoeas (see). Gonokokki get into a soft meninx in the hematogenous way from the center of primary localization at an urethritis, conjunctivitis, a blepharitis. M. Etiol is clinically similar with meningococcal, the diagnosis is established by detection of gonokokk in cerebrospinal liquid. Treatment is same, as well as at meningococcal M. (see. Meningococcal infection ).

The meningitis caused by a pyocyanic stick met very seldom earlier. Increase in number of cases of M. caused by a pyocyanic stick (Pseudomonas aeruginosa) is connected with the broad use of antibiotics leading to dysbacteriosis, at Krom less steady bacteria disappear and steady types, including a pyocyanic stick survive. In most cases pyocyanic M. — display of the sepsis arising as superinfection after various operative measures (especially on a skull) or manipulations (punctures, catheterization), and also at the persons of old age having malignant diseases of blood.

The long wavy current of M. is more often observed, but cases of an acute current with quickly coming lethal outcome are described.

Cerebrospinal liquid muddy, sometimes greenish-blue shade. The pleocytosis (neutrophylic) reaches several thousand, protein content is increased, sugar is reduced.

The diagnosis is made on the basis of symptomatology and bacterial, researches of cerebrospinal liquid.

Prolonged treatment. The activator is steady against the majority of antibiotics. Polymyxin, gentamycin, karbenitsillin, concerning nek-ry strains — tetracycline, streptomycin are preferable. Polymyxin or gentamycin enter endolyumbalno. Pathogenetic therapy — as well as at M. of other etiology.

The forecast is heavy, a lethality high.

Salmonellezny meningitis meets seldom, more often at children is the first six months of life, especially at newborns, but also adults sometimes are ill.

V. I. Pokrovsky (1965) of 5550 cases of meningitis observed five cases salmonellezny (3 children and 2 adults). The disease is registered more often in maternity hospitals, children's hospitals where sick children, mothers, personnel can be a source of salmonellas. The contributing factor at newborns is the birth trauma.

The m, apparently, can be caused by any serotype of salmonellas.

At adult M. develops sharply with typical for salmonellosis (see) a picture of a gastroenteritis. The meningeal syndrome comes to light from the first days of a disease. At children, on the contrary, the disease develops gradually, the dispeptic phenomena are absent or are expressed moderately. Toxicosis, a septicaemia or a septicopyemia, increase in a liver and spleen, rash, a hyperleukocytosis of blood are characteristic. Often develop cerebral hypotension (see. Hypotensive syndrome ) and eksikoz.

The diagnosis is confirmed by detection of salmonellas in cerebrospinal liquid and blood, increase in a caption of specific antibodies.

Prolonged treatment: levomycetinum parenterally in a dose of 50 — 75 mg on 1 kg of body weight a day; ampicillin on 500 — 1000 mg on 1 kg of body weight a day. The combination of antibiotics, administration of streptomycin, levomycetinum endolyumbalno is possible. Fight against toxicosis is obligatory.

The forecast is heavy, a lethality high.

Typroid (paratyphoid) meningitis meets seldom. The disease develops more often in the acute period of a typhoid (see). Existence of meningeal symptoms against the background of a wedge, the symptoms characteristic of a typhoid, positive takes bacterial, and serol, blood analyses give the grounds to think of typroid M. Odnako the final diagnosis of M. can be made only at allocation of the activator from cerebrospinal liquid. It is necessary to consider that at patients with severe forms of a typhoid the meningism is quite often noted, and also otogenic M.'s accession, napr, a coccal etiology is possible.

Treatment is similar to salmonellezny M.'s treatment, and the forecast more favorable.

Collibacillary meningitis occurs seldom, preferential at children of early age, especially at newborns as display of sepsis (see. Koliinfektion ). At newborns it more often pathogenetic is connected with umbilical sepsis, at adults — with postoperative or with gynecologic. Current heavy.

The diagnosis is confirmed by detection of the activator in cerebrospinal liquid.

Treatment is directed to increase in protective forces of an organism. Definition of sensitivity of the allocated strain to antibiotics is obligatory. Before treatment is carried out by ampicillin in massive doses or tetracyclines in combination with cephalosporins or aminoglycosides. However efficiency of therapy is often small since big percent of strains of colibacillus rezistenten to many antibiotics.

The forecast is extremely serious.

Listeriozny meningitis. A tank listerell in the nature are rodents. Infection of the person occurs in the alimentary way more often (see. Listeriosis ). The disease develops sharply. The meningeal syndrome is expressed sharply, symptoms are often noted encephalitis (see). Cerebrospinal liquid can be transparent or muddy, opalescent. The pleocytosis of the mixed structure varies from several hundred to several thousand. Protein content is increased.

The diagnosis is made on the basis a lab. data: allocation listerell from cerebrospinal liquid, serol, a blood analysis.

Treatment: ampicillin, Kanamycinum. The lethal outcome in the first days of a disease is possible, but to M.'s thicket accepts a long current.

Serous meningitis

Serous meningitis can develop at various inf. diseases bacterial (tuberculosis, syphilis, leptospirosis, etc.), virus (acute lymphocytic choriomeningitis, parotitis, poliomyelitis, Koksaki-and ESNO-infection) nature, injury, tumor of a head or spinal cord, otitises, pansinusites, parasitic diseases of a brain. Cerebrospinal liquid at most of patients is transparent or opalestsirut, is colourless. Pressure it is increased. Pleocytosis — from several tens to 200 — 700 cells in 1 mkl; in a tsitogramma from the first days of a disease lymphocytes prevail. Protein content is normal or a little increased, the sugar content depends on an etiology of M. At tubercular M. the sugar content is often lowered, at virus M. — normal.

===== the Bacterial ===== forms

Tubercular meningitis is known since Hippocrates. Its activator was allocated from cerebrospinal liquid of the patient in 1893.

For years of the Soviet power incidence of tubercular M., as well as tuberculosis (see), considerably decreased, especially among children. Tubercular M. is registered usually during the whole year, but is more often during the winter and spring period.

In most cases tubercular M. develops as a result of hematogenous dissimination. From primary center in lungs, limf, nodes or kidneys the activator gets to a nervous system and strikes covers of a brain. According to D. S. Futer, only at 3% of patients clinically and sektsionno it was not possible to establish primary center; the last can be in various stages of development: the center of a fresh caseous necrosis encapsulated or petrifitsirovanny.

Sometimes M. is the first a wedge, display of tuberculosis and can be the only localization of active tubercular process. At 1/3 patients tubercular M. proceeds against the background of the disseminated pulmonary tuberculosis, to-ry, as a rule, comes to light along with a meningeal tuberculosis. Value of a fibrous and cavernous pulmonary tuberculosis as tubercular M.'s source considerably decreased (apprx. 10%), but in isolated cases of M. can develop at such patients after long specific therapy.

The course of a disease is quite often preceded by a prodromal stage — an indisposition, slackness, decrease in working capacity, appetite, a sleep disorder, irritability, non-constant subfebrile temperature. The prodromal stage gradually is replaced by the developed picture of a disease. A constant symptom of M. is temperature increase (from subfebrile to high gektichesky type), a cut precedes emergence of a headache more often or arises along with it. Tubercular M. is characterized by gradual development of a meningeal syndrome. But also the acute course of a disease, especially occurs at children of younger age. One of the earliest symptoms of M. is the headache of different intensity which, as a rule, is accruing, not passing at reception of analgetics. Nek-ry patients note also pains in chest or lumbar departments of a backbone, testimonial of defeat of covers and roots of a spinal cord. Morbidity at effleurage of vertebrae and a palpation of intervertebral points is at the same time noted. At a number of patients with such complaints the typical picture of spinal defeat develops further. Nek-ry patients in the first days of a disease complain also of numbness of a half of the face, language, extremities, paresthesias, dizzinesses. Vomiting, as a rule, joins a headache on 5 — the 8th day from an onset of the illness and arises at meal or drugs, at fast changing of position of a body; vomiting is often preceded by nausea. In the next days vomiting becomes more intensive. Meningeal symptoms are expressed in the beginning poorly therefore the patient continues to go, and quite often even to work. On 5 — the 7th day from an onset of the illness these symptoms become accurate and their intensity increases. In the next days patients accept a typical meningeal pose with the thrown-back head and legs given to a stomach. Only at certain patients, it is preferential with a basal encephalomeningitis, Meningeal symptoms are absent or are poorly expressed; their dissociation can be observed — at sharply expressed stiff neck there is no Kernig's sign or on the contrary.

Tubercular M. always proceeds as an encephalomeningitis or a meningomyelitis. Disturbances of mentality, various focal symptoms depending generally on localization of process are typical for it.

On the 1st week of a disease the general slackness, apathy, an adynamia, a headache is noted, to-rye every day of a disease amplify. On the 2nd week of development of M. patients are pale, pupils are often expanded. The general hyperesthesia is noted. Apathy, an oglushennost increases, delirious or oneiric states develop (see. Delirious syndrome , Oneiric syndrome ). Easing of memory on current events is observed; patients cannot report the anamnesis of a disease, gradually lose orientation in the place and time, they often have confabulations (false memoirs). Tubercular M. often is followed by damage of cranial nerves, a cut, as a rule, comes to light at the end of the 1st — the beginning of the 2nd week of a disease. Paresis III, IV, VII pairs of cranial nerves (isolated or in a combination), quickly progressing owing to a prelum the increasing exudate, and also as a result of a direct injury a nerve inflammatory process is most characteristic. Defeat of diencephalic area causes development of a number of vegetovascular symptoms: bradycardia, vasomotor reactions, red dermographism (see), Trusso's spots, sleep disorder. Signs of congestive disks of optic nerves appear and accrue (see. Congestive nipple ). Motive disturbances also develop gradually; they are quite often preceded by paresthesias of those extremities, in to-rykh paresis and paralyzes can develop further (see Paralyses, paresis). Then on the 2nd week of a disease also disturbances of tendon jerks and a muscle tone, patol, Babinski's reflexes, Rossolimo, Oppengeym, etc. come to light. The expressed paresis and paralyzes of extremities at not receiving specific therapy develop on 3 — the 4th week. Aphasia (see) at paralyzes it is noted at 25% of patients. Together with paralyzes less often separately meet hyperkinesias (see), choreoathetosis, the torsion dystonia, hemiballism. At children of early age and at elderly a hemiparesis is observed more often, sometimes in the first days of a disease. In some cases they are combined with spasms that is explained by defeat of substance of a konveksitalny surface of a brain. Spinal defeats are characteristic of later period of tubercular M. In rare instances the disease begins with spinal symptoms, and the general manifestations of M. arise later. Within the 3rd week the condition of patients with tubercular M. continues to worsen progressively. The condition of an oglushennost passing in prekomatozny and then and in coma accrues. Patients lie not movably, only sometimes plaintively groan. Tendon and pupillary jerks die away, or the resistant or periodically arising syndrome of a cerebrate rigidity develops (see), for to-rogo the persistent hypertension of muscles of hands and legs is typical: flexion and extensive or only flexion.

Depending on localization of process various wedge, tubercular M.'s options, early symptoms, a current meet and outcomes to-rykh have the distinctiveness.

A basal tubercular encephalomeningitis — the most often found form (85 — 90%) which is characterized by localization of serofibrinous exudative inflammatory process in the field of the basis of a brain around the intercrural tank. The gradual beginning with the accruing headache and temperature increase is characteristic of a basal encephalomeningitis. At the end of the 1st week of a disease vomiting joins, at the beginning of the 2nd week damage of cranial nerves, at the end of the 2nd week — dysfunction of pelvic bodies and confusion of consciousness, within the 3rd week — the oglushennost passing into a coma, a cerebrate rigidity is observed.

The diffuse konveksitalny encephalomeningitis begins more sharply with a headache and temperature increase, consciousness is quickly broken. In cerebrospinal liquid neutrophilic leukocytes can prevail. At a limited konveksitalny encephalomeningitis process is localized in the field of the central crinkles of a brain. Initial symptoms of a disease — paresthesias, a hemiparesis, aphasia, epileptic seizures against the background of the increasing temperature and a headache. At such localization of M. can accept a long current with remissions and aggravations. Sooner or later the basal encephalomeningitis joins.

Tubercular meningoentsefalomiyelit (a cerebrospinal form of tubercular M.) can be descending and ascending. At ascending the first displays of a disease — symptoms of a meningoradikulonevrit with dysfunction of pelvic bodies; Meningeal symptoms join later (at treated sometimes in several weeks). The descending form is characterized by bystry distribution of process from the basis of a brain on covers of a spinal cord and dominance in a wedge, a picture of a disease of symptoms of defeat of covers and substances of a spinal cord.

The diagnosis is made on the basis a wedge, pictures, data of the anamnesis and a lab. diagnoses. Data in the anamnesis on contact with the TB patient, a disease of tuberculosis, and also detection in cerebrospinal liquid of mycobacteria of tuberculosis are important for diagnosis. To find the activator by method of flotation, by means of crops and infection of Guinea pigs it is possible only at 1/5 patients therefore diagnostic value of these techniques is small especially as in most cases it is necessary to wait for results up to 2 months. Absence in cerebrospinal liquid of the activator does not exclude the diagnosis of tubercular M.

Cerebrospinal liquid, as a rule, transparent or opalescent, colourless (at spinal forms with the block of likvorny ways — xanthochromatic). ’ Its pressure in spinal (central, T.) the channel at uncured tubercular M. it is usually raised (more than 300 — 500 mm w.g.).

Increase in content of crude protein on average to 1 — 3,3 °/00 (is characteristic at spinal forms much higher — 30 — 60%0 and more). Pleocytosis within 100 — 500 cells with nek-ry fluctuations in this or that party. Only at certain patients it reaches 1000 — 2000. As a rule, a pleocytosis of the mixed structure with noticeable dominance of lymphocytes; preferential neutrophylic pleocytosis meets seldom, does not reach such high figures as at purulent M., and quickly is replaced by preferential lymphocytic. At children neutrophylic character of a pleocytosis is rather often observed (to 80 — 90%), especially at children of early age at an acute current, at retests dominance of lymphocytes is noted.

The sugar content in cerebrospinal liquid at tubercular M. often decreases to 0,3 g/l and below, but maybe normal (0,5 — 0,6 g/l). Decrease in a sugar content quite often correlates with weight of a condition of the patient and can have predictive value as well as the decrease in content of chlorides to 5,0 — 6,0 g/l (norm of 7,2 — 7,5 g/l) observed, as a rule, at heavy patients. Loss of a fibrinny film during the standing of cerebrospinal liquid within a day is typical for tubercular M. Repeated researches of cerebrospinal liquid in 3 — 4 days since tubercular M. is characterized by the increasing protein content, a resistant pleocytosis are necessary.

In blood the changes inherent to active tuberculosis are noted: leukocytosis (10 — 12 thousand) or the normal maintenance of leukocytes, in a leukocytic formula is more often a moderate lymphopenia, a monocytosis, small shift to the left — to 10% of band leukocytes, ROE remains on normal figures or is moderately accelerated.

The heavy current of M. and lethal outcomes are generally connected with untimely diagnosis and late begun treatment. During the performing adequate therapy it is possible to interrupt further development of process, however the tendency to improvement is planned only 3 — 7 days later from an initiation of treatment. At first vegetative frustration weaken, intoxication decreases. On 3 — the 4th day of treatment clears up consciousness. The patient becomes more active, contact. Temperature decreases, there is an appetite, vomiting stops. Gradually decreases and in 2 — 4 weeks the headache disappears. However, as a rule, it is still long subfebrile condition, a stiff neck and a Kernig's sign (up to 1 — 5 month), changes in cerebrospinal liquid remain (up to 5 — 6 months and more). Focal symptoms of defeat of c. N of page regress in different terms.

Treatment of patients with tubercular M. complex. Specific antituberculous remedies and fortifying drugs, a sanatorium therapy are used. The main specific drugs are derivatives of hydrazide isonicotinic to - you (drugs GINK, an isoniazid, Ftivazidum, metazid), to-rye get through a blood-brain barrier in bacteriostatic concentration. In modern a wedge, the practician Endo lumbar administration of streptomycin is not applied. The isoniazid (Tubazidum) is appointed in a daily dose at the rate of 15 — 20 mg to 1 kg of body weight of the patient; the dose of 20 mg is appointed to children of early age and the patient with a heavy current of M. Doz of Ftivazidum makes 20 — 30 mg on 1 kg of body weight for adults and 40 — 60 mg on 1 kg of body weight for children. To children of early age and about 60 — 80 mg are appointed arrived in a serious condition in the acute period to 1 kg of body weight a day. The daily dose of an isoniazid and Ftivazidum is divided usually into three receptions and given in 20 min. prior to food. At difficulties of swallowing, persistent vomiting the isoniazid can be entered rektalno in candles or intravenously kapelno.

The patient who was not treated by earlier antitubercular drugs appoint surely an isoniazid or Ftivazidum, streptomycin in combination with one of himiopreparat (Etioniamidum, Prothionamidum, Ethambutolum, rifampicin), PASK (sodium salt p-aminosalicylic to - you). Streptomycin is entered intramusculary daily once adult on 1 g, teenagers and children on 20 mg on 1 kg of body weight. PASK is appointed in a daily dose of adult 10,0 — 12,0 g (thrice reception) after food, to teenagers and children at the rate of 150 — 200 mg to 1 kg of body weight. At the expressed dispeptic frustration of PASK appoint after their elimination. Ethambutolum is appointed at the rate of 20 — 25 mg to 1 kg of body weight (on average adult 1200 — 1400 mg, and to children and teenagers to 1 g a day in one step). Treatment by Ethambutolum needs to be carried out at systematic control from the oculist. Rifampicin (Benemycinum) is applied in a daily dose of 600 mg (0,6 g) by the adult and 8 — 10 mg on 1 kg of body weight (no more than 0,45 g) to teenagers and children in one step. Treatment by rifampicin and Ethambutolum is appointed with medicinal stability of mycobacteria to drugs I of a row or their bad portability sick, at prevalence of the basic tubercular process and expressiveness of inflammatory process in a meninx, in cases of insufficient efficiency of treatment drugs I and II of a row (see. Antituberculous remedies ), at late diagnosis of M.

At late diagnosis of tubercular M. and serious condition of patients also use of corticosteroid hormones in a dose of 0,5 — 1 mg on 1 kg of body weight a day is shown to children and 15 — 30 mg on 1 kg of body weight by the adult during 3 — 4 weeks with gradual drug withdrawal. Favorable effect of hormones is expressed in bystry improvement of a condition of patients, decrease in temperature, reduction of a meningeal syndrome. Tuberculostatic therapy shall be combined with administration of vitamins: B6, B1 (inside or intramusculary), ascorbic to - you, glutaminic to - you in the standard doses. The important place in treatment of patients with tubercular meningitis is taken by fight against hydrocephaly. Apply lasixum (furosemide), Diacarbum (Fonuritum), hypothiazid. In hard cases injection of a mannitol is shown (intravenously 15% solution at the rate of 1 g of nonvolatile solid on 1 kg of body weight).

In the presence of motive disturbances (paresis, paralyzes) it is recommended after mitigation of a meningeal syndrome (in 3 — 4 weeks) to appoint massage, to lay down. gymnastics in combination with injections of a prozerin (1 ml of 0,05% of solution subcutaneously daily within 1 — 2 month) and other means. At neuritis optic nerve (see) — the corresponding treatment against the background of antibacterial therapy.

In the course of treatment control endolumbar punctures are carried out (see. Spinal puncture ). TB patients brain .obolochek shall be 1,5 — 2 months on a high bed rest before improvement of the general state, decrease in temperature, reduction of manifestations of a meningeal syndrome in the acute period of a disease, before emergence of the expressed positive dynamics at a research of cerebrospinal liquid. In the subsequent, in process of improvement of the general state, the mode becomes more active — in 2 months it is allowed to sit down on beds, to eat food sitting. If activation of the mode does not worsen a condition of the patient, and the composition of cerebrospinal liquid improves gradually, allowed to go on chamber, and in process of adaptation to the changed mode to make walks on air.

The extract from a hospital can be carried out after disappearance a wedge, M.'s manifestations and normalization of cerebrospinal liquid, at treatment or considerable regressing of tubercular process in other bodies not earlier than in 6 months from an initiation of treatment. From a hospital of patients for continuation of treatment send to specialized sanatorium. Duration of antibacterial therapy shall be not less than 6 months from the moment of full sanitation of cerebrospinal liquid and average at easy disease of 10 months, at medium-weight — 12 months, at heavy — 14 — 16 months taking into account weight of dynamics of tubercular process and in other bodies. At the same time streptomycin is appointed intramusculary in the absence of local changes in bodies or the calmed-down tubercular process within 3 — 4 months, at common forms of pulmonary and extra pulmonary tuberculosis — within 5 — 6 months. Drugs GINK are shown during all course of treatment.

At early diagnosis of M., as a rule, there occurs recovery; at the late beginning of specific treatment development is possible epilepsies (see), compensated hydrocephaly (see), permanent preservation of paresis. The expressed edema of a brain, the block of likvorny ways, cholesteatomas which were often developing at treatment of tuberculosis endolumbar administration of streptomycin meet seldom.

Syphilitic meningitis can be observed in all stages of syphilis, but a thicket in secondary and tertiary.

Early neurosyphilis lasts on average from 2 to 3 years. The m developing in this period of a disease carry to early, M. developing in later period of neurosyphilis — to late syphilitic M. Syphilitic defeats of a soft meninx can proceed sharply, subacutely and chronically.

Unlike M. of other etiology syphilitic M. often proceeds clinically asymptomatically that formed the basis for allocation of a special form of early neurosyphilis — the hidden syphilitic M., at Krom neither objective, nor subjective symptoms of defeat of a nervous system are found, but there are changes of cerebrospinal liquid: a pleocytosis (from single to 300 and more preferential lymphocytic cells in 1 mkl) at normal or small increase in protein content (to 0,45 — 0,6%0); globulinovy and colloid reactions slabopolozhitelny or negative, specific serol, reactions at most of patients positive; pressure of cerebrospinal liquid is usually increased. Such changes are noted to 6 months after infection in 8,1% of cases, till 1 year — in 33%, up to 2 years — in 25,8% and up to 3 years — in 22,8% of cases. The great influence on changes in cerebrospinal liquid is exerted by treatment by specific antisyphilitic drugs.

At a number of patients with the hidden M. at inspection it is possible to reveal the erased symptomatology of defeat of c. N of page: a headache, dizziness, extremity pains, decrease in painful sensitivity standing, limited epileptiform neuralgias, the erased focal defeats. The m arising in the first one and a half years of a disease in 1 — 1,5 month after the termination of a course of specific treatment is defined as a neurorelapse and demonstrates defective treatment. The hidden M. can develop at patients with late latent syphilis.

Manifest M. (acute feverish syphilitic cerebral) is characterized by the acute or subacute beginning, temperature increase (is more often to subfebrile figures) expressed Meningeal by a syndrome, variety of focal defeats of a nervous system. The headache, vomiting, the general hyperesthesia are noted, epileptic seizures are possible. At a number of patients mental disturbances — a depression or emotional disinhibition, psychomotor excitement are observed. Rather often paresis III, IV, VII pairs of cranial nerves, developments of stagnation on an eyeground meets. In cerebrospinal liquid the pleocytosis reaches 1000 — 2000 cells in 1 mkl, lymphocytes prevail, but there are also neutrocytes, the amount of protein is increased; loss of a fibrinous film is possible. Serol, reactions in cerebrospinal liquid in most cases positive, sometimes find a pale treponema. Allocate the following forms of manifest M.: 1) acute syphilitic hydrocephaly owing to occlusion at the level of a back cranial pole with developments of stagnation on an eyeground, headaches and vomiting; 2) the konveksitalny acute M. proceeding with epileptic seizures and mental disturbances; 3) basal M. with damage of cranial nerves; 4) spinal M., at Krom a soft meninx is surprised either diffuzno, or also substances of a spinal cord (a meningomyelitis, a meningoradiculitis) are more often in chest department with simultaneous defeat of roots.

Manifest syphilitic M.'s current differs in big variability: in one cases bystry, in others slow, sometimes recurrent. It in many respects depends on treatment. At patients with infectious forms of syphilis of M. before treatment it is characterized slowly, within several months, by the progressing meningeal phenomena, and after treatment — absence or weak expressiveness of all-brain and meningeal symptoms.

At M. children is quite frequent display of inborn syphilis. The meningeal syndrome is expressed unsharply, in cerebrospinal liquid are noted a moderate lymphocytic pleocytosis (100 — 150 cells in 1 mkl), the increased protein content, positive serol, reactions. Sometimes liquid hemorrhagic. On an eyeground the atrophy of optic nerves is noted. Separate cranial nerves are surprised. Transition of inflammatory process to substance of a brain causes a wedge, a picture of an encephalomeningitis, at Krom there are focal symptoms and spasms.

The diagnosis is based on klinikolaboratorny data.

Syphilitic M.' treatment is carried out according to the accepted schemes (see. Syphilis ).

The forecast at timely and full treatment favorable.

Brucellous meningitis proceeds, generally as a meningomyelitis or an encephalomeningitis (see. Brucellosis ).

Tulyaremiyny meningitis meets extremely seldom.

Mycoplasmal meningitis is described rather recently. Lerer and Kalavsky (R. J. Lerer, S. The m of Kalavsky, 1973) report about 50, Mari (E. Murray, 1975) with soavt, about 29 cases, S. V. Prozorovsky et al. (1978) about 19 cases of defeat of c. N of page at patients mycoplasmal infection (see). This form M. meets at any age.

The disease proceeds in the form of M. and an encephalomeningitis more often. It begins with symptoms of an acute respiratory disease and subfebrile temperature; in 3 — 14 days the sharp headache, the Meningeal syndrome develop. Cerebrospinal liquid remains transparent or becomes opalescent; the pleocytosis makes 20 — 3500 cells in 1 mkl with dominance of polinuklear (60 — 95%). Protein content normal or slightly increased, sugar — normal. The meningeal syndrome, as a rule, weakens gradually and symptoms disappear to 7 — to the 20th day of a disease. Focal symptoms of defeat of c. N of page can remain is longer.

The diagnosis is made on the basis a wedge, symptoms. The mycoplasmal etiology comes to light bacteriological.

Treatment is carried out by tetracycline drugs, erythromycin, semi-synthetic penicillin.

Forecast: Gesnikh (Gesnich, 1956) described 12 lethal outcomes. However, according to Mari's data, lethal outcomes from M. or an encephalomeningitis confirmed with allocation of the activator it is not described.

Leptospirozny meningitis can be caused by any serotype leptospir.

M at hay fever (see) it is observed at 10 — 15% of patients. Meningeal symptoms can develop both from the first days of a disease, and during the second and even the third feverish wave. Along with a headache pains in eyeglobes, a photophobia, excitement are noted. Focal nevrol, symptoms can be absent or are expressed moderately.

Cerebrospinal liquid more often transparent or opalescent, at certain patients — purulent. In the first days of a disease even at patients with a meningeal syndrome of a pleocytosis still can not be; quite often it appears only to 4 — to the 5th day of a disease, as a rule, within 100 — 400 cells in 1 mkl, but maybe lower and higher. In a tsitogramma lymphocytes, but impurity of neutrocytes considerable prevail more often, in rare instances they even prevail. Protein content is moderately increased. Sometimes in cerebrospinal liquid it is possible to find leptospira. Normalization of cerebrospinal liquid occurs after disappearance of meningeal) a syndrome and other symptoms of a disease.

The diagnosis is made on the basis of cliques, features of a disease, data epidemiol, the anamnesis (bathing in a reservoir, work in the boggy area) and is confirmed bacterial, and serol, by researches.

Treatment: penicillin in massive doses, tetracycline drugs, heterogeneous antileptospirozny gamma-globulin.

Forecast: lethal outcomes are rare; the disease, as a rule, comes to an end without the expressed focal defeats of a nervous system.

===== the Virus ===== forms

the Acute high-quality lymphocytic choriomeningitis (a synonym acute serous meningitis of Armstrong) — an infectious disease from group zoonoz (see). The activator concerns to group arenovirus (see). In an experiment on animals it causes a serous inflammation of a soft meninx with lymphocytic infiltration and considerable changes in vascular textures of a brain (from here and the name «lymphocytic choriomeningitis»). The disease at the person can proceed with various a wedge, syndromes (the most often grippopodobny and meningeal) N asymptomatically. It is described hron, the current of a lymphocytic choriomeningitis (up to 10 years), a cut begins the same as acute, with a meningeal syndrome, but encephalitis can develop further.

A tank and a source of a virus in the nature are nek-ry animal species, from to-rykh the greatest epid, the gray domestic mouse (Mus musculus) matters. The virus gets to an organism through respiratory tracts with the dust containing the dried-up excrement of rodents more often, but also other ways of transfer are possible. Both sporadic cases, and small epid are observed, flashes, are more often in the winter and in the spring, but there is no expressed seasonality. Adults and children of advanced age are ill preferential.

The disease begins sharply — with sharp rise in temperature, repeated vomiting and the most severe headache: also pain and pressure sense in eyeglobes are characteristic. The diffuse, constant headache, as a rule, proceeds within 7 — 12 days, in the subsequent 3 — 5 weeks it becomes pristupoobrazny. Vomiting stops earlier, than the headache, but at height of attacks of headache it repeats.

Meningeal symptoms are expressed from the first day of a disease. At most of patients they remain 10 — 14 days, and sometimes and more. Fever lasts 1 — 2 week, then temperature lytically decreases to norm, at certain patients subfebrile condition long remains. Also wavy character of a temperature curve is described. In the first days of a disease the oglushennost is quite often noted and easy, unstable encephalitic symptoms — a tendinous anizorefleksiya, Babinsky's symptom from one or two parties, an easy ataxy and a lack of coordination, paresis of separate cranial nerves appear. At 30 — 50% of patients on an eyeground easy developments of stagnation are observed: expansion and crimpiness of veins, slight hypostasis and smazannost of borders of disks of optic nerves. All these symptoms in process of subsiding of process gradually disappear. Palindromias and cases of a long current are possible.

Sharp increase in intracranial pressure — to 300 — 400 mm w.g. is characteristic. Cerebrospinal liquid colourless, transparent or opalescent. The pleocytosis from the first day of a disease lymphocytic (96 — 100%), reaches 200 — 2000 cells in 1 mkl. Protein content is more often increased to 0,6 — 1,2 °/00, but maybe normal. The sugar content and chlorides normally or is a little increased. The described changes remain is long also after normalization of temperature and disappearance of a meningeal syndrome.

The diagnosis is based on epidemiol. yielded and results a lab. researches — allocation of a virus from cerebrospinal liquid and blood, increase of credits of complement-linked and virus neutralizing antibodies more than by 4 times.

Treatment of the meningitis and meningoentsefalit caused by various viruses including an acute high-quality lymphocytic choriomeningitis, first of all is directed to decrease in cerebral hypertensia. Furosemide is for this purpose appointed, is more often inside (to adults and children of advanced age on 0,04 — 0,16 g a day in two-three inclusion with intervals in 6 hours, at heavier current — intravenously and intramusculary on 0,02 — 0,04 g).

At wet brain, spasms it is possible to enter intravenously 20% solution of Mannitolum at the rate of 1,5 g on 1 kg of body weight, 25% solution of albumine on 50 — 80 ml, the concentrated plasma. Appoint also a complex of vitamins. The condition of the patient improves after spinal punctures. The question of purpose of corticosteroid drugs (on 30 — 40 mg inside in days within 2 — 5 days), to-rye is recommended by certain clinical physicians, decides individually; quickly reducing temperature and reducing pains, they at the same time speed up bacterial complications (pneumonia, pyelocystites), terms of normalization of cerebrospinal liquid detain. At a lymphocytic choriomeningitis reception of corticosteroids increases a possibility of development of a recurrence. Corticosteroids are more shown at a serous encephalomeningitis. At development of symptoms of defeat of a nervous system (paresis, paralyzes) carry out the corresponding treatment. At development of bacterial superinfections appoint antibiotics. The bed rest shall be observed before normalization of temperature.

The forecast more often favorable, but is data on a possibility of a long persistirovaniye of the activator in c. N of page and a possibility of death at development of encephalitis.

The meningitis caused by a virus of epidemic parotitis of a virus etiology occurs among M. most often and develops at 10 — 15% of patients with epidemic parotitis (see. Parotitis epidemic ). Generally children of preschool and school age and young people are ill. At most of patients M.'s symptoms are shown in 3 — 5 days after swelling of sialadens, but this term can be and big. Approximately at 1/5 patients M., parotitis and pancreatitis at the same time develop. At nek-ry sick M. arises for 3 — 7 days before an inflammation of sialadens or proceeds without parotitis.

The m develops sharply: high temperature, vomiting, headache. Meningeal symptoms appear from the first days of a disease, but they are expressed unsharply and there do not correspond weights of a condition of the patient. Dissociation of meningeal symptoms is often observed: at the expressed stiff neck Kernig's signs and Brudzinsky are absent.

From the first days of a disease many patients, especially at children of the first years have lives, drowsiness and an oglushennost is noted. The loss of consciousness or a condition of psychomotor excitement, sometimes the general spasms are possible. Paresis VI, VII, VIII pairs of cranial nerves, a cerebellar ataxy, passing paresis of extremities is observed. Cases of polyradiculoneurites, meningoradikulomiyelit are described.

Sometimes changes in cerebrospinal liquid are noted at patients with epidemic parotitis without wedge, M. Zhidkost's signs transparent or opalescent, follows under pressure of 300 — 400 mm w.g. The pleocytosis usually within several hundred, but can reach 1000 and more cells in 1 mkl, preferential lymphocytic, but in the first days of a disease the considerable percent of polinuklear reaching sometimes to 30 — 50 is often observed. Protein content is moderately increased. Sugar content and chlorides normal. During the standing of liquid the fibrinous film occasionally drops out. The pleocytosis at repeated researches decreases, but normalization of cerebrospinal liquid happens more slowly, than the wedge, symptoms disappear: the increased maintenance of cells is noted at the general good shape of the patient and total disappearance of meningeal symptoms.

Treatment is similar to virus M.' treatment other etiology. In hard cases with the expressed symptoms of an encephalomeningitis, a polyradiculoneuritis antihistaminic and corticosteroid drugs in usual age doses are shown.

M.'s current, as a rule, favorable and in 2 — 3 weeks a disease comes to an end with recovery. However it is long there are phenomena of a psychasthenia. In cases with the expressed focal symptoms of defeat of a nervous system recovery slower.

The meningitis caused by enteroviruses (poliomyelitis viruses, the ECHO viruses and Koksaki) — one of a wedge, forms of enteroviral infections of the person (see. Enteroviral diseases ), proceeding with defeat of covers of a brain. The disease affects preferential children, teenagers and persons of young age. Sporadic cases and epidemics are observed. Regarding cases the disease proceeds as an encephalomeningitis. The m can be caused by any enterovirus, but the greatest number of large epidemics is caused by the ECHO 9, 6, 4, 11, 16, 30, 71 viruses; Koksaki's viruses B5. The flash can be caused at the same time by several enteroviruses.

Clinically M. caused by different types of poliomyelitis viruses, Koksaki's viruses and ECHO cannot practically be distinguished. For specification of an etiology allocate viruses from blood and cerebrospinal liquid of patients, reveal increase of an antiserum capacity to them.

An incubation interval of a disease — from 2 to 12 days. Begins sharply — with sharp rise in temperature, a severe headache and repeated vomiting, in some cases with disturbance of consciousness, spasms. Feverish period of 3 — 10 days; temperature is more often a constant, sometimes two-wave, decreases critically.

The face of the patient is hyperemic, with a pale nasolabial triangle, conjunctivitis and an injection of vessels of scleras is expressed. The hyperemia of a pharynx, especially in the field of handles is characteristic. The herpetic rash at a nose and lips is sometimes noted. 10 — 25% of patients on face skin, trunks, extremities have a rozeolezny, spotty or papular rash disappearing sometimes in several hours. Bradycardia, locks, a deviation to the left with a moderate leukocytosis or without it, the eosinophilia developing to 6 — to the 7th day of a disease, the accelerated ROE are possible. The liver and a spleen increase seldom. Meningeal symptoms appear on 2 — Z-y day of a disease. They are preceded by the headache of various intensity, vomiting connected with sharply arising syndrome of increase in intracranial pressure. At most of patients the scattered, easy and quickly passing symptoms of organic lesion of a nervous system are noted: revival of tendon jerks, anizorefleksiya, Babinsky's symptoms. Oppengeyma, central paresis VII, XII pairs of cranial nerves, cerebellar ataxy, etc.

Cerebrospinal liquid transparent, colourless, follows under supertension. In the first days of a disease the pleocytosis which is often mixed sometimes with dominance of neutrophils. Further (to 3 — to the 5th day of a disease) it becomes lymphocytic. In most cases the pleocytosis reaches 100 — 700 cells in 1 mkl. Protein content more often normal, but can be increased (to 1 per mille) or lowered (less than 0,1 per milles). Content of chlorides and sugar is also more often normal.

Wedge, enteroviral M.' symptoms are expressed less, than changes in cerebrospinal liquid. At 15 — 30% of patients they are absent in the presence of the expressed inflammatory changes of cerebrospinal liquid.

Enteroviral M.' current high-quality. Normalization of cerebrospinal liquid happens gradually: the pleocytosis decreases with 3 — the 10th day, the cytosis on 20 — is finally normalized the 30th day.

The diagnosis is based on epidemiol. data, wedge, and virusol, researches.

Treatment is similar to treatment of viral meningitis of other etiology.

Forecast favorable.

At the nek-ry patients who transferred M. the postinfectious asthenic syndrome is observed. A recurrence is possible (in 10 — 25% of cases). The recurrence usually proceeds easier.

Herpetic meningitis and an encephalomeningitis, to-rye can be caused by a virus both a herpes simplex, and surrounding meet seldom, but proceed hard. Prevalence of herpetic rashes does not correspond to expressiveness of meningeal and focal symptoms. The encephalomeningitis at the surrounding herpes develops more often against the background of defeat cerebral gangliyev and spinal nodes. Fever keeps within 5 — 10 days. Cerebrospinal liquid transparent. The lymphocytic pleocytosis fluctuates from several tens to hundreds of cells in 1 mkl. Protein content is moderately increased (to 0,6 — 1,2 per milles).

The diagnosis is made on the basis a wedge, pictures and data of a virologic research. Treatment is similar to virus M.' treatment other ethnology (see also Herpes ).

Entsefaliticheskne and the Meningeal phenomena, as a rule, regress rather quickly, but lethal outcomes are described.

Influenzal meningitis. A consensus about existence of M. caused by an influenza virus, no. In most cases defeat of a nervous system at flu is connected with the expressed circulator disturbances of blood circulation in a brain and its covers. Nek-ry authors acknowledge the possibility of development of the serous M. caused by an influenza virus, to-ry proceeds with the expressed lymphocytic pleocytosis of cerebrospinal liquid (within 200 — 300 cells in 1 mkl), low protein content, and sometimes availability of blood in it. Normalization of cerebrospinal liquid happens during 5 — 10 days.

Treatment is similar to treatment of other virus M.

The forecast at the «isolated» influenzal M. favorable, at development of the hemorrhagic phenomena, hemorrhagic meningoentsefalit serious.

The serous and purulent meningitis caused by fungi and protozoa

Blastomikozny meningitis develops at cryptococcosis (see). M.'s symptoms appear gradually, symptoms of encephalitis often develop: damages of cranial nerves, spasms. Cases with development of epilepsy of jacksonian type are described (see. Jacksonian epilepsy ), hemiparesis. Disease is reminded by tubercular M. Davleniye to cerebrospinal liquid is raised. It can be transparent, muddy or xanthochromatic. The pleocytosis is moderate, is more often within 200 — 800 cells in 1 mkl, can p be higher, the mixed character, but lymphocytes prevail more often; the sugar content is lowered.

The diagnosis is made at detection of the activator.

An effective remedy of treatment is Amphotericinum In, to-ry enter slowly, hours, intravenously and into the spinal canal. A daily dose of 200 — 1000 PIECES on 1 kg of body weight. Are effective 5-ftortsitozin and flutsitozin.

Forecast heavy. Lethality high.

Koktsidioidozny meningitis is a complication of a coccidioidosis of lungs (see. Coccidioidosis ) and very seldom proceeds without their expressed defeat. Meets in the desert hot regions of America. Inflammatory process in covers of a brain is characterized by formation of the multiple miliary small knots similar to tubercular granulomas. Substance of a brain is often involved in process.

On a wedge. to a picture the disease is similar to tubercular M. Techeniye M. and an encephalomeningitis chronic, for several months. In cerebrospinal liquid the pleocytosis reaches several hundred in 1 mkl, on structure it is preferential lymphocytic. Protein content is increased.

The diagnosis is made on the basis of detection in cerebrospinal liquid of the activator.

Treatment is carried out by Amphotericinum In, to-ry is entered intravenously, into the spinal canal and suboktsipitalno. In the big tank the drug is administered not more often than two weekly in the doses which are not exceeding 500 PIECES on 1 kg of body weight. Fortifying therapy is obligatory.

Forecast adverse.

Toksoplazmenny meningitis and encephalomeningitis develop both at inborn, and at the acquired toxoplasmosis. The m on a current can be acute and chronic. Headaches are noted, it is preferential in a nape and in a forehead, dizziness, various focal symptoms: damages of cranial nerves, paresis of extremities, cerebellar and neuroendocrinal frustration. Meningeal symptoms are a little expressed. Generalized or local spasms, myoclonias, damages of eyes, existence on the roentgenogram of a skull of calcifications of various form are characteristic of an inborn form. Damages of eyes at the acquired toxoplasmosis can not be, calcificats in a brain are absent. Pressure of cerebrospinal liquid and protein content in it are increased, the xanthochromia is possible. The pleocytosis is more often small, but can reach even 1500 cells in 1 mkl, with dominance of lymphocytes. In the draft of cerebrospinal liquid after coloring are found toxoplasma; introduction allows to allocate to her animals strains toksoplazm.

The diagnosis is confirmed by reaction of binding complement, Seybin's test — Feldman, a positive intracutaneous allergy test (see. Toxoplasmosis ).

Treatment is similar to treatment of other generalized forms of a toxoplasmosis.

The forecast is adverse, especially at an inborn form.

Candidosis meningitis can be caused by any kind Candida — Candida albicans, tropicalis, krusei, etc. Process is characterized by formation of infiltrates of a meninx from lymphocytes, histiocytes and epithelial cells, hemorrhages and the centers of a necrosis. Often defeat of covers is combined with defeat of tissue of brain (in the form of abscesses). Candidosis M. develops at the persons having pulmonary or renal candidiasis or candidosis sepsis more often. Its symptomatology depends on localization of defeat. Allocate diffusion M., basal M., an encephalomeningitis. On a wedge, candidosis M. reminds a current tubercular M. or abscess of a brain. In cerebrospinal liquid, quite often transparent or opalescent, the quantity of leukocytes (neutrophils, mononuklear, lymphocytes) increases up to 100 — 1000 cells in 1 mkl, protein content to 1 — 2 per mille. The diagnosis is based on detection of the activator in cerebrospinal liquid.

Treatment is similar to treatment of visceral and septic forms candidiasis (see).

Forecast heavy.

Mukorozny meningitis meets seldom. Is caused various look by fungi of the sorts Absidia, Mucor and Rhizopus combined in this. Mucoraceae. Mukorozny M. and an encephalomeningitis usually develop for the second time owing to hematogenous innidiation from primary center in lungs, a nose, a nasopharynx. From a nasopharynx process on veins through bones of a skull can reach a cavernous sine. Mukorozny M. develops at patients with severe forms of diabetes more often.

Cerebrospinal liquid, as a rule, transparent, contains single erythrocytes and leukocytes; the amount of protein is increased.

The diagnosis is based on detection of the activator in cerebrospinal liquid or allocations from a nose.

Treatment is similar to koktsidioidozny M. V treatment early stages perhaps an operative measure in a nasopharynx.

Forecast bad.

See also Mould mycoses .

Amoebic meningitis (encephalomeningitis) caused by amoebas of the Limax group for the first time is described by Fowler and Carter (M. Fowler, R. F. Carter) in 1965. Activators are potentially pathogenic amoebas of the Limax — Naegleria fowleri Carter group, 1970 from this. Valcampliidae and several types akantameb, including Acanthamoeba culbertsoni, A. astronyxis, A. polyphaga, etc. from this. Acanthamoebidae Sawyer and Griffin, 1975.

Infection with negleriya is connected with bathing in the lakes, ponds opened and the closed swimming pools. The meningoentsefalita caused by negleriya are registered in the form of sporadic cases and small epid, flashes in warm season in all latitudes. Children and persons of young age get sick. The m caused by akantameba in the form of sporadic cases are registered at persons of different age with an immunodeficiency or weakened heavy hron, diseases. Infection with these amoebas occurs through water, the soil, dust is more rare. Entrance gate — a nasopharynx, and for akantameb, perhaps, lungs.

An incubation interval at infection with negleriya — 3 — 7, akantamebam — 10 and more days. Meningoentsefalita, caused by negleriya, are characterized by the sudden beginning and an acute current. The severe headache, disturbance of consciousness, temperature increase, anorexia, vomiting, muscle tension of a nape is noted, motor and touch disturbances, a coma develop. The focal symptomatology (spasms, paralyzes, etc.) soon joins meningeal symptoms owing to development of encephalitis. Death comes on 2 — the 7th days of a disease.

The encephalomeningitis caused by akantameba is characterized by the gradual beginning and hron, a current. At the beginning of a disease the headache, elevated temperature, muscle tension of a nape, an ataxy are noted, then the lethargic state, a coma develops. Death comes in 5 — 50 and more days from the beginning of a disease.

Cerebrospinal liquid transparent, is noted a neutrophylic pleocytosis, high content of protein and low — sugar. Amoebas are found at microscopy of fresh cerebrospinal liquid, its crops and pieces of tissues of brain of a corpse on a hungry agar with a bacterial lawn.

Treatment is not developed, antibiotics are sometimes effective (Amphotericinum In).

Forecast adverse.

Prevention is not developed, bathing in the reservoirs infected with amoebas of the Limax group is forbidden.

Otogenic and rhinogenic meningitis — the acute inflammation of a meninx, a cut is connected with purulent process in an ear (otogenic M.), in a nose and its adnexal bosoms (rhinogenic M.). Among all otogenic intracranial complications otogenic M. makes, according to different authors, from 9.4 to 25,1%.

Rhinogenic M., as well as rhinogenic intracranial complications, meets much less often, and in literature there are only descriptions of separate observations of this disease. Rhinogenic intracranial complications meet 12 — 15 times less often than otogenic. Otogenic and rhinogenic M.'s activators most often are streptococci, pneumococci and other microorganisms, and also adenoviruses and mycoplasmas. The big role in otogenic and rhinogenic M.'s development is played by changes of local and general body resistance, its reactivity. A source of infection at otogenic M. are most often hron, purulent average otitis, especially an attic disease (see. Otitis ), complicated cholesteatoma (see), acute purulent average otitis is more rare. Frequency of complications hron, purulent average otitis of M., according to literary data, fluctuates from 0,5 to 3,6%.

The infection from tympanic cavities can get into a head cavity contact, hematogenous and lymphogenous in the ways. At contact distribution of process the infection gets in the ways or anatomically already existing, or on again formed patol, process. In the first case — it is vascular connections, preformirovanny anatomic messages in the form of openings and channels, labyrinth windows, internal acoustical pass, water supply systems of a snail and a threshold, mastoidal cells; children of early age in conjunctions of components of a temporal bone have open cracks, to-rye can long remain open and with the adult. Ways of spread of an infection in the second case are the fistulas which are formed owing to caries of walls of a middle ear. At hron, purulent average otitis fistulas are more often formed in the field of a roof of a drum cavity and a mastoidal cave, and also on an internal wall of a mastoid. If the infection extends through an inner ear, then such M. is called labirintogenny if through a middle ear — timpanogenny.

The labyrinth way of spread of an infection meets more than at 50% of all otogenic M. Otogenic M. can be caused also by other intracranial complications — subdural abscess, a sinus thrombosis, abscess of a brain and cerebellum. The factors promoting penetration of an infection into a head cavity. are concussion of the head at blow, falling, at operative measures a «molotkovy» way on the sclerosed mastoid, and also weakening of an organism infectious diseases.

Rhinogenic M. develop owing to penetration of an infection into a subarachnoid space from adnexal bosoms of a nose (a thicket frontal) or from a nasal cavity. The infection gets through fistulas of thin cerebral walls of adnexal bosoms at hron, an inflammation, through veins of a mucous membrane of a trellised labyrinth on the existing anastomosis into veins of a firm meninx, and also on covers of an olfactory nerve. Rhinogenic M.'s development at surgical interventions in a nose and paranasal sinuses is possible. More often it is observed at endonasal opening of a trellised labyrinth and frontal sinus.

Patomorfol, changes at otogenic and rhinogenic M. are characterized by formation of inflammatory exudate in a subarachnoid space. In character exudate can be serous or purely purulent; depending on it distinguish serous and purulent M. Accumulations of exudate can be limited and be localized by hl. obr. in the place of transition of an infection from cavities of an ear in a head cavity that is promoted by formation of commissures between a soft meninx at hron, the course of a disease. In this case the limited purulent M is observed. If inflammatory exudate spreads to big spaces, passing to other hemisphere and a cerebellum, then the diffusion purulent M develops.

Otogenic and rhinogenic M.'s symptoms are various and caused by the disease which caused them, localization of process, extent of increase in intracranial pressure. The main complaint of the patient are severe headaches of the poured or localized character. There is a stiff neck, a meningeal pose. The general hyperesthesia of skin, a photophobia is noted, sensitivity to sounds becomes aggravated. Clonic and tonic myotonia of extremities and the person, and also symptoms of damage of cranial nerves (especially often oculomotor, front, wandering, trigeminal) in the form of paralyzes, paresis, disorders of sensitivity and secretory disturbances can be observed. At localization patol, process in a back cranial pole delay of breath is possible; sometimes develops cheynstoksovo breath (see. Cheyna — Stokes breath ).

At distribution of process on a spinal cord functions of pelvic bodies are broken, appear patol, Babinski's reflexes, Gordon, Rossolimo, Oppengeym (see. Babinsky reflex , Gordon reflexes , Rossolimo reflex ), to-rye can be shown not always in full and not always to be distinctly expressed.

Especially rapid current with high fever, the expressed headaches, persistent vomiting, unconsciousness is characteristic of the purulent M. caused by hematogenous distribution of process at acute purulent average otitis. A symptom of ohms of otogenic or rhinogenic M. changes in cerebrospinal liquid are constant: increase in its pressure, sometimes to 700 — 800 mm w.g.; it is opalescent, sometimes muddy. At a research of cellular composition of cerebrospinal liquid the pleocytosis, hl is found. obr. at the expense of polinuklear. Protein content increases, sugar and chlorides goes down. In blood the leukocytosis (to 20 — 25 thousand in 1 mkl), a neutrocytosis is found; ROE is accelerated. Temperature reaction, as a rule, happens expressed and a constant. Serous M.'s symptoms are much less expressed, and disease less heavy.

Otogenic and rhinogenic M.'s diagnosis is based on data of the anamnesis, inspection and a research of cerebrospinal liquid. Establishment of communication of purulent M. with a disease of an ear or a nose is very important. If at hron, purulent average otitis there are ear pains, the otorrhea amplifies, there are fever and Meningeal symptoms, then it is necessary to assume existence of otogenic M. The same should be assumed if the corresponding symptomatology appears at a disease of a nose and its adnexal bosoms or after operative measures on these bodies. At acute purulent average otitis of pain in an ear, the elevated temperature and an otorrhea are inherent also to a basic disease and the differential diagnosis becomes more difficult. Results of a research of cerebrospinal liquid, existence of a meningeal syndrome resolve an issue.

At differential diagnosis of purulent otogenic and rhinogenic M. about meningococcal M. detection in cerebrospinal liquid of a meningokokk is of great importance.

Otogenic and rhinogenic M.'s treatment shall be complex — etiological, pathogenetic and symptomatic. A priority action is removal inf. the center irrespective of weight of a condition of the patient. Operation is made against the background of purpose of antibacterial therapy; it is previously necessary to define character of microflora and its sensitivity to antibiotics. The way of introduction of antibiotics depending on weight of a condition of the patient can be intramuscular, intravenous, intrakarotidny, endolumbar. From antibiotics penicillin in a dose from 10 to 20 million is more often applied. The piece a day, is more rare Sigmamycinum, Oleandomycinum on 1,0 g a day, etc. Endolumbar administration of penicillin is admissible at serious condition of the patient; at the same time it is possible to use only its sodium salt. Duration of introduction of antibiotics depends on the nature of disease. Along with antibiotics nystatin, streptocides is appointed, Disintoxication, dehydrational and symptomatic therapy is carried out.

The forecast at otogenic and rhinogenic M. before introduction to practice of streptocides and antibiotics was heavy, the lethal outcome was observed in 75 — 97% of cases. At observance of complex correct treatment the lethality does not exceed 20%.

Prevention of otogenic and rhinogenic meningitis consists in timely diagnosis and the correct treatment of purulent diseases of an ear, nose and its adnexal bosoms.

Mental disorders at meningitis

Mental disorders at M. concern to group symptomatic psychoses (see). At M. of a different etiology they are quite same.

In a prodromal stage of M. the mental exhaustion, fatigue, the suppressed mood with tearfulness and a capriciousness, a hyperesthesia, frustration of a dream, headaches are noted. At height of a disease conditions of stupefaction (devocalization, confusion, delirious, oneiric states) inherent to acute symptomatic psychoses are generally observed.

At children of younger age slackness, an adynamia, drowsiness, devocalization with the periods of motive concern prevail. At the expressed toxicosis convulsive attacks are possible.

The most expressed mental disorders are observed at purulent M. V the acute period devocalization with episodes of delirious and amental stupefaction prevails, in the most hard cases development soporous and coma is possible (see. Devocalization ).

In serous M.' (meningoentsefalit) group the most accurately expressed mental disorders can be observed at tubercular M. In this case the prodromal stage is characterized by the suppressed mood, indifference, sleep disorders. In the acute period devocalization can alternate with short-term delirious and oneiric episodes when patients experience the figurative fantastic experiences which are combined with visual and acoustical hallucinations (see), metamorphopsias (the distorted perception of size, a form and spatial relationship of objects), disturbances of a body scheme, false recognition of relatives.

Serous M. at epidemic parotitis quite often is followed by the expressed drowsiness, slackness, psychosensorial frustration without the phenomena of clear stupefaction.

The nek-ry patients who had psychosis after escaping of a condition of the dulled consciousness can have transitional syndromes, napr, depressive and paranoid states, a passing anamnestic syndrome, to-rye last of 1 week up to 3 months

Krom of therapy of a basic disease, at the expressed psychomotor initiation, alarming agitation, deception of perception at patients with stupefaction appoint intramuscular injections of aminazine and drugs of dehydrating action (an injection of sulfate magnesia). Dehydrating agents in combination with neuroleptics are used also at transitional syndromes.

The forecast of mental disorders at M. is various. In cases of a heavy current of M., especially at children of younger age, residual encephalopathy with weak-mindedness, symptomatic epilepsy or a psychopatholike state can develop.

Prevention of mental disorders at meningitis consists in early recognition and adequate treatment of a basic disease.

Features of meningitis

M. at children occurs at children more often than at adults that is connected with more wide spread occurance at them inf. diseases, hyperpermeability blood-brain barrier (see) and features immunol, reactivity (see. Reactivity of an organism ).

Among serous M. at children the main place is taken by M. caused by a virus of epidemic parotitis and intestinal viruses of Koksaki and ECHO. These M. are especially frequent at children of preschool and younger school age. At children of the first year of life they are extremely rare; at this age purulent M. U of newborn M. always purulent are especially frequent and often arise against the background of a birth trauma and sepsis. At children of early age secondary purulent meningitis at sepsis of various etiology is especially frequent. At the senior children considerably otogenic and rhinogenic purulent meningitis meets more often.

Serous M. of a virus etiology at children begin sharply — with rise in temperature to high figures, emergence of a headache, repeated vomiting, meningeal symptoms of various expressiveness. At nek-ry children Meningeal symptoms can not be defined that in most cases is the reason of diagnostic mistakes. Expressiveness of meningeal symptoms and weight of a current usually depend on the size of intracranial pressure, a cut can reach 300 mm w.g. above. Children of preschool age have an intracranial pressure and a pleocytosis reach higher figures, than at the senior children. Cerebrospinal liquid protein content is normal or is moderately increased. The acute period of serous virus M. proceeds 3 — 5 days, cerebrospinal liquid is normalized to 12 — to the 16th day of a disease.

Purulent M. of any etiology, especially primary, usually begin at children sharply with a fever, temperature increase, emergence of vomiting, a headache, all-brain disturbances. Quickly Meningeal symptoms accrue, the hyperesthesia is expressed. At children of early age kloniko-tonic spasms are frequent, the integument has a grayish shade, the phenomena of intoxication with short wind, tachycardia, deaf cardiac sounds are expressed, parenteral dyspepsia is possible. From meningeal symptoms at this age tension, the strengthened pulsation of a fontanel and Meytus's symptom has special value. At the senior children consciousness is often broken, block, forced situation with the thrown-back head and the bent legs appears. The meningeal syndrome is accurately expressed, tendon jerks are strengthened, reflexes can be caused patol. In blood a high leukocytosis, a neutrocytosis; ROE is accelerated. Cerebrospinal liquid muddy or purulent, protein content in it is increased, the pleocytosis of neutrophylic character reaches several thousand cells in 1 mkl.

Purulent M. against the background of it is purulent - septic diseases, treated antibiotics, begins subacutely and often, especially at children of early age more often, presents great difficulties for diagnosis. Existence at the child of gektichesky temperature, periodically arising general concern with a shriek, a cut alternates with slackness and an adynamia, failure from food, periodic vomiting, sometimes spasms * permanent acceleration ROE and a neutrocytosis in blood are the basis for carrying out a diagnostic lumbar puncture even in the absence of meningeal symptoms. At the same time it is necessary to consider that use of antibiotics can lead to decrease in a pleocytosis and neutrophylic lymphocytic its structure. Decrease in a sugar content in cerebrospinal liquid indicates the long current of purulent M.

Techeniye of purulent M. and emergence of complications in many respects depend on correctness and timeliness of treatment. It is necessary to carry hydrocephaly, various motive disturbances, damages of cranial nerves, a convulsive syndrome to number of complications. The resistant psychasthenia and a gipertenzionny syndrome are frequent. At a favorable current the state gradually improves, toxicosis disappears, Meningeal symptoms cease to be defined. The leukocytosis and a leukocytic formula are normalized at the accelerated ROE. To 12 — to the 14th day, sometimes later, cerebrospinal liquid is normalized.

Serous M.' therapy at children is directed to cerebral decompression for what within 7 — 10 days carry out dehydrating therapy (Mannitolum, Diacarbum, lasixum). Also desensibilizing and fortifying means, vitamins are appointed. On 2 — 3 weeks the bed rest is necessary. For the purpose of the prevention of complications (a gipertenzionno-gidrotsefalny syndrome, a psychasthenia), to-rye a thicket are noted at children of advanced age, for 3 months the sparing mode is set.

Purulent M.' treatment first of all etiotropic — antibiotics, selection to-rykh is caused by an etiology of a disease. Pathogenetic therapy — desintoxication by administration of plasma, Haemodesum, a reopoliglyukin, glyukozopoliionny solutions, correction of the arising exchange and hormonal disturbances, sufficient vitaminization, etc. is necessary. Treatment shall be carried out in a complex.

The forecast depends on timeliness of treatment, at serous M. it is optimum. At purulent M. the lethality, especially at early age, remains rather high.

PREVENTION

M.'s Prevention consists in timely and correct treatment of a basic disease, and also prevention inf. diseases, against the background of to-rykh M.

the MAIN DIFFERENTIAL DIAGNOSTIC CHARACTERS of VARIOUS FORMS of MENINGITIS

Group of meningitis develops combines a large number nosologically of the independent diseases differing on an etiology, a pathogeny, the nature of morphological changes in covers of a head and spinal cord, a clinical picture, sharpness and weight of a current, the forecast. Differential diagnosis between them quite often presents certain difficulties and demands the accounting of all set of clinical signs and these special methods of a research. In this regard in addition to the main article «Meningitis» it is brought the table including the main differential diagnostic characters of various forms of meningitis .



Bibliography: Weinstein I. G. and Grashchenkov N. I. Meningitis, M., 1962, bibliogr.; Garshin M. I. Otogenic meningitis, L., 1963, bibliogr.; Davydovsky I. V. Pathological anatomy and pathogeny of diseases of the person, t. 1, page 493, M., 1956; Dadiomova M. A. and Pratuse-v and p P. M. Acute serous meningitis and encephalitis at children, D., 1974, bibliogr.; Clinical psychiatry, under the editorship of G. Grule, etc., the lane with it., page 288, M., 1967; The Multivolume guide to pathological anatomy, under the editorship of A. N. Strukov and P. P. Dvizhkov, t. 9, page 584, M., 1964; Patomorfologiya of a nervous system, under the editorship of. I. Ni-kulesku, the lane from Romanians., Bucharest, 1963; The Pokrovsk V. I., F and in about r about in and L. A. and Kostyukov N. N. Meningococcal infection, M., 1976; Preobrazhensky B. of Page and P about p about in and G. N. Angina, an adenoid disease and the general diseases interfaced to them, page 163, M., 1970; Prozorovsky S. V., Pok-r about in with to and y V. I. and In and with and l e in and V.P, the Mycoplasma of pneumonia infection, M., 1978; Reznik B. Ya. and With p and l of e to S. F., Meningitis at children, M., 1971, bibliogr.; The guide to infectious diseases, under the editorship of A. F. Bilibin and G. P. Rudnev, page 335, M., 1967; Suprunov V. K., About treatment of patients with otogenic meningitis in Loruchrezhdeniyakh of the USSR, Vestn, otorinolar., JsTs 6, page 3, 1962; D. S Footer. Diseases of a nervous system at children, page 56, M., 1965; Tsuker M. B. Infectious diseases of a nervous system at children, page 5, M., 1963; it, Meningitis and encephalitis at children, M., 1.975, bibliogr.; it, Clinical neuropathology of children's age, M., 1978; Sh and p about in and l And. H. Aseptic meningitis, L., 1971, bibliogr.; Adams R. D. a. Victor M. Principles of neurology, p. 619, N. Y., 1977; Appelbaum E. Purulent forms of meningitis, in book: The Cyclopedia of medicine, surgery, specialties, v. 8, p. 975, Philadelphia, 1956; Handbook of clinical neurology, ed. by P. J. Vinken a. G. W. Bruyn, y. 35, p. 260, 321, Amsterdam a. o., 1978; Y e s n i with k L. Central nervous system complications of primary atypical pneumonia, Arch, intern. Med., v. 97, p. 93, 1956. V. I. Pokrovsky, L. O. Badalyan;


E. S. Bondarenko, V. I. Freydkov (ped.), L. M. Gordeeva (paraz.), V. V. Kovalyov (psikhiat.), N. I. Kostrov, V. P. Fomina-Kosolapov (ENT specialist.), A. M. Nesvetov (stalemate. An.).

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