From Big Medical Encyclopedia

MIOSITIS (myositis; grech, mys, my[os] a muscle + - itis) — the inflammation of muscles of various etiology which is shown a pain syndrome, development of muscular weakness and sometimes an atrophy of the struck muscular groups. On M.'s etiology divide on infectious (purulent and not purulent), parasitic, toxic. Due to the nek-ry features patomorfol, pictures and a wedge, symptoms allocate a neuromyositis, a polyfibromyositis, ossifying M., and also professional M.

On M.'s current can be acute, subacute and chronic, on prevalence — localized and diffusion.

Pathological anatomy

Morfol. changes at M. are presented by alterativny, exudative and proliferative processes in muscular tissue (see. Inflammation ).

At purulent M. strepto-or a staphylococcal etiology the widespread necrotic changes delimited by a massive leukocytic shaft come to light. The inflammation can be diffusion as phlegmonous M. and limited by the piogenic capsule with formation of abscess. At a pyocyanic infection ichorization of nekrotizirovanny fabrics is noted. In muscles, adjacent to a necrosis, heavy circulatory disturbances in the form of a sharp plethora, staz, hemorrhages and massive fibrinous exudate with a small amount of polinuklear come to light.

Not purulent inf. M can be serous, perenkhimatozno-intersticial, proliferative, diffusion sclerous. Serous M. usually develops as a reactive inflammation patol around. process (e.g., at tuberculosis, tumors). Vacuolar dystrophy, segmented coagulative necrosis with a macrophagic resorption of muscle fibers, melkoochagovy limfoplazmotsitarny infiltration are characteristic of virus M. Electronic microscopically in single muscle fibers subsarkolemmalny paracrystal virus inclusions come to light.

Fig. 1. Microdrug of muscular tissue at an acute polymiositis (longitudinal section): dystrophy and necrosis of muscle fibers (1), lymphoid and macrophagic infiltration (2); X 280.
Fig. 2. Microdrug of muscular tissue at a chronic polymiositis (cross section): a raznokalibernost of muscle fibers, a sclerosis endo-and a perimysium (it is specified by shooters); x 280.

The m at tuberculosis proceeds as intersticial with tubercular granulomas or cold abscess forms (see. Natechnik ), in Krom the center of a coagulative necrosis and granulyatsionny tubercular fabric is defined. Diffusion sclerous process is characteristic of syphilitic M., less often in the thickness of muscles gummas meet. The m at rheumatism depending on activity patol, process can proceed with dominance of exudative, destructive or proliferative changes and existence of typical rheumatic granulomas. At a polyfibromyositis the serous exudate, lymphoid and histiocytic infiltrates, focal dystrophic and necrotic changes in muscle fibers with the subsequent sclerosis endo-and a perimysium histologically come to light. At a polymiositis macroscopically muscles edematous, pale, with the centers of necroses and hemorrhages; at the chronic course of a disease they are condensed owing to growth of fibrous fabric. Histologically at an acute polymiositis the parenchymatous and intersticial inflammation with expressed dystrophic (granular, gidropichesky, fatty) and necrotic (mio l from, a coagulative necrosis) changes of muscle fibers and preferential perivascular macrofocal lymphoid makrsfagalnoy infiltration (fig. 1) is observed. Signs of a macrophagic resorption and intracellular regeneration with proliferation of subsarkolemmalny kernels come to light. At hron, a polymiositis (fig. 2) the combination of processes of an atrophy, a hypertrophy and destruction of muscle fibers, a sclerosis and a lipomatoz endo-and a perimysium is noted. A part of muscle fibers is exposed to calcification. Involvement in inflammatory process of a perineurium leads to destruction of myelin covers and axial cylinders of nervous trunks with development of a neuromyositis.

Parasitic M. at trichinosis (see), cysticercosis (see), echinococcosis (see) are characterized by inflammatory infiltration from lymphocytes, neutrophylic and eosinophilic granulocytes, dystrophic changes and a necrosis of muscle fibers, adjacent to a parasite. Around parasites the fibrous capsule from the outcome develops in calcification. Toxoplasma are located in muscle fibers and usually inflammatory changes at them are expressed poorly. At the granulematozny miositis representing a muscular form of a sarcoidosis find nodular or diffusion infiltrates from epithelial cells, histiocytes, lymphocytes and single colossal cells like Pirogov — Langkhansa (see. Colossal cells ).

At toxic M. necrotic changes of muscle fibers (a myolysis, a coagulative necrosis) with preservation of a sarcolemma and scanty inflammatory reaction in endo-and perimysiums prevail. At the professional M. caused long physical. tension, focal dystrophic and atrophic changes of muscle fibers, a sclerosis endo-and a perimysium are defined.

The heterotopic ossification which is patol, a form of an osteogenesis (see. Bone ), can develop in many fabrics and bodies, including and in muscles. The most important form of heterotopic ossification is the ossifying M. At traumatic ossifying M. in the center of the centers of consolidation young connecting fabric decides on actively proliferating fibroblasts, on peripheries — calcific main substance, unripe and mature bone crossbeams. Ossifying M. of not traumatic genesis represents universal calcification of muscles (see. Calcification ), to-rogo the fibrodisplaziya is the cornerstone. Histologically in nodes of consolidation at early stages patol, process find actively proliferating fibroblastopodobny cells. Their cytoplasm contains a large number of a glycoprotein rich with mannose. Electronic microscopically cells remind tumoral (hyperchromic kernels, a giperplazirovanny cytoplasmatic reticulum and a lamellar complex). In interstitial fabric accumulation of glikozaminoglikan is noted (hyaluronic and chondroitinsulphuric to - you). The created node has zonal structure: in the center — fibrous fabric from fibroblastopodobny cells, on the periphery — sites of osteoid. Further in neogenic bone crossbeams lime is laid. Except a metaplasia of connecting fabric in bone, the metaplasia it in a cartilage with the subsequent endostosis is noted. Bone sites take the branchy form with a spongy structure in internal departments and compact in outside. In old bone educations marrow appears.

Separate clinical forms of a miositis

Purulent miositis is caused most often by staphylococcus, and also a streptococcus, a pneumococcus, a mephitic gangrene and other activators. Develops usually sharply against the background of focal purulent process or in connection with a septicopyemia (see. Sepsis ). Sometimes damage of muscles arises later a nek-swarm time after subsiding of the inflammatory phenomena in primary center. Various pustulous diseases of skin, carious teeth, purulent processes in almonds, adnexal nasal cavities can be sources of infections (okolonosovy, T.), a middle ear, at women — in genitalias, etc. Most often purulent M. happens localized though also the multiple centers of defeat are observed. At the heart of a pathogeny — development of an inflammation in muscular tissue in response to a purulent infection. Cooling or an injury can promote localization of inflammatory process in this or that muscle.

The wedge, a picture is characterized by local pains, intensity to-rykh quickly increases. Pains sharply amplify at the movements causing reduction of the affected muscles and also at a palpation. There is a swelling, puffiness of soft tissues; sometimes dermahemia. The protective muscle tension, restriction of movements in joints develops. As a rule, the general symptoms in the form of high temperature, a fever, a headache, and also increase regional limf, nodes are noted. In blood — a leukocytosis with shift to the left, the raised ROE. In the place of the developing infiltrate in several days fluctuation can appear, at a puncture receive pus. Acute purulent M.' treatment: antibiotics, physical therapy, operative measure. The forecast at the correct and timely treatment favorable.

Infectious not purulent miositis arises as a complication after flu, respiratory diseases, a typhoid, and also at rheumatism and against the background of such hron, infections as tuberculosis, a brucellosis, syphilis. Special forms inf. The m is the Bornholm disease, edges is caused by a virus from Koksaki's group (see. Pleurodynia epidemic ), and also so-called muscular rheumatism. Pathogeny inf. M — emergence of inflammatory changes in muscular tissue of specific or nonspecific character. At tubercular M. specific process extends to muscles limfogenno or gematogenno. Syphilitic M. is characterized by local defeat of any muscular group as a result of a solitary gumma or diffusion defeat with development of a sclerous form M.

Inf. The m can develop sharply, subacutely or to have hron, a current. For a wedge, pictures the hl is characteristic. obr. local pain syndrome. Pains as spontaneous, and at a palpation and the active movements. Places of an attachment of muscles are especially painful. The swelling and muscular tension can be noted. Mobility of the corresponding part of a body is sharply limited. At a palpation of the affected muscles in the place of the most expressed pathology of muscular tissue it is possible to find painful, mobile to the touch, dense educations by the size from prosyany grain to a bean, rounded or irregular shape (Cornelius's syndrome). Sometimes, especially in buttock, gastrocnemius, trapezoid, deltoid muscles, the painful consolidations changing the form (a syndrome of a hyper tone of Müller) during the pressing are defined. In average or deep layers of muscles it is possible to find also round or oblong consolidations of a gelatinous consistence — a miogeloza.

In addition to pains the skin hyperesthesia in the affected muscles can be noted. Muscular weakness — secondary and usually develops in connection with existence of a pain syndrome. An atrophy of muscles for this form M. of a malokharaktern. The general symptoms, as a rule, are absent though depending on an etiology manifestations of the general inf can be observed. process (especially at hron, infections).

Rheumatic M. is characterized by the pulling, quite often «flying» pains in skeletal muscles, at a palpation to-rykh sharp morbidity is noted. Pains can amplify at night or at a weather changing. Rheumatic M.'s current — subacute or chronic. At this form the atrophy of muscles which is usually moderately expressed can develop.

Treatment at inf. M — sedatives, drugs like Rheopyrinum, in some cases antibiotics. At rheumatism, and also at tubercular or syphilitic M. specific therapy is carried out. Forecast favorable.

Polymiositis — inflammatory damage of muscles, to-rogo is the cornerstone infectious and allergic process (see. Infectious allergy ). Along with inflammatory reactions in muscular tissue also dystrophic changes develop. The first message on a case of a polymiositis was made by E. L. Wagner in 1863.

The polymiositis meets at any age, but the thicket is from 5 to 15 years old and from 50 to 60 years. Women are ill twice more often than men. There are data on growth of frequency of this form M.

The etiology and a pathogeny of process are up to the end not found out. It is not excluded that a polymiositis — a polyetiological disease as there is a number of the factors preceding development a wedge, symptoms. So, various infections (especially quinsy), an injury, massive insolation, use of large numbers of various medicines, in particular streptocides and antibiotics, are considered as the factors leading to development of hypersensitivity (see. Allergy ). Endocrine shifts matter during pregnancy, childbirth, a climax. Most of scientists allocate the leading place in a pathogeny of a polymiositis to autoimmune processes with antibody formation to muscular tissue. Clinically the disease is shown by a pain syndrome (see. Mialgiya ), usually moderately expressed, and muscular weakness. Paresis is localized preferential in proximal departments of muscles of hands and legs, in muscles of pelvic and humeral belts. In muscles there can be consolidations, the moderate atrophy sometimes develops. Tendon jerks (see) usually decrease, sometimes drop out. Objective disorders of sensitivity are not noted, symptoms of a tension are absent. Klien, a picture can remind a myodystrophy like Erba (see. Myopathy ). In nek-ry cases the muscle tension and even their sharp consolidation (induration) develops. In late stages of process tendinous appear contractures (see), is more often in a biceps of a shoulder and in Achilles (calcaneal, T.) sinews. Visceral defeats are rare. Hypotonia of muscles of a gullet is sometimes noted. At a part of patients the polymiositis proceeds very easily. Patients note only pains, muscular weakness and fatigue. At the same time the heavy, sharply proceeding forms with bystry increase of sharply expressed weakness up to a tetraplegia can take place.

At children the picture meets more often dermatomyositis (see) in the form of acute or hron, forms. Quite often at hron, a current in the affected muscles calcificats are formed. At adults the polymiositis can be combined with a carcinoma or be a component of clinic of a «dry» syndrome of Shegren (hyposecretion of the lacrimal, salivary, gastric and intestinal glands, polyarthritis). In hard cases of an acute polymiositis in blood the leukocytosis, a neutrophilia, increase in ROE is noted, quite often there is a creatinuria and reduction of excretion to urine of creatinine. In blood serum there can be a hyperactivity of enzymes, especially kreatinfosfokinaza, zymohexases, transaminases. In protein fractions increase alfa2-and gamma-globulins is sometimes noted. In mild cases of a polymiositis of biochemical shifts can not be. On EMG with use of needle electrodes (see. Electromyography ) the characteristic triad of changes comes to light: 1) short, low polyphase potentials of motive units, 2) potentials of fibrillations and an irritation on introduction of an electrode, 3) fancy high-frequency discharges.

Very important gistol, confirmation of the diagnosis of M. At a biopsy the necrosis, phagocytosis, an atrophy and dystrophy of fibers I and II of types, accurate inflammatory infiltration, a picture of vasculites comes to light. The polymiositis should be differentiated from other muscular syndromes which are followed by pains, and first of all from endocrine myopathies (at a hyperparathyreosis, a hypocorticoidism, a thyrotoxicosis). Hron, the polymiositis at adults needs to be distinguished from sporadic forms of a myopathy and spinal amyotrophy (see), myasthenias (see), Mac-Ardla's diseases (see. Glycogenoses ), and also granulematozny M. (muscular form of a sarcoidosis).

At easy forms of a polymiositis apply the desensibilizing means, Butadionum, Resochinum, delagil in combination with ATP, ascorbic to - that, vitamin E, at a zatikhaniye of the inflammatory phenomena — massage, LFK. At the expressed forms with accurate biochemical, shifts, especially in combination with damage of internals, carry out treatment by steroid hormones. Purpose of Prednisolonum since other drugs can aggravate damage of muscles (a steroid Myopathy) is preferable. The good effect is gained during the use of high doses of Prednisolonum by a discontinuous method (the two-day dose in number of 80 — 100 mg is accepted during 1 — 2 hour every other day at once)! Duration of a course of treatment depends on weight of process, portability of drug, a wedge, effect. As a rule, the maximum dose of drug is appointed within 5 — 6 months then it gradually, is very slowly reduced. The maintenance dose of 10 — 20 mg is appointed up to 1,5 years.

If muscular weakness does not disappear at treatment by Prednisolonum within 2 months, its combination with a methotrexate in an initial dose of 10 — 15 mg intravenously is recommended. At good tolerance the dose is gradually increased to 30 — 50 mg. Interval between injections of 5 — 7 days. Duration of therapy is 12 — 15 months. Day reception of Prednisolonum in these cases gradually decreases (to 20 mg in 6 months and to 10 mg in 12 months).

Along with reception of Prednisolonum appoint antiacid means (see), drugs of potassium, exercise control of the ABP, level of sugar of blood. By-effects at a discontinuous method of steroid therapy, as a rule, do not arise or are poorly expressed. The forecast at easy forms favorable, at heavy depends on full value and timeliness of treatment.

Parasitic miositis in most cases it is necessary to consider as a polymiositis. It trichinosis, cysticercosis, Toxoplasmosis, seldom Echinococcosis are the reason. The disease is considered as toksiko-allergic process with development of inflammatory reactions in places of implementation of parasites in muscular tissue. More often proximal departments of hands and legs suffer. Patients complain of pains, fatigue of muscles. Quite often there are general symptoms: subfebrile temperature, changes from blood (an eosinophilia, a lymphocytosis, etc.), skin manifestations (urticaria, an itch). Process quite often has wavy character that is connected with a cycle of life activity of parasites. In muscles pseudo-cysts and kaltsinata are found that can be established at rentgenol, or gistol, a research.

Treatment — the desensibilizing means, antiparasitic drugs. The absolute recovery comes seldom.

Toxic miositis it is observed at a number of intoxications. So, at heavy alcoholism painful hypostases of muscles with paresis, a myoglobinuria and a secondary renal failure can take place. Can lead use to damage of muscles nek-ry pharmakol. means (colchicine, Vincristinum, etc.), and also stings of nek-ry animals and insects, especially in the tropical countries.

Treatment — it is necessary to exclude action of the factor which caused toxic M. and to carry out disintoxication therapy. At process of an alcoholic etiology purpose of thiol drugs (Unithiolum, sodium thiosulphate), and also high doses of vitamin B is shown 1 . In hard cases make a hemodialysis. The forecast is rather favorable.

Neuromyositis it is allocated from sheathe groups M. because at this form, in addition to inflammatory changes in muscular tissue, there are changes in intramuskulyarny nerve fibrils, and sometimes and in distal departments of axons of nerves.

Clinically this form is characterized by the expressed pain syndrome; pains sharply amplify at a palpation, painful points of Vallée can be noted (see. Diagnostic painful points ). Slabopolozhitelna symptoms of a tension. Confirmation of the diagnosis (in addition to data of a biopsy) is helped by EMG, on a cut elements of denervatsionny changes are noted.

Treatment — analgetics, anti-inflammatory drugs, physical therapy (thermal procedures, Bernard's currents), sometimes local novocainic blockade. The forecast is rather favorable.

Polyfibromyositis nek-ry scientists treats general diseases, at to-rykh inflammatory changes in muscles are followed by the expressed reaction from connecting fabric with development in it fibrous changes.

Clinically the disease is shown by pains at the movements, sharp morbidity in points of an attachment of muscles, formation of consolidations in the form of small knots, tyazhy. Sinews of muscles can suffer, they become sharply painful, contractures quite often are thickened, develop. Very severe forms of a disease are described, at to-rykh in connection with development of rough fibrosis of muscles there comes the progressing restriction of movements, especially in muscles of a back, a shoulder girdle, and formation of pathological poses. Confirmation of widespread fibroziruyushchy process, in addition to data gistol, researches, lack of relaxation of the affected muscles is during sleep and during the carrying out the general anesthesia. Hron, a form of a polyfibromyositis can be a consequence of a polymiositis or extensive traumatic miositis.

Treatment — anti-inflammatory drugs, injections of a lidaza, massage, LFK, physiotherapeutic procedures, a balneoterapiya. The forecast depends on severity and prevalence of process.

Ossifying miositis (Myunkhmeyer's disease) — metaplastic process, at Krom happens calcification, and in the subsequent true ossification of connective tissue layers in the thickness of muscles, and also fastion, aponeuroses, sinews. There are several hypotheses of a pathogeny of an extra skeletal osteogenesis — heterotopic ossification: inflammatory, trophoneurotic, endocrine, embriogenetichesky (as anomaly of development of a mesenchyma). Ossifying M., or heterotopic ossificates, can be independent educations, but arise also owing to an injury. Ossifying M. can sometimes be an initial stage dermatomyositis (see).

Ossifying M. — the progressing disease, a cut is observed preferential at children's age, very seldom after 20 years. More often males suffer. The wedge, a picture is characterized by gradual restriction of movements, constraint of muscles of a neck, back, proximal departments of extremities, sometimes muscles of the head. The bearing changes, poses develop patol. At a palpation of muscles dense formations of various size and a form are defined. Additional injuries aggravate local ossifications).

Ossifying traumatic M. should be considered as the intramuscular fibrositis arising in the form of response to damage of soft tissues. It can develop as a result of a single injury or owing to often repeating traumatization of the same muscle, napr, at sports activities. At first after M.'s injury it is shown by symptomatology of a bruise of soft tissues in the form of limited and their painful consolidation, local temperature increase of skin, its reddening and dysfunction of all extremity or is more often than its one segment. Gradually acute phenomena abate, there comes the painless period proceeding sometimes several weeks and even months. In the subsequent through various time terms patients pay attention to the firm education which sometimes is densely connected with a bone and close adjacent to hypodermic cellulose. Cases when to rentgenol, researches these dense educations in muscles mistakenly were accepted to sarcomas of bones or soft tissues, especially to paraossalny sarcoma are known. Favourite localization of ossifying traumatic M. is the area of a humeral muscle, group of muscles at the level of a diaphysis of a femur and a rump.

Except ossifying M., heterotopic ossification can be shown in the form of calcification and ossification of sinews at places of their attachments to bones or circumarticular ossificates. There are typical localizations of ossificates, napr, Pellegrini's disease — Shtida (see. Pellegrini-Shtida disease ), elbow «spur», so-called posttraumatic stones in adductors of a hip at equestrians, in a biceps of a shoulder, in a deltoid muscle at gymnasts etc. These educations should not be mixed with calcifications in mucous bags.

The progressing (multiple) ossifying M. has very characteristic rentgenol, a picture. Shadows of the irregular korallopodobny shape on the roentgenogram are noted at the beginning of a disease in muscles of a back, a neck, a nape, and further in muscles of extremities and a stomach.

At ossifying M. of trophoneurotic genesis (at tabes, a myelosyringosis, injuries of a spinal cord and large nervous trunks, a cross myelitis, polyneurites) rentgenol, changes come to light in the form of low-intensive flocculent shadows, to-rye further become more dense. They are localized usually at hip, knee joints, along a fibular bone. Such longitudinal arrangement of shadows should be taken into account at ossifying M.'s differentiation, e.g., with sarcoma, at a cut of a shadow of calcifications are located preferential in transverse direction to a longitudinal axis of a bone.

Trophoneurotic osteogeneses are quite often combined with uzura, destructions of bones, e.g., of big spits, sciatic hillocks and other speakers of bone educations.

Rentgenol, ossifying traumatic M.'s picture is in most cases expressed by a shadow of irregular shape with indistinct outlines. In the beginning the shadow of a malointensivn, an oblakovidn, but eventually it is condensed, and afterwards in it the bone structure often differs. The shadow of ossification usually lies separately from a bone of an extremity, but afterwards quite often merges with a shadow of a bone. Especially considerable ossification is observed in muscles of area of an elbow joint, in a humeral muscle.

Treatment of the ossifying progressing M. is ineffective. There are attempts to influence exchange of calcium of use of complexons (Tetacinum-calcium). Earlier applied operation of removal of epithelial bodies is not effective.

At ossifying traumatic M. in the presence hematomas (see) appoint cold, a compressing bandage for the prevention of increase of hemorrhage, in 2 — 3 days for a rassasyvaniye of a hematoma dry heat is recommended. In early stages of formation of heterotopic ossification apply applications of ozokerite, physiotherapeutic treatment using ultrasound, a hydrocortisone. Conservative treatment of ossificates is inefficient. After maturing to bone density education does not grow, as a rule, back does not develop, but can decrease in volume. The most radical method of treatment is an operative measure. As indications to it serve dysfunction of a joint, a prelum and irritation of a nervous trunk or a prelum and a close arrangement of ossificate at the main vessels. After removal of ossificate the immobilization of an extremity up to 10 days is necessary.

Forecast favorable. A recurrence without repeated injuries does not happen.

Traumatic ossifying M.'s prevention is a careful attitude to soft tissues, especially at sports activities and at professional loads of certain segments of a skeleton.

Professional miositis develops owing to disturbance of a trophicity of the muscles which are exposed to an intensive overstrain in the course of work, especially during the performance of the uniform differentiated movements or at a steady static stress. It is characterized by pain, decrease in an animal force, development of fibrous educations in certain groups of muscles in the form of small knots, tyazhy (fibrosites, cellulitises), usually is followed by damage of tendinous vaginas (tendovaginitis). More often muscles of upper extremities and a shoulder girdle suffer.

Treatment — massage, local thermal procedures (paraffin, heat baths), a diathermy, an electrophoresis. However it is difficult to achieve full treatment.

Bibliography: Biochemical changes in an organism at an injury, under the editorship of H. N. Priorov and B. S. Kasavina, page 115, M., 1959; To Gauja m of An ov a-P etrusevich And. Muscular diseases, the lane with polsk., Warsaw, 1971; Demidov P. V. ipo-Tomsk L. 3. A muscular syndrome at a chronic polymiositis, Zhurn, a neuropath, and psikhiat., t. 76, century 2, page 204, 1976; Dyachenko V. A. Radiodiagnosis of calcifications and heterogeneous okosteneniye, M., 1960; Eremina L. A. and Tseshkovsky M. S. An ossifying miositis (a parostalny ossifying hematoma), in book: Tumors of the musculoskeletal device, under the editorship of H. N. Trapeznikov and L. A. Eremina, century 5, page 174, M., 1976; A. A Cake layer. Heterotopic traumatic ossifications, M., 1963, bibliogr.; Kupilova Yu. S. and A. I Ila-shev. The progressing multiple ossifying miositis, Pediatrics, No. 7, page 77, 1972; M at t and S. S. N and With IS and d and Ya. A N. Infectious and allergic miositis, Klin. medical, t. 43, No. 5, page 130, 1965; Proskura V. I. and Kostenko I. N. About the multiple progressing ossifying miositis, the Doctor, business, No. 4, page 114, 1973; With t r at-to about in A. I. and the Spear-in and T. N. Dermatomyositis, Arkh. patol., t. 30, No. 9, page 3, 1968; At about t with about N Jones of River. Fractures of bones and injury of joints, the lane with English, page 45, M., 1972; Yumashev G. S. Traumatology and orthopedics, page 368, M., 1977; Bethlem J. Muscle pathology, Amsterdam — L., 1970; Dermatomyosites and polymyositis, ed. by W. F. Lever, N. Y., 1974; Disorders of voluntary muscle, ed. by J. N. Walton, Edinburgh, 1974; DubowitzY. Brooke M. H. Muscle biopsy, L., 1973; M an i r W. G. P. a. Tome F. M. S. Atlas of the ultrastructure of diseased human muscle, Edinburgh — L., 1972; Pearson C. M. Polymyositis, Ann. Rev. Med., v. 17, p. 63, 1966; Ricker K., Seitz D. Tro-stdorf E. Myositis fibrose generalisata and of «stiff-man» syndrome, Europ. Neurol., v. 3, p. 13, 1970.

H. A. Ilyina; V. A. Dyachenko (rents.), M. K. Klimova (injuries.), T. N. Kopyeva (stalemate. An.).