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Electroneuromyography and electromyography were performed in 48 and 102 patients, respectively, with Lyme disease-induced algic and amyotrophic syndromes. Electromyographic and clinical findings in the regions of the tick suction correlated. Multiple lesions of the nervous system may be considered as meningoencephalomyeloradiculoneuropathy as well as subclinical multiple mononeuropathy. Pronounced changes in the nerve potential against minimal shifts in peripheral nervous conduction reflect infectious-toxic nature of the condition.

The authors describe a 16-year-old patient suffering from facial scapulohumeral myopathy. The given case is regarded as sporadic. The disease was characterized by an early debut and rapid progression of neuromuscular disorders. Marked myasthenia and muscular atrophy of the face, shoulders, thighs, as well as contractures in the knee joints, hands and feet were noted. By 15 years the patient demonstrated a noticeable progress of motor disorders: she was unable to stand up from the chair, experienced difficulties in walking along the ward, and had a waddle gait. The given symptom-complex corresponds with the infantile variety of facial scapulohumeral myodystrophy.

The authors have developed an enzyme immunoassay test system for measurements of the specific cerebral alpha 2-glycoprotein (alpha 2-GP), whose sensitivity limit is 0.8 ng/ml. Blood serum alpha 2-GP level is 7 ng/ml, cerebrospinal fluid level is 12.8 ng/ml in health; detection of alpha 2-GP in these biological fluids in concentrations surpassing such values indicates impairment of the hematoencephalic barrier permeability and active release of the cerebral proteins into the blood. The hematoencephalic barrier is most frequently disrupted in the brain-blood direction in purulent meningitis, encephalitis, open craniocerebral injuries; such impairments may be detected with the use of alpha 2-GP measurements. A direct correlation between the blood serum alpha 2-GP level and the severity of the disease clinical course has been revealed.

The paper treats of a case of progressive myodystrophy coupled with multiple contractures of the large joints. In an Uzbek family placed under observation and living in the Uzbek SSR, the disease was revealed in 3 members of the family (in mother and two children). Contractures of the large joints grew on parallel with the myodystrophic process. The pattern of myodystrophy seen in the family was characterized by a number of unusual clinical features and by pronounced clinical pleomorphism. The differences of the clinical manifestations within the family lay in variability of the debut, localization and intensity of the contractures, and in the rate of the myodystrophy course.

The paper concerns a family in which father and sibs (two brothers and a sister) suffered from rapid-progressing myodystrophy. Clinically, the disease was marked by a debut in the pubertal period (at 12 to 13 years), derangement of the muscles of the limb girdles, proximal parts of the legs and arms, and distal parts of the legs. The given case was also characterized by the impairment of the cervical and facial muscles as well as by associated neuromuscular lesions and neurosensory hypoacusis. The case described supports the clinical pleomorphism of the facial scapulohumeral form of Landouzy-Dejerine myopathy.

Vitamin B12 deficiency is often attended by neuropsychic disorders. In the geriatric population, the level of vitamin B12 is mostly reduced. However, the clinical manifestations and pathogenesis are not completely specified. The authors describe a female patients in whom vitamin B12 deficiency was coupled with manifest neuropsychic disorders. Provide a detailed depiction of the clinical status, the disease course and laboratory findings. Relate the most typical neuropsychic manifestations of vitamin B12 deficiency.

The authors describe a family living in the Dagestan where three relative sibs, girls, suffered from familial spastic paraplegia. The variety described is marked by early debut, pronounced intrafamilial polymorphism of the disease course, autosomal recessive type of inheritance which, according to the reported data, is marked by frequently occurring combination with damage to other organs and systems (the familial spastic paraplegia "plus"). The "pure" disease variety seen in autosomal recessive type of inheritance, detection of the disease symptoms since the birth indicate that the case in question is a rare clinical variety of familial spastic paraplegia.

A family in which 9 persons in three generations suffered from "pure" Strümpell's disease is described. The disease made is debut in early childhood and was characterized by slightly marked intrafamilial polymorphism. An electromyographic study was made. It has been proved that the pattern described is a "pure" disease variety inherited by the autosomal dominant type, with an early development of the clinical manifestations and slow progress of motor disturbances (up to 25 years). The nosology of the given disease pattern is under discussion.

The authors summarize the results of a follow-up study (clinico-electrophysiological) of the S. family living in the Namangan region of the Uzbek SSR. The familial anamnesis data provide evidence in favour of a probable autosomal recessive type of inheritance. A combination of the disease signs has been defined: spasticity, deafness, ataxia and speech disorders. To specify the problem of the given syndrome nosology, further studies into gene mapping are required.

A rare case of Eulenburg's paramyotonia and periodic paralysis combination is described in one family. The question of whether the disease presents a nosological entity is discussed with due consideration of its clinical polymorphism and the data of literature. Mapping the genes determining the disease would be decisive in this respect.

The authors describe a familial case of Kennedy's spinal amyotrophy. In three brothers of the R. family, the disease was marked by the appearance in the 4th-5th decade of life of myasthenia in the proximal parts of the limbs and of bulbar symptoms, which will run a slow-progressive course. Since the young age all the patients manifested gynecomastia. Besides, later one of the brothers developed scirrhus of the left mammary gland. Clinically, Kennedy's spinal amyotrophy in the R. family manifested itself by asymmetric distribution of myotrophies (more pronounced in the left limbs), bilateral Dupuytren's contractures in the hands. Apart from the signs of injuries to motoneurons of the anterior horns, electromyography and electroneuromyography have shown the peripheral nerves to be involved into the pathological process.

The authors describe a familial form of childhood spinal amyotrophy. Among 7 patients in the M. family, 5 were diagnosed to suffer from type II spinal amyotrophy and 2 from type III. It is of interest to mention that type II was observed only in boys whereas type III in girls. The data of the clinical and electromyographic examination of two M. siblings of male and female sexes have been analyzed. Possible mechanisms of the clinical polymorphism of childhood spinal amyotrophy are under discussion.

A clinico-electrophysiological study of motor-coordinatory impairments was carried out in 117 patients with infantile cerebral paralysis. The results obtained suggest a possibility of a slow rate of myelinization, inadequate development of the coordinatory systems due to early damage to the brain associated with the systemic localization of the defect, and the obligatory involvement of extrapyramidal impairments in the realization of pathological dyskinesias. The clinical and electrophysiological examination made it possible to sum up all clinical manifestations of the pathology under a heading "discoordinatory extrapyramidal dyskinesias".