In the review, we present the main pathogenetic mechanisms of the development of phantom limb pain (PLP) after limb amputation, the prevalence of which can reach 87%. The exact mechanism of PLP remains unknown. The involvement of peripheral and central mechanisms of the formation of PLP is assumed. Peripheral mechanisms include increased excitability and the formation of ectopic activity in the amputation neuromas and in the ganglion cells of the dorsal roots of the spinal cord. The central mechanisms are represented by central sensitization in the dorsal horns of the spinal cord with the development of the “wind up” phenomenon, reorganization processes in the thalamus and cortex with thalamic and cortical remapping, and proprioceptive memory. Also significant is the neuromatrix theory, the reduction of feedback from the visual and other sensory systems after deafferentation. PLP therapy methods focused on central mechanisms are: spinal cord stimulation, transcutaneous electrical neurostimulation, deep brain stimulation, non-invasive and invasive methods of cerebral cortex stimulation, mirror therapy, virtual and augmented reality technologies, movement representation and its modification “phantom exercises”. In addition, pharmacologic treatment options based on PLP mechanisms can be used: NMDA receptor antagonists, anticonvulsants, tricyclic antidepressants, opioids.

Rationale. Despite a large number of studies on the effectiveness of various pharmacological and non- pharmacological therapies, PLP treatment tactics have not yet been developed, which is largely due to the complex mechanism of the formation of this pathology. Although PLP is classified as neuropathic pain, standard methods of neuropathic pain therapy are not always effective for this syndrome. To optimize the regimens of existing methods of PLP treatment, as well as the search and clinical trials of new therapeutic approaches, it is necessary to take into account the currently available evidence base.

Material and methods. Our analysis included publications on phantom pain treatment methods with a high level of evidence (randomized controlled trials, systematic reviews and meta-analyses). Literature search was performed in Medline PubMed and eLIBRARY systems.

Results. The review provides an evidence base for pharmacotherapy methods (opioids, NMDA-receptor antagonists, tricyclic antidepressants, anticonvulsants, local anesthetics), for methods based on the phantom illusion (mirror therapy, motion representation, virtual reality), for non-invasive (transcutaneous electrical neurostimulation, transcranial magnetic stimulation, transcranial electrical stimulation) and invasive (deep brain stimulation, motor cortex stimulation, spinal cord stimulation, dorsal root ganglion stimulation) neuromodulation. Data on the most studied dosing regimens of different methods of pharmacological and non-pharmacological therapy are presented.

Alzheimer’s disease (AD) is a progressive neurological disease that causes cognitive impairment in old aged persons. It is the cause of a wide spectrum of neurodegenerative disturbances including tauopathies, which are responsible for progressive neuronal degeneration and impaired cognitive functions. Although drug discovery researchers and pharmaceutical companies are meticulously working to develop novel drugs for AD, establishing their safety and efficacy proofs are major challenges for them. In this review, we have discussed about AD and its causes mainly focusing on molecular targets with their physiological and pathophysiological roles, therapeutic approaches, and their future perspectives. We have compiled the information about novel and promising drug targets and lead data bases that will help to select appropriate target and design novel drug molecules for the treatment of Alzheimer.

Botulinum toxin type A (BTA) has taken a strong place in the rehabilitation of patients with impaired function of mimic muscles in both acute and late post-paralytic periods.

Aim: to highlight the main stages of the development of botulinum therapy (BT) in the treatment of mimic muscles dysfunctions in Russia.

Methods. Published data were searched in the electronic database Medline (PubMed) and eLibrary.

Results. The role of BT in the treatment of mimic muscles dysfunctions, synkinesis (which can be interpreted clinically as secondary hemifacial spasm), lacrimation, dry eye syndrome, as well as the role of BT in the formation of protective ptosis, was analyzed. The stages of the BT formation in Russia as a method of restoring the function of mimic muscles by specialists of various profiles (neurologists, maxillofacial surgeons, rehabilitation specialists, etc.) are described.

Conclusion. Currently, there is a BT school in Russia, which based on extensive clinical experience, developed algorithms and methods for administering BT to patients with facial nerve disorders of various etiologies.

Introduction. The rarity of chronic acquired polyneuropathies (PNP) with the demyelinating nature of peripheral nerve damage causes the difficulties of their differential diagnosis that persist in our country and abroad. Objective: to identify significant clinical, neurophysiological and sonographic differential diagnostic markers in chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) and non-IgM paraproteinemic demyelinating polyneuropathies (PDP).

Material and methods: 80 patients were included in the study: 30 with CIDP, 30 with non-IgM-PDP associated with monoclonal gammapathy of unclear significance (PDP-MGUS), and 20 with non-IgM-PDP associated with lymphoproliferative disease (PDP-LPD). The patients included in the study underwent clinical evaluation of neurological disorders according to the MRC, NIS, VAS, INCAT, IRODS, SARA scales; ENMG and ultrasound studies of peripheral nerves.

Results. The predominance of men in all groups was noted (p > 0.05). Compared with patients with CIDP, patients with PDP were significantly older, they were more likely to have neuropathic pain syndrome and trophic disorders (p < 0.05). In patients with PDP-LPD, in contrast to CIDP and PDP-MGUS, there was a predominance of the distal pattern of muscle weakness distribution and a greater severity of sensitive ataxia (p < 0.05). During NCV studies in patients with CIDP, compared with patients with PDP, blocks of conduction and dispersion of M-waves were signifi -cantly more often recorded in the study of motor fibers of the nerves of the hands (p < 0.05); and in the study of motor nerves of the legs, non-excitability of motor fibers was significantly less often noted (p < 0.05). Ultrasound examination of peripheral nerves showed no significant differences between patients (p > 0.05).

Conclusion. Clinical phenotype, neurophysiological and sonographic changes in patients with CIDP and PDP do not have highly specific differences. Electrophoresis of serum proteins with immunofixation makes it possible to differentiate CIDP and PDP, and further examination by an oncohematologist with paraproteinemia makes it possible to distinguish MGUS from LPD.

There are two clinical cases. In the first case, the stroke began with a monosymptom — cervical dystonia. The second case had a more complex movement disorder with symptoms of dystonia. In the first clinical case, the patient was young. He had symptoms of involuntary movements in the neck. The course of the stroke was mild. It resulted in complete regression of the neurological defect. In the second case, the patient was elderly. If not given the right help it would have been fatal. In both cases, the focus of ischemia in the brain was verified by neuroimaging.

Conclusion. An acutely developed syndrome of involuntary movements requires a mandatory CT scan of the brain, and in the absence of pathology on the CT scan, an MRI of the brain.

A description of a clinical case of Tolosa–Hunt syndrome (THS) and a brief review of the literature are presented. The described clinical case is characterized by three features that have not received sufficient attention in the literature: 1) the presence of recurrent pain outside the orbit in combination with ptosis without diplopia several years before the development of a typical episode of THS; 2) insufficient and unstable clinical response to standard doses of glucocorticoids with high efficiency of pulse therapy with methylprednisolone followed by oral administration of prednisolone; 3) a longer than required according to the international classification of headaches (ICHD-3) time interval between the development of cephalalgia and the appearance of oculomotor disorders. This clinical observation expands the understanding of the clinical picture and treatment of THS.

The aim of this research was to demonstrate the relevance of personalised nutritional support for patients at the 2nd stage of neurorehabilitation. The study involved work with patients in the neurorehabilitation. The nutritional status of the patient was assessed according to the data of protein fractions. Individual calculation of calorie intake was performed via the Harris–Benedict formula. The observation has established the necessity of application of the “Nutritional status assessment scale” for all patients entering the neurorehabilitation course. An algorithm for patient examination in nutritional deficiency has been tested: evaluation of protein fractions, calculation of calories intake with determination of the amount of proteins, fats and carbohydrates.

Conclusion. It is quite difficult to calculate energy expenditure in the process of neurorehabilitation for every manipulation. However, through application of the common standard of nutritional status assessment for patients on admission, it is possible to distinguish the patients requiring nutritional support. This will make it possible to avoid development of protein deficiency and “exhaustion” of patients in the process of the sessions.

The incidence of malnutrition in stroke patients varies widely and amounts to 6.1–62%. Risk factors for malnutrition in stroke patients are diverse and include the type and severity of stroke, gender, age, dysphagia, cognitive impairment, polysensory insufficiency, severe comorbid conditions, lack of adequate care, etc. At the same time, both the previous and the malnutrition that developed as a result of the stroke is the reason for a longer stay in the hospital, deterioration of functional results and an increase in mortality rates. The metabolic response to stress in stroke patients is represented by the hypermetabolism-hypercatabolism syndrome and is an essential component of the systemic inflammatory response, the development and progression of which leads to infectious complications, multiple organ dysfunction, increased hospitalization and increased mortality. Currently, clinical nutrition, or nutritional support (NS), is considered not only as a process of providing the body with energy and plastic material for the prevention and treatment of malnutrition, but also as an opportunity to influence structural, functional and metabolic processes in order to increase the adaptive reserves of the body, which is necessary for the recovery and rehabilitation of patients. The objectives of this review are the analysis of modern scientific data on clinical nutrition strategies and the development of an optimal algorithm of actions for the implementation of NS in clinical practice in the treatment and rehabilitation of stroke patients.