Neuropathic pain is an acute or chronic pain caused by damage to or dysfunction of the peripheral and/or central nervous system. Neuropathic pain is a direct sequel of damage to or disease of the somatosensory nervous system. The paper presents the definition, international diagnostic criteria, clinical and diagnostic features, and causes of neuropathic pain syndrome, differences between nociceptive and neuropathic pain, the classification of major neuropathic pain syndromes, and the DN4 questionnaire to identify neuropathic pain. It shows a substantial clinical and pathophysiological similarity of neuropathic pain and fibromyalgia and gives preliminary diagnostic criteria for fibromyalgia. 

The differential diagnosis of neuropathic, nociceptive, and psychogenic pain and the determination of the level of damage to the nervous system and a leading pathogenetic mechanism of neuropathic pain syndrome require not only meticulous clinical examination of the sensory sphere, but also neurophysiological examination including electroneuromyography, somatosensory evoked potential recording, quantitative sensory testing, and, in a number of cases, neuroimaging (magnetic resonance imaging) or morphological (intraepidermal nerve fiber density examination) verification of injury somatosensory afferents. 

Objective: to study the specific features of development of cognitive impairments (CIs), the role of traditional cardiovascular risk factors and renal failure-induced factors in patients with Stages I–IV chronic kidney disease (CKD) and to assess an association of CIs with the signs of vascular wall remodeling in them.
Patients and methods. Fifty-one patients aged 53±10 years with CKD were examined. Among them, there were 20 patients with Stages I–II CKD: a glomerular filtration rate (GFR) of і60 ml/min/1.73 m2, signs of renal lesion; 20 with Stages III CKD: a GFR of <60–30 ml/min/1.73 m2, and 11 with Stages VI CKD: a GFR of <30–15 ml/min/1.73 m2. 
Results and discussion. CIs were more common in the patients with Stages III–IV than in those with Stages I–II, as shown by the scores of the mini-mental state examination (p<0.001), the frontal assessment battery (p=0.001), and the regulatory function test (p<0.001). These tests showed that the magnitude of CIs increased with the higher stage of CKD. Stages III–IV CKD is an independent predictor of CIs in persons with predialysis-stage kidney lesion. CIs were found to be related to hyperhomocysteinemia, anemia, abdominal obesity, left ventricular hypertrophy, and patient age. The signs of atherosclerotic lesion of the common carotid arteries and the indicators of arterial stiffness were also associated with the incidence and magnitude of CIs in CKD. 

The detection of CIs in patients with early CKD allows one to timely initiate adequate therapy aimed particularly at improving cerebral circulation, eliminating the impact of risk factors, and slowing down the vascular remodeling. The management tactics for patients with CKD must involve the identification and correction of cardiovascular risk factors, and duplex scanning of the wall of the common carotid arteries may be used as a noninvasive method to assess the risk of the development and progression of CIs in predialysis CKD. 

Objective: to analyze the quality of diagnosis and treatment of primary headache (HA) in different social groups of the Ural Region.
Patients and methods. The study enrolled 3124 persons who were divided into three groups: 1) 1042 students; of them there were 719 women; mean age 20.6 years; range 17–40 years; 2) 1075 workers; of them there were 146 women; mean age 40.4 years; range 21–67 years; 3) 1007 blood donors; of them there were 484 women; mean age, 34.1 years; range 18–64 years. Semi-structured interviews involving the characteristics of HA and its prior diagnosis and treatment were conducted face-to-face in all those included in the study. HA was diagnosed using the International Classification of Headache Disorders, 3rd edition, beta version.
Results and discussion. The following factors decreasing the quality of diagnosis and treatment of HA were identified in all the study groups: 1) low physician visit rates. Despite the high prevalence of all types of primary HA in 3 groups (67%), only 496 (23%) out of 2110 participants with HA visited their physician with this problem. Among the patients with HA, physicians were visited most often by 342 (35%) out of 968 students, least often by 60 (13%) out of 457 workers and by 94 (14%) out of 685 donors; 2) inadequate diagnosis of HA. Only 12 and 11.7% of the patients were correctly diagnosed with migraine and tension HA (THA), respectively; 3) the practically complete absence of preventive treatment for HA. The majority of patients used drugs to arrest HA attacks; preventive treatment for migraine was performed in 2 (0.4%) and not performed in any of the patients with THA. 

It is necessary to improve the diagnosis and treatment of primary HA and to elaborate new Russian clinical guidelines for patient management on the basis of international standards. 

Objective: to estimate the time course of changes in foot biomechanical function as multiple sclerosis (MS) progresses in patients with different degrees of disability compared to a control group.
Patients and methods. To estimate the time course of changes in gait disorders in MS, changes in foot biomechanical function were explored in 30 patients with relapsing-remitting MS. Their neurological status was evaluated using the expanded disability status scale (EDSS); pedographic examination was made applying a plantar pressure distribution system; all the patients were examined twice. During the first examination, the patients were divided into two groups: 1) minimal neurological disorders (EDSS scores of < 3.0) and 2) moderate ones (EDSS scores of ≥3.0). 

Results and discussion. The patients with a mild neurological deficit showed increases in foot load and its lateralization by elevating pressure on the heads of the fourth and fifth metatarsal bones, as evidenced by a significant rise in mean pressure, maximum force, and force-time integral. These changes occurred in the absence of the patients’ complaints of changes in movements.
Pedographic examination revealed the changes indicating an enlarged anterior transverse arch and the lower role of the hallux in body weight transfer in the patients with a moderate neurological deficit despite the fact that there were no further visible negative changes in a motor process or progression in neurological deficit. 

The pedographic examination makes it possible to estimate the degree of gait disorders caused by pyramidal and/or cerebellar lesions and to identify a leading role of this or that functional system in their genesis. Pyramidal dysfunction has impact on the pressurization of the heads of the second and third metatarsal bones. Computed pedography can identify clinically subtle movement changes and estimate the time course of changes in movement disorders in MS patients, including those to evaluate the efficiency of therapy and rehabilitation measures. 

Hemorrhagic transformation of an infarction focus is the most common and menacing complication of systemic thrombolytic therapy (TLT) for ischemic stroke (IS).
Objective: to analyze the rates of hemorrhagic transformation of infarction and to search for the risk factors of hemorrhagic transformation of an ischemic area after systemic TLT. 
Patients and methods. The data of 469 IS patients who had received systemic thrombolysis at the primary vascular departments of the Sverdlovsk Region in 2009 to 2013 were analyzed. In accordance with the selection criteria, a study group comprised 143 patients from 4 vascular centers of the Sverdlovsk Region, who were analyzed for the incidence of reperfusion hematomas. Neurological deficit was evaluated by the National Institutes of Health Stroke Scale (NIHSS) and self-care abilities were assessed by the modified Rankin scale (mRS). Brain computed tomography was carried out before, on days 1 and 7 after TLT, and when the patient displayed any deterioration in his/her condition. Analysis of TLT complications involved estimation of the rate of hemorrhagic transformation in accordance with the ECASS II criteria.
Results and discussion. According to the ECASS II criteria, the clinically obvious bleeding rate was 4.9%. Hemorrhagic transformation was found to affect the time course of changes and degree of neurological deficit regression and self-care ability recovery. Logistic regression analysis has established that disability index on admission and diastolic blood pressure on admission and during TLT are the most important risk factors of reperfusion hematoma.

There is outpatient hyperdiagnosis of dyscirculatory encephalopathy (DE) frequently masked by other diseases.
Objective: to improve the differential diagnosis of DE on the basis of a comprehensive patient examination, including neuropsychological testing. Patients and methods. Fifty patients, including 10 men and 40 women, aged 45 to 75 years (mean age 68.8±9.0 years), who had been followed up at the polyclinic with a diagnosis of DE for an average of 1.5 years, were examined. All the patients underwent evaluations of cognitive functions and emotional status and otoneurological examination (in case of headache); a psychiatrist consulted patients with anxiety and/or depressive disorders.
Results and discussion. Only 9 (18%) patients were found to have vascular cognitive impairments (CIs) and signs of cerebrovascular lesions, as shown by neuroimaging, which may be regarded as DE. Five (10%) patients had CIs and neuroimaging changes that were more characteristic of Alzheimer’s disease (AD) than those of DE. The remaining 36 (72%) patients were established to have other diseases (primary headache, peripheral vestibulopathy, primary anxiety and depressive disorders, etc.), in which CIs were not detected. The diagnosis and effective treatment of these diseases yielded a rapid positive result in most cases. The management of patients with DE and AD was aimed at preventing stroke and improving cognitive functions; moreover, akatinol memantine was noted to be effective in the combination therapy of both DE and AD. 

The impact of the pattern of atherosclerotic stenotic lesion on the clinical presentation of cognitive impairments (CIs) has been inadequately investigated.
Objective: to estimate the impact of the degree and site of an atherosclerotic stenotic process on cerebral perfusion and cognitive functions.
Patients and methods. A total of 123 patients (65 men and 58 women) aged 50 to 75 years with brachiocephalic artery stenosis of at least 40%, without hypertension, diabetes mellitus, or other systemic vascular pathology were examined. The structural state of the brain substance and the state of cerebral blood flow were evaluated by magnetic resonance imaging and magnetic resonance angiography. The scale described by P. Scheltens et al. was used to determine changes in the white matter. The site and degree of a stenotic process were estimated by extracranial and transcranial duplex scanning. CIs were identified applying a set of neuropsychological assessment scales. The Hamilton hospital depression rating scale was also employed. 
Results and discussion. Varying degrees of CIs were detected in the majority of the examinees with brachiocephalic artery atherosclerosis. The most severe CIs were associated with the involvement of parietal and frontal lobes. There was significant deterioration in cognitive functions with a higher percentage of stenosis: more severe CIs were seen in the presence of stenosis in the carotid system than in those in the vertebrobasilar bed. In addition, the patients with concomitant stenoses and tandem stenoses were observed to have more pronounced CIs than those with single artery stenosis. Cerebral atherosclerosis is shown to be one of the major risk factors for CIs. Not only the degree of stenoses, but also to a greater extent their site was observed to impact the occurrence of CIs accompanied by the development of a perfusion deficit in the specific vascular beds. The determination of the pattern of a stenotic process will be able to predict the development of CIs in patients with atherosclerosis and to choose an appropriate treatment policy. 

About 20% of all road traffic accidents may be associated with falling asleep while driving. This may be caused by sleep disorders leading to daytime sleepiness, the most common of which is obstructive sleep apnea syndrome (OSAS).
Objective: to study somatic and mental health, sleep disorders, OSAS in particular, in the population of Russian drivers (Sverdlovsk Region).
Patients and methods. The descriptive cohort «Dangerous Sleep» (DS-1) study of 20 professional drivers having more than 5-year driving experience was conducted at the Clinical Institute of the Brain. The mean age of the drivers was 45.8 years. They underwent somatic evaluation for cardiovascular risk factors and a psychological examination involving a risk readiness diagnostic procedure, the Zung Self-Rating Depression Scale, the Beck Depression Inventory, and an electroencephalographic examination. A somnological examination assumed testing using the Epworth sleepiness scale, polysomnography, or overnight pulse metry. 
Results and discussion. 30% of the drivers were found to have marked attention disorders and an inability to adapt to extreme conditions, which create a risk for professional duties. The predisposing factors were noted to be alcohol addiction, overweight, and OSAS, the rate of the latter proved to be higher than that in the general population of able-bodied men. It was shown that a somnological examination should be obligatorily performed while hiring professional drivers, particularly to long hauliers. The drivers having a long length of experience, in whom a periodic examination detects sleep disorders, should be treated for somatic diseases and should also have individual working schedules to rule out their long night-time driving. 

Objective: to study the causes of dizziness and instability in patients during an outpatient specialized appointment and to analyze and improve typical management tactics for these patients.
Patients and methods. In 2009 to 2014, neurologists, dizziness specialists, examined 300 patients (122 men and 178 women) aged 18 to 85 years, who complained of dizziness and instability. Prior to the examination, the patients had been diagnosed as having dyscirculatory encephalopathy (46%), vertebrobasilar insufficiency (30%), cervical osteochondrosis (12%), and vegetative dystonia (7%). 
Results and discussion. The examination established the causes of dizziness: benign paroxysmal positional vertigo (BPPV) (34%), phobic postural instability (22%), multiple sensory insufficiency (15%), Meniere's disease (7%), migraine-associated vertigo (5%), vestibular neuronitis (4%), acute cerebrovascular accident (4%), and other diseases (9%). In accordance with the established diagnosis, adequate treatment which could completely eliminate or substantially reduce the magnitude of dizziness in the majority of cases was performed. 

The paper describes two clinical cases (BPPV and Meniere's disease). Betahistine dihydrochloride (vesticap, betaserc) were most commonly used in a dose of 48 mg/day to treat vestibular vertigo. It gives the results of comparative treatment (with vesticap or betaserc) for vestibular vertigo in 62 patients.
The authors note the low level of diagnosis and effective treatment in patients with dizziness in outpatient practice. They show the expediency of a specialized examination, the efficiency and safety of current treatments, including medication therapy with betahistine dihydrochloride (betaserc and vesticap) and rehabilitation on a stabiligraphic platform with biofeedback, for vestibular vertigo. 

The paper presents historical prerequisites for designing antidepressants from a group of selective serotonin neuronal reuptake inhibitors (SSRIs): to determine a lower serotonin concentration in the different tissues of depressed patients; to establish a higher serotonin concentration in the treatment of depressed patients with tricyclic antidepressants, and to formulate the serotonergic theory of depression. It also provides a consecutive account of the history of clinical introduction of individual SSRI representatives, such as fluoxetine, zimelidine, fluvoxamine, indalpine, citalopram, sertraline, paroxetine, and escitalopram. There are data from the history of studying the mechanism of SSRI action: from the theory of the importance of an increase in the concentration of serotonin in the synaptic cleft to the current understanding of complex successive intracellular rearrangements at the level of the postsynaptic neuron. The history of studying the efficacy of SSRIs in treating depression is considered in detail. Emphasis is laid on the reasons for a paradoxical difference in the evaluations of the efficiency of therapy with SSRIs versus other groups of antidepressants at different developmental stages of psychopharmacology. The role of marketing technologies in disseminating the data on the efficacy of this or that group of antidepressants is described. The practical significance of differences in individual SSRI representatives (the potency of serotonin uptake inhibition; the degree of selectivity and activity against the serotonergic system; the likelihood of an unfavorable pharmacokinetic interaction with other drugs; the half-life of elimination; the quickness of achieving a therapeutic dose) is analyzed. Whether it is possible and reasonable to differentially choose different SSRI representatives in the treatment of depressions at the present stage is discussed. The authors state their belief that researches should be continued to specify the place of SSRIs among other groups of current antidepressants for the treatment of depressions. 

The paper generalizes the experience with one of the main original drugs for the treatment of multiple sclerosis (MS) – glatiramer acetate (GA, Copaxone®, Teva) in large Russian MS centers. The performed analysis of clinical trials suggests the high efficacy and favorable safety profile of the drug. The fact that patents for a number of effective and widely used original drugs, including those for agents from a group of immunomodulators, used to treat MS expire is one of the features of the current development of medicine. Due to the fact that most of them belong to interferons-β, i.e. biologicals, or structurally close to nonbiological complex drugs, the authors discuss the need to conduct comparative clinical trials of the original drug and follow-on glatiramoids with measured endpoints that can be used to establish their efficacy, safety, and evidence for therapeutic equivalence in order to examine their potential interchangeability. 

The paper considers the main causes and pathogenetic, clinical, and therapeutic aspects of cardioembolic stroke (CES). The latter is emphasized to be a group of conditions, which is highly heterogeneous in its etiology, pathogenesis, course, and prognosis. Their major risk factors are atrial fibrillation (AF), myocardial infarction (MI), and heart valve apparatus pathology. The leading diagnostic method for CES is brain computed tomography or magnetic resonance imaging, which most commonly visualize a well-defined wedge-shaped area of ischemia on the gray and white matter boundary, as well as cardiological examination. The results of electrocardiography, among them the detection of AF or MI, and echocardiography are of key value for correct diagnosis. Patients with CES are managed by the common principles applied to ischemic stroke. Oral anticoagulants, the efficacy and safety of which have been proven in large clinical trials, are most widely used to prevent recurrent CES. The patients who are at risk for CEA must be followed up by both a cardiologist and a neurologist. Adequate and individualized therapy can substantially reduce the likelihood of cerebrovascular disorders in this category of patients. 

Aging is a physiological process that may develop long without manifestations of comorbidities. In the meantime a high proportion of elderly people very often experience limitations in daily life due to impairments in memory and other cognitive functions. Non-cognitive neuropsychiatric disorders, most commonly stress-related anxiety disorders, are a major contribution to maladaptation in these patients. The present studies of the neurobiology of aging enable one to decipher not only the mechanisms that underlie the physiology of brain aging, but also the factors that influence cognitive aging and aggravate the manifestations of cognitive dysfunction and neurodegenerative disease. The process of brain aging is known to presume the long-term preservation of functional neuroplasticity that is greatly influenced by different lifestyle factors, such as daily social and physical activities, the pattern and amount of food taken, cognitive activity, and stressful life events. These lifestyle factors are supposedly a potent tool to maintain physiological brain aging and a delayed cognitive diminution in elderly people. At the same time, studies of the possibility of pharmacologically correcting age-related (both cognitive and non-cognitive) impairments are promising to improve everyday function in elderly people. 

The problem of cerebrovascular lesions takes on even greater significance with the higher prevalence of both acute and chronic forms of cerebrovascular diseases (CVD). Cognitive dysfunctions that have a pronounced negative impact on the quality of life in patients hold a special place among the various neurological symptoms resulting from cerebrovascular lesions. The incidence of vascular dementia increases with age.
The paper considers the main issues of the etiology, pathogenesis and classification of vascular cognitive impairments (VCIs). It proposes criteria for the diagnosis of VCIs in the early stages of the disease. 

Potentially modifiable factors, such as hypertension, coronary heart disease, orthostatic hypotension, diabetes mellitus, hypercholesterolemia, hyperhomocysteinemia, obesity, et al., are indicated to have a special place among the main etiological causes of VCIs. The timely detection of etiological factors and the assessment of their role in the development of cognitive impairments (CI) in CVD form the basis for managing these patients. 

The issues of treating CI no dementia in patients with CVD are considered. These included the administration of nootropic, vasoactive drugs, as well as agents that exert a modulatory effect on the cholinergic and glutamatergic systems. The use of neuroprotective and neurotrophic drugs is noted to be promising in terms of the multicomponent mechanism of their action. 

Chronic cerebrovascular attack (CCVA) is a brain lesion caused by vascular factors. CCVA appears as cognitive impairments (CIs), affective (emotional) disorders and focal syndromes. Treatment for CCVA requires a comprehensive approach. Effective combination therapy for CCVA involves secondary prevention of stroke and CIs; treatment of CIs; treatment of depression and other affective disorders; and neuroprotective therapy. Basic therapy for CCVA includes modification of risk factors, antihypertensive, hypolipidemic, and antithrombotic therapies. Central acetylcholinesterase inhibitors (galantamine, rivastigmine, donepezil) and a reversible NMDA receptor blocker (memantine) are symptomatically used at a stage of vascular and mixed dementia. There are no unique guidelines for the therapy of mild and moderate vascular nondementia-related CIs. Drug use, based on the neurochemical mechanisms underlying the development of vascular CIs, is substantiated. When choosing psychotropic agents, it is necessary to take into account the causes and clinical manifestations of neuromediator deficiency. Antidepressants are used as essential drugs. Neuroleptics and tranquilizers are additionally administered in complex-pattern syndromes, such as depression with marked anxiety. Prescription of neuroprotectors may be effective in treating both stroke and CCVA. These medicaments are most effective when a damaging factor acts, i.e. neuroprotectors should be given in a risk situation and to reduce damage. Citicoline is one of the most test drugs in a group of neuroprotectors. 

Cerebrovascular diseases (CVD) are major causes of disability and death in Russia. Stroke is the third significant cause of higher death rates after cardiovascular disease and cancer. The prevalence of circulatory diseases, such as atherosclerosis and hypertension, is on the rise. Therapy for CVD must be aimed at the underlying disease in which vascular catastrophe (atherosclerosis, hypertension, heart disease, etc.) develops, at the regression of neurological and psychopathological syndromes, and at the improvement of cerebral blood flow and metabolic processes. Neuroprotective agents, whose efficacy has been established in uncontrolled and small placebo-controlled trials, are widely used in our country. The prescription of these medications is substantiated by the important role of the pathogenetic mechanisms underlying cerebral ischemia. This paper gives data on the clinical use of L-lysine escinate for ischemic stroke (IS), hypertensive crisis, and chronic cerebral circulatory disorders and discusses the mechanism of this drug's action and the pathogenetic mechanisms of cerebrovascular lesions. A number of investigations have shown it expedient to incorporate L-lysine escinate in the combined neuroprotective therapy of patients with IS, cerebral hypertensive crisis, and hypertensive encephalopathy, which is associated with its antiedematous effect, particularly in preventing vasogenic brain edema, in enhancing the tone of cerebral veins, and in improving venous outflow. It is stated that there is a need for an individualized approach to treating CVD, by taking into consideration the existing risk factors and somatic and neurological diseases. 

Compression of the spinal nerve root, giving rise to pain and sensory and motor disorders in the area of its innervation is the most vivid manifestation of herniated intervertebral disk. Different treatment modalities, including neurosurgery, for evolving these conditions are discussed. There has been recent evidence that spontaneous regression of disk herniation can regress. The paper describes a female patient with large lateralized disc extrusion that has caused compression of the nerve root S1, leading to obvious myotonic and radicular syndrome. Magnetic resonance imaging has shown that the clinical manifestations of discogenic radiculopathy, as well myotonic syndrome and morphological changes completely regressed 8 months later. The likely mechanism is inflammation-induced resorption of a large herniated disk fragment, which agrees with the data available in the literature. A decision to perform neurosurgery for which the patient had indications was made during her first consultation. After regression of discogenic radiculopathy, there was only moderate pain caused by musculoskeletal diseases (facet syndrome, piriformis syndrome) that were successfully eliminated by minimally invasive techniques.