The main issues of the epidemiology and the early and late clinical manifestations of Alzheimer’s disease (AD), the most common cause of dementia in the elderly, are discussed. Current data on the pathogenesis of, new treatment strategies for AD, and investigator’s altered views on the course of the disease are given. The fact that AD is a long-term, progressive disease that develops long before the occurrence of the first clinical symptoms is beyond question now. This necessitates the design of new diagnostic criteria and methods that allow the disease to be diagnosed as early as possible. The main aspects of basic symptomatic therapy for AD are discussed in detail. The basic principles of its correct treatment using new dosage forms that permit a complete therapeutic effect to be achieved are given.

The author gives the data available in the literature and her materials on the prevalence and degree of noncognitive neuropsychological disorders (NNPDs) in dyscirculatory encephalopathy (DE) with non-dementia cognitive impairments (CI) and in Alzheimer’s disease (AD) with mild to moderate stage dementia. Memantine (akatinol) therapy-induced changes in NNPDs are shown. It is emphasized that the significance of NNPDs in the general disease picture is now underestimated; in this connection their adequate therapy is not performed. This may result in a rapider progression of CI and a more significant reduction in daily activities in the patient. The high prevalence and multisymptom
pattern of NNPD are determined in both patients with DE and non-dementia CI and in those with AD and mild to moderate stage dementia. The degree of NNPDs correlates with the severity of cognitive defect and the low quality of life. Akatinol is noted to be clinically efficacious in DE and moderate CI against not only CI, but also NNPDs. In AD, symptomatic antidementia drugs (galantine, memantine, or their combination) arrest NNPDs in the first 3 months of therapy. Combined therapy should be recognized as best. The data available in the literature and the results of the authorХs studies show the need for further investigations of NNPDs in patients with CI in order to optimize the diagnosis and treatment of neurogeriatric diseases.

The authors give the data available in the literature on and the results of their studies of the epidemiology, risk factors, pathogenesis, diagnosis, and treatment of poststroke cognitive impairment (PSCI). The latter occurs in 35—83% of patients; poststroke does in 6—40%. Different mechanisms of PSCI are under discussion; these are a single infarct in a strategic area of the brain; multiple focal lesion of the brain substance in restrokes; cerebral white-matter lesion as leukoaraiosis; the presence of concomitant Alzheimer’s disease (AD). The capacities for the diagnosis of concomitant AD in PSCI are analyzed. The treatment of the latter involves secondary prevention of stroke and specific therapy for cognitive, emotional-affective, and behavioral disorders. The experience with akatinol memantine used in postischemic dementia has been found to be positive.

The affliction of basal ganglia and their associations, which underlies extrapyramidal diseases, leads not only to diverse movements, but also to a broad spectrum of neuropsychological disorders, including cognitive, emotional-personality, and psychotic ones. The basis for these disorders are most commonly dysfunction of one or a few parallel frontostriatal circuits combining the basal ganglia with the thalamus, limbic structures, frontal and other cortical regions into the uniform functional system. The pattern of neuropsychological disorders has both specific and common features, the discussion of which is the subject matter of this paper. Analysis of the specific features of neuropsychological and behavioral disorders allows one to specify the localization of a pathological process and its extent, which may be of important differential diagnostic value. Cognitive and emotional-personality impairments sometimes develop earlier than motor disorders and their detection may be of significance for the early diagnosis of Parkinson’s disease or Huntington’s disease in persons who are predisposed to these diseases. Moreover, to establish the nature of mental disorders and the degree of their disadapting effect and to identify the affected and preserved components in the psychic processes are important for the choice of adequate pharmacotherapy and the elaboration of neuropsychological rehabilitation programs.

The epidemiology, clinical presentation, morphology, and pathogenesis of central nervous system lesion in types 1 and 2 diabetes mellitus (DM) are considered, by using the results of experimental and clinical studies. The definition of diabetic encephalopathy is given. Whether there is a relationship between diabetic encephalopathy and diabetic polyneuropathy is considered. It is concluded that it is expedient to identify diabetic encephalopathy as a complication of DM. The capacities of pathogenetic treatment for diabetic encephalopathy are shown.

The state-of-the-art of Russian neuropsychiatry and priority developments in different psychopathological syndromes in severe brain injuries are assessed. Many cognitive and emotional impairments are explained in terms of the idea on the organization of psychic activity over time. It is emphasized that to achieve the premorbid levels of an interhemispheric interaction and functional asymmetry of the cerebral hemispheres affords psychic activity recovery. The experience in investigating, classifying, and treating various mental disorders occurring after severe brain injuries is generalized. The basic principles of psychopharmacotherapy and rehabilitation of victims are stated.

untington’s disease (HD) is one of the most severe and fatal hereditary diseases of the nervous system. The paper outlines the history of studies of the disease, its key features and development mechanisms in terms of recent advances in molecular biology. The neuropsychiatric manifestations of HD, which are a major disabling factor, are characterized. Mental and emotional-volitional disorders are systematized; possible methods for correction of the clinical manifestations of HD are presented. A special emphasis is made on the fact that cooperation between different specialists and with a patient’s relatives is of importance in achieving the best treatment results. The authors present their experience in studying the psychopathological manifestations of HD at the Neurology Research Center, Russian Academy of Medical Sciences, and the results of an integrated study of cognitive and neuropsychological characteristics of at-risk asymptomatic HD gene carriers, by using a battery of psychological tests and the newest methods of electroneurophysiology and neuroimaging, and conclude that there is a preclinical disease stage. The authors’ experience with pharmacotherapy for neuropsychiatric manifestations and cognitive deficit in HD patients is described.

The authors give the results of their investigations of and the generalized data available in the literature on the significance of neuroimaging techniques in the diagnosis of cognitive impairment of different origins. Special attention is given to the importance of applying current diagnostic methods for functional neuroimaging both in early and advanced dementias: in Alzheimer's disease, vascular dementia, and mixed pathology.

The paper considers the clinical features and mechanisms of recovery of motor and cognitive functions after stroke. It is emphasized that the earliest therapy of stroke appreciably determines the success of further rehabilitation measures. There may be the most significant recovery in the first 3 months after stroke and generally only an insignificant improvement following 6 months. However, the process of recovery can last longer in a number of patients. Data are given on the use of nicergoline (sermion) in this category of patients.

The outpatient records of 147 patients followed up for diagnosed vascular dementia were analyzed to assess the relationship between affective disorders and severe cognitive impairments. It was found that 7% of the examinees had a history of depressive states. Estimating the development time for vascular dementia could divide the patients into 2 groups: 1) 60% of the patients in whom cognitive impairments began to determine its clinical picture just within the first 2 years after identification of affective disorders and 2) 40%, in whom cognitive impairments occurred 10—20 years later. In both groups, mental disorders occurred at an equal age in the presence of depressive disorders; in Group 1, vascular dementia developed nearly twice as often as that in Group 2. At the same time, the occurrence of cognitive impairments in Group 1 patients just in the early disease stages is indicative of the organic genesis of affective disorders, as confirmed by the moderately rapid progression of psychopathological symptoms, such as sharpening of personality traits, increased rigidity of psychic processes, emotional lability, variations in affective symptomatology, inadequate remissions, and the presence of neurological symptoms. Another type of a ratio of depressive to severe cognitive disorders was found in the elderly persons in Group 2. The long existence of affective disorders without signs of cognitive diminution leads one to say that they have recurrent depressive disorder with further addition of a comorbid vascular process. These patients showed a fairly high severity of affective pathology that was responsible for more frequent admissions, as well as a phase course with relatively pure remissions without any clear intellectual-mnestic reduction and a predominance of hysterical character traits.

The paper gives the results of a long-term comparative therapeutic study of a large cohort of more than 500 liquidators of the consequences of the accident at the Chernobyl nuclear power plant in 1986. The patients were followed up (and periodically treated at hospital) 5 years or more, usually 10—15 years. The study confirmed mainly the cerebrovascular nature of disorders following the pattern seen in moderate psychoorganic syndrome. Therapy with cerebroprotective agents having vascular vegetotropic properties could yield certain therapeutic results and, to some extent, preserve social functioning capacity in these patients.

Neuropsychological, ultrasonographic, and neuroimaging characteristics were comparatively analyzed in 72 women (mean age 64.3±1.0 years) and 48 age- and education-matched men (mean age 65.0±1.2 years) with early manifestations of dyscirculatory encephalopathy (DE). It was shown that there was a preponderance of cognitive impairments (mainly those of attention, verbal memory, and praxis) in the men with DE and that of emotional and insomniac disorders in the women. A probable relationship was found between the decreased serum level of cerebral neutrotrophic factor and the degree of depression and cognitive impairments in the patients with DE, in the men in particular. The findings may be of importance for individualized therapy.

Neurocognitive deficit is considered to be the third key group of symptoms in schizophrenia. A series of studies concerning various aspects of neurocognitive impairments was conducted at the First Psychosis Episode Clinic, Department of Extrahospital Psychiatry and Organization of Psychiatric Care, Moscow Research Institute of Psychiatry over 10 years (2001—2010). In patients with varying schizophrenia progression, neurocognitive functions were shown to have both the approximate form of the cognitive profile (which serves to consider the disease in terms of a unified pathogenetic mechanism) and great differences primarily in the degree of involvement of brain structures into the pathological process, as well as neurocognitive deficit changes in the course of the disease. A study of the impact of therapy with atypical antipsychotics on the time course of changes in neurocognitive impairments in patients with the first psychotic episodes revealed a number of characteristic features of these drugs, which enables one to tell that the spectrum of their psychotropic activity is different. However, therapy for cognitive impairments cannot be limited only by the use of drugs: of great importance in these patients are psychosocial therapeutic and rehabilitation measures that are aimed not only at reducing their symptoms, but also at enhancing social competence in the patient.

The paper discusses the state of development of acquired hyperkinetic disorder in psychotic forms of autistic spectrum disorders. Attention deficit hyperactivity disorder (ADHD) in childhood autism (childhood psychosis) has pathopsychological markers as cognitive disontogenesis with delays in fine motor activity and visual motor coordination, neurophysiological markers as a high index of sensor motor rhythm, and immunological markers as preserved higher parameters of innate immunity in remission (the activity of leukocytic elastase, the level of acute phase proteins, such as α1-PI and C-reactive protein). The heterogeneity of ADHD requires that its nosological entities be identified to create clear differentiated habilitation algorithms in accordance with the principles of evidence-based medicine, by applying the multidisciplinary clinical and biological characteristics.