Vol 11, No 2 (2017)

Introduction. Sleep-disordered breathing (SDB) is detected in 70% of stroke patients and impedes functional rehabilitation; it also increases the length of hospital stay and the risk of stroke recurrence and fatal outcome.

Objective: to study the dynamics of SDB in its correlation with neurological disorders in stroke patients and to develop the approaches to optimization of early rehabilitation.

Materials and methods. A total of 78 patients with acute ischemic stroke were examined. SDB was verified by cardiorespiratory monitoring; the neurological deficit was assessed using the NIHSS and mRS scales. Examination was carried out upon admission (days 2–5 post stroke) and again after 3 weeks. The effect of SDB correction on effectiveness of neurological recovery was studied using positional therapy (position elevated by 30^о) in combination with oxygen therapy (insufflation of O₂ with the saturation level maintained no less than 95% under control of a digital sensor).

Results. Upon admission, SDB was revealed in 88% of patients; moderate and severe disorders being predominant (the apnea/hypopnea index (AHI) ≥15 h^-1), most frequently presenting as obstructive apnea. In patients with AHI < 15 h^-1, the positive dynamics of neurological disorders (p<0.04) were observed along with stable SDB parameters. Neurological improvement (р<0.05) was observed in patients with AHI ≥ 15 h^-1, which was associated with decreased severity of SDB. A direct correlation between the severity of neurological disorders and AHI after 3 weeks was revealed: R_NIHSS/AHI = 0.45 (р=0.003), R_mRS/AHI = 0.44 (р=0.004). Patients with AHI ≥ 15 h^-1 were distributed into 2 groups: group A (without corrective interventions) and group B (the use of positional and oxygen therapy during the night sleep during 7 days). A positive effect of the course of corrective therapy on restoration of neurological functions, along with a decrease in AHI, was revealed.

Conclusions. SDB is a frequent and persistent disorder in patients with ischemic stroke. Early detection and correction of SDB should be regarded as an important component of post-stroke rehabilitation.

Introduction. Investigation of systemic organization of goal-directed behavior and analysis of the physiological mechanisms ensuring productive activity in epilepsy patients are the variants of the integrative approach to study the mechanisms of epilepsy.

Objective. To refine the mechanisms of simulated goal-directed activity among epilepsy patients in its relationship with clinical characteristics of the disease.

Materials and methods. A total of 72 virtually healthy persons and 163 epilepsy patients were examined. Seizure frequency, the levels of cognitive and emotional impairments, and the number of administered anticonvulsants were assessed. Electroencephalograms, parameters of visual and auditory evoked potentials, the cognitive evoked P300 potential, parameters of the motor systems, and autonomous maintenance of activity were recorded. Division into groups was performed by clustering analysis using the results of the Schulte–Gorbov test.

Results. The high- (99 patients) and low-effectiveness (64 patients) groups of epilepsy patients were revealed. The low-effectiveness group of patients was characterized by predominantly symptomatic forms of the diseases. High cross-correlation values, reduced frequencies of EEG alpha oscillations, reduction in the amplitude of the components of visual evoked potentials and the P300 potential, an increase in N2 and P3 peak latency in the low-effectiveness group of epilepsy patients were determined. Increased amplitude of the wave of conditionally negative deviation, slower latency of sensorimotor responses, reduced variability of heart rate, and increased respiratory rate group of patients were observed in this group of patients.

Conclusions. The inadequate performance in epilepsy patients is associated with the reduced activity of specific afferent associative subsystems and mechanisms of motor-based maintenance of performance, as well as with excessive activity of stress-inducing mechanisms, which increases the physiological costs and reduces the effectiveness of simulated activity.

Introduction. The model involving injection of quinolinic acid (QA) into the rat striatum simulates many clinical and morphological characteristics of Huntington’s disease (HD). Searching for effective treatment methods is rather topical because of the fatality of HD. One of such methods is to create a neuroprotective environment to slow down the current degenerative process and/or replace dead neurons. In particular, this can be performed by transplantation of cells capable of undergoing neuronal differentiation and integration into the proper structural and functional brain networks.

Objective. To assess effectiveness and safety of transplantation of neural progenitors differentiated from induced pluripotent stem cells (iPSCs) harvested from a healthy donor into the striatum with QA-induced model of HD.

Materials and methods. The effects of neurotransplantation on reproduction of the conditioned passive avoidance reflex were studied in rats with the model of HD induced by injection of QA into the caudate nuclei of the striatum. In the study group (n=8), human neural progenitors (1×10⁶ per 10 µl of normal saline unilaterally, on the injured side) derived from iPSCs harvested from a healthy donor were injected into the caudate nuclei as the transplanted material; normal saline was injected in the control group. The conditioned passive avoidance responses were tested using the ShutАvoid 1.8.03 software on a Harvard apparatus (Panlab, Spain).

Results. When testing the reproduction of the passive avoidance responses, we found that injection of QA into the caudate nuclei of the rat brain reliably reduced the conditioned responses. Neurotransplantation of neural progenitors derived from iPSCs had a clear therapeutic effect and reinforced the passive avoidance reflex. During the entire testing period (7 days after exposure to the pain stimulus), the experimental animals either did not visit the dark compartment at all or visited it with a long latency period.

Conclusions. Experimental neurotransplantation using iPSC derivatives allowance to improve storage of trace memory in rats with QA-induced model of HD, which contributes to correction of cognitive impairments caused by administration of the neurotoxin.

Abstract. Amyotrophic lateral sclerosis (ALS) is a fatal progressive central nervous system disorder affecting the upper and lower motor neurons. It is important to study the features of the course and progression of neurodegeneration in ALS, since no effective methods for treating this disease have been developed yet. Despite the clear evidence that brain lesions in ALS are of multisystem nature, there are no objective biomarkers of lesions of the upper motor neuron and the extramotor areas of the brain. Structural and functional neuroimaging, such as MR brain morphometry, diffusion tensor imaging, MR spectroscopy, functional MRI, positron emission tomography (PET), etc., have recently been playing a significant role in studying ALS. The results of neuroimaging studies are analyzed in this review in the context of using them to diagnose, predict, and monitor the course of ALS. Diffusion tensor imaging, MR spectroscopy, PET, combination of several neuroimaging methods and their combination with transcranial magnetic stimulation are the most sensitive and specific techniques to be used to diagnose the disease. Diffusion tensor imaging and MR spectroscopy can be used to monitor and predict the disease course. The main limitations and shortcomings of the performed studies, as well as the possible outlook for using neuroimaging in ALS, are discussed.

Resting-state functional magnetic resonance imaging (R-fMRI) assesses the state of low-frequency fluctuations of the BOLD-signal showing spontaneous neuronal activity in different areas of the brain. Hence, R-fMRI allows one to visualize the synchronicity of generation of certain neurophysiological phenomena in different regions of the central nervous system, including the ones being remote from one another, by linking them into a functional network and assessing brain connectivity in normal state and in pathology. This technique has proved itself in the study of neurodegenerative diseases. In this review, we present the results of using R-fMRI for the most common forms of primary focal dystonia (blepharospasm and cervical dystonia) compared to the data of task-based fMRI and some other neuroimaging technologies such as positron emission tomography and voxel-based morphometry. It has been demonstrated in many studies that R-fMRI allows to assess disturbances in cerebral architecture and complex rearrangements in the neural network in patients with focal dystonia, including those after administration of botulinum toxin. This makes it possible to study more thoroughly the pathophysiological foundations of focal dystonia and the variety of mechanisms of botulinum toxin therapy in patients with these pathologies, including the central (indirect) mechanisms of action of botulinum toxin.

Abstract: Agenesis of the corpus callosum (ACC) is detected in patients with cerebral dysgenesis associated with various hereditary syndromes. It is conventionally subdivided into total (the absence of commissural fibers) and partial (agenesis of the rostral and caudal areas of the corpus callosum) ACC. The disorder can either be individual or associated with other developmental brain malformations. Isolated pathologies of the corpus callosum can be clinically occult, thus significantly impeding diagnosis of this pathology. AAC can be verified using various neuroimaging data, including fetal brain ultrasonography. In this study, we report two cases of patients with ACC associated with hereditary syndromes from our own clinical experience. In one case, the course of the disease was relatively favorable. The severe infantile form with fatal outcome is reported in the second case. The detailed autopsy data and results of morphological examination of the brain are presented. Special attention is paid to the issues associated with analysis of clinical phenotypes, as well as lifetime and postmortem diagnosis of the disease.