Neurological Deficiency Research Articles

Usefulness of eye tracking systems in multiple sclerosis

Multiple sclerosis (MS) is a chronic disease of the central nervous system characterized by inflammation and neurodegeneration. It represents the leading cause of nontraumatic disability in young adults in many places around the world.Currently, for the objective quantification of the damage of the visual pathway swept‐source OCT (SS‐OCT) is considered the most appropriate technique. Additionally, during the course of the disease multiple neurological deficiencies can appear, including eye motility disorders.Patients may develop various ocular motor disorders (OMDs) affecting visual function and significantly increasing disability. These alterations involve visual function and may decrease quality of life perceived by patients because they affect, among other functions, reading capability.OMDs, can be analysed by several recording systems, although they have not been incorporated into the practice routine clinic due to its complexity, high costs and also because the value of these alterations is probably not known.It is possible that an accurate examination of motility eye, may have a substantial impact on the diagnosis and management of those patients. OMDs has been suggested as potential biomarker of early neurological deterioration and its evaluation could contribute to obtaining progression and response to treatments, facilitating translational development of so‐called precision medicine.Eye trackers are state‐of‐the‐art tools that can obtain valuable information of OMDs in neurological degenerations. In MS, oculomotor alterations as saccadic dysmetria, saccadic intrusions, nystagmus, fixational deficits, smooth pursuit impairment, skew deviation, optokinetic and vestibulo‐ocular reflex impairments, may go unnoticed because systematic examination of the oculomotor systems do not use routinely these techniques.As mentioned, objective recordings of eye movements through eye‐tracking systems are not currently performed widely, despite that they have been described as an important adjunct in diagnosis, documentation, and management of different neurologic conditions.In addition, eye tracking is also a capable method to investigate the relationship between behaviour and neural mechanisms. Eye motion recordings provide a measure of functional preservation of the nervous system, which should be recognized to be of significant importance in assessing a disease in which disability is manifested by disruption of normal neuronal functions.In fact, it has been described that eye tracking tasks (especially saccadic tasks) are often used as an adjunct to traditional scales for cognitive assessment. In addition, eye tracking data confirmed that MS is characterized by attention deficits.In conclusion, there is a growing interest in the use of eye tracking systems as biomarkers for MS. Specifically in this work we have analysed a large series MS patients to detect if any of the anomalies that patients refer to, such as reading difficulties, are related to disorders of the ocular motor systems.

Shexiang Tongxin dropping pills protect against ischemic stroke-induced cerebral microvascular dysfunction via suppressing TXNIP/NLRP3 signaling pathway

Ethnopharmacological relevancePatients with ischemic stroke (IS) often continue to exhibit cerebral microcirculatory dysfunction even after receiving thrombolytic therapy. Enhancing the function of cerebral microvascular endothelia represents a pivotal advancement in the therapeutic strategy for ischemic microcirculatory disturbances. A traditional Chinese medicinal formulation named Shexiang Tongxin Dropping Pills (STDP), has been clinically employed to ameliorate microcirculatory abnormalities. Existing literature attests to the beneficial role of STDP on endothelial cells (ECs). Nevertheless, specific impacts and underlying mechanisms of STDP in rectifying IS-induced cerebral microvascular dysfunction warrant further exploration. Aim of the studyThis investigation seeks to delineate the effects of STDP on cerebral microvascular endothelial damage induced by ischemic stroke and to elucidate the underlying mechanism involved. Materials and methodsMiddle cerebral artery occlusion and reperfusion (MCAO/R) technique was employed to established ischemic stroke model in mice. The therapeutic efficacy of STDP on cerebral microvascular function was assessed through laser speckle contrast imaging, behavioral assays, and histological evaluations. Biochemical markers in the brain tissue, including GSH, SOD, MDA, and ROS, were quantified using specific assay kits. In vitro study, oxygen-glucose deprivation and reperfusion (OGD/R) was performed in bEnd.3 cells. The cytoprotective potential of STDP was then evaluated by measuring cell viability, LDH activity, endothelial permeability, and oxidative stress parameters. Important targets in critical pathway were verified by immunoblotting and immunofluorescence both in mice brain slices and bEnd.3 cells. ResultsSTDP decrease brain infarct size, repaired microvascular cerebral blood flow and attenuated neurological deficiency in MCAO/R mice. Moreover, STDP abolished MCAO/R-induced oxidative stress which was reflected by rescuing GSH content, restoration of SOD activity and T-AOC, reduction of MDA and ROS. Ex vivo, STDP increased cerebral microvascular endothelial cells viability, abolished oxidative stress and decreased their permeability after ODG/R. Mechanistically, STDP significantly suppressed endothelial ROS-TXNIP mediated the activation of NLRP3 inflammasome in vivo and in vitro. ConclusionSTDP improves ischemic stroke-induced cerebral microcirculatory deficits by regulating cerebral microvascular endothelial ROS/TXNIP/NLRP3 signaling pathway.

HDLC as an indicator of severity of neurological deficiency in ischemic stroke in Dagestan women

HDLC as an indicator of severity of neurological deficiency in ischemic stroke in Dagestan women

Protective effects of pyrroloquinoline quinone in brain folate deficiency

BackgroundFolates (Vitamin B9) are critical for normal neurodevelopment and function, with transport mediated by three major pathways: folate receptor alpha (FRα), proton-coupled folate transporter (PCFT), and reduced folate carrier (RFC). Cerebral folate uptake primarily occurs at the blood-cerebrospinal fluid barrier (BCSFB) through concerted actions of FRα and PCFT, with impaired folate transport resulting in the neurological disorder cerebral folate deficiency (CFD). Increasing evidence suggests that disorders associated with CFD also present with neuroinflammation, oxidative stress, and mitochondrial dysfunction, however the role of brain folate deficiency in inducing these abnormalities is not well-understood. Our laboratory has identified the upregulation of RFC by nuclear respiratory factor 1 (NRF-1) at the blood–brain barrier (BBB) once indirectly activated by the natural compound pyrroloquinoline quinone (PQQ). PQQ is also of interest due to its anti-inflammatory, antioxidant, and mitochondrial biogenesis effects. In this study, we examined the effects of folate deficiency and PQQ treatment on inflammatory and oxidative stress responses, and changes in mitochondrial function.MethodsPrimary cultures of mouse mixed glial cells exposed to folate-deficient (FD) conditions and treated with PQQ were analyzed for changes in gene expression of the folate transporters, inflammatory markers, oxidative stress markers, and mitochondrial DNA (mtDNA) content through qPCR analysis. Changes in cellular reactive oxygen species (ROS) levels were analyzed in vitro through a DCFDA assay. Wildtype (C57BL6/N) mice exposed to FD (0 mg/kg folate), or control (2 mg/kg folate) diets underwent a 10-day (20 mg/kg/day) PQQ treatment regimen and brain tissues were collected and analyzed.ResultsFolate deficiency resulted in increased expression of inflammatory and oxidative stress markers in vitro and in vivo, with increased cellular ROS levels observed in mixed glial cells as well as a reduction of mitochondrial DNA (mtDNA) content observed in FD mixed glial cells. PQQ treatment was able to reverse these changes, while increasing RFC expression through activation of the PGC-1α/NRF-1 signaling pathway.ConclusionThese results demonstrate the effects of brain folate deficiency, which may contribute to the neurological deficits commonly seen in disorders of CFD. PQQ may represent a novel treatment strategy for disorders associated with CFD, as it can increase folate uptake, while in parallel reversing many abnormalities that arise with brain folate deficiency.

Study on the anti-mitochondrial apoptosis mechanism of Erigeron breviscapus injection based on UPLC-Q-TOF-MS metabolomics and molecular docking in rats with cerebral ischemia-reperfusion injury

Ethnopharmacological relevanceErigeron breviscapus is a common medicine of eight ethnic minorities, including Miao, Naxi, and Yi. As early as the Ming Dynasty (AD 1368–1644), Lanmao's Materia Medica of Southern Yunnan (AD 1436) recorded that the medicine is used for the treatment of “Zuo tan you huan.” In modern pharmacological research, Erigeron breviscapus injection is the most commonly used preparation in the treatment of ischemic stroke caused by acute cerebral infarction, but its mechanism of action in the treatment of ischemic stroke is not well understood. Aim of the studyIn this study, a metabonomics study based on ultraperformance liquid chromatography–quadrupole time-of-flight tandem mass spectrometry (UPLC-QTOF-MS) was used in investigating the effect of a traditional Chinese medicine preparation Erigeron breviscapus injection on the rat model of focal cerebral ischemia-reperfusion and the affinity of its main components with the targets of mitochondrial apoptotic pathways. Materials and methodsThis study used molecular docking technology to verify the effective binding ability of main effective components of Erigeron breviscapus injection to target proteins related to mitochondrial apoptosis pathway. This study developed a metabonomics method based on the ultra-performance liquid chromatography combined with quadrupole time-of-flight tandem mass spectrometry (UPLC Q-TOF MS) to evaluate the efficacy and study the mechanism of traditional Chinese medicine preparation. With pattern recognition analysis (principal component analysis and partial least squares-discriminate analysis) of urinary metabolites, a clear separation of focal cerebral ischemia-reperfusion model group and healthy control group was achieved. ResultsErigeron breviscapus injection can significantly reduce the area of cerebral infarction, improve tissue morphological lesion in rats, and can increase the number of Nissl bodies. It may be a promoting factor by inhibiting hippocampal nerve cell apoptosis and Bax protein expression and by exerting effects against ischemia reperfusion after the induction of apoptosis. Thus, it plays a role in brain protection. Moreover, it can considerably promote the recovery of neurological deficiency signs in advance. Meanwhile, Erigeron breviscapus decreased malondialdehyde content and T-NOS activity. Its curative effect from strong to weak order: low dose > high dose > medium dose. The representative components of Erigeron breviscapus have good affinity with the active sites of mitochondrial apoptosis-related proteins. Metabolomics found that the potential biomarkers regulated by breviscapine are kynurequinolinic acid, succinylornithine, and leucine proline. It is speculated that it may participate in TRP–kynurequinolinic acid and succinylornithine–urea cycle–NO metabolic pathways. ConclusionsThis paper revealed the potential biomarkers and metabolic pathways regulated by Erigeron breviscapus. It was speculated that the mechanism is related to its inhibition of mitochondrion-mediated apoptosis. Erigeron breviscapus could restore the metabolic profiles of the model animals to normal animal levels. The mechanism may be related to the potential biomarkers of quinolinic acid, succinylornithine, and leucine proline and the metabolic pathways involved. However, the exact mechanism by which Erigeron breviscapus inhibits mitochondrion-mediated apoptosis remains to be further explored.

Neuromuscular diseases in intensive care

Guillain-Barre syndrome and myasthenia gravis are common in the Intensive Care Unit (ICU) and are not always easy to diagnose in the emergency department. The short-term risk is the occurrence of respiratory muscle paralysis, which must be monitored by repeated measurement of vital capacity, and the existence of respiratory impairment requires transfer to intensive care. Apart from specific therapeutic options (plasma exchange, intravenous immunoglobulins and anticholinesterase agents), management is mainly symptomatic. Our work is a retrospective study, concerning 23 cases of neuromuscular diseases in the ICU from a period from 2018 to 2022. The various epidemiological, clinical, paraclinical, therapeutic, and evolutionary data were collected from the files of the Intensive Care Department A1 of the Hassan II University Hospital of Fez for the study. Osteomas of the paranasal sinuses are benign, often asymptomatic, tumors that progress very slowly. Endocranial development of an osteoma can breach the dura mata, allowing air to enter the cranium producing pneumocephalia which leads to severe neurological deficiencies. Pneumocephalia is an exceptional complication of osteoma.

Active tuberculosis of spine: Current updates

BackgroundSpinal tuberculosis (TB) is the most common extrapulmonary form of tuberculosis. In both developing and developed countries, TB has been on the rising trend due to factors such as increasing HIV coinfection, multidrug resistance of the organism, and global migration. Spinal TB, which most often affects the lower thoracic and thoracolumbar area, accounts for 50% of all musculoskeletal tuberculosis. MethodsUsing the Cochrane Database of Systematic Reviews, EMBASE, and PubMed, a systematic computerized literature search was performed. Analyses of studies published within the past 10 years were conducted. The searches were performed using Medical Subject Headings terms, with “spinal tuberculosis,” “diagnosis,” “epidemiology,” and “etiology”,“management,” “surgery,” and “therapy” as subheadings. ResultsProgressive collapse, kyphosis, and neurological deficiency are hallmarks of the disease because of its destructive effect on the intervertebral disc and adjacent vertebral bodies. The condition may be identified using laboratory testing and distinctive imaging features, but the gold standard for diagnosis is tissue diagnosis using cultures, histology, and polymerase chain reaction. Uncomplicated spinal TB is today a medical condition that can be adequately treated by multidrug ambulatory chemotherapy. Surgery is reserved for individuals who have instability, neurological impairment, and deformity correction. Debridement, deformity correction, and stable fusion are the cornerstones of surgical treatment. ConclusionsClinical results for the treatment of spinal TB are generally satisfactory when the disease is identified and treated early. However, the major health issue and the biggest obstacle in achieving the goals of the “End TB strategy” is the recent rise in the emergence of drug resistance. Hence strict vigilance and patient perseverance in the completion of the treatment is the main need of the hour.

A rare clinical case of syringomyelia progression in the presence of Chiari I malformation following the surgery

Today, an Arnold-Chiari malformation is defined as a developmental pathology of the craniovertebral junction manifested by a discrepancy between the volume and contents of the posterior cranial fossa, which in turn leads to compression of neurological structures and changes in the cerebrospinal fluid circulation. There are several theories of the correlation between Chiari malformation and syringomyelia, but the exact mechanism of syringomyelia development remains unclear.This article describes a clinical case of treatment of a child with Chiari I malformation and syringomyelia within the cervical and thoracic segments of the spinal cord; after complete posterior fossa decompression, syringomyelia progressed in the early postoperative period with the development of a severe neurological deficiency. Since there is no standard treatment of such postoperative complications, a decision was made on the expectant management of the patient. From the twentieth day of the postoperative period, the patient showed complete regression of the neurological deficiency and positive MRI dynamics of syringomyelia.The presented clinical case raises such issues as not only the pathophysiology of syringomyelia progression after complete posterior fossa decompression, but also the determination of patient management tactics in case of a complicated postoperative course of the disease.The presented clinical case is of interest due to the rarely described aggravation of syringomyelia with enhancing neurological symptoms in the early postoperative period after complete posterior fossa decompression. Our observation suggests that the expectant management of the patient, despite syringomyelia progression with neurological deficiency aggravation after posterior fossa decompression, allowed a favorable long-term outcome of Chiari I malformation.

Hydrophobic Polystyrene-Modified Gelatin Enhances Fast Hemostasis and Tissue Regeneration in Traumatic Brain Injury.

Hemostatic sealant is required to deal with blood loss, especially in the scenario of traumatic brain injury (TBI), which presents high rates of morbidity and disability. Hemostasis in surgery with traditional gelatin-based sealants often leads to blood loss and other issues in brain because of the hydrophilic gelatin swelling. Herein, hydrophobic effects on the hemostasis in TBI surgery are studied by tuning the chain length of polystyrene (PS) onto methylacrylated gelatin (Gel-MA). The hydrophobicity and hemostatic efficiency can be tuned by controlling the length of PS groups. The platelet activation of modified sealants Gel-MA-2P, Gel-MA-P, and Gel-MA-0.5P is as much as 17.5, 9.1, and 2.1 times higher than Gel-MA in vitro. The hemostatic time of Gel-MA-2P, Gel-MA-P, and Gel-MA-0.5P groups is 2.0-, 1.6-, and 1.1-folds faster than that in Gel-MA group in TBI mice. Increased formation of fibrins and platelet aggregation can also be observed in vitro by scanning electron microscopy. Animal's mortality is lowered by 46%, neurologic deficiency is reduced by 1.5 times, and brain edema is attenuated by 10%. Protein expression is further investigated to exhibit toxic iron-related processes caused by delayed hemostasis and activation of platelets via PI3K/PKC-α signaling. The hydrophobic Gel-MA has the potential in hemostatic TBI and promotes nervous system recovery in brain with the potentials in clinics.

Multisystem inflammatory syndrome in a child associated with COVID-19: a clinical case report

Multisystem inflammatory syndrome in children (MIS-C) who contracted COVID-19 remains an urgent problem. Mortality due to this disease among children ranges from 0.8 % to 2.0 %. According to reports found in the literature, MIS-C can develop both in children who have experienced COVID-19 without clinical manifestations, and in those who have had a severe course of the disease. To date, there are no well-defined factors that allow predicting the risk of developing MIS-C in children after experiencing COVID-19, and the spectrum of clinical manifestations can be quite diverse. Aim: on the example of a specific case, to examine and analyze the features of the course and the range of diagnostic measures in children with MIS-C using an analytical method and a systemic approach. Materials and methods. The material was a clinical case of MIS-C, methods of instrumental diagnosis and objective analysis. The diagnosis of MIS-C was based on the WHO 2021 criteria for the diagnosis of MIS-C associated with COVID-19. Results. The clinical case of MIS-C associated with COVID-19 in a child with congenital thymus pathology that resulted in rapid, aggressive, and worsening multiple organ failure was studied. The manifestations were dominated by liver failure, respiratory failure, circulatory failure, and neurological deficiency, that led to the child’s death. Conclusions. Multisystem inflammatory syndrome in children associated with SARS-CoV-2 infection can lead to serious and life-threatening complications in previously clinically healthy children. Physicians need to be more alert to children of different age groups with manifestations of respiratory infections as potential COVID-19 and to test for its presence, which will subsequently allow timely identification of children with MIS-C associated with SARS-CoV-2. Considering the probable role of the thymus in the pathogenesis and course of MIS-C associated with SARS-CoV-2, we recommend an ultrasound examination of the thymus for all children under 3 years of age with confirmed COVID-19 and followed by examination of T-cellular response if changes are detected.

Ethmoidal sinus osteoma associated with Pneumocephalus

The most common causes of intracranial air are head trauma and neurosurgical procedures. Less common etiologies include infection due to gas-forming organisms, mucoceles, tumors, congenital neuroenteric cysts, and dural defects. Here, we present a case of an ethmoidal sinus osteoma associated with pneumocephalus. Osteomas of the paranasal sinuses are benign, often asymptomatic, tumors that progress very slowly. Endocranial development of an osteoma can breach the dura mata, allowing air to enter the cranium producing pneumocephalia which leads to severe neurological deficiencies. Pneumocephalia is an exceptional complication of osteoma.

The Relevance of Osteoscintigraphy Technique in Early Detection of Bone Metastatic Lesions: a Systematic Review

Background. Due to intensive blood supply to the red bone marrow, as well as high adhesive abilities of tumor cells, bone tissue is a perfect structure for the metastatic process. Timely identification of the pathological process is highly relevant, since data from numerous sources on the use of radiation methods at later stages indicate the development of severe pathological conditions leading to neurological deficiency and significant decrease in a patient’s quality of life. Objective: to summarize data on the diagnostic effectiveness of osteoscintigraphy (OSG), as well as to conduct a comparative analysis of various diagnostic methods in bone metastases detection. Material and methods. The review was performed according to PRISMA standard (Preferred Reporting Items for Systematic Reviews and Meta-Analyses). It included only full-text articles published in the period from 2015 to 2022, as well as particularly important publications from 2005 to 2014. The search for articles was carried out independently using CyberLeninka, eLibrary, Google Scholar, PubMed/MEDLINE databases, by key terms without the use of language restrictions: “osteoscintigraphy”, “radiology’, “tumors”, “bones”, “diagnosis”. Results. The final analysis included 56 scientific articles by a qualitative indicator. The advantages and disadvantages of the methods, as well as indications for the use of various diagnostic techniques in bone metastatic lesions detection were presented. It was shown that OSG will cost 6 times cheaper than positron emission tomography (PET), and 3 times cheaper than magnetic resonance imaging (MRI). The analysis of using radiation methods demonstrated that the specificity of computed tomography and radiography was at a high level, but this techniques had less pronounced sensitivity, and MRI, OSG and PET had greater sensitivity, but insufficient specificity. In the initial stage of the disease, OSG is one of the main methods of metastatic lesions visualization, but not the only way of diagnosis in diversification strategy aspect. Conclusion. OSG is an effective and informative technique for early detection of bone metastases, allowing to assess the functional state of the tumor and its surrounding tissues, even before the appearance of structural disorders visible by other diagnostic methods. To improve the accuracy of the study, it is advisable to use a set of radiation diagnostic techniques. The choice of a particular method is determined by its technical capability and financial availability.

Ginkgo biloba extract (EGb-761) confers neuroprotection against ischemic stroke by augmenting autophagic/lysosomal signaling pathway

Ginkgo biloba extract (EGb-761) is well-recognized to have neuroprotective properties. Meanwhile, autophagy machinery is extensively involved in the pathophysiological processes of ischemic stroke. The EGb-761 is widely used in the clinical treatment of stroke patients. However, its neuroprotective mechanisms against ischemic stroke are still not fully understood. The present study was conducted to uncover whether the pharmacological effects of EGb-761 can be executed by modulation of the autophagic/lysosomal signaling axis. A Sprague-Dawley rat model of ischemic stroke was established by middle cerebral artery occlusion (MCAO) for 90 min, followed by reperfusion. The EGb-761 was then administered to the MCAO rats once daily for a total of 7 days. Thereafter, the penumbral tissues were acquired to detect proteins involved in the autophagic/lysosomal pathway including Beclin1, LC-3, SQSTM1/p62, ubiquitin, cathepsin B, and cathepsin D by western blot and immunofluorescence, respectively. Subsequently, the therapeutic outcomes were evaluated by measuring the infarct volume, neurological deficits, and neuron survival. The results showed that the autophagic activities of Beclin1 and LC3-II in neurons were markedly promoted by 7 days of EGb-761 therapy. Meanwhile, the autophagic cargoes of insoluble p62 and ubiquitinated proteins were effectively degraded by EGb-761-augmented lysosomal activity of cathepsin B and cathepsin D. Moreover, the infarction size, neurological deficiencies, and neuron death were also substantially attenuated by EGb-761 therapy. Taken together, our study suggests that EGb-761 exerts a neuroprotective effect against ischemic stroke by promoting autophagic/lysosomal signaling in neurons at the penumbra. Thus, it might be a new therapeutic target for treating ischemic stroke.

Thoracic spinal tuberculosis in a 2.5-year-old child treated by surgical procedure with a transthoracic approach: a case report.

A 2-year-old and 6-month-old boy was admitted with fever and unspecific generalized pain, the examination revealed mild hyperreflexia in the lower extremities, isotope scan showed increased uptake in the T8 vertebra. MRI demonstrated destruction in the T8 vertebra with kyphotic deformity and abscess anterior to T7, T8, and T9 levels with an epidural abscess at the T8 level extending to the spinal canal and compressing the spinal cord. The patient underwent a surgical procedure with a transthoracic approach, the decompression of the spinal canal was performed through T8 corpectomy, the reduction of kyphosis was performed and the internal fixation with a dynamic cylinder and lateral titanium plate was carried out. Microbiologic examination suggests Mycobacterium tuberculosis. Pott's disease (spinal TB) is extremely rare in the young children population, and surgical treatment is reported only in a few reports, and it is considered a technical challenge. There are several surgical approaches during childhood, for upper thoracic spinal TB, the posterior approach is easy, minimally invasive, safe, reliable, and effective. But it had the worst outcomes. In contrast, the anterior approach provides direct access to the lesions. More research are needed to detect the best choice in the management of thoracic spinal TB in children.

Policies Affecting Pregnant Women with Substance Use Disorder

Policies Affecting Pregnant Women with Substance Use Disorder

Relationships between stroke prevalence, health literacy, and oral health-related quality of life in middle-aged and older adults: a national survey study

BackgroundStroke may cause debilitating neurological deficiencies that result in motor, sensory, and cognitive deficits and poorer psychosocial functioning. Prior studies have provided some initial evidence for the significant roles of health literacy and poor oral health for old people. However, few studies have focused on the health literacy of individuals who had a stroke; therefore, the relationships between the health literacy and oral health-related quality of life (OHRQoL) among middle-aged and older adults who had a stroke are unknown. We aimed to assess the relationships between stroke prevalence, health literacy status, and OHRQoL in middle-aged and older adults.MethodsWe retrieved the data from The Taiwan Longitudinal Study on Aging, a population-based survey. For each eligible subject, we gathered data in 2015 on age, sex, level of education, marital status, health literacy, the activity daily living (ADL), stroke history and OHRQoL. We evaluated the respondents’ health literacy by using a nine-item health literacy scale and categorized their health literacy level as low, medium, or high. OHRQoL was identified based on the Taiwan version of the Oral Health Impact Profile (OHIP-7T).ResultsThe final study contained 7702 community-based dwelling elderly people (3630 male and 4072 female) were analysis in our study. Stroke history was reported in 4.3% of participants, 25.3% reported low health literacy, and 41.9% had at least one ADL disability. Furthermore, 11.3% of participants had depression, 8.3% had cognitive impairment, and 3.4% had poor OHRQoL. Age, health literacy, ADL disability, stroke history, and depression status were significantly associated with poor OHRQoL after sex and marital status was adjusted. Medium (odds ratio [OR] = 1.784, 95% confidence interval [CI] = 1.177, 2.702) to low health literacy (OR = 2.496, 95% CI = 1.628, 3.828) was significantly associated with poor OHRQoL.ConclusionsBase our study results, people with stroke history had poor OHRQoL. Lower health literacy and ADL disability were associated with worse QHRQoL. Further studies are necessary to define practical strategies for reducing the risk of stroke and oral health with constantly lower health literacy, thereby improving the quality of life and providing health care of older people.

The course of post intensive care syndrome in patients with severe cerebral insufficiency and predictors of recovery. Clinical observation

Post-intensive care syndrome (PICS) is currently a problem affecting the entire intensive care strategy. The study of its mechanisms becomes most relevant in regard to the prevention of its development and influence on the disease course in patients with impaired respiratory function, neuromuscular transmission and cognitive disorders requiring long-term protection of the vital functions. The severity of the systemic inflammatory response as an individual reaction of the body has a significant influence on the PICS development and severity, that predetermines the degree of neurological and psychological deficiency. The presence of background somatic diseases, such as diabetes mellitus (including that in the framework of metabolic syndrome), significantly aggravates the course of PICS and contributes to the deceleration of the recovery process. The earliest possible start of rehabilitation with both passive and active measures on the basis of an intensive care unit, followed by an expanded individual rehabilitation program on the basis of a specialized department, leads to the most favorable prognosis for the restoration of both impaired vital functions and for the emerging disorders in the cognitive, motor, and affective spheres. Such an approach reduces the length of stay in the hospital and improves the patients quality of life after the discharge from the hospital.
 The article describes three clinical cases of PIT syndrome. Based on the analysis of the course and severity of this syndrome, the conclusions are drawn about the relationship between the course of the inflammatory process and its effect on the restoration of the impaired functions.

Late answers in the electroneuromyography of patients with degenerative-dystrophic spine disorders

We carried out electroneuromyography of 78 patients with degenerative-dystrophic cervical and lumbar spine disorders, which were treated at the neurosurgical department of the Irkutsk Scientific Centre of Surgery and Traumatology. The results of the study of late ENMG phenomena such as H-reflex, F-waves and A-reflex were obtained at different stages of the disease using “Neuromyan” neuromyoanalyzer. The predictable changes in late answers at different stages of the process were determined. For example, in patients with radiculopathy, the degree of neurological deficiency was minimal, and in patients with a combination of nerve root syndrome and stenotic changes, the neurological deficiency had the character of a pronounced bilateral pathology. The severity of changes in neurophysiological indicators depends on the degree of spinal stenosis. Determination of N-reflex and F-wave parameters allows us to identify subclinical forms of loss both at the level of peripheral nerves and of spinal cord segments, and the appearance of axon reflex is an evidence of a demyelinizing pathology and chronic process.

Different Ways to Die: Cell Death Pathways and Their Association With Spinal Cord Injury.

Cell death is a systematic/nonsystematic process of cessation of normal morphology and functional properties of the cell to replace and recycle old cells with new also promoting inflammation in some cases. It is a complicated process comprising multiple pathways. Some are well-explored, and others have just begun to be. The research on appropriate control of cell death pathways after acute and chronic damage of neuronal cells is being widely researched today due to the lack of regeneration and recovering potential of a neuronal cell after sustaining damage and the inability to control the direction of neuronal growth. In the progression and onset of various neurological diseases, impairments in programmed cell death signaling processes, like necroptosis, apoptosis, ferroptosis, pyroptosis, and pathways directly or indirectly linked, like autophagy as in nonprogrammed necrosis, are observed. Spinal cord injury (SCI) involves the temporary or permanent disruption of motor activities due to the death of a neuronal and glial cell in the spinal cord accompanied by axonal degeneration. Recent years have seen a significant increase in research on the intricate biochemical interactions that occur after a SCI. Different cell death pathways may significantly impact the subsequent damage processes that lead to the eventual neurological deficiency after an injury to the spinal cord. A better knowledge of the molecular basis of the involved cell death pathways might help enhance neuronal and glial survival and neurological deficits, promoting a curative path for SCI.

Synergic neurotoxic and paraneoplastic neurological syndrome during cysplatin chemotherapy in case of transplanted experimental rat lymphoma

The aim of the study is assessment of combined effect of homotransplanted rat lymphoma (Pliss Lymphosrcoma) growth and antitumor therapy (cysplatin) upon the functioning of the nervous system was accomplished in 160 male Wistar rats, divided into four groups: intact animals, rats treated with cysplatin, rats with transplanted lymphoma, and rats with transplanted lymphoma that received cysplatin treatment. The neurologic deficiency degree as well as basic myelin protein peripheral blood level (nervous system impairment hematological marker) were comparatively assessed. Tumor development was accompanied with emergence and subsequent growth of neurologic deficit in locomotory, sensory and coordinative spheres as well as pronounced growth of basic myeline protein plasma level thus making this model a valid test-system for studying paraneoplastic neurologic syndrome. Cysplatin has produced a non-selective toxic effect upon the nervous system of the experimental animals within its therapeutic window range documented by neurotoxic syndrome. Subsequently along with elimination of cysplatin and its derivates from the organism, systemic neurotoxic effect intensity decreased and the nervous system functional state parameters returned to control values. Using cysplatin for the treatment of homotransplanted experimental rat lymphoma results in synergic neurotoxic and paraneoplastic neurological syndrome through combined injury of the nervous system.