Impaired Nervous System Function Research Articles

Mikroglijos reikšmė išsėtinės sklerozės patogenezėje ir sąsajos su imunomoduliuojančiu gydymu

Multiple sclerosis is a chronic autoimmune disease of the central nervous system. Multiple sclerosis causes demyelination, impaired nervous system function, and eventually neurodegeneration. Microglia are cells of the central nervous system that develop from yolk sac macrophages during embryogenesis. These cells perform important functions in the development of the central nervous system and the retina, in the formation of synapses, protect against pathogens, and are involved in the removal of damaged structures. In response to environmental factors, microglia can acquire an inflammatory or anti-inflammatory phenotype. Microglia also play an important role in the pathogenesis of multiple sclerosis, and these cells are thought to be involved in both demyelination and remyelination processes. Microglial cells phagocytose harmful myelin remnants, promote remyelination, and control the proper response of peripheral immune cells, but disruption of these functions can lead to demyelination and neurodegeneration. Many of the disease-modifying drugs used to treat multiple sclerosis also affect microglial cells and inhibit their inflammatory response. Currently, new drugs are being researched that could be used to treat multiple sclerosis promoting the transition of microglia to an anti-inflammatory phenotype. The latest advanced cell therapy drugs have a broader spectrum of action – they inhibit inflammation, promote angiogenesis, perform trophic function, and inhibit oxidative damage.

The effect of extended continuous nursing strategy applied to patients with mild brain injury on their quality of life and self-efficacy.

Postoperative rehabilitation of craniocerebral injury requires a long process and has many complications. In addition, patients with severe craniocerebral injury are usually accompanied by impaired nervous system function, which will affect the patients’ normal life and work in a period of time after surgery. Reasonable rehabilitation nursing plays an active role in restructuring central nervous system function and coordinating muscle and joint activities. Since the rehabilitation of cerebral trauma is a long process, how to ensure the patients to carry out limb and brain function as well as self-care ability and self-care skills according to the rehabilitation exercise plan and intervention measures formulated before discharge has aroused hot debate. This study analyzed the impact of out-of-hospital continuous nursing strategy applied to patients with mild cerebral trauma on their quality of life and self-efficacy level.

Adrenoleukodystrophy and other peroxisomal disorders that affect the nervous system, including new observations on L-pipecolic acid oxidase in primates

Impaired nervous system function in childhood is encountered in 10 separate disorders of the peroxisome. Peroxisomal disorders are subdivided into three major groups. In group 1 there is failure to form the organelle and impairment of multiple peroxisomal functions. In group 3 peroxisome structure is intact and the defect involves a single enzyme. In group 2 (rhizomelic chondrodysplasia punctata) peroxisome structure is probably intact, but at least 2 peroxisomal enzymes fail to function normally. We present an overview of this newly recognized field which is so pertinent to brain development. In addition, we present recent and new data about the biochemical defect, genetics and therapy of X-linked adrenoleukodystrophy; about the normal metabolism of L-pipecolic acid in primates and its disturbance in the Zellweger syndrome, and about the prenatal diagnosis of peroxisomal disorders.

Sequelae of carbon monoxide-induced hypoxia in the rat.

Rats were exposed to carbon monoxide, and conduction velocity of ventral caudal nerve (VCN), visual cortical evoked potential (VEP), electroencephalogram, and vital functions were determined in relation to the degree of CO-induced hypoxia. The conduction velocity of VCN and VEP (latency of P2 [second positive deflection of the visual evoked response]) were unaffected until carboxyhemoglobin (COHb) levels reached between 60% and 70%. These levels were maintained for approximately one hour before decreased conduction velocity or increased latency of P2 occurred. Decrease in mean arterial blood pressure resulted in impaired neurological function. Recovery of conduction velocity was discontinuous. Conduction was lost and recovered again within a three-hour period after exposure. It decreased again 9 to 13 days later, recovering in approximately four days. Data on P2 latency after exposure were fragmentary, but suggest that later increases might occur. Similar effects of CO-induced hypoxia on peripheral and central nervous systems were found. Decrease of mean arterial blood pressure was consistently associated with impaired nervous system function.