A Clinical And Basic Study Of Myelin Damage Mechanism In Carbon Monoxide Poisoning Deiayed Neurological Sequelae

After a period of latent phase, the phenomena of nervous system function occurs againon the patients those who got Acute carbon monoxide poisoning, ACOP. We name it asDelayed neuropsychological Sequelae，(DNS). Clinically, it has been found that the mainreason which cause this disease is alba demyelination. But there are so many kinds ofhypothesis about the theory of demyelination. Moreover, the observation on albademyelination is just based on CT or MRI, which only provides perceptual cognizance ofpicture and lack of objective evaluation standard, so the development and progression ofalba demyelination is not sufficient enough, which cause there is no clinical standard. Thisarticle will be with a view to improve the acknowledge of alba demyelination fromperceptual cognizance to rational level. It aims to fund the pathogenesis of albademyelination according to the way of clinic conclusions, objective examination andanimal test.The fist step is the collection of clinical data. The data of122patients those who have5years of DNS from2007to2012in our hospital HPO department has been selected. WeMainly review the feature of condition change and the time and results of brain CT, MRI inorder to form the initial impression of development of the DNS patients with albademyelination. Through data sorting,34patients get the examination of head CT or MRIduring their period of counterfeit recovery.12of them have not been found albademyelination. And the examination time is3.7±1.2d;22of them have been found h albademyelination.And the examination time is10.9±6.3d110patients can be found alba demyelination changing by the more than times ofexamination of head CT or MRI during early and developing period of DNS morbidity.The results of examination of17patients among them tells that “the condition is betterthan before”, and according to the iconography, we can see that the phenomena of albademyelination disappeared only happens on4patients from the period of3to97days afterintoxication. The above results of patients with DNS, white matter demyelinationperformance may not appear immediately after poisoning, but a longer duration.. The above results give us a hint that it is nor certain to appear that alba demyelination of DNSpatients after intoxication but it will last for a long duration.Step two is Clinical trial design,the acknowledge of the DNS alba demyelination istransferred from subjective evaluation into objective analysis. Image logical examinationwith selected data of Diffusion tensor imaging,(DTI) and Magnetic resonancespectroscopy,(MRS) can quantitatively evaluate the condition of alba demyelination andnerve cellular metabolism of DNS patients. According to the actual work, we select thedata of DTI+MRS, and extract disease area ADC and FA values, NAA and Cho on thetime which of two points. One is the period of aggravation; the other is the period of onemonth cure Combining with Mini-Mental State Examination, MMSE) and (Activities ofdaily living, ADL), we grade for the performance of patient’s symptom objectively. Theresult shows that the grade of MMSE and ADL increase in one month later after cure, andADC value observed by DTI and FA value does change little, NAA/Cr observed by MRSapparently increase after cure, Cho/Cr change little. From this analysis, demyelinationDNS patients need a long time for recovery. These results prompted factors that COpoisoning may influent the recovery.Step threes to design animal test. Nervous centralis myelin is formed by thatoligodendrocyte cells, OLs surround axons of nerve cell, and the differentiation ofoligodendrocyte precursor cells OPCs is the key step of myelination. By using WesternBlot to examine MBP corresponding to Ols and NG2protein expression levelcorresponding to OPCs cell in the brain of rat, the development of myelin damage after COpoisoning can be revealed by evaluating the condition of Ols and OPCs. We select36SDmale rats around400g.they were divided randomly into the normal group and the COpoisoning group after basic training in Morris water maze.18of the rats were made severepoisoning model after employed with CO intraperitoneal injections. After the Morris WaterMaze of the above rats, it evaluated that the rats which were intraperitoneal injected withCO gas appear obvious toxic symptom, and parts of them died. Detected by Morris watermaze, the rats of poisoning dramatically decline in memory and capability of studying. After1,3,7,14,21,30days later, we take3brains from poisoning group and control group,and use WB method to examine MBP and NG2expression. WB test results show thatMBP and NG2expression from poisoning group reduce in three days, and NG2reduceobviously;14days after the MBP has risen again, but the expression of NG2stillinsufficient. As to the decrease of MBP and NG2of poisoning group, there are significantdifferences in comparison with the control group.Conclusion: After CO poisoning mainly OPCs cell is damaged, causing generation ofOLs inadequate. OLs cells can maintain normal neurological function for a time in the caseof no added supplementary when its dying, which is called the period of counterfeitrecovery. Until the Reduce of OLs to a certain extent, the performance of nerve damagegradually emerges. The state of illness of patients is delayed and the performance of albadamaged is always associated with the slow recovery of OPCs cells. After neuronalfunction recovery, patient may use of the remaining intact neural pathways to partiallycompensate nerve function, but demyelination performance will last longer. The findingsmay explain the situation pre-medical statistics and clinical test, which is maybe the reasonof DNS generation.