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Study On The Level Of NO,SOD,MDA In Cerebrospinal Fluid From Patients With Cerebral Cysticercosis In Acute Stage

Posted on:2004-02-28Degree:MasterType:Thesis
Country:ChinaCandidate:X M ShengFull Text:PDF
GTID:2144360092999681Subject:Neurology
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Purpose:Cerebral cysticercosis is a common but severe central nervous system parasitic disease caused by encystment of the larvae of taenia solium, and in China it has 60%~80% incidence in the all cysticercosis cases. Cysticercosis belongs to an allergic disease.The larvae of taenia solium has its regular living pattern in brain tissue and which leads to different pathological processes. According to the pathological changes, it is divided into three stages: alive stage, the degeno-death stage (early and late stage) and the calcification (static) stage. The acute stage of cerebral cysticercosis is the degeno-death stage that is from larvae deterioration to their death. The clinical mannifestations of patients with cerebral cysticercosis are complicated and varied. The major symptoms include seizures,headache and mental disorders.The clinical symptoms are mainly related to the site, scope and number of cysticerci, to the living condition of the larvae of taenia solium, to the extent of tissue inflammation, and to the disfunction of blood and cerebrospinal fluid circulation. Epilepsy presents in up to 67.5% of cases. The pathophysiology mechanism thatinduces seizures is very complicated. Epilepsy is related not only to the location where cysticerci lie but also to the extent of brain edema. The edema is concerned with body allergy caused by the large quantity of toxin and protein released from denatured and dead cysticercus. The main methanism that leads to neuron injury is the immuno-inflammatory reaction which causes metabolic acidosis, intracelluar calcium ion (Ca2+) overload,exicitating amino acid (EAA) toxicity,lipoid metabolic disorder and free radicals mediating cell death, cytokine inducing neuron damage, etc. In the patients with cerebral cysticercosis in acute phage macrophage is activated due to the cysticercus' denaturation and death which leads to some metabolites and protein releasing. Thus the activated macrophage secretes inducible nitric oxide synthetase (iNOS) and a large quantity of Nitric oxide (NO) is produced. It is not completely known about the mechanism of NO anti-parasite. It has been suggested that NO may inhibite the cysticercus'living and help to kill parasite by different means. NO is a highly reactive signal molecule. In one hand, it acts as an immune modulator and makes parasite deteriorate; in the other hand, it could damage brain tissue to display many clinical mannifestations. It has been widely accepted that NO is involved in the phathophysiology of seizures, but definite mechanism is not known. At present, there are two kinds of argument: one is that NO can induce seizures, the other is that NO isanti-epileptic. The aim of our study is to assess whether NO is invovled in seizures in patients with cerebral cysticercosis in acute stage. The active oxygen theroy is widely invovled in a diversity of pathophysiological processes in the body. Central nervous system is easily damaged by active oxygen because of its high oxygen metabolism, high density of non-saturated fatty acid and integrated synaptic circuit. As a sort of metal proteinase super oxide dismutase (SOD) is a major defensive factor against free radicals. SOD can make free radical change into H2O2 and H2O2 is changed into H2O by glutathine peroxidase. Active oxygen may be involved in the regulating expression of SOD mRNA. Mental and intelligence obstacles may be related to the conditions of expression and regulation of SOD mRNA in hippocampus regions. The brain edema and the large quantity of free radicals make CuZnSOD decrease quickly in field CA1 while MnSOD in CA3 maintains high density for a long time. So cone cells in field CA1 are more easily damaged than that in field CA3. Malondialldehyde (MDA) is the final metabolism product of lipoid peroxidation and it can indirectly show the extent of oxygen radical mediating lipoidic super-oxidated. NO, SOD and MDA are complicatedly involved in the immunopathophysiology mechanism of cerebral cysticercosis. The aim of this study is to provi...
Keywords/Search Tags:cerebral cysticercosis, seizure, cerebro- spinal fluid, nitric oxide (NO), malondialdehyde (MDA), superoxide dismutase (SOD)
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