Objective To study the efficacy as well as side effects of the Nimotop in the treatment of benign memory disorders with oral tab. Method 38 patients with benign memory disorders as treatment group, taking Nimotop oral tab 30mg, Tid for 6 weeks and anathr 34patients with benign memory disorders taking Pyrrolidone Acetamide oral tab 0. 8, Tid as control group. Result The total efficiency were 73.6% in treatment group, while 47% in control group. Although some improvement in the memory scale and memory quotient were found in both groups, but the treatment group is obviously superior to control group ( P ＜ 0. 05) . Conclusion Nimotop has positive effect on the treatment of benign memory disorders.

ObjectiveTo explore the effect of brain derived neurotrophic factor(BDNF) on regeneration of distal axon in sciatic nerve after cfrush injury. MethodDistal axon was assessed by quantitavtive and qualitative analysis of pathology ResultLight microscope indicated thedensity of large diameter of peroneal-nerve was higher in study group compared with control group( P ＜0.01 ). No differences in density of littlediameter fiber were found between study and control group. EM showed the density of non-medullated fibers with diameter ＜0.5μm in studygroup was higher than that of control group. The numbers of layer in myelin was positively related to transverse axonal area( P ＜0.01 ) . The re-gression codfficient in study group wsa higher compared with control group( P = 0. 0023).ConclusionBDNF may promoted maturation ofsensoy nerve and formation of the myeline.

Objective :To observate the axon changes in pathology of Ola mice,compared with those of 6Jmice. Methods:The peroneal nerve and sural nerve were studied by light-microscope and electronmi-croscope. Results :In light-microscope,the total transverse fascicular area was significantly large ;density ofmyelinated fibers was significantly less;the maximal diameter of myelinated fibers was significantly less;minimal diameter of myelinated fibers had no changens in 6J mice. The Ola mice were nomal. In electronmi-croscope observation, the neurofilament was accumulated within axons. Conclusion: In Ola mice treatedwith ACR,the like-Wallerian degeneration wes delayed. However,in 6J mice the neurofilament and mito-chondria accumulation was found within axons.

BACKGROUND:Ola rats is a kind of rats with genovariation, who displays Wallerian degeneration after peripheral neuroaxonal damage that is slower than that normal 6J rats, thereby additional damage factor may help fully understand the property of Ola rats.OBJECTIVE: To observe the effect of acrylamide on the degeneration and regeneration of sciatic nerve medullated fibers following crush injury of C57BL/Ola (Ola) rat and C57BL/6J (6J) rat.DESIGN: Randomized controlled experiment.SETTING: Department of Neurology,Second People's hospital of Shenzhen; Department of Neurology of First hospital of Jilin University MATERIALS: This experiment was carried out in the neurological department in the University of Occupational and Environmental, Japan from January to June 1996. Twelve adult Ola rats and 6J rats were adopted and evenly randomly divided into experimental group and comparison group.METHODS: Rats were subjected to general anaesthesia, and then the proximal section of sciatic nerve was exposed and frustrated with hemostatic forceps for 10 s before suture. Rats in the experimental group were given intraperitoneal injection of acrylamide in a total dosage of 350 mg, which replaced by the same volume of physiological saline in comparison group.At 14 days after sciatic nerve torsion injury, all rats were anaesthetized again and the distal section of sciatic nerve was obtained and cut into slices, meanwhile the cross sectional area, the density and size frequency distribution of medullated fibers, as well as the number of medullated fibers in each nerve were determined.MAIN OUTCOME MEASURES: The density and size frequency distribution of sciatic nerve medullated fibers, as well as the number, the maximum diameter and the mean diameter of medullated fibers in two group of 0la rats and 6J rats.RESULTS: Totally 12 Ola rats and 6J rats entered the result analysis.① No Ola rat displayed Wallerian degeneration; But medullated fiber degeneration and following neonatal small diameter medullated fibers could be observed in 6J rats. ②In the experimental group, the total density of sciatic nerve medullated fibers in 6J rats was lower than that of Ola rat (P ＜ 0.05) ;with the total number of medullated fibers in 6J rats also less than that of Ola rat (P ＜ 0.01 ), which predominated by obviously reduced big diameter fibers (P ＜ 0.01); The mean diameter of medullated fiber in 6J rats was also obviously smaller than that of 0la rat (P ＜ 0.01 ).CONCLUSION: The Wallerian degeneration is extremely slow in Ola rat after torsion injury, which cannot be affected by acrylamide; while acrylamide has obvious inhibition on the axonal neogenesis in 6J rat after torsion injury.

Objective To investigate whether there are correlations between working memory impairmentand fractional anisotropy values and to explore the neuropathology underlying that the patients of depression suffered from memory impairment.Methods Thirty depression patients and 30 healthy controls group-matched by age,educational level were conducted the study.Mean correct reaction time(mRT)was recorded when they performed a One-Back Working Memory Task and fractional anisotropy(FA)values was recorded when they performed the diffusion tensor imaging.Statistics analysis was done respectively for mRT and FA values between two groups.Results Relative to mean correct reaction time((612.45±54.08)ms)of controls,the mean correct reaction time ((720.25±57.02)ms)of patients with depression was much longer(P＜0.05)and the patients with depression had a lower FA values in the white matter of both frontal lobe,anterior cingulate gyrus,supramarginal gyrus,splenium of corpus callosum(P＜0.05),and the FA values in the white matter of both frontal lobe were significantly negative correlated with mRT(r=-0.604,P＜0.05).Conclusion The impairment of white matter region may be one of the neuropathology underlying that the depression patients suffer from memory impairment.

Objective To investigate the characteristics and relative pathogenesis of cognitive impairment in people with depression.Methods 24 people with depression and 24 healthy controls were evaluated respectively with HAMD scale,the WCST test,N-BACK task P300 and fMRI.Results (1) The WCST scores,N-back reaction (MRT),the P300 incubation period in depression group were significantly different from those in control group(P300 wave amplitude(4.12± 1.51) μV vs (6.42± 1.73) μV ; P300 latency(392.02±23.60) ms vs (309.43± 21.39) ms,t=4.922,P＜0.01 ; t=12.726,P＜0.01).(2) The illness course had positive correlation with Rep(r=0.596,P＜0.01) and mRT(r=0.518,P＜0.01).The P300 latency had positive correcation with Rpe(r=0.929,P＜ 0.01) and mRT(r=0.939,P＜0.01).(3)Compared with control group,the decreased activation area in patients with depression were as follows:bilateral frontal gyrus,left middle frontal gyrus,inferior frontal gyrus and superior parietal lobule.Conclusion The depressive patients exist cognitive impairment mainly in frontal lobe.The longer with the illness,the wose with the impairment.P300 incubation period is a sensitive indicator of the frontal executive function.

Objective　To observe the differential pathological changes in Purkinje cells of the cerebellum in Ola mice and 6J mice after acrylamide intoxication. Methods　Purkinje cells were studied by light microscope and electron microscope. Results　Under light microscope,Purkinje cells in 6J mice were densely stained and irregular in cell shape.Under electron microscope,parts of the plasma membrane projection containing some smooth tubular endoplasmic reticula were found occasionally,and the membrane became split and thickened.These abnormal changes were not found in Ola mice. Conclusion　Acrylamide intoxication may induce pathological changes in Purkinje cells of 6J mice which may be the pathological basis of ataxia.

Objective　To observe the differential pathological changes in Purkinje cells of the cerebellum in Ola mice and 6J mice after acrylamide intoxication. Methods　Purkinje cells were studied by light microscope and electron microscope. Results　Under light microscope,Purkinje cells in 6J mice were densely stained and irregular in cell shape.Under electron microscope,parts of the plasma membrane projection containing some smooth tubular endoplasmic reticula were found occasionally,and the membrane became split and thickened.These abnormal changes were not found in Ola mice. Conclusion　Acrylamide intoxication may induce pathological changes in Purkinje cells of 6J mice which may be the pathological basis of ataxia.

OBJECTIVETo explore the changes of brain energy metabolism following acrylamide (ACR) poisoning.

METHODSCreatie kinase (CK), adenosine triphosphate (ATP), adenosine diphosphate(ADP), adenosine 5'-monophosphate(AMP) and glucose contents in brain were observed in O1a mice and 6J mice following ACR intoxication by enzyme analytical method.

RESULTSATP, CK and glucose levels decreased transiently in O1a mice, while ATP level in 6J mice was significantly decreased (1.76 mumol/g, P < 0.01), as compared to the control (2.53 mumol/g) but ADP and AMP were increased, glucose was decreased. The activity of CK in poisoned group (1.13 mumol/g, P < 0.01) was lower than that of control (3.16 mumol/g and lasted for 5 weeks).

CONCLUSIONThe influence of ACR on O1a mice was slight and reversible but on 6J mice was severe and lasting. There was severe damage to the potential energy supply compensation, which might be the biochemical basis of neuron damage induced by acrylamide.

Acrylamide ; poisoning ; Adenosine Triphosphate ; analysis ; Animals ; Brain ; drug effects ; metabolism ; Creatine Kinase ; analysis ; Energy Metabolism ; drug effects ; Glucose ; analysis ; Mice

Objective To describe the chnical, neuroimagine, pathological and genetic features in a case with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS)/Leigh overlap syndrome.Methods The ease was a 22-year-old woman with recurrent headache, loss of visual acuity and general seizures over 11 years.MRI demonstrated symmetrical high T2-weighted signals in occipital and parietal lobes, in the late stage of the disease, the above imagine changes on MRJ were also shown in the bilateral basal ganglion and brainstem.She died of status epilepticus at age of 22.Brain autopsy and mitochondrial DNA (mtDNA) analysis were performed in the patient.Results The main neuropathological findings were muhifocal and lamilar spongiform in the cortex of the whole brain, the basal ganglion and middle brain.Gliosis, macrophagie reaction and capillary endothelial proliferation were observed in these areas.All 6 layers of the cortex and subcortical white matter in occipital and parietal lobes were severely affected.GI3513A mutation was found in the gene of mitochondria encoded NADH dehydrogenase subunit 5 (MTNDS).Conclusions MELAS/Leigh overlap syndrome presents the symptoms predominantly affecting the cerebral cortex.Neuroimagines suggested that the lesion initially involves the cerebral cortex and in the late stage implicates the basal ganglion and the brainstem, possibly caused by pathological changes of spongiform with capillary proliferation in these areas.