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@#Nonarteritic anterior ischemic optic neuropathy(NAION)is caused by ischemia of the short posterior ciliary artery that supplies the lamina area of the optic disc. It usually occurs in over 50-year-old people. It is acute optic neuropathy and featured with acute, monocular, and painless vision loss, which frequently results in severe permanent vision damage and visual field defects. This disease is attracting increased attention of clinical researchers. This paper overviews the current molecular pathology of NAION from these aspects, including pathogenesis, pathological changes, relevant protein molecules and susceptibility genes in previous studies. This paper lays a theoretical foundation for future research on the pathological mechanism and the treatment of NAION.
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Leukoaraiosis (LA) has important clinical significance;however, the neurobiological mechanism was still unclear. In this pa-per, we reviewed literatures about the clinical symptoms, pathology and imaging of LA in order to improve the understanding of the patho-logic mechanism, recognize the reversible pathological change in the earliest stage, which can help to prevent dementia.
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BackgroundWith the number of diabetics increases,people pay more attention to the diabetic keratopathy.The major mechanism leading to diabetic keratopathy is diabetic corneal neuropathy.So it is significant to observe pathologic mechanism of diabetic corneal neuropathy. Objective To investigate the protective effects of edaravone( a free radical scavenger) on corneal nerve of rats with experimental diabetic corneal neuropathy,then explain the effects of oxidative stress in the pathologic mechanism of diabetic corneal neuropathy. Methods Seventy Sprague-Daxley male rats were taken as experimental subjects and 20 of them were used as normal control group.The remaining 50 were induced to be diabetic mellitus by a single intraperitoneal injection of streptozotocin and divided into 2 groups randomly:edaravone treated group and diabetic control group.In the edaravone treated group,edaravone(0.2 g/L) eye drops were used 3 times a day until the animal was killed.Five rats in each group were sacrificed at 6,8,10 and 12 weeks respectively.Then the corneal sensation,number of corneal nerve fibers,morphology,content of malondialdehyde(MDA) and activity of superoxide dismutase(SOD) in the corneal tissue were detected.ResultsIn the diabetic control group,the corneal sensation and the number of corneal nerve fibers were decreased,the density of neural network for cluster was sparse,the nerve activity was decreased,the content of MDA in the corneal tissue was significantly increased,the activity of SOD in the corneal tissue was significantly decreased (P＜0.01 ).Accompany with the course of disease,the above change was obvious day after day.Compared with the diabetic control group,the corneal sensation and the morphological abnormalities in corneal nerve of edaravone group were improved significantly which had the partial branches to the 12th week,the content of MDA in the corneal tissue was significantly decreased,the activity of SOD in the corneal tissue was significantly increased (P＜0.01).Conclusions Edaravone can lower diabetic corneal nerve of rats with experimental diabetic corneal neuropathyinjury,Oxidative stress may be a critical pathologic mechanism of diabetic corneal neuropathy.
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@#ObjectiveTo investigate the pathologic mechanism of motor aphasia.Methods25 patients with cerebral infarction and motor aphasia were examined by magnetic resonance spectroscopy (MRS) and perfusion weighted imaging (PWI) at Broca's areas, the results were compared with that of the mirror side.ResultsMRS showed that the N-acetyl aspartate, choline in Broca's areas reduced than that of the mirror side ( P<0.05); while PWI showed that the regional cerebral blood volume and regional cerebral blood flow of damaged Broca's areas decreased significantly than that of the right hemisphere ( P<0.01). Mean transit time and time to peak of damaged Broca's areas prolonged than that of mirror side ( P<0.05).ConclusionHypoperfusion and hypometabolism revealed in Broca's areas of patients with motor aphasia may be one of the mechanisms of motor aphasia.