A retrospective analysis was performed for the clinical data of a patient with GFAP astrocytopathy that was initially misdiagnosed as viral encephalitis， and the diagnostic and therapeutic experience of this disease was summarized through a literature review.The female patient， aged 39 years， presented with headache and fever after diarrhea for 1 day， with the main manifestations of distending pain in the brain， nausea， vomiting， low‑grade fever， and right‑sided ataxia. Physical examination showed papilledema in both eyes and neck stiffness； contrast-enhanced cranial MRI showed extensive leptomeningeal enhancement； cerebrospinal fluid （CSF） analysis showed a significant increase in opening pressure and lymphocytic‑predominant pleocytosis. The patient was tested negative for common infectious pathogens and autoimmune encephalitis antibodies， and therefore， she was once misdiagnosed with viral encephalitis. After unsuccessful antiviral and antibiotic therapies， CSF and serum samples were tested positive for GFAP‑IgG antibodies， and the patient was finally diagnosed with GFAP astrocytopathy. The patient symptoms were rapidly relieved after pulse therapy with methylprednisolone （1 g/day）， and imaging reexamination showed the disappearance of leptomeningeal enhancement， with significant improvements in both intracranial pressure and CSF parameters. The patient remained asymptomatic till the last follow‑up in July 2025， and negative conversion was observed for CSF GFAP antibodies.GFAP astrocytopathy lacks specific clinical manifestations， with leptomeningeal enhancement and lymphocytic predominance in CSF as crucial clues for early diagnosis， and detection of GFAP IgG antibodies in CSF and serum is the key to a confirmed diagnosis. This disease is highly sensitive to glucocorticoid therapy， and early identification followed by standardized treatment can help to achieve a good prognosis. This disease should be differentiated from common central nervous system infections such as viral encephalitis in clinical practice to avoid treatment delay due to missed diagnosis or misdiagnosis.

Stroke is one of the most important diseases in the world with high mortality and disability rate. Acute ischemic stroke (AIS) is more than 80% in total. At present, the main treatments for AIS include intravenous thrombolysis and endovascular mechanical thrombectomy. Cognitive impairment is a common or potentially disabling effect of stroke, but the optimal treatment of post-stroke cognitive impairment remains controversial. This article reviews the effects of treatments for acute ischemic stroke on cognitive function.

Objective To investigate the effects of low dose of gamma knife irradiation on the expression of N-methyl-D-aspartate (NMDA) receptor subunits in cortex and hippocampus of epileptic rats. Methods The rats were randomly divided into 4 groups: control group, GK group, pentylenetetrazole (PTZ) group and GK+ PTZ group. The rats were injected intraperitoneally with PTZ to establish the epileptic models. Gamma knife irradiation was performed on bilateral frontal cortex of rats at a peripheral dose of 15Gy. After irradiation, the changes of the seizure and behaviors were observed and recorded. The rats were killed on the 12th week after irradiation, Immunohistochemstry and western blotting were used to detect the relative expression levels of NMDAR subunits (NR1, NR2A, and NR2B) in the cortex and hippocampus. Results There were no epileptic seizures in the control group and the GK group. Compared with the PTZ group, the epileptic seizures of rats in the GK+PTZ group were significantly reduced after low dose gamma knife irradiation (P<0.05). Compared with control group, the protein expression levels of NR1, NR2A and NR2B in the PTZ group increased significantly in the cortex and hippocampus, and so were the positive neurons and their average absorbance value (P<0.05). Compared with PTZ group, the protein expression levels of NR1, NR2A and NR2B of the GK+PTZ group decreased remarkably in the cortex and hippocampus (P<0.05). Protein expression levels of NR1, NR2A and NR2B were not significantly different between control group and GK group (P＞0.05). Conclusion Epileptic rats exhibited an increase in the protein expression levels of NR1, NR2A and NR2B in the cortex and hippocampus while low dose of gamma knife irradiation can decrease expression levels of NMDA receptor subunits in the cortex and hippocampus of epileptic rats, which might represent a possible mechanism underlying the therapeutic effects of gamma knife irradiation on epileptic seizure.

Objective To investigate the lesionsin theleft thalamus and to explore their correlation with executive functionin patients with subcortical ischemic vascular disease(SIVD)by using 1H magnetic resonance spectroscopy (1H-MRS) and diffusion tensor imaging (DTI). Methods Fourteen patients with vascular dementia (VaD), 14 patients with vas-cular cognitive impairment without dementia(VCIND)and 14 normal controls (NC) were recruited. The quantitative analy-sis of N-acetylaspartate (NAA), Choline (Cho), myoinositol (MI) and Creatine (Cr) resonance signals in region of interests (ROI) in the left thalamus were measured. Fractional anisotropy (FA) and mean diffusivity (MD) values in the same region were examined by using DTI. The relationship were analyzedamong the MRS, DTI ratios and cognitive impairment reflect-ed in MMSE and trail making test(TMT). Results The NAA/Cr ratio showed a gradual decrease in the left thalamus of VaD andVCIND patients compared with controls(F=3.656, P=0.038). There was no significant difference in NAA/Cr ra- tiobetween VaD and VCIND patients.Compared with controls, patients with VaD and VCIND demonstrated increased MD value in the left thalamus(F=3.882, P=0.030).There was no significant difference in MD value between VaD and VCIND patients (P>0.05). There were no correlations between NAA/Cr, MI/Cr, Cho/Cr value and DTI parameters in the ROI (P>0.05). TMTb time was positively associated with Cho/Cr(r=0.520,P=0.001 ) and with MD value in the left thalamus (r=0.305, P=0.044). Conclusions Combination of 1H-MRS with DTI can provide the valuable informationon the potential lesions in the thalamus in patients with SIVD. The Cho/Cr and MD values in the leftthalamus may be correlated with ex-ecutive function.

Vascular cognitive impairment refers to the learning and memory impairments caused by cerebrovascular lesions.Studies in recent years have shown that oxidative stress plays an important role in vascular cognitive impairment.This article reviews the mechanisms and the prevention and treatment of oxidative stress in vascular cognitive impairment.

Objective To investigate the expressions of protein kinase B (PKB/Akt) and glycogen synthase kinasc-3β in the hippocampus in mice with vascular dementia (VaD) induced by repetitive bilateral common carotid artery occlusion.Methods Forty-eight healthy adult male C57B1/6 mice were randomly allocated into 3 group:normal group,sham operation group,and model group (n =16 in each group).A mouse VaD model was induced by intermittent blocking the bilateral common carotid artery for 3 times in the model group.The sham group only separated the bilateral common carotid artery,but did not block it.The normal group did not receive any treatment.The behavioral changes of the mice were observed using the water maze and step-down tests at 4 weeks after procedure.HE staining was used to observe the histopathological changes of hippocampal tissue.The Western blotting was used to detect the expressions of Akt,p-Akt (Ser473),GSK3β and p-GSK3β (Ser9) proteins.Results In the water maze test,the time of swimming the entire distance was prolonged at the learning stage and memory stage (learning stage:F =19.389,P ＜0.05; memory stage:F =27.929,P ＜ 0.05),the number of errors increased (learning stage:F =7.228,P ＜ 0.05; memory stage:F =21.189,P＜0.05) in the model group.In the step-down test,the response time was prolonged (F=19.162,P ＜0.05) at learning stage and the number of errors increased (F =6.562,P ＜ 0.05),the latency time was shortened (F=10.634,P＜0.05) and the number of errors increased (F=12.890,P＜0.05) in the model group.At the same time,HE staining showed the reduction of neurons and the proliferation of glial cells in the hippocampal CA1 region in the model group; p-Akt (Ser473) (F=37.849,P＜0.05) and p-GSK3β (Ser9)(F =67.725,P ＜0.05) protein expressions were up-regulated significantly (F =37.849,P ＜0.05; F =67.725,P＜0.05) at 4 weeks after procedure compared to those in the sham operation group,while there were no significant differences in Akt (F =1.004,P ＞0.05) and GSK3β(F =0.329,P ＞0.05) total protein expressions among all groups.Conclusions The repetitive bilateral common carotid artery occlusion may result in learning and memory impairment and severe damage in the hippocampus in mice.The Akt and GSK3β expressions may be involved in the mechanism of VaD.

Vascular cognitive impairment (VCI) is a large class syndrome caused by a variety of cerebrovascular diseases from mild cognitive impairment to dementia.In the VCI animal experiments,choosing a reliable test method is particularly important for evaluating animal cognitive function and the improving the quality of animal models.

Ischemic cerebrovascular disease results in electrophysiological changes of the cerebral cortex.Magnetoencephalography (MEG) can objectively and sensitively detect cortical magnetic field.It has a very high temporal and spatial resolution,and locates the magnetic field source.At present,MEG is mainly used for the detection of spontaneous wave and the detection of somatosensory evoked magnetic fields,auditory evoked magnetic fields,visual evoked magnetic fields,and event-related magnetic fields,and provides valuable information for cortex function changes of ischemic cerebrovascular disease.However,further study is still needed.

Vascular cognitive impaiment (VCI) refers to a large class of clinical syndromes caused by vascular risk factors,obvious or not obvious cerebrovascular diseases from mild cognitive impairment to dementia.Looking for a physiologically controllable and repeatable animal model is critical for the systematic research of the VCI pathophysiological processes and the evaluation of new treatment methods.

Subcortical ischemic vascular disease (SIVD) is one of the most common subtypes in vascular cognitive impairment.This article reviews the research progress in the aspects of its pathogenesis,neuropsychological performance,imaging changes,and biological markers of SIVD.