Vascular cognitive impairment(VCI)is a continuum including early cognitive impairment to dementia caused by cerebral vascular disease.VCI was introduced to identify cognitive decline in early stage for valid treatment.There is inconsistence about the cognitive impairment profile in VCI.This paper reviewed the neuropsychological features of VCI.The problems existed in researches were also discussed.

Objective To determine the cognitive profile of mild cognitive impairment due to subcortieal small vessel disease(MCI-SSVD)and mild cognitive impairment caused by Alzheimer's disease(MCI-AD)and to establish the best way of differentiating.Methods Extensive neuropsychological tests covenng 5 cognitive domains were performed on 45 MCI-SSVD patients,30 MCI-AD patients,and 61healthy controls.The impaired domains in patient groups were determined.Tests valuable in discriminating MCI-SSVD and MCI-AD were established using logistie regression analysis.Results Both patient groups showed impairments in multiple cognitive domains.The auditory verbal learning test immediate recall(control group 55.48±5.33;MCI-SSVD group 38.55±8.04;MCI-AD group 34.93±8.79;F=113.407,P=0.000),short time delayed recall(control group 13.34±1.38;MCI-SSVD group 8.47±2.18;MCI-AD group 4.06±2.87;F=216.284,P=0.000),and long time delayed recall(control group13.18±1.19;MCI-SSVD group 8.58±2.02;MCI-AD group 3.93±2.84;F=239.394,P=0.000)impaired most.Compared with MCI-SSVD,MCI-AD patients did worse in memory assessments(P=0.000),but better in mental processing and visuoconstruction(P=0.000-0.023).Two tests tapping memory and processing speed in combination could identify 93.3%MCI-SSVD patients and 93.3% MCI-AD patients correctly.Conclusions Current study indicates that both MCI-SSVD and MCI-AD,varying significantly in memory and mental processing speed,have a multiple-domain cognitive deficit,with memory impaired most seriously.Tests involving these 2 domains might be useful in differentiating MCI-SSVD from MCI-AD.

OBJECTIVE: To investigate the mechanism of the pulmonary injury in rats caused by chronic intermittent hypoxia (CIH) and to investigate the intervention effect of Edaravone. METHOD: Ninety-six male Wistar rats were divided into four groups randomly: the control group (NC), chronic intermittent hypoxia group (CIH), chronic intermittent hypoxia normal saline matched group (NS), chronic intermittent hypoxia edaravone treatment group (NE). The four groups were also divided into 1, 2, 3, 4 W time subgroups, and each time subgroup had 6 rats. After the experiment, sections of pulmonary were stained with hematoxylin-eosin (HE) and the level of SOD, MDA, PO2 and Ang II mRNA in rat homogenate pulmonary were measured. RESULT: Pulmonary histology revealed that the CIH group showed high levels of interstitial edema, alveolar atelectasis, inflammatory cell infiltration of alveolar epithelial cell, pulmonary injury were serious in 1, 2, 3, 4 W. But the pulmonary histology of the UC group and the NS group was normal. Compared with the NS group, pulmonary injury of NE group 1, 2, 3, 4 W, significantly decreased. Compared with the NC group, the levels of PO2 in the CIH group were decreased; while the compared with the NS group, the levels of PO2 in the NE group were increased. Compared with the UC group and NS group, the levels of Ang II mRNA in each time point in CIH group were increased gradually (P < 0.05), the content of MDA were increased in 1, 2, 3, 4 W (P < 0.05), they had reached the peak all at 4 W; while the SOD in each time point in CIH group were decreased gradually (P < 0.05) compared with that in UC group and NS group; The Ang II mRNA levels of CIH in pulmonary showed positive correlation with MDA [r = 0.782,P < 0.01]; while the Ang II mRNA levels of CIH in pulmonary showed negative correlation with SOD [r = - 0.904, P < 0.01]. CONCLUSION CIH can cause pulmonary injury through oxidative stress and activating Ang II, and Edaravone could prevent pulmonary injury induced by CIH through scavenging oxygen free radicals.
Angiotensin II ; metabolism ; Animals ; Antipyrine ; analogs & derivatives ; pharmacology ; Edaravone ; Free Radical Scavengers ; metabolism ; Hypoxia ; physiopathology ; Lung ; pathology ; Lung Injury ; physiopathology ; Male ; Malondialdehyde ; metabolism ; Oxidative Stress ; Rats ; Rats, Wistar ; Superoxide Dismutase ; metabolism

Objective To explore the clinical,neuroimage,and neuropsychological profiles of semantic dementia (SD).Methods Detailed medical history were collected on 18 SD patients.Brain MRI scans were administered.Neuropsychological evaluation taping semantic memory (things naming),overall cognitive function ( Mini-mental State Examination,MMSE),visuoconstructive skill ( Clock Drawing Test,CDT), daily functional ability (Activities of Daily Living, ADL), neuropsychiatric symptoms (Neuropsychiatric Inventory,NPI),and disease severity (Frontotemporal Lobar Degeneration Modified Clinical Dementia Rating Scale,FTLD-CDR) were performed on all patients.Results The mean age at onset was (60.6 ± 8.5 ) years,with 5 cases over 65. All patients developed progressive word-finding difficulty and anomic speech.Ten patients complained significant memory impairment and 14 experienced behavioral disturbance.Five patients were previously diagnosed as Alzheimer' s disease (AD) and 1 as schizophrenia.All patients developed marked semantic memory impairment both for living things and nonliving things.The mean score on MMSE was 10.94 ± 8.86,with 16 cases performed incorrectly on naming.Mean score on CDT copy was 4.61 ±0.85,with 14 cases scored normally.Mean score on ADL was 29.72 ± 8.75.Cases with a 5-year course showed a significant overall decline.Fourteen cases presented behavior symptoms and scored 8.00 ± 7.22 on NPI.All patients scored worst on language domain among all the domains evaluated in FTLD-CDR.Atrophy,typically involving the left anterior temporal was shown on MRI scans.However,predominantly right temporal atrophy was observed in one patient.Atrophy confined to the temporal lobe in patients with early stage and extended to the contralateral temporal,frontal lobe,and parietal lobe as disease progression. Conclusions Current study suggested that SD tend to develop in presenile age.However,about 1/3 cases develop the disease after 65 years. Deficit in language is the earliest and most prominent symptom. Behavior change is prevalent as well. Patients are commonly misdiagnosed as AD or lack a definite diagnosis.Visuoconstructive skill and other abilities are relatively preserved in the early stage.With progression into the 5th years,overall decline comes inevitably.Brain scans can reflect the disease characteristics and progression. Of note,there exists individual with right dominant atrophy.

Objective To review the experience of multiple modality endovascular treatment for intracranial venous thrombosis, and to evaluate the efficacy and risk of endovascular thrombolysis for intracranial venous thrombosis.Methods From October, 2000 to October, 2001, 12 patients with intracranial venous thrombosis confirmed by CT, MRI, MRV, and/or DSA were treated with multiple modality endovascular thrombolysis including intravenous thrombolysis, mechanical thrombus maceration, intraarterial thrombolysis, and stenting.After thrombolysis, treatment aimed at the primary diseases was continued and warfarin was used for 6 months.The patients were followed-up for 17-29 months, averaged 23 months.Results Of the twelve patients, all underwent transvenous thrombolysis, ten underwent combined transvenous thrombolysis and clot maceration, seven underwent transvenous infusion of urokinase combined with transarterial infusion of urokinase.Two underwent transvenous infusion of urokinase combined with transarterial infusion of urokinase.The thrombolysis duration was from one to three days.The infusion dose of urokinase was 800 000 to 2 900 000 IU, the averaging dosage of urokinase was less than 1 000 000 IU per day.All patients achieved from recanalization of sinuses as confirmed on postprocedural angiography, MRI, and MRV studies prior to hospital discharge.At discharge, all the patients improved neurologically, and GCS improved from averaged 12 of pre-operation to 14 of post-operation.During the averaging 23 months follow-up, no patient recurred. Conclusion Combined multiple modality endovascular treatment is an effective and safe procedure for potentially catastrophic intracranial venous thrombosis.