The present study aimed to summarize the clinical characteristics and experiences of misdiagnoses of cerebral venous thrombosis (CVT). A total of 18 patients with CVT who received treatment between September 2009 and August 2011 were enrolled. Of the patients, 13 were females and 5 were males with an average age of 39 years. Clinical manifestations and characteristics according to cerebrospinal fluid examination and imaging were summarized retrospectively. CVT principally manifested as headaches, papilledema, psychiatric symptoms, impaired consciousness and seizure disorders, with or without neurological defects. A combination of magnetic resonance imaging (MRI) and venography (MRV) was demonstrated to be an effective method for CVT diagnosis. Of the 18 patients, 8 were misdiagnosed, as a result of the lack of further examination due to undefined etiology, atypical clinical manifestations and ambiguous neuroimaging direct signs. The clinical symptoms of CVT are aspecific, as a result of which misdiagnosis tends to occur. For patients with intracranial hypertension accompanied with or without neurological defects, MRI combined with MRV can improve the accuracy of CVT diagnosis.

BackgroundEarly diagnosis of tuberculous meningitis (TBM) is still a challenge; the present study aimed to establish a method of detecting the antigen early secreted antigenic target 6 (ESAT-6) in cerebrospinal fluid (CSF) by an indirect enzyme-linked immunosorbance assay (ELISA) protocol and to study the value of detecting ESAT-6 in CSF in the early diagnosis of TBM.MethodsAn indirect ELISA protocol was used, employing a monoclonal antibody (mAb) against ESAT-6, which was used to demonstrate ESAT-6 in the CSF from TBM patients and non-TBM controls. CSF was obtained from 100 patients: confirmed TBM, clinically diagnosed TBM, disease controls, and healthy controls (n = 10). Pure recombinant ESAT-6 (standard product) was used in serial dilutions to detect the absorbance and to establish a standard curve from the data; the concentration was on the X axis vs. absorbance on the Y axis, and the standard curve was used to interpolate the concentration of ESAT-6 in samples.ResultsThe indirect ELISA method provided 88 % sensitivity and 92 % specificity for the diagnosis of TBM using a mAb to ESAT-6. The mean concentration of ESAT-6 in TBM patients was significantly higher than that of the non-TBM groups. There was also a significant difference in the mean ESAT-6 expression between the confirmed TBM patients and the clinically diagnosed TBM patients (p < 0.01).ConclusionsDetection of ESAT-6 in the CSF of TBM patients by indirect ELISA protocol gives a reliable early diagnosis and can be used to develop an immunodiagnostic assay with increased sensitivity and specificity.

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Background and Purpose: Whether imaging parameters would independently predict stroke recurrence in low-risk minor ischemic stroke (MIS) or transient ischemic attack (TIA) according to traditional score system (such as ABCD 2 score, which was termed on the basis of the initials of the five factors: age, blood pressure, clinical features, duration, diabetes) remains unclear. We sought to evaluate the association between imaging parameters and 1-year stroke recurrence in patients with TIA or MIS in different risk stratum stratified by ABCD 2 score. Methods: We included patients with TIA and MIS (National Institutes of Health Stroke Scale score ≤3) with complete baseline vessel and brain imaging data from the Third China National Stroke Registry III. Patients were categorized into different risk groups based on ABCD 2 score (low risk, 0–3; moderate risk, 4–5; and high risk, 6–7). The primary outcome was stroke recurrence within 1 year. Multivariable Cox proportional-hazards regression models were used to assess whether imaging parameters (large artery stenosis, infarction number) were independently associated with stroke recurrence. Results: Of the 7140 patients included, 584 patients experienced stroke recurrence within 1 year. According to the ABCD 2 score, large artery stenosis was associated with higher stroke recurrence in both low-risk (adjusted hazard ratio, 1.746 [95% CI, 1.200–2.540]) and moderate-risk group (adjusted hazard ratio, 1.326 [95% CI, 1.042–1.687]) but not in the high-risk group ( P >0.05). Patients with multiple acute infarctions or single acute infarction had a higher risk of recurrent stroke than those with no infarction in both low- and moderate-risk groups, but not in the high-risk group. Conclusions: Large artery stenosis and infarction number were independent predictors of 1-year stroke recurrence in low-moderate risk but not in high-risk patients with TIA or MIS stratified by ABCD 2 score. This finding emphasizes the importance of early brain and vascular imaging evaluation for risk stratification in patients with TIA or MIS.

Background: The purpose of this study was to investigate the impact of fucoidan (FUC) on the oxidative stress response and lysosomal apoptotic pathways in the Parkinson disease (PD) cell model.Methods: The Dopaminergic nerve precursor cell line(MN9D) cells that served as a PD model in this study underwent damage induced by 100 μM 1-methyl-4-phenyl pyridine (MPP+). Cell viability was assessed after FUC treatment and intracellular SOD GSH was measured via immunofluorescence assay. Cellular changes in cathepsin D, Autophagy marker Light Chain 3-II (LC3-II), and apoptotic protein Bax were assessed by Western blot. The expression of Cat D, LC3-II, and B cell lymphoma-2-associated x protein (Bax) was also measured after addition of the cathepsin inhibitor, pepstatin A.Results: The results indicated that MN9D cell viability decreased by 50% within 24 h after 100 μM MPP+ induced toxicity. Pretreatment with 100 μM Fucoidan reduced cellular expression of LC3-II and CatD in 3 h and suppressed the induction of Bax protein. After pepstatin A treatment, Bax expression was significantly downregulated.FUC reversed the reduction of superoxide dismutase (SOD) L-Glutathione(GSH), decreased cell viability, and apoptosis induced by MPP+ in 6 h, suggesting that Fucoidan can attenuate damage to MN9D cells induced by MPP+.Conclusions: Fucoidan protected lysosomes, reduced the expression of LC3-II, inhibited the expression of CatD-Bax and the oxidative stress response, suppressed apoptosis, and thus conferred protective effects for dopaminergic neural cells. FUC may have neuroprotective effects on PD and further research is needed.