ObjectiveCerebral venous sinus thrombosis (CVST) is a rare cerebrovascular disease affecting young adults. The majority of the patients are female. The aim of this study is to assess the clinical associations, risk factors and outcomes of the patients with CVST.MethodsThe data of 75 patients with CVST admitted to our hospital between 2006 and 2016 were reviewed. Demographic and clinical features and the thrombophilic risk factors of the patients were recorded. The localizations of the thrombi were determined and modified Rankin score at the time of onset and discharge were calculated.ResultsThe majority of our patients (78.7%) were female. Median age was 35 years (16–76). The most common symptom was headache (86.7%). In 82.6% of our patients, inherited or acquired risk factors for thrombosis were detected. Transverse sinus was the most common site of thrombosis followed by sigmoid and superior sagittal sinuses. Two thirds of the patients had involvement of multiple sinuses. The patients with the involvement of sagittal sinus had better disability at the time of admittance (p = 0.013) while the number of involved sinuses was correlated worse disability (p = 0.015). The neurologic states in the majority of the patients were improved by the end of the hospitalization period (p = 0.001). There was no significant difference in disability score at discharge between men and women (p = 0.080). No patient with CVST died in the hospitalization period.ConclusionsThis study is one of the largest cohort studies on CVST in our region. The results of the study disclosed that CVST had wide range of clinical manifestations and non-specific symptoms at the beginning. For that reason, in especially high risk groups for thrombosis, the diagnosis of CVST should be kept in mind.
Parkinson's disease (PD) is one of the common neurodegenerative disorders. Oxidative stress is considered as a contributing factor to the development of PD. The present study aims to investigate serum oxidative stress status in patients with PD. Oxidative stress was assessed by measuring serum nitric oxide levels, lipid hydroperoxide concentrations, and nitric oxide synthase activity. In addition, total serum antioxidant capacity (TAC) was evaluated using the serum 2,2-Diphenyl-1-picryl-hydrazyl (DPPH) free-radical scavenging method in 32 patient with Parkinson's disease and 32 control subjects. Our results indicated that serum nitric oxide and lipid hydroperoxide levels were significantly lower in patients with PD than controls. Moreover, nitric oxide levels were found to be negatively correlated with Unified Parkinson's Disease Rating Scale (UPDRS). However, no statistical difference was observed in total serum antioxidant capacities and nitric oxide synthase activities between patients and controls. The present study indicates that although antioxidant capacity was not changed, lipid hydroperoxide (LPO) level was found decreased. This might show pre-oxidative process in these patients. In addition, decreased nitric oxide (NO) level and negative correlation observed between NO level and disease rating scale implicated a role for NO in the disease process.
Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by loss of dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc). Oxidative stress has been hypothesized to play a major role in the development of PD in various studies. This study assessed to investigate oxidative and anti-oxidative status in PD patients. We evaluated oxidant/antioxidant status by measuring serum malondialdehyde (MDA) levels, xanthine oxidase (XO) activities, and activities of antioxidant enzymes, namely, glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD). The study included 29 patients with PD and 32 healthy subjects as controls. Comparison of oxidative parameters in the patient and control groups revealed significantly higher GSH-Px and XO activities in the patient group. Serum MDA and SOD activities in PD patients were not significantly different from the controls. MDA was negatively correlated with duration of the PD and positively with age of onset. There was a negative correlation between SOD and Hoehn and Yahr (H&Y) stage. According to these results, we suggest that oxidative stress may contribute to the development of PD.
MG has an increased frequency of coexisting ADs. Autoantibodies that are characteristic for ADs can be found in the patients without the presence of any of the clinical findings of ADs. Clinical attention towards the management of ADs is especially needed during the follow-up of patients with MG.
Small fiber neuropathy (SFN), due to loss of A-delta and unmyelinated C fibers, is a cause of neuropathic pain. Although the patients with vitamin B12 deficiency are included in SFN studies in the literature, there is no histopathological study investigating the small fiber loss solely in patients with vitamin B12 deficiency. In this pilot study, we aim to demonstrate the intraepidermal nerve fiber density (IENFD) in skin punch biopsy of patients with vitamin B12 deficiency. Ten patients with vitamin B12 deficiency suffering from neuropathic pain and as control group ten patients with vitamin B12 deficiency without neuropathic pain were included. Neurological examination, electrophysiological evaluation, and DN4 questionnaire were performed. Subsequently, skin punch biopsy 10 cm above the lateral malleolus was done. The biopsy samples were stained with PGP9.5 antibody, and IENFD was determined. IENFD was low in two groups compared to their age normative values. The median of IENFD was 3.345 (1.12-5.32) in patients with neuropathic pain and 6. 20 (4.6-9.8) in controls (p < 0.001). Our pilot study showed that vitamin B12 deficiency causes symptomatic as well as asymptomatic small fiber loss like diabetes mellitus.
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