Our study has shown that Turkish stroke survivors have sexual health needs during the rehabilitation process, though this has not been addressed previously. Sexual health needs seem to be affected by cultural factors and biases.

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We found no data in the literature related to oxidative stress index (OSI), total oxidative status (TOS) and prolidase activity in patients with diabetic neuropathy (DN). In this study, we aimed to evaluate the oxidative status of DN patients via measurement of TOS and serum total antioxidant status (TAS) and estimation of OSI using new automated methods. Thirty-eight healthy participants, 40 diabetic patients without neuropathy, and 39 patients with DN were included. Electrophysiological and neurological examinations were performed. The activity of prolidase and levels of TOS and TAS were determined in the serum of patients. The level of TAS was lower, while the levels of TOS and OSI, and activity of prolidase were higher in both DN and diabetic control groups compared with the healthy subjects (p < 0.05). Prolidase activity was found to be higher in the DN group than in the diabetic control group (p = 0.001). In conclusion, the presence of high TOS and OSI levels together with low levels of TAS in diabetic patients with or without neuropathy may support a role of oxidative stress in the pathogenesis of diabetes mellitus. In addition, increased serum prolidase activity in DN may be interpreted as evidence of increased collagen turnover.

We found serum albumin levels were significantly lower and the NLR was significantly higher in the acute period of CSE. Neutrophil-mediated inflammation may be important in the aetiopathogenesis of CSE.

Many studies in the literature have clearly shown the increase in creatine kinase-myocardial subfraction (CK-MB) levels and changes in electrocardiography (ECG) after stroke. However, the studies on cardiac troponin T (cTnT) which is more sensitive and specific to myocardium after stroke are relatively scarce. Moreover, its associations with volume of stroke lesions and type of stroke have not been investigated thoroughly. Thus, the aims of this study were to investigate a predictive value of cTnT in assessing myocardial injury and cardiac dysfunction in different types of stroke (hemorrhagic or ischemic stroke) and its relationship with stroke size and volume. This study included 62 patients (30 males and 32 females) with acute stroke confirmed by computed tomography (CT). Blood samples were obtained within 24 hours of stroke onset to measure the serum levels of creatin kinase (CK), CK-MB, lactate dehydrogenate (LDH), and cTnT. ECG and echocardiography were performed to assess myocardial function and left ventricular ejection fraction (LVEF). Of all patients included in the study, 20 patients (32%) demonstrated elevations in cTnT, while 28 patients (45%) had increased CK-MB levels. Serum levels of cTnT were positively correlated with stroke volume (r = 0.65, p < 0.0001), while inversely correlated with LVEF (r = −0.53, p < 0001). Serum levels of both CK-MB and cTnT were higher in patients with hemorrhagic stroke than those with ischemic stroke but this difference was not significant (p > 0.05). As a conclusion, cTnT has a higher specificity and sensitivity in detecting myocardial injury after stroke of both ischemic and hemorrhagic origins. Measurement of the serum levels of cTnT is of clinical importance in evaluating myocardial injury and provides a useful aid in estimating the volume of stroke lesions. cardiac troponin T; creatine kinase-MB; stroke; myocardial injury; stroke volume © 2005 Tohoku University Medical PressStroke is defined as the primer pathology of brain vascular system that temporarily or permanently affects brain functions as a result of ischemia or hemorrhage. Due to consequent high mortality and morbidity rates, stroke is to become a major community health problem for whole

This study investigated correlations between mortality, stroke subtype and stroke severity with serum osteoprotegerin (OPG) and S-100 protein levels prior to the treatment of patients admitted to the emergency department and diagnosed with ischaemic stroke. Pretreatment serum samples were collected from patients (n = 90) to determine OPG and S-100 protein levels. Age- and sex-matched healthy individuals (n = 16) served as controls. Compared with controls, OPG and S-100 protein levels were significantly higher in the cardioembolic and atherothrombotic stroke groups. Within the stroke group, OPG levels were significantly higher in the cardioembolic and atherothrombotic stroke groups compared with the transient ischaemic attack (TIA) group. S-100 protein levels were significantly higher in the atherothrombotic stroke group than in the lacunar stroke and TIA groups, and in the cardioembolic stroke group compared with the lacunar stroke group. Serum OPG and S-100 protein levels were significantly higher in patients who died compared with survivors. In predicting stroke subtype and severity, although both OPG and S-100 protein levels were indicators, S-100 protein was more valuable for mortality prediction.

Chemotherapeutic drugs are the most common toxic agents for peripheral nerves. Vincristine is a vinca alkaloid drug that is used for the treatment of several malignancies in combination with other chemotherapeutic agents. Treatment with intravenous (IV) vincristine at doses above 5 mg leads to a dose-dependent neuropathy with sensory symptoms but higher cumulative doses at around 30 to 50 mg are needed for the development of motor symptoms. The standard maximum adult IV vincristine dose is 2 mg IV per dose given at weekly intervals. However, administration of a single 2-mg dose IV vincristine may rarely result in the development of peripheral neuropathy. Few case reports have been presented on vincristine-associated severe paralysis in patients with preexisting hereditary neuropathy like Charcot-Marie Tooth (CMT) disease, who received doses even lower than 2 mg. Herein, we reported a Hodgkin lymphoma patient who developed severe polyneuropathy after receiving 2 mg vincristine treatment and was subsequently found to carry the CMT1A duplication responsible for CMT disease.