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David Thaler

Publications and source records attributed to David Thaler.

3 recordsLinked to original sources

Decreased levels of plasma vitamin C and increased concentrations of inflammatory and oxidative stress markers after stroke.

BACKGROUND AND PURPOSE: Inflammatory response is a critical component of the complex pathophysiological response to stroke. Vitamin C has been shown to have important roles in cell performance and vascular function. In this study, we compared the nutritional status and levels of inflammatory markers between stroke cases and controls and assessed which antioxidant was associated with levels of inflammatory markers and oxidative stress among cases and controls. METHODS: We evaluated the nutritional status and measured plasma levels of vitamins C and E, uric acid, serum levels of C-reactive protein (CRP), the cytokines tumor necrosis factor-alpha and interleukin-1beta, intercellular adhesion molecule-1 (ICAM-1) and chemokine monocyte chemoattractant protein-1 (MCP-1), prostaglandins PGE2 and PGI2, and 8-isoprostanes (8-epiPGF2alpha) for 15 patients with ischemic stroke within 2 to 5 days after stroke onset and for 24 control subjects. RESULTS: Stroke patients had significantly lower plasma levels of vitamin C than did controls. Among stroke patients, CRP was significantly elevated, as were the ICAM-1, MCP-1, and 8-epiPGF2alpha, but the prostaglandins PGE2 and PGI2 were significantly reduced. Interestingly, vitamin C concentration was significantly inversely correlated with the levels of CRP and 8-epiPGF2alpha among stroke patients, and 8-epiPGF2alpha was significantly associated with the levels of CRP. Uric acid was also elevated among stroke patients. CONCLUSIONS: Lower vitamin C concentration, higher serum levels of inflammatory (CRP, ICAM-1, MCP-1) and oxidative stress (8-epiPGF2alpha) markers, and lower PGI2 and PGE2 concentrations among stroke patients indicate the presence of an inflammatory response associated with stroke.

Aged↗

Transcatheter closure of patent foramen ovale associated with paradoxical embolism using the amplatzer PFO occluder: initial and intermediate-term results of the U.S. multicenter clinical trial.

Closure of patent foramen ovale (PFO) has been proposed as an alternative to anticoagulation in patients with presumed paradoxical emboli. We report the immediate and mid-term results of the phase 1 U.S. Multicenter Clinical Trial of patients who underwent transcatheter PFO closure for paradoxical embolism using the new Amplatzer PFO device. Fifty patients (28 male/22 female) underwent catheter closure of their PFOs at a mean age of 41 +/- 11 years. Thirty-six patients had ischemic stroke, 10 had transient ischemic attack, and 4 had peripheral embolism. Seventeen patients had atrial septal aneurysm. The implantation procedure was successful in 49/49 patients; one patient did not have a PFO. Complete closure was seen immediately after the procedure in 26/49 patients; 17 had minimal residual shunt, 4 had moderate and 2 had large residual shunts. The median fluoroscopy time was 10.5 min (2.8-43 min). There were no complications related to the device. One patient developed an arteriovenous fistula at the catheter site requiring surgical repair. At a mean follow-up interval of 16.5 +/- 7.2 months, there were no deaths or recurrent neurological or peripheral embolic events. Eight patients reported an episode of dizziness or palpitations (four of them within 18 days of the procedure). No episodes of atrial dysrhythmias were noted. Contrast bubble study at last follow-up documented complete closure in 45/48 patients; one patient had minimal, one had moderate residual shunt, and one had a large shunt. One patient was lost to follow-up. We conclude that catheter closure of PFO associated with stroke/transient ischemic attack or peripheral embolism using the new Amplatzer PFO device is a safe and effective method in preventing recurrence of such episodes. Randomized clinical trials comparing device closure versus continued medical therapy are underway.

Adult↗

Case report: hypoglycemia and diffusion-weighted imaging.

The effect of severe hypoglycemia on the brain is well known, ranging from alterations of mental status to profound coma and death. We describe a case of global diffusion abnormalities eventually resulting in death. This otherwise healthy patient presented with seizures and a serum glucose level less than 20 mg/dL. Testing suggested that the hypoglycemia was likely caused by exogenous insulin or perhaps insulin receptor antibodies. Magnetic resonance imaging on the day after admission showed regions of restricted diffusion in the temporal and occipital lobes as well as in the basal ganglia. Despite the large body of literature concerning the pathophysiology of hypoglycemia and its clinical implications, little is known regarding its radiologic correlations.

Brain↗