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Unconsciousness clinical trials

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NCT ID: NCT01011192 Completed - Unconsciousness Clinical Trials

Performance of Two Different ke0s in the Same Pharmacokinetic Propofol Model

Start date: September 2009
Phase: N/A
Study type: Observational

The aim of this study was to assess the clinical performance of two different ke0s (fast and slow) in terms of propofol effect-site concentration (Ce) during the loss and recovery of consciousness, using Marsh's pharmacokinetic model.The hypothesis to be tested was that the Ce of propofol predicted by the slow ke0 in the loss and recovery of consciousness is similar, differently from the fast ke0.

NCT ID: NCT00869154 Completed - Clinical trials for Traumatic Brain Injury With Brief Loss of Consciousness

Multidisciplinary Treatment in Patients With Mild Traumatic Brain Injury

Start date: March 1, 2009
Phase: N/A
Study type: Interventional

The aim of the study is to compare a multidisciplinary examination and follow up by rehabilitation program with a multidisciplinary examination, good advice and follow up by the family doctor. Further on we will examine if there were differing clinical characteristics between patients who attended a planned follow-up session and those that failed to and Prognostic factors in mild traumatic brain injury patients after discharge from hospital.

NCT ID: NCT00793741 Completed - Type 1 Diabetes Clinical Trials

Measurement of Glucose Metabolism in Humans Using Magnetic Resonance at 4 Tesla. Substudy: Hypoglycemia Unawareness

Start date: December 2007
Phase: N/A
Study type: Observational

The purpose of this study is to determine whether islet transplantation alters brain glucose concentrations in patients with type 1 diabetes, recurrent hypoglycemia, and hypoglycemia unawareness when compared to that measured prior to transplant in the same subjects.

NCT ID: NCT00160056 Completed - Diabetes Clinical Trials

The Effect of Antecedent Hypoglycaemia on β2-adrenergic Sensitivity

Start date: April 2005
Phase: N/A
Study type: Interventional

Hypoglycaemia unawareness is a common complication in patients with type 1 diabetes and with insulin-treated type 2 diabetes of long duration. The loss of autonomic symptoms to hypoglycemia does not solely depend on loss of adrenaline responses.Differences in sensitivity to catecholamines may also be involved. Reconciling the data on β2-adrenergic receptor polymorphism to those on loss of β-adrenergic sensitivity in diabetic patients with hypoglycemia unawareness, we hypothesize that hypoglycemia unawareness is at least partly the result of desensitization of the β2-adrenergic receptor and that patients who are homozygous for arginine at codon 16 are particularly susceptible for this desensitization process, whereas patients who are homozygous for glycine at codon 16 are resistant for desensitization. Objectives 1. To determine whether, and if so to what extent, antecedent hypoglycemia reduces β2-adrenergic sensitivity in healthy subjects with Arg16 homozygosity. 2. To investigate whether or not healthy subjects with Gly16 homozygosity are resistant to desensitization 3. To confirm that antecedent hypoglycemia reduces the heart rate response to isoproterenol and to assess to what extent this reduced response is mediated by impairments in baroreflex sensitivity.