129 research outputs found

    Are some brain injury patients improving more than ohers?

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    Predicting the evolution of individuals is a rather new mining task with applications in medicine. Medical researchers are interested in the progress of a disease and in the evolution of individuals subjected to treatment. We investigate the evolution of patients on the basis of medical tests before and during treatment after brain trauma: we want to understand how similar patients can become to healthy participants. We face two challenges. First, we have less information on healthy participants than on the patients. Second, the values of the medical tests for patients, even after treatment started, remain well-separated from those of healthy people; this is typical for neurodegenerative diseases, but also for further brain impairments. Our approach encompasses methods for modelling patient evolution and for predicting the health improvement of different patient subpopulations, dealing with the above challenges. We test our approach on a cohort of patients treated after brain trauma and a corresponding cohort of controls

    Data mining applied to the cognitive rehabilitation of patients with acquired brain injury

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    Acquired brain injury (ABI) is one of the leading causes of death and disability in the world and is associated with high health care costs as a result of the acute treatment and long term rehabilitation involved. Different algorithms and methods have been proposed to predict the effectiveness of rehabilitation programs. In general, research has focused on predicting the overall improvement of patients with ABI. The purpose of this study is the novel application of data mining (DM) techniques to predict the outcomes of cognitive rehabilitation in patients with ABI. We generate three predictive models that allow us to obtain new knowledge to evaluate and improve the effectiveness of the cognitive rehabilitation process. Decision tree (DT), multilayer perceptron (MLP) and general regression neural network (GRNN) have been used to construct the prediction models. 10-fold cross validation was carried out in order to test the algorithms, using the Institut Guttmann Neurorehabilitation Hospital (IG) patients database. Performance of the models was tested through specificity, sensitivity and accuracy analysis and confusion matrix analysis. The experimental results obtained by DT are clearly superior with a prediction average accuracy of 90.38%, while MLP and GRRN obtained a 78.7% and 75.96%, respectively. This study allows to increase the knowledge about the contributing factors of an ABI patient recovery and to estimate treatment efficacy in individual patients

    Artificial metaplasticity prediction model for cognitive rehabilitation outcome in acquired brain injury patients

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    Objective The main purpose of this research is the novel use of artificial metaplasticity on multilayer perceptron (AMMLP) as a data mining tool for prediction the outcome of patients with acquired brain injury (ABI) after cognitive rehabilitation. The final goal aims at increasing knowledge in the field of rehabilitation theory based on cognitive affectation. Methods and materials The data set used in this study contains records belonging to 123 ABI patients with moderate to severe cognitive affectation (according to Glasgow Coma Scale) that underwent rehabilitation at Institut Guttmann Neurorehabilitation Hospital (IG) using the tele-rehabilitation platform PREVIRNEC©. The variables included in the analysis comprise the neuropsychological initial evaluation of the patient (cognitive affectation profile), the results of the rehabilitation tasks performed by the patient in PREVIRNEC© and the outcome of the patient after a 3–5 months treatment. To achieve the treatment outcome prediction, we apply and compare three different data mining techniques: the AMMLP model, a backpropagation neural network (BPNN) and a C4.5 decision tree. Results The prediction performance of the models was measured by ten-fold cross validation and several architectures were tested. The results obtained by the AMMLP model are clearly superior, with an average predictive performance of 91.56%. BPNN and C4.5 models have a prediction average accuracy of 80.18% and 89.91% respectively. The best single AMMLP model provided a specificity of 92.38%, a sensitivity of 91.76% and a prediction accuracy of 92.07%. Conclusions The proposed prediction model presented in this study allows to increase the knowledge about the contributing factors of an ABI patient recovery and to estimate treatment efficacy in individual patients. The ability to predict treatment outcomes may provide new insights toward improving effectiveness and creating personalized therapeutic interventions based on clinical evidence

    Simplifying the use of prognostic information in traumatic brain injury. Part 2: Graphical Presentation of Probabilities

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    Objective: Clinical features such as those included in the Glasgow Coma Scale (GCS) score, pupil reactivity, and patient age, as well as CT findings, have clear established relationships with patient outcomes due to neurotrauma. Nevertheless, predictions made from combining these features in probabilistic models have not found a role in clinical practice. In this study, the authors aimed to develop a method of displaying probabilities graphically that would be simple and easy to use, thus improving the usefulness of prognostic information in neurotrauma. This work builds on a companion paper describing the GCS-Pupils score (GCS-P) as a tool for assessing the clinical severity of neurotrauma. Methods: Information about early GCS score, pupil response, patient age, CT findings, late outcome according to the Glasgow Outcome Scale, and mortality were obtained at the individual adult patient level from the CRASH (Corticosteroid Randomisation After Significant Head Injury; n = 9045) and IMPACT (International Mission for Prognosis and Clinical Trials in TBI; n = 6855) databases. These data were combined into a pooled data set for the main analysis. Logistic regression was first used to model the combined association between the GCS-P and patient age and outcome, following which CT findings were added to the models. The proportion of variability in outcomes “explained” by each model was assessed using Nagelkerke’s R2. Results: The authors observed that patient age and GCS-P have an additive effect on outcome. The probability of mortality 6 months after neurotrauma is greater with increasing age, and for all age groups the probability of death is greater with decreasing GCS-P. Conversely, the probability of favorable recovery becomes lower with increasing age and lessens with decreasing GCS-P. The effect of combining the GCS-P with patient age was substantially more informative than the GCS-P, age, GCS score, or pupil reactivity alone. Two-dimensional charts were produced displaying outcome probabilities, as percentages, for 5-year increments in age between 15 and 85 years, and for GCS-Ps ranging from 1 to 15; it is readily seen that the movement toward combinations at the top right of the charts reflects a decreasing likelihood of mortality and an increasing likelihood of favorable outcome. Analysis of CT findings showed that differences in outcome are very similar between patients with or without a hematoma, absent cisterns, or subarachnoid hemorrhage. Taken in combination, there is a gradation in risk that aligns with increasing numbers of any of these abnormalities. This information provides added value over age and GCS-P alone, supporting a simple extension of the earlier prognostic charts by stratifying the original charts in the following 3 CT groupings: none, only 1, and 2 or more CT abnormalities. Conclusions: The important prognostic features in neurotrauma can be brought together to display graphically their combined effects on risks of death or on prospects for independent recovery. This approach can support decision making and improve communication of risk among health care professionals, patients, and their relatives. These charts will not replace clinical judgment, but they will reduce the risk of influences from biases

    Hyperglycemia in bacterial meningitis: a prospective cohort study

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    ABSTRACT: BACKGROUND: Hyperglycemia has been associated with unfavorable outcome in several disorders, but few data are available in bacterial meningitis. We assessed the incidence and significance of hyperglycemia in adults with bacterial meningitis. METHODS: We collected data prospectively between October 1998 and April 2002, on 696 episodes of community-acquired bacterial meningitis, confirmed by culture of CSF in patients >16 years. Patients were dichotomized according to blood glucose level on admission. A cutoff random non-fasting blood glucose level of 7.8 mmol/L (140 mg/dL) was used to define hyperglycemia, and a cutoff random non-fasting blood glucose level of 11.1 mmol/L (200 mg/dL) was used to define severe hyperglycemia. Unfavorable outcome was defined on the Glasgow outcome scale as a score <5. We also evaluated characteristics of patients with a preadmission diagnosis of diabetes mellitus. RESULTS: 69% of patients were hyperglycemic and 25% severely hyperglycemic on admission. Compared with non-hyperglycemic patients, hyperglycemia was related with advanced age (median, 55 yrs vs. 44 yrs, P<0.0001), preadmission diagnosis of diabetes (9% vs. 3%, P=0.005), and distant focus of infection (37% vs. 28%, P=0.02). They were more often admitted in coma (16% vs. 8%; P=0.004) and with pneumococcal meningitis (55% vs. 42%, P=0.007). These differences remained significant after exclusion of patients with known diabetes. Hyperglycemia was related with unfavorable outcome (in a hockey stick-shaped curve) but this relation did not remain robust in a multivariate analysis. Factors predictive for neurologic compromise were related with higher blood glucose levels, whereas factors predictive for systemic compromise were related with lower blood glucose levels. Only a minority of severely hyperglycemic patients were known diabetics (19%). The vast majority of these known diabetic patients had meningitis due to Streptococcus pneumoniae (67%) or Listeria monocytogenes (13%) and they were at high risk for unfavorable outcome (52%). CONCLUSIONS: The majority of patients with bacterial meningitis have hyperglycemic blood glucose levels on admission. Hyperglycemia can be explained by a physical stress reaction, the central nervous system insult leading to disturbed blood-glucose regulation mechanisms, and preponderance of diabetics for pneumococcal meningitis. Patients with diabetes and bacterial meningitis are at high risk for unfavorable outcom

    Stratification of the severity of critically ill patients with classification trees

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    <p>Abstract</p> <p>Background</p> <p>Development of three classification trees (CT) based on the CART (<it>Classification and Regression Trees</it>), CHAID (<it>Chi-Square Automatic Interaction Detection</it>) and C4.5 methodologies for the calculation of probability of hospital mortality; the comparison of the results with the APACHE II, SAPS II and MPM II-24 scores, and with a model based on multiple logistic regression (LR).</p> <p>Methods</p> <p>Retrospective study of 2864 patients. Random partition (70:30) into a Development Set (DS) n = 1808 and Validation Set (VS) n = 808. Their properties of discrimination are compared with the ROC curve (AUC CI 95%), Percent of correct classification (PCC CI 95%); and the calibration with the Calibration Curve and the Standardized Mortality Ratio (SMR CI 95%).</p> <p>Results</p> <p>CTs are produced with a different selection of variables and decision rules: CART (5 variables and 8 decision rules), CHAID (7 variables and 15 rules) and C4.5 (6 variables and 10 rules). The common variables were: inotropic therapy, Glasgow, age, (A-a)O2 gradient and antecedent of chronic illness. In VS: all the models achieved acceptable discrimination with AUC above 0.7. CT: CART (0.75(0.71-0.81)), CHAID (0.76(0.72-0.79)) and C4.5 (0.76(0.73-0.80)). PCC: CART (72(69-75)), CHAID (72(69-75)) and C4.5 (76(73-79)). Calibration (SMR) better in the CT: CART (1.04(0.95-1.31)), CHAID (1.06(0.97-1.15) and C4.5 (1.08(0.98-1.16)).</p> <p>Conclusion</p> <p>With different methodologies of CTs, trees are generated with different selection of variables and decision rules. The CTs are easy to interpret, and they stratify the risk of hospital mortality. The CTs should be taken into account for the classification of the prognosis of critically ill patients.</p

    Control of hyperglycaemia in paediatric intensive care (CHiP): study protocol.

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    BACKGROUND: There is increasing evidence that tight blood glucose (BG) control improves outcomes in critically ill adults. Children show similar hyperglycaemic responses to surgery or critical illness. However it is not known whether tight control will benefit children given maturational differences and different disease spectrum. METHODS/DESIGN: The study is an randomised open trial with two parallel groups to assess whether, for children undergoing intensive care in the UK aged <or= 16 years who are ventilated, have an arterial line in-situ and are receiving vasoactive support following injury, major surgery or in association with critical illness in whom it is anticipated such treatment will be required to continue for at least 12 hours, tight control will increase the numbers of days alive and free of mechanical ventilation at 30 days, and lead to improvement in a range of complications associated with intensive care treatment and be cost effective. Children in the tight control group will receive insulin by intravenous infusion titrated to maintain BG between 4 and 7.0 mmol/l. Children in the control group will be treated according to a standard current approach to BG management. Children will be followed up to determine vital status and healthcare resources usage between discharge and 12 months post-randomisation. Information regarding overall health status, global neurological outcome, attention and behavioural status will be sought from a subgroup with traumatic brain injury (TBI). A difference of 2 days in the number of ventilator-free days within the first 30 days post-randomisation is considered clinically important. Conservatively assuming a standard deviation of a week across both trial arms, a type I error of 1% (2-sided test), and allowing for non-compliance, a total sample size of 1000 patients would have 90% power to detect this difference. To detect effect differences between cardiac and non-cardiac patients, a target sample size of 1500 is required. An economic evaluation will assess whether the costs of achieving tight BG control are justified by subsequent reductions in hospitalisation costs. DISCUSSION: The relevance of tight glycaemic control in this population needs to be assessed formally before being accepted into standard practice

    Traumatic brain injury and peripheral immune suppression: primer and prospectus

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    Nosocomial infections are a common occurrence in patients following traumatic brain injury (TBI) and are associated with an increased risk of mortality, longer length of hospital stay and poor neurological outcome. Systemic immune suppression arising as a direct result of injury to the central nervous system (CNS) is considered to be primarily responsible for this increased incidence of infection, a view strengthened by recent studies that have reported novel changes in the composition and function of the innate and adaptive arms of the immune system post TBI. However, our knowledge of the mechanisms that underlie TBI-induced immune suppression is equivocal at best. Here, after summarising our current understanding of the impact of TBI on peripheral immunity and discussing CNS-mediated regulation of immune function, we propose roles for a series of novel mechanisms in driving the immune suppression that is observed post TBI. These mechanisms, which have never been considered before in the context of TBI-induced immune paresis include the CNS-driven emergence into the circulation of myeloid derived suppressor cells and suppressive neutrophil subsets, and the release from injured tissue of nuclear and mitochondria-derived damage associated molecular patterns. Moreover, in an effort to further our understanding of the mechanisms that underlie TBI-induced changes in immunity, we pose throughout the review a series of questions, which if answered would address a number of key issues such as establishing whether manipulating peripheral immune function has potential as a future therapeutic strategy by which to treat and/or prevent infections in the hospitalised TBI patient
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