Effort Test Performance in Non-litigating Brain Injury Populations

Over recent years there has been increasing interest in personal gain as a threat to the validity of neuropsychological testing. As a result, clinicians have begun to use specialist measures in an attempt to identify how much ‘effort’ a person is putting in and therefore whether they may be feigning or exaggerating their difficulties. Such effort tests have become commonplace within a medico-legal context and their use is also increasing within clinical settings. However, thorough investigation of the performance and classification accuracy of such measures is limited and questions have been raised regarding the rates of false positives in clinical populations. Assessing how people with genuine injuries perform on effort tests is critical for the valid interpretation of test scores, as clinicians have a duty of care not to label people as having a brain injury if they are malingering, or diagnosing someone as malingering when they have a genuine brain injury or are legitimately unwell. Therefore, the current thesis investigated the base rates of failure on a number of effort tests in a genuinely brain-injured population with no identifiable incentives to feign in order to provide further evaluation of the measures. The main focus was on the Word Memory Test, as the author claims that this measure is “virtually insensitive to all but the most extreme forms of impairment of learning and memory” (Green, Lees-Haley & Allen, 2002, p. 99).A total of 47 participants were recruited to the study, including 20 people in residential community rehabilitation services, 16 outpatients with intractable epilepsy, and 11 people in post-acute inpatient rehabilitation. Each participant was administered a battery of tests, including measures of effort, pre-morbid IQ, memory, speed of processing, and mood. Analyses of pass/fail rates across effort tests indicated that the rates of false positives within a genuine clinical sample with no incentive to feign were much higher than those proposed within the validation research of the tests. In addition, further statistical analyses identified a number of factors that contributed to scores on tests in addition to effort. Relationships with these factors varied depending on the particular effort test being assessed, with significant associations being identified with memory, depression, processing speed, age and participant subgroup. These findings are consistent with recent research that suggests people with genuine brain injuries can fail effort tests for reasons related to ability rather than effort. The implications for clinical assessment and intervention are discussed, and potential future research is suggested

Soluble GPVI is elevated in injured patients: shedding is mediated by fibrin activation of GPVI

Soluble glycoprotein VI (sGPVI) is shed from the platelet surface and is a marker of platelet activation in thrombotic conditions. We assessed sGPVI levels together with patient and clinical parameters in acute and chronic inflammatory conditions, including patients with thermal injury and inflammatory bowel disease and patients admitted to the intensive care unit (ICU) for elective cardiac surgery, trauma, acute brain injury, or prolonged ventilation. Plasma sGPVI was measured by enzyme-linked immunosorbent assay and was elevated on day 14 after thermal injury, and was higher in patients who developed sepsis. sGPVI levels were associated with sepsis, and the value for predicting sepsis was increased in combination with platelet count and Abbreviated Burn Severity Index. sGPVI levels positively correlated with levels of D-dimer (a fibrin degradation product) in ICU patients and patients with thermal injury. sGPVI levels in ICU patients at admission were significantly associated with 28- and 90-day mortality independent of platelet count. sGPVI levels in patients with thermal injury were associated with 28-day mortality at days 1, 14, and 21 when adjusting for platelet count. In both cohorts, sGPVI associations with mortality were stronger than D-dimer levels. Mechanistically, release of GPVI was triggered by exposure of platelets to polymerized fibrin, but not by engagement of G protein-coupled receptors by thrombin, adenosine 5′-diphosphate, or thromboxane mimetics. Enhanced fibrin production in these patients may therefore contribute to the observed elevated sGPVI levels. sGPVI is an important platelet-specific marker for platelet activation that predicts sepsis progression and mortality in injured patients.The research was part funded by the National Institute for Health Research (NIHR) Surgical Reconstruction and Microbiology Research Centre. The authors also thank the Scar Free Foundation and the British Heart Foundation for funding. S.P.W. holds a BHF Chair (CH/03/003/15571). This project was initiated during a sabbatical visit by E.E.G. supported by the Institute for Advanced Studies at the University of Birmingham. The project was also supported by funding from National Health and Medical Research Council Australia and the Fonds National pour la Recherche Scientifique Belgium (FNRS-FRSM 3.4611.11, CDR J.0043.13) and by the French Community of Belgium (FSRC-12/13, ARC-SF 12/14-05). C.L. was a postdoctoral researcher at the FNRS. C.D. was supported by a “Fond pour la recherche industrielle et agricole” fellowship. C.O. is a senior research associate at the Fonds National pour la Recherche Scientifique

Soluble GPVI is elevated in injured patients: shedding is mediated by fibrin activation of GPVI.

Soluble glycoprotein VI (sGPVI) is shed from the platelet surface and is a marker of platelet activation in thrombotic conditions. We assessed sGPVI levels together with patient and clinical parameters in acute and chronic inflammatory conditions, including patients with thermal injury and inflammatory bowel disease and patients admitted to the intensive care unit (ICU) for elective cardiac surgery, trauma, acute brain injury, or prolonged ventilation. Plasma sGPVI was measured by enzyme-linked immunosorbent assay and was elevated on day 14 after thermal injury, and was higher in patients who developed sepsis. sGPVI levels were associated with sepsis, and the value for predicting sepsis was increased in combination with platelet count and Abbreviated Burn Severity Index. sGPVI levels positively correlated with levels of D-dimer (a fibrin degradation product) in ICU patients and patients with thermal injury. sGPVI levels in ICU patients at admission were significantly associated with 28- and 90-day mortality independent of platelet count. sGPVI levels in patients with thermal injury were associated with 28-day mortality at days 1, 14, and 21 when adjusting for platelet count. In both cohorts, sGPVI associations with mortality were stronger than D-dimer levels. Mechanistically, release of GPVI was triggered by exposure of platelets to polymerized fibrin, but not by engagement of G protein-coupled receptors by thrombin, adenosine 5'-diphosphate, or thromboxane mimetics. Enhanced fibrin production in these patients may therefore contribute to the observed elevated sGPVI levels. sGPVI is an important platelet-specific marker for platelet activation that predicts sepsis progression and mortality in injured patients

UMD Clark Engineering WIE Science and Technology Policy Papers

Science and Technology Policy Papers produced by students enrolled in the Women in Engineering program Flexus/Virtus living learning community for women, men, and non-binary engineering students

Health-status outcomes with invasive or conservative care in coronary disease

BACKGROUND In the ISCHEMIA trial, an invasive strategy with angiographic assessment and revascularization did not reduce clinical events among patients with stable ischemic heart disease and moderate or severe ischemia. A secondary objective of the trial was to assess angina-related health status among these patients. METHODS We assessed angina-related symptoms, function, and quality of life with the Seattle Angina Questionnaire (SAQ) at randomization, at months 1.5, 3, and 6, and every 6 months thereafter in participants who had been randomly assigned to an invasive treatment strategy (2295 participants) or a conservative strategy (2322). Mixed-effects cumulative probability models within a Bayesian framework were used to estimate differences between the treatment groups. The primary outcome of this health-status analysis was the SAQ summary score (scores range from 0 to 100, with higher scores indicating better health status). All analyses were performed in the overall population and according to baseline angina frequency. RESULTS At baseline, 35% of patients reported having no angina in the previous month. SAQ summary scores increased in both treatment groups, with increases at 3, 12, and 36 months that were 4.1 points (95% credible interval, 3.2 to 5.0), 4.2 points (95% credible interval, 3.3 to 5.1), and 2.9 points (95% credible interval, 2.2 to 3.7) higher with the invasive strategy than with the conservative strategy. Differences were larger among participants who had more frequent angina at baseline (8.5 vs. 0.1 points at 3 months and 5.3 vs. 1.2 points at 36 months among participants with daily or weekly angina as compared with no angina). CONCLUSIONS In the overall trial population with moderate or severe ischemia, which included 35% of participants without angina at baseline, patients randomly assigned to the invasive strategy had greater improvement in angina-related health status than those assigned to the conservative strategy. The modest mean differences favoring the invasive strategy in the overall group reflected minimal differences among asymptomatic patients and larger differences among patients who had had angina at baseline

Initial invasive or conservative strategy for stable coronary disease

BACKGROUND Among patients with stable coronary disease and moderate or severe ischemia, whether clinical outcomes are better in those who receive an invasive intervention plus medical therapy than in those who receive medical therapy alone is uncertain. METHODS We randomly assigned 5179 patients with moderate or severe ischemia to an initial invasive strategy (angiography and revascularization when feasible) and medical therapy or to an initial conservative strategy of medical therapy alone and angiography if medical therapy failed. The primary outcome was a composite of death from cardiovascular causes, myocardial infarction, or hospitalization for unstable angina, heart failure, or resuscitated cardiac arrest. A key secondary outcome was death from cardiovascular causes or myocardial infarction. RESULTS Over a median of 3.2 years, 318 primary outcome events occurred in the invasive-strategy group and 352 occurred in the conservative-strategy group. At 6 months, the cumulative event rate was 5.3% in the invasive-strategy group and 3.4% in the conservative-strategy group (difference, 1.9 percentage points; 95% confidence interval [CI], 0.8 to 3.0); at 5 years, the cumulative event rate was 16.4% and 18.2%, respectively (difference, 121.8 percentage points; 95% CI, 124.7 to 1.0). Results were similar with respect to the key secondary outcome. The incidence of the primary outcome was sensitive to the definition of myocardial infarction; a secondary analysis yielded more procedural myocardial infarctions of uncertain clinical importance. There were 145 deaths in the invasive-strategy group and 144 deaths in the conservative-strategy group (hazard ratio, 1.05; 95% CI, 0.83 to 1.32). CONCLUSIONS Among patients with stable coronary disease and moderate or severe ischemia, we did not find evidence that an initial invasive strategy, as compared with an initial conservative strategy, reduced the risk of ischemic cardiovascular events or death from any cause over a median of 3.2 years. The trial findings were sensitive to the definition of myocardial infarction that was used