Takotsubo Cardiomyopathy in Traumatic Brain Injury

Background

Takotsubo cardiomyopathy (TC) is a well-known complication after aneurysmal subarachnoid hemorrhage and has been rarely described in patients with traumatic brain injury (TBI).

Methods

Case report and review of literature.

Results

Here, we report a 73-year-old woman with mild traumatic brain injury (TBI) presenting in cardiogenic shock. Takotsubo cardiomyopathy (TC) was diagnosed by repeated echocardiography. Cardiovascular support by inotropic agents led to hemodynamic stabilization after initiation of levosimendan. Cardiac function fully recovered within 21 days. We performed an in-depth literature review and identified 16 reported patients with TBI and TC. Clinical course and characteristics are discussed in the context of our patient.

Conclusion

Takotsubo cardiomyopathy is under-recognized after TBI and may negatively impact outcome if left untreated.

     

Association of Early Hemodynamic Profile and the Development of Systolic Dysfunction Following Traumatic Brain Injury

Background

While systolic dysfunction has been observed following traumatic brain injury (TBI), the relationship between early hemodynamics and the development of systolic dysfunction has not been investigated. Our study aimed to determine the early hemodynamic profile that is associated with the development of systolic dysfunction after TBI.

Methods

We conducted a prospective cohort study among patients under 65 years old without cardiac comorbidities who sustained moderate–severe TBI. Transthoracic echocardiography was performed within the first day after TBI to assess for systolic dysfunction. Hourly systolic blood pressure (SBP), mean arterial pressure (MAP), heart rate, and confounding clinical variables (sedatives, fluid balance, vasopressors, and osmotherapy) were collected during the first 24 h following admission. Multivariable linear mixed models assessed the early hemodynamic profile in patients who developed systolic dysfunction, compared to patients who did not develop systolic dysfunction.

Results

Thirty-two patients were included, and 7 (22 %) developed systolic dysfunction after TBI. Patients who developed systolic dysfunction experienced early elevation of SBP, MAP, and heart rate, compared to patients who did not develop systolic dysfunction (p < 0.01 for all comparisons). Patients who developed systolic dysfunction experienced a greater rate of decrease in SBP [?10.2 mmHg (95 % CI ?16.1, ?4.2)] and MAP [?9.1 mmHg (95 % CI ?13.9, ?4.3)] over the first day of hospitalization, compared to patients who did not develop systolic dysfunction (p < 0.01 for both comparisons). All sensitivity analyses revealed no substantial changes from the primary model.

Conclusions

Patients who develop systolic dysfunction following TBI have a distinctive hemodynamic profile, with early hypertension and tachycardia, followed by a decrease in blood pressure over the first day after TBI. This profile suggests an early maladaptive catecholamine-excess state as a potential underlying mechanism of TBI-induced systolic dysfunction.

     

Progesterone Provides the Pleiotropic Neuroprotective Effect on Traumatic Brain Injury Through the Nrf2/ARE Signaling Pathway

Objective

This study was to investigate the role of Nrf2/ARE signaling pathway in the pleiotropic neuroprotective effect of progesterone (PROG) on traumatic brain injury (TBI).

Methods

The Nrf2-knockout (Nrf2?/?) and C57 mice were respectively subjected to a lateral cortical impact injury caused by a free-falling object and randomly divided into three groups: sham-operated, trauma, and trauma + PROG treatment group. The PROG treatment group was given PROG (32 mg/kg of body weight, intraperitoneal injection) immediately after injury. For all groups, a series of brain samples were obtained after trauma at 24 and 72 h, respectively. The cerebral edema was evaluated; the expression of IL-1β, IL-6, and TNF-α was measured using ELISA array, and the apoptosis index was detected by TUNEL. Flow cytometry was used to detect the intracellular calcium concentration.

Results

The water content, the apoptosis index, the levels of inflammatory cytokine, and the intracellular calcium ion were significantly decreased with the PROG treatment in C57 mice with TBI model. However, the effect of PROG on TBI was not found in the Nrf2?/? mouse model of TBI.

Conclusions

PROG reduced cerebral edema, apoptosis, inflammatory reaction, and intracellular calcium ion overload effects after TBI. These beneficial effects were not seen in the Nrf2?/? mouse model of TBI. The results from this study suggested that the Nrf2/ARE signal pathway may be involved in the pleiotropic neuroprotective effect of PROG on TBI.

     

Severe Leukoaraiosis Portends a Poor Outcome After Traumatic Brain Injury

Background and Purpose

It is now well accepted that traumatic white matter injury constitutes a critical determinant of post-traumatic functional impairment. However, the contribution of preexisting white matter rarefaction on outcome following traumatic brain injury (TBI) is unknown. Hence, we sought to determine whether the burden of preexisting leukoaraiosis of presumed ischemic origin is independently associated with outcome after TBI.

Methods

We retrospectively analyzed consecutive, prospectively enrolled patients of ≥50 years (n = 136) who were admitted to a single neurological/trauma intensive care unit. Supratentorial white matter hypoattenuation on head CT was graded on a 5-point scale (range 0–4) reflecting increasing severity of leukoaraiosis. Outcome was ascertained according to the modified Rankin Scale (mRS) and Glasgow outcome scale (GOS) at 3 and 12 months, respectively.

Results

After adjustment for other factors, leukoaraiosis severity was significantly associated with a poor outcome at 3 and 12 months defined as mRS 3–6 and GOS 1–3, respectively. The independent association between leukoaraiosis and poor outcome remained when the analysis was restricted to patients who survived up to 3 months, had moderate-to-severe TBI [enrollment Glasgow Coma Scale (GCS) ≤12; p = 0.001], or had mild TBI (GCS 13–15; p = 0.002), respectively.

Conclusion

We provide first evidence that preexisting cerebral small vessel disease independently predicts a poor functional outcome after closed head TBI. This association is independent of other established outcome predictors such as age, comorbid state as well as intensive care unit complications and interventions. This knowledge may help improve prognostic accuracy, clinical management, and resource utilization.

     

Thromboelastography After Murine TBI and Implications of Beta-Adrenergic Receptor Knockout

Background

The source of coagulopathy in traumatic brain injury (TBI) is multifactorial and may include adrenergic stimulation. The aim of this study was to assess coagulopathy after TBI using thromboelastography (TEG), and to investigate the implications of β-adrenergic receptor knockout.

Methods

Adult male wild type c57/bl6 (WT) and β₁/β₂-adrenergic receptor knockout (BKO) mice were assigned to either TBI (WT-TBI, BKO-TBI) or sham injury (WT-sham, BKO-sham). Mice assigned to TBI were subject to controlled cortical impact (CCI). At 24 h post-injury, whole blood samples were obtained and taken immediately for TEG.

Results

At 24 h after injury, a trend toward increased fibrinolysis was seen in WT-TBI compared to WT-sham although this did not reach significance (EPL 8.1 vs. 0 %, p = 0.18). No differences were noted in fibrinolysis in BKO-TBI compared to BKO-sham (LY30 2.6 vs. 2.5 %, p = 0.61; EPL 3.4 vs. 2.9 %, p = 0.61). In addition BKO-TBI demonstrated increased clot strength compared to BKO-sham (MA 76.6 vs. 68.6, p = 0.03; G 18.2 vs. 11.3, p = 0.03).

Conclusions

In a mouse TBI model, WT mice sustaining TBI demonstrated a trend toward increased fibrinolysis at 24 h after injury while BKO mice did not. These findings suggest β-blockade may attenuate the coagulopathy of TBI and minimize progression of intracranial hemorrhage by reducing fibrinolysis and increasing clot strength.

     

Sleep Disturbance After TBI

Purpose of Review

Present relevant literature to update knowledge on sleep science, identify common sleep disturbances seen in TBI, discuss evidence for available treatment options, and illuminate future areas for research.

Recent Findings

Sleep disturbances, including insomnia, circadian rhythm disturbances, and sleep apnea, are prevalent for all severities of traumatic brain injury (TBI), can be chronic, and affect both rehabilitation and recovery from the TBI.

Summary

New knowledge of basic sleep mechanisms and neurochemistry has exploded in the last decade. In addition to known effects on mood and cognition from sleep deprivation in persons with TBI, new evidence indicates potential deleterious effects on neurorecovery and acceleration of long-term neurodegeneration.

     

Systemic Inflammatory Response Syndrome (SIRS) Score Independently Predicts Poor Outcome in Isolated Traumatic Brain Injury

Introduction

Systemic inflammatory response syndrome (SIRS) is frequently observed after various types of acute cerebral injury and has been linked to clinical deterioration in non-traumatic brain injury (TBI). SIRS scores have also been shown to be predictive of length of stay and mortality in trauma patients. We aimed to determine the prognostic utility of SIRS present at admission in trauma patients with isolated TBI.

Methods

This was a 5-year retrospective cohort study of adults (≥18 years) with isolated TBI admitted to a Level II trauma center. The prognostic value of SIRS, total SIRS scores, and each SIRS criterion was examined by Χ ² and logistic regression analyses.

Results

Of the 330 patients identified, 50 (15.2%) met SIRS criteria. SIRS was significantly associated with poor outcome (P < 0.001). Relative risk of poor outcome was 2.7 times higher in patients with a SIRS score of 2 on admission (P = 0.007) and increased significantly to 6.5 times in patients with a SIRS score of 3 (P = 0.002). Logistic regression demonstrated SIRS and each criterion to be significant independent prognostic factors (SIRS, P = 0.030; body temperature, P = 0.006; tachypnea, P = 0.022, tachycardia P = 0.023).

Conclusion

SIRS at admission is an independent predictor of poor outcome in isolated TBI patients. These data demonstrate SIRS to be an important clinical tool that may be used in facilitating prognostication, particularly in elderly trauma patients. Future prospective studies aimed at therapeutic interventions to mitigate SIRS in TBI patients are warranted.

Level of Evidence

Prognostic, Level III.

     

Autophagy Biomarkers Beclin 1 and p62 are Increased in Cerebrospinal Fluid after Traumatic Brain Injury

Background

Autophagy is a process that recycles damaged proteins and organelles. Beclin 1 is involved in the nucleation phase, while p62 is consumed during the elongation phase. We hypothesized that these autophagy biomarkers are increased in cerebrospinal fluid (CSF) after traumatic brain injury (TBI) in children and associated with unfavorable outcome.

Methods

Thirty children with severe TBI had CSF collected on days 1, 3, and 7. Patients without TBI or meningoencephalitis served as controls. Beclin 1 and p62 were measured by ELISA. Outcome was assigned 6 months after injury (Glasgow Outcome Scale score; GOS).

Results

Mean and peak CSF beclin 1 and p62 levels were increased compared to controls (P < 0.05). Peak p62 levels were higher in patients with unfavorable versus favorable outcome (0.79 ± 1.03 vs. 0.17 ± 0.54 ng/ml, respectively; mean ± SD, P = 0.002) and were independently associated with outcome when controlling for age and initial Glasgow Coma Scale score (P = 0.019; AUC 0.88, 95% CI 0.76, 1.00).

Conclusions

Beclin 1 and p62 are increased in CSF after TBI, suggesting increased autophagy with impairment of, and/or exceeding the capacity for, autophagic flux. The association of increased p62 with unfavorable outcome suggests that autophagy in excess of the capacity to clear degradation products may be deleterious after TBI.

     

Relationship of Coagulopathy and Platelet Dysfunction to Transfusion Needs After Traumatic Brain Injury

Background

Coagulopathy and platelet dysfunction commonly develop after traumatic brain injury (TBI). Thromboelastography (TEG) and platelet function assays (PFAs) are often performed at the time of admission; however, their roles in assessing post-TBI coagulopathy have not been investigated. We hypothesized that compared to blunt TBI, penetrating TBI would (1) demonstrate greater coagulopathy by TEG, (2) be associated with abnormal PFA results, and (3) require more blood product transfusions.

Methods

We performed a retrospective study of patients admitted to the neuroscience intensive care unit of a level 1 trauma center from 2013 to 2015 with head Abbreviated Injury Scale ≥3. Patients were compared by mechanism of injury (blunt vs. penetrating). Admission demographics, injury characteristics, and laboratory parameters were evaluated. VerifyNow^® Aspirin and P2Y12 tests were used for platelet function analysis.

Results

Five hundred and thirty-four patients were included in the analysis. There were no differences between groups in platelet count or international normalized ratio; however, patients with penetrating TBI were more coagulopathic by TEG, with all of the TEG parameters being significantly different except for R time. Patients with penetrating head trauma were not more likely than their blunt counterparts to have abnormal PFA results, and PFA results did not correlate with any TEG parameter in either group. The penetrating cohort received more units of blood products in the first 4 and 24 h than the blunt cohort.

Conclusions

Patients presenting with penetrating TBI demonstrated increased coagulopathy compared to those with blunt TBI as measured by TEG and need for transfusion. PFA results did not correlate with TEG findings in this population.

     

Further Controversies About Brain Tissue Oxygenation Pressure-Reactivity After Traumatic Brain Injury

Background

Continuous monitoring of cerebral autoregulation is considered clinically useful due to its ability to warn against brain ischemic insults, which may translate to a relationship with adverse outcome. It is typically performed using the pressure reactivity index (PRx) based on mean arterial pressure and intracranial pressure. A new ORx index based on brain tissue oxygenation and cerebral perfusion pressure (CPP) has been proposed that similarly allows for evaluation of cerebrovascular reactivity. Conflicting results exist concerning its clinical utility.

Methods

Retrospective analysis was performed in 85 patients with traumatic brain injury (TBI). ORx was calculated using three time windows of 5, 20, and 60 min. Correlation coefficients and individual “optimal CPP” (CPP_opt) were calculated using both PRx and ORx, and relation to patient outcome investigated.

Results

Correlation coefficients for all comparisons between PRx and ORx indicated poor association between these indices (range from ?0.04 to 0.07). PRx was significantly lower in patients with good outcome (p = 0.01), while none of the ORx indices proved to be significantly different in the two outcome groups. Higher mortality related to average CPP < CPP_opt was found regardless of which index was used to calculate CPP_opt.

Conclusion

In the TBI setting, ORx does not appear to correlate with vascular pressure reactivity as assessed with PRx. Its potential use for individualizing CPP thresholds remains unclear.

     

Cerebrospinal Fluid NLRP3 is Increased After Severe Traumatic Brain Injury in Infants and Children

Background

Inflammasome-mediated neuroinflammation may cause secondary injury following traumatic brain injury (TBI) in children. The pattern recognition receptors NACHT domain-, Leucine-rich repeat-, and PYD-containing Protein 1 (NLRP1) and NLRP3 are essential components of their respective inflammasome complexes. We sought to investigate whether NLRP1 and/or NLRP3 abundance is altered in children with severe TBI.

Methods

Cerebrospinal fluid (CSF) from children (n = 34) with severe TBI (Glasgow coma scale score [GCS] ≤8) who had externalized ventricular drains (EVD) placed for routine care was evaluated for NLRP1 and NLRP3 at 0–24, 25–48, 49–72, and >72 h post-TBI and was compared to infection-free controls that underwent lumbar puncture to rule out CNS infection (n = 8). Patient age, sex, initial GCS, mechanism of injury, treatment with therapeutic hypothermia, and 6-month Glasgow outcome score were collected.

Results

CSF NLRP1 was undetectable in controls and detected in 2 TBI patients at only <24 h post-TBI. CSF NLRP3 levels were increased in TBI patients compared with controls at all time points, p < 0.001. TBI patients ≤4 years of age had higher peak NLRP3 levels versus patients >4 (15.50 [3.65–25.71] vs. 3.04 [1.52–8.87] ng/mL, respectively; p = 0.048). Controlling for initial GCS in multivariate analysis, peak NLRP3 >6.63 ng/mL was independently associated with poor outcome at 6 months.

Conclusions

In the first report of NLRP1 and NLRP3 in childhood neurotrauma, we found that CSF NLRP3 is elevated in children with severe TBI and independently associated with younger age and poor outcome. Future studies correlating NLRP3 with other markers of inflammation and response to therapy are warranted.

     

Onset of bladder and motor symptoms in multiple system atrophy: differences according to phenotype

Purpose

To compare the order of presentation of bladder and motor symptoms between multiple system atrophy phenotypes.

Methods

Medical records were retrospectively reviewed in 144 patients.

Results

Bladder symptoms occurred either before or within 12 months after onset of motor symptoms in significantly more patients with the cerebellar phenotype than the parkinsonian phenotype (80 vs. 53%, p = 0.003); similar results were observed for urinary incontinence (79 vs. 45%, p = 0.001).

Conclusions

Urinary dysfunction is more likely to appear either before or shortly after motor symptoms in the cerebellar phenotype than in the parkinsonian phenotype.

     

In-Hospital Mortality with Use of Percutaneous Endoscopic Gastrostomy in Traumatic Brain Injury Patients: Results of a Nationwide Population-Based Study

Background

Percutaneous endoscopic gastrostomy (PEG) is a frequently performed invasive procedure that has been associated with high short-term mortality. Its use of special interest in traumatic brain injury (TBI) patients as nutrition support constitutes important issues in intensive care of this group. We used a national database to determine the incidence of, and factors associated with, in-hospital mortality among TBI patients undergoing PEG.

Methods

We conducted a retrospective study using the US nationwide inpatient sample to analyze data from all hospitalizations in 2008 with International Classification of Diseases, Ninth Revision, diagnostic and procedure codes identifying patients with TBI and hemorrhagic stroke who received PEG. Bivariate and multivariate logistic regression analyses were performed using demographic and clinical variables to identify predictors of in-hospital mortality in this patient population. Patients who did not undergo PEG were used as control.

Results

In-hospital mortality after PEG was 6% (95% CI, 0.05–0.76%) among the TBI population with 0.2% occurring in the first 7 days and 2% occurring in the first 14 days. These patients had a higher incidence of other trauma-related comorbidities and were classified as high-risk stratification based on SRRi score compared to the non-PEG group. Factors strongly predictive of in-hospital mortality were age >51 years, not receiving a PEG, and having a high comorbidity burden of >2.

Conclusion

Understanding the rate of mortality associated with PEG in this patient population and identifying factors that increase and decrease the risk of death will improve patient selection for those most likely to benefit from this procedure.

     

Structure,Process, and Culture Differences of Pediatric Trauma Centers Participating in an International Comparative Effectiveness Study of Children with Severe Traumatic Brain Injury

Background

Traumatic brain injury (TBI) is an important worldwide cause of death and disability for children. The Approaches and Decisions for Acute Pediatric TBI (ADAPT) Trial is an observational, cohort study to compare the effectiveness of six aspects of TBI care. Understanding the differences between clinical sites—including their structure, clinical processes, and culture differences—will be necessary to assess differences in outcome from the study and can inform the overall community regarding differences across academic centers.

Methods

We developed a survey and queried ADAPT site principal investigators with a focus on six domains: (i) hospital, (ii) pediatric intensive care unit (PICU), (iii) medical staff characteristics, (iv) quality of care, (v) medication safety, and (vi) safety culture. Summary statistics were used to describe differences between centers.

Results

ADAPT clinical sites that enrolled a subject within the first year (32 US-based, 11 international) were studied. A wide variation in site characteristics was observed in hospital and ICU characteristics, including an almost sevenfold range in ICU size (8–55 beds) and more than fivefold range of overall ICU admissions (537–2623). Nursing staffing (predominantly 1:1 or 1:2) and the presence of pharmacists within the ICU (79 %) were less variable, and most sites “strongly agreed” or “agreed” that Neurosurgery and Critical Care teams worked well together (81.4 %). However, a minority of sites (46 %) used an explicit protocol for treatment of children with severe TBI care.

Conclusions

We found a variety of inter-center structure, process, and culture differences. These intrinsic differences between sites may begin to explain why interventional studies have failed to prove efficacy of experimental therapies. Understanding these differences may be an important factor in analyzing future ADAPT trial results and in determining best practices for pediatric severe TBI.

     

A Self-Regulatory Intervention for Patients with Head and Neck Cancer: Pilot Randomized Trial

Background

Research is yet to investigate whether psychological interventions delivered early after diagnosis can benefit patients with head and neck cancer (HNC).

Purpose

The aim of this study was to investigate the effectiveness of a brief self-regulatory intervention (targeting illness perceptions and coping) at improving HNC patient health-related quality of life (HRQL).

Methods

A pilot randomized controlled trial was conducted, in which 64 patients were assigned to receive three sessions with a health psychologist in addition to standard care or standard care alone. Participants completed questionnaires assessing HRQL, general distress, and illness perceptions at baseline and again 3 and 6 months later.

Results

Compared to the control group, patients who received the intervention had increased treatment control perceptions at 3 months (p = .01), and increased social quality of life at 6 months (p = .01). The intervention was particularly helpful for patients exhibiting distress at baseline.

Conclusion

A brief psychological intervention following HNC diagnosis can improve patient perceptions of treatment and social quality of life over time. Such interventions could be targeted to patients who are distressed in order to confer the greatest benefit.

Trial Registration Number

12614000813684.

     

Suicidal deaths in elementary school students in Korea

Background

The purpose of this study was to determine the characteristics of childhood suicidal deaths among elementary school students that occurred from 2011 to 2015 in Korea.

Methods

The report form of each suicide case by the teacher in charge to the Education Ministry was reviewed retrospectively.

Results

There were 19 suicidal deaths (12 boys, 7 girls) in elementary school students. The youngest case was a third grader (n = 1). Jumping from heights (n = 12) was the most frequently used method. Most suicides (n = 12) were committed in their homes.

Conclusion

These results highlight the alarming trend of early suicidal deaths and the importance of early suicide prevention strategies, especially in schools.

     

Sensory Sensitivity in TBI: Implications for Chronic Disability

Purpose of Review

This review investigates the relationship between sensory sensitivity and traumatic brain injury (TBI), and the role sensory sensitivity plays in chronic disability.

Recent Findings

TBI is a significant cause of disability with a range of physical, cognitive, and mental health consequences. Sensory sensitivities (e.g., noise and light) are among the most frequently reported, yet least outwardly recognizable symptoms following TBI. Clinicians and scientists alike have yet to identify consistent nomenclature for defining noise and light sensitivity, making it difficult to accurately and reliably assess their influence. Noise and light sensitivity can profoundly affect critical aspects of independent function including communication, productivity, socialization, cognition, sleep, and mental health.

Summary

Research examining the prevalence of sensory sensitivity and evidence for the association of sensory sensitivity with TBI is inconclusive. Evidence-based interventions for sensory sensitivity, particularly following TBI, are lacking.

     

EEG Monitoring and Antiepileptic Drugs in Children with Severe TBI

Background

Traumatic brain injury (TBI) causes substantial morbidity and mortality in US children. Post-traumatic seizures (PTS) occur in 11–42% of children with severe TBI and are associated with unfavorable outcome. Electroencephalographic (EEG) monitoring may be used to detect PTS and antiepileptic drugs (AEDs) may be used to treat PTS, but national rates of EEG and AED use are not known. The purpose of this study was to describe the frequency and timing of EEG and AED use in children hospitalized after severe TBI.

Methods

Retrospective cohort study of 2165 children at 30 hospitals in a probabilistically linked dataset from the National Trauma Data Bank (NTDB) and the Pediatric Health Information Systems (PHIS) database, 2007–2010. We included children (age <18 years old at admission) with linked NTDB and PHIS records, severe (Emergency Department [ED] Glasgow Coma Scale [GCS] <8) TBI, hospital length of stay >24 h, and non-missing disposition. The primary outcomes were EEG and AED use.

Results

Overall, 31.8% of the cohort had EEG monitoring. Of those, 21.8% were monitored on the first hospital day. The median duration of EEG monitoring was 2.0 (IQR 1.0, 4.0) days. AEDs were prescribed to 52.0% of the cohort, of whom 61.8% received an AED on the first hospital day. The median duration of AED use was 8.0 (IQR 4.0, 17.0) days. EEG monitoring and AED use were more frequent in children with known risk factors for PTS. EEG monitoring and AED use were not related to hospital TBI volume.

Conclusion

EEG use is relatively uncommon in children with severe TBI, but AEDs are frequently prescribed. EEG monitoring and AED use are more common in children with known risk factors for PTS.

     

Neuroleptic Malignant Syndrome: Complications,Outcomes, and Mortality

Objective

Our study objective was to identify real-world rates of complications, mortality, and outcomes in patients with neuroleptic malignant syndrome (NMS) over the last decade in the United States.

Methods

A total of 1346 patients were obtained from the nationwide inpatient sample for the years 2002–2011. Common complications known to be associated with NMS were identified. Multivariable regression analyses were used to identify predictors of mortality.

Results

The most prevalent complication was rhabdomyolysis (30.1 %). Other common complications were acute respiratory failure (16.1 %), acute kidney injury (17.7 %), sepsis (6.2 %), and other systemic infections. Unadjusted mortality rate was 5.6 %. Older age, acute respiratory failure, acute kidney injury, sepsis, and comorbid congestive heart failure were significant predictors of mortality. Acute respiratory failure was the strongest independent mortality predictor (p < 0.001).

Conclusion

In our large sample population-based study on NMS, we were able to identify the rates of several preselected complications and the mortality. The identification of independent mortality predictors in this study can guide physicians in the management and prognostication of this rare syndrome.

     

Monetary Incentive Interventions Can Enhance Psychological Factors Related to Fruit and Vegetable Consumption

Background

Incentive interventions have gained popularity to motivate health behavior change, but some psychological theorists caution that they may have deleterious effects on factors that potentiate behavior maintenance. Importantly, no empirical study has tested whether incentives indeed have iatrogenic effects on key psychological constructs associated with health behavior change and maintenance.

Purpose

The study aims to explore the effects of monetary incentives on theoretically informed psychological constructs and fruit and vegetable consumption.

Methods

Individuals reporting insufficient fruit and vegetable consumption were randomly assigned to receive either daily monetary incentives, delayed monetary incentives, or no incentives for their fruit and vegetable consumption during a 3-week intervention period. Behavior engagement and psychological factors were measured at baseline, at the end of the intervention, and 2 weeks following the cessation of the intervention.

Results

Participants in the daily incentive condition demonstrated the greatest increase in self-reported consumption during the intervention and at the follow-up. Moreover, increases in consumption during the intervention period were associated with increases in attitudes and self-efficacy, which, in turn, predicted behavior maintenance at follow-up. Intrinsic motivation to consume fruits and vegetables increased over time across the entire sample but did not differ between groups.

Conclusions

Monetary incentives can alter health behavior engagement without decreasing intrinsic motivation or other relevant cognitive and motivational constructs. Further, although incentives may serve as a vehicle to initiate behavior change, increased experience with the behavior may then lead to enhancements in key psychological constructs that serve as mechanisms to potentiate behavior maintenance following the cessation of incentives.

Trial Registration Number

The trial was registered with the ClinicalTrials.gov database (NCT02594319) https://www.clinicaltrials.gov/ct2/show/NCT02594319.