Infant Modified Constraint-Induced Movement Therapy Paired With Neuromuscular Electrical Stimulation: A Feasibility Study.

PURPOSE: To determine the feasibility of modified constraint-induced movement therapy (mCIMT) paired with neuromuscular electrical stimulation (NMES) for infants with asymmetrical hand function (AHF). METHODS: Five infants received an experimental ABA design: (A1) 3 weeks of our Standard AHF Care, (B) 3 weeks mCIMT-NMES, and (A2) 3 weeks of our Standard AHF Care. Parents tracked key data in a daily log, and infants were assessed 4 times using the Hand Assessment for Infants and Peabody Developmental Motor Scale-2. RESULTS: There was a high level of participant enrollment, visit frequency adherence, and compliance with the treatment protocol. No adverse events were reported. Mean Hand Assessment for Infants Both Hands measure scores changed more after mCIMT-NMES than after our Standard AHF Care. CONCLUSIONS: mCIMT-NMES is a feasible early intervention for infants with AHF at risk for unilateral cerebral palsy. A future study in a larger sample should examine the efficacy of mCIMT-NMES in this population.

Characterizing the effects of muscle-specific GSK3α/ß reduction on murine muscle contractility and metabolism in female mice.

Dysregulation of skeletal muscle morphology and metabolism is associated with chronic diseases such as obesity and type 2 diabetes. The enzyme glycogen synthase kinase 3 (GSK3) is highly involved in skeletal muscle physiology and metabolism, acting as a negative regulator of muscle size, strength, adaptive thermogenesis, and glucose homeostasis. Correspondingly, we have shown that partial knockdown (∼40%) of GSK3 specifically in skeletal muscle increases lean mass, reduces fat mass, and activates muscle-based adaptive thermogenesis via sarco(endo)plasmic reticulum Ca2+ (SERCA) uncoupling in male mice. However, the effects of GSK3 knockdown in female mice have yet to be investigated. Here, we examined the effects of muscle-specific GSK3 knockdown on body composition, muscle size and strength, and whole body metabolism in female C57BL/6J mice. Our results show that GSK3 content is higher in the female soleus versus the male soleus; however, there were no differences in the extensor digitorum longus (EDL). Furthermore, muscle-specific GSK3 knockdown did not alter body composition in female mice, nor did it alter daily energy expenditure, glucose/insulin tolerance, mitochondrial respiration, or the expression of the SERCA uncouplers sarcolipin and neuronatin. We also did not find any differences in soleus muscle size, strength, or fatigue resistance. In the EDL, we found that an increase in absolute and specific force production, but there were no differences in fatigability. Therefore, our study highlights sex differences in the response to genetic reduction of gsk3, with most of the effects previously observed in male mice being absent in females.NEW & NOTEWORTHY Here we show that partial GSK3 knockdown has minimal effects on whole body metabolism and muscle contractility in female mice. This is partly inconsistent with previous results found in male mice, which reveal a potential influence of biological sex.

Influence of metabolic stress and metformin on synaptic protein profile in SH-SY5Y-derived neurons.

Insulin resistance (IR) is associated with reductions in neuronal proteins often observed with Alzheimer's disease (AD), however, the mechanisms through which IR promotes neurodegeneration/AD pathogenesis are poorly understood. Metformin (MET), a potent activator of the metabolic regulator AMPK is used to treat IR but its effectiveness for AD is unclear. We have previously shown that chronic AMPK activation impairs neurite growth and protein synthesis in SH-SY5Y neurons, however, AMPK activation in IR was not explored. Therefore, we examined the effects of MET-driven AMPK activation with and without IR. Retinoic acid-differentiated SH-SY5Y neurons were treated with: (1) Ctl: 24 h vehicle followed by 24 h Vehicle; (2) HI: 100 nM insulin (24 h HI followed by 24 h HI); or (3) MET: 24 h vehicle followed by 24 h 2 mM metformin; (4) HI/MET: 24 h 100 nM insulin followed by 24 h 100 nM INS+2 mM MET. INS and INS/MET groups saw impairments in markers of insulin signaling (Akt S473, mTOR S2448, p70s6k T389, and IRS-1S636) demonstrating IR was not recovered with MET treatment. All treatment groups showed reductions in neuronal markers (post-synaptic marker HOMER1 mRNA content and synapse marker synaptophysin protein content). INS and MET treatments showed a reduction in the content of the mature neuronal marker NeuN that was prevented by INS/MET. Similarly, increases in cell size/area, neurite length/area observed with INS and MET, were prevented with INS/MET. These findings indicate that IR and MET impair neuronal markers through distinct pathways and suggest that MET is ineffective in treating IR-driven impairments in neurons.

Memory impairment in the D2.mdx mouse model of Duchenne muscular dystrophy is prevented by the adiponectin receptor agonist ALY688.

NEW FINDINGS: What is the central question of this study? Can adiponectin receptor agonism improve recognition memory in a mouse model of Duchenne muscular dystrophy? What is the main finding and its importance? Short-term treatment with the new adiponectin receptor agonist ALY688 improves recognition memory in D2.mdx mice. This finding suggests that further investigation into adiponectin receptor agonism is warranted, given that there remains an unmet need for clinical approaches to treat this cognitive dysfunction in people with Duchenne muscular dystrophy. ABSTRACT: Memory impairments have been well documented in people with Duchenne muscular dystrophy (DMD). However, the underlying mechanisms are poorly understood, and there is an unmet need to develop new therapies to treat this condition. Using a novel object recognition test, we show that recognition memory impairments in D2.mdx mice are completely prevented by daily treatment with the new adiponectin receptor agonist ALY688 from day 7 to 28 of age. In comparison to age-matched wild-type mice, untreated D2.mdx mice demonstrated lower hippocampal mitochondrial respiration (carbohydrate substrate), greater serum interleukin-6 cytokine content and greater hippocampal total tau and Raptor protein contents. Each of these measures was partly or fully preserved after treatment with ALY688. Collectively, these results indicate that adiponectin receptor agonism improves recognition memory in young D2.mdx mice.

Exercise training and BDNF injections alter amyloid precursor protein (APP) processing enzymes and improve cognition.

Exercise reduces cognitive aging, neurodegeneration, and Alzheimer's disease (AD) risk. Acute exercise reduces the activity of ß-site amyloid precursor protein-cleaving enzyme 1 (BACE1), the rate-limiting enzyme in the production of Aß. However, mechanisms mediating these effects remain largely unknown. Work has implicated brain-derived neurotrophic factor (BDNF) in the processing of amyloid precursor protein (APP). BDNF is an exercise-induced neurotrophin known for its role in synaptic plasticity, neurite growth, and neuronal survival. Previously, our lab has shown using an ex vivo model that treatment of the prefrontal cortex with BDNF reduced BACE1 activity, highlighting a BDNF to BACE1 link. The purpose of this research was to examine whether BDNF treatments resulted in similar biochemical adaptations to APP processing as exercise training. Male C57BL6/J mice were assigned into one of four groups (n = 12/group): 1) control; 2) exercise training (progressive treadmill training 5 days/wk); 3) BDNF (0.5 mg/kg body mass subcutaneous injection 5 days/wk); or 4) endurance training and BDNF, for an 8-wk intervention. Recognition memory was measured with a novel object recognition test. Serum, the prefrontal cortex, and hippocampus were collected. BDNF improved recognition memory to a similar extent as endurance training. BDNF and exercise decreased BACE1 activity and increased ADAM10 activity in the prefrontal cortex, indicating a shift in APP processing. Our novel results indicate that BDNF exerts similar beneficial effects on cognition and APP processing as exercise training. Future evidence-based preventative or therapeutic interventions that increase BDNF and reduce BACE1 will be of value for populations that are at risk of AD.NEW & NOTEWORTHY Our study presents the novel findings that chronic peripheral BDNF injections result in regulation of APP processing enzymes and improved cognition to a similar extent as exercise training. These findings highlight the potential efficacy of using BDNF as a therapeutic intervention in the prevention of neurodegenerative diseases (i.e., Alzheimer's disease). Furthermore, future evidence-based preventative or therapeutic interventions that increase BDNF and reduce BACE1 will be of value for populations that are at risk of AD.

Declining Rates of Legg-Calvé-Perthes Surgery in the United States: National Trends Using the Kids' Inpatient Database and Pediatric Health Information System.

BACKGROUND: In 2004 and 2008 two large prospective, multicenter studies were published which resulted in improved understanding of operative indications for the treatment of Legg-Calvé-Perthes disease (LCPD) based on patient age, disease severity, and resultant radiographic outcomes. The primary aim of this study is to evaluate the trends in surgical management of LCPD in the United States prior, and subsequent to, the publication of these landmark studies. METHODS: Cross-sectional retrospective analysis of US pediatric hospitalizations for the surgical management of LCPD was conducted using the Kids' Inpatient Database from 2000 to 2016. Patients 12 years of age and younger were included who had a primary admission diagnosis of LCPD and a LCPD-related procedure during the hospitalization. Data was subsequently weighted to produce national-level estimates and variables pertaining to patient age group, procedure, demographics, and hospital characteristics were analyzed. In a post hoc analysis, the results of the Kids' Inpatient Database were also corroborated with the Pediatric Health Information System database. RESULTS: A weighted sample of 2786 LCPD surgical admissions met inclusion and exclusion criteria; 11.2% of surgical admissions were patients below 6 years of age, 35.9% were 6 to 8 years of age, and 52.9% were above 8 years of age. There was a significant decrease in admissions for surgical management of LCPD in all age groups over time, however there was no appreciable change in the proportion of LCPD surgical admissions performed among the above 8 to below 12, above 6 to below 8, or below 6 years age groups. Femoral osteotomy remained the most common surgical procedure, while other osteotomy types, including pelvic and unspecified osteotomies involving the hip, decreased over time ( P <0.001). CONCLUSIONS: There is a decreasing rate of hospital admissions for LCPD surgery since 2000, perhaps indicating a decline in incidence of disease. Furthermore, despite evidence supporting LCPD surgical outcomes related to patient age, there has been no change in the proportion of patients undergoing surgery by age group over time. LEVEL OF EVIDENCE: Level III-retrospective study.

Acute interleukin-6 modulates key enzymes involved in prefrontal cortex and hippocampal amyloid precursor protein processing.

Exercise has been shown to be beneficial for individuals with Alzheimer's disease (AD). In rodent models of AD, exercise decreases the amyloidogenic processing of the amyloid precursor protein (APP). Although it remains unclear as to how exercise is promoting this shift away from pathological APP processing, there is emerging evidence that exercise-induced factors released from peripheral tissues may facilitate these alterations in brain APP processing. Interleukin-6 (IL-6) is released from multiple organs into peripheral circulation during exercise and is among the most characterized exerkines. The purpose of this study is to examine whether acute IL-6 can modulate key enzymes responsible for APP processing, namely, a disintegrin and metalloproteinase 10 (ADAM10) and ß-site amyloid precursor protein-cleaving enzyme 1 (BACE1), which initiate the nonamyloidogenic and amyloidogenic cascades, respectively. Male 10-wk-old C57BL/6J mice underwent acute treadmill exercise bout or were injected with either IL-6 or a PBS control 15 min prior to tissue collection. ADAM10 and BACE1 enzyme activity, mRNA, and protein expression, as well as downstream markers of both cascades, including soluble APPα (sAPPα) and soluble APPß (sAPPß), were examined. Exercise increased circulating IL-6 and brain IL-6 signaling (pSTAT3 and Socs3 mRNA). This occurred alongside a reduction in BACE1 activity and an increase in ADAM10 activity. IL-6 injection reduced BACE1 activity and increased sAPPα protein content in the prefrontal cortex. In the hippocampus, IL-6 injection decreased BACE1 activity and sAPPß protein content. Our results show that acute IL-6 injection increases markers of the nonamyloidogenic cascade and decreases markers of the amyloidogenic cascade in the cortex and hippocampus of the brain.NEW & NOTEWORTHY It is becoming evident that exercise modulates APP processing and can reduce amyloid-beta (Aß) peptide production. Our data help to explain this phenomenon by highlighting IL-6 as an exercise-induced factor that lowers pathological APP processing. These results also highlight brain regional differences in response to acute IL-6.

Low-Dose Lithium Supplementation Influences GSK3ß Activity in a Brain Region Specific Manner in C57BL6 Male Mice.

BACKGROUND: Lithium, a commonly used treatment for bipolar disorder, has been shown to have neuroprotective effects for other conditions including Alzheimer's disease via the inhibition of the enzyme glycogen synthase kinase-3 (GSK3). However, dose-dependent adverse effects of lithium are well-documented, highlighting the need to determine if low doses of lithium can reliably reduce GSK3 activity. OBJECTIVE: The purpose of this study was to evaluate the effects of a low-dose lithium supplementation on GSK3 activity in the brain of an early, diet-induced Alzheimer's disease model. METHODS: Male C57BL/6J mice were divided into either a 6-week or 12-week study. In the 6-week study, mice were fed a chow diet or a chow diet with lithium-supplemented drinking water (10 mg/kg/day) for 6 weeks. Alternatively, in the 12-week study, mice were fed a chow diet, a high-fat diet (HFD), or a HFD with lithium-supplemented drinking water for 12 weeks. Prefrontal cortex and hippocampal tissues were collected for analysis. RESULTS: Results demonstrated reduced GSK3 activity in the prefrontal cortex as early as 6 weeks of lithium supplementation, in the absence of inhibitory phosphorylation changes. Further, lithium supplementation in an obese model reduced prefrontal cortex GSK3 activity as well as improved insulin sensitivity. CONCLUSION: Collectively, these data provide evidence for low-dose lithium supplementation to inhibit GSK3 activity in the brain. Moreover, these results indicate that GSK3 activity can be inhibited despite any changes in phosphorylation. These findings contribute to an overall greater understanding of low-dose lithium's ability to influence GSK3 activity in the brain and its potential as an Alzheimer's disease prophylactic.

Nightmare on CIL Street: A Simulation Series to Increase Confidence and Skill in Responding to Clinical Emergencies.

Background: The Central Texas Veterans Health Care System (CTVHCS) in Temple, a 189-bed teaching hospital, recently opened its Center for Innovation and Learning for simulation-based learning. CTVHCS built a rapid response simulation curriculum to improve preparedness for internal medicine residents, medical students, and physician assistant students that exploits newly developed medical education technology. Observations: The Center for Innovation and Learning curriculum was created based on the most common rapid response calls received over the previous 3 years. Cardiac, respiratory, and neurological simulations were implemented. Learners approach each scenario as if they were on night service alone without specialist help. Learners must identify tachyarrhythmia, impending respiratory failure, and a patient with encephalopathy requiring transfer. Conclusions: Sixteen learners were surveyed before the simulation and after addressing each educational objective was completed and showed improvement. Educating trainees on rapid response scenarios by using a simulation curriculum provides many benefits. Trainees reported improvement in addressing cardiac, respiratory, and neurological rapid response scenarios after experiencing the simulation.

Voluntary wheel running alters markers of amyloid-beta precursor protein processing in an ovarian hormone depleted model.

Introduction: Aberrant cleavage of the transmembrane protein, amyloid-beta precursor protein (ABPP), results in the overproduction of amyloid-beta (AB) peptides which can form senile plaques in the brain. These plaques can get lodged within synapses and disrupt neuronal communication ultimately leading to rampant neuron death. The rate-limiting enzyme in AB production is beta-site ABPP cleaving enzyme 1 (BACE1). In females, estrogen loss is associated with increases in AB and BACE1 content and activity. Exercise is known to have anti-amyloidogenic effects and may be able to alter BACE1 in cases of ovarian hormone depletion. This study aimed to examine the effects of physical activity on BACE1 in intact and ovariectomized female mice. Methods: Female C57BL/6 mice (24 weeks old) underwent bilateral ovariectomy (OVX; n=20) or SHAM surgery (SHAM; n=20). Mice were assigned to one of four groups (n=10/group) for 8 weeks: (1) sham (SHAM), (2) sham with a wheel (SHAM VWR), (3) ovariectomized (OVX), or (4) ovariectomized with a wheel (OVX VWR). Results: Novel object recognition testing demonstrated that OVX mice had a lower percentage of novel object investigation time compared to SHAM. OVX mice also had higher prefrontal cortex BACE1 activity compared to SHAM (p<0.0001), while the OVX+VWR activity was not different from SHAM. Discussions: Our results demonstrate that voluntary wheel running in an ovariectomized model prevented increases in BACE1 activity, maintained memory recall, and may provide a method of slowing the progression of Alzheimer's disease.

Low-dose lithium supplementation promotes adipose tissue browning and sarco(endo)plasmic reticulum Ca2+ ATPase uncoupling in muscle.

Sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) uncoupling in skeletal muscle and mitochondrial uncoupling via uncoupling protein 1 (UCP1) in brown/beige adipose tissue are two mechanisms implicated in energy expenditure. Here, we investigated the effects of glycogen synthase kinase 3 (GSK3) inhibition via lithium chloride (LiCl) treatment on SERCA uncoupling in skeletal muscle and UCP1 expression in adipose. C2C12 and 3T3-L1 cells treated with LiCl had increased SERCA uncoupling and UCP1 protein levels, respectively, ultimately raising cellular respiration; however, this was only observed when LiCl treatment occurred throughout differentiation. In vivo, LiCl treatment (10 mg/kg/day) increased food intake in chow-fed diet and high-fat diet (HFD; 60% kcal)-fed male mice without increasing body mass-a result attributed to elevated daily energy expenditure. In soleus muscle, we determined that LiCl treatment promoted SERCA uncoupling via increased expression of SERCA uncouplers, sarcolipin and/or neuronatin, under chow-fed and HFD-fed conditions. We attribute these effects to the GSK3 inhibition observed with LiCl treatment as partial muscle-specific GSK3 knockdown produced similar effects. In adipose, LiCl treatment inhibited GSK3 in inguinal white adipose tissue (iWAT) but not in brown adipose tissue under chow-fed conditions, which led to an increase in UCP1 in iWAT and a beiging-like effect with a multilocular phenotype. We did not observe this beiging-like effect and increase in UCP1 in mice fed a HFD, as LiCl could not overcome the ensuing overactivation of GSK3. Nonetheless, our study establishes novel regulatory links between GSK3 and SERCA uncoupling in muscle and GSK3 and UCP1 and beiging in iWAT.

Postexercise serum from humans influences the biological tug of war of APP processing in human neuronal cells.

Neurodegenerative diseases such as Alzheimer's disease (AD) are becoming more prevalent in our aging society. One specific neuropathological hallmark of this disease is the accumulation of amyloid-ß (Aß) peptides, which aggregate to form extraneuronal plaques. Increased Aß peptides are often observed well before symptoms of AD develop, highlighting the importance of targeting Aß-producing pathways early on in disease progression. Evidence indicates that exercise has the capacity to reduce Aß peptide production in the brain; however, the mechanisms remain unknown. Exercise-induced signaling mediators could be the driving force behind some of the beneficial effects observed in the brain with exercise. The purpose of this study was to examine if postexercise serum and the factors it contains can alter neuronal amyloid precursor protein (APP) processing. Human SH-SY5Y neuronal cells were differentiated with retinoic acid for 5 days and treated with 10% pre- or postexercise serum from humans for 30 min. Cells were collected for analysis of acute (30 min; n = 6) or adaptive (24 h posttreatment; n = 6) responses. There were no statistical differences in a disintegrin and metalloproteinase 10 (ADAM10) and ß-site amyloid precursor protein cleaving enzyme 1 (BACE1) mRNA or protein expression with postexercise serum treatment at either time point. However, there was an increase in the ratio of soluble amyloid precursor protein α (sAPPα) to soluble amyloid precursor protein ß (sAPPß) protein content (P = 0.05) after 30 min of postexercise serum treatment. In addition, 30 min of postexercise serum treatment increased ADAM10 (P = 0.01) and BACE1 (P = 0.02) activity. These findings suggest that postexercise serum modulates important enzymes involved in APP processing, potentially pushing the cascade toward the nonamyloidogenic arm.

Creatine Monohydrate Supplementation Increases White Adipose Tissue Mitochondrial Markers in Male and Female Rats in a Depot Specific Manner.

White adipose tissue (WAT) is a dynamic endocrine organ that can play a significant role in thermoregulation. WAT has the capacity to adopt structural and functional characteristics of the more metabolically active brown adipose tissue (BAT) and contribute to non-shivering thermogenesis under specific stimuli. Non-shivering thermogenesis was previously thought to be uncoupling protein 1 (UCP1)-dependent however, recent evidence suggests that UCP1-independent mechanisms of thermogenesis exist. Namely, futile creatine cycling has been identified as a contributor to WAT thermogenesis. The purpose of this study was to examine the efficacy of creatine supplementation to alter mitochondrial markers as well as adipocyte size and multilocularity in inguinal (iWAT), gonadal (gWAT), and BAT. Thirty-two male and female Sprague-Dawley rats were treated with varying doses (0 g/L, 2.5 g/L, 5 g/L, and 10 g/L) of creatine monohydrate for 8 weeks. We demonstrate that mitochondrial markers respond in a sex and depot specific manner. In iWAT, female rats displayed significant increases in COXIV, PDH-E1alpha, and cytochrome C protein content. Male rats exhibited gWAT specific increases in COXIV and PDH-E1alpha protein content. This study supports creatine supplementation as a potential method of UCP1-independant thermogenesis and highlights the importance of taking a sex-specific approach when examining the efficacy of browning therapeutics in future research.

Significant Pain Reduction in Hospitalized Patients Receiving Integrative Medicine Interventions by Clinical Population and Accounting for Pain Medication.

Background: Prior research has reported that integrative medicine (IM) therapies reduce pain in inpatients, but without controlling for important variables. Here, the authors extend prior research by assessing pain reduction while accounting for each patient's pain medication status and clinical population. Methods: The initial data set consisted of 7,106 inpatient admissions, aged ≥18 years, between July 16, 2012, and December 15, 2014. Patients' electronic health records were used to obtain data on demographic, clinical measures, and pain medication status during IM. Results: The final data set included first IM therapies delivered during 3,635 admissions. Unadjusted average pre-IM pain was 5.33 (95% confidence interval [CI]: 5.26 to 5.41) and post-IM pain was 3.31 (95% CI: 3.23 to 3.40) on a 0-10 scale. Pain change adjusted for severity of illness, clinical population, sex, treatment, and pain medication status during IM was significant and clinically meaningful with an average reduction of -1.97 points (95% CI: -2.06 to -1.86) following IM. Adjusted average pain was reduced in all clinical populations, with largest and smallest pain reductions in maternity care (-2.34 points [95% CI: -2.56 to -2.14]) and orthopedic (-1.71 points [95% CI: -1.98 to -1.44]) populations. Pain medication status did not have a statistically significant association on pain change. Decreases were observed regardless of whether patients were taking narcotic medications and/or nonsteroidal anti-inflammatory drugs versus no pain medications. Conclusions: For the first time, inpatients receiving IM reported significant and clinically meaningful pain reductions during a first IM session while accounting for pain medications and across clinical populations. Future implementation research should be conducted to optimize identification/referral/delivery of IM therapies within hospitals. Clinical Trials.gov #NCT02190240.

Regionalization of Isolated Pediatric Femur Fracture Treatment: Recent Trends Observed Using the Kids' Inpatient Database.

BACKGROUND: Isolated pediatric femur fractures have historically been treated at local hospitals. Pediatric referral patterns have changed in recent years, diverting patients to high volume centers. The purpose of this investigation was to assess the treatment location of isolated pediatric femur fractures and concomitant trends in length of stay and cost of treatment. METHODS: A cross-sectional analysis of surgical admissions for femoral shaft fracture was performed using the 2000 to 2012 Kids' Inpatient Database. The primary outcome was hospital location and teaching status. Secondary outcomes included the length of stay and mean hospital charges. Polytrauma patients were excluded. Data were weighted within each study year to produce national estimates. RESULTS: A total of 35,205 pediatric femoral fracture cases met the inclusion criteria. There was a significant shift in the treatment location over time. In 2000, 60.1% of fractures were treated at urban, teaching hospitals increasing to 81.8% in 2012 (P<0.001). Mean length of stay for all hospitals decreased from 2.59 to 1.91 days (P<0.001). Inflation-adjusted total charges increased during the study from $9499 in 2000 to $25,499 in 2012 per episode of treatment (P<0.001). Total charges per hospitalization were ∼$8000 greater at urban, teaching hospitals in 2012. CONCLUSIONS: Treatment of isolated pediatric femoral fractures is regionalizing to urban, teaching hospitals. Length of stay has decreased across all institutions. However, the cost of treatment is significantly greater at urban institutions relative to rural hospitals. This trend does not consider patient outcomes but the observed pattern appears to have financial implications. LEVEL OF EVIDENCE: Level III-case series, database study.

Repeated episodes of pediatric constraint induced movement therapy with a gross motor training component: A prospective cohort study.

PURPOSE: To examine the results of repeated episodes of 21-day pediatric constraint induced movement therapy (PCIMT) paired with gross motor training (GMT). METHODS: Nineteen children, age 14 months - 6 years with unilateral upper extremity impairment enrolled in this cohort study to receive repeated episodes of 21 day PCIMT-GMT. Outcome measures included the Peabody Developmental Motor Scales-2 (PDMS-2), the Assisting Hand Assessment (AHA) and the Canadian Occupational Performance Measure (COPM). RESULTS: All children demonstrated improvement in raw scores following each episode of PCIMT-GMT with a statistically significant change in the least squares estimated mean for all measures except the PDMS-2 total motor raw score and gross motor quotient for the preferred hand in the fourth episode (p< 0.05). Gains were noted on the Scaled Score for the AHA for 39/39 episodes, all greater than the smallest detectable difference. COPM Performance and Satisfaction scores for 17/17 episodes were above the clinically meaningful threshold. Additional improvements in scores were noted in all children with each repeated episode. CONCLUSION: Children with unilateral upper extremity impairment demonstrate improvements in fine motor, gross motor, and bimanual skills, along with functional changes in participation in daily life, following PCIMT-GMT. Participation in repeated episodes can lead to further improvements.

Comparison of Pediatric Tracheostomy Stoma Cleaning Solutions.

BACKGROUND: In the limited literature on cleaning tracheostomy stoma sites, there is no standard guideline for the cleaning solution. The objective of this study was to determine whether signs of stoma-site infection were different among a hospitalized pediatric population when using sterile water, sterile saline solution, or 0.25% acetic acid solution for tracheostomy stoma cleaning. METHODS: A retrospective chart review was completed and included nursing and physician notes. The subjects were <1 y of age, in the neonatal ICU, and received a tracheostomy within the previous 30 days. Clinical signs of infection were visually observed by the providers and documented in the medical record. The subjects were divided into 3 groups, those prescribed 0.25% acetic acid, those prescribed sterile water, and those prescribed sterile saline solution for twice daily tracheostomy stoma care. We compared the rate of signs of infection of the tracheostomy stoma site across the 3 treatments by using a chi-square test. RESULTS: In the 102 subjects included, there were significantly more signs of infection in the subjects for whom 0.25% acetic acid was not used for daily stoma cleaning (P = .03). There were no differences in signs of infection between those cleaned with saline solution (39%) and those cleaned with sterile water (31%) for daily stoma cleaning. Overall, there were 29% fewer signs of infection when 0.25% acetic acid was used than either sterile water or saline solution. CONCLUSIONS: Analysis of our findings indicated that a 0.25% acetic acid solution used for stoma cleaning may be associated with fewer signs of infection than sterile water or sterile saline solution. More research is warranted toward establishing a standard practice.