Fitness and fatness in childhood obesity : implications of physical activity

Overweight and obesity are a significant cause of poor health worldwide, particularly in conjunction with low levels of physical activity (PA). PA is health-protective and essential for the physical growth and development of children, promoting physical and psychological health while simultaneously increasing the probability of remaining active as an adult. However, many obese children and adolescents have a unique set of physiological, biomechanical, and neuromuscular barriers to PA that they must overcome. It is essential to understand the influence of these barriers on an obese child's motivation in order to exercise and tailor exercise programs to the special needs of this population. Chapter Outline • Introduction • Defining Physical Activity, Exercise, and Physical Fitness • Physical Activity, Physical Fitness, And Motor Competence In Obese Children • Physical Activity and Obesity in Children • Physical Fitness in Obese Children • Balance and Gait in Obese Children • Motor Competence in Obese Children • Physical Activity Guidelines for Obese Children • Clinical Assessment of the Obese Child • Physical Activity Characteristics: Mode • Physical Activity Characteristics: Intensity • Physical Activity Characteristics: Frequency • Physical Activity Characteristics: Duration • Conclusion

Pre-Admission and Post-Hospital Management of Heart Failure in Patients not Enrolled in Specialist Programs

Aim: To review the management of heart failure in patients not enrolled in specialist multidisciplinary programs. Method: A prospective clinical audit of patients admitted to hospital with either a current or past diagnosis of heart failure and not enrolled in a specialist heart failure program or under the direct care of the cardiology unit. Results: 81 eligible patients were enrolled (1 August to 1 October 2008). The median age was 81 9.4 years and 48% were male. Most patients (63%) were in New York Heart Association Class II or Class III heart failure. On discharge, 59% of patients were prescribed angiotensin converting enzyme inhibitors and 43% were prescribed beta-blockers. During hospitalisation, 8.6% of patients with a past diagnosis of heart failure were started on an angiotensin converting enzyme inhibitor and 4.9% on a beta-blocker. There was evidence of suboptimal dosage on admission and discharge for angiotensin converting enzyme inhibitors (19% and 7.4%) and beta-blockers (29% and 17%). The results compared well with international reports regarding the under-treatment of heart failure. Conclusion: The demonstrated practice gap provides excellent opportunities for the involvement of pharmacists to improve the continuation of care for heart failure patients discharged from hospital in the areas of medication management review, dose titration and monitoring.

What We Have Here is a Failure to Communicate! Improving Communication between Tertiary to Primary Care for Chronic Heart Failure Patients

Background:  The aims of this study were to determine the documentation of pharmacotherapy optimization goals in the discharge letters of patients with the principal diagnosis of chronic heart failure. Methods:  A retrospective practice audit of 212 patients discharged to the care of their local general practitioner from general medical units of a large tertiary hospital. Details of recommendations regarding ongoing pharmacological and non-pharmacological management were reviewed. The doses of medications on discharge were noted and whether they met current guidelines recommending titration of angiotensin-converting enzyme inhibitors and beta-blockers. Ongoing arrangements for specialist follow up were also reviewed. Results:  The mean age of patients whose letters were reviewed was 78.4 years (standard deviation ± 8.6); 50% were men. Patients had an overall median of six comorbidities and eight regular medications on discharge. Mean length of stay for each admission was 6 days. Discharge letters were posted a median of 4 days after discharge, with 25% not posted at 10 days. No discharge letter was sent in 9.4% (20) of the cases. Only six (2.8%) letters had any recommendations regarding future titration of angiotensin-converting enzyme inhibitors and 6.6% (14) for beta-blockers. Recommendations for future non-pharmacological management, for example, diuretic action plans, regular weight monitoring and exercise plans were not found in the letters in this audit. Conclusion:  Hospital discharge is an opportunity to communicate management plans for treatment optimization effectively, and while this opportunity is spurned, implementation gaps in the management of cardiac failure will probably remain.

Rural and Urban Differentials in Primary Care Management of Chronic Heart Failure: New Data from the CASE Study

Objective: To determine whether primary care management of chronic heart failure (CHF) differed between rural and urban areas in Australia. Design: A cross-sectional survey stratified by Rural, Remote and Metropolitan Areas (RRMA) classification. The primary source of data was the Cardiac Awareness Survey and Evaluation (CASE) study. Setting: Secondary analysis of data obtained from 341 Australian general practitioners and 23 845 adults aged 60 years or more in 1998. Main outcome measures: CHF determined by criteria recommended by the World Health Organization, diagnostic practices, use of pharmacotherapy, and CHF-related hospital admissions in the 12 months before the study. Results: There was a significantly higher prevalence of CHF among general practice patients in large and small rural towns (16.1%) compared with capital city and metropolitan areas (12.4%) (P < 0.001). Echocardiography was used less often for diagnosis in rural towns compared with metropolitan areas (52.0% v 67.3%, P < 0.001). Rates of specialist referral were also significantly lower in rural towns than in metropolitan areas (59.1% v 69.6%, P < 0.001), as were prescribing rates of angiotensin-converting enzyme inhibitors (51.4% v 60.1%, P < 0.001). There was no geographical variation in prescribing rates of β-blockers (12.6% [rural] v 11.8% [metropolitan], P = 0.32). Overall, few survey participants received recommended “evidence-based practice” diagnosis and management for CHF (metropolitan, 4.6%; rural, 3.9%; and remote areas, 3.7%). Conclusions: This study found a higher prevalence of CHF, and significantly lower use of recommended diagnostic methods and pharmacological treatment among patients in rural areas.

Prevalence of malnutrition in Parkinson's disease : a systematic review

Parkinson's disease (PD) patients may be at higher risk of malnutrition because of the symptoms associated with the disease and the side effects of the medication used to manage it. A decline in nutritional status is associated with many adverse outcomes related to health and quality of life. It is not clear, however, to what extent this population is currently affected by malnutrition. The objective of this review was to systematically assess the methodology and outcomes of studies reporting the prevalence of malnutrition in PD patients. Studies that attempted to classify participants with PD into nutritional risk and/or malnutrition categories using body mass index, weight change, anthropometric measures, and nutritional screening and assessment scores were included. The prevalence of malnutrition ranged from 0% to 24% in PD patients, while 3–60% of PD patients were reported to be at risk of malnutrition. There was a large degree of variation among studies in the methods chosen, the definition of malnutrition using those methods, and the detail in which the methodological protocols were reported. The true extent of malnutrition in the PD population has yet to be accurately quantified. It is important, however, to screen for malnutrition at the time of PD diagnosis.

Hamstring strain injuries : factors that lead to injury and re-injury

Hamstring strain injuries (HSIs) are common in a number of sports and incidence rates have not declined in recent times. Additionally, the high rate of recurrent injuries suggests that our current understanding of HSI and re-injury risk is incomplete. Whilst the multifactoral nature of HSIs is agreed upon by many, often individual risk factors and/or causes of injury are examined in isolation. This review aims to bring together the causes, risk factors and interventions associated with HSIs to better understand why HSIs are so prevalent. Running is often identified as the primary activity type for HSIs and given the high eccentric forces and moderate muscle strain placed on the hamstrings during running these factors are considered to be part of the aetiology of HSIs. However, the exact causes of HSIs remain unknown and whilst eccentric contraction and muscle strain purportedly play a role, accumulated muscle damage and/or a single injurious event may also contribute. Potentially, all of these factors interact to varying degrees depending on the injurious activity type (i.e. running, kicking). Furthermore, anatomical factors, such as the biarticular organization, the dual innervations of biceps femoris (BF), fibre type distribution, muscle architecture and the degree of anterior pelvic tilt, have all been implicated. Each of these variables impact upon HSI risk via a number of different mechanisms that include increasing hamstring muscle strain and altering the susceptibility of the hamstrings to muscle damage. Reported risk factors for HSIs include age, previous injury, ethnicity, strength imbalances, flexibility and fatigue. Of these, little is known, definitively, about why previous injury increases the risk of future HSIs. Nevertheless, interventions put in place to reduce the incidence of HSIs by addressing modifiable risk factors have focused primarily on increasing eccentric strength, correcting strength imbalances and improving flexibility. The response to these intervention programmes has been mixed with varied levels of success reported. A conceptual framework is presented suggesting that neuromuscular inhibition following HSIs may impede the rehabilitation process and subsequently lead to maladaptation of hamstring muscle structure and function, including preferentially eccentric weakness, atrophy of the previously injured muscles and alterations in the angle of peak knee flexor torque. This remains an area for future research and practitioners need to remain aware of the multifactoral nature of HSIs if injury rates are to decline.

Osteopenia in a teenage boy presenting with previously undiagnosed guanidinoacetate methyltransferase (GAMT) deficiency and response to creatine supplementation

A 16 y.o. fully ambulant boy born to consanguineous Indian parents, presented for assessment of a fragility femoral neck fracture sustained against a background of autism and moderately severe intellectual disability. He had a past history of infantile eczema, and epilepsy treated with anticonvulsants from 2 to 10 years of age, with no further seizures following cessation of anticonvulsants. He had a thin body habitus (see Table 1) with long fingers and a high arched palate. He had no speech and negligible social interaction, but physical examination was otherwise unremarkable. Positive investigations revealed an undetectable serum creatinine and a urinary metabolic screen which showed an elevated GUA:Phe of 160 (< 36) and a decreased creatinine of 0.3 mmol/l (1.2–29.5) consistent with the diagnosis of guanidinoacetate methyltransferase(GAMT) deficiency. He was commenced on oral creatine 5 g three times daily. Despite improvement in physical activity, height and bone density, there was no discernable improvement in his intellectual functioning. Proton and phosphorous brain and leg magnetic resonance spectroscopy(MRS) was performed at baseline and showed an increased inorganic phosphorus peak and decreased phosphocreatine synthesis in brain and decreased creatine concentration in muscle. Following creatine treatment total brain creatine(1H-MRS) and phosphocreatine/ATP ratio (31P-MRS) content increased to 30% and 60% of control values, respectively. Brain GUA returned to normal levels.

Benign Epilepsy with Centro-temporal Spikes: Spike Triggered fMRI Shows Somato-sensory Cortex Activity

Summary:  Objective: We performed spike triggered functional MRI (fMRI) in a 12 year old girl with Benign Epilepsy with Centro-temporal Spikes (BECTS) and left-sided spikes. Our aim was to demonstrate the cerebral origin of her interictal spikes. Methods: EEG was recorded within the 3 Tesla MRI. Whole brain fMRI images were acquired, beginning 2–3 seconds after spikes. Baseline fMRI images were acquired when there were no spikes for 20 seconds. Image sets were compared with the Student's t-test. Results: Ten spike and 20 baseline brain volumes were analysed. Focal activiation was seen in the inferior left sensorimotor cortex near the face area. The anterior cingulate was more active during baseline than spikes. Conclusions: Left sided epileptiform activity in this patient with BECTS is associated with fMRI activation in the left face region of the somatosensory cortex, which would be consistent with the facial sensorimotor involvement in BECT seizures. The presence of BOLD signal change in other regions raises the possibility that the scalp recorded field of this patient with BECTs may reflect electrical change in more than one brain region.

Myoinositol Abnormalities in Temporal Lobe Epilepsy

Purpose: This study used magnetic resonance spectroscopy (MRS) to examine metabolite abnormalities in the temporal and frontal lobe of patients with temporal lobe epilepsy (TLE) of differing severity. Methods: We investigated myoinositol in TLE by using short-echo MRS in 34 TLE patients [26 late onset (LO-TLE), eight hippocampal sclerosis (HS-TLE)], and 16 controls. Single-voxel short-echo (35 ms) MR spectra of temporal and frontal lobes were acquired at 1.5 T and analyzed by using LCModel. Results: The temporal lobe ipsilateral to seizure origin in HS-TLE, but not LO-TLE, had reduced N-acetylaspartate (NA) and elevated myoinositol (MI; HS-TLE NA, 7.8 ± 1.9 mM, control NA, 9.2 ± 1.3 mM; p < 0.05; HS-TLE MI, 6.1 ± 1.6 mM, control mI 4.9 ± 0.8 mM, p< 0.05). Frontal lobe MI was low in both patient groups (LO-TLE, 4.3 ± 0.8 mM; p < 0.05; HS-TLE, 3.6 ±.05 mM; p < 0.001; controls, 4.8 ± 0.5 mM). Ipsilateral frontal lobes had lower MI (3.8 ± 0.7 mM; p < 0.01) than contralateral frontal lobes (4.3 ± 0.8 mM; p < 0.05). Conclusions: MI changes may distinguish between the seizure focus, where MI is increased, and areas of seizure spread where MI is decreased.

Delta opioid-receptor function in the dorsal striatum plays a role in high levels of ethanol consumption in rats

Binge-like patterns of excessive drinking during young adulthood increase the propensity for alcohol use disorders (AUDs) later in adult life; however, the mechanisms that drive this are not completely understood. Previous studies showed that the δ-opioid peptide receptor (DOP-R) is dynamically regulated by exposure to ethanol and that the DOP-R plays a role in ethanol-mediated behaviors. The aim of this study was to determine the role of the DOP-R in high ethanol consumption from young adulthood through to late adulthood by measuring DOP-R-mediated [(35)S]GTPγS binding in brain membranes and DOP-R-mediated analgesia using a rat model of high ethanol consumption in Long Evans rats. We show that DOP-R activity in the dorsal striatum and DOP-R-mediated analgesia changes during development, being highest during early adulthood and reduced in late adulthood. Intermittent access to ethanol but not continuous ethanol or water from young adulthood leads to an increase in DOP-R activity in the dorsal striatum and DOP-R-mediated analgesia into late adulthood. Multiple microinfusions of naltrindole into the dorsal striatum or multiple systemic administration of naltrindole reduces ethanol consumption, and following termination of treatment, DOP-R activity in the dorsal striatum is attenuated. These findings suggest that DOP-R activity in the dorsal striatum plays a role in high levels of ethanol consumption and suggest that targeting the DOP-R is an alternative strategy for the treatment of AUDs.

The relationship between Bayesian motor unit number estimation and histological measurements of motor neurons in wild-type and SOD1 G93A mice

Objective: To assess the relationship between Bayesian MUNE and histological motor neuron counts in wild-type mice and in an animal model of ALS. Methods: We performed Bayesian MUNE paired with histological counts of motor neurons in the lumbar spinal cord of wild-type mice and transgenic SOD1 G93A mice that show progressive weakness over time. We evaluated the number of acetylcholine endplates that were innervated by a presynaptic nerve. Results: In wild-type mice, the motor unit number in the gastrocnemius muscle estimated by Bayesian MUNE was approximately half the number of motor neurons in the region of the spinal cord that contains the cell bodies of the motor neurons supplying the hindlimb crural flexor muscles. In SOD1 G93A mice, motor neuron numbers declined over time. This was associated with motor endplate denervation at the end-stage of disease. Conclusion: The number of motor neurons in the spinal cord of wild-type mice is proportional to the number of motor units estimated by Bayesian MUNE. In SOD1 G93A mice, there is a lower number of estimated motor units compared to the number of spinal cord motor neurons at the end-stage of disease, and this is associated with disruption of the neuromuscular junction. Significance: Our finding that the Bayesian MUNE method gives estimates of motor unit numbers that are proportional to the numbers of motor neurons in the spinal cord supports the clinical use of Bayesian MUNE in monitoring motor unit loss in ALS patients. © 2012 International Federation of Clinical Neurophysiology.

Wide-field assessment of the human corneal subbasal nerve plexus in diabetic neuropathy using a novel mapping technique

To develop a rapid optimized technique of wide-field imaging of the human corneal subbasal nerve plexus. A dynamic fixation target was developed and, coupled with semiautomated tiling software, a rapid method of capturing and montaging multiple corneal confocal microscopy images was created. To illustrate the utility of this technique, wide-field maps of the subbasal nerve plexus were produced in 2 participants with diabetes, 1 with and 1 without neuropathy. The technique produced montages of the central 3 mm of the subbasal corneal nerve plexus. The maps seem to show a general reduction in the number of nerve fibers and branches in the diabetic participant with neuropathy compared with the individual without neuropathy. This novel technique will allow more routine and widespread use of subbasal nerve plexus mapping in clinical and research situations. The significant reduction in the time to image the corneal subbasal nerve plexus should expedite studies of larger groups of diabetic patients and those with other conditions affecting nerve fibers. The inferior whorl and the surrounding areas may show the greatest loss of nerve fibers in individuals with diabetic neuropathy, but this should be further investigated in a larger cohort.