Boosting the traditional physiotherapist approach for stroke spasticity using a sensorized ankle foot orthosis: a pilot study

Background: Spasticity is a motor disorder that is commonly treated manually by a physical therapist (PhT) stretching the muscles. Recent data on learning have demonstrated the importance of human-to-human interaction in improving rehabilitation: cooperative motor behavior engages specific areas of the motor system compared with execution of a task alone.

Objectives: We hypothesize that PhT-guided therapy that involves active collaboration with the patient (Pt) through shared biomechanical visual biofeedback (vBFB) positively impacts learning and performance by the Pt during ankle spasticity treatment. A sensorized ankle foot orthosis (AFO) was developed to provide online quantitative data of joint range of motion (ROM), angular velocity, and electromyographic activity to the PhT and Pt during the treatment of ankle spasticity.

Methods: Randomized controlled clinical trial. Ten subacute stroke inpatients, randomized into experimental (EXP) and control (CTRL) groups, underwent six weeks of daily treatment. The EXP group was treated with an active AFO, and the CTRL group was given an inactive AFO. Spasticity, ankle ROM, ankle active and passive joint speed, and coactivation index (CI) were assessed at enrollment and after 15–30 sessions.

Results: Spasticity and CI (p < 0.005) decreased significantly after training only in the EXP group, in association with a significant rise in active joint speed and active ROM (p < 0.05). Improvements in spasticity (p < 0.05), active joint speed (p < 0.001), and CI (p < 0.001) after treatment differed between the EXP and CTRL groups.

Conclusions: PhT–Pt sharing of exercise information, provided by joint sensorization and vBFB, improved the efficacy of the conventional approach for treating ankle spasticity in subacute stroke Pts.     

Variability of platelet indices and function: acquired and genetic factors

Each individual has an inherent variable risk of bleeding linked to genetic or acquired abnormal platelet number or platelet dysfunction. In contrast, it is less obvious that the variability of platelet phenotypes (number, mean platelet volume, function) may contribute to the variable individual risk of thrombosis. Interindividual variability of platelet indices or function may be either due to acquired factors, such as age, sex, metabolic variables, smoke, dietary habits, and ongoing inflammation, or due to genetic factors. Acquired variables explain a small portion of the heterogeneity of platelet parameters. Genetic factors, instead, appear to play a major role, although a consistent portion of such a genetic variance has not yet been attributed to any specific genetic factor, possibly due to the high number of DNA loci potentially involved and to the limited effect size of each individual SNP. A portion of variance remains thus unexplained, also due to variability of test performance. A major contradiction in present platelet knowledge is, indeed, the difficulty to reconcile the universally accepted importance of platelet indices or function and the lack of reliable platelet parameters in cardiovascular risk prediction models. Trials on antiplatelet drugs were generally designed to select a homogeneous sample, whose results could be applied to an "average subject," tending to exclude the deviation/extreme values. As the current indications for antiplatelet treatment in primary or secondary prevention of ischemic vascular disease still derive from the results of such clinical trials where platelet function and its variability was not investigated, we cannot at present rely upon any current platelet test to either initiate, or monitor, or modify or stop treatment with any antiplatelet drug. Evidence is, however, increasing that traditional platelet aggregometry and other more recently developed platelet function assays could be useful to optimize antiplatelet therapy and to predict major adverse cardiac events.The observation of interindividual differences in platelet response to antiplatelet drugs has enlarged the spectrum and the possible clinical relevance of the variability of platelet indices or function. The development of "personalized medicine" will benefit from the concepts discussed in this chapter.     

Impairment of methyl cycle affects mitochondrial methyl availability and glutathione level in Down's syndrome

In Down's syndrome there is evidence that increased gene expression coding for specific cystathionine beta-synthase translates directly into biochemical aberrations, which result in a biochemical and metabolic imbalance of the methyl status. This event is destined to impact mitochondrial function since methylation is a necessary event in mitochondria and relies on the availability and uptake of the methyl donor S-adenosylmethionine. Indeed mitochondrial dysfunctions have been widely described in Down's syndrome, but they have never been correlated to a possible mitochondrial methyl unbalance. In the present study we find that the mitochondrial levels of S-adenosylmethionine are reduced in Down's syndrome compared to control cells demonstrating the effect of the methyl unbalance on mitochondria. The possible role of methylation in mitochondria is discussed and some preliminary results on a possible methylation target are presented.     

Metabolic syndrome,hypertension, and nervous system injury: Epidemiological correlates

Metabolic syndrome (MetS) is a common and complex disorder combining hypertension, obesity, dyslipidemia, and insulin resistance. MetS represents a risk factor for changes in cognitive functions in older age, and several studies have suggested that MetS may be linked to dementia. This article reviews the main evidences about the relationship between MetS and neurodegenerative disease. Starting from an epidemiological point of view, the article analyzes medico-social aspects related to MetS, considering the reduction of work capacity and the condition of disability that it involves. Some authors affirm that on the basis of current Italian legislation, it is possible to consider the syndrome as a disability. This is because all the diseases that make up MetS are high-risk clinical pathological conditions. For these reasons, a joint action is required to contain the incidence of MetS, the high social costs, and the loss of productivity related to the syndrome. In conclusion, healthcare initiatives could be adopted in order to increase the understanding of the pathogenic contributions of each element on MetS and how they can be modified. These actions will be useful to reduce healthcare costs and can lead to more effective prevention of metabolic disease, thus promoting good health.

Abbreviations: MetS: Metabolic syndrome; WHO: World Health Organization; CVD: cerebrovascular diseases; AD: Alzheimer’s Disease; VaD: Vascular Dementia; IDF: International Diabetes Federation; T2DM: type 2 diabetes mellitus; CAD: coronary artery disease; MCI: mild cognitive impairment; NCDs: Non Communicable Diseases; BMI: Body Mass Index; ICIDH: International classification of impairments, disabilities and handicaps     

2009 Influenza A H1N1 infections: delays in starting treatment with oseltamivir were associated with a more severe disease

Respiratory failure has been the main severe complication described in pediatric patients with influenza A H1N1 2009 (pandemic H1N1) infection. We describe the pandemic H1N1 2009 disease in children who required hospital admission and the patients' data associated with pediatric intensive care unit admission. Respiratory failure was the main complication. Extrapulmonary manifestations were also observed. Of the 127 patients, 24 required pediatric intensive care unit admission. Four patients died. Patients admitted with chronic conditions and those in whom oseltamivir was delayed more than 72 hours had a more severe disease.