The Strathclyde Brain Computer Interface (S-BCI) : the road to clinical translation

In this paper, we summarise the state of development of the Strathclyde Brain Computer Interface (S-BCI) and what has been so far achieved. We also briefly discuss our next steps for translation to spinal cord injured patients and the challenges we envisage in this process and how we plan to address some of them. Projections of the S-BCI project for the coming few years are also presented

Reversed cortical over-activity during movement imagination following neurofeedback treatment for central neuropathic pain

Objective: One of the brain signatures of the central neuropathic pain (CNP) is the theta band over-activity of wider cortical structures, during imagination of movement. The objective of the study was to investigate whether this over-activity is reversible following the neurofeedback treatment of CNP. Methods: Five paraplegic patients with pain in their legs underwent from twenty to forty neurofeedback sessions that significantly reduced their pain. In order to assess their dynamic cortical activity they were asked to imagine movements of all limbs a week before the first and a week after the last neurofeedback session. Using time–frequency analysis we compared EEG activity during imagination of movement before and after the therapy and further compared it with EEG signals of ten paraplegic patients with no pain and a control group of ten able-bodied people. Results: Neurofeedback treatment resulted in reduced CNP and a wide spread reduction of cortical activity during imagination of movement. The reduction was significant in the alpha and beta band but was largest in the theta band. As a result cortical activity became similar to the activity of other two groups with no pain. Conclusions: Reduction of CNP is accompanied by reduced cortical over-activity during movement imagination. Significance: Understanding causes and consequences mechanism through which CNP affects cortical activity

The mechanism of neurofeedback training for treatment of central neuropathic pain in paraplegia : a pilot study

Central neuropathic pain has a prevalence of 40% in patients with spinal cord injury. Electroencephalography (EEG) studies showed that this type of pain has identifiable signatures, that could potentially be targeted by a neuromodulation therapy. The aim of the study was to investigate the putative mechanism of neurofeedback training on central neuropathic pain and its underlying brain signatures in patients with chronic paraplegia. Patients’ EEG activity was modulated from the sensory-motor cortex, electrode location C3/Cz/C4/P4 in up to 40 training sessions Results. Six out of seven patients reported immediate reduction of pain during neurofeedback training. Best results were achieved with suppressing Ɵ and higher β (20–30 Hz) power and reinforcing α power at C4. Four patients reported clinically significant long-term reduction of pain (>30 %) which lasted at least a month beyond the therapy. EEG during neurofeedback revealed a wide spread modulation of power in all three frequency bands accompanied with changes in the coherence most notable in the beta band. The standardized low resolution electromagnetic tomography analysis of EEG before and after neurofeedback therapy showed the statistically significant reduction of power in beta frequency band in all tested patients. Areas with reduced power included the Dorsolateral Prefrontal Cortex, the Anterior Cingulate Cortex and the Insular Cortex. Neurofeedback training produces both immediate and longer term reduction of central neuropathic pain that is accompanied with a measurable short and long term modulation of cortical activity. Controlled trials are required to confirm the efficacy of this neurofeedback protocol on treatment of pain. The study is a registered UKCRN clinical trial Nr 9824

Isometric hip and knee torque measurements as an outcome measure in robot assisted gait training

Strength changes in lower limb muscles following robot assisted gait training (RAGT) in subjects with incomplete spinal cord injury (ISCI) has not been quantified using objective outcome measures. To record changes in the force generating capacity of lower limb muscles (recorded as peak voluntary isometric torque at the knee and hip), before, during and after RAGT in both acute and subacute/chronic ISCI subjects using a repeated measures study design. Eighteen subjects with ISCI participated in this study (Age range: 26–63 years mean age = 49.3 ± 11 years). Each subject participated in the study for a total period of eight weeks, including 6 weeks of RAGT using the Lokomat system (Hocoma AG, Switzerland). Peak torques were recorded in hip flexors, extensors, knee flexors and extensors using torque sensors that are incorporated within the Lokomat. All the tested lower limb muscle groups showed statistically significant (p < 0.001) increases in peak torques in the acute subjects. Comparison between the change in peak torque generated by a muscle and its motor score over time showed a non-linear relationship. The peak torque recorded during isometric contractions provided an objective outcome measure to record changes in muscle strength following RAGT

Palmoplantar keratoderma along with neuromuscular and metabolic phenotypes in Slurp1-deficient mice.

Mutations in SLURP1 cause mal de Meleda, a rare palmoplantar keratoderma (PPK). SLURP1 is a secreted protein that is expressed highly in keratinocytes but has also been identified elsewhere (e.g., spinal cord neurons). Here, we examined Slurp1-deficient mice (Slurp1(-/-)) created by replacing exon 2 with β-gal and neo cassettes. Slurp1(-/-) mice developed severe PPK characterized by increased keratinocyte proliferation, an accumulation of lipid droplets in the stratum corneum, and a water barrier defect. In addition, Slurp1(-/-) mice exhibited reduced adiposity, protection from obesity on a high-fat diet, low plasma lipid levels, and a neuromuscular abnormality (hind-limb clasping). Initially, it was unclear whether the metabolic and neuromuscular phenotypes were due to Slurp1 deficiency, because we found that the targeted Slurp1 mutation reduced the expression of several neighboring genes (e.g., Slurp2, Lypd2). We therefore created a new line of knockout mice (Slurp1X(-/-) mice) with a simple nonsense mutation in exon 2. The Slurp1X mutation did not reduce the expression of adjacent genes, but Slurp1X(-/-) mice exhibited all of the phenotypes observed in the original line of knockout mice. Thus, Slurp1 deficiency in mice elicits metabolic and neuromuscular abnormalities in addition to PPK

PGC-1α is coupled to HIF-1α-dependent gene expression by increasing mitochondrial oxygen consumption in skeletal muscle cells

Mitochondrial biogenesis occurs in response to increased cellular ATP demand. The mitochondrial electron transport chain requires molecular oxygen to produce ATP. Thus, increased ATP generation after mitochondrial biogenesis results in increased oxygen demand that must be matched by a corresponding increase in oxygen supply. We found that overexpression of peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α), which increases mitochondrial biogenesis in primary skeletal muscle cells, leads to increased expression of a cohort of genes known to be regulated by the dimeric hypoxia-inducible factor (HIF), a master regulator of the adaptive response to hypoxia. PGC-1α-dependent induction of HIF target genes under physiologic oxygen concentrations is not through transcriptional coactivation of HIF or up-regulation of HIF-1α mRNA but through HIF-1α protein stabilization. It occurs because of intracellular hypoxia as a result of increased oxygen consumption after mitochondrial biogenesis. Thus, we propose that at physiologic oxygen concentrations, PGC-1α is coupled to HIF signaling through the regulation of intracellular oxygen availability, allowing cells and tissues to match increased oxygen demand after mitochondrial biogenesis with increased oxygen supply

Incorporating translation into sociolinguistic research: translation policy in an international non-governmental organisation

This article explores aspects of translation, multilingualism and language policy in the field of transnational civil society. By focusing on translation policies at Amnesty International, an international non-governmental organisation that performs a key role in global governance, this article seeks to contribute to a globalisation-sensitive sociolinguistics. It argues that combining a sociolinguistic approach, more precisely linguistic ethnography, with translation studies leads to an increased understanding of the language practices under study. Furthermore, the article calls for more interdisciplinary research, stating that there is a space for sociolinguistics and translation studies to contribute to research in international relations and development studies by highlighting the role of multilingualism and challenging the traditionally powerful position of English in transnational civil society

A life in progress: motion and emotion in the autobiography of Robert M. La Follette

This article is a study of a La Follette’s Autobiography, the autobiography of the leading Wisconsin progressive Robert M. La Follette, which was published serially in 1911 and, in book form, in 1913. Rather than focusing, as have other historians, on which parts of La Follette’s account are accurate and can therefore be trusted, it explains instead why and how this major autobiography was conceived and written. The article shows that the autobiography was the product of a sustained, complex, and often fraught series of collaborations among La Follette’s family, friends, and political allies, and in the process illuminates the importance of affective ties as well as political ambition and commitment in bringing the project to fruition. In the world of progressive reform, it argues, personal and political experiences were inseparable

The medical student

The Medical Student was published from 1888-1921 by the students of Boston University School of Medicine