Search

Objective: The aim of the study is to evaluate the safety and efficacy of a physiatrist-led clinical pathway to expedite rehabilitation transitions for stroke patients with dysphagia requiring nasogastric tube or percutaneous endoscopic gastrostomy. Design: This is a retrospective single-center observational study in 426 adults with stroke and dysphagia admitted to the acute hospital. Physican Medicine and Rehabilitation (PM&R) was consulted to determine dysphagia prognosis and candidacy for rehabilitation admission with nasogastric tube or percutaneous endoscopic gastrostomy. The proportion of patients accepted with nasogastric tube versus percutaneous endoscopic gastrostomy, progression to total oral diet during rehabilitation, and lengths of stay were tracked. Results: The rate of recovery to total oral diet for patients accepted with nasogastric tube was 38/44 = 86.3% versus 29/75 = 38.6% with percutaneous endoscopic gastrostomy. There was a significant difference in mean time to total oral diet with nasogastric tube (20.37 days) versus percutaneous endoscopic gastrostomy (34.46 days): t(43) = 4.49, P < 0.001. The acute hospital length of stay was significantly shorter with nasogastric tube (12.9 days) versus percutaneous endoscopic gastrostomy (20.4 days): t(117) = 4.16, P < 0.001. Rehabilitation length of stay did not differ significantly between groups (26.9 vs. 32.0 days). Conclusion: Physiatrist-led initiatives to evaluate stroke patients with dysphagia can expedite rehabilitation transitions, prevent unnecessary invasive procedures, and reduce acute hospital length of stay. [ABSTRACT FROM AUTHOR]

Numerous biological mechanisms contribute to outcome after stroke, including brain injury, inflammation, and repair mechanisms. Clinical genetic studies have the potential to discover biological mechanisms affecting stroke recovery in humans and identify intervention targets. Large sample sizes are needed to detect commonly occurring genetic variations related to stroke brain injury and recovery. However, this usually requires combining data from multiple studies where consistent terminology, methodology, and data collection timelines are essential. Our group of expert stroke and rehabilitation clinicians and researchers with knowledge in genetics of stroke recovery here present recommendations for harmonizing phenotype data with focus on measures suitable for multicenter genetic studies of ischemic stroke brain injury and recovery. Our recommendations have been endorsed by the International Stroke Genetics Consortium. [ABSTRACT FROM AUTHOR]

There are now a large number of technological and methodological approaches to the rehabilitation of motor function after stroke. It is important to employ these approaches in a manner that is tailored to specific patient impairments and desired functional outcomes, while avoiding the hype of overly broad or unsubstantiated claims for efficacy. Here we review the evidence for poststroke plasticity, including therapy-related plasticity and functional imaging data. Early demonstrations of remapping in somatomotor and somatosensory representations have been succeeded by findings of white matter plasticity and a focus on activity-dependent changes in neuronal properties and connections. The methods employed in neurorehabilitation have their roots in early understanding of neuronal circuitry and plasticity, and therapies involving large numbers of repetitions, such as robotic therapy and constraint-induced movement therapy (CIMT), change measurable nervous systems properties. Other methods that involve stimulation of brain and peripheral excitable structures have the potential to harness neuroplastic mechanisms, but remain experimental. Gaps in our understanding of the neural substrates targeted by neurorehabilitation technology and techniques remain, preventing their prescriptive application in individual patients as well as their general refinement. However, with ongoing research—facilitated in part by technologies that can capture quantitative information about motor performance—this gap is narrowing. These research approaches can improve efforts to attain the shared goal of better functional recovery after stroke. [ABSTRACT FROM AUTHOR]

Background and purpose: The preponderance of evidence from recent studies in human subjects supports a negative effect of the BDNF Val66Met polymorphism on motor outcomes and motor recovery. However prior studies have generally reported the effect of the Met allele in older stroke patients, while potential effects in younger stroke patients have remained essentially unexamined. The lack of research in younger patients is significant since aging effects on CNS repair and functional recovery after stroke are known to interact with the effects of genetic polymorphisms. Here we present a study of first-ever ischemic stroke patients aged 15–49 years that examines the effect of Met carrier status on functional disability. Methods: 829 patients with a first ischemic stroke (Average age = 41.4 years, SD = 6.9) were recruited from the Baltimore-Washington region. Genotyping was performed at the Johns Hopkins University Center for Inherited Disease Research (CIDR). Data cleaning and harmonization were done at the GEI-funded GENEVA Coordinating Center at the University of Washington. Our sample contained 165 Met carriers and 664 non-Met carriers. Modified Rankin scores as recorded at discharge were obtained from the hospital records by study personnel blinded to genotype, and binarized into "Good" versus "Poor" outcomes (mRS 0–2 vs. 3+), with mRS scores 3+ reflecting a degree of disability that causes loss of independence. Results: Our analysis showed that the Met allele conveyed a proportionally greater risk for poor outcomes and disability-related loss of independence with mRS scores 3+ (adjusted OR 1.73, 95% CI 1.13–2.64, p = 0.01). Conclusions: The BDNF Val66Met polymorphism was negatively associated with functional outcomes at discharge in our sample of 829 young stroke patients. This finding stands in contrast to what would be predicted under the tenets of the resource modulation hypothesis (i.e. that younger patients would be spared from the negative effect of the Met allele on recovery since it is posited to arise as a manifestation of age-related decline in physiologic resources). [ABSTRACT FROM AUTHOR]

The development of clinical vectors to correct genetic mutations that cause inherited myopathies and related disorders of skeletal muscle is advancing at an impressive rate. Adeno-associated virus vectors are attractive for clinical use because (1) adeno-associated viruses do not cause human disease and (2) these vectors are able to persist for years. New vectors are now becoming available as gene therapy delivery tools, and recent preclinical experiments have demonstrated the feasibility, safety, and efficacy of gene therapy with adeno-associated virus for long-term correction of muscle pathology and weakness in myotubularin-deficient canine and murine disease models. In this review, recent advances in the application of gene therapies to treat inherited muscle disorders are presented, including Duchenne muscular dystrophy and x-linked myotubular myopathy. Potential areas for therapeutic synergies between rehabilitation medicine and genetics are also discussed. [ABSTRACT FROM AUTHOR]