Purpose: This longitudinal study investigated long-term effects of a multidisciplinary rehabilitation program consisting of resistance and sensorimotor training, patient education, and stress management over 6 months in patients with chronic low back pain.
Methods: Ninety-six patients with chronic recurrent low back pain performed a multidisciplinary rehabilitation program. We assessed pain-free lumbar spine range of motion (ROM), strength of the lumbar extensor muscles, and pain by visual analog scale (VAS). Furthermore, the Roland-Morris (RM) questionnaire and SF-36 were used. The examinations were performed before and after rehabilitation, and a long-term follow-up was performed after 18 months.
Results: All outcome measurements (ROM, VAS, RM, muscle strength, and SF-36 scores) improved significantly from baseline to the post-rehabilitation evaluation. These improvements were found to persist until a follow-up evaluation 18 months after cessation of the intervention.
Conclusions: Our findings confirm the results of former studies evaluating the short-term effects of multidisciplinary rehabilitation programs. In addition, our data demonstrate that well-balanced outpatient rehabilitation programs may induce persistent improvements in muscle strength, pain, function and quality of life in patients with chronic low back pain.
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http://dx.doi.org/10.1007/s00586-013-3156-z | DOI Listing |
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View Article and Find Full Text PDFAlzheimers Dement
December 2024
NYU Grossman School of Medicine, New York, NY, USA; NYU, New York City, NY, USA.
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View Article and Find Full Text PDFBackground: There are no cures for Alzheimer's disease (AD), a progressive neurodegenerative disorder characterized by elevation of beta-amyloid and tau proteins besides neuronal death and causing cognitive impairment. Phosphodiesterase 5 (PDE5) is a cyclic guanosine monophosphate-degrading enzyme involved in numerous biological pathways including those relevant to memory formation. PDE5 inhibition offers the potential to attenuate AD progression by acting at the downstream level of beta-amyloid and tau elevation.
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