Frequent computer-related activities are an independent risk factor for NSP and LBP. Daily use of computers exceeding 2-3 h seems to be a threshold for NSP and exceeding 5 h for LBP. Computer-related activities may explain the increase of NSP and LBP in the 1990s and the beginning of 2000.

Results Prevalence of pain in the back and neck was greater in the 1990s than in the 1980s and increased steadily from 1993 to 1997. Pain of the neck and shoulder and pain of the lower back was much more common in 1999 than in 1991 and in 2001 than in 1999. Pain was more common among girls and older groups: pain of the neck and shoulder affected 24% of girls and 12% of boys in 14 year olds, 38% of girls and 16% of boys in 16 year olds, and 45% of girls and 19% of boys in 18 year olds; pain in the lower back affected 8% of girls and 7% of boys in 14 year olds, 14% of girls and 11% of boys in 16 year olds, and 17% of boys and 13% of girls in 18 year olds. Conclusion Pain in the neck, shoulder, and lower back is becoming more common in Finnish adolescents. This pain suggests a new disease burden of degenerative musculoskeletal disorders in future adults.

No abstract

No abstract

The progressive myoclonus epilepsies, featuring the triad of myoclonus, seizures, and ataxia, comprise a large group of inherited neurodegenerative diseases that remain poorly understood and refractory to treatment. The Cystatin B gene is mutated in one of the most common forms of progressive myoclonus epilepsy, Unverricht-Lundborg disease (EPM1). Cystatin B knockout in a mouse model of EPM1 triggers progressive degeneration of cerebellar granule neurons. Here, we report impaired redox homeostasis as a key mechanism by which Cystatin B deficiency triggers neurodegeneration. Oxidative stress induces the expression of Cystatin B in cerebellar granule neurons, and EPM1 patient-linked mutation of the Cystatin B gene promoter impairs oxidative stress induction of Cystatin B transcription. Importantly, Cystatin B knockout or knockdown sensitizes cerebellar granule neurons to oxidative stress-induced cell death. The Cystatin B deficiency-induced predisposition to oxidative stress in neurons is mediated by the lysosomal protease Cathepsin B. We uncover evidence of oxidative damage, reflected by depletion of antioxidants and increased lipid peroxidation, in the cerebellum of Cystatin B knock-out mice in vivo. Collectively, our findings define a pathophysiological mechanism in EPM1, whereby Cystatin B deficiency couples oxidative stress to neuronal death and degeneration, and may thus provide the basis for novel treatment approaches for the progressive myoclonus epilepsies.