Relationship between Barkhof criteria and the clinical features of multiple sclerosis in northern Japan

Background and Objective: We previously reported that the prevalence of MS in Tokachi Province of Hokkaido has increased from 8.6 to 13.1 per 100,000 individuals between 2001 and 2006. Here, we studied the frequency of MS patients who fulfill the Barkhof criteria and identified their common features. Subjects: All 47 subjects in our previous study, who fulfilled Poser's criteria, were included in this study. Results: Of these, 33 satisfied the Barkhof criteria. In 2006, 9.2 per 100,000 MS patients fulfilled the Barkhof criteria; the percentage of patients who fulfilled these criteria was significantly higher among patients born after 1960 than among those born before 1960 (84.3% and 40.0%, respectively). The proportion of patients with conventional MS (C-MS) who fulfilled the Barkhof criteria was higher than that of patients with opticospinal MS (OS-MS) who fulfilled these criteria (93.9% and 71.4%, respectively). Longitudinally extensive spinal cord lesions (LESCLs) were not associated with the brain lesions defined in the Barkhof criteria (Barkhof brain lesions). Conclusion: In Tokachi Province, the increased percentage of MS patients who fulfill the Barkhof criteria was associated with increased C-MS incidence and increase in the proportion of C-MS patients with Barkhof brain lesions among people born after 1960

TNF-alpha contributes to the death of NGF-dependent neurons during development

Many sympathetic and sensory neurons depend on a supply of nerve growth factor (NGF) from their targets during development, and neurons that fail to obtain sufficient NGF die by apoptosis. Here we show that tumor necrosis factor alpha (TNF) is involved in bringing about the death of NGF-deprived neurons. Function-blocking antibodies against either TNF or TNF receptor 1 (TNFR1) rescued many sympathetic and sensory neurons following NGF deprivation in vitro. Fewer sympathetic and sensory neurons died during the phase of naturally occurring neuronal death in TNF-deficient embryos, and neurons from these embryos survived in culture better than wild-type neurons. These neurons coexpress TNF and TNFR1 during this stage of development, suggesting that TNF acts by an autocrine loop