RESUMEN
AIM: Sports activities provide social interaction for humans. Commitment to a given team is a salient feature of being a sports fan and becomes a prominent part of self-identification for fanatics. Emotion, subjective hedonic experience, and non-romantic love are related to fan behaviors. Few studies have evaluated the neural basis of sports fanaticism. METHODS: Thirty men, including 16 football fanatics and 14 non-fanatics, with a mean age of 27.4 ± 6.4 years (range, 20-48 years) were enrolled. Subjects underwent functional MRI while watching a set of goals scored by favorite, rival, and neutral teams. RESULTS: The analysis of variance in a general linear model revealed a significant Group × Condition interaction effect in the bilateral dorsal anterior cingulate cortex (dACC) that was more prominent in the left hemisphere. In the post-hoc comparisons, fanatics showed increased activation in bilateral dACC, supplementary motor area, superior frontal cortex, right dorsolateral prefrontal cortex, and right insula for Favorite > Neutral contrast and an increased activation in bilateral dACC and supplementary motor area for Rival > Neutral contrast. Seed-based connectivity analyses using the areas with significant activation differences revealed increased connectivity between dACC and several regions, including the left posterior lateral temporal area, insula, bilateral medial temporal area, and medial superior frontal area as well as the basal ganglia in fanatics compared to non-fanatics. CONCLUSION: Our results suggest that football fanatics exhibit a different brain activation and connectivity pattern from non-fanatics, both under favorable and unfavorable conditions. This brain activity and connectivity pattern under emotionally laden conditions may represent higher responses to rewards, higher emotional valence attribution, and stronger motivational state of football fanatics, which might underlie their unusual behavioral responses.
Asunto(s)
Ganglios Basales/fisiología , Emociones/fisiología , Giro del Cíngulo/fisiología , Corteza Motora/fisiología , Corteza Prefrontal/fisiología , Fútbol/psicología , Adulto , Ganglios Basales/diagnóstico por imagen , Giro del Cíngulo/diagnóstico por imagen , Humanos , Imagen por Resonancia Magnética , Masculino , Persona de Mediana Edad , Corteza Motora/diagnóstico por imagen , Corteza Prefrontal/diagnóstico por imagen , Adulto JovenRESUMEN
Familial Mediterranean fever (FMF) is an autosomal recessive autoinflammatory disease of childhood and adulthood. Development of systemic amyloidosis and frequent attack influence quality of life and survival. There is sporadic evidence indicating subclinical inflammation in patients with FMF. We aimed to assess subclinical inflammation using neutrophil to lymphocyte ratio (NLR), platelet to lymphocyte ratio (PLR), and C-reactive protein (CRP) in pediatric patients with FMF in the attack-free period. In this retrospective study, we reviewed the files of all FMF patients in our pediatric rheumatology outpatient clinic in a tertiary center and enrolled those with sufficient clinical and laboratory data. We also enrolled 73 controls. We grouped the patients according to being in attack period or attack-free period. We compared CRP, NLR, PLR, and WBC (white blood cell) levels between different mutations and polymorphisms. We also compared patients in the attack period with those in attack-free period. We enrolled 61 patients in attack period, 509 patients in attack-free period, and 73 controls. There was no difference between patients with different mutations with respect to NLR or PLR levels in the attack-free period. However, CRP levels were higher in patients with homozygous exon 10 mutations, especially those with homozygous M694V mutations compared with other mutations. However, CRP levels were mostly normal in these patients. Our data are against the reported fact that patients with FMF have higher NLR or PLR levels in attack-free periods. However, CRP levels were higher in the presence of homozygous exon 10 mutations (in particular homozygous M694V mutations).