The consequences of traumatic brain injury from the classroom to the courtroom: understanding pathways through structural equation modelling

Purpose: Paediatric traumatic brain injury (TBI) can have resultant ongoing significant impairments which can impact life outcomes. The primary aim of this research was to explore whether TBI contributes to the relationship between poor educational outcomes and offending trajectories. Materials and methods: Through analysis of a dataset consisting of self-reported health, educational, and offending histories of 70 incarcerated young males, structural equation modelling was used to explore the mediation of educational outcomes and patterns in offending behaviour by chronic symptoms following TBI. Results: Symptoms related to TBI significantly mediated the relationship between decreased educational attainment and more frequent convictions. It did not mediate any relationships involving age at first conviction. Conclusions: Traumatic brain injury appears to have more influence over frequency of offending patterns than age at first conviction. However, TBI remains a pervasive factor in both higher rates of offending and poorer educational attainment. In order to tackle this effect on adverse social outcomes, greater attention to the impact of TBI is required in education and criminal justice systems. IMPLICATIONS FOR REHABILITATION Highlights traumatic brain injury as a contributory factor in some education to offending pathways, suggesting that greater focus on rehabilitation within the education and criminal justice systems is required. Reinforces that greater understanding of educational pathways post-injury is needed to better facilitate rehabilitation within the school system

Hyper-IgG4 disease: report and characterisation of a new disease

BACKGROUND: We highlight a chronic inflammatory disease we call 'hyper-IgG4 disease', which has many synonyms depending on the organ involved, the country of origin and the year of the report. It is characterized histologically by a lymphoplasmacytic inflammation with IgG4-positive cells and exuberant fibrosis, which leaves dense fibrosis on resolution. A typical example is idiopathic retroperitoneal fibrosis, but the initial report in 2001 was of sclerosing pancreatitis. METHODS: We report an index case with fever and severe systemic disease. We have also reviewed the histology of 11 further patients with idiopathic retroperitoneal fibrosis for evidence of IgG4-expressing plasma cells, and examined a wide range of other inflammatory conditions and fibrotic diseases as organ-specific controls. We have reviewed the published literature for disease associations with idiopathic, systemic fibrosing conditions and the synonyms: pseudotumour, myofibroblastic tumour, plasma cell granuloma, systemic fibrosis, xanthofibrogranulomatosis, and multifocal fibrosclerosis. RESULTS: Histology from all 12 patients showed, to varying degrees, fibrosis, intense inflammatory cell infiltration with lymphocytes, plasma cells, scattered neutrophils, and sometimes eosinophilic aggregates, with venulitis and obliterative arteritis. The majority of lymphocytes were T cells that expressed CD8 and CD4, with scattered B-cell-rich small lymphoid follicles. In all cases, there was a significant increase in IgG4-positive plasma cells compared with controls. In two cases, biopsies before and after steroid treatment were available, and only scattered plasma cells were seen after treatment, none of them expressing IgG4. Review of the literature shows that although pathology commonly appears confined to one organ, patients can have systemic symptoms and fever. In the active period, there is an acute phase response with a high serum concentration of IgG, and during this phase, there is a rapid clinical response to glucocorticoid steroid treatment. CONCLUSION: We believe that hyper-IgG4 disease is an important condition to recognise, as the diagnosis can be readily verified and the outcome with treatment is very good

Factors associated with vitamin D deficiency in a multicultural inflammatory bowel disease cohort.

OBJECTIVE: The aim of this study was to determine the prevalence of vitamin D deficiency in a multicultural inflammatory bowel disease (IBD) cohort and determine predictors of deficiency including ethnicity. DESIGN: Patients with IBD were recruited into a dedicated database over a 6-month period and evaluated retrospectively. SETTING: Department of Gastroenterology, St George's University Hospital, London, UK. OUTCOMES MEASURED: Clinical data including demographics, ethnic group, disease phenotype by the Montreal classification, vitamin D level and season tested were recorded from clinical and electronic medical records. Vitamin D levels were classified as normal (≥50 nmol/l) and deficient (<50 nmol/l). RESULTS: 168 patients had a vitamin D level measured subsequent to diagnosis. There was no significant difference in the median vitamin D level between patients with Crohn's disease (CD) and ulcerative colitis (UC) (39 nmol/l (IQR 23-56) vs 28 nmol/l (IQR 17-51), p=0.35). Overall the median vitamin D level was significantly lower in non-Caucasians (Asian and Black) versus Caucasians (28 nmol/l (IQR 17-41) vs 41 nmol/l (IQR 25-63), p<0.0001). Multiple regression analysis revealed IBD related surgery (OR 2.9) and ethnicity (OR 6.0 non-Caucasian vs Caucasian) in CD and ethnicity (OR 5.0 non-Caucasian vs Caucasian) in UC were independently associated with vitamin D deficiency. CONCLUSIONS: Vitamin D deficiency is common in IBD patients; therefore, we suggest monitoring of vitamin D levels and correction with supplements especially in non-Caucasians and those with a history of IBD related surgery