Self-generated expressions of residual complaints following brain injury

Following brain injury there is often a prolonged period of deteriorating psychological condition, despite neurological stability or improvement. This is presumably consequent to the remission of anosognosia and the realisation of permanently worsened status. This change is hypothesised to be directed partially by the socially mediated processes which play a role in generating self-awareness and which here direct the reconstruction of the self as a permanently injured person. However, before we can understand this process of redevelopment, we need an unbiassed technique to monitor self-awareness. Semi-structured interviews were conducted with 30 individuals with long-standing brain injuries to capture their spontaneous complaints and their level of insight into the implications of their difficulties. The focus was on what the participants said in their own words, and the extent to which self-knowledge of difficulties was spontaneously salient to the participants. Their responses were subjected to content analysis. Most participants were able to say that they had brain injuries and physical difficulties, many mentioned memory and attentional problems and a few made references to a variety of emotional disturbances. Content analysis of data from unbiassed interviews can reveal the extent to which people with brain injuries know about their difficulties. Social constructionist accounts of self-awareness and recovery are supported.

Recovery from brain injury: Finding the missing bits of the puzzle

Background: One basic problem found during rehabilitation is that people with brain injuries lack awareness of their difficulties. Research into this phenomenon has often disregarded the voices of those affected by the trauma and do not give an insider's perspective on the process through which a person with a brain injury develops awareness of their difficulties.

A comparative study of nursing attitudes towards young male survivors of brain injury: A questionnaire survey.

Background The attitudes members of the nursing profession hold towards survivors of brain injury may impact on the level of help, and degree of involvement they are willing to have. Given that the manner in which an individual receives their brain injury has been shown to impact on public prejudices, the importance of exploring nursing attitudes to this vulnerable group, and the subsequent impact this may have on the caring role, requires investigation. Objective To investigate the attitudes held by members of the nursing profession towards young male survivors of brain injury whose behaviour either contributed, or did not contribute, to their injury. Design Independent groups design. Setting and participants Ninety trainee and sixty-nine qualified nurses respectively drawn from a university in the south west of England and the emergency, orthopaedic and paediatric Departments of the Royal Devon and Exeter Hospital, UK. Methods Participants were randomly assigned to one of four fictional brain injury scenarios. A young male character was portrayed as sustaining a brain injury as a result of either an aneurysm, or through drug taking, with their behaviour being either a contributory or non-contributory factor. On reading these, participants were asked to complete the prejudicial evaluation scale, the social interaction scale and the helping behaviour scale. Results Analysis of variance showed that qualified nurses held more prejudicial attitudes than student nurses towards survivors of brain injury. Mean scores indicated that individuals seen as contributing towards their injury were likely to experience more prejudice (blame total = 42.35 vs. no blame total = 38.34), less social interaction (blame total = 37.54 vs. no blame total = 41.10), and less helping behaviour (blame total = 21.49 vs. no blame total = 22.34) by both groups. Conclusions Qualified nurses should be mindful of the impact their attitudes and judgements of survivors of brain injury may have on the subsequent care they provide. Greater emphasis on the effects of negative attitudes on patient interactions during training may provide nurses with the understanding to recognise and avoid challenges to their caring role in the future.

BACE1 mRNA Expression in Alzheimer's Disease Postmortem Brain Tissue

ß-site AßPP cleaving enzyme 1 (BACE1) catalyses the rate-limiting step for production of amyloid-ß (Aß) peptides, involved in the pathological cascade underlying Alzheimer's disease (AD). Elevated BACE1 protein levels and activity have been reported in AD postmortem brains. Our study explored whether this was due to elevated BACE1 mRNA expression. RNA was prepared from five brain regions in three study groups: controls, individuals with AD, and another neurodegenerative disease group affected by either Parkinson's disease (PD) or dementia with Lewy bodies (DLB). BACE1 mRNA levels were measured using quantitative realtime PCR (qPCR) and analyzed by qbasePLUS using validated stably-expressed reference genes. Expression of glial and neuronal markers (glial fibrillary acidic protein (GFAP) and neuron-specific enolase (NSE), respectively) were also analyzed to quantify the changing activities of these cell populations in the tissue. BACE1 mRNA levels were significantly elevated in medial temporal and superior parietal gyri, compared to the PD/DLB and/or control groups. Superior frontal gryus BACE1 mRNA levels were significantly increased in the PD/DLB group, compared to AD and control groups. For the AD group, BACE1 mRNA changes were analyzed in the context of the reduced NSE mRNA, and strongly increased GFAP mRNA levels apparent as AD progressed (indicated by Braak stage). This analysis suggested that increased BACE1 mRNA expression in remaining neuronal cells may contribute to the increased BACE1 protein levels and activity found in brain regions affected by AD.

Retinopathy is reduced during experimental diabetes in a mouse model of outer retinal degeneration

PURPOSE. Diabetic patients who also have retinitis pigmentosa (RP) appear to have fewer and less severe retinal microvascular lesions. Diabetic retinopathy may be linked to increased inner retinal hypoxia, with the possibility that this is exacerbated by oxygen usage during the dark-adaptation response. Therefore, patients with RP with depleted rod photoreceptors may encounter proportionately less retinal hypoxia, and, when diabetes is also present, there may be fewer retinopathic lesions. This hypothesis was tested in rhodopsin knockout mice (Rho(-/-)) as an RP model in which the diabetic milieu is superimposed. The study was designed to investigate whether degeneration of the outer retina has any impact on hypoxia, to examine diabetes-related retinal gene expression responses, and to assess lesions of diabetic retinopathy.

Clinical risk factors for age-related macular degeneration: a systematic review and meta-analysis

Background: Age-related macular degeneration (AMD) is the leading cause of blindness in Western countries. Numerous risk factors have been reported but the evidence and strength of association is variable. We aimed to identify those risk factors with strong levels of evidence which could be easily assessed by physicians or ophthalmologists to implement preventive interventions or address current behaviours.

Systematic review and meta-analysis of the association between complement component 3 and age-related macular degeneration: A HUGE review and meta-analysis

We performed a meta-analysis to estimate the magnitude of C3 gene polymorphism effects, and their possible mode of action, on age-related macular degeneration (AMD). The meta-analysis included 16 studies for rs2230199 and 7 studies for rs1047286. Data extraction and risk of bias assessments were performed in duplicate, and heterogeneity and publication bias were explored. There was moderate evidence for association between both polymorphisms and AMD in individuals of European descent. For rs2230199, patients with CG and GG genotypes were 1.44 (95% CI: 1.33 – 1.56) and 1.88 (95% CI: 1.59 – 2.23) times more likely to have AMD than patients with CC genotype. For rs1047286, those with GA and AA genotypes had 1.27 (95% CI: 1.15 – 1.41) and 1.70 (95% CI: 1.27 – 2.11) times higher risk of AMD than those with GG genotypes. These gene effects suggested an additive model. The population attributable risks for the GG/GC and AA/GA genotypes are approximately 5-10%. Stratification of studies on the basis of ethnicity indicates that these variants are very infrequent in Asian populations and the significance of the effect observed is based largely on the high frequency of these variants within individuals of European descent. This meta-analysis supports the association between C3 and AMD and provides a robust estimate of the genetic risk.