Being mindful of mindfulness interventions in cancer: A systematic review of intervention reporting and study methodology.

OBJECTIVES: While mindfulness-based stress reduction (MBSR) and mindfulness-based cognitive therapy (MBCT) have demonstrated efficacy in clinical populations, the potential therapeutic benefit of mindfulness in the context of cancer is less clear. The aim of this review was to critically appraise mindfulness intervention reporting and study methodology. METHODS: Studies using randomized control trial design and/or a control arm were included. PubMed, Medline, PsycINFO, CINAHL, and Embase databases between January 1999 and April 2017 were searched. Studies were assessed on (1) reported theoretical framework, (2) intervention description, and (3) justification of modifications to standardized MBSR/MBCT. The overall quality of study design and research methodology were also assessed. RESULTS: Of 30 studies identified, none adhered to MBSR. Modified versions of MBSR were reported in 19 studies. Five studies reported variants of MBCT, 1 used a combination of MBSR/MBCT, and 5 inadequately documented the intervention/ theoretical framework. Overall, component and timeline modifications were poorly documented and justified. Mean intervention contact time was less than standardized MBSR/MBCT protocols. Target outcomes were poorly justified, and 12 studies failed to identify a primary aim, reporting multiple outcomes. Only 9 of 15 studies recruiting clinical populations included clinical cutoffs, and an active therapeutic control was included in 4 studies. CONCLUSIONS: Mindfulness is increasingly considered a standard therapy in psycho-oncology. While many studies proclaim benefits, considerable variability, modification to standardized protocols, and claims of benefit often reflect decreases in sub-clinical supportive care symptomology rather than therapeutic relief of clinically significant psychological disorders.

Negative neuroplasticity in chronic traumatic brain injury and implications for neurorehabilitation.

Based on growing findings of brain volume loss and deleterious white matter alterations during the chronic stages of injury, researchers posit that moderate-severe traumatic brain injury (TBI) may act to "age" the brain by reducing reserve capacity and inducing neurodegeneration. Evidence that these changes correlate with poorer cognitive and functional outcomes corroborates this progressive characterization of chronic TBI. Borrowing from a framework developed to explain cognitive aging (Mahncke et al., Progress in Brain Research, 157, 81-109, 2006a; Mahncke et al., Proceedings of the National Academy of Sciences of the United States of America, 103(33), 12523-12528, 2006b), we suggest here that environmental factors (specifically environmental impoverishment and cognitive disuse) contribute to a downward spiral of negative neuroplastic change that may modulate the brain changes described above. In this context, we review new literature supporting the original aging framework, and its extrapolation to chronic TBI. We conclude that negative neuroplasticity may be one of the mechanisms underlying cognitive and neural decline in chronic TBI, but that there are a number of points of intervention that would permit mitigation of this decline and better long-term clinical outcomes.

Examining moderators of cognitive recovery trajectories after moderate to severe traumatic brain injury.

OBJECTIVES: To examine the influence of cognitive reserve-related moderator variables on recovery trajectories during the first year after traumatic brain injury (TBI). Using mixed effects models, we measured (1) the level of cognitive function at 2 and 12 months postinjury and (2) the trajectories of cognitive recovery during the first 12 months postinjury. DESIGN: Repeated-measures design with neuropsychological testing at 2, 5, and 12 months postinjury. SETTING: Large, urban inpatient neurorehabilitation program. PARTICIPANTS: Patients (N=75) with moderate-to-severe TBI. INTERVENTIONS: Not applicable. PRIMARY OUTCOMES: neuropsychological composite scores including simple speed of processing, complex speed of processing, memory, untimed executive functions, and attention span. Primary predictors: age, estimated premorbid intelligence quotient (IQ), and years of education. RESULTS: Only age significantly moderated trajectories. Decreasing age significantly enhanced recovery of speed of processing, both simple (2-12mo postinjury, P<.001) and complex (2-12mo postinjury, P<.05; 5-12mo postinjury, P<.005). Decreasing age and increasing estimated premorbid IQ were associated with higher performance at 2 and 12mo postinjury for simple speed of processing (premorbid IQ, 2 and 12mo), complex speed of processing (age, 2 and 12mo), untimed executive functions (premorbid IQ, 2 and 12mo), and memory (premorbid IQ, 2 and 12mo). CONCLUSIONS: Recovery of speed of processing (both simple and complex) was favorably moderated by younger age. Older age is associated with more neuronal loss and less integrity of white matter, and speed of processing is associated with white matter networks. The recuperative effects of younger age may therefore be attributable to greater reserve capacity (as indexed by white matter integrity). Lower age and higher estimated premorbid IQ were associated with higher functioning on a variety of cognitive outcomes. This may reflect the buffering effects of reserve capacity or premorbid differences in age and IQ-related cognitive functioning. Implications for rehabilitation and recovery mechanisms are discussed.

Traumatic brain injury and post-acute decline: what role does environmental enrichment play? A scoping review.

OBJECTIVES: While a growing number of studies provide evidence of neural and cognitive decline in traumatic brain injury (TBI) survivors during the post-acute stages of injury, there is limited research as of yet on environmental factors that may influence this decline. The purposes of this paper, therefore, are to (1) examine evidence that environmental enrichment (EE) can influence long-term outcome following TBI, and (2) examine the nature of post-acute environments, whether they vary in degree of EE, and what impact these variations have on outcomes. METHODS: We conducted a scoping review to identify studies on EE in animals and humans, and post-discharge experiences that relate to barriers to recovery. RESULTS: One hundred and twenty-three articles that met inclusion criteria demonstrated the benefits of EE on brain and behavior in healthy and brain-injured animals and humans. Nineteen papers on post-discharge experiences revealed that variables such as insurance coverage, financial, and social support, home therapy, and transition from hospital to home, can have an impact on clinical outcomes. CONCLUSION: There is evidence to suggest that lack of EE, whether from lack of resources or limited ability to engage in such environments, may play a role in post-acute cognitive and neural decline. Maximizing EE in the post-acute stages of TBI may improve long-term outcomes for the individual, their family and society.