Computational and Mathematical Methods in Medicine

The theory of affordances, a conceptual pillar of the ecological approach to perception and action, has the potential to become a guiding principle for research on perception and action in sport. Affordances are opportunities for action. They describe the environment in terms of behaviors that are possible at a given moment under a given set of conditions. Affordances capture the tight coupling between perception and action, and allow for the prospective and moment-to-moment control of activity that is characteristic of fluent, fast-paced behavior on the playing field. We begin with an overview of the ecological approach and the principle of direct perception, using past research on interceptive action to illustrate how this principle has been put to work to capture information-movement relations in perceptualmotor skill. We then review theory and research on body-scaled, action-scaled, and social affordances, highlighting outstanding questions that provide opportunities for new research on affordances in the context of sport. We conclude with consideration of affordances as providing a functional semantics for sports.

Information, affordances, and the control of action in sport.

The benefits of regular exercise, physical fitness and sports participation on cardiovascular and brain health are undeniable. Physical activity reduces the risk for cardiovascular disease, type 2 diabetes, hypertension, obesity, and stroke, and produces beneficial effects on cholesterol levels, antioxidant systems, inflammation, and vascular function. Exercise also enhances psychological health, reduces age-related loss of brain volume, improves cognition, reduces the risk of developing dementia, and impedes neurodegeneration. Nonetheless, the play of sports is associated with risks, including a risk for mild TBI (mTBI) and, rarely, catastrophic traumatic injury and death. There is also growing awareness that repetitive mTBIs, such as concussion and subconcussion, can occasionally produce persistent cognitive, behavioral, and psychiatric problems as well as lead to the development of a neurodegeneration, chronic traumatic encephalopathy (CTE). In this review, we summarize the beneficial aspects of sports participation on psychological, emotional, physical and cognitive health, and specifically analyze some of the less common adverse neuropathological outcomes, including concussion, second-impact syndrome, juvenile head trauma syndrome, catastrophic sudden death, and CTE. CTE is a latent neurodegeneration clinically associated with behavioral changes, executive dysfunction and cognitive impairments, and pathologically characterized by frontal and temporal lobe atrophy, neuronal and axonal loss, and abnormal deposits of paired helical filament (PHF)-tau and 43 kDa TAR deoxyribonucleic acid (DNA)-binding protein (TDP-43). CTE often occurs as a sole diagnosis, but may be associated with other neurodegenerative disorders, including motor neuron disease (CTE-MND). Although the incidence and prevalence of CTE are not known, CTE has been reported most frequently in American football players and boxers. Other sports associated with CTE include ice hockey, professional wrestling, soccer, rugby, and baseball.

http://i2.cdn.turner.com/cnn/2014/images/02/28/mckee.neuropath.of.sport.2014.acta.copy.pdf

The neuropathology of sport

Aging, hypertension, diabetes, hypoxia/obstructive sleep apnea (OSA), obesity, vitamin B12/folate deficiency, depression, and traumatic brain injury synergistically promote diverse pathological mechanisms including cerebral hypoperfusion and glucose hypometabolism. These risk factors trigger neuroinflammation and oxidative-nitrosative stress that in turn decrease nitric oxide and enhance endothelin, Amyloid-β deposition, cerebral amyloid angiopathy, and blood-brain barrier disruption. Proinflammatory cytokines, endothelin-1, and oxidative-nitrosative stress trigger several pathological feedforward and feedback loops. These upstream factors persist in the brain for decades, upregulating amyloid and tau, before the cognitive decline. These cascades lead to neuronal Ca2+ increase, neurodegeneration, cognitive/memory decline, and Alzheimer's disease (AD). However, strategies are available to attenuate cerebral hypoperfusion and glucose hypometabolism and ameliorate cognitive decline. AD is the leading cause of dementia among the elderly. There is significant evidence that pathways involving inflammation and oxidative-nitrosative stress (ONS) play a key pathophysiological role in promoting cognitive dysfunction. Aging and several comorbid conditions mentioned above promote diverse pathologies. These include inflammation, ONS, hypoperfusion, and hypometabolism in the brain. In AD, chronic cerebral hypoperfusion and glucose hypometabolism precede decades before the cognitive decline. These comorbid disease conditions may share and synergistically activate these pathophysiological pathways. Inflammation upregulates cerebrovascular pathology through proinflammatory cytokines, endothelin-1, and nitric oxide (NO). Inflammation-triggered ONS promotes long-term damage involving fatty acids, proteins, DNA, and mitochondria; these amplify and perpetuate several feedforward and feedback pathological loops. The latter includes dysfunctional energy metabolism (compromised mitochondrial ATP production), amyloid-β generation, endothelial dysfunction, and blood-brain-barrier disruption. These lead to decreased cerebral blood flow and chronic cerebral hypoperfusion- that would modulate metabolic dysfunction and neurodegeneration. In essence, hypoperfusion deprives the brain from its two paramount trophic substances, viz., oxygen and nutrients. Consequently, the brain suffers from synaptic dysfunction and neuronal degeneration/loss, leading to both gray and white matter atrophy, cognitive dysfunction, and AD. This Review underscores the importance of treating the above-mentioned comorbid disease conditions to attenuate inflammation and ONS and ameliorate decreased cerebral blood flow and hypometabolism. Additionally, several strategies are described here to control chronic hypoperfusion of the brain and enhance cognition. © 2016 Wiley Periodicals, Inc.

Cerebral hypoperfusion and glucose hypometabolism: Key pathophysiological modulators promote neurodegeneration, cognitive impairment, and Alzheimer's disease.

Stroke survivors often adapt to the loss of upper-limb function by adopting compensatory strategies. Jones discusses evidence that these compensatory strategies may influence the neural remodelling processes that occur after the initial stroke and can have mixed effects on functional outcome of the paretic limb.

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Motor compensation and its effects on neural reorganization after stroke

Although a proportion of individuals report chronic cognitive difficulties after mild traumatic brain injury (mTBI), results from behavioral testing have been inconsistent. In fact, the variability inherent to the mTBI population may be masking subtle cognitive deficits. We hypothesized that this variability could be reduced by accounting for post-concussion syndrome (PCS) in the sample. Thirty-six participants with mTBI (>1 year post-injury) and 36 non-head injured controls performed information processing speed (Paced Visual Serial Addition Task, PVSAT) and working memory (n-Back) tasks. Both groups were split by PCS diagnosis (4 groups, all n = 18), with categorization of controls based on symptom report. Participants with mTBI and persistent PCS had significantly greater error rates on both the n-Back and PVSAT, at every difficulty level except 0-Back (used as a test of performance validity). There was no difference between any of the other groups. Therefore, a cognitive deficit can be observed in mTBI participants, even 1 year after injury. Correlations between cognitive performance and symptoms were only observed for mTBI participants, with worse performance correlating with lower sleep quality, in addition to a medium effect size association (falling short of statistical significance) with higher PCS symptoms, post-traumatic stress disorder (PTSD), and anxiety. These results suggest that the reduction in cognitive performance is not due to greater symptom report itself, but is associated to some extent with the initial injury. Furthermore, the results validate the utility of our participant grouping, and demonstrate its potential to reduce the variability observed in previous studies.

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Long-term effects of mild traumatic brain injury on cognitive performance

Primary objective: To compare the prevalence of persistent post-concussion syndrome (PCS; >1 year post-injury) in participants with mild traumatic brain injury (mTBI) and those without head injury. Research design: A cross-sectional sample of 119 participants with mTBI and 246 without previous head injury. Methods: Online questionnaires collected data about post-concussion symptoms, cognitive failures, anxiety, depression, sleep behaviour and post-traumatic stress disorder. Variability within the sample was addressed by splitting by PCS diagnosis to create four groups: mTBI + PCS, mTBI-PCS, Control + PCS and Control-PCS. PCS was diagnosed using ICD-10 criteria in all groups, with controls not requiring previous head injury. Main outcomes and results: PCS was present to a similar extent in participants with no head injury (34%) compared to those with mTBI (31%). Only report of headaches, which could be caused by expectation bias, distinguished between mTBI + PCS and Control + PCS groups. In addition, significantly higher cognitive problems were observed in participants with mTBI compared with the control group. Conclusions: Persistent PCS, as currently defined, is not specific to mTBI. These data suggest that somatic and cognitive symptoms are most likely to be able to distinguish PCS after mTBI from that present in the general population. Further research is necessary into these factors in order to create more specific PCS diagnostic criteria.

Post-concussion syndrome: Prevalence after mild traumatic brain injury in comparison with a sample without head injury

To investigate sustained structural changes in the long-term (>1 year) after mild traumatic brain injury (mTBI) and their relationship to ongoing post-concussion syndrome (PCS).

Long-term structural changes after mTBI and their relation to post-concussion symptoms

Motor disorders increase dramatically with age; however, little is known about non-clinical ageing of motor control mechanisms and their respective neural correlates. With the present experiment we aimed to study age effects on advance movement preparation, a key characteristic of motor behaviour that is known to involve premotor and primary motor circuits. The respective brain regions are subject to age-related brain atrophy of grey and white matter, and we therefore hypothesized that motor preparation mechanisms
may be altered in older persons.Using a motor priming paradigm, performance data and event-related potentials were recorded in older (68–83 years) and younger (21–25 years) participants. The effect pattern observed for the younger group fully replicated previous findings, showing significant reaction time benefits and greater foreperiod activity for valid trials, as well as lateralized
activation over motor regions. In older participants, the validity effect was insignificant, which corresponded to markedly reduced foreperiod amplitudes and the absence of lateralized activity. At the same time, the event-related potential showed a frontocentrally distributed positive component peaking in the P300 latency range after presentation of the prime. The amplitude of this potential was enhanced in elderly compared with young participants.The data suggest that the information processing related to the anticipation and preparation of an upcoming response changes substantially with age. In contrast to younger participants, older participants show
no indication of effector-specific activation and recruit frontal areas in anticipation of a response signal. It is therefore not only movement execution that changes with age but also motor cognition.

Keywords: ageing, contingent negative variation, electroencephalography, event-related laterality, lateralised readiness potential,
movement preparation

Neural correlates of movement preparation in healthy ageing.

Background: Persistent postconcussion syndrome (PCS) occurs in around 5– 10% of individuals after mild traumatic brain injury (mTBI), but research into the underlying biology of these ongoing symptoms is limited and inconsistent. One reason for this could be the heterogeneity inherent to mTBI, with individualized injury mechanisms and psychological factors. A multimodal imaging study may be able to characterize the injury better. Aim: To look at the relationship between functional (fMRI), structural (diffusion tensor imaging), and metabolic (magnetic resonance spectroscopy) data in the same participants in the long term (>1 year) after injury. It was hypothesized that only those mTBI participants with persistent PCS would show functional changes, and that these changes would be related to reduced structural integrity and altered metabolite concentrations. Methods: Functional changes associated with persistent PCS after mTBI (>1 year postinjury) were investigated in participants with and without PCS (both n = 8) and non-head injured participants (n = 9) during performance of working memory and attention/processing speed tasks. Correlation analyses were performed to look at the relationship between the functional data and structural and metabolic alterations in the same participants. Results: There were no behavioral differences between the groups, but participants with greater PCS symptoms exhibited greater activation in attention-related areas (anterior cingulate), along with reduced activation in temporal, default mode network, and working memory areas (left prefrontal) as cognitive load was increased from the easiest to the most difficult task. Functional changes in these areas correlated with reduced structural integrity in corpus callosum and anterior white matter, and reduced creatine concentration in right dorsolateral prefrontal cortex. Conclusion: These data suggest that the top-down attentional regulation and deactivation of task-irrelevant areas may be compensating for the reduction in working memory capacity and variation in white matter transmission caused by the structural and metabolic changes after injury. This may in turn be contributing to secondary PCS symptoms such as fatigue and headache. Further research is required using multimodal data to investigate the mechanisms of injury after mTBI, but also to aid individualized diagnosis and prognosis.

https://www.onlinelibrary.wiley.com/doi/pdf/10.1002/brb3.292

Philip J. A. Dean

Papers

Long-term effects of mild traumatic brain injury on cognitive performance

Post-concussion syndrome: Prevalence after mild traumatic brain injury in comparison with a sample without head injury

Long-term structural changes after mTBI and their relation to post-concussion symptoms

Neural correlates of movement preparation in healthy ageing.

Multimodal imaging of mild traumatic brain injury and persistent postconcussion syndrome