Identification of Chronic Postural Stability Impairments Associated With History of Concussion

Concussion is the most common form of traumatic brain injury (TBI). However, there is a disproportionate level of understanding between the acute and chronic impairments associated with traumatic brain injury. Specifically, problems maintaining balance during standing and walking are cardinal signs of acute concussion, but the temporal extent to which postural control deficits remain following the initial injury are not well defined or understood. The purpose of the projects composing this dissertation was to examine the long-term effects of a prior history of concussion on static (i.e. standing) and dynamic (i.e. gait) postural control. To address this, healthy adults aged 18-45 reporting a prior history of concussion(s) as well as age-matched controls with no documented concussion history were recruited to participate. Static postural control was assessed using a force plate system to track each participant’s center-of-pressure during standing. Spatiotemporal parameters as well as head stability during gait were assessed using a pressure-sensitive walkway and accelerometers placed at the head, neck, and lower trunk, respectively. The findings of these projects indicate that concussion has detrimental effects on both static and dynamic postural stability years after the initial injury and clinical determination of recovery. Specifically, individuals with a prior history of concussion demonstrated greater postural sway displacement and reduced sway regularity under dual-task conditions compared to the control group. In addition, previously concussed individuals demonstrated less variability in their gait cadence and step length, which suggests a reduction in the complexity of the neural networks contributing to postural control. Lastly, individuals with a history of concussion demonstrated greater triaxial accelerations at the head during gait, indicating a reduced ability to attenuate gait-related oscillations and stabilize the head. Collectively, these findings indicate that concussion is associated with impaired postural control that persists for years after the initial injury and well beyond the point where clinical testing protocols can identify deficits in maintaining balance. Future efforts should be directed toward incorporating more sophisticated measures and analyses of postural stability in concussion screenings to improve clinicians’ abilities to identify the scope in which concussion negatively impacts the function of the central nervous system

Influence of carbacetam on neurologic destruction processes under the experimental traumatic brain injury

Objective of the research. Provide the research of the influence of Carbacetam on the neurologic destruction processes in paraventricular and supraoptic nuclei of the hypothalamus under the experimental traumatic brain injury (TBI).Materials and methods of the research. The research was held by means of white outbred male rats weighing 200±10 g. The modulation of the traumatic brain injury was based on the method of V.M. Eslki and S.V. Ziablitsev (2008), where the TBI was caused due to gravity load on animals with the strike energy of 0.52 J. The lethal outcome during the first 5 days after the TBI was 84%. The control group (n=10) was administered 1 ml of saline intraperitoneally within the 10 days after TBI. The rats of experimental group (n=10) were provided Carbacetam (5 mg per 1 kg) in 1 ml of saline. After the experiment, the animals were decapitated followed by the removal of the brain, and the histological medicines were produced by means of Microtome after the appropriate histological processing. Some sections were stained with hematoxylin and eosin, others - properly prepared before applying the neuromarkers NSE, S-100 and GFAP. The morphological and immune histochemical evaluation of neurodegenerative changes in the nerve tissue were done by the produced medicines.Outcomes and discussion of them. The outcomes of the research show that Carbacetam influences the decrease of the degenerative processes in the neural tissue of paraventricular and supraoptic nuclei of the hypothalamus. The neurons of the animals after TBI being administered with the Carbacetam, are characterized by the restoration of the normal morphological features unlike the rats that did not receive the medicine. Immune histochemical research of the brain neuronal markers confirms the functional recovery of the neurons and astrocytes in the researched areas of the hypothalamus of the rats after administration of Carbacetam. The decrease in the expression of glial markers GFAP and S-100 has been observed, showing the reduction of degenerative changes in the neural tissue. Meanwhile, the expression of neuronal marker NSE has increased, showing high metabolic activity of the nerve cells. However, changes in the expression of the neural markers and glia feature the restoring of normal neuronal activity due to the administration of Carbacetam.Therefore, further research of Carbacetam effects is promising in terms of restoring the neuronal destruction under TBI

Preventing Neurodegenerative Memory Loss in Hopfield Neuronal Networks Using Cerebral Organoids or External Microelectronics

Developing technologies have made significant progress towards linking the brain with brain-machine interfaces (BMIs) which have the potential to aid damaged brains to perform their original motor and cognitive functions. We consider the viability of such devices for mitigating the deleterious effects of memory loss that is induced by neurodegenerative diseases and/or traumatic brain injury (TBI). Our computational study considers the widely used Hopfield network, an autoassociative memory model in which neurons converge to a stable state pattern after receiving an input resembling the given memory. In this study, we connect an auxiliary network of neurons, which models the BMI device, to the original Hopfield network and train it to converge to its own auxiliary memory patterns. Injuries to the original Hopfield memory network, induced through neurodegeneration, for instance, can then be analyzed with the goal of evaluating the ability of the BMI to aid in memory retrieval tasks. Dense connectivity between the auxiliary and Hopfield networks is shown to promote robustness of memory retrieval tasks for both optimal and nonoptimal memory sets. Our computations estimate damage levels and parameter ranges for which full or partial memory recovery is achievable, providing a starting point for novel therapeutic strategies

Expert consensus document: Mind the gaps—advancing research into short-term and long-term neuropsychological outcomes of youth sports-related concussions

Sports-related concussions and repetitive subconcussive exposure are increasingly recognized as potential dangers to paediatric populations, but much remains unknown about the short-term and long-term consequences of these events, including potential cognitive impairment and risk of later-life dementia. This Expert Consensus Document is the result of a 1-day meeting convened by Safe Kids Worldwide, the Alzheimer\u27s Drug Discovery Foundation, and the Andrews Institute for Orthopaedics and Sports Medicine. The goal is to highlight knowledge gaps and areas of critically needed research in the areas of concussion science, dementia, genetics, diagnostic and prognostic biomarkers, neuroimaging, sports injury surveillance, and information sharing. For each of these areas, we propose clear and achievable paths to improve the understanding, treatment and prevention of youth sports-related concussions

Investigating the neural basis of self-awareness deficits following traumatic brain injury

Self-awareness deficits are a common and disabling consequence of traumatic brain injury (TBI). ‘On-line’ awareness is one facet of self-awareness that can be studied by examining how people monitor their performance and respond to their errors. Performance monitoring, like many of the cognitive functions disrupted after TBI, is believed to depend on the coordinated activity of neural networks. The fronto-parietal control network (FPCN) is one such network that contains a sub-network called the salience network (SN). The SN consists of the dorsal anterior cingulate (dACC) and bilateral insulae cortex and is thought to monitor salient events (e.g. errors). I used advanced structure and function MRI techniques to investigate these networks and test two overarching hypotheses: first, performance monitoring is regulated by regions within the FPCN; and second, dysfunction of the FPCN leads to impaired self-awareness after TBI. My first study demonstrated two distinct frontal networks that respond to different error types. Predictable/internally signalled errors caused SN activation; whereas unpredictable/externally signalled errors caused activation of the ventral attentional network, a network thought to respond to unexpected events. This suggested the presence of parallel performance monitoring systems within the FPCN. My second study established that the ‘driving’ input into the SN originated in right anterior insula and subsequent behavioural adaptation was regulated by enhanced effective connectivity from the dACC to the left anterior insula. In my third study I identified a large group of TBI patients with impaired performance monitoring. These patients had additional metacognitive evidence of impaired self-awareness and demonstrated reduced functional connectivity between the dACC and the remainder of the FPCN at ‘rest’, and abnormally large insulae activation in response to errors. These studies clarified how the brain monitors and responds to salient events; and, provided evidence that self-awareness deficits after TBI are due to FPCN dysfunction, identifying this network as a potential target for future treatments.Open Acces

Neural and cognitive biomarkers of binge and heavy drinking

BACKGROUND: Theories suggest two motivations that drive people to consume alcohol at pathological levels: (1) seeking of short-term pleasurable effects and (2) alleviation of unpleasant states. The former is associated with binge drinking (BD; i.e. high intake during fewer occasions) and the latter with heavy drinking (HD; substantial intake during more occasions). Although direct comparisons have not been made, BD has been associated with impairments in top-down executive control (related to frontal-parietal regions) and HD has been linked to bottom-up changes in internal mentation (related to the default mode network anatomical structure and function). This dissertation compares the two drinking patterns with the goal of testing for differential neurocognitive and neuroanatomical characteristics that would be indicative of two disorder subtypes. METHODS: The sample consisted of adult participants with a history of adolescent onset: BD (N = 16), HD (N = 15), and Healthy Controls (HC; N = 21). All groups were equated on age, education, amount of lifetime alcohol consumed (BD and HD groups), as well as other factors. The study compared group performance on an affective go/no go task and group differences in brain volume and cortical thickness based on structural MRI. RESULTS: Behavioral results showed a higher number of errors for the HD group, in comparison to other groups. Volumetric results indicated a smaller bilateral ventral diencephalon in both BD and HD, in comparison to the HC, and smaller bilateral globus pallidus in BD only. Cortical thickness analyses revealed a thinner left superior parietal region (overlapping with the dorsal attention and fronto-parietal networks) in BD, whereas a left medial occipito-parietal region was thicker in HD (overlapping mainly with the visual network). CONCLUSION: These data, interpreted in the context of prior studies, suggest that BD findings might be indicative of an executive control dysregulation that could contribute to continued BD. HD findings might be indicative of tissue damage due to frequent drinking. Prior research has found the occipital region to have the highest concentration γ-Aminobutyric acid receptors that are affected by alcohol, which might explain the thicker occipital region findings in the HD group

Do informal caregivers of people with dementia mirror the cognitive deficits of their demented patients?:A pilot study

Recent research suggests that informal caregivers of people with dementia (ICs) experience more cognitive deficits than noncaregivers. The reason for this is not yet clear. Objective: to test the hypothesis that ICs ‘mirror' the cognitive deficits of the demented people they care for. Participants and methods: 105 adult ICs were asked to complete three neuropsychological tests: letter fluency, category fluency, and the logical memory test from the WMS-III. The ICs were grouped according to the diagnosis of their demented patients. One-sample ttests were conducted to investigate if the standardized mean scores (t-scores) of the ICs were different from normative data. A Bonferroni correction was used to correct for multiple comparisons. Results: 82 ICs cared for people with Alzheimer's dementia and 23 ICs cared for people with vascular dementia. Mean letter fluency score of the ICs of people with Alzheimer's dementia was significantly lower than the normative mean letter fluency score, p = .002. The other tests yielded no significant results. Conclusion: our data shows that ICs of Alzheimer patients have cognitive deficits on the letter fluency test. This test primarily measures executive functioning and it has been found to be sensitive to mild cognitive impairment in recent research. Our data tentatively suggests that ICs who care for Alzheimer patients also show signs of cognitive impairment but that it is too early to tell if this is cause for concern or not