scholarly journals Integrative CNS Plasticity With Exercise in MS: The PRIMERS (PRocessing, Integration of Multisensory Exercise-Related Stimuli) Conceptual Framework

2018 ◽  
Vol 32 (10) ◽  
pp. 847-862 ◽  
Author(s):  
Brian M. Sandroff ◽  
Robert W. Motl ◽  
William R. Reed ◽  
Aron K. Barbey ◽  
Ralph H. B. Benedict ◽  
...  

There is a proliferation of research examining the effects of exercise on mobility and cognition in the general population and those with neurological disorders as well as focal research examining possible neural mechanisms of such effects. However, there is seemingly a lack of focus on what it is about exercise, in particular, that drives adaptive central nervous system neuroplasticity. We propose a novel conceptual framework (ie, PRIMERS) that describes such adaptations as occurring via activity-dependent neuroplasticity based on the integrative processing of multisensory input and associated complex motor output that is required for the regulation of physiological systems during exercise behavior. This conceptual framework sets the stage for the systematic examination of the effects of exercise on brain connectivity, brain structure, and molecular/cellular mechanisms that explain improvements in mobility and cognition in the general population and persons with multiple sclerosis (MS). We argue that exercise can be viewed as an integrative, systems-wide stimulus for neurorehabilitation because impaired mobility and cognition are common and co-occurring in MS.

2018 ◽  
Vol 120 (5) ◽  
pp. 2453-2465 ◽  
Author(s):  
Mintao Zhao

Studies of human and rodent navigation often reveal a remarkable cross-species similarity between the cognitive and neural mechanisms of navigation. Such cross-species resemblance often overshadows some critical differences between how humans and nonhuman animals navigate. In this review, I propose that a navigation system requires both a storage system (i.e., representing spatial information) and a positioning system (i.e., sensing spatial information) to operate. I then argue that the way humans represent spatial information is different from that inferred from the cellular activity observed during rodent navigation. Such difference spans the whole hierarchy of spatial representation, from representing the structure of an environment to the representation of subregions of an environment, routes and paths, and the distance and direction relative to a goal location. These cross-species inconsistencies suggest that what we learn from rodent navigation does not always transfer to human navigation. Finally, I argue for closing the loop for the dominant, unidirectional animal-to-human approach in navigation research so that insights from behavioral studies of human navigation may also flow back to shed light on the cellular mechanisms of navigation for both humans and other mammals (i.e., a human-to-animal approach).


2018 ◽  
Author(s):  
Anil Seth

At the birth of psychology as a science, consciousness was its central problem. But throughout the twentieth century, ideological and methodological concerns pushed the explicit empirical study of consciousness to the sidelines. Since the 1990s, studying consciousness has regained a legitimacy and impetus befitting its status as the central feature of our mental lives. Nowadays consciousness science encompasses a rich interdisciplinary mixture drawing together philosophical, theoretical, computational, experimental, and clinical perspectives. While solving the metaphysically ‘hard’ problem of why consciousness is part of the universe may seem as intractable as ever, scientists have learned a great deal about the neural mechanisms underlying conscious states. Further progress will depend on specifying closer explanatory mappings between (first person subjective) phenomenological descriptions and (third person objective) descriptions of biological and physical processes. Such progress will help reframe our understanding of our place in nature, and may also accelerate clinical approaches to a wide range of psychiatric and neurological disorders.


2019 ◽  
Vol 16 (2) ◽  
pp. 265-285
Author(s):  
Christina Fawcett ◽  
Steven Kohm

The action-adventure video games Batman: Arkham Asylum (2009) and Batman: Arkham City (2011) draw on familiar comic book narratives, themes and characters to situate players in a world of participatory violence, crime and madness. In the first game, the player-as-Batman is situated in Arkham Asylum, a high-security facility for the criminally insane and supervillains that also temporarily houses a general population of prisoners from Blackgate Penitentiary. The elision of criminality and mental illness becomes amplified in the second game with the establishment of Arkham City, a combined facility that conflates asylum and prison, completely dissolving any distinction between crime and madness. We draw on Rafter’s conceptual framework of popular criminology to seriously interrogate the representation of violence, crime and madness in these games. More than simply texts offering popular explanations for crime, the games directly implicate the player in violence enacted upon the bodies of criminals and patients alike. Violence is necessary to move the action of the game forward and evokes a range of emotional responses from players who draw from personal experience and other cultural and media representations as they navigate the game. We argue that while the game celebrates violence and the brutal conditions of incarceration, it also offers possibilities for subversive and critical readings. While working to affirm assumptions about crime and mental illness, the game also provides a visceral and visual critique of excessive punishment by the state as a source of injustice for those deemed mad or bad.


Autism ◽  
2020 ◽  
pp. 136236132095137 ◽  
Author(s):  
Pei-Yin Pan ◽  
Sven Bölte ◽  
Preet Kaur ◽  
Sadia Jamil ◽  
Ulf Jonsson

The etiological significance of neurological disorders in autism is debated, but it is clear that they complicate support provision and clinical management, and can have negative impact on outcomes. This systematic review and meta-analysis explored the full range of co-occurring neurological disorders in autism. We estimated the odds of having neurological complications compared to the general population and other neurodevelopmental conditions, as well as the overall prevalence of different neurological disorders. Seventy-nine articles were eligible for the systematic review, including 28 case-control studies, 43 prevalence studies, and 8 cohort studies. Findings were heterogeneous across studies. Overall, autistic individuals were significantly more likely than the general population to exhibit epilepsy, macrocephaly, hydrocephalus, cerebral palsy, migraine/headache, and congenital abnormalities of the nervous system, with prevalence estimates ranging from 1.1% (0%–3.3%; hydrocephalus) to 14.2% (11.3%–17.2%; epilepsy). Epilepsy was also more common in autism than in attention-deficit/hyperactivity disorder (odds ratio [95% confidence interval] = 4.06 [2.81–5.88]). Findings indicate that awareness of neurological disorders and neurological check-ups are indicated in autism to ensure adequate physical health care and support. Prospective studies of neurological disorders in children diagnosed with or at risk of autism might further enhance our understanding of causal pathways. Lay abstract Neurological disorders, such as epilepsy and cerebral palsy, have been reported to occur among individuals with autism beyond chance and may have an impact on daily living across the lifespan. Although there has been research investigating neurological disorders in autism, the findings are not always conclusive. Previous summaries of existing studies have not evaluated the full range of neurological disorders. This study aimed to comprehensively explore the neurological problems appearing in autism to provide updated information that is needed for better healthcare and support in this population. We looked at already published studies focusing on risk or frequency of neurological disorders in autism. Our results suggest that individuals with autism are more likely than the general population to have a range of neurological disorders, including epilepsy, macrocephaly, hydrocephalus, cerebral palsy, migraine/headache, and inborn abnormalities of the nervous system. In order to provide individualized healthcare and support of high quality to individuals diagnosed with autism, health care professionals and other support providers need to be attentive to neurological complications. To further improve our understanding about the link between autism and neurological disorders, future research should follow the neurological health of children who are diagnosed with or are at increased likelihood of autism.


2009 ◽  
Vol 184 (1) ◽  
pp. 31-44 ◽  
Author(s):  
Alexandre Méjat ◽  
Valérie Decostre ◽  
Juan Li ◽  
Laure Renou ◽  
Akanchha Kesari ◽  
...  

The LMNA gene encodes lamins A and C, two intermediate filament-type proteins that are important determinants of interphase nuclear architecture. Mutations in LMNA lead to a wide spectrum of human diseases including autosomal dominant Emery-Dreifuss muscular dystrophy (AD-EDMD), which affects skeletal and cardiac muscle. The cellular mechanisms by which mutations in LMNA cause disease have been elusive. Here, we demonstrate that defects in neuromuscular junctions (NMJs) are part of the disease mechanism in AD-EDMD. Two AD-EDMD mouse models show innervation defects including misexpression of electrical activity–dependent genes and altered epigenetic chromatin modifications. Synaptic nuclei are not properly recruited to the NMJ because of mislocalization of nuclear envelope components. AD-EDMD patients with LMNA mutations show the same cellular defects as the AD-EDMD mouse models. These results suggest that lamin A/C–mediated NMJ defects contribute to the AD-EDMD disease phenotype and provide insights into the cellular and molecular mechanisms for the muscle-specific phenotype of AD-EDMD.


2017 ◽  
Vol 372 (1715) ◽  
pp. 20160157 ◽  
Author(s):  
Melanie A. Gainey ◽  
Daniel E. Feldman

We compare the circuit and cellular mechanisms for homeostatic plasticity that have been discovered in rodent somatosensory (S1) and visual (V1) cortex. Both areas use similar mechanisms to restore mean firing rate after sensory deprivation. Two time scales of homeostasis are evident, with distinct mechanisms. Slow homeostasis occurs over several days, and is mediated by homeostatic synaptic scaling in excitatory networks and, in some cases, homeostatic adjustment of pyramidal cell intrinsic excitability. Fast homeostasis occurs within less than 1 day, and is mediated by rapid disinhibition, implemented by activity-dependent plasticity in parvalbumin interneuron circuits. These processes interact with Hebbian synaptic plasticity to maintain cortical firing rates during learned adjustments in sensory representations. This article is part of the themed issue ‘Integrating Hebbian and homeostatic plasticity’.


2021 ◽  
Vol 13 ◽  
Author(s):  
Morgan Crewe ◽  
Ram Madabhushi

The nervous system is vulnerable to genomic instability and mutations in DNA damage response factors lead to numerous developmental and progressive neurological disorders. Despite this, the sources and mechanisms of DNA damage that are most relevant to the development of neuronal dysfunction are poorly understood. The identification of primarily neurological abnormalities in patients with mutations in TDP1 and TDP2 suggest that topoisomerase-mediated DNA damage could be an important underlying source of neuronal dysfunction. Here we review the potential sources of topoisomerase-induced DNA damage in neurons, describe the cellular mechanisms that have evolved to repair such damage, and discuss the importance of these repair mechanisms for preventing neurological disorders.


2021 ◽  
Author(s):  
Nuttida Rungratsameetaweemana ◽  
Claudia Lainscsek ◽  
Sydney S Cash ◽  
Javier O Garcia ◽  
Terrence J Sejnowski ◽  
...  

Dynamic functional brain connectivity facilitates adaptive cognition and behavior. Abnormal alterations within such connectivity could result in disrupted functions observed across various neurological conditions. As one of the most common neurological disorders, epilepsy is defined by the seemingly random occurrence of spontaneous seizures. A central but unresolved question concerns the mechanisms by which extraordinarily diverse dynamics of seizures emerge. Here, we apply a graph-theoretical approach to assess dynamic reconfigurations in the functional brain connectivity before, during, and after seizures that display heterogeneous propagation patterns despite sharing similar origins. We demonstrate unique reconfigurations in globally-defined network properties preceding seizure onset that predict propagation patterns of impending seizures, and in locally-defined network properties that differentiate post-onset dynamics. These results characterize quantitative network features underlying the heterogeneity of seizure dynamics and the accompanying clinical manifestations. Decoding these network properties could improve personalized preventative treatment strategies for epilepsy as well as other neurological disorders.


2021 ◽  
Author(s):  
Marius Zimmermann ◽  
Arianna Schiano Lomoriello ◽  
Ivana Konvalinka

We often perform actions while observed by others, yet the behavioural and neural signatures of audience effects remain understudied. Performing actions while being observed has been shown to result in more emphasized movements in musicians and dancers, as well as during communicative actions. Here we investigate the behavioural and neural mechanisms of observed actions in relation to individual actions in isolation and interactive joint actions. Movement kinematics and EEG were recorded in 42 participants (21 pairs) during a mirror game paradigm, while participants produced improvised movements alone, while observed by a partner, or by synchronizing movements with the partner. Participants produced largest movements when being observed; and observed actors and dyads in interaction produced slower and less variable movements in contrast to acting alone. On a neural level, we observed increased mu suppression during interaction, as well as to a lesser extent during observed actions, relative to individual actions. Moreover, we observed increased functional brain connectivity during observed actions relative to both individual and interactive actions, suggesting increased intra-individual monitoring and action-perception integration as a result of audience effects. These results suggest that observed actors take observers into account in their action plans by increasing self-monitoring; and on a behavioural level, observed actions are similar to emergent interactive actions, characterized by slower and more predictable movements.


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