Pub Date : 2024-05-01eCollection Date: 2024-01-01DOI: 10.3389/fnetp.2024.1392701
Drew C Gottman, Bradford J Smith
Introduction: Acute respiratory distress syndrome (ARDS) presents a significant clinical challenge, with ventilator-induced lung injury (VILI) being a critical complication arising from life-saving mechanical ventilation. Understanding the spatial and temporal dynamics of VILI can inform therapeutic strategies to mitigate lung damage and improve outcomes.
Methods: Histological sections from initially healthy mice and pulmonary lavage-injured mice subjected to a second hit of VILI were segmented with Ilastik to define regions of lung injury. A scale-free network approach was applied to assess the correlation between injury regions, with regions of injury represented as 'nodes' in the network and 'edges' quantifying the degree of correlation between nodes. A simulated time series analysis was conducted to emulate the temporal sequence of injury events.
Results: Automated segmentation identified different lung regions in good agreement with manual scoring, achieving a sensitivity of 78% and a specificity of 85% across 'injury' pixels. Overall accuracy across 'injury', 'air', and 'other' pixels was 81%. The size of injured regions followed a power-law distribution, suggesting a 'rich-get-richer' phenomenon in the distribution of lung injury. Network analysis revealed a scale-free distribution of injury correlations, highlighting hubs of injury that could serve as focal points for therapeutic intervention. Simulated time series analysis further supported the concept of secondary injury events following an initial insult, with patterns resembling those observed in seismological studies of aftershocks.
Conclusion: The size distribution of injured regions underscores the spatially heterogeneous nature of acute and ventilator-induced lung injury. The application of network theory demonstrates the emergence of injury 'hubs' that are consistent with a 'rich-get-richer' dynamic. Simulated time series analysis demonstrates that the progression of injury events in the lung could follow spatiotemporal patterns similar to the progression of aftershocks in seismology, providing new insights into the mechanisms of injury distribution and propagation. Both phenomena suggest a potential for interventions targeting these injury 'hubs' to reduce the impact of VILI in ARDS management.
{"title":"A scale-free model of acute and ventilator-induced lung injury: a network theory approach inspired by seismology.","authors":"Drew C Gottman, Bradford J Smith","doi":"10.3389/fnetp.2024.1392701","DOIUrl":"https://doi.org/10.3389/fnetp.2024.1392701","url":null,"abstract":"<p><strong>Introduction: </strong>Acute respiratory distress syndrome (ARDS) presents a significant clinical challenge, with ventilator-induced lung injury (VILI) being a critical complication arising from life-saving mechanical ventilation. Understanding the spatial and temporal dynamics of VILI can inform therapeutic strategies to mitigate lung damage and improve outcomes.</p><p><strong>Methods: </strong>Histological sections from initially healthy mice and pulmonary lavage-injured mice subjected to a second hit of VILI were segmented with Ilastik to define regions of lung injury. A scale-free network approach was applied to assess the correlation between injury regions, with regions of injury represented as 'nodes' in the network and 'edges' quantifying the degree of correlation between nodes. A simulated time series analysis was conducted to emulate the temporal sequence of injury events.</p><p><strong>Results: </strong>Automated segmentation identified different lung regions in good agreement with manual scoring, achieving a sensitivity of 78% and a specificity of 85% across 'injury' pixels. Overall accuracy across 'injury', 'air', and 'other' pixels was 81%. The size of injured regions followed a power-law distribution, suggesting a 'rich-get-richer' phenomenon in the distribution of lung injury. Network analysis revealed a scale-free distribution of injury correlations, highlighting hubs of injury that could serve as focal points for therapeutic intervention. Simulated time series analysis further supported the concept of secondary injury events following an initial insult, with patterns resembling those observed in seismological studies of aftershocks.</p><p><strong>Conclusion: </strong>The size distribution of injured regions underscores the spatially heterogeneous nature of acute and ventilator-induced lung injury. The application of network theory demonstrates the emergence of injury 'hubs' that are consistent with a 'rich-get-richer' dynamic. Simulated time series analysis demonstrates that the progression of injury events in the lung could follow spatiotemporal patterns similar to the progression of aftershocks in seismology, providing new insights into the mechanisms of injury distribution and propagation. Both phenomena suggest a potential for interventions targeting these injury 'hubs' to reduce the impact of VILI in ARDS management.</p>","PeriodicalId":73092,"journal":{"name":"Frontiers in network physiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11097687/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140960390","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-08eCollection Date: 2024-01-01DOI: 10.3389/fnetp.2024.1356653
Yupeng Tian, Srikar Saradhi, Edward Bello, Matthew D Johnson, Gabriele D'Eleuterio, Milos R Popovic, Milad Lankarany
Introduction: Closed-loop control of deep brain stimulation (DBS) is beneficial for effective and automatic treatment of various neurological disorders like Parkinson's disease (PD) and essential tremor (ET). Manual (open-loop) DBS programming solely based on clinical observations relies on neurologists' expertise and patients' experience. Continuous stimulation in open-loop DBS may decrease battery life and cause side effects. On the contrary, a closed-loop DBS system uses a feedback biomarker/signal to track worsening (or improving) of patients' symptoms and offers several advantages compared to the open-loop DBS system. Existing closed-loop DBS control systems do not incorporate physiological mechanisms underlying DBS or symptoms, e.g., how DBS modulates dynamics of synaptic plasticity. Methods: In this work, we propose a computational framework for development of a model-based DBS controller where a neural model can describe the relationship between DBS and neural activity and a polynomial-based approximation can estimate the relationship between neural and behavioral activities. A controller is used in our model in a quasi-real-time manner to find DBS patterns that significantly reduce the worsening of symptoms. By using the proposed computational framework, these DBS patterns can be tested clinically by predicting the effect of DBS before delivering it to the patient. We applied this framework to the problem of finding optimal DBS frequencies for essential tremor given electromyography (EMG) recordings solely. Building on our recent network model of ventral intermediate nuclei (Vim), the main surgical target of the tremor, in response to DBS, we developed neural model simulation in which physiological mechanisms underlying Vim-DBS are linked to symptomatic changes in EMG signals. By using a proportional-integral-derivative (PID) controller, we showed that a closed-loop system can track EMG signals and adjust the stimulation frequency of Vim-DBS so that the power of EMG reaches a desired control target. Results and discussion: We demonstrated that the model-based DBS frequency aligns well with that used in clinical studies. Our model-based closed-loop system is adaptable to different control targets and can potentially be used for different diseases and personalized systems.
{"title":"Model-based closed-loop control of thalamic deep brain stimulation.","authors":"Yupeng Tian, Srikar Saradhi, Edward Bello, Matthew D Johnson, Gabriele D'Eleuterio, Milos R Popovic, Milad Lankarany","doi":"10.3389/fnetp.2024.1356653","DOIUrl":"https://doi.org/10.3389/fnetp.2024.1356653","url":null,"abstract":"<p><p><b>Introduction:</b> Closed-loop control of deep brain stimulation (DBS) is beneficial for effective and automatic treatment of various neurological disorders like Parkinson's disease (PD) and essential tremor (ET). Manual (open-loop) DBS programming solely based on clinical observations relies on neurologists' expertise and patients' experience. Continuous stimulation in open-loop DBS may decrease battery life and cause side effects. On the contrary, a closed-loop DBS system uses a feedback biomarker/signal to track worsening (or improving) of patients' symptoms and offers several advantages compared to the open-loop DBS system. Existing closed-loop DBS control systems do not incorporate physiological mechanisms underlying DBS or symptoms, e.g., how DBS modulates dynamics of synaptic plasticity. <b>Methods:</b> In this work, we propose a computational framework for development of a model-based DBS controller where a neural model can describe the relationship between DBS and neural activity and a polynomial-based approximation can estimate the relationship between neural and behavioral activities. A controller is used in our model in a quasi-real-time manner to find DBS patterns that significantly reduce the worsening of symptoms. By using the proposed computational framework, these DBS patterns can be tested clinically by predicting the effect of DBS before delivering it to the patient. We applied this framework to the problem of finding optimal DBS frequencies for essential tremor given electromyography (EMG) recordings solely. Building on our recent network model of ventral intermediate nuclei (Vim), the main surgical target of the tremor, in response to DBS, we developed neural model simulation in which physiological mechanisms underlying Vim-DBS are linked to symptomatic changes in EMG signals. By using a proportional-integral-derivative (PID) controller, we showed that a closed-loop system can track EMG signals and adjust the stimulation frequency of Vim-DBS so that the power of EMG reaches a desired control target. <b>Results and discussion:</b> We demonstrated that the model-based DBS frequency aligns well with that used in clinical studies. Our model-based closed-loop system is adaptable to different control targets and can potentially be used for different diseases and personalized systems.</p>","PeriodicalId":73092,"journal":{"name":"Frontiers in network physiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11033853/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140871646","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-03-07eCollection Date: 2024-01-01DOI: 10.3389/fnetp.2024.1302499
Siva Venkadesh, Asmir Shaikh, Heman Shakeri, Ernest Barreto, John Darrell Van Horn
Transient synchronization of bursting activity in neuronal networks, which occurs in patterns of metastable itinerant phase relationships between neurons, is a notable feature of network dynamics observed in vivo. However, the mechanisms that contribute to this dynamical complexity in neuronal circuits are not well understood. Local circuits in cortical regions consist of populations of neurons with diverse intrinsic oscillatory features. In this study, we numerically show that the phenomenon of transient synchronization, also referred to as metastability, can emerge in an inhibitory neuronal population when the neurons' intrinsic fast-spiking dynamics are appropriately modulated by slower inputs from an excitatory neuronal population. Using a compact model of a mesoscopic-scale network consisting of excitatory pyramidal and inhibitory fast-spiking neurons, our work demonstrates a relationship between the frequency of pyramidal population oscillations and the features of emergent metastability in the inhibitory population. In addition, we introduce a method to characterize collective transitions in metastable networks. Finally, we discuss potential applications of this study in mechanistically understanding cortical network dynamics.
{"title":"Biophysical modulation and robustness of itinerant complexity in neuronal networks.","authors":"Siva Venkadesh, Asmir Shaikh, Heman Shakeri, Ernest Barreto, John Darrell Van Horn","doi":"10.3389/fnetp.2024.1302499","DOIUrl":"10.3389/fnetp.2024.1302499","url":null,"abstract":"<p><p>Transient synchronization of bursting activity in neuronal networks, which occurs in patterns of metastable itinerant phase relationships between neurons, is a notable feature of network dynamics observed <i>in vivo</i>. However, the mechanisms that contribute to this dynamical complexity in neuronal circuits are not well understood. Local circuits in cortical regions consist of populations of neurons with diverse intrinsic oscillatory features. In this study, we numerically show that the phenomenon of transient synchronization, also referred to as metastability, can emerge in an inhibitory neuronal population when the neurons' intrinsic fast-spiking dynamics are appropriately modulated by slower inputs from an excitatory neuronal population. Using a compact model of a mesoscopic-scale network consisting of excitatory pyramidal and inhibitory fast-spiking neurons, our work demonstrates a relationship between the frequency of pyramidal population oscillations and the features of emergent metastability in the inhibitory population. In addition, we introduce a method to characterize collective transitions in metastable networks. Finally, we discuss potential applications of this study in mechanistically understanding cortical network dynamics.</p>","PeriodicalId":73092,"journal":{"name":"Frontiers in network physiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10954887/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140186465","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-12-22DOI: 10.3389/fnetp.2023.1271042
Debora Kaiser-Graf, Angela Schulz, Eva Mangelsen, Michael Rothe, Juliane Bolbrinker, Reinhold Kreutz
Background: Glomerular hyperfiltration (GH) is an important mechanism in the development of albuminuria in hypertension. The Munich Wistar Frömter (MWF) rat is a non-diabetic model of chronic kidney disease (CKD) with GH due to inherited low nephron number resulting in spontaneous albuminuria and podocyte injury. In MWF rats, we identified prostaglandin (PG) E2 (PGE2) signaling as a potential causative mechanism of albuminuria in GH.Method: For evaluation of the renal PGE2 metabolic pathway, time-course lipidomic analysis of PGE2 and its downstream metabolites 15-keto-PGE2 and 13-14-dihydro-15-keto-PGE2 was conducted in urine, plasma and kidney tissues of MWF rats and albuminuria-resistant spontaneously hypertensive rats (SHR) by liquid chromatography electrospray ionization tandem mass spectrometry (LC/ESI-MS/MS).Results: Lipidomic analysis revealed no dysregulation of plasma PGs over the time course of albuminuria development, while glomerular levels of PGE2 and 15-keto-PGE2 were significantly elevated in MWF compared to albuminuria-resistant SHR. Overall, averaged PGE2 levels in glomeruli were up to ×150 higher than the corresponding 15-keto-PGE2 levels. Glomerular metabolic ratios of 15-hydroxyprostaglandin dehydrogenase (15-PGDH) were significantly lower, while metabolic ratios of prostaglandin reductases (PTGRs) were significantly higher in MWF rats with manifested albuminuria compared to SHR, respectively.Conclusion: Our data reveal glomerular dysregulation of the PGE2 metabolism in the development of albuminuria in GH, resulting at least partly from reduced PGE2 degradation. This study provides first insights into dynamic changes of the PGE2 pathway that support a role of glomerular PGE2 metabolism and signaling for early albuminuria manifestation in GH.
{"title":"Tissue lipidomic profiling supports a mechanistic role of the prostaglandin E2 pathway for albuminuria development in glomerular hyperfiltration","authors":"Debora Kaiser-Graf, Angela Schulz, Eva Mangelsen, Michael Rothe, Juliane Bolbrinker, Reinhold Kreutz","doi":"10.3389/fnetp.2023.1271042","DOIUrl":"https://doi.org/10.3389/fnetp.2023.1271042","url":null,"abstract":"Background: Glomerular hyperfiltration (GH) is an important mechanism in the development of albuminuria in hypertension. The Munich Wistar Frömter (MWF) rat is a non-diabetic model of chronic kidney disease (CKD) with GH due to inherited low nephron number resulting in spontaneous albuminuria and podocyte injury. In MWF rats, we identified prostaglandin (PG) E2 (PGE2) signaling as a potential causative mechanism of albuminuria in GH.Method: For evaluation of the renal PGE2 metabolic pathway, time-course lipidomic analysis of PGE2 and its downstream metabolites 15-keto-PGE2 and 13-14-dihydro-15-keto-PGE2 was conducted in urine, plasma and kidney tissues of MWF rats and albuminuria-resistant spontaneously hypertensive rats (SHR) by liquid chromatography electrospray ionization tandem mass spectrometry (LC/ESI-MS/MS).Results: Lipidomic analysis revealed no dysregulation of plasma PGs over the time course of albuminuria development, while glomerular levels of PGE2 and 15-keto-PGE2 were significantly elevated in MWF compared to albuminuria-resistant SHR. Overall, averaged PGE2 levels in glomeruli were up to ×150 higher than the corresponding 15-keto-PGE2 levels. Glomerular metabolic ratios of 15-hydroxyprostaglandin dehydrogenase (15-PGDH) were significantly lower, while metabolic ratios of prostaglandin reductases (PTGRs) were significantly higher in MWF rats with manifested albuminuria compared to SHR, respectively.Conclusion: Our data reveal glomerular dysregulation of the PGE2 metabolism in the development of albuminuria in GH, resulting at least partly from reduced PGE2 degradation. This study provides first insights into dynamic changes of the PGE2 pathway that support a role of glomerular PGE2 metabolism and signaling for early albuminuria manifestation in GH.","PeriodicalId":73092,"journal":{"name":"Frontiers in network physiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138944830","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-12-15DOI: 10.3389/fnetp.2023.1285658
Arcady A. Putilov
Introduction: Several widely held explanations of the mechanisms underlying the responses of endogenous sleep–wake-regulating processes to early weekday wakeups have been proposed. Here, they were briefly reviewed and validated against simulations based on the rhythmostatic version of a two-process model of sleep–wake regulation.Methods: Simulated sleep times on weekdays and weekends were compared with the times averaged over 1,048 samples with either earlier or later weekday risetimes. In total, 74 paired samples were collected before and during lockdown, and 93 paired samples were collected during early and later school start times.Results: The counterintuitive predictions of the simulations included the following: 1) only one night of ad lib sleep is sufficient to restore the endogenously determined sleep times after 1 day/5 days of larger/smaller reduction/extension of the sleep/wake phase of the circadian sleep–wake cycle; 2) sleep loss on weekdays is irrecoverable; 3) irrespective of the amount of such deadweight loss, sleep on weekends is not prolonged; and 4) the control of the circadian clocks over the sleep–wake cyclicity is not disrupted throughout the week.Discussion: The following popular explanations of the gaps between weekends and weekdays in sleep timing and duration were not supported by these simulations: 1) early weekday wakeups cause “social jetlag,” viewed as the weekend and weekday (back and forth) shifts of the sleep phase relative to the unchanged phase of the circadian clocks, and 2) early weekday wakeups cause an accumulation of “sleep debt paid back” on weekends, or, in other terms, people can “catch-up” or “compensate” sleep on weekends.
{"title":"Reaction of the endogenous regulatory mechanisms to early weekday wakeups: a review of its popular explanations in light of model-based simulations","authors":"Arcady A. Putilov","doi":"10.3389/fnetp.2023.1285658","DOIUrl":"https://doi.org/10.3389/fnetp.2023.1285658","url":null,"abstract":"Introduction: Several widely held explanations of the mechanisms underlying the responses of endogenous sleep–wake-regulating processes to early weekday wakeups have been proposed. Here, they were briefly reviewed and validated against simulations based on the rhythmostatic version of a two-process model of sleep–wake regulation.Methods: Simulated sleep times on weekdays and weekends were compared with the times averaged over 1,048 samples with either earlier or later weekday risetimes. In total, 74 paired samples were collected before and during lockdown, and 93 paired samples were collected during early and later school start times.Results: The counterintuitive predictions of the simulations included the following: 1) only one night of ad lib sleep is sufficient to restore the endogenously determined sleep times after 1 day/5 days of larger/smaller reduction/extension of the sleep/wake phase of the circadian sleep–wake cycle; 2) sleep loss on weekdays is irrecoverable; 3) irrespective of the amount of such deadweight loss, sleep on weekends is not prolonged; and 4) the control of the circadian clocks over the sleep–wake cyclicity is not disrupted throughout the week.Discussion: The following popular explanations of the gaps between weekends and weekdays in sleep timing and duration were not supported by these simulations: 1) early weekday wakeups cause “social jetlag,” viewed as the weekend and weekday (back and forth) shifts of the sleep phase relative to the unchanged phase of the circadian clocks, and 2) early weekday wakeups cause an accumulation of “sleep debt paid back” on weekends, or, in other terms, people can “catch-up” or “compensate” sleep on weekends.","PeriodicalId":73092,"journal":{"name":"Frontiers in network physiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138998748","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-12-05eCollection Date: 2023-01-01DOI: 10.3389/fnetp.2023.1279646
Louis-David Lord, Timoteo Carletti, Henrique Fernandes, Federico E Turkheimer, Paul Expert
In recent years, brain imaging studies have begun to shed light on the neural correlates of physiologically-reversible altered states of consciousness such as deep sleep, anesthesia, and psychedelic experiences. The emerging consensus is that normal waking consciousness requires the exploration of a dynamical repertoire enabling both global integration i.e., long-distance interactions between brain regions, and segregation, i.e., local processing in functionally specialized clusters. Altered states of consciousness have notably been characterized by a tipping of the integration/segregation balance away from this equilibrium. Historically, functional MRI (fMRI) has been the modality of choice for such investigations. However, fMRI does not enable characterization of the integration/segregation balance at sub-second temporal resolution. Here, we investigated global brain spatiotemporal patterns in electrocorticography (ECoG) data of a monkey (Macaca fuscata) under either ketamine or propofol general anesthesia. We first studied the effects of these anesthetics from the perspective of band-specific synchronization across the entire ECoG array, treating individual channels as oscillators. We further aimed to determine whether synchrony within spatially localized clusters of oscillators was differently affected by the drugs in comparison to synchronization over spatially distributed subsets of ECoG channels, thereby quantifying changes in integration/segregation balance on physiologically-relevant time scales. The findings reflect global brain dynamics characterized by a loss of long-range integration in multiple frequency bands under both ketamine and propofol anesthesia, most pronounced in the beta (13-30 Hz) and low-gamma bands (30-80 Hz), and with strongly preserved local synchrony in all bands.
{"title":"Altered dynamical integration/segregation balance during anesthesia-induced loss of consciousness.","authors":"Louis-David Lord, Timoteo Carletti, Henrique Fernandes, Federico E Turkheimer, Paul Expert","doi":"10.3389/fnetp.2023.1279646","DOIUrl":"10.3389/fnetp.2023.1279646","url":null,"abstract":"<p><p>In recent years, brain imaging studies have begun to shed light on the neural correlates of physiologically-reversible altered states of consciousness such as deep sleep, anesthesia, and psychedelic experiences. The emerging consensus is that normal waking consciousness requires the exploration of a dynamical repertoire enabling both global integration i.e., long-distance interactions between brain regions, and segregation, i.e., local processing in functionally specialized clusters. Altered states of consciousness have notably been characterized by a tipping of the integration/segregation balance away from this equilibrium. Historically, functional MRI (fMRI) has been the modality of choice for such investigations. However, fMRI does not enable characterization of the integration/segregation balance at sub-second temporal resolution. Here, we investigated global brain spatiotemporal patterns in electrocorticography (ECoG) data of a monkey (<i>Macaca fuscata</i>) under either ketamine or propofol general anesthesia. We first studied the effects of these anesthetics from the perspective of band-specific synchronization across the entire ECoG array, treating individual channels as oscillators. We further aimed to determine whether synchrony within spatially localized clusters of oscillators was differently affected by the drugs in comparison to synchronization over spatially distributed subsets of ECoG channels, thereby quantifying changes in integration/segregation balance on physiologically-relevant time scales. The findings reflect global brain dynamics characterized by a loss of long-range integration in multiple frequency bands under both ketamine and propofol anesthesia, most pronounced in the beta (13-30 Hz) and low-gamma bands (30-80 Hz), and with strongly preserved local synchrony in all bands.</p>","PeriodicalId":73092,"journal":{"name":"Frontiers in network physiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10728865/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138814333","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-11-30eCollection Date: 2023-01-01DOI: 10.3389/fnetp.2023.1297345
Yulia Novitskaya, Matthias Dümpelmann, Andreas Schulze-Bonhage
Over the past decades, studies of human brain networks have received growing attention as the assessment and modelling of connectivity in the brain is a topic of high impact with potential application in the understanding of human brain organization under both physiological as well as various pathological conditions. Under specific diagnostic settings, human neuronal signal can be obtained from intracranial EEG (iEEG) recording in epilepsy patients that allows gaining insight into the functional organisation of living human brain. There are two approaches to assess brain connectivity in the iEEG-based signal: evaluation of spontaneous neuronal oscillations during ongoing physiological and pathological brain activity, and analysis of the electrophysiological cortico-cortical neuronal responses, evoked by single pulse electrical stimulation (SPES). Both methods have their own advantages and limitations. The paper outlines available methodological approaches and provides an overview of current findings in studies of physiological and pathological human brain networks, based on intracranial EEG recordings.
{"title":"Physiological and pathological neuronal connectivity in the living human brain based on intracranial EEG signals: the current state of research.","authors":"Yulia Novitskaya, Matthias Dümpelmann, Andreas Schulze-Bonhage","doi":"10.3389/fnetp.2023.1297345","DOIUrl":"https://doi.org/10.3389/fnetp.2023.1297345","url":null,"abstract":"<p><p>Over the past decades, studies of human brain networks have received growing attention as the assessment and modelling of connectivity in the brain is a topic of high impact with potential application in the understanding of human brain organization under both physiological as well as various pathological conditions. Under specific diagnostic settings, human neuronal signal can be obtained from intracranial EEG (iEEG) recording in epilepsy patients that allows gaining insight into the functional organisation of living human brain. There are two approaches to assess brain connectivity in the iEEG-based signal: evaluation of spontaneous neuronal oscillations during ongoing physiological and pathological brain activity, and analysis of the electrophysiological cortico-cortical neuronal responses, evoked by single pulse electrical stimulation (SPES). Both methods have their own advantages and limitations. The paper outlines available methodological approaches and provides an overview of current findings in studies of physiological and pathological human brain networks, based on intracranial EEG recordings.</p>","PeriodicalId":73092,"journal":{"name":"Frontiers in network physiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10723837/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138814454","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-11-23eCollection Date: 2023-01-01DOI: 10.3389/fnetp.2023.1298228
Michael Rosenblum, Arkady Pikovsky
We review an approach for reconstructing oscillatory networks' undirected and directed connectivity from data. The technique relies on inferring the phase dynamics model. The central assumption is that we observe the outputs of all network nodes. We distinguish between two cases. In the first one, the observed signals represent smooth oscillations, while in the second one, the data are pulse-like and can be viewed as point processes. For the first case, we discuss estimating the true phase from a scalar signal, exploiting the protophase-to-phase transformation. With the phases at hand, pairwise and triplet synchronization indices can characterize the undirected connectivity. Next, we demonstrate how to infer the general form of the coupling functions for two or three oscillators and how to use these functions to quantify the directional links. We proceed with a different treatment of networks with more than three nodes. We discuss the difference between the structural and effective phase connectivity that emerges due to high-order terms in the coupling functions. For the second case of point-process data, we use the instants of spikes to infer the phase dynamics model in the Winfree form directly. This way, we obtain the network's coupling matrix in the first approximation in the coupling strength.
{"title":"Inferring connectivity of an oscillatory network via the phase dynamics reconstruction.","authors":"Michael Rosenblum, Arkady Pikovsky","doi":"10.3389/fnetp.2023.1298228","DOIUrl":"https://doi.org/10.3389/fnetp.2023.1298228","url":null,"abstract":"<p><p>We review an approach for reconstructing oscillatory networks' undirected and directed connectivity from data. The technique relies on inferring the phase dynamics model. The central assumption is that we observe the outputs of all network nodes. We distinguish between two cases. In the first one, the observed signals represent smooth oscillations, while in the second one, the data are pulse-like and can be viewed as point processes. For the first case, we discuss estimating the true phase from a scalar signal, exploiting the protophase-to-phase transformation. With the phases at hand, pairwise and triplet synchronization indices can characterize the undirected connectivity. Next, we demonstrate how to infer the general form of the coupling functions for two or three oscillators and how to use these functions to quantify the directional links. We proceed with a different treatment of networks with more than three nodes. We discuss the difference between the structural and effective phase connectivity that emerges due to high-order terms in the coupling functions. For the second case of point-process data, we use the instants of spikes to infer the phase dynamics model in the Winfree form directly. This way, we obtain the network's coupling matrix in the first approximation in the coupling strength.</p>","PeriodicalId":73092,"journal":{"name":"Frontiers in network physiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10704096/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138814449","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-11-21eCollection Date: 2023-01-01DOI: 10.3389/fnetp.2023.1227861
Mariana R C Aquino, Joshua J Liddy, C Dane Napoli, Sérgio T Fonseca, Richard E A van Emmerik, Michael A Busa
Background: Fatigue is associated with increased injury risk along with changes in balance control and task performance. Musculoskeletal injury rates in runners are high and often result from an inability to adapt to the demands of exercise and a breakdown in the interaction among different biological systems. This study aimed to investigate whether changes in balance dynamics during a single-leg squat task following a high-intensity run could distinguish groups of recreational runners who did and did not sustain a running-related injury within 6 months. Methods: Thirty-one healthy recreational runners completed 60 s of single-leg squat before and after a high-intensity run. Six months after the assessment, this cohort was separated into two groups of 13 matched individuals with one group reporting injury within this period and the other not. Task performance was assessed by the number of repetitions, cycle time, amplitude, and speed. To evaluate balance dynamics, the regularity and temporal correlation structure of the center of mass (CoM) displacements in the transverse plane was analyzed. The interaction between groups (injury, non-injured) and time (pre, post) was assessed through a two-way ANOVA. Additionally, a one-way ANOVA investigated the percent change difference of each group across time. Results: The injured group presented more regular (reduced entropy; 15.6%) and diffusive (increased short-term persistence correlation; 5.6%) CoM displacements after a high-intensity run. No changes were observed in the non-injured group. The within-subject percent change was more sensitive in demonstrating the effects of fatigue and distinguishing the groups, compared to group absolute values. No differences were observed in task performance. Discussion: Runners who were injured in the future demonstrate changes in balance dynamics compared to runners who remain injury-free after fatigue. The single-leg squat test adopted appears to be a potential screening protocol that provides valuable information about balance dynamics for identifying a diminished ability to respond to training and exercise.
{"title":"Changes to balance dynamics following a high-intensity run are associated with future injury occurrence in recreational runners.","authors":"Mariana R C Aquino, Joshua J Liddy, C Dane Napoli, Sérgio T Fonseca, Richard E A van Emmerik, Michael A Busa","doi":"10.3389/fnetp.2023.1227861","DOIUrl":"https://doi.org/10.3389/fnetp.2023.1227861","url":null,"abstract":"<p><p><b>Background:</b> Fatigue is associated with increased injury risk along with changes in balance control and task performance. Musculoskeletal injury rates in runners are high and often result from an inability to adapt to the demands of exercise and a breakdown in the interaction among different biological systems. This study aimed to investigate whether changes in balance dynamics during a single-leg squat task following a high-intensity run could distinguish groups of recreational runners who did and did not sustain a running-related injury within 6 months. <b>Methods:</b> Thirty-one healthy recreational runners completed 60 s of single-leg squat before and after a high-intensity run. Six months after the assessment, this cohort was separated into two groups of 13 matched individuals with one group reporting injury within this period and the other not. Task performance was assessed by the number of repetitions, cycle time, amplitude, and speed. To evaluate balance dynamics, the regularity and temporal correlation structure of the center of mass (CoM) displacements in the transverse plane was analyzed. The interaction between groups (injury, non-injured) and time (pre, post) was assessed through a two-way ANOVA. Additionally, a one-way ANOVA investigated the percent change difference of each group across time. <b>Results:</b> The injured group presented more regular (reduced entropy; 15.6%) and diffusive (increased short-term persistence correlation; 5.6%) CoM displacements after a high-intensity run. No changes were observed in the non-injured group. The within-subject percent change was more sensitive in demonstrating the effects of fatigue and distinguishing the groups, compared to group absolute values. No differences were observed in task performance. <b>Discussion:</b> Runners who were injured in the future demonstrate changes in balance dynamics compared to runners who remain injury-free after fatigue. The single-leg squat test adopted appears to be a potential screening protocol that provides valuable information about balance dynamics for identifying a diminished ability to respond to training and exercise.</p>","PeriodicalId":73092,"journal":{"name":"Frontiers in network physiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10699445/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138814441","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-11-08DOI: 10.3389/fnetp.2023.1276401
Hildegard Meyer-Ortmanns
Heteroclinic networks are a mathematical concept in dynamic systems theory that is suited to describe metastable states and switching events in brain dynamics. The framework is sensitive to external input and, at the same time, reproducible and robust against perturbations. Solutions of the corresponding differential equations are spatiotemporal patterns that are supposed to encode information both in space and time coordinates. We focus on the concept of winnerless competition as realized in generalized Lotka–Volterra equations and report on results for binding and chunking dynamics, synchronization on spatial grids, and entrainment to heteroclinic motion. We summarize proposals of how to design heteroclinic networks as desired in view of reproducing experimental observations from neuronal networks and discuss the subtle role of noise. The review is on a phenomenological level with possible applications to brain dynamics, while we refer to the literature for a rigorous mathematical treatment. We conclude with promising perspectives for future research.
{"title":"Heteroclinic networks for brain dynamics","authors":"Hildegard Meyer-Ortmanns","doi":"10.3389/fnetp.2023.1276401","DOIUrl":"https://doi.org/10.3389/fnetp.2023.1276401","url":null,"abstract":"Heteroclinic networks are a mathematical concept in dynamic systems theory that is suited to describe metastable states and switching events in brain dynamics. The framework is sensitive to external input and, at the same time, reproducible and robust against perturbations. Solutions of the corresponding differential equations are spatiotemporal patterns that are supposed to encode information both in space and time coordinates. We focus on the concept of winnerless competition as realized in generalized Lotka–Volterra equations and report on results for binding and chunking dynamics, synchronization on spatial grids, and entrainment to heteroclinic motion. We summarize proposals of how to design heteroclinic networks as desired in view of reproducing experimental observations from neuronal networks and discuss the subtle role of noise. The review is on a phenomenological level with possible applications to brain dynamics, while we refer to the literature for a rigorous mathematical treatment. We conclude with promising perspectives for future research.","PeriodicalId":73092,"journal":{"name":"Frontiers in network physiology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135393102","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}