Frontiers in Integrative Neuroscience最新文献

Cingulotomy is therapeutic in OCD, but what are the possible mechanisms? Computer models that formalize cortical OCD abnormalities and anterior cingulate cortex (ACC) function can help answer this. At the neural dynamics level, cortical dynamics in OCD have been modeled using attractor networks, where activity patterns resistant to change denote the inability to switch to new patterns, which can reflect inflexible thinking patterns or behaviors. From that perspective, cingulotomy might reduce the influence of difficult-to-escape ACC attractor dynamics on other cortical areas. At the functional level, computer formulations based on model-free reinforcement learning (RL) have been used to describe the multitude of phenomena ACC is involved in, such as tracking the timing of expected outcomes and estimating the cost of exerting cognitive control and effort. Different elements of model-free RL models of ACC could be affected by the inflexible cortical dynamics, making it challenging to update their values. An agent can also use a world model, a representation of how the states of the world change, to plan its actions, through model-based RL. OCD has been hypothesized to be driven by reduced certainty of how the brain's world model describes changes. Cingulotomy might improve such uncertainties about the world and one's actions, making it possible to trust the outcomes of these actions more and thus reduce the urge to collect more sensory information in the form of compulsions. Connecting the neural dynamics models with the functional formulations can provide new ways of understanding the role of ACC in OCD, with potential therapeutic insights.

The laws of physics and mathematics describe the world we live in as internally consistent. As these rules provide a very effective description, and our interaction with the world is also very effective, it seems self-evident that our perception follows these laws. As a result, when trying to explain imperfections in perception, we tend to impose consistency and introduce concepts such as deformations of visual space. In this review, we provide numerous examples that show that in many situations we perceive related attributes to have inconsistent values. We discuss how our tendency to assume consistency leads to erroneous conclusions on how we process sensory information. We propose that perception is not about creating a consistent internal representation of the outside world, but about answering specific questions about the outside world. As the information used to answer a question is specific for that question, this naturally leads to inconsistencies in perception and to an apparent dissociation between some perceptual judgments and related actions.

Many studies have documented cognitive deficits, especially spatial cognitive deficits, in patients with some form of vestibular loss. Almost 20 years ago, hippocampal (HPC) atrophy was reported to be correlated with spatial memory deficits in such patients and the idea has gradually emerged that HPC atrophy may be causally responsible for the cognitive deficits. However, the results of studies of HPC volume following vestibular loss have not always been consistent, and a number of studies have reported no evidence of HPC atrophy. This paper argues that HPC atrophy, if it does occur following vestibular loss, may not be directly, causally responsible for the cognitive deficits, and that it is more likely that rapid functional changes in the HPC are responsible, due to the interruption of the transmission of vestibular information to the HPC. The argument presented here rests on 3 tranches of evidence: (1) Cognitive deficits have been observed in humans even in the absence of HPC atrophy; (2) HPC atrophy has not been reported in animal studies following vestibular loss, despite cognitive deficits; and (3) Animal studies have shown that the interruption of the transmission of vestibular information to the HPC has immediate consequences for HPC place cells, far too quickly to be explained by HPC atrophy. It is possible that HPC atrophy, when it does occur, is related to the longer-term consquences of living with vestibular loss, which are likely to increase circulating cortisol.

The last two decades have seen a surge of interest in the mechanisms underpinning bodily self-consciousness (BSC). Studies showed that BSC relies on several bodily experiences (i.e., self-location, body ownership, agency, first-person perspective) and multisensory integration. The aim of this literature review is to summarize new insights and novel developments into the understanding of the neural bases of BSC, such as the contribution of the interoceptive signals to the neural mechanisms of BSC, and the overlap with the neural bases of conscious experience in general and of higher-level forms of self (i.e., the cognitive self). We also identify the main challenges and propose future perspectives that need to be conducted to progress into the understanding of the neural mechanisms of BSC. In particular, we point the lack of crosstalk and cross-fertilization between subdisciplines of integrative neuroscience to better understand BSC, especially the lack of research in animal models to decipher the neural networks and systems of neurotransmitters underpinning BSC. We highlight the need for more causal evidence that specific brain areas are instrumental in generating BSC and the need for studies tapping into interindividual differences in the phenomenal experience of BSC and their underlying mechanisms.

The comprehension of the neural elements interacting in the spinal cord affected by vestibular input will contribute to the understanding of movement execution in normal and pathological conditions. In this context, Hoffman's reflex (H-reflex) has been used to evaluate transient excitability changes on the spinal cord descending pathways. The post-activation depression (P-AD) of the H-reflex consists of evoking consecutive responses (>1 Hz) provoking an amplitude depression, which has been shown to diminish in pathological conditions (i.e., spasticity, diabetic neuropathy). Galvanic Vestibular Stimulation (GVS) is a non-invasive method that activates the vestibular afferents and has been used to study the excitability of the H-reflex applied as a conditioning pulse. To our knowledge, there are no reports evaluating the P-AD during and after GVS. Our primary aim was to determine if GVS alters the P-AD evoked by stimulating the tibial nerve at 0.1, 1, 5, and 10 Hz, recording in the gastrocnemius and soleus muscles. Direct current stimulation of 2.0 ± 0.6 mA with the cathode ipsilateral (Ipsi) or contralateral (Contra) to the H-reflex electrode montage was applied bilaterally over the mastoid process in 19 healthy subjects. The P-AD's immediate post-GVS response (P Ipsi, P Contra) was also analyzed. Secondarily, we analyzed the excitability of the H-reflex during GVS. Responses evoked at 0.1 Hz with GVS, post-GVS, and a Control (no GVS) condition were used for comparisons. Our results show that P-AD persisted in all subjects despite increased excitability induced by GVS: statistical significance was found when comparing P-AD at 1, 5, and 10 Hz with the corresponding condition (Control, Ipsi, P Ipsi, Contra, P Contra) at 0.1 Hz (p < 0.001). Additionally, the increase in excitability produced by GVS was quantified for the first H-reflex of each P-AD stimulation frequency. The percentage change for all GVS conditions surpassed the Control by at least 20%, being statistically significant for Contra compared to Control (p < 0.01). In summary, although GVS increases the excitability of the vestibulospinal pathway at a premotor level, the neural inhibitory mechanism present in P-AD remains unaltered in healthy subjects.

Background: One factor which influences the speech intelligibility of cochlear implant (CI) users is the number and the extent of the functionality of spiral ganglion neurons (SGNs), referred to as "cochlear health." To explain the interindividual variability in speech perception of CI users, a clinically applicable estimate of cochlear health could be insightful. The change in the slope of the electrically evoked compound action potentials (eCAP), amplitude growth function (AGF) as a response to increased interphase gap (IPG) (IPGE_slope) has been introduced as a potential measure of cochlear health. Although this measure has been widely used in research, its relationship to other parameters requires further investigation.

Methods: This study investigated the relationship between IPGE_slope, demographics and speech intelligibility by (1) considering the relative importance of each frequency band to speech perception, and (2) investigating the effect of the stimulus polarity of the stimulating pulse. The eCAPs were measured in three different conditions: (1) Forward masking with anodic-leading (FMA) pulse, (2) Forward masking with cathodic-leading (FMC) pulse, and (3) with alternating polarity (AP). This allowed the investigation of the effect of polarity on the diagnosis of cochlear health. For an accurate investigation of the correlation between IPGE_slope and speech intelligibility, a weighting function was applied to the measured IPGE_slopes on each electrode in the array to consider the relative importance of each frequency band for speech perception. A weighted Pearson correlation analysis was also applied to compensate for the effect of missing data by giving higher weights to the ears with more successful IPGE_slope measurements.

Results: A significant correlation was observed between IPGE_slope and speech perception in both quiet and noise for between-subject data especially when the relative importance of frequency bands was considered. A strong and significant correlation was also observed between IPGE_slope and age when stimulation was performed with cathodic-leading pulses but not for the anodic-leading pulse condition.

Conclusion: Based on the outcome of this study it can be concluded that IPGE_slope has potential as a relevant clinical measure indicative of cochlear health and its relationship to speech intelligibility. The polarity of the stimulating pulse could influence the diagnostic potential of IPGE_slope.

Fragile X syndrome (FXS) is a neurodevelopmental disorder caused by a repeat expansion mutation in the promotor region of the FMR1 gene resulting in transcriptional silencing and loss of function of fragile X messenger ribonucleoprotein 1 protein (FMRP). FMRP has a well-defined role in the early development of the brain. Thus, loss of the FMRP has well-known consequences for normal cellular and synaptic development leading to a variety of neuropsychiatric disorders including an increased prevalence of amygdala-based disorders. Despite our detailed understanding of the pathophysiology of FXS, the precise cellular and circuit-level underpinnings of amygdala-based disorders is incompletely understood. In this review, we discuss the development of the amygdala, the role of neuromodulation in the critical period plasticity, and recent advances in our understanding of how synaptic and circuit-level changes in the basolateral amygdala contribute to the behavioral manifestations seen in FXS.

Background: Brain aneurysms represent a significant cause of hemorrhagic stroke. Prior research has demonstrated links between stress and stroke, including brain aneurysms. We aimed to determine relationships between select psychiatric disorders and aneurysms and aneurysmal SAH.

Methods: We performed retrospective, case-control study of a National Veterans Affairs population with two experimental groups (aneurysm-only and aneurysmal SAH) and 10-fold controls per group matched by age, date, and clinical data source. The studied the presence of 4 psychiatric disorders: Posttraumatic stress disorder (PTSD), major depressive disorder (MDD), generalized anxiety disorder (GAD), and other mood disorders. Our main outcomes Unadjusted and multivariable adjusted ORs of PTSD, MDD, GAD, and mood disorders within aneurysm-only and aSAH groups.

Results: In 6,320,789 US Veterans who were enrolled for at least 5 years in Medicare and/or the Veterans Health Administration, we identified 35,094 cases of aneurysm without SAH and 5,749 cases of aneurysm with SAH between 1/2005 and 12/2019. In analyses adjusted for sex, hypertension, and tobacco use, patients with aneurysm were more likely than matched controls to have a history of PTSD (OR 1.48), MDD (OR 1.33), GAD (OR 1.26), and other mood disorders (OR 1.34) (all p-values < 0.0001). Similarly, patients with aSAH were more likely than controls to have a history of PTSD (OR 1.35), MDD (OR 1.38), GAD (OR 1.18), and other mood disorders (OR 1.30) (all p-values < 0.0001).

Conclusion: The study, the largest of its kind, further suggests links between psychiatric disorders and stroke. This is important as patients with aneurysms are not routinely screened for such psychiatric risk factors. Additional research on this topic could lead to novel strategies to improve stroke prevention.