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Working memory (WM) involves the capacity to maintain and manipulate information over short periods. Previous research has suggested that fronto-parietal activities play a crucial role in WM. However, there remains no agreement on the effect of working memory load (WML) on neural activities and haemodynamic responses. Here, our study seeks to examine the effect of WML through simultaneous electroencephalography (EEG) and functional near-infrared spectroscopy (fNIRS). In this study, a delay change detection task was conducted on 23 healthy volunteers. The task included three levels: one item, three items and five items. The EEG and fNIRS were simultaneously recorded during the task. Neural activities and haemodynamic responses at prefrontal and parietal regions were analysed using time-frequency analysis and weighted phase-lag index (wPLI). We observed a significant enhancement in prefrontal and parietal ß suppression as WML increased. Furthermore, as WML increased, there was a notable enhancement in fronto-parietal connectivity (FPC), as evidenced by both EEG and fNIRS. Correlation analysis indicated that as WML increased, there was a potential for enhancement of neurovascular coupling (NVC) of FPC.
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BACKGROUND: Pernicious anemia (PA) is believed to be highly prevalent in Western countries but has rarely been reported in China. The study explores whether PA, an autoimmune disease, is an uncommon cause of cobalamin (vitamin B12) deficiency anemia in China. METHODS: Clinical and hematological data were collected from 90 cobalamin deficiency-caused megaloblastic anemia (MA) patients between July 2014 and December 2021. Through anti-intrinsic factor antibody (IFA) and anti-parietal cell antibody (PCA) testing, PA was distinguished from other causes of cobalamin deficiency leading to MA. Meanwhile, 30 healthy controls (HCs) were included to estimate the positive rates of IFA and PCA. RESULTS: Of the 30 HCs, only one tested positive for IFA, and all 30 tested negative for PCA. Among the 90 patients with cobalamin deficiency-caused MA, 76.7% were positive for IFA, and 47.8% were positive for PCA; a total of 76 patients (84.4%) were diagnosed with PA. The mean follow-up time was 41.0 ± 16.3 months. During the follow-up period, no case relapsed among the continuous cobalamin-supply treatment patients, while 24.4% of patients relapsed due to the interruption of maintenance cobalamin-supplement therapy (the median recurrence time was 54.0 ± 17.7 months). CONCLUSIONS: The proportion of PA in cobalamin deficiency-caused MA patients in Hainan province was higher than 80%, which was more common than expected. Therefore, screening for IFA, PCA, endoscopic biopsy, and thyroid-related parameters are recommended for all cobalamin deficiency-caused MA patients. Furthermore, maintenance cobalamin-supplement therapy is important for PA patients.
This research examines pernicious anemia (PA), a type of anemia caused by vitamin B12 deficiency, which has been widely reported in Western countries but is less known in China. The study focuses on determining if PA is also a significant cause of this deficiency in Hainan, China. Researchers gathered data from patients with megaloblastic anemia (a blood disorder) due to lack of vitamin B12, comparing them with healthy individuals to see how common PA is. The findings reveal that a very high percentage of the patients studied have PA, much higher than expected. This suggests that PA is not as rare in this region of China as previously thought. The study also highlights the importance of continuous treatment with vitamin B12 to prevent the recurrence of the anemia. Based on these results, the researchers recommend that all patients with vitamin B12 deficiency should be tested for PA and continuously receive vitamin B12 supplements to maintain their health once diagnosed with PA. This strategic insight is of paramount importance to medical practitioners in China, potentially paving the way for enhanced clinical management protocols for individuals afflicted by this ailment.
Subject(s)
Anemia, Megaloblastic , Anemia, Pernicious , Vitamin B 12 Deficiency , Humans , Anemia, Pernicious/epidemiology , Anemia, Pernicious/blood , Anemia, Pernicious/complications , Anemia, Megaloblastic/etiology , Anemia, Megaloblastic/epidemiology , Vitamin B 12 Deficiency/complications , Female , China/epidemiology , Male , Middle Aged , Adult , Vitamin B 12/blood , Aged , Young Adult , AdolescentABSTRACT
BACKGROUND: Grating orientation discrimination (GOD) is commonly used to assess somatosensory spatial processing. It allows discrimination between parallel and orthogonal orientations of tactile stimuli applied to the fingertip. Despite its widespread application, the underlying mechanisms of GOD, particularly the role of cortico-cortical interactions and local brain activity in this process, remain elusive. Therefore, we aimed to investigate how a specific cortico-cortical network and inhibitory circuits within the primary somatosensory cortex (S1) and secondary somatosensory cortex (S2) contribute to GOD. METHODS: In total, 51 healthy young adults were included in our study. We recorded resting-state magnetoencephalography (MEG) and somatosensory-evoked magnetic field (SEF) in participants with open eyes. We converted the data into a source space based on individual structural magnetic resonance imaging. Next, we estimated S1- and S2-seed resting-state functional connectivity (rs-FC) at the alpha and beta bands through resting-state MEG using the amplitude envelope correlation method across the entire brain (i.e., S1/S2-seeds × 15,000 vertices × two frequencies). We assessed the inhibitory response in the S1 and S2 from SEFs using a paired-pulse paradigm. We automatically measured the GOD task in parallel and orthogonal orientations to the index finger, applying various groove widths with a custom-made device. RESULTS: We observed a specific association between the GOD threshold (all P < 0.048) and the alpha rs-FC in the S1-superior parietal lobule and S1-adjacent to the parieto-occipital sulcus (i.e., lower rs-FC values corresponded to higher performance). In contrast, no association was observed between the local responses and the threshold. DISCUSSION: The results of this study underpin the significance of specific cortico-cortical networks in recognizing variations in tactile stimuli.
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Introduction: Abnormal brain structure and function have been reported in individuals with attention deficit hyperactivity disorder (ADHD). This study investigated the parietal lobe structure and function alteration in individuals with ADHD. Methods: In this systematic review, we searched English papers in accordance with the PRISMA (the preferred reporting items for systematic reviews and meta-analyses) approach. Studies were published between January 2010 and May 2021. Our search was conducted in two parts. Our first search was in July 2020, and our final search was in June 2021. A literature search identified 20 empirical experiments. Results: Functional magnetic resonance imaging (MRI) studies generally reported low activity and poor connectivity; structural MRI studies reported less gray matter in this lobe, and an echo study reported atrophy. In addition, electroencephalographic studies reported less connectivity of the parietal lobes in ADHD. Furthermore, the transcranial direct current stimulation intervention has shown that activation of this lobe improves attention and executive functions in children with ADHD. Finally, a deep transcranial magnetic stimulation study has demonstrated that activation of this lobe improves working memory. Conclusion: Functional and structural alteration of the parietal cortex has been reported in ADHD, which has a causal relationship with cognitive impairments. In sum, all included studies reported abnormal structure, function, or connectivity of the parietal lobe or improvement of cognitive functions with parietal lobe stimulation.
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Symbolic numeracy first emerges as children learn the meanings of number words and how to use them to precisely count sets of objects. This development starts before children enter school and forms a foundation for lifelong mathematics achievement. Despite its importance, exactly how children acquire this basic knowledge is unclear. Here we test competing theories of early number learning by measuring event-related brain potentials during a novel number word-quantity comparison task in 3-4-year-old preschool children (N = 128). We find several qualitative differences in neural processing of number by conceptual stage of development. Specifically, we find differences in early attention-related parietal electrophysiology (N1), suggesting that less conceptually advanced children process arrays as individual objects and more advanced children distribute attention over the entire set. Subsequently, we find that only more conceptually advanced children show later-going frontal (N2) sensitivity to the numerical-distance relationship between the number word and visual quantity. The nature of this response suggested that exact rather than approximate numerical meanings were being associated with number words over frontal sites. No evidence of numerical distance effects was observed over posterior scalp sites. Together these results suggest that children may engage parallel individuation of objects to learn the meanings of the first few number words, but, ultimately, create new exact cardinal value representations for number words that cannot be defined in terms of core, nonverbal number systems. More broadly, these results document an interaction between attentional and general cognitive mechanisms in cognitive development. RESEARCH HIGHLIGHTS: Conceptual development in numeracy is associated with a shift in attention from objects to sets. Children acquire meanings of the first few number words through associations with parallel attentional individuation of objects. Understanding of cardinality is associated with attentional processing of sets rather than individuals. Brain signatures suggest children attribute exact rather than approximate numerical meanings to the first few number words. Number-quantity relationship processing for the first few number words is evident in frontal but not parietal scalp electrophysiology of young children.
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OBJECTIVE: The right posterior parietal cortex is the core brain region of emotional processing and executive control network in the human brain, and the function of the right posterior parietal cortex is decreased in patients with major depressive disorder. This study aims to preliminarily investigate whether the excitation of the right posterior parietal cortex by transcranial direct current stimulation (tDCS) could improve their clinical symptoms. METHODS: In this study, 12 patients with major depressive disorder were given tDCS treatment at Xuanwu Hospital of Capital Medical University and the First Hospital of Hebei Medical University. The stimulating electrode (anode) was placed on the patients' right parietal cortex, whereas the reference electrode (cathode) was placed on the patients' left mastoid. The stimulation intensity was set as 2.0 mA. The patients with depressive disorder were treated for 20 min at a time twice a day for 14 consecutive days. The severity of the clinical symptoms was evaluated using the Hamilton Depression Rating Scale-17 (HDRS-17) and the Hamilton Anxiety Rating Scale (HARS) at before and right after treatment. RESULTS: The HDRS-17 scores of patients with depressive disorder decreased significantly following the tDCS treatment compared with those before treatment (p < .001). Further analysis revealed that the patients' anxiety/somatization, cognitive deficit, retardation, and sleep disorder scores all decreased significantly after the tDCS treatment (p < .05), although there was no significant change in their weight. Moreover, the patients' HARS scores decreased significantly after the tDCS treatment when compared with those before treatment (p < .01). CONCLUSION: The right parietal cortex may be another key stimulation targets to improving the efficacy of tDCS treatment to the patients with major depressive disorder.
Subject(s)
Depressive Disorder, Major , Parietal Lobe , Transcranial Direct Current Stimulation , Humans , Transcranial Direct Current Stimulation/methods , Parietal Lobe/physiopathology , Male , Female , Adult , Depressive Disorder, Major/therapy , Depressive Disorder, Major/physiopathology , Middle Aged , Treatment OutcomeABSTRACT
Objective: Recent studies have shown that transcutaneous vagal nerve stimulation (tVNS) holds promise as a treatment for neurological or psychiatric disease through the ability to modulate neural activity in some brain regions without an invasive procedure. The objective of this study was to identify the neural correlates underlying the effects of tVNS. Methods: Twenty right-handed healthy subjects with normal hearing participated in this study. An auricle-applied tVNS device (Soricle, Neurive Co., Ltd., Gyeongsangnam-do, Republic of Korea) was used to administer tVNS stimulation. A session consisted of 14 blocks, including 7 blocks of tVNS stimulation or sham stimulation and 7 blocks of rest, and lasted approximately 7 min (1 block = 30 s). Functional magnetic resonance imaging (fMRI) was performed during the stimulation. Results: No activated regions were observed in the fMRI scans following both sham stimulation and tVNS after the first session. After the second session, tVNS activated two clusters of brain regions in the right frontal gyrus. A comparison of the activated regions after the second session of each stimulation revealed that the fMRI following tVNS exhibited four surviving clusters. Additionally, four clusters were activated in the overall stimulated area during both the first and second sessions. When comparing the fMRI results after each type of stimulation, the fMRI following tVNS showed four surviving clusters compared to the fMRI after sham stimulation. Conclusion: tVNS could stimulate some brain regions, including the fronto-parietal network. Stimulating these regions for treating neurological or psychiatric disease might require applying tVNS for at least 3.5 min.
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Mathematical operations are cognitive actions we take to calculate relations among numbers. Arithmetic operations, addition, subtraction, multiplication, and division are elemental in education. Addition is the first one taught in school and is most popular in functional magnetic resonance imaging (fMRI) studies. Division, typically taught last is least studied with fMRI. fMRI meta-analyses show that arithmetic operations activate brain areas in parietal, cingulate and insular cortices for children and adults. Critically, no meta-analysis examines concordance across brain correlates of separate arithmetic operations in children and adults. We review and examine using quantitative meta-analyses data from fMRI articles that report brain coordinates separately for addition, subtraction, multiplication, and division in children and adults. Results show that arithmetic operations elicit common areas of concordance in fronto-parietal and cingulo-opercular networks in adults and children. Between operations differences are observed primarily for adults. Interestingly, higher within-group concordance, expressed in activation likelihood estimates, is found in brain areas associated with the cingulo-opercular network rather than the fronto-parietal network in children, areas also common between adults and children. Findings are discussed in relation to constructivist cognitive theory and practical directions for future research.
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Brain-behavior relationships are complex. For instance, one might know a brain region's function(s) but still be unable to accurately predict deficit type or severity after damage to that region. Here, I discuss the case of damage to the angular gyrus (AG) that can cause left-right confusion, finger agnosia, attention deficit, and lexical agraphia, as well as impairment in sentence processing, episodic memory, number processing, and gesture imitation. Some of these symptoms are grouped under AG syndrome or Gerstmann's syndrome, though its exact underlying neuronal systems remain elusive. This review applies recent frameworks of brain-behavior modes and principles from modern lesion-symptom mapping to explain symptomatology after AG damage. It highlights four major issues for future studies: (1) functionally heterogeneous symptoms after AG damage need to be considered in terms of the degree of damage to (i) different subdivisions of the AG, (ii) different AG connectivity profiles that disconnect AG from distant regions, and (iii) lesion extent into neighboring regions damaged by the same infarct. (2) To explain why similar symptoms can also be observed after damage to other regions, AG damage needs to be studied in terms of the networks of regions that AG functions with, and other independent networks that might subsume the same functions. (3) To explain inter-patient variability on AG symptomatology, the degree of recovery-related brain reorganisation needs to account for time post-stroke, demographics, therapy input, and pre-stroke differences in functional anatomy. (4) A better integration of the results from lesion and functional neuroimaging investigations of AG function is required, with only the latter so far considering AG function in terms of a hub within the default mode network. Overall, this review discusses why it is so difficult to fully characterize the AG syndrome from lesion data, and how this might be addressed with modern lesion-symptom mapping.
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Mammalian cell membranes are very dynamic where they respond to several environmental stimuli by rearranging the membrane composition by basic biological processes, including endocytosis. In this context, receptor-mediated endocytosis, either clathrin-dependent or caveolae-dependent, is involved in different physiological and pathological conditions. In the last years, an important amount of evidence has been reported that kidney function involves the modulation of different types of endocytosis, including renal protein handling. In addition, the dysfunction of the endocytic machinery is involved with the development of proteinuria as well as glomerular and tubular injuries observed in kidney diseases associated with hypertension, diabetes, and others. In this present review, we will discuss the mechanisms underlying the receptor-mediated endocytosis in different glomerular cells and proximal tubule epithelial cells as well as their modulation by different factors during physiological and pathological conditions. These findings could help to expand the current understanding regarding renal protein handling as well as identify possible new therapeutic targets to halt the progression of kidney disease.
Subject(s)
Endocytosis , Humans , Animals , Kidney Diseases/metabolism , Kidney Diseases/pathology , Kidney/metabolism , Kidney/pathology , Receptors, Cell Surface/metabolismABSTRACT
OBJECTIVE: Repeated spaced sessions of repetitive transcranial magnetic stimulation (TMS) to the human primary motor cortex can lead to dose-dependent increases in motor cortical excitability. However, this has yet to be demonstrated in a defined cortical circuit. We aimed to examine the effects of repeated spaced cortical paired associative stimulation (cPAS) on excitability in the motor cortex. METHODS: cPAS was delivered to the primary motor cortex (M1) and posterior parietal cortex (PPC) with two coils. In the multi-dose condition, three sessions of cPAS were delivered 50-min apart. The single-dose condition had one session of cPAS, followed by two sessions of a control cPAS protocol. Motor-evoked potentials were evaluated before and up to 40 min after each cPAS session as a measure of cortical excitability. RESULTS: Compared to a single dose of cPAS, motor cortical excitability significantly increased after multi-dose cPAS. Increasing the number of cPAS sessions resulted in a cumulative, dose-dependent effect on excitability in the motor cortex, with each successive cPAS session leading to notable increases in potentiation. CONCLUSION: Repeated spaced cPAS sessions summate to increase motor cortical excitability induced by single cPAS. SIGNIFICANCE: Repeated spaced cPAS could potentially restore abilities lost due to disorders like stroke.
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Parietal cell autoantibodies (PCAs), which recognize the enzyme H+/K+-ATPase as a target, are considered to be a diagnostic marker of autoimmune gastritis and pernicious anemia; these conditions are characterized by the presence of corpus atrophic gastritis. Circulating PCAs can be detected using several analytical methods that are commonly available in the clinical laboratory. Traditionally, indirect immunofluorescence (IIF) on rodent or primate stomach tissue is used as a screening test for the detection of PCAs. However, IIF suffers from a high inter-observer variability and lacks standardization. In addition, like immunoblotting, results are expressed only in a qualitative or semi-quantitative manner. Based on the few available studies that are reviewed herein, quantitative enzyme-linked immunosorbent assays (ELISAs) and fluorescence enzyme immunoassays (FEIAs) using purified H+/K+-ATPase perform better than IIF in the detection of PCAs, displaying higher sensitivity and utility in monitoring the disease. In light of their higher diagnostic accuracy, these solid-phase methods should be preferred to IIF in the screening of autoimmune atrophic gastritis. The use of methods to detect antibodies versus a specific subunit of H+/K+-ATPase (α or ß) is currently confined to the world of research. Further investigation is required to define the clinical utility of H+/K+-ATPase subunit detection.
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BACKGROUND: Chronic Low Back Pain (cLBP) poses a significant health challenge, leading to functional disability and reduced quality of life. Osteopathic Manipulative Treatment (OMT) is emerging as a therapeutic option for cLBP, but the brain mechanisms underlying its analgesic effect remain unclear. MATERIALS AND METHODS: Thirty cLBP patients were randomly exposed to either four weekly sessions of OMT (N=16) or Sham treatment (N=14). Resting-state Magnetic Resonance Imaging (rs-MRI) scans and pain perception questionnaires were collected before and after treatment. A voxel-wise, rs-fMRI data-driven analysis was conducted to identify changes in the intrinsic functional connectivity across the whole brain that were associated with the OMT. Spearman's correlations were used to test for the association between changes in intrinsic connectivity and individual reports of pain perception. RESULTS: Compared to the Sham group, participants who received OMT showed significant alterations in the functional connectivity of several regions belonging to the pain matrix. Specifically, OMT was associated with decreased connectivity of a parietal cluster that includes the somatosensory cortex and an increase of connectivity of the right anterior insula and ventral and dorsal anterolateral prefrontal areas. Crucially, the change in connectivity strength observed in the ventral anterolateral prefrontal cortex, a putative region of the affective-reappraisive layer of the pain matrix, correlates with the reduction in pain perception caused by the OMT. CONCLUSIONS: This study offers insights into the brain mechanisms underlying the analgesic effect of OMT. Our findings support a link between OMT-driven functional cortical architecture alterations and improved clinical outcomes.
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Chronic stress is well known to erode cognitive functions. Yet, our understanding of how repeated stress exposure impacts one of the fundamental bases of cognition: sensory processing, remains limited. The posterior parietal cortex (PPC) is a high order visual region, known for its role in visually guided decision making, multimodal integration, attention, and working memory. Here, we used functional measures to determine how repeated exposure to multiple concurrent stressors (RMS) affects sensory processing in the PPC in adult male mice. A longitudinal experimental design, repeatedly surveying the same population of neurons using in vivo two-photon imaging, revealed that RMS disrupts the balanced turnover of visually responsive cells in layer 2/3 of the PPC. Across the population, RMS-induced changes in visual responsiveness followed a bimodal distribution suggesting idiosyncratic stress effects. In cells that maintained their responsiveness across recording sessions, we found that stress reduced visual response magnitudes and feature selectivity. While we did not observe stress-induced elimination of excitatory synapses, noise correlation statistics indicated that RMS altered visual input to the neuronal population. The impact of RMS was restricted to visually evoked responses and was not evident in neuronal activity associated with locomotion onset. Together, our results indicate that despite no apparent synaptic reorganization, stress exposure in adulthood can disrupt sensory processing in the PPC, with the effects showing remarkable individual variation.
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The brain in the genus Homo expanded rapidly during evolution, accelerated by a reciprocated interaction between neural, cognitive, and ecological niches (triadic niche construction, or TNC). This biologically costly expansion incubated latent cognitive capabilities that, with a quick and inexpensive rewiring of brain areas in a second phase of TNC, provided the basis for Homo sapiens specific abilities. The neural demands for perception of the human body in interaction with tools and the environment required highly integrated sensorimotor domains, inducing the parietal lobe expansion seen in humans. These newly expanded brain areas allowed connecting the sensations felt in the body to the actions in the world through the cognitive function of "projection". In this opinion article, we suggest that as a relationship of equivalence between body parts, tools and their external effects was established, mental mechanisms of self-objectification might have emerged as described previously, grounding notions of spatial organization, idealized objects, and their transformations, as well as socio-emotional states in the sensing agent through a self-in-the-world map. Therefore, human intelligence and its features such as symbolic thought, language, mentalizing, and complex technical and social behaviors could have stemmed from the explicit awareness of the causal relationship between the self and intentional modifications to the environment.
Subject(s)
Brain , Humans , Animals , Brain/physiology , Primates/physiology , Biological Evolution , Cognition/physiologyABSTRACT
[This corrects the article DOI: 10.3389/fnins.2023.1255124.].
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The cerebellum has been involved in social abilities and autism. Given that the cerebellum is connected to the cortex via the cerebello-thalamo-cortical loop, the connectivity between the cerebellum and cortical regions involved in social interactions, that is, the right temporo-parietal junction (rTPJ) has been studied in individuals with autism, who suffer from prototypical deficits in social abilities. However, existing studies with small samples of categorical, case-control comparisons have yielded inconsistent results due to the inherent heterogeneity of autism, suggesting that investigating how clinical dimensions are related to cerebellar-rTPJ functional connectivity might be more relevant. Therefore, our objective was to study the functional connectivity between the cerebellum and rTPJ, focusing on its association with social abilities from a dimensional perspective in a transdiagnostic sample. We analyzed structural magnetic resonance imaging (MRI) and functional MRI (fMRI) scans obtained during naturalistic films watching from a large transdiagnostic dataset, the Healthy Brain Network (HBN), and examined the association between cerebellum-rTPJ functional connectivity and social abilities measured with the social responsiveness scale (SRS). We conducted univariate seed-to-voxel analysis, multivariate canonical correlation analysis (CCA), and predictive support vector regression (SVR). We included 1404 subjects in the structural analysis (age: 10.516 ± 3.034, range: 5.822-21.820, 506 females) and 414 subjects in the functional analysis (age: 11.260 ± 3.318 years, range: 6.020-21.820, 161 females). Our CCA model revealed a significant association between cerebellum-rTPJ functional connectivity, full-scale IQ (FSIQ) and SRS scores. However, this effect was primarily driven by FSIQ as suggested by SVR and univariate seed-to-voxel analysis. We also demonstrated the specificity of the rTPJ and the influence of structural anatomy in this association. Our results suggest that there is a complex relationship between cerebellum-rTPJ connectivity, social performance and IQ. This relationship is specific to the cerebellum-rTPJ connectivity, and is largely related to structural anatomy in these two regions. PRACTITIONER POINTS: We analyzed cerebellum-right temporoparietal junction (rTPJ) connectivity in a pediatric transdiagnostic sample. We found a complex relationship between cerebellum and rTPJ connectivity, social performance and IQ. Cerebellum and rTPJ functional connectivity is related to structural anatomy in these two regions.
Subject(s)
Cerebellum , Magnetic Resonance Imaging , Humans , Cerebellum/diagnostic imaging , Cerebellum/physiopathology , Cerebellum/pathology , Male , Female , Young Adult , Adult , Connectome/methods , Social Skills , Adolescent , Nerve Net/diagnostic imaging , Nerve Net/physiopathology , Parietal Lobe/diagnostic imaging , Parietal Lobe/physiopathology , Temporal Lobe/diagnostic imaging , Temporal Lobe/physiopathology , Neural Pathways/physiopathology , Neural Pathways/diagnostic imagingABSTRACT
Discrete neural states are associated with reaching movements across the fronto-parietal network. Here, the Hidden Markov Model (HMM) applied to spiking activity of the somato-motor parietal area PE revealed a sequence of states similar to those of the contiguous visuomotor areas PEc and V6A. Using a coupled clustering and decoding approach, we proved that these neural states carried spatiotemporal information regarding behaviour in all three posterior parietal areas. However, comparing decoding accuracy, PE was less informative than V6A and PEc. In addition, V6A outperformed PEc in target inference, indicating functional differences among the parietal areas. To check the consistency of these differences, we used both a supervised and an unsupervised variant of the HMM, and compared its performance with two more common classifiers, Support Vector Machine and Long-Short Term Memory. The differences in decoding between areas were invariant to the algorithm used, still showing the dissimilarities found with HMM, thus indicating that these dissimilarities are intrinsic in the information encoded by parietal neurons. These results highlight that, when decoding from the parietal cortex, for example, in brain machine interface implementations, attention should be paid in selecting the most suitable source of neural signals, given the great heterogeneity of this cortical sector.
Applying HMMs to spiking activity recorded from the somato-motor parietal area PE revealed discrete neural states related to reaching movements. These states were extremely similar to those present in the neighbouring visuomotor areas PEc and V6A. Our decoding approach showed that these states conveyed spatiotemporal behaviour information across all three posterior parietal areas. However, decoding accuracy was lower in PE compared to V6A and PEc, with V6A excelling in target inference. These differences held true even when changing the decoding algorithm, indicating intrinsic dissimilarities in information encoding by parietal different areas. These findings highlight the importance of selecting the appropriate neural signal sources in applications such as brain machine interfaces and pave the way for further investigation of the nontrivial diversity within the parietal cortex.
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Wide-range thermoreceptive neurons (WRT-EN) in monkey cortical area 7b that encoded innocuous and nocuous cutaneous thermal and threatening visuosensory stimulation with high fidelity were studied to identify their multisensory integrative response properties. Emphasis was given to characterizing the spatial and temporal effects of threatening visuosensory input on the thermal stimulus-response properties of these multisensory nociceptive neurons. Threatening visuosensory stimulation was most efficacious in modulating thermal evoked responses when presented as a downward ("looming"), spatially congruent, approaching and closely proximal target in relation to the somatosensory receptive field. Both temporal alignment and misalignment of spatially aligned threatening visual and thermal stimulation significantly increased mean discharge frequencies above those evoked by thermal stimulation alone, particularly at near noxious (43°C) and mildly noxious (45°C) temperatures. The enhanced multisensory discharge frequencies were equivalent to the discharge frequency evoked by overtly noxious thermal stimulation alone at 47°C (monkey pain tolerance threshold). A significant increase in behavioral mean escape frequency with shorter escape latency was evoked by multisensory stimulation at near noxious temperature (43°C), which was equivalent to that evoked by noxious stimulation alone (47°C). The remarkable concordance of elevating both neural discharge and escape frequency from a nonnociceptive and prepain level by near noxious thermal stimulation to a nociceptive and pain level by multisensory visual and near noxious thermal stimulation and integration is an elegantly designed defensive neural mechanism that in effect lowers both nociceptive response and pain thresholds to preemptively engage nocifensive behavior and, consequently, avert impending and actual injurious noxious thermal stimulation.NEW & NOTEWORTHY Multisensory nociceptive neurons in cortical area 7b are engaged in integration of threatening visuosensory and a wide range of innocuous and nocuous somatosensory (thermoreceptive) inputs. The enhancement of neuronal activity and escape behavior in monkey by multisensory integration is consistent and supportive of human psychophysical studies. The spatial features of visuosensory stimulation in peripersonal space in relation to somatic stimulation in personal space are critical to multisensory integration, nociception, nocifensive behavior, and pain.
Subject(s)
Macaca mulatta , Nociceptors , Animals , Nociceptors/physiology , Male , Nociception/physiology , Hot Temperature , Visual Perception/physiology , Pain Threshold/physiology , Photic Stimulation , Escape Reaction/physiology , Thermoreceptors/physiologyABSTRACT
Objectives: : Despite the frequent occurrence of visual cognitive impairment after anoxic encephalopathy, only a few studies have analyzed gaze movements following encephalopathy. This study determined the visual cognitive characteristics of patients with anoxic encephalopathy using an eye-tracking system. Methods: : This study included ten patients with anoxic encephalopathy and ten age/sex-matched controls. Factors for anoxic encephalopathy onset and brain imaging findings were extracted from medical records. An eye-tracking system was used to track eye movements during three visual search tasks (pop-out, serial search, and saliency) in patient and healthy control groups. The average target search time, number of saccades, and number of fixations to salient stimuli were compared. Results: : Stagnant blood flow, observed in six of ten patients, was the most common cause of disease onset, four of whom exhibited hypoperfusion in bilateral occipital or parietal lobes on single-photon emission computed tomography. The patient group required longer search times during all visual search tasks and a higher number of saccades during pop-out and serial search tasks. However, no significant difference was observed between the two groups for the number of fixations to salient stimuli during the saliency task. Conclusions: : Following anoxic encephalopathy, bottom-up (pop-out task) and top-down (serial search task) gaze control were considered impaired because of extensive parieto-occipital lobe damage after blood flow stagnation. Patients exhibited reduced top-down function for finding targets (serial search task) but relatively retain inhibitory function for salient stimuli (saliency task). Gaze analysis can be used to reveal the clinical characteristics of anoxic encephalopathy.