Joint low-rank tensor fusion and cross-modal attention for multimodal physiological signals based emotion recognition.

Objective. Physiological signals based emotion recognition is a prominent research domain in the field of human-computer interaction. Previous studies predominantly focused on unimodal data, giving limited attention to the interplay among multiple modalities. Within the scope of multimodal emotion recognition, integrating the information from diverse modalities and leveraging the complementary information are the two essential issues to obtain the robust representations.Approach. Thus, we propose a intermediate fusion strategy for combining low-rank tensor fusion with the cross-modal attention to enhance the fusion of electroencephalogram, electrooculogram, electromyography, and galvanic skin response. Firstly, handcrafted features from distinct modalities are individually fed to corresponding feature extractors to obtain latent features. Subsequently, low-rank tensor is fused to integrate the information by the modality interaction representation. Finally, a cross-modal attention module is employed to explore the potential relationships between the distinct latent features and modality interaction representation, and recalibrate the weights of different modalities. And the resultant representation is adopted for emotion recognition.Main results. Furthermore, to validate the effectiveness of the proposed method, we execute subject-independent experiments within the DEAP dataset. The proposed method has achieved the accuracies of 73.82% and 74.55% for valence and arousal classification.Significance. The results of extensive experiments verify the outstanding performance of the proposed method.

Protective effects of docosahexaenoic acid supplementation on cognitive dysfunction and hippocampal synaptic plasticity impairment induced by early postnatal PM2.5 exposure in young rats.

PM2.5 exposure is a challenging environmental issue that is closely related to cognitive development impairment; however, currently, relevant means for prevention and treatment remain lacking. Herein, we determined the preventive effect of docosahexaenoic acid (DHA) supplementation on the neurodevelopmental toxicity induced by PM2.5 exposure. Neonatal rats were divided randomly into three groups: control, PM2.5, and DHA + PM2.5 groups. DHA could ameliorate PM2.5-induced learning and memory dysfunction, as well as reverse the impairment of hippocampal synaptic plasticity, evidenced by enhanced long-term potentiation, recovered synaptic ultrastructure, and increased expression of synaptic proteins. Moreover, DHA increased CREB phosphorylation and BDNF levels and attenuated neuroinflammation and oxidative stress, reflected by lower levels of IBA-1, IL-1ß, and IL-6 and increased levels of SOD1 and Nrf2. In summary, our findings demonstrated that supplementation of DHA effectively mitigated the cognitive dysfunction and synaptic plasticity impairment induced by early postnatal exposure to PM2.5. These beneficial effects may be attributed to the upregulation of the CREB/BDNF signaling pathway, as well as the reduction of neuroinflammation and oxidative stress.

Anticonvulsant Effect of Carbenoxolone on Chronic Epileptic Rats and Its Mechanism Related to Connexin and High-Frequency Oscillations.

Objective: This study was designed to investigate the influence and mechanism of gap junction carbenoxolone (CBX) on dynamic changes in the spectral power of ripples and fast ripples (FRs) in the hippocampus of chronic epileptic rats. Methods: The lithium-pilocarpine (PILO) status epilepticus (SE) model (PILO group) and the CBX pretreatment model (CBX + PILO group) were established to analyze dynamic changes in the spectral power of ripples and FRs, and the dynamic expression of connexin (CX)26, CX32, CX36, and CX43 in the hippocampus of chronic epileptic rats. Results: Within 28 days after SE, the number of spontaneous recurrent seizures (SRSs) in the PILO group was significantly higher than that in the CBX + PILO group. The average spectral power of FRs in the PILO group was significantly higher than the baseline level at 1 and 7 days after SE. The average spectral power of FRs in the PILO group was significantly higher than that in the CBX + PILO group at 1, 7, and 14 days after SE. Seizures induced an increase in CX43 expression at 1 and 7 days after SE, but had no significant effect on CX26, CX36, or CX32. CBX pretreatment did not affect the expression of CXs in the hippocampus of normal rats, but it inhibited the expression of CX43 in epileptic rats. The number of SRSs at 2 and 4 weeks after SE had the highest correlation with the average spectral power of FRs; the average spectral power of FRs was moderately correlated with the expression of CX43. Conclusion: The results of this study indicate that the energy of FRs may be regulated by its interference with the expression of CX43, and thus, affect seizures. Blocking the expression of CX43 thereby reduces the formation of pathological high-frequency oscillations (HFOs), making it a promising strategy for the treatment of chronic epilepsy.

Clinical Characteristics of Children With Anti-N-Methyl-d-Aspartate Receptor Encephalitis After Japanese Encephalitis.

BACKGROUND: Viral encephalitis is an important trigger for anti-N-methyl-d-aspartate receptor (NMDAR) encephalitis. We analyzed the clinical characteristics of anti-NMDAR encephalitis after Japanese encephalitis (JE) in children. METHODS: Clinical data of 185 children with anti-NMDAR encephalitis were retrospectively reviewed. Patients with a history of viral encephalitis other than JE or who were identified with other autoantibodies were excluded. RESULTS: Twenty children with anti-NMDAR encephalitis after JE were enrolled with a median age of 6 years and 10 months (interquartile range [IQR]: 3 years to 11 years and 5 months). The median time from JE to anti-NMDAR encephalitis was 29 (IQR: 25 to 32) days. At 12 months, most patients (17 of 18) recovered to at least their baseline modified Rankin scale (mRS) scores caused by JE. One hundred forty two children with classical anti-NMDAR encephalitis were enrolled. Compared with classical anti-NMDAR encephalitis, patients after JE had significantly more decreased level of consciousness (50% vs 18.3%, P = 0.003), more autonomic dysfunction (30.0% vs 9.9%, P = 0.021), fewer psychiatric or behavioral symptoms (70.0% vs 90.8%, P = 0.016), fewer seizures (25.0% vs 68.3%, P < 0.001), lesser improvement 4 weeks after immunotherapy (35.0% vs 73.2%, P = 0.001), and worse outcomes at 12 months (median mRS: 1 vs 0, P < 0.001). CONCLUSIONS: Anti-NMDAR encephalitis after JE in children mainly occurred within two months. Their clinical manifestation may differ from classical anti-NMDAR encephalitis. The prognosis of children with anti-NMDAR encephalitis after JE probably depends on the neurological sequelae after JE.

Postural Balance in Individuals With Knee Osteoarthritis During Stand-to-Sit Task.

Objective: Stand-to-sit task is an important daily function, but there is a lack of research evidence on whether knee osteoarthritis (knee OA) affects the postural balance during the task. This study aimed to compare individuals with knee OA and asymptomatic controls in postural balance and identify kinematic and lower extremity muscle activity characteristics in individuals with knee OA during the stand-to-sit task. Methods: In total, 30 individuals with knee OA and 30 age-matched asymptomatic controls performed the 30-s Chair Stand Test (30sCST) at self-selected speeds. Motion analysis data and surface electromyography (sEMG) were collected while participants performed the 30sCST. To quantify postural balance, the displacement of the center of mass (CoM) and the peak instantaneous velocity of the CoM were calculated. The kinematic data included forward lean angles of the trunk and pelvic, range of motion (RoM) of the hip, knee, and ankle joints in the sagittal plane. The averaged activation levels of gluteus maximus, vastus lateralis, vastus medialis, rectus femoris, biceps femoris (BF), tibialis anterior (TA), and medial head of gastrocnemius muscles were indicated by the normalized root mean square amplitudes. Results: Compared with the asymptomatic control group, the knee OA group prolonged the duration of the stand-to-sit task, demonstrated significantly larger CoM displacement and peak instantaneous CoM velocity in the anterior-posterior direction, reduced ankle dorsiflexion RoM, greater anterior pelvic tilt RoM, and lower quadriceps femoris and muscles activation level coupled with higher BF muscle activation level during the stand-to-sit task. Conclusion: This study indicates that individuals with knee OA adopt greater pelvic forward lean RoM and higher BF muscle activation level during the stand-to-sit task. However, these individuals exist greater CoM excursion in the anterior-posterior direction and take more time to complete the task. This daily functional activity should be added to the rehabilitation goals for individuals with knee OA. The knee OA group performs reduced ankle dorsiflexion RoM, quadriceps femoris, and TA activation deficit. In the future, the rehabilitation programs targeting these impairments could be beneficial for restoring the functional transfer in individuals with knee OA.

Clinical and genetic characteristics of epilepsy of infancy with migrating focal seizures in Chinese children.

OBJECTIVE: Epilepsy of infancy with migrating focal seizures (EIMFS) is a rare and severe developmental epileptic encephalopathy. The aim of this study was to improve our understanding of EIMFS by using phenotype-genotype correlation. METHODS: We recruited, performed clinical genetic testing, and summarized the clinical features and genetic characteristics in five patients with EIMFS in China. RESULTS: The five recruited patients included 2 males and 3 females. The median age of seizure onset was 2 months (range, day 3 to 3 months). All patients exhibited the characteristics of clinically migrating focal motor (tonic or clonic) seizures. Typical migrating ictal electrical patterns were found in 1 patient; the remaining four patients presented with overlapping seizures with different areas of ictal onset in differing hemispheres. All the patients had the associated variants, including KCNT1, SCN1A, SCN2A, TBC1D24 and ALG1. All patients received two or more antiseizure medications, and 1 patient became seizure-free, 1 reported >75 % seizure reduction, 2 reported >50 % seizure reduction, and 1 patient showed no improvement. Varying degrees of psychomotor developmental delays were observed in all patients. CONCLUSIONS: The course of EIMFS could be related to the type of gene variant present, and different genes may have specific clinical features. Larger cohorts are required to elucidate such potential phenotype-genotype correlations.

Autoimmune encephalitis after Japanese encephalitis in children: A prospective study.

OBJECTIVE: To explore anti-neuronal surface antibodies and identify associated serum predictors of autoimmune encephalitis after Japanese encephalitis (JE). METHODS: This prospective study first detected anti-neuronal surface antibodies and cytokines in the serum and cerebrospinal fluid (CSF) of JE patients within one week of symptom onset. Anti-neuronal surface antibodies and cytokines in the serum were detected on day 21 post-JE. If the patients relapsed during the convalescent phase, we simultaneously detected JE virus RNA and cytokines in the CSF, as well as anti-neuronal surface antibodies in the serum and CSF. RESULTS: All 31 patients were negative for anti-neuronal surface antibodies at the onset of JE in the serum and CSF. During the convalescent phase, five patients developed autoimmune encephalitis (two had anti-N-methyl-d-aspartate receptor [NMDAR] antibodies, one had γ-aminobutyric acid-B receptor [GABABR] antibodies, and two had other antibodies against unknown neuronal surface antigens). Patients who developed autoimmune encephalitis experienced more severe outcomes than those who did not at the one-year follow-up (p = 0.044). The levels of serum CXCL13 and IL-6, as well as CXCL13, BAFF, CXCL10, and MMP-9 in the CSF were increased in the convalescent phase compared to the acute phase in patients who developed autoimmune encephalitis (p < 0.05). CONCLUSION: In addition to anti-NMDAR antibodies, anti-GABABR antibodies and antibodies against unknown neuronal surface antigens can trigger autoimmune encephalitis following JE. Patients who developed autoimmune encephalitis had a poorer prognosis at the one-year follow-up. Serum CXCL13 may represent a predictor of autoimmune encephalitis after JE.

Role of PKA/CREB/BDNF signaling in PM2.5-induced neurodevelopmental damage to the hippocampal neurons of rats.

Exposure to fine particulate matter (PM2.5) is implicated in neurodevelopmental disorders including cognitive decline, attention-deficit/hyperactivity disorder, and autism spectrum disorder. However, the specific molecular mechanisms by which PM2.5 impacts neurodevelopment are poorly understood. Accordingly, in the present study, the role of protein kinase A (PKA)/cAMP response element binding protein (CREB)/brain-derived neurotrophic factor (BDNF) signaling in PM2.5-induced neurodevelopmental damage was investigated using primary cultured hippocampal neurons. When hippocampal neurons cultured for 3 days in vitro (DIV3) were exposed to PM2.5 for 24 h and 96 h, neuronal viability decreased by 18.8% and 32.7% respectively, percentage of TUNEL-positive neurons increased by 78.5% and 64.0% separately, caspase-9 expression increased, lower postsynaptic density and shorter active zones were observed by transmission electron microscopy, expression of synapse-related proteins including postsynaptic density-95 (PSD95), growth associated protein-43 (GAP43), and synaptophysin (SYP) were decreased, and the phosphorylation levels of PKA, CREB, and BDNF expression also decreased. However, the PM2.5-induced neuronal damage could be ameliorated or aggravated to varying degrees by up- or down-regulation of the PKA/CREB/BDNF signaling pathway, respectively. Our results indicate that PM2.5 exposure exerts neurodevelopmental toxicity as indicated by lower viability, apoptosis, and synaptic damage in primary cultured hippocampal neurons, and that the PKA/CREB/BDNF pathways could play a vital role in PM2.5-mediated neurodevelopmental toxicity.

Dynamic alteration of dendrites and dendritic spines in the hippocampus and microglia in mouse brain tissues after kainate-induced status epilepticus.

PURPOSE: To study the alteration of microglial subtypes, the representative markers of microglia, and the morphology of dendrites and dendritic spines after acute status epilepticus (SE) and during recurrent seizures. METHODS: A mouse kainate-induced SE model was used. Dendrites and dendritic spines of granule neurons in the dentate gyrus (DG) subregion and pyramidal neurons in the cornu ammonis (CA)1 and cornu ammonis (CA)3 subregions of the hippocampus were visualized by Golgi staining. Synaptic proteins were evaluated by Western blot analysis, and microglia and their markers were evaluated by flow cytometry. RESULTS: Extensive partial spine loss was observed in the dendrites of granule and pyramidal cells in the acute and early chronic stages of SE. In terms of spine loss, the thin and mushroom types predominated. Accompanying the spine loss in these two stages, the proportion of M1 microglia increased significantly with high CX3CR1 expression and low CD200R expression. However, at the transiting stage, the proportion of M2 microglia was increased dramatically, and high expression levels of CXCR3 on all microglia and CD68 on M1 microglia were observed. Morris water maze tests revealed significant learning and memory impairment in the chronic phase of epilepsy. CONCLUSION: Dendritic spines in the hippocampus and microglia in the central nevus system are dynamically altered in epilepsy during the establishment and maintenance of spontaneous seizures. Microglia may contribute to the spine loss and related learning and memory impairment.

Efficacy and safety of levetiracetam in the off-label treatment of neonatal seizures.

Background: Treatment of neonatal seizures includes etiotropic and anticonvulsant treatments. However, anticonvulsant use in neonates is off-label and requires ethical review.Objective: To investigate the efficacy and safety of levetiracetam for neonatal seizures and to establish a predictive model.Methods: We retrospectively analyzed 125 neonatal seizure cases (phenobarbital 66 cases, levetiracetam 59 cases). The efficacy, safety and tolerability of levetiracetam were evaluated by cox regression survival analysis and a regression tree prediction model for the 16-week time point.Results: There was no significant difference between phenobarbital and levetiracetam treatment group in short-term efficacy (p > 0.05). But the cumulative survival function suggested that levetiracetam treatment group was better than phenobarbital (p = 0.026) in long-term efficacy evaluation. Neurodevelopmental assessments at 16 weeks showed that levetiracetam had better effect on the neurodevelopmental level (Gesell scores in response) than phenobarbital (p = 0.011). The main adverse events with levetiracetam were irritability and anorexia. According to the regression tree prediction model, the top three factors influencing the therapeutic effect were pre-treatment seizure frequency, age of onset and etiological classification.Conclusion: Levetiracetam shows good efficacy, safety and tolerability for the long-term neonatal seizure treatment.

Effects of gap junctions blockers on fast ripples and connexin in rat hippocampi after status epilepticus.

OBJECTIVE: To assess the dynamic changes in the average and peak spectral power of fast ripples (FRs) in the hippocampi after interventions with valproate sodium (VPA), carbenoxolone (CBX) and quinine (QUIN). METHOD: Adult rats were used to establish a lithium-pilocarpine (pilo) epileptic model, and were assigned to a lithium-pilocarpine (PILO), VPA + PILO, QUIN + PILO or CBX + PILO group. Intracranial electroencephalography was performed before and after status epilepticus (SE). The hippocampal connexin (CX) 43, CX32 and CX36 expressions were analyzed via western blotting. RESULTS: The time required for the disappearance of SE after chloral hydrate injection was lower in the intervention groups than in the PILO group (p < 0.05). Seizures induced CX43 expression, but had no significant effects on CX36 or CX32 expressions. Pretreatment with VPA, QUIN and CBX inhibited CX43, CX36 and CX32 expression after SE. The average spectral power of the FRs was significantly lower in the VPA + PILO and QUIN + PILO groups than in the PILO group at 10 min after SE, 10 min before chloral hydrate injection, and 10 min after chloral hydrate injection (p < 0.05). The average spectral power of FRs was lower in the CBX + PILO group than in the PILO group at 10 min after SE (p < 0.05). The average spectral power of FRs in the 3 intervention groups recovered to the baseline level at 10 min after chloral hydrate injection and persisted for 3 days after SE. The dynamic changes in the average and peak spectral power of FRs were similar. SIGNIFICANCE: After SE, CX may participate in pathological FR generation by establishing abnormal electrical synaptic transmission. Gap junction blockers can inhibit various CX expressions, and thus decrease FR energy and alleviate the degree of seizure. These findings could contribute to the development of new anti-epileptic drugs with novel mechanistic targets.

Dynamic Changes in Spectral and Spatial Signatures of High Frequency Oscillations in Rat Hippocampi during Epileptogenesis in Acute and Chronic Stages.

OBJECTIVE: To analyze spectral and spatial signatures of high frequency oscillations (HFOs), which include ripples and fast ripples (FRs, >200 Hz) by quantitatively assessing average and peak spectral power in a rat model of different stages of epileptogenesis. METHODS: The lithium-pilocarpine model of temporal lobe epilepsy was used. The acute phase of epilepsy was assessed by recording intracranial electroencephalography (EEG) activity for 1 day after status epilepticus (SE). The chronic phase of epilepsy, including spontaneous recurrent seizures (SRSs), was assessed by recording EEG activity for 28 days after SE. Average and peak spectral power of five frequency bands of EEG signals in CA1, CA3, and DG regions of the hippocampus were analyzed with wavelet and digital filter. RESULTS: FRs occurred in the hippocampus in the animal model. Significant dynamic changes in the spectral power of FRS were identified in CA1 and CA3. The average spectral power of ripples increased at 20 min before SE (p < 0.05), peaked at 10 min before diazepam injection. It decreased at 10 min after diazepam (p < 0.05) and returned to baseline after 1 h. The average spectral power of FRs increased at 30 min before SE (p < 0.05) and peaked at 10 min before diazepam. It decreased at 10 min after diazepam (p < 0.05) and returned to baseline at 2 h after injection. The dynamic changes were similar between average and peak spectral power of FRs. Average and peak spectral power of both ripples and FRs in the chronic phase showed a gradual downward trend compared with normal rats 14 days after SE. SIGNIFICANCE: The spectral power of HFOs may be utilized to distinguish between normal and pathologic HFOs. Ictal average and peak spectral power of FRs were two parameters for predicting acute epileptic seizures, which could be used as a new quantitative biomarker and early warning marker of seizure. Changes in interictal HFOs power in the hippocampus at the chronic stage may be not related to seizure occurrence.