Synchronization Of Neuronal Activity Research Articles

Common Causes of Neonatal Seizure among Neonates Admitted to Neonatal Care Unit at Al Ramadi Teaching Hospital for Maternity and Children

Neonatal seizures are the transient occurrence of signs and symptoms due to an abnormal excessive or synchronous neuronal activity in the neural cells causing paroxysmal electro clinical changes. Neonates are at high risk for seizures as compared to other age groups. The aim of this study was to identify the common causes that lead to neonatal seizure during the period from first of October 2020 to the end of July 2021using history, physical examination, and investigations in Al Ramadi teaching hospital for maternity and children. The total number of neonates diagnosed as neonatal seizure during the period of study in Al Ramadi teaching hospital for maternity and childhood was 64 cases. Total number of admissions to neonatal care unit was 4102 so the prevalence in neonatal care unit was 15.6 per 1000 live births. 30 (47.1 %) cases were diagnosed as perinatal asphyxia, 18 (28 %) cases were diagnosed as metabolic, 6 (9.4 %) cases were diagnosed as infections, seizures, 4 (6.3%) cases were diagnosed as intracranial hemorrhage, 3(4.6%) cases were diagnosed as CNS malformation, while 3 cases (4.6 %) were Unknown etiology. 38 (59.3%) of studied neonatal seizures were male, while 26 (40.7%) were female. Male to female ratio was (1.4:1). 37 (57.8%) were term babies (≥37 gestational age), while 27 (42.2%) were preterm babies (<37 gestational age). 41 (64%) of studied neonatal seizure cases were born by normal vaginal delivery, while 23 (36%) of cases were born by caesarian section delivery. The most common cause of neonatal seizure was perinatal asphyxia followed by metabolic causes then infection, intracranial hemorrhage, CNS malformations and unknown causes. Male are more common than female. In term neonates more common than preterm and in normal vaginal delivery more than cesarean section.

Heterogeneity in oligodendrocyte precursor cell proliferation is dynamic and driven by passive bioelectrical properties

Oligodendrocyte precursor cells (OPCs) generate myelinating oligodendrocytes and are the main proliferative cells in the adult central nervous system. OPCs are a heterogeneous population, with proliferation and differentiation capacity varying with brain region and age. We demonstrate that during early postnatal maturation, cortical, but not callosal, OPCs begin to show altered passive bioelectrical properties, particularly increased inward potassium (K+) conductance, which correlates with G1 cell cycle stage and affects their proliferation potential. Neuronal activity-evoked transient K+ currents in OPCs with high inward K+ conductance potentially release OPCs from cell cycle arrest. Eventually, OPCs in all regions acquire high inward K+ conductance, the magnitude of which may underlie differences in OPC proliferation between regions, with cells being pushed into a dormant state as they acquire high inward K+ conductance and released from dormancy by synchronous neuronal activity. Age-related accumulation of OPCs with high inward K+ conductance might contribute to differentiation failure.

Unveiling the hidden connection: the blood-brain barrier's role in epilepsy.

Epilepsy is characterized by abnormal synchronous electrical activity of neurons in the brain. The blood-brain barrier, which is mainly composed of endothelial cells, pericytes, astrocytes and other cell types and is formed by connections between a variety of cells, is the key physiological structure connecting the blood and brain tissue and is critical for maintaining the microenvironment in the brain. Physiologically, the blood-brain barrier controls the microenvironment in the brain mainly by regulating the passage of various substances. Disruption of the blood-brain barrier and increased leakage of specific substances, which ultimately leading to weakened cell junctions and abnormal regulation of ion concentrations, have been observed during the development and progression of epilepsy in both clinical studies and animal models. In addition, disruption of the blood-brain barrier increases drug resistance through interference with drug trafficking mechanisms. The changes in the blood-brain barrier in epilepsy mainly affect molecular pathways associated with angiogenesis, inflammation, and oxidative stress. Further research on biomarkers is a promising direction for the development of new therapeutic strategies.

Aberrant neural oscillations in poststroke aphasia.

Neural oscillations are electrophysiological indicators of synchronous neuronal activity in the brain. Recent work suggests aberrant patterns of neuronal activity in patients with poststroke aphasia. Yet, there is a lack of systematic explorations of neural oscillations in poststroke aphasia. Investigating changes in the dynamics of neuronal activity after stroke may be helpful to identify neural markers of aphasia and language recovery and increase the current understanding of successful language rehabilitation. This review summarizes research on neural oscillations in poststroke aphasia and evaluates their potential as biomarkers for specific linguistic processes. We searched the literature through PubMed, Web of Science, and EBSCO, and selected 31 studies that met the inclusion criteria. Our analyses focused on neural oscillation activity in each frequency band, brain connectivity, and therapy-induced changes during language recovery. Our review highlights potential neurophysiological markers; however, the literature remains confounded, casting doubt on the reliability of these findings. Future research must address these confounds to confirm the robustness of cross-study findings on neural oscillations in poststroke aphasia.

Shaping the olfactory map: cell type-specific activity patterns guide circuit formation.

The brain constructs spatially organized sensory maps to represent sensory information. The formation of sensory maps has traditionally been thought to depend on synchronous neuronal activity. However, recent evidence from the olfactory system suggests that cell type-specific temporal patterns of spontaneous activity play an instructive role in shaping the olfactory glomerular map. These findings challenge traditional views and highlight the importance of investigating the spatiotemporal dynamics of neural activity to understand the development of complex neural circuits. This review discusses the implications of new findings in the olfactory system and outlines future research directions.

Serotonin modulates infraslow oscillation in the dentate gyrus during Non-REM sleep.

Synchronous neuronal activity is organized into neuronal oscillations with various frequency and time domains across different brain areas and brain states. For example, hippocampal theta, gamma and sharp wave oscillations are critical for memory formation and communication between hippocampal subareas and the cortex. In this study, we investigated the neuronal activity of the dentate gyrus (DG) with electrophysiological and optical imaging tools during sleep-wake cycles. We found that the activity of major glutamatergic cell populations in the DG is organized into in-fraslow oscillations (0.01 - 0.03 Hz) during NREM sleep. Although the DG is considered a sparsely active network during wakefulness, we found that 50% of granule cells and about 25% of mossy cells exhibit increased activity during NREM sleep. Further experiments revealed that the infraslow oscillation in the DG is modulated by rhythmic serotonin release during sleep, which oscillates at the same frequency but in an opposite phase. Genetic manipulation of 5-HT receptors revealed that this neuromodulatory regulation is mediated by 5-HT1a receptors and the knockdown of these receptors leads to memory impairment. Together, our results provide novel mechanistic insights into how the 5-HT system can influence hippocampal activity patterns during sleep.

Diagnostic and therapeutic approach to patients with first seizure episode

Seizures are transient episodes of signs and/or symptoms resulting from abnormal, excessive or synchronous neuronal activity in the brain. About 8% to 10% of people will experience a seizure at some point in their lives, and of that group, about 2% to 3% will develop epilepsy. Given the impact that epilepsy can have on a person's quality of life and related medical, cognitive, or psychiatric conditions, it is crucial to perform a detailed evaluation when a patient presents an unprovoked first seizure episode. A seizure crisis must be distinguished from other events with a similar presentation, as the possible causes must be determined, to establish the need for adequate treatment, and establish a long-term prognosis.

Somatostatin interneurons control the timing of developmental desynchronization in cortical networks

Synchronous neuronal activity is a hallmark of the developing brain. In the mouse cerebral cortex, activity decorrelates during the second week of postnatal development, progressively acquiring the characteristic sparse pattern underlying the integration of sensory information. The maturation of inhibition seems critical for this process, but the interneurons involved in this crucial transition of network activity in the developing cortex remain unknown. Using invivo longitudinal two-photon calcium imaging during the period that precedes the change from highly synchronous to decorrelated activity, we identify somatostatin-expressing (SST+) interneurons as critical modulators of this switch in mice. Modulation of the activity of SST+ cells accelerates or delays the decorrelation of cortical network activity, a process that involves regulating the maturation of parvalbumin-expressing (PV+) interneurons. SST+ cells critically link sensory inputs with local circuits, controlling the neural dynamics in the developing cortex while modulating the integration of other interneurons into nascent cortical circuits.

Analysis of hippocampal local field potentials by diffusion mapped delay coordinates

Spatial navigation through novel spaces and to known goal locations recruits multiple integrated structures in the mammalian brain. Within this extended network, the hippocampus enables formation and retrieval of cognitive spatial maps and contributes to decision making at choice points. Exploration and navigation to known goal locations produce synchronous activity of hippocampal neurons resulting in rhythmic oscillation events in local networks. Power of specific oscillatory frequencies and numbers of these events recorded in local field potentials correlate with distinct cognitive aspects of spatial navigation. Typically, oscillatory power in brain circuits is analyzed with Fourier transforms or short-time Fourier methods, which involve assumptions about the signal that are likely not true and fail to succinctly capture potentially informative features. To avoid such assumptions, we applied a method that combines manifold discovery techniques with dynamical systems theory, namely diffusion maps and Takens’ time-delay embedding theory, that avoids limitations seen in traditional methods. This method, called diffusion mapped delay coordinates (DMDC), when applied to hippocampal signals recorded from juvenile rats freely navigating a Y-maze, replicates some outcomes seen with standard approaches and identifies age differences in dynamic states that traditional analyses are unable to detect. Thus, DMDC may serve as a suitable complement to more traditional analyses of LFPs recorded from behaving subjects that may enhance information yield.

Chronic Hyponatremia and Brain Structure and Function Before and After Treatment

Rationale & ObjectiveHyponatremia is the most common electrolyte disorder and is associated with significant morbidity and mortality. This study investigated neurocognitive impairment, brain volume, and alterations in MRI-based measures of cerebral function in patients before and after treatment for hyponatremia. Study DesignProspective cohort study. Setting & ParticipantsPatients with presumed chronic hyponatremia without signs of hypo- or hypervolemia treated in the Emergency Department of a German tertiary care hospital. ExposureHyponatremia ([Na+] <125 mmol/L) before and after treatment leading to [Na+] >130 mmol/L. OutcomesStandardized neuropsychological testing (Mini-Mental-State examination [MMSE], DemTect, Trail-Making Test [TMT] A/B, Beck’s Depression Inventory, Timed Up and Go) and resting-state MRI were performed prior to and following treatment of hyponatremia to assess volumes of total brain, white and gray matter, as well as neuronal activity and its synchronization. Analytical ApproachChanges in outcomes after treatment for hyponatremia assessed using bootstrapped confidence intervals and Cohen’s d. Associations between parameters were assessed using correlation analyses. ResultsDuring a 3.7-year period, 26 patients were enrolled. Complete data were available for 21 patients. Mean [Na+] was 118.4 mmol/L before treatment and 135.5 mmol/L following treatment. Most measures of cognition improved significantly. Comparison of MRI studies showed a decrease in brain tissue volumes, neuronal activity, and synchronization across all gray matter after normalization of [Na+]. Volume effects were particularly prominent in the hippocampus. During hyponatremia, synchronization of neuronal activity was negatively correlated with [Na+] (r=-.836, [-.979, -.446]) and cognitive function (MMSE: r=-.523, [-.805, -.069]; DemTect: r=-.744, [-.951, -.385] and TMT-A: r=.692, [.255, .922]). LimitationsSmall sample size, insufficient quality of several MRI scans due to motion artifact. ConclusionsResolution of hyponatremia was associated with improved cognition and reductions in brain volumes and neuronal activity. Impaired cognition during hyponatremia is closely linked to increased neuronal activity rather than to tissue volumes. Furthermore, the hippocampus appears to be particularly susceptible to hyponatremia, exhibiting pronounced changes in tissue volume.

Adansonia digitata L. Stem Bark Attenuates Epileptic Seizure, Depression, and Neurodegeneration by Mediating GABA and Glutamate in Pentylenetetrazol-Kindled Rats.

Epilepsy is a neurological condition characterized by repeated seizures attributable to synchronous neuronal activity in the brain. The study evaluated the effect of acetone extract of Adansonia digitata stem bark (ASBE) on seizure score, cognition, depression, and neurodegeneration as well as the level of Gamma-Aminobutyrate acid (GABA) and glutamate in Pentylenetetrazol-kindled rats. Thirty-five rats were assigned into five groups (n = 7). Groups 1-2 received normal saline and 35 mg/kg PTZ every other day. Groups 3-4 received 125 mg/kg and 250 mg/kg ASBE orally while group 5 received 5 mg/kg diazepam daily for twenty-six days. Group 3-5 received PTZ every other day, 30 mins after ASBE and diazepam. The results showed that Pentylenetetrazol (PTZ) induces seizure, reduces mobility time in force swim test and decreases the normal cell number in the brain. It also significantly decreases (p < 0.05) catalase, superoxide dismutase and reduced glutathione activities compared to the ASBE pre-treated rats. Pre-treatment with ASBE reportedly decreases seizure activities significantly (p < 0.05) and increases mobility time in the force swim test. ASBE also significantly elevate (p < 0.05) the normal cell number in the hippocampus, temporal lobe, and dentate gyrus. ASBE reduced seizure activity and prevented depression in PTZ-treated rats. It also prevented neurodegeneration by regulating glutamate and GABA levels in the brain as well as preventing lipid peroxidation.

Optogenetic stimulation suppresses ictal activity in a 4-aminopyridine model of epileptic activity &lt;i&gt;in vitro&lt;/i&gt;

The WHO estimates that nearly 1% of the population suffers from epilepsy. Despite advances in the development of new antiepileptic drugs, seizures cannot be completely eliminated in nearly one-third of patients. One promising approach to the treatment of epilepsy may be gene therapy. Because epileptic activity is caused by an imbalance between excitation and inhibition, researchers have focused primarily on regulating neuronal excitability. Initially, the main approaches were based on the hyperexpression of inhibitory peptides such as galanin or NPY, or the suppression of neuronal excitability by the hyperexpression of potassium channels in neurons. However, these effects should be well calculated and strictly dosed, as it is difficult to correct the expression later. If the expression is too low, the anticonvulsant effect will not be achieved, and if the expression is too high, the neuronal networks will be impaired due to strong inhibition. For this reason, methodological approaches to treatment in which the effect on the neuronal excitability in the epileptic focus can be controlled are of great interest. Optogenetic methods offer such an advantage. Optogenetics uses light to alter the excitability of specific neuronal populations and can also be used in a biofeedback paradigm in which the light source is activated only at the risk of generating seizure activity. A number of optogenetic tools have now been developed, including light-activated cationic (e.g., ChR2) and anion channels (ACR), metabotropic receptors, pumps (NpHR, Arch), and enzymes. However, the optogenetic approach has a number of technical difficulties in delivering the light source and the risk of developing an immune response to the expression of rhodopsins. This report reviews the experience of practical application of optogenetic tools in the use of 4-aminopyridine in vitro model of epileptiform activity in experiencing slices of the entorhinal cortex. We tested the efficacy of suppressing ictal activity using several variants of optogenetic stimulation: (1) activation of excitatory and inhibitory neurons (in Thy1-ChR2-YFP mice), (2) activation of inhibitory interneurons only (in PV-Cre mice after virus injection with the channelodopsin-2 gene), hyperpolarization of excitatory neurons after expression of (3) archaeodopsin or (4) a light-dependent sodium pump. We found that ictal activity was successfully suppressed when low-frequency optogenetic stimulation induced regular interictal activity. Usually, interictal activity was induced by rhythmic synchronous activation of the principal neurons of the entorhinal cortex. In other cases, the ictal activity was preserved, although its characteristics may have changed. We determined the parameters of optogenetic stimulation that were most effective in suppressing ictal activity. The availability of a wide range of gene therapy approaches for epilepsy that have demonstrated efficacy in preclinical studies suggests that clinical trials of some of these approaches will begin in the next few years.

Neuropsychiatric and cognitive comorbidities in epilepsy

The epileptic crisis is characterized by a momentary episode of signs and symptoms that are caused by abnormal excessive or synchronous neuronal activity in the brain. On the other hand, epileptic syndrome is defined, according to the International League Against Epilepsy (ILAE), by “a group of clinical and neuroimaging characteristics in electroencephalographic (EEG) findings, many times, supported by specific etiologic findings (structural, genetic, metabolic, immunological and infectious)”. Accordingly, epilepsy patients have multiple neuropsychiatric comorbidities, being depressive disorders the most common, a condition that affects the quality of life and is influenced by numerous external factors. The present study aims to conduct a literature review based on the analysis of articles published from 2010 to 2022 in the PubMed (Medline) and Science Direct databases on epilepsy, its cognitive compromising and its neuropsychiatric comorbidities, using the terminology indicated by the System of Descriptors in Health Sciences (DeCS) and a set of predetermined criteria to select the best articles on the subject. Therefore, approaching psychiatric comorbidities, such as depressive disorders and cognitive deficiencies, in epilepsy is essential in light of its high prevalence and the negative repercussions in the patient's life. Consequently, more in-depth studies are necessary to provide a better prognosis for epilepsy patients and to evaluate the side effects and the clinical repercussions of Anti-Epileptic Drugs (AEDs).

Pharmacological inhibition of ictal and interictal epileptiform discharges

Background: Epilepsy is a brain disorder characterized by an enduring predisposition to generate epileptic seizures. Seizures are a transient occurrence of signs and/or symptoms due to abnormal excessive and synchronous neuronal activity in the brain. Electroencephalogram (EEG), a non-invasive instrumental test, has an important role in the diagnosis of epilepsy, as well as in monitoring the results and long-term treatment because it can detect interictal and ictal discharges that are crucial for confirmation and classification of seizures. Antiepileptic drugs are the first treatment option in patients with epilepsy, although the effectiveness of such drugs is limited only to symptom control and requires a regular intaking by the patient. These drugs exploit the cell membrane channels, modifying their permeability, allowing either an increase in the inhibitory neurotransmission or the reduction in the excitatory one, by hyperpolarizing neurons and avoiding the recurrence of the epileptic seizures without reversing or stopping the underlying mechanism of epileptogenesis. Materials and Methods: The internship took place in the Neurophysiopathology department of the Antonio, Biagio and Cesare Arrigo’s hospital in Alessandria, from October 2022 to March 2023. During this period, it was possible to attend the emergency treatment of prolonged and recurrent epileptic seizures during EEGrafic recording and the consequential amendments of the ictal discharges induced by the administration of antiepileptic drugs. Follow up EEG was also performed to investigate the modifications of interictal activity after a period of treatment with antiepileptic drugs. The patient who has been analyzed in this paper, underwent EEG recordings obtained by using bridge electrodes placed on the scalp according to the international 10-20 system. Objectives: The aim of this study is to analyze the mechanisms of action of the main antiepileptic drugs, in relation to the physiological cellular mechanisms regulating the neuronal excitability and their effect on the ictal and interictal epileptiform discharges in the EEG recordings.

Altered Spontaneous Brain Activity and Its Predictive Role in Patients with Central Retinal Artery Occlusion Using fMRI and Machine Learning.

To investigate spontaneous neuronal activity changes in patients with central retinal artery occlusion (CRAO) using the resting-state functional magnetic resonance imaging (fMRI) and detect whether these brain functional alterations can represent an objective biomarker of clinical response using a machine learning algorithm. Eighteen patients with CRAO and eighteen healthy controls (HCs) were recruited. The regional homogeneity (ReHo) method of resting-state fMRI was conducted to evaluate the synchronous brain activity alterations between two groups. Differences of ReHo values between two groups were compared using the independent two-sample t-test. The support vector machine algorithm was to distinguish patients of CRAO from HCs based on the two groups' whole-brain ReHo patterns. The accuracy, sensitivity, and specificity for the classification were calculated. The classification performance was evaluated using the non-parametric permutation test. Compared to HCs, individuals with CRAO showed significantly lower ReHo in the right cerebellum and precuneus. Meanwhile, significant higher ReHo values were observed in the left superior temporal gyrus, postcentral gyrus, and precentral gyrus in the CRAO group compared to HCs. Furthermore, our results suggested that 77.78% individuals with CRAO could be successfully distinguished from HCs by the machine learning, with a sensitivity of 72.22% and a specificity of 83.33%, respectively. The area of receiver operating characteristic curve was calculated to be 0.85. This study uncovered individuals with CRAO exhibited disturbed synchronous neuronal activities in multiple brain areas using neuroimaging techniques. The ReHo variability could distinguish individuals with CRAO from HCs with high accuracy.

Emergence of preparatory dynamics in VIP interneurons during motor learning

To determine what actions to perform in each context, animals must learn how to execute motor programs in response to sensory cues. In rodents, the interface between sensory processing and motor planning occurs in the secondary motor cortex (M2). Here, we investigate dynamics in vasointestinal peptide (VIP) and somatostatin (SST) interneurons in M2 during acquisition of a cue-based, reach-to-grasp (RTG) task in mice. We observe the emergence of preparatory activity consisting of sensory responses and ramping activation in a subset of VIP interneurons during motor learning. We show that preparatory and movement activities in VIP neurons exhibit compartmentalized dynamics, with principal component 1 (PC1) and PC2 reflecting primarily movement and preparatory activity, respectively. In contrast, we observe later and more synchronous activation of SST neurons during the movement epoch with learning. Our results reveal how VIP population dynamics might support sensorimotor learning and compartmentalization of sensory processing and movement execution.

THE GREAT PRETENDER: COULD A PHEOCHROMOCYTOMA MANIFEST ITSELF AS A SEIZURE?

Objective: Seizures are defined as transient occurrence of signs or symptoms due to the abnormally excessive or synchronous neuronal activity in the cerebral cortex. Pheochromocytomas and paragangliomas (PPGL) are chromaffin cell tumors arising from the adrenal medulla in 80–85% of patients and from extra-adrenal sympathetic tissue in 10–20% of patients. PPGL has been referred to as ‘‘the great mimic’’ disease. We present a patient with pheochromocytoma possibly disguised as seizures. Design and method: A 44 years old woman was referred to University Clinic of Endocrinology by radiologist. Two years earlier she had syncopal crises . She complained of headache, heart palpitation and malaise, heart palpitations and fatigue during exertion and sense of panic. The maximal self-measured blood pressure was 160/100 mmHg, the pulse is 90-100 beats per min. Abdominal US: a hyperechoic change, 76x65mm was seen, then described in the right lobe of the liver. The following year she had two commotional crises of consciousness and spasms of the extremities . She had a non-specific slowing of FC on EEG on the right for 1-2 seconds. MSCT abdomenal : in the right adrenal gland, a mass 144 x 90mm, with clear borders, pressing into the liver and pushing the right kidney,. The 24h urine was collected, which confirmed a norepinephrine secreting pheochromocytoma. We administered long acting alpha blocking agent preoperatively. The complete surgical excision of the right adrenal mass was done, pathohistological diagnosis: Pheochromocytoma. The last EEG after sleep deprivation performed 2 months postoperatively was described as normal. The patient had no headache or seizure. Results: PPGLs have a notable ability of boosting NE levels systemically and hypertension, the most common sign of PPGL could facilitate the permeability of blood brain barrier to NE. Studies showed NE could play its anticonvulsant property at an appropriate concentration but has a proconvulsant effect in either too high or too low concentrations . Conclusions: The definite pathogenetic mechanisms explaining how PPGL can cause seizures are far from being clearly understood, though “the great pretender” should be considered as a possible etiological factor of seizures.

Intrinsic brain activity alterations in patients with Parkinson’s disease

ObjectiveThe objective of this study is to explore the brain activity alterations in Parkinson’s disease (PD) from the perspectives of neuronal activity, synchronization of neuronal activity, and coordination of whole-brain activity. MethodsIn this study, we recruited 38 PD patients and 35 matched healthy controls (HCs). We explored intrinsic brain activity alterations in PD by comparing resting-state functional magnetic resonance imaging (rs-fMRI) metrics of the amplitude of low-frequency of fluctuation (ALFF), the fractional amplitude of low-frequency fluctuation (fALFF), percent amplitude of fluctuation (PerAF), regional homogeneity (ReHo), and degree centrality (DC). Two-sample t-tests were used to determine the differences between the two groups. Spearman correlation analysis was used to explore the relationships between abnormal ALFF, fALFF, PerAF, ReHo, and DC values and clinical indicators such as the Movement Disorder Society’s Unified Parkinson’s Disease Rating Scale (MDS-UPDRS), Hoehn and Yahr (H&Y) stage, and duration of disease. ResultsCompared with the HCs, PD had increased ALFF,fALFF, and PerAF in the temporal lobe and cerebellum, and decreased ALFF,fALFF, and PerAF in the occipital-parietal lobe in the neuronal activity. In the synchronization of neuronal activity, PD patients had increased ReHo in the right inferior parietal lobule and decreased ReHo in the caudate. In the coordination of whole-brain activity, PD patients had increased DC in the cerebellum and decreased DC in the occipital lobe. Correlation analysis showed that there is a correlation between abnormal brain regions and clinical indicators in PD. Notably, the changes in occipital lobe brain activity were found in ALFF, fALFF, PerAF, and DC, and were most correlated with the clinical indicators of PD patients. ConclusionsThis study found that intrinsic brain function in several occipital-temporal-parietal and cerebellum regions was altered in PD patients, potentially related to the clinical indicators of PD. These results may enhance our understanding of the underlying neural mechanisms of PD and may contribute to further exploring the selection of therapeutic targets in PD patients.

CLINICO-ETIOLOGICAL PROFILE OF FIRST EPISODE OF SEIZURE AND ITS CORRELATION WITH ELECTROENCEPHALOGRAM AND IMAGING SPECTRUM IN CHILDREN AGED ABOVE 5 YEARS OF AGE IN A TERTIARY CARE HOSPITAL: A PROSPECTIVE OBSERVATIONAL STUDY

Seizures, a transient occurrence of signs and/or symptoms resulting from abnormal excessive or synchronous neuronal activity in the brain [1, 2].Seizure is one of the commonest neurological illnesses. About 4-10% of children experience at least one episode in the rst 16 years of life. Where 1/5th of total children with unprovoked seizures may develop epilepsy. Risk is approximately 20% if neurological examination, electroencephalogram (EEG) and neuroimaging is normal[1]. EEG abnormalities can be detected in up to 59% of children with rst afebrile seizure and can identify subtle focality in presence of normal magnetic resonance imaging of brain[1]. Neuroimaging has an important role in children with focal seizure, persistent seizure activity, focal neurologic decit, neurocutaneous disorder etc.Right assessment and scrutiny of rst seizure is crucial, not only for abortion of acute attack but also for long term control of epilepsy. Aim and methods- The objective of the study is to determine the age of onset, etiology of rst episode of seizure in children between the age group of above 5 yearsto15 years and the pattern of EEG changes and MRI ndings in the above group of children. In a prospective single centre observational study at GIMS GADAG, around 60 children who were admitted with rst episode of seizure at age group of above 5 years to 15 years to our emergency department between October 2021 to July-2022 (10 months) were studied. Seizures dened using international league against epilepsy (ILAE). EEG and MRI were done in all 60 children and their records were analysed. Results- A total of 60 children presenting with rst episode of seizures were included in the study. 9-12 year age group were major portion of our study with male gender predominance. Generalized seizures were more common accounting for 78%. Idiopathic seizure was the most common etiology identied (40%), followed by meningitis (27%) and other causes. EEG abnormality was seen in 50% of the children.

Monocular transcorneal electrical stimulation induces ciliary muscle thickening in contralateral eye

Transcorneal electrical stimulation (TES) is used as therapy for retinal diseases such as retinitis pigmentosa (RP) and was suggested for assessing retinal sensitivity by determining phosphene thresholds, subjective luminance impressions caused by retinal stimulation. Further applications concerned the accommodation process, revealing an improved accommodative amplitude in presbyopic eyes after TES treatment. The respective changes of the ciliary muscle (CM), the structure most important for near vision, during TES are yet unknown. In a pilot study, we aimed to assess whether monocular TES leads to morphological and functional CM changes and whether central accommodation control is affected. Ten healthy, near-emmetropic adults participated in the trial (4 females, age 26.3 ± 3.6 years). Using a wavefront and a stimulus generator, a biphasic square-wave stimulus (2 s positive and 6 s negative amplitude) of 0 μA average current was produced and transferred to the eye by means of a Dawson-Trick & Litzkow electrode. Prior to the stimulation, an individual determination of phosphene thresholds served to define individual TES current amplitudes, which ranged between 60 and 100 μA. Optical coherence tomography (OCT) imaging of the right eye's temporal ciliary muscle was performed before and during ipsi- as well as contralateral monocular TES in randomized order in the morning and afternoon of the same day. During imaging, subjects fixated a target at 4 m distance and refraction was simultaneously recorded via eccentric infrared photorefraction. OCT images were assessed using previously published custom-developed software, allowing the definition of selective CM thickness (CMT) readings, and plotting of continuous CMT profiles along the muscle border. CMT profiles revealed that both stimulations, on the ipsi- and contralateral eye, induced a thickening of the CM compared to the non-stimulated state. The selective CMT readings confirmed a significant increase with ipsi- (31 ± 30 μm; p = 0.010) and contralateral (25 ± 16 μm; p = 0.001) TES. However, refraction during far vision was not significantly affected by either stimulation (ipsilateral [n = 5]: median Δw/-w/o = 0 D; contralateral [n = 7]: Δw/-w/o = 0.13 D). Pupil size on average increased during TES, but without reaching significance (ipsilateral [n = 5] median Δw/-w/o = 0.23 mm, contralateral [n = 7] Δw/-w/o = 0.39 mm). Ipsilateral CM thickening could be explained by local changes within the stimulated ciliary muscle, such as increased blood flow or interstitial fluid rise induced by TES. However, the CMT increase in the right eye when TES was performed contralaterally, on the left eye, indicates an involvement of the central control circuit of accommodation. Further possible explanations for this finding are a synchronization of neuronal activities in the visual pathway, the release of vasoactive neuropeptides, or effects on the central blood pressure regulation. Given a neuromodulation effect on the CM function, TES might have implications for children with accommodation insufficiencies and as additional therapy in myopia control management, e.g. in combination with multifocal contact lens treatment. Our study is important for the clinical application of TES, and the outcome might add crucial knowledge to the current understanding of the accommodation process and inform research and treatment of both myopia and presbyopia.