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Purpose: Advancements in medical treatments and increased access to healthcare have significantly extended the life expectancy of children with neurological disorders. However, this has also led to a higher incidence of secondary health issues, such as nephrolithiasis. This review aims to analyze the risk factors, management, and treatment outcomes for stone disease in children with neurological disorders and focus on specific risk factors such as immobilization, urinary tract infections, and metabolic abnormalities to identify key points in the occurrence of nephrolithiasis. Methods: A comprehensive literature search was conducted across two primary databases, PubMed and Ovid Medline, to identify studies on urolithiasis in children with neurological disorders. A total of 771 articles were initially identified. After removing four duplicate articles, 729 were excluded following title and abstract screening due to irrelevance. Thirty-eight articles were selected for full-text review, and after further exclusions, 11 articles were included in this review. Results: The studies mainly consisted of small-scale, single-center investigations. Nephrolithiasis were reported in 5–54% of patients across the studies. The most commonly identified risk factors were immobilization, urinary tract infections (UTIs), and hypercalciuria. Treatment options for urinary stones included medical expulsive therapy (MET), extracorporeal shock wave lithotripsy (ESWL), endoscopic surgery (RIRS), and percutaneous nephrolithotomy (PCNL). Conclusion: Key steps in managing these patients include monitoring bone mineral density, conducting a 24-h urine analysis to assess metabolic components (despite challenges in obtaining this), and encouraging physical activity as much as the patient's condition permits. [ABSTRACT FROM AUTHOR]

The common cold is the primary cause of illness in the community, with over 200 viral strains identified, and rhinovirus infections being the most prevalent. Coronavirus Disease 19 (COVID-19) is also a significant cause of severe illness. The burden of acute respiratory infections has a significant impact on the economy, resulting in absenteeism from work and school. Rhinovirus infections can exacerbate asthma and other chronic diseases, leading to hospitalization. The objective of this study is to investigate the factors associated with death and survival in patients hospitalized for rhinovirus in Brazil in 2022. This is a retrospective cohort study using data from the national surveillance of Severe Acute Respiratory Syndrome (SARS) in 2022 in Brazil, with all the norrifications. We analysed and compared clinical and epidemiological factors and outcomes between survivors and deaths in patients hospitalised for rhinovirus. The absolute and relative frequencies were calculated according to the states. Bivariate analysis was performed using chi-squared test and Fisher's exact test, while multivariate analysis was performed using COX regression. Out of 8,130 cases of SARS caused by rhinovirus, 291 (3.58%) resulted in death while 7839 (96.47%) patients survived. The factors associated with death were invasive ventilation (p- < 0.001 HR 4.888 CI 95% 3.816–6.262), bocavirus (p- < 0.001 HR 4.204 CI 95% 2.595–6.812), immunodepression/Immunosuppression (p- < 0.001 HR 2.417 CI 95% 1. 544–3, 786), COVID-19 (p- < 0.001 HR 2.167 CI 95% 1.495–3.142), chronic neurological diseases (p-0.007 HR 1.610 CI 95% 1.137–2.280), abdominal pain (p-0.005 HR 1.734 CI 95% 1.186–2.537), age (p- < 0.001 HR 1.038 CI 95% 1.034–1.042). The survival factors identified in this study were dyspnea (p = 0.005; HR 0.683; CI 95% 0.524–0.889), cough (p < 0.001; HR 0.603; CI 95% 0.472–0.769), and asthma (p = 0.052; HR 0.583; CI 95% 0.339–1.004). Additionally, the study found that receiving a COVID-19 booster dose was also a significant survival factor (p = 0.001; HR 0.570; CI 95% 0.415–0.784). The factors associated with death were similar to those in the literature, and the factors associated with survival were also similar, except for the booster dose of the COVID-19 vaccine, which we didn't find in any studies. Our study is the first to associate the full course of the COVID-19 vaccine with survival in those hospitalized for rhinovirus, regardless of COVID-19 and rhinovirus co-detection. [ABSTRACT FROM AUTHOR]

Oropouche virus is the aetiological agent of Oropouche fever. At present, this is currently considered one of the most important vector-borne diseases in Latin America. On 27 May 2024, the Ministry of Public Health of Cuba reported the first ever outbreak of Oropouche fever. In this report, we describe three human cases of Oropouche virus infection with symptoms and signs of neurological disease and clinical diagnosis of Guillain-Barré Syndrome. This study offers insights regarding that Oropouche virus is a causal agent of neurological disorders and it could be involved in the etiology of the Guillain-Barré Syndrome. [ABSTRACT FROM AUTHOR]

Mycoplasma pneumoniae, a frequent respiratory pathogen, can cause neurological disease manifestations. We here present a case of M. pneumoniae as cause of meningitis and occurrence of an intracranial abscess as a complication of mastoiditis with septic cerebral venous sinus thrombosis in a patient with multiple sclerosis on anti-CD20 therapy. [ABSTRACT FROM AUTHOR]

Critical alterations in the brain and psyche are often triggered by critical points and feedback effects in closely networked systems. Such crises can occur in the form of neurological disorders, such as epilepsy or mental disorders, such as bipolar disorder and depression. A central mechanism is the excitation-inhibition (EI) balance in the brain, which is responsible for an optimal processing of information. Disruptions in this balance can lead to pathological conditions. The concept of attractors, which represent the stable conditions in neuronal networks, helps to explain the consolidation of memories, behavioral patterns and mental states. These attractor states can be triggered by external stimuli and may become anchored in pathological contexts. Advances in measurement technologies and methods of artificial intelligence enable a deeper analysis of neuronal dynamics and open up new pathways for targeted therapeutic interventions for the treatment of mental disorders. [ABSTRACT FROM AUTHOR]

Migraine is a disabling neurological disorder that affects more than one billion people worldwide. The clinical presentation is characterized by recurrent headache attacks, which are often accompanied by photophobia, phonophobia, nausea and vomiting. Although the pathogenesis of migraine remains incompletely understood, mounting evidence suggests that specific signalling molecules are involved in the initiation and modulation of migraine attacks. These signalling molecules include pituitary adenylate cyclase-activating polypeptide (PACAP), a vasoactive peptide that is known to induce migraine attacks when administered by intravenous infusion to people with migraine. Discoveries linking PACAP to migraine pathogenesis have led to the development of drugs that target PACAP signalling, and a phase II trial has provided evidence that a monoclonal antibody against PACAP is effective for migraine prevention. In this Review, we explore the molecular and cellular mechanisms of PACAP signalling, shedding light on its role in the trigeminovascular system and migraine pathogenesis. We then discuss emerging therapeutic strategies that target PACAP signalling for the treatment of migraine and consider the research needed to translate the current knowledge into a treatment for migraine in the clinic. Pituitary adenylate cyclase-activating polypeptide signalling has been linked to migraine pathogenesis. In this Review, Ashina and co-workers explore the molecular and cellular mechanisms of pituitary adenylate cyclase-activating polypeptide signalling and discuss emerging therapeutic strategies to target this pathway for migraine treatment. Key points: Pituitary adenylate cyclase-activating polypeptide (PACAP) signalling has been identified as an important pathogenic contributor to migraine, supported by evidence from both animal and human studies. PACAP causes vasodilation and influences immune cell recruitment and activation, which are processes implicated in the pathophysiology of migraine. Intravenous infusion of PACAP can induce migraine attacks in humans, highlighting its direct role in migraine pathogenesis. A monoclonal antibody against PACAP signalling has shown promise in a phase II trial for migraine prevention, indicating potential therapeutic benefits. The complexity of the role that PACAP has in migraine is underscored by its interaction with multiple receptors and the trigeminovascular system; further research is needed to fully understand the therapeutic potential of targeting PACAP signalling. [ABSTRACT FROM AUTHOR]

Chronic inflammatory demyelinating polyneuropathy (CIDP) is a rare autoimmune neurological disorder seen in both pediatric and adult populations. CIDP typically presents with progressive and persistent weakness over at least 4 weeks in addition to sensory symptoms in the extremities. Although CIDP shares common clinical features between children and adults, it sometimes presents as a distinct clinical entity in children that requires close attention and recognition. A major caveat when diagnosing a child with CIDP is the clinical and diagnostic overlap with inherited neuropathies, most commonly Charcot–Marie–Tooth disease (CMT). Demyelinating CMT (dCMT) and CIDP might share similar clinical presentations, and sometimes it might be difficult to differentiate them on the basis of the electrodiagnostic findings or cerebrospinal fluid (CSF) albumino-cytological dissociation. This indeed merits early consideration for genetic testing in patients who do not respond to conventional CIDP therapies. Current treatment options for CIDP include intravenous immunoglobulins (IVIG), corticosteroids (CS), and plasmapheresis (PLEX). The need for novel therapies is essential in instances where patients continue to have symptoms despite the standard therapies or due to adverse effects of long-term use of standard therapies such as CS. This paper reviews the challenges in the diagnosis of CIDP in children and the current as well as novel therapies for CIDP. [ABSTRACT FROM AUTHOR]

Objective: To analyze the association of neurological disorders (ND) and head and neck cancer (HNC) with dysphagia severity and aspiration pneumonia occurrence. Method: Retrospective cohort study conducted at a university dysphagia center) for two consecutive years. Patients with ND or HNC were included if they had undergone a flexible endoscopic swallowing evaluation (FEES) at the dysphagia center, and at least one food consistency had been sampled and recorded. Outcomes of interest were swallowing safety, highest penetration-aspiration-score (PASmax), way of food intake, presence of a tracheal tube, and occurrence of pneumonia within the past two years. Results: Of 257 consecutive patients, 199 were enrolled in the study and classified according to their underlying diagnosis into ND (120 patients) or HNC (79 patients). Forty-three HNC patients (54.4%) and 54 ND patients (45%) showed critical dysphagia in FEES (PAS ≥ 6). Binary logistic regression comparing both groups showed patients with ND to be 2.31 times more likely to develop pneumonia. However, if the 32 stroke patients were excluded from the calculation, PASmax remains the only significant variable affecting pneumonia risk in both groups. Liquids were the main challenge for ND patients, while aspirating HNC patients struggled with all consistencies. Conclusions: The study shows that patients with HNC and ND differ in pneumonia risk only if stroke patients are included in the ND group. If they are excluded, the PAS score is the only remaining risk factor for pneumonia. Thickening liquids may not be suitable for all dysphagic patients; individually tailored measures might be more helpful, especially for HNC patients. [ABSTRACT FROM AUTHOR]

Pediatric palliative care is a holistic care of children suffering from life-threatening or life-limiting illnesses and encompasses care of a child's body, mind, and spirit and involves giving support to the family. According to the Global Atlas of Palliative Care, 6% of the global need for palliative care is in children. In order to provide palliative care, one needs to identify and diagnose the conditions requiring palliative care. There has always been a confusion in identifying pediatric conditions requiring palliative care. There is a lot of inconsistency in the diagnosis of such conditions particularly in pre-verbal patients. This study attempts to generate more data about the common palliative care conditions and complaints with which the children present to tertiary care hospitals. To study the socio-demographic details, clinical profile, CCC (complex chronic conditions) designation, and the ACT/ RCPCH (Association for Children with Life-threatening or Terminal Conditions and the Royal College of Pediatrics and Child Health) classification of children suffering from chronic conditions requiring palliative care. The study was conducted as a single-center retrospective observational study of pediatric patients enrolled for palliative care at a tertiary care hospital in a metropolitan city in India from 01.06.2021 to 31.06.2022. The total sample size was 400. The socio-demographic data and the clinical profile were recorded from the case records of all the 400 patients. Classification of the conditions was done as per the CCC as well as the ACT/ RCPCH classification system. The mean age in our study was 5.15 years and there was a slighter male (59.5%) preponderance. They presented in OPDs with acute symptoms such as fatigue and fever, and they had other symptoms like tightness of the body, constipation, seizures, and difficulty in swallowing. Majority of the children (55%) were suffering from neurologic and neuromuscular conditions as per CCC followed by hematologic and immunologic conditions (10%). Category 4 (irreversible but non-progressive conditions causing severe disability, leading to susceptibility to health) was reported as the most common category according to the ACT/RCPCH. Conclusion: Children suffering from chronic disease conditions requiring palliative care usually suffer from multiple symptoms which affect their daily life. As most of the patients belong to category 4 according to ACT/RCPCH which is an irreversible but non-progressive life-limiting condition, the course of the disease is prolonged, therefore requiring comprehensive care and services for a long time. It is necessary to establish more pediatric palliative care units to address the needs of such children. What is known: • Pediatric palliative care is a specialized area within palliative care, which focusses on the needs of children with life-limiting illnesses. • Data on pediatric palliative care has largely been limited to oncological conditions. There is a paucity of literature documenting the needs among children suffering from non-cancerous chronic conditions. What is new: • This study provides vital information with respect to palliative care burden among children mainly suffering from non-oncological conditions. • It also provides clinical and socio-demographic profile of the children suffering from chronic life-limiting conditions requiring palliative care in a tertiary hospital setting in a LMIC (low- or middle-income country). [ABSTRACT FROM AUTHOR]

Precise control of norepinephrine (NE) levels and NE-receptor interaction is crucial for proper function of the brain. Much evidence for this view comes from experimental studies that indicate an important role for NE in the pathophysiology and treatment of various conditions, including cognitive dysfunction, Alzheimer's disease, Parkinson's disease, multiple sclerosis, and sleep disorders. NE provides neuroprotection against several types of insults in multiple ways. It abrogates oxidative stress, attenuates neuroinflammatory responses in neurons and glial cells, reduces neuronal and glial cell activity, promotes autophagy, and ameliorates apoptotic responses to a variety of insults. It is beneficial for the treatment of neurodegenerative diseases because it improves the generation of neurotrophic factors, promotes neuronal survival, and plays an important role in the regulation of adult neurogenesis. This review aims to present the evidence supporting a principal role for NE in neuroprotection, and molecular mechanisms of neuroprotection. [ABSTRACT FROM AUTHOR]

Neuropathic pain (NPP) is a refractory pain syndrome, caused by damage or disease of the somatosensory nervous system and characterized by spontaneous pain, hyperalgesia, abnormal pain and sensory abnormality. Non-coding RNAs (ncRNAs), including microRNA (miRNA), long non-coding RNA (lncRNA), circular RNA (circRNA) and Piwi interacting RNA (piRNA), play a notable role in initiation and maintenance of NPP. In this review, we summarize the role of ncRNAs in NPP and their underlaying mechanism. Generally, ncRNAs are interacted with mRNA, protein or DNA to regulate the molecules and signals assciated with neuroinflammation, ion channels, neurotrophic factors and others, and then involved in the occurrence and development of NPP. Therefore, this review not only contributes to deepen our understanding of the pathophysiological mechanism of NPP, but also provides theoretical basis for the development of new therapy strategies for this disorder. [ABSTRACT FROM AUTHOR]

Background: Monoclonal antibodies (mAbs) are pivotal in treating various diseases, including cancers and autoimmune disorders. Despite their therapeutic benefits, mAb therapy has been associated with neurological toxicity. Objectives: This study aimed to assess the occurrence of neuronal toxicity associated with mAbs, utilizing data from the FDA Adverse Event Reporting System (FAERS) safety database. The study also sought to delineate the medical characteristics of the reported cases. Methods: A comprehensive analysis of neurological adverse events reported in the FAERS database was conducted, employing computational methodologies such as proportional relative risk (PRR), information component (IC025), and chi-square (χ2). Individual case safety reports (ICSRs) pertaining to neurological disorders linked to mAbs from the date of first global marketing authorization until June 30, 2023, were meticulously examined. Results: The FAERS safety database contains 79,022 ICSRs linking mAbs to nervous system disorders. Rituximab, bevacizumab, denosumab, nivolumab, and trastuzumab were frequently cited. Reported adverse events include headache, peripheral neuropathy, dizziness, and cerebrovascular accident. Most ICSRs (85.81%) were serious, mainly affecting females (57.04%) with a 14.09% fatality rate. Panitumumab, atezolizumab, bevacizumab, and trastuzumab showed strong drug-event associations. Signal disproportionate reporting (SDR) analysis flagged myasthenia gravis, peripheral neuropathy, and neurotoxicity across multiple mAbs, suggesting potential signals. Conclusions: Interdisciplinary collaboration between oncologists and neurologists is crucial for safe mAb use. Our study enhances understanding of mAb neurological safety. Disproportionality signal analysis provides valuable evidence for risk mitigation. [ABSTRACT FROM AUTHOR]

Temporal Lobe Epilepsy (TLE) is a severe neurological condition characterized by recurrent seizures that often do not respond well to available anti-seizure medications. TLE has been associated with epileptogenesis, a process that starts during the latent period following a neurologic insult and is followed by chronic phase. Recent research has linked canonical Wnt signaling to the pathophysiology of epileptogenesis and TLE. Our previous study demonstrated differential regulation of canonical Wnt signaling during early and late stage post status epilepticus (SE) induction. Building on these findings, our current study utilized Wnt modulators: GSK-3β inhibitor 6-bromoindirubin-3'-oxime (6-Bio) and disheveled inhibitor niclosamide and investigated their impact on canonical Wnt signaling during the early (30 days) and later stages (60 days) following SE induction. We assessed several parameters, including seizure frequency, astrogliosis, synaptic density, and neuronal counts in hippocampal tissue. We used immunohistochemistry and Nissl staining to evaluate gliosis, synaptic density, and neuronal counts in micro-dissected hippocampi. Western blotting was used to examine the expression of proteins involved in canonical Wnt/β-catenin signaling, and real-time PCR was conducted to analyze their relative mRNA expression. Wnt modulators, 6-Bio and Niclosamide were found to reduce seizure frequency and various other parameters including behavioral parameters, hippocampal morphology, astrogliosis and synaptic density at different stages of TLE. [ABSTRACT FROM AUTHOR]

Originally sourced from plants, Bergenin has been used as a medicinal compound in traditional medicine for centuries, and anecdotal reports suggest a wide range of therapeutic uses. Naturally-occurring and lab-synthesized Bergenin, as well as some of its related compounds, have been shown in in vivo and in vitro studies to alter activity of several enzymes and proteins critical in cellular functioning, including reelin, GSK-3β, Lingo-1, Ten-4, GP-43, Aβ 1-42, P-tau, SOD1,2, GPx, Glx1, NQO1, HO1, PPAR-ɣ, BDNF, VEGF, and STAT6. Additionally, Bergenin alters levels of several cytokines, such as IL-6, IL-1β, TNF-α, and TGF-β. Behavioral and cellular effects of Bergenin have been shown to involve PI3K/Akt, NF-κB, PKC, Nrf2, and Sirt1/FOXO3a pathways. These pathways, enzymes, and proteins have been shown to be important in normal neurological functioning, and/or dysfunctions in these pathways and proteins have been shown to be important in several neuro-based disorders or diseases, which suggests that Bergenin could be therapeutic in management of neuropsychiatric conditions or neurological disorders. In preclinical studies, Bergenin has been shown to be useful for the management of Alzheimer's disease, Parkinson's disease, anxiety, depression, addiction, epilepsy, insomnia, stroke, and potentially, state control. Our review aims to summarize current evidence supporting the conclusion that Bergenin could play a role in treating various neuro-based disorders and that future studies should be conducted to evaluate the mechanisms by which Bergenin could exert its therapeutic effects. [ABSTRACT FROM AUTHOR]

Background: Multiple sclerosis is a chronic autoimmune-mediated demyelinating disease of the central nervous system that is usually associated with varying degrees of progressive disability. Free Kappa light chain (FKLC) has attracted growing attention as a significant diagnostic marker of MS. Our aim was to study the diagnostic utility of cerebrospinal fluid free Kappa light chain and related indices in a sample of Egyptian MS patients vs. CSF IgG oligoclonal bands. It was a prospective case–control study of MS patients carried in our hospital during the period from January 2021 till January 2022. Our study carried on 30 patients with multiple sclerosis and other inflammatory neurologic diseases and 20 age and sex matched controls. The study measured FKLC in the CSF and serum sample pairs of patients and control group. Indices calculated using FKLC measured in CSF and serum included; FKLC index, FKLC intrathecal fraction and quotient of FKLC. Indices were used to assess intrathecal synthesis of FKLC considering blood–CSF barrier function. Receiver operating characteristic curve analysis was used to determine diagnostic performance of FKLC and related indices in comparison to CSF–OCB testing. Results: Measured FKLC levels as well as its calculated indices have shown statistically significant higher values among MS patients against OIND patients and healthy control group. Both FKLC index and FKLC IF were similarly showing 100% diagnostic sensitivity and 100% diagnostic specificity for MS diagnosis. Conclusions: FKLC biomarkers are proposed to be highly sensitive and easy to detect first-line markers of intrathecal immunoglobulin synthesis with accurate performance and low cost that might prove to be promising diagnostic markers of MS. [ABSTRACT FROM AUTHOR]

Background: Local recurrent brain metastases are defined as lesions that recur in the brain at the same site after a previous local therapy. In patients already submitted to surgery, a second operation may be potentially challenging due to scar formation, infiltration of cerebral vessels or eloquent brain areas and local effect of previous radiotherapy. The aim of this study is to retrospectively review the results and complications of a second surgical treatment in a series of local recurrent lesions and to review the literature on this topic. Methods: 37 patients submitted to surgery for a local, histologically confirmed, recurrent brain metastases between 2000 and 2022 were retrospectively analyzed with respect to the following parameters: age, histology, anatomic location, time to recurrence, previous radiotherapy, size of recurrent tumors, preoperative and postoperative Karnofsky Performance Status (KPS) score, recursive partitioning analysis (RPA) class and graded prognostic assessment (GPA) score, surgery-related complications and the presence of further cerebral metastases. Overall survival (OS) was calculated using the Kaplan-Meier method. A multivariate Cox proportional hazard model was developed using stepwise regression (forwards selection) with predictive variables that were significant in the univariate analyses. Results: A significant improvement of post-operative KPS status was obtained after second surgery. At multivariate analysis better results in terms of OS were achieved in patients with a pre-operative KPS ≥ 70 and in patients who had received radiotherapy after the initial surgery. No significant postoperative complications related to previous treatments were observed. Conclusions: Surgical resection of local recurrent brain metastases may improve patients ́ neurologic conditions allowing more time for systemic therapies to act with a low incidence of surgery-related morbidity and mortality. However, careful patient selection with a fair pre-operative clinical status seems mandatory to achieve the best post-operative results, since uniform treatment-paradigms cannot be established yet, due to the highly heterogeneous patient cohort. [ABSTRACT FROM AUTHOR]

Variants in mitochondrial genomes (mtDNA) can cause various neurological and mitochondrial diseases such as mitochondrial myopathy, encephalopathy, lactic acidosis, stroke-like episodes (MELAS). Given the 16 kb length of mtDNA, continuous sequencing is feasible using long-read sequencing (LRS). Herein, we aimed to show a simple and accessible method for comprehensive mtDNA sequencing with potential diagnostic applications for mitochondrial diseases using the compact and affordable LRS flow cell "Flongle." Whole mtDNA amplification (WMA) was performed using genomic DNA samples derived from four patients with mitochondrial diseases, followed by LRS using Flongle. We compared these results to those obtained using Cas9 enrichment. Additionally, the accuracy of heteroplasmy rates was assessed by incorporating mtDNA variants at equimolar levels. Finally, mtDNA from 19 patients with Parkinson's disease (PD) was sequenced using Flongle to identify disease risk-associated variants. mtDNA variants were detected in all four patients with mitochondrial diseases, with results comparable to those obtained from Cas9 enrichment. Heteroplasmy levels were accurately detected (r2 > 0.99) via WMA using Flongle. A reported variant was identified in three patients with PD. In conclusion, Flongle can simplify the traditionally cumbersome and expensive mtDNA sequencing process, offering a streamlined and accessible approach to diagnosing mitochondrial diseases. [ABSTRACT FROM AUTHOR]

Background: The prevalence of cognitive diseases, including Alzheimer's disease and other forms of dementia, poses a significant global health challenge due to the limited availability of effective therapeutic options. Recent years have witnessed a growing emphasis in research on the exploration of natural compounds and their derivatives as prospective therapeutic agents for cognitive impairments. Main body Xanthotoxin, a furanocoumarin compound derived from botanical sources, exhibits promising therapeutic promise in several neurological conditions such as depression, neuronal inflammation, Alzheimer's disease, vascular cognitive impairment, epilepsy, and Parkinson's disease. This potential stems from its notable neuroprotective, antioxidant, and anti-inflammatory characteristics. The present study offers a comprehensive examination of the acquisition of XAT from both natural sources and synthetic means. It delves into the significance of XAT in the treatment of cognitive disorders and delineates potential avenues for future research in the domain of XAT and cognitive disorders. Conclusion: Ongoing research and advancements in the field of XAT have the potential to enhance its use as a potent therapeutic intervention for cognitive impairments, consequently enhancing the holistic welfare of those afflicted by these incapacitating disorders. [ABSTRACT FROM AUTHOR]

Electroencephalography (EEG) is a well-known modality in neuroscience and is widely used in identifying and classifying neurological disorders. This paper investigates how EEG data can be used along with knowledge distillation-based deep learning models to detect mental disorders like epilepsy and sleep disorders. The EEG signals are converted into time–frequency plots using short-time Fourier transforms. Further, we propose a novel methodology for using knowledge distillation-based transfer learning (KDTL). Knowledge distillation is becoming quite prevalent in the machine learning field and is associated with various applications in our work; we propose its use in the detection of mental disorders from EEG spectrograms. We convert the EEGs using short-term Fourier transform to obtain time–frequency representation and apply teacher-student by first training a large teacher model and use knowledge distillation to train a student model. In our experiments, we found that ConvNext teacher and MobileNet student combination obtained better results. Our proposed KDTL approach is tested on two datasets with multiple cases, namely the Bonn and ISRUC datasets and obtain 98% and 95% accuracies, respectively. Further experimental results show that the overall KDTL methodology can obtain high classification accuracy across both datasets in binary and multiclass classifications and proves to be better than multiple prior works. Further, our KDTL approach provides a way to train lightweight models which have a smaller number of trainable parameters and thereby constitute lower training time overall. Our proposed KDTL-based approach obtained accurate results in diagnosing mental disorders from EEG spectrograms. Compared to other related methods, KDTL outperformed across tasks with obtained good results in both binary and multiclass classifications. [ABSTRACT FROM AUTHOR]

The neurological condition epilepsy is demanding and even fatal. Electroencephalogram (EEG)-based epilepsy detection still faces various difficulties. EEG readings fluctuate, and different patients have various seizure activity patterns. EEG signal detection is time-consuming and labour-intensive, which puts a strain on medical staff and raises the possibility of erroneous detections. Usually, electrodes are inserted into the scalp or inside the brain for a brief period of time in order to obtain EEG data. It is essential to research efficient cross-patient automatic epilepsy detection techniques. The multi-head self-attention mechanism recognises long-distance dependencies with the same proficiency as it does temporal dynamic correlations between short-term temporal pattern characteristics and sequential relationships. The contextual representations are inputted into a bidirectional long short-term memory network (BiLSTM) so that information can be extracted in both directions. Classification and training are carried out utilising the log SoftMax algorithm. The experiments utilised scalp EEG data from the CHB-MIT database. Sensitivity, specificity, F1-score, and accuracy were computed to be 96.5 percent, 97.04 percent, 96.6 percent, and 96.2 percent, respectively. The results of the experiment show how well the technique works for detecting seizures in several patients utilising multi-channel EEG recordings. The results also demonstrate the method's improved generalisation capabilities and resilience and consistency in collecting seizure patterns. This is particularly critical for the tertiary diagnosis of epilepsy, and the findings indicate that the proposed method significantly improves the accuracy of detection. [ABSTRACT FROM AUTHOR]

Offset responses are traditionally viewed as indicators of sound cessation. Here, we investigate offset responses to auditory click trains, examining how they are modulated by inter-click intervals (ICIs) and train duration. Using extracellular recordings and electrocorticography (ECoG) in non-human primates, alongside electroencephalography (EEG) in humans, we show that offset responses are significantly influenced by both ICI and train length, thereby establishing them as markers of temporal integration. We introduce the concept of the 'Neuronal Integrative Window' (NIW), defined as the temporal span during which neurons integrate stimuli to produce or modulate the temporal integration signal. Our data reveal that on the neuronal level, the auditory cortex (AC) exhibits a more expansive NIW than the medial geniculate body (MGB), integrating stimuli over longer durations and showing a preference for larger ICIs. Furthermore, our results indicate that offset responses could serve as potential biomarkers for neurological and psychiatric conditions, highlighted by their sensitivity to pharmacological modulation with ketamine. This study advances our understanding of auditory temporal processing and proposes a novel approach for assessing and monitoring brain health. Offset responses to auditory click trains reveal temporal integration in the auditory cortex, introducing the 'Neuronal Integrative Window' concept and suggesting offset responses as potential biomarkers for assessing and monitoring brain health. [ABSTRACT FROM AUTHOR]

Migraine is a common and complex neurological disorder that has a high impact on quality of life. Recent advances with drugs that target the neuropeptide calcitonin gene-related peptide (CGRP) have helped, but treatment options remain insufficient. CGRP is released from trigeminal sensory fibers and contributes to peripheral sensitization, perhaps in part due to actions on immune cells in the trigeminovascular system. In this review, we will discuss the potential of cannabinoid targeting of immune cells as an innovative therapeutic target for migraine treatment. We will cover endogenous endocannabinoids, plant-derived phytocannabinoids and synthetically derived cannabinoids. The focus will be on six types of immune cells known to express multiple cannabinoid receptors: macrophages, monocytes, mast cells, dendritic cells, B cells, and T cells. These cells also contain receptors for CGRP and as such, cannabinoids might potentially modulate the efficacy of current CGRP-targeting drugs. Unfortunately, to date most studies on cannabinoids and immune cells have relied on cell cultures and only a single preclinical study has tested cannabinoid actions on immune cells in a migraine model. Encouragingly, in that study a synthetically created stable chiral analog of an endocannabinoid reduced meningeal mast cell degranulation. Likewise, clinical trials evaluating the safety and efficacy of cannabinoid-based therapies for migraine patients have been limited but are encouraging. Thus, the field is at its infancy and there are significant gaps in our understanding of the impact of cannabinoids on immune cells in migraine. Future research exploring the interactions between cannabinoids and immune cells could lead to more targeted and effective migraine treatments. [ABSTRACT FROM AUTHOR]

The retina plays a crucial role in processing and decoding visual information, both in normal development and during myopia progression. Recent advancements have introduced a library-independent approach for data-independent acquisition (DIA) analyses. This study demonstrates deep proteome identification and quantification in individual mice retinas during myopia development, with an average of 6,263 ± 86 unique protein groups. We anticipate that the use of a predicted retinal-specific spectral library combined with the robust quantification achieved within this dataset will contribute to a better understanding of the proteome complexity. Furthermore, a comprehensive mice retinal-specific spectral library was generated, encompassing a total identification of 9,401 protein groups, 70,041 peptides, 95,339 precursors, and 761,868 transitions acquired using SWATH-MS acquisition on a ZenoTOF 7600 mass spectrometer. This dataset surpasses the spectral library generated through high-pH reversed-phase fractionation by data-dependent acquisition (DDA). The data is available via ProteomeXchange with the identifier PXD046983. It will also serve as an indispensable reference for investigations in myopia research and other retinal or neurological diseases. [ABSTRACT FROM AUTHOR]

The increasing prevalence of neurological disorders such as Alzheimer's, Parkinson's, and multiple sclerosis presents a significant global health challenge. Despite extensive research, the precise mechanisms underlying these conditions remain elusive, with current treatments primarily addressing symptoms rather than root causes. Emerging evidence suggests that gut permeability and the kynurenine pathway are involved in the pathogenesis of these neurological conditions, offering promising targets for novel therapeutic and preventive strategies. Gut permeability refers to the intestinal lining's ability to selectively allow essential nutrients into the bloodstream while blocking harmful substances. Various factors, including poor diet, stress, infections, and genetic predispositions, can compromise gut integrity, leading to increased permeability. This condition facilitates the translocation of toxins and bacteria into systemic circulation, triggering widespread inflammation that impacts neurological health via the gut–brain axis. The gut–brain axis (GBA) is a complex communication network between the gut and the central nervous system. Dysbiosis, an imbalance in the gut microbiota, can increase gut permeability and systemic inflammation, exacerbating neuroinflammation—a key factor in neurological disorders. The kynurenine pathway, the primary route for tryptophan metabolism, is significantly implicated in this process. Dysregulation of the kynurenine pathway in the context of inflammation leads to the production of neurotoxic metabolites, such as quinolinic acid, which contribute to neuronal damage and the progression of neurological disorders. This narrative review highlights the potential and progress in understanding these mechanisms. Interventions targeting the kynurenine pathway and maintaining a balanced gut microbiota through diet, probiotics, and lifestyle modifications show promise in reducing neuroinflammation and supporting brain health. In addition, pharmacological approaches aimed at modulating the kynurenine pathway directly, such as inhibitors of indoleamine 2,3-dioxygenase, offer potential avenues for new treatments. Understanding and targeting these interconnected pathways are crucial for developing effective strategies to prevent and manage neurological disorders. [ABSTRACT FROM AUTHOR]

Background: Peripheral veno-arterial extracorporeal membrane oxygenation (pECMO) has become the first-line device in refractory cardiogenic shock (rCS). Some pECMO complications can preclude any bridging strategies and a peripheral-to-central ECMO (cECMO) switch can be considered as a bridge-to-decision. We conducted this study to appraise the in-hospital survival and the bridging strategies in patients undergoing peripheral-to-central ECMO switch. Methods: This retrospective monocenter study included patients admitted to a ECMO-dedicated intensive care unit from February 2006 to January 2023. Patients with rCS requiring pECMO switched to cECMO were included. Patients were not included when the cECMO was the first mechanical circulatory support. Results: Eighty patients, with a median [IQR25-75] age of 44 [29–53] years at admission and a female-to-male sex ratio of 0.6 were included in the study. Refractory pulmonary edema was the main switching reason. Thirty patients (38%) were successfully bridged to: heart transplantation (n = 16/80, 20%), recovery (n = 10/80, 12%) and ventricle assist device (VAD, n = 4/30, 5%) while the others died on cECMO (n = 50/80, 62%). The most frequent complications were the need for renal replacement therapy (76%), hemothorax or tamponade (48%), need for surgical revision (34%), mediastinitis (28%), and stroke (28%). The in-hospital and one-year survival rates were 31% and 27% respectively. Myocardial infarction as the cause of the rCS was the only variable independently associated with in-hospital mortality (HR 2.5 [1.3–4.9], p = 0.009). Conclusions: The switch from a failing pECMO support to a cECMO as a bridge-to-decision is a possible strategy for a very selected population of young patients with a realistic chance of heart function recovery or heart transplantation. In this setting, cECMO allows patients triage preventing from wasting expensive and limited resources. [ABSTRACT FROM AUTHOR]

Purpose: To describe the clinical presentation and urodynamic findings in detrusor underactivity (DU) patients and investigate the association between DU and straining related complications such as pelvic organ prolapse (POP), inguinal hernia, and hemorrhoids. Methods: We retrospectively reviewed all consecutive patients who underwent urodynamic studies (UDS) from 2012 to 2023, divided into two groups: those with evidence of DU (n = 573), and control subjects with normal voiding parameters (n = 522). Exclusion criteria were patients who lacked sufficient data, those with obstructive voiding parameters, and those who had received intravesical botulinum toxin injections within the previous nine months. Demographic information, clinical presentation, straining related complications, and UDS findings were compared between the two groups using univariate statistical analysis. Results: The male DU group had a statistically significant higher prevalence of spinal disease and previous cerebrovascular accidents, while the female DU group had a statistically significant higher prevalence of spinal disease, multiple sclerosis, diabetes, previous colorectal surgery, previous transabdominal gynecological surgery, POP surgery, and recurrent UTIs. Female DU patients had a higher prevalence of pronounced vaginal bulging symptoms, recurrent POP, inguinal hernia, and hemorrhoids. The predominant LUTS were voiding symptoms (81.2% in males and 77.9% in females), followed closely by storage symptoms (66.2% in males and 74.7% in females). The median Qmax, PdetQmax, and PVR were 6 ml/sec, 18 cmH2O, 190 ml for male DU patients, and 8 ml/sec, 11 cmH2O, and 200 ml for female DU patients, respectively. Conclusion: Risk factors for DU that were identified include age, neurological diseases (spinal disease, CVA in men, MS in women), diabetes and transabdominal surgery (colorectal, gynecological) that can cause pelvic denervation in women. DU patients commonly present with both voiding and storage symptoms. There is approximately twice the risk of having POP surgery and inguinal hernia, an eight-fold risk of hemorrhoids, and a three-fold risk of recurrent UTIs for females. This is thought to be secondary to increased intra-abdominal pressure during urinary straining. [ABSTRACT FROM AUTHOR]

Neurodevelopmental disorders (NDDs) are among the most common health issues in childhood and adolescence. Psychiatric disorders are known to be overrepresented among children using child welfare services and placed in out-of-home care (OHC). Child- and parent-related determinants for OHC among a national population with NDDs were evaluated utilising longitudinal register data from the national Finnish Birth Cohort 1997 (n = 58,802) from birth to 18 years (1997–2015). The cohort members with NDDs (n = 5,143, 9% of total cohort) formed our study population. Based on their history of OHC, cohort members with NDD were categorised to OHC (n = 903) and non-OHC groups (n = 4,240). Of all cohort members with NDDs, 17.6% had a history of OHC. Within NDDs, a significant excess of ADHD diagnosis was observed in the OHC group compared to the non-OHC group (49% vs. 26%). The OHC group with NDDs was significantly characterised by having comorbid psychiatric diagnosis for conduct and oppositional disorders (adj. RR 2.21), substance use disorders (adj. RR 1.61) and depression and anxiety disorders (adj. RR 1.60). Of all parent-related determinants, the most prevailing in the OHC group compared to the non-OHC group, was social assistance received by parent (88% vs. 44.5%). The longer the period (in years) for received social assistance, the greater the likelihood for OHC (adj. RRs range from 2.41 for one year to 5.24 for over 4 years). Further, significantly associating determinants for OHC were parental psychiatric disorders (adj. RR 1.42) and parental death (adj. RR 1.23). Our findings from the population-based cohort of children and adolescents with NDDs highlight the importance of screening and assessment of family situation. Also, effective prevention and treating of comorbid psychiatric disorders, especially conduct and oppositional disorders is essential. [ABSTRACT FROM AUTHOR]

Short-term exposure to air pollution has previously been studied in relation to certain neurological disorders, but there is still a lack of convincing data linking air pollution to epileptic seizures. The study's goal was to investigate how exposure to ambient nitrogen dioxide (NO2) affected the number of patients seeking assistance at the Wuhan Emergency Medical Center due to epileptic seizures. We gathered data on medical emergency calls (MECs), daily ambient air pollution concentrations (SO2, NO2, PM2.5, PM10, CO, and O3), and meteorological variables in Wuhan, China, spanning from January 1, 2017, to November 30, 2019. To investigate the potential influence of ambient nitrogen dioxide on MECs for epileptic seizures, we carried out a time-series investigation using the general additive model (GAM). Additionally, analyses stratified by season, age, and gender were performed. A total of 8989 records of MECs for epileptic seizures were enrolled in our study during the period. Statistical analysis indicates that a rise of 10 μg/m3 in NO2 concentration is linked to a 0.17% increase in daily MECs for epileptic seizures (95% confidence interval [CI]: 0.02%, 0.32%). Furthermore, people aged 14–59 years were more susceptible(2.25%, P < 0.05). The short-term effects of NO2 exposure on daily MECs for epileptic seizures were stronger in warm seasons than in cool seasons (0.55% vs. -0.10%, P < 0.0001). Our findings suggests that short-term exposure to ambient NO2 was positively correlated with daily MECs for epileptic seizures in Wuhan, China. Additionally, we observed that these associations were stronger in patients aged above 14 but under 60 years and the warmer seasons (from April to September). [ABSTRACT FROM AUTHOR]

Autosomal recessive spinocerebellar ataxia 13 (SCAR13) is a neurological disease characterized by psychomotor delay, mild to profound intellectual disability with poor or absent language, nystagmus, stance ataxia, and, if walking is acquired, gait ataxia. Epilepsy and polyneuropathy have also been documented in some patients. Cerebellar atrophy and/or ventriculomegaly may be present on brain MRI. SCAR13 is caused by pathogenic variants in the GRM1 gene encoding the metabotropic receptor of glutamate type 1 (mGlur1), which is highly expressed in Purkinje cerebellar cells, where it plays a fundamental role in cerebellar development. Here we discuss the case of an 8-year-old patient who presented with a severe neurodevelopmental disorder with balance disturbance, absence of independent walking, absence of language, diffuse hypotonia, mild nystagmus, and mild dysphagia. Whole-exome sequencing revealed a compound heterozygosity for two likely pathogenic variants in the GRM1 gene, responsible for the patient's phenotype, and made it possible to diagnose autosomal recessive spinocerebellar ataxia SCAR13. The detected (novel) variants appear to be causative of a particularly severe picture with regard to neurodevelopment, in the context of the typical neurological signs of spinocerebellar ataxia. [ABSTRACT FROM AUTHOR]

Purpose: Pelvic osteotomies present a surgical option to restore pelvic alignment, improve function and pain in sequelae of pelvic ring fractures. Understanding the three-dimensional deformity is a crucial step within preoperative planning; furthermore, accurate intraoperative execution of the planning can be challenging. In recent years, patient-specific guides and 3D modeling have emerged as promising technologies in orthopedic and trauma surgery to enhance surgical precision and facilitate intraoperative decision-making. Methods: We present the case of a 41-year-old male patient with a pelvic malunion, resulting from a vertical shear fracture occurring 8 years prior. The patient presented with a 4-cm cranial displacement of the right hemipelvis, accompanied by pubic symphysis disruption and fusion of S1 to L5 vertebra. Severely altered posture in the coronal and sagittal plane was associated with sitting imbalance, impaired gait, and chronic pain. Results: We analyzed the deformity and planned the surgical correction on a 3D interactive virtual model. Moreover, we developed 2 patient-specific cutting guides and one patient-specific reduction guide, allowing accurate bilateral pelvic osteotomies, subsequent realignment, and restoration of the pelvic anatomy. Conclusion: For the first time, 3D modeling and 3D-printed patient-specific guides were effectively employed in pelvic malunion surgery, enhancing the precision of preoperative planning, and providing valuable assistance during intraoperative procedures. [ABSTRACT FROM AUTHOR]

Migraine, a complex disorder, is characterized by recurrent headache episodes. The production of melatonin in the pineal gland, which is crucial for controlling circadian rhythms and sleep–wake cycles, is altered in various conditions, including neurological disorders such as migraine. Recent studies underscore the significance of serum melatonin levels in patients with chronic and episodic migraine, the focus of this study. This case‒control study, conducted from September 2017 to June 2020 in Tehran, Iran, selected potential participants aged 18–65 years from a headache clinic at Sina Hospital (affiliated with Tehran University of Medical Sciences). Both episodic migraine and chronic migraine were diagnosed following the diagnostic criteria in the International Classification of Headache Disorders' third edition. Melatonin levels were measured according to the instructions of the ELISA kits. There were significant differences in the frequency of headache days and the duration of abortive medication usage between the two groups (P value < 0.001). Besides, analysis revealed significantly lower serum melatonin levels in patients with episodic ((80.45–45.06) 72.83) and chronic migraine ((154.34–63.34) 70.38, P value < 0.001) than in healthy controls (281.25–160.86) 280). Although no considerable differences were found between episodic and chronic migraine patients, the current study demonstrated that serum melatonin levels were substantially greater in healthy controls than in patients with migraine. [ABSTRACT FROM AUTHOR]

This document is a letter published in the Journal of Neurology discussing the use of tocilizumab as a treatment for acute necrotizing encephalopathy (ANE). ANE is a severe neurological condition that can occur after systemic infections. The letter reports a case of a 17-year-old female patient with ANE who was successfully treated with tocilizumab in addition to standard therapy. The patient showed significant clinical improvement and had minimal residual symptoms at a follow-up visit. The authors recommend considering tocilizumab as a treatment option for severe ANE, along with genetic testing for patients with ANE and preventive measures such as vaccinations. [Extracted from the article]

Background: Neurology trials typically rely on composite scales for measuring symptom severity. Completing all items in a long scale can be burdensome for patients, caregivers, and trial personnel. Objectives: To test the hypothesis that sparse item testing, aided by item-response modelling, can preserve the power for detecting treatment effect in a controlled trial. Methods: UPDRS (Unified Parkinson's Disease Rating Scale) Part III (motor examinations) data from a placebo-controlled trial (N = 391) of ropinirole were analysed with a longitudinal item-response model. Symptom severity was estimated directly from item scores as a latent variable, without needing the total score. This enabled sparse item testing. With the symptom severity as a clinical endpoint, the potential power loss for detecting treatment effect due to the sparse testing was assessed by simulation. Results: When each patient took 18 of all 27 tests in UPDRS Part III at each study visit, there was no appreciable power loss. Reducing four visits to three also had negligible effects on power. A threefold reduction of the total tests that each patient needed to do throughout the trial, from 108 to 27, only compromised power slightly, e.g., from 92 to 87% at N = 160. Conclusions: These findings show that using the symptom severity derived from item scores as the endpoint allows sparse testing to drastically reduce trial burden without incurring major power loss. This benefit would multiply for indications like Alzheimer's disease where modern trials often require patients to be tested on multiple scales at several times. [ABSTRACT FROM AUTHOR]

Objective: Which theoretical and practical competences do the neurological and psychiatric case histories of the Hippocratic Corpus convey? Material and methods: The 431 Hippocratic case histories have been studied for reports and communication on the diagnostics, treatment and prognosis of single persons and groups of patients suffering from neurological and psychiatric diseases. Results: In the 7 books of the Hippocratic Epidemics, a total of 128 patients with neurological and psychiatric symptoms are described. Epidemic fever and its variants were the leading predisposing conditions and the main symptoms were delirium, coma, insomnia, headache, speech disorders and convulsions. A number of patients with phrenitis and opisthotonos are also reported. The majority of the sick persons were male, were teenagers or adults and 47 of them are mentioned by name. The patient's information about the course is often just as informative as the doctor's observations. Treatment was limited to physical and dietary measures. Discussion: The Hippocratic physician diagnosed and attempted to treat a large number of neurological and psychiatric diseases. The often almost continuous observations of the patients led to astonishingly precise predictions of the course and the prospects of recovery. Numerous symptoms described in the case studies, including carphologia and opisthotonus, have entered the neurological vocabulary. The retrospective etiological analysis of the reports leads to the almost explicit identification of neurosyphilis and encephalitis lethargica. The therapeutic measures described by the author were, as the changeable course of the diseases shows, only of limited effectiveness despite a very differentiated application over time, both against the underlying diseases and the neurological and psychiatric complications. [ABSTRACT FROM AUTHOR]

Background: Neurodegenerative diseases represent an increasing challenge in ageing societies, as only limited treatment options are currently available. Objective: New research methods and interdisciplinary interaction of different disciplines have changed the way neurological disorders are viewed and paved the way for the comparatively new field of neuroimmunology, which was established in the early 1980s. Starting from neurological autoimmune diseases, such as multiple sclerosis, knowledge about the involvement of immunological processes in other contexts, such as stroke or traumatic brain injury, has been significantly expanded in recent years. Material and methods: This review article provides an overview of the role of the immune system and the resulting potential for novel treatment approaches. Results: The immune system plays a central role in fighting infections but is also able to react to the body's own signals under sterile conditions and cause inflammation and subsequent adaptive immune responses through the release of immune mediators and the recruitment and differentiation of certain immune cell types. This can be beneficial in initiating healing processes; however, chronic inflammatory conditions usually have destructive consequences for the tissue and the organism and must be interrupted. Conclusion: It is now known that different cells of the immune system play an important role in neurological diseases. Regulatory mechanisms, which are mediated by regulatory T cells or Th2 cells, are usually associated with a good prognosis, whereas inflammatory processes and polarization towards Th1 or Th17 have a destructive character. Novel immunomodulators, which are also increasingly being used in cancer treatment, can now be used in a tissue-specific manner and therefore offer great potential for use in neurological diseases. [ABSTRACT FROM AUTHOR]

Rare neurological diseases as a whole share peculiar features as motor and/or cognitive impairment, an elevated disability burden, a frequently chronic course and, in present times, scarcity of therapeutic options. The rarity of those conditions hampers both the identification of significant prognostic outcome measures, and the development of novel therapeutic approaches and clinical trials. Collection of objective clinical data through digital devices can support diagnosis, care, and therapeutic research. We provide an overview on recent developments in the field of digital tools applied to rare neurological diseases, both in the care setting and as providers of outcome measures in clinical trials in a representative subgroup of conditions, including ataxias, hereditary spastic paraplegias, motoneuron diseases and myopathies. [ABSTRACT FROM AUTHOR]

The present work investigates whether financial abilities can be associated with numerical abilities and with general cognitive abilities. We compared performance on numerical and financial tests, and on tests routinely used to measure general cognitive performance, in healthy controls and in a group of people with heterogeneous pathological conditions including mild cognitive impairment, amyotrophic lateral sclerosis, traumatic brain injury, and schizophrenia. Patients showed lower performances in both numerical and financial abilities compared to controls. Numerical and financial skills were positively correlated in both groups, but they correlated poorly with measures of general cognitive functioning. Crucially, only basic financial tasks -such as counting currencies- but not advanced ones -like financial judgments- were associated with numerical or general cognitive functioning in logistic regression analyses. Conversely, advanced financial abilities, but not basic ones, were associated with abstract reasoning. At a qualitative analysis, we found that deficits in numerical and financial abilities might double dissociate. Similarly, we observed double dissociations between difficulties in financial abilities and cognitive deficits. In conclusion, financial abilities may be independent of numerical skills, and financial deficits are not always related to the presence of cognitive difficulties. These findings are important for both clinical and legal practice. [ABSTRACT FROM AUTHOR]

Parkinson's disease (PD) is an age-related chronic neurological condition characterized by progressive degeneration of dopaminergic neurons and the presence of Lewy bodies, primarily composed of alpha-synuclein and ubiquitin. The pathophysiology of PD encompasses alpha-synuclein aggregation, oxidative stress, neuroinflammation, mitochondrial dysfunction, and impaired autophagy and ubiquitin–proteasome systems. Among these, the Keap1–Nrf2 pathway is a key regulator of antioxidant defense mechanisms. Nrf2 has emerged as a crucial factor in managing oxidative stress and inflammation, and it also influences ubiquitination through p62 expression. Keap1 negatively regulates Nrf2 by targeting it for degradation via the ubiquitin–proteasome system. Disruption of the Nrf2–Keap1 pathway in PD affects cellular responses to oxidative stress and inflammation, thereby playing a critical role in disease progression. In addition, the role of neuroinflammation in PD has gained significant attention, highlighting the interplay between immune responses and neurodegeneration. This review discusses the various mechanisms responsible for neuronal degeneration in PD, with a special emphasis on the neuroprotective role of the Nrf2–Keap1 pathway. Furthermore, it explores the implications of inflammopharmacology in modulating these pathways to provide therapeutic insights for PD. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is a progressive and irreversible neurological condition that occurs with age and poses a significant global public health concern, is distinguished by the degeneration of neurons and synapses in various regions of the brain. While the exact processes behind the neurodegeneration in AD are not completely known, it is now acknowledged that inflammation may have a significant impact on the beginning and advancement of AD neurodegeneration. The severity of many neurological illnesses can be influenced by the equilibrium between pro-inflammatory and anti-inflammatory mediators. The IL-1 family of cytokines is linked to innate immune responses, which are present in both acute inflammation and chronic inflammatory diseases. Research on the role of the IL-1 family in chronic neurological disease has been concentrated on AD. In this context, there is indirect evidence suggesting its involvement in the development of the disease. This review aims to provide a summary of the contribution of every IL-1 family member in AD pathogenesis, current immunotherapies in AD disease, and present treatment possibilities for either targeting or boosting these cytokines. [ABSTRACT FROM AUTHOR]

Background: Epilepsy ranks among the most prevalent neurological conditions worldwide. Cannabidiol (CBD) has received authorization for epilepsy treatment, yet utilizing CBD is linked to a variety of adverse events (AEs). This umbrella review aims to explore risk and frequency of AEs in epilepsy patients undergoing treatment with CBD. Methods: International electronic databases comprising Scopus, PubMed, and Web of Science were extensively searched from the most ancient data accessible until May 2024. In line with fundamental principle of the Preferred Reporting Items for Systematic Reviews and Meta-analysis (PRISMA), this umbrella review was executed. RStudio software version 2023.03.1 along with R software 4.3.2 was used for our statistical analyses. Results: Thirteen meta-analyses and systematic reviews were included. CBD use in epileptic patients compared to controls can be meaningfully linked with 10.87% becoming seizure-free (RD: 10.87%, 95%CI: 2.39%, 19.34%; I2 = 80%). Compared to controls, a meaningful 73% increase in 50% or greater reduction in seizure frequency was observed (RR: 1.73, 95%CI: 1.47, 2.03; I2 = 0%). In epileptic individuals who using CBD with the dosage of 20 mg/kg/d, a higher incidence of treatment withdrawal was detected (RR: 4.39, 95%CI: 2.46, 7.83; I2 = 0%). Conclusion: In this umbrella review of meta-analyses and systematic reviews, CBD use in epileptic patients was linked to an increased risk of ample AEs. Further research, specifically targeting various epilepsy categories, is essential to fully understand the effectiveness and potential side effects of CBD across different epilepsy forms. [ABSTRACT FROM AUTHOR]

Introduction: Migraine is a recurrent, disabling neurological disorder with a substantial global disease burden. However, limited real-world data are available on the patient characteristics, treatment patterns, comorbidities, and economic burden of migraine in the United Arab Emirates (UAE). In this study, we evaluated the disease burden, comorbidities, treatment patterns, specialties involved in migraine diagnosis, and healthcare resource utilization (HCRU) and associated costs in patients with migraine in Dubai, UAE. Methods: A retrospective, secondary database cohort study was conducted from 01 January 2014 to 31 March 2022 using the Dubai Real-World Database. Patients aged ≥ 18 years with at least one diagnosis claim for migraine with continuous enrollment during the study period were included. Patients were stratified into treatment sub-cohorts. Outcomes were evaluated in terms of clinical characteristics, comorbidities, specialists visited, treatment patterns, and HCRU. Results: The study included 203,222 patients (mean age: 40 years), with male predominance (55.4%). About 13.4% of patients had specific cardiovascular comorbidities. Frequently prescribed drug classes were nonsteroidal anti-inflammatory drugs (84.4%), triptans (29.8%), and beta-blockers (12.8%), while only 1.0% of patients with migraine were prescribed newer medications like calcitonin gene-related peptide antagonists. General medicine was the most frequently visited specialty on the index date (51.5%). The all-cause and migraine-specific median gross costs during the 12-month post-index period were US $1252.6 (2.4–564,740.7) and US $198.1 (0–168,903.3) respectively, with maximum contribution from inpatients. The contribution of migraine-specific median costs to all-cause median costs was highest for the diagnosis-related group (64.9%), followed by consumables (35.2%), medications (32.0%), procedures (24.5%), and services (24.5%). Conclusion: Migraine significantly impacts healthcare costs in the UAE. The role of newer therapies in migraine management should be explored to reduce the associated socioeconomic burden and improve patients' quality of life. [ABSTRACT FROM AUTHOR]

Introduction: Seizures are common reasons to call an ambulance, and this study aims to analyze the burden of seizures in the prehospital setting based on incidence, hospital admission rate, and costs. Methods: This was a population-based, cross-sectional analysis of prehospital emergency medical services (EMS) data on suspected seizure cases from the federal state of Hesse, Germany, in 2019. Results: A total of 6534 suspected seizure cases were identified, of which most were those with a known seizure disorder. Incidence rate for epilepsy-related seizures (ES; pediatric epilepsy, first seizure [1stS], seizure with known seizure disorder [SEPI]) was 205.7 per 100,000 inhabitants and incidence rate for pediatric febrile seizures (PFS) was 36.7 per 100,000 inhabitants, corresponding to 171,275 ES and 28,500 PFS (99.3% < 18 years) cases in Germany. A prehospital EMS physician was involved in 40.0% (SEPI) to 54.4% (PFS) of suspected seizure cases. Depending on the type of seizure, 70.7% (SEPI) to 80.9% (1stS) were admitted to hospital for inpatient stay of ≥ 24 h. An additional 4% (PFS) to 16% (1stS) of cases needed immediate intervention at hospital. Prehospital EMS staff needed 8:24 min:s (SD 7:24; n = 5004) after the emergency call to arrive at the scene of the ES and 10:58 min:s (SD 27:39; n = 321) for PFS. ES and PFS cases caused estimated costs of 48.5 and 8.1 million euros for Germany in 2019, respectively, not including hospital treatment-related costs. Conclusion: This study identified a high number of suspected seizure-related emergency cases and proportion of patients admitted to hospitals, as well as high associated costs in Germany. [ABSTRACT FROM AUTHOR]

Background: Clinical management of persons with disorders of consciousness (DoC) is dedicated largely to optimizing recovery. However, selecting a measure to evaluate the extent of recovery is challenging because few measures are designed to precisely assess the full range of potential outcomes, from prolonged DoC to return of preinjury functioning. Measures that are designed specifically to assess persons with DoC are often performance-based and only validated for in-person use. Moreover, there are no published recommendations addressing which outcome measures should be used to evaluate DoC recovery. The resulting inconsistency in the measures selected by individual investigators to assess outcome prevents comparison of results across DoC studies. The National Institute of Neurological Disorders and Stroke (NINDS) common data elements (CDEs) is an amalgamation of standardized variables and tools that are recommended for use in studies of neurologic diseases and injuries. The Neurocritical Care Society Curing Coma Campaign launched an initiative to develop CDEs specifically for DoC and invited our group to recommend CDE outcomes and endpoints for persons with DoCs. Methods: The Curing Coma Campaign Outcomes and Endpoints CDE Workgroup, consisting of experts in adult and pediatric neurocritical care, neurology, and neuroscience, used a previously established five-step process to identify and select candidate CDEs: (1) review of existing NINDS CDEs, (2) nomination and systematic vetting of new CDEs, (3) CDE classification, (4) iterative review and approval of panel recommendations, and (5) development of case report forms. Results: Among hundreds of existing NINDS outcome and endpoint CDE measures, we identified 20 for adults and 18 for children that can be used to assess the full range of recovery from coma. We also proposed 14 new outcome and endpoint CDE measures for adults and 5 for children. Conclusions: The DoC outcome and endpoint CDEs are a starting point in the broader effort to standardize outcome evaluation of persons with DoC. The ultimate goal is to harmonize DoC studies and allow for more precise assessment of outcomes after severe brain injury or illness. An iterative approach is required to modify and adjust these outcome and endpoint CDEs as new evidence emerges. [ABSTRACT FROM AUTHOR]

The article discusses the Lance-Adams Syndrome, a rare condition characterized by intention or action myoclonus that occurs as a result of hypoxic encephalopathy. The syndrome was first described in a seminal article in 1963 by James Lance and Raymond Adams. The article provides details about the archetypal cases of the syndrome, its clinical features, and the neuropathological findings associated with it. The treatment for Lance-Adams Syndrome has evolved over time, with current options including clonazepam and/or levetiracetam. The article also explores the prevalence of the syndrome and its differentiation from other forms of myoclonus. [Extracted from the article]

Neuropsychiatric and neurological disorders pose a significant global health burden, highlighting the need for innovative therapeutic approaches. Fingolimod (FTY720), a common drug to treat multiple sclerosis, has shown promising efficacy against various neuropsychiatric and neurological disorders. Fingolimod exerts its neuroprotective effects by targeting multiple cellular and molecular processes, such as apoptosis, oxidative stress, neuroinflammation, and autophagy. By modulating Sphingosine-1-Phosphate Receptor activity, a key regulator of immune cell trafficking and neuronal function, it also affects synaptic activity and strengthens memory formation. In the hippocampus, fingolimod decreases glutamate levels and increases GABA levels, suggesting a potential role in modulating synaptic transmission and neuronal excitability. Taken together, fingolimod has emerged as a promising neuroprotective agent for neuropsychiatric and neurological disorders. Its broad spectrum of cellular and molecular effects, including the modulation of apoptosis, oxidative stress, neuroinflammation, autophagy, and synaptic plasticity, provides a comprehensive therapeutic approach for these debilitating conditions. Further research is warranted to fully elucidate the mechanisms of action of fingolimod and optimize its use in the treatment of neuropsychiatric and neurological disorders. [ABSTRACT FROM AUTHOR]

The functioning of several cellular processes in neuron cells relies on the interplay between multiple systems, such as calcium ([Ca2+]), inositol 1, 4, 5-trisphosphate (IP3), and dopamine. But, their individual dynamics provide very little insight into the various regulatory and dysregulatory cellular processes. The interaction of two systems dynamics offers some useful information about cell functioning in neurons. But, no attempt has been noted in the literature about the cooperation of three systems dynamics of [Ca2+], IP3, and dopamine in neurons. A mathematical model was utilized to examine the dynamic interactions of [Ca2+], IP3, and dopamine in neurons, considering their spatiotemporal aspects. Numerical findings were obtained using the finite element technique in conjunction with the Crank–Nicholson scheme. The effects of different component events like IP3-receptor (IP3R), sodium–calcium exchanger (NCX), calbindin-D28K buffer, etc. on the synergetic calcium, IP3, and dopamine dynamics have been studied in neuronal cells. The present model offers novel insights into the effects of regulation and dysregulation in different mechanisms like IP3R, NCX, calbindin-D28K, etc. on the synergetic systems of [Ca2+], IP3 and dopamine in neurons and their association with multiple neurological disorders, including Alzheimer's disease and Parkinson's disease. [ABSTRACT FROM AUTHOR]

Ferroptosis is a programmed cell death that relies on iron and lipid peroxidation. It differs from other forms of programmed cell death such as necrosis, apoptosis and autophagy. More and more evidence indicates that ferroptosis participates in many types of diseases, such as neurodegenerative diseases, ischemia-reperfusion injury, cardiovascular diseases and so on. Hence, clarifying the role and mechanism of ferroptosis in diseases is of great significance for further understanding the pathogenesis and treatment of some diseases. Hydrogen sulfide (H2S) is a colorless and flammable gas with the smell of rotten eggs. Many years ago, H2S was considered as a toxic gas. however, in recent years, increasing evidence indicates that it is the third important gas signaling molecule after nitric oxide and carbon monoxide. H2S has various physiological and pathological functions such as antioxidant stress, anti-inflammatory, anti-apoptotic and anti-tumor, and can participate in various diseases. It has been reported that H2S regulation of ferroptosis plays an important role in many types of diseases, however, the related mechanisms are not fully clear. In this review, we reviewed the recent literature about the role of H2S regulation of ferroptosis in diseases, and analyzed the relevant mechanisms, hoping to provide references for future in-depth researches. Highlights: Whether H2S can regulate cell ferroptosis through selective autophagy other than ferritinophagy is a topic worth studying in the future; The role and mechanism of H2S regulation of ferroptosis in various tumors require future research to elucidate. Further researches are needed to determine whether different concentrations of H2S can promote ferroptosis in different tissues and disease types. [ABSTRACT FROM AUTHOR]

TRAF2 and NCK interacting kinase (TNIK), a critical interacting protein kinase, is currently receiving wide attention. TNIK is found in various human body organs and tissues and participates in cell motility, proliferation, and differentiation. On the one hand, its aberrant expression is related to the onset and progression of numerous malignant tumors. On the other hand, TNIK is important in neuronal growth, proliferation, differentiation, and synaptic formation. Thus, the novel therapeutic strategies for targeting TNIK offer a promising direction for cancer, neurological or psychotic disorders. Here, we briefly summarized the biological information of TNIK, reviewed the role and regulatory mechanism in cancer and neuropsychiatric diseases, and introduced the research progress of inhibitors targeting TNIK. Taken together, this review hopes to contribute to the in-depth understanding of the function and regulatory mechanism of TNIK, which is of great significance for revealing the role of TNIK in the occurrence and treatment of diseases. [ABSTRACT FROM AUTHOR]

Chronobiological rhythms, such as the circadian rhythm, have long been linked to neurological disorders, but it is currently unknown how pathological processes affect the expression of biological rhythms in the brain. Here, we use the unique opportunity of long-term, continuous intracranially recorded EEG from 38 patients (totalling 6338 hours) to delineate circadian (daily) and ultradian (minute to hourly) rhythms in different brain regions. We show that functional circadian and ultradian rhythms are diminished in pathological tissue, independent of regional variations. We further demonstrate that these diminished rhythms are persistent in time, regardless of load or occurrence of pathological events. These findings provide evidence that brain pathology is functionally associated with persistently diminished chronobiological rhythms in vivo in humans, independent of regional variations or pathological events. Future work interacting with, and restoring, these modulatory chronobiological rhythms may allow for novel therapies. The role of long-term fluctuations in intracranial EEG signals in epilepsy is currently unclear. Here the authors show that the circadian rhythm as well as various ultradian rhythms are diminished in brain regions thought to be central in epilepsy. [ABSTRACT FROM AUTHOR]