Navigating the Complexities: A Rare Case of Intrahepatic Cholestasis of Pregnancy With Placenta Previa Manifesting With Seizures.

Intrahepatic cholestasis of pregnancy (ICP) is a prevalent and reversible liver disorder that occurs during pregnancy. It is primarily characterized by itching, especially on the palms and soles, and elevated levels of transaminases and bile acids. Some patients may also exhibit hyperbilirubinemia. This condition generally has a good maternal prognosis. The patient, in this case, presented with severe itching, elevated liver enzymes and bile acids, and an ultrasound indicated placenta previa. Uniquely, she experienced an episode of seizure and high blood pressure following surgery. This case report underscores the need for vigilant monitoring of patients with ICP, not only during pregnancy due to the risk of adverse perinatal outcomes but also for antenatal and postpartum complications.

Isolated Partial Absence of the Septum Pellucidum: A Case Report.

The septum pellucidum is an important thin, membranous structure in the brain that separates the anterior horns of the lateral ventricles, essential for maintaining brain anatomy and function. Here, we describe a case of a 38-year-old male with a 20-year history of seizures, occurring approximately three to four times annually and lasting 30 minutes to one hour per episode, who presented with a recent seizure three days prior. Magnetic resonance imaging (MRI) of the brain revealed an absence of the septum pellucidum in its posterior portion, mild prominence of both lateral ventricles, and an abnormal course of the crura of the fornix, leading to a diagnosis of partial absence of the septum pellucidum. This case underscores the importance of comprehensive neuroimaging in detecting structural brain anomalies, which is crucial for effective diagnosis, management, and improving patient outcomes, particularly in long-standing seizure disorders.

Identifying serious underlying diagnoses among patients with brief resolved unexplained events (BRUEs): a Canadian cohort study.

OBJECTIVE: To describe the demographics and clinical outcomes of infants with brief resolved unexplained events (BRUE). DESIGN: A retrospective cohort study. SETTING: 11 centres within the Canadian Paediatric Inpatient Research Network. PATIENTS: Patients presenting to the emergency department (ED) following a BRUE (2017-2021) were eligible, when no clinical cause identified after a thorough history and physical examination. MAIN OUTCOME MEASURES: Serious underlying diagnosis (requiring prompt identification) and event recurrence (within 90 days). RESULTS: Of 1042 eligible patients, 665 were hospitalised (63.8%), with a median stay of 1.73 days. Diagnostic tests were performed on 855 patients (82.1%), and 440 (42.2%) received specialist consultations. In total, 977 patients (93.8%) were categorised as higher risk BRUE per the American Academy of Pediatrics guidelines. Most patients (n=551, 52.9%) lacked an explanatory diagnosis; however, serious underlying diagnoses were identified in 7.6% (n=79). Epilepsy/infantile spasms were the most common serious underlying diagnoses (2.0%, n=21). Gastro-oesophageal reflux was the most common non-serious underlying diagnosis identified in 268 otherwise healthy and thriving infants (25.7%). No instances of invasive bacterial infections, arrhythmias or metabolic disorders were found. Recurrent events were observed in 113 patients (10.8%) during the index visit, and 65 patients had a return to ED visit related to a recurrent event (6.2%). One death occurred within 90 days. CONCLUSIONS: There is a low risk for a serious underlying diagnosis, where the majority of patients remain without a clear explanation. This study provides evidence-based risk for adverse outcomes, critical information to be used when engaging in shared decision-making with caregivers.

Functional analysis of a novel nonsense PPP1R12A variant in a Chinese family with infantile epilepsy.

BACKGROUND: Defects in PPP1R12A can lead to genitourinary and/or brain malformation syndrome (GUBS). GUBS is primarily characterized by neurological or genitourinary system abnormalities, but a few reported cases are associated with neonatal seizures. Here, we report a case of a female newborn with neonatal seizures caused by a novel variant in PPP1R12A, aiming to enhance the clinical and variant data of genetic factors related to epilepsy in early life. METHODS: Whole-exome and Sanger sequencing were used for familial variant assessment, and bioinformatics was employed to annotate the variant. A structural model of the mutant protein was simulated using molecular dynamics (MD), and the free binding energy between PPP1R12A and PPP1CB was analyzed. A mutant plasmid was constructed, and mutant protein expression was analyzed using western blotting (WB), and the interaction between the mutant and PPP1CB proteins using co-immunoprecipitation (Co-IP) experiments. RESULTS: The patient experienced tonic-clonic seizures on the second day after birth. Genetic testing revealed a heterozygous variant in PPP1R12A, NM_002480.3:c.2533 C > T (p.Arg845Ter). Both parents had the wild-type gene. MD suggested that loss of the C-terminal structure in the mutant protein altered its structural stability and increased the binding energy with PPP1CB, indicating unstable protein-protein interactions. On WB, a low-molecular-weight band was observed, indicating that the protein was truncated. Co-IP indicated that the mutant protein no longer interacted with PPP1CB, indicating an effect on the structural stability of the myosin phase complex. CONCLUSION: The PPP1R12A c.2533 C > T variant may explain the neonatal seizures in the present case. The findings of this study expand the spectrum of PPP1R12A variants and highlight the potential significance of truncated proteins in the pathogenesis of GUBS.

A Two-Hit Approach Inducing Flurothyl Seizures in Fmr1 Knockout Mice Impacts Anxiety and Repetitive Behaviors.

BACKGROUND: Fragile X Syndrome (FXS) is the leading monogenetic cause of autism spectrum disorder (ASD) and is associated with seizures. We examined the impact of repeated seizures on the behavioral and molecular changes in male Fmr1 knockout (KO) mice and wild-type (WT) mice. METHODS: Seizures were induced by administering three flurothyl seizures per day across postnatal days (PD) 7-11, for a total of 15 seizures. In adulthood, mice were tested in a battery of behavioral tasks to assess long-term behavioral deficits. RESULTS: The two-hit impact of a Fmr1 knockout and seizures resulted in decreased anxiety-like behavior in the elevated plus maze test and a longer latency to their first nose poke (repetitive behavior). Seizures resulted in decreased activity, decreased repetitive behavior (grooming and rearings), and decreased social behavior, while they also increased habituation to auditory stimuli and increased freezing in delayed fear conditioning in both KO and control mice. KO mice displayed increased repetitive behavior in the open field task (clockwise revolutions) and repeated nose pokes, and decreased anxiety in the open field test. No differences in mTOR signaling were found. CONCLUSIONS: These findings further illuminate the long-term effects of synergistic impact of two hits on the developing brain.

Utility of Quantitative EEG in Neurological Emergencies and ICU Clinical Practice.

The electroencephalogram (EEG) is a cornerstone tool for the diagnosis, management, and prognosis of selected patient populations. EEGs offer significant advantages such as high temporal resolution, real-time cortical function assessment, and bedside usability. The quantitative EEG (qEEG) added the possibility of long recordings being processed in a compressive manner, making EEG revision more efficient for experienced users, and more friendly for new ones. Recent advancements in commercially available software, such as Persyst, have significantly expanded and facilitated the use of qEEGs, marking the beginning of a new era in its application. As a result, there has been a notable increase in the practical, real-world utilization of qEEGs in recent years. This paper aims to provide an overview of the current applications of qEEGs in daily neurological emergencies and ICU practice, and some elementary principles of qEEGs using Persyst software in clinical settings. This article illustrates basic qEEG patterns encountered in critical care and adopts the new terminology proposed for spectrogram reporting.

Mortality-Associated Factors in a Traumatic Brain Injury Population in Mexico.

BACKGROUND: Traumatic brain injury (TBI) is a major cause of death and disability, with a rising incidence in recent years. Factors such as age, sex, hypotension, low score on the Glasgow Coma Scale, use of invasive mechanical ventilation and vasopressors, etc., have been associated with mortality caused by TBI. The aim of this study was to identify the clinical and sociodemographic characteristics that influence the mortality or survival of patients with TBI in a tertiary care hospital in Mexico. METHODS: A sample of 94 patients aged 18 years or older, from both sexes, with an admitting diagnosis of mild-to-severe head trauma, with initial prehospital treatment, was taken. Data were extracted from the Single Registry of Patients with TBI at the Ixtapaluca Regional High Specialty Hospital (HRAEI). Normality tests were used to decide on the corresponding statistical analysis. RESULTS: No factors associated with mortality were found; however, survival analysis showed that the presence of seizures, aggregate limb trauma, and subjects with diabetes mellitus, heart disease or patients with four concomitant comorbidities had 100% mortality. In addition, having seizures in the prehospital setting increased the risk of mortality four times. Although they did not have a direct association with mortality, they significantly decreased survival. A larger sample size is probably required to obtain an association with mortality. CONCLUSIONS: These results reflect the severity of the clinical situation in this population and, although no risk factors were identified, they enlighten us about the conditions presented by patients who died.

Association of SCN1A Polymorphisms rs3812718 and rs2298771 with Epilepsy.

Background/Objectives: Epilepsy is a brain disease with both environmental and genetic inputs. Ion channel dysfunction seems to be of great significance for abnormal neuronal behavior during epileptic seizures. Within neurons, the voltage-gated sodium channels are crucial proteins contributing to the initiation and propagation of action potentials. The voltage-gated sodium channel α subunit 1 (SCN1A) gene encodes for the α subunit of a voltage-gated ion channel. The aim of the study was to investigate the relation of two common SCN1A variants, i.e., rs3812718 and rs2298771, with distinct epileptic phenotypes in a South-Eastern European population. Methods: DNA was extracted from 214 unrelated participants with focal onset, focal to bilateral tonic-clonic, or generalized onset epileptic seizures and genotyped using real-time PCR (LightSNiP assays) followed by melting curve analysis. Statistical analysis of the results was performed using IBM SPSS Statistics software (version 29.0 for Windows). Results: Genotype frequency distribution analysis indicated an association for the A-allele-containing genotypes of both rs3812718 and rs2298771 polymorphisms of SCN1A with generalized onset seizures and focal to bilateral tonic-clonic seizures versus focal onset seizures. Conclusions: Consequently, the study provides evidence that supports a potential association of the investigated SCN1A polymorphisms with distinct seizure subtype susceptibility in South-Eastern Europeans.

Development of Seizures Following Traumatic Brain Injury: A Retrospective Study.

Objectives: The multifaceted impact of Traumatic brain injury (TBI) encompasses complex healthcare costs and diverse health complications, including the emergence of Post-Traumatic Seizures (PTS). In this study, our goal was to discern and elucidate the incidence and risk factors implicated in the pathogenesis of PTS. We hypothesize that the development of PTS following TBI varies based on the type and severity of TBI. Methods: Our study leveraged the Nationwide Inpatient Sample (NIS) to review primary TBI cases spanning 2016-2020 in the United States. Admissions featuring the concurrent development of seizures during the admission were queried. The demographic variables, concomitant diagnoses, TBI subtypes, hospital charges, hospital length of stay (LOS), and mortality were analyzed. Results: The aggregate profile of TBI patients delineated a mean age of 61.75 (±23.8) years, a male preponderance (60%), and a predominantly White demographic (71%). Intriguingly, patients who encountered PTS showcased extended LOS (7.5 ± 9.99 vs. 6.87 ± 10.98 days, p < 0.001). Paradoxically, PTS exhibited a reduced overall in-hospital mortality (6% vs. 8.1%, p < 0.001). Notably, among various TBI subtypes, traumatic subdural hematoma (SDH) emerged as a predictive factor for heightened seizure development (OR 1.38 [1.32-1.43], p < 0.001). Conclusions: This rigorous investigation employing an extensive national database unveils a 4.95% incidence of PTS, with SDH accentuating odds of seizure risk by OR: 1.38 ([1.32-1.43], p < 0.001). The paradoxical correlation between lower mortality and PTS is expected to be multifactorial and necessitates further exploration. Early seizure prophylaxis, prompt monitoring, and equitable healthcare provision remain pivotal avenues for curbing seizure incidence and comprehending intricate mortality trends.

Ultrastructural Analysis of the Large Neuronal Perikarya in an Injured Dentate Nucleus Using an Experimental Model of Hyperthermia-Induced Convulsions: The First Qualitative and Quantitative Study.

Background: Febrile seizures are a common form of convulsions in childhood, with poorly known cellular mechanisms. The objective of this pioneering study was to provide qualitative and quantitative ultrastructural research on the large neuronal perikarya in the cerebellar dentate nucleus (DN), using an experimental model of hyperthermia-induced seizures (HSs), comparable to febrile seizures in children. Methods: The study used young male Wistar rats, divided into experimental and control groups. The HSs were evoked by a hyperthermic water bath at 45 °C for 4 min for four consecutive days. Specimens (1 mm3) collected from the DN were routinely processed for transmission electron microscopy studies. Results: The ultrastructure of the large neurons in the DN affected by hyperthermic stress showed variously pronounced lesions in the perikarya, including total cell disintegration. The most pronounced neuronal lesions exhibited specific morphological signs of aponecrosis, i.e., dark cell degeneration ('dark neurons'). In close vicinity to the 'dark neurons', the aponecrotic bodies were found. The findings of this qualitative ultrastructural study correspond with the results of the morphometric analysis of the neuronal perikarya. Conclusions: Our results may constitute interesting comparative material for similar submicroscopic observations on large DN neurons in HS morphogenesis and, in the future, may help to find potential treatment targets to prevent febrile seizures or reduce recurrent seizures in children.

Case Report: Cerebral folate deficiency caused by FOLR1 variant.

Background: Cerebral folate transport deficiency (CFD) is a rare neurological disease characterized by a deficiency in 5-methyltetrahydrofolate (5-MTHF) in the cerebrospinal fluid, with a normal peripheral total folate level. Late infantile-onset refractory seizures, ataxia, movement disorders, hypotonia, developmental delays, and developmental regression characterize CFD. Some patients present with visual and hearing impairments and autism-like manifestations. This study aimed to elucidate the clinical features, diagnostic approach, and therapeutic outcomes in siblings with CFD due to FOLR1 variants, highlighting the importance of early diagnosis and treatment. Case presentation: We reported the cases of two siblings with CFD caused by a new variant in FOLR1. They presented with intractable epilepsy, developmental regression, and ataxia, and the younger sibling developed autism. Whole-exon sequencing revealed a c.148G>A homozygous variant, resulting in a change in the amino acid sequence (p.Glu50Lys). Low 5-MTHF levels were detected in the cerebrospinal fluid. Conclusions: This report illustrates that CFD was caused by FOLR1 variants in two siblings. They had intractable epilepsy, developmental regression, and ataxia, and a diagnosis of CFD was confirmed by a c.148G>A (p.Glu50Lys) variant in FOLR1, a new pathogenic variant in FOLR1. Early diagnosis is essential and can improve outcomes in affected patients.

Clinical Insights Into Eating-Induced Reflex Epilepsy: A Case Report of an Eight-Year-Old Girl.

Eating epilepsy is a rare condition in children where seizures are triggered by the act of eating. An eight-year-old girl presented with seizures occurring primarily during mealtimes, characterized by a fixed gaze, jaw hypotonia, and impaired awareness. These seizures began at age seven, were initially uninvestigated, and progressively worsened over the year, reaching up to 20-30 episodes per meal. Diagnostic tests, including blood work, upper gastrointestinal endoscopy, psychiatric evaluation, and magnetic resonance imaging (MRI), were normal. The EEG showed generalized epileptiform activity, suggesting a seizure disorder, but the exact cause was unclear. After ruling out more common conditions with similar symptoms, such as gastroesophageal reflux disease, Sandifer syndrome, and psychogenic non-epileptic seizures, the diagnosis of reflex eating epilepsy was made in the end through a process of elimination, combining clinical features with EEG findings and through reviewing the literature. Treatment with oral sodium valproate monotherapy led to significant symptomatic improvement, reducing the frequency of seizures during meals.

[Epilepsy or functional neurological disorder. Diagnostic strategies]. / Epilepsia o trastorno neurológico funcional. Estrategias para el diagnóstico.

A seizure is the manifestation of symptoms or signs produced by excessive or synchronous neuronal activity in the brain. It usually presents as brief, self-limited episodes of involuntary movements that can affect a part or the entire body and that are sometimes accompanied by loss of consciousness and sphincter control. Epilepsy may be considered after a single unprovoked seizure in a patient with a high risk of recurrence. Paroxysmal non-epileptic disorders are defined as episodes of sudden onset and short duration that imitate an epileptic seizure, caused by a brain dysfunction of diverse origin that, unlike epilepsy, is not due to excessive neuronal discharge. Its incidence is much higher than epilepsy and it can appear at any age. It is important for diagnosis to analyze the triggering factors, the details of each episode, physical examination and only proceed to basic complementary tests such as video-electroencephalogram in case of doubt or for diagnostic confirmation. There is a tendency to overdiagnose epilepsy and excessive use of anticonvulsant drugs. Those that can most frequently be confused are syncope, "daydreams" and pseudoseizures.

Una convulsión es la manifestación de signos o síntomas producidos por una actividad neuronal excesiva o sincrónica en el cerebro. Suele presentarse como episodios breves, autolimitados, de movimientos involuntarios que pueden afectar a una parte del cuerpo o su totalidad y que, en ocasiones, se acompañan de pérdida de la conciencia y control de esfínteres. Puede considerarse epilepsia una sola crisis no provocada en un paciente con un elevado riesgo de recurrencia. Los trastornos paroxísticos no epilépticos se definen como episodios de aparición brusca y de breve duración que imitan a una crisis epiléptica, originados por una disfunción cerebral de origen diverso que a diferencia de la epilepsia no obedecen a una descarga neuronal excesiva. Su incidencia es mucho más elevada que la epilepsia y pueden aparecer a cualquier edad. Es importante para el diagnóstico analizar los factores desencadenantes, los pormenores de cada episodio, examen físico y solamente proceder a los exámenes complementarios básicos como video-electroencefalograma en caso de duda o para confirmación diagnóstica. Existe la tendencia a sobrediagnosticar epilepsia y al uso excesivo de fármacos anticonvulsivos. Los que con mayor frecuencia se pueden confundir son los síncopes, ensoñaciones y las pseudocrisis.

[Neonatal epileptics syndromes]. / Síndromes epilépticos neonatales.

Neonatal epileptic syndromes are part of the genetic and metabolic epilepsies in this age group. Although they are not the most frequent cause of neonatal seizures, their early recognition allows for better diagnostic and therapeutic approaches. These syndromes can be classified into self-limited neonatal syndromes and early infantile epileptic and developmental encephalopathies (EIDEE). While they may share semiology in some types of seizures, such as sequential, and even share alterations in common genes in their etiology, their evolution is very different. In self-limited neonatal syndromes, seizures typically resolve within the first months of life with normal psychomotor development, giving rise to the term self-limited. However, the term benign should not be used as some may present recurrence of seizures, movement disorders, or learning disorders. In the case of EIDEE, seizures are usually refractory to treatment, affecting brain functions and neurodevelopment. In this review, our aim was to describe the electroclinical phenotype of neonatal epileptic syndromes, the most frequently involved genes and their clinical spectrum, their diagnostic approach, as well as the recommended treatments.

Los síndromes epilépticos neonatales hacen parte de las epilepsias de origen genético y metabólico en este grupo edad y aunque no son la causa más frecuente de crisis neonatales, su reconocimiento temprano permite dirigir mejor su enfoque diagnóstico y tratamiento. Pueden clasificarse en síndromes neonatales autolimitados y encefalopatías epilépticas y del desarrollo infantil temprano (EIDEE). Aunque pueden mostrar semiología similar en algunos tipos de crisis, como las secuenciales, e incluso comparten alteraciones en genes comunes en su etiología, su evolución es muy diferente. En los síndromes autolimitados, las crisis remiten en los primeros meses de vida alcanzando un desarrollo psicomotor normal, lo que da su nombre de autolimitado; sin embargo, el término benigno no debe utilizarse dado que algunos pueden presentar recurrencia de crisis, trastornos del movimiento o trastornos del aprendizaje. En las EIDEE las crisis suelen ser refractarias al tratamiento y se comprometen funciones cerebrales y el neurodesarrollo. En esta revisión describiremos el fenotipo electroclínico de los síndromes epilépticos neonatales, los genes más frecuentemente involucrados y su espectro clínico, su enfoque diagnóstico, así como los tratamientos recomendados.

Electrographic Seizures and Predictors of Epilepsy after Pediatric Arteriovenous Malformation Rupture.

OBJECTIVE: To assess clinical and electroencephalogram (EEG) predictors of epilepsy and to describe the percentage of electrographic seizures (ES) and development of epilepsy among patients with spontaneous intracerebral hemorrhage (ICH) due to arteriovenous malformation (AVM) rupture. STUDY DESIGN: Retrospective review of patients admitted to the pediatric intensive care unit with ICH secondary to AVM rupture over 11 years. Clinical variables were collected by review of the electronic medical record. Seizures were described as acute symptomatic (7 days after AVM rupture), subacute (7-30 days after AVM rupture) and remote (greater than 30 days after AVM rupture). Outcome metrics included mortality, and the development of epilepsy post discharge. Descriptive statistics were used. RESULTS: Forty-three patients met inclusion criteria with a median age of 12.2 years (IQR 7.3-14.8) and 49% (21/43) were female. Sixteen percent (7/43) presented with a clinical seizure prior to EEG placement. EEG was performed in 62% (27/43) of patients; one had electrographic status epilepticus without clinical signs. Sixteen percent (7/43) of patients were diagnosed with epilepsy, with a median time to diagnosis of 1.34 years (IQR 0.55-2.07) after AVM rupture. One-year epilepsy free survival was 84% (95% CI 70%-98%) and two-year epilepsy free survival was 79% (95% CI 63%-95%) Remote seizures were associated with epilepsy (p<0.001), but acute symptomatic seizures were not (p=0.16). CONCLUSIONS: EEG-confirmed seizures are uncommon in patients with ICH secondary to AVM rupture; however when identified, the seizure burden appears to be high. Patients with seizures 30 days after AVM rupture are more likely to develop epilepsy.

Intractable seizures after cranioplasty, a dreadful post-operative complication managed efficiently from Nepal: A case series.

INTRODUCTION AND IMPORTANCE: Cranioplasty is an elective neurosurgical procedure following decompressive craniectomy, often associated with post-operative complications such as hemorrhage, seizures, infection, hydrocephalus, and bone resorption. While seizures post-cranioplasty is not uncommon, Intractable seizures are rare but a dreadful complication following cranioplasty. CASE SUMMARY: A 23 and 17-year-old male underwent decompression craniectomy for traumatic brain injury and subsequently underwent titanium mesh and acrylic cranioplasty respectively, During the post-operative period both patients developed intractable seizures. Initially seizures were refractory to multiple anti-epileptic drugs and benzodiazepine induced coma. Intractable seizures were controlled gradually with few anti-epileptic drugs after the removal of cranioplasty. During 2 years' follow-up, there was no new episode of seizures complained by patients. DISCUSSION: Elective cranioplasty following decompressive craniectomy after traumatic head injury is one of the commonest surgical modality carried out globally as a life saving measure. But post-operative complications following cranioplasty such as wound infection, implant displacement, bone resorption, hydrocephalus, epidural hematoma are the commonest observed complications whereas post-operative seizure is the most dreadful complication needing immediate intervention. Along with it intractable seizure is rarer during post- operative period. CONCLUSION: Intractable seizures post-cranioplasty, though rare, are serious and often linked to cerebral edema from negative pressure drainage and dysregulation of cerebral blood flow. Removing the cranioplasty can restore blood flow regulation, stabilize brain tissue, and resolve seizures. Care providers should be aware of this rare complication and to be counselled the patient and the family before the surgery.

Nonictal electroencephalographic measures for the diagnosis of functional seizures.

OBJECTIVE: Functional seizures (FS) look like epileptic seizures but are characterized by a lack of epileptic activity in the brain. Approximately one in five referrals to epilepsy clinics are diagnosed with this condition. FS are diagnosed by recording a seizure using video-electroencephalography (EEG), from which an expert inspects the semiology and the EEG. However, this method can be expensive and inaccessible and can present significant patient burden. No single biomarker has been found to diagnose FS. However, the current limitations in FS diagnosis could be improved with machine learning to classify signal features extracted from EEG, thus providing a potentially very useful aid to clinicians. METHODS: The current study has investigated the use of seizure-free EEG signals with machine learning to identify subjects with FS from those with epilepsy. The dataset included interictal and preictal EEG recordings from 48 subjects with FS (mean age = 34.76 ± 10.55 years, 14 males) and 29 subjects with epilepsy (mean age = 38.95 ± 13.93 years, 18 males) from which various statistical, temporal, and spectral features from the five EEG frequency bands were extracted then analyzed with threshold accuracy, five machine learning classifiers, and two feature importance approaches. RESULTS: The highest classification accuracy reported from thresholding was 60.67%. However, the temporal features were the best performing, with the highest balanced accuracy reported by the machine learning models: 95.71% with all frequency bands combined and a support vector machine classifier. SIGNIFICANCE: Machine learning was much more effective than using individual features and could be a powerful aid in FS diagnosis. Furthermore, combining the frequency bands improved the accuracy of the classifiers in most cases, and the lowest performing EEG bands were consistently delta and gamma.

Temporal and Potential Predictive Relationships between Sleep Spindle Density and Spike-and-Wave Discharges.

Spike-and-wave discharges (SWDs) and sleep spindles are characteristic electroencephalographic (EEG) hallmarks of absence seizures and nonrapid eye movement sleep, respectively. They are commonly generated by the cortico-thalamo-cortical network including the thalamic reticular nucleus (TRN). It has been reported that SWD development is accompanied by a decrease in sleep spindle density in absence seizure patients and animal models. However, whether the decrease in sleep spindle density precedes, coincides with, or follows, the SWD development remains unknown. To clarify this, we exploited Pvalb-tetracycline transactivator (tTA)::tetO-ArchT (PV-ArchT) double-transgenic mouse, which can induce an absence seizure phenotype in a time-controllable manner by expressing ArchT in PV neurons of the TRN. In these mice, EEG recordings demonstrated that a decrease in sleep spindle density occurred 1 week before the onset of typical SWDs, with the expression of ArchT. To confirm such temporal relationship observed in these genetic model mice, we used a gamma-butyrolactone (GBL) pharmacological model of SWDs. Prior to GBL administration, we administered caffeine to wild-type mice for 3 consecutive days to induce a decrease in sleep spindle density. We then administered low-dose GBL, which cannot induce SWDs in normally conditioned mice but led to the occurrence of SWDs in caffeine-conditioned mice. These findings indicate a temporal relationship in which the decrease in sleep spindle density consistently precedes SWD development. Furthermore, the decrease in sleep spindle activity may have a role in facilitating the development of SWDs. Our findings suggest that sleep spindle reductions could serve as early indicators of seizure susceptibility.

Midazolam-Induced Seizure-Like Activity in Five Neonates: A case series.

An intravenous (IV) administration of midazolam may result in seizure-like activity or movement. This report describes 5 neonates who developed seizure-like movements after IV midazolam injection. The patients presented between 2019 and 2022 and were admitted to a neonatal intensive care unit located within an academic centre in Muscat, Oman. The abnormal movements occurred shortly after IV bolus administration of midazolam. None of the patients experienced seizure-like movements after receiving midazolam infusions. The seizure-like movements were aborted either spontaneously or by antiseizure medications. In addition, seizure recurrence was not observed in any of the infants during the later stages of their treatment. Since this adverse effect might be related to the speed of the bolus administration, IV midazolam must be given as a slow bolus over 2-3 minutes followed by a slow flush of normal saline. To prevent midazolam's potential adverse effect on newborns, neonatal caregivers must be aware of it.

Traumatic encephalocele in the nasal cavity after 6 years of trauma: a case report.

BACKGROUND: Encephalocele refers to protrusion of the meninges and brain tissue through a skull bone defect. It results from congenital, traumatic, neoplastic, or spontaneous reasons. Traumatic encephalocele occurs because of the posttraumatic fracture of the skull bone or iatrogenic causes. The manifestations vary a lot, such as rhinorrhea, seizures, headaches, and focal neurological deficits. CASE PRESENTATION: A 20-year-old Syrian male presented to our department with the complaint of clear cerebrospinal fluid drainage from his right nostril, which started 6 years ago after a head trauma, moderate headache, and episodes of tonic-clonic seizures without any response to medical treatment. Then, 2 months ago, the patient had meningoencephalitis, so he was admitted to the intensive care unit and treated for a month until he was cured. The patient underwent radiological investigations, which showed that he had a base fracture with an encephalocele in the nasal cavity. The brain tissues with the meninges herniated through the skull base fracture with a significant expansion of the subarachnoid spaces in the right hemisphere. He was advised to undergo surgical repair at that time, but he refused the surgery. During this visit, surgery was indicated. The surgery was done by a specialist who returned the herniated brain tissues to their normal location, repaired the meninges, and reconstructed the skull base with bone cement and bio-glue. The patient's recovery after the surgery was uneventful. CONCLUSION: Traumatic encephalocele is a rare and unexpected complication of trauma, but we should keep it in mind when the patient comes with head trauma because of its life-threatening consequences. This complication can happen after years of trauma if the patient refuses treatment, therefore, we must educate patients about the dangerous results of neglecting cerebrospinal fluid leakage and skull fractures.