Drosophila models used to simulate human ATP1A1 gene mutations that cause Charcot-Marie-Tooth type 2 disease and refractory seizures

Certain amino acids changes in the human Na^(+)/K^(+)-ATPase pump,ATPase Na^(+)/K^(+)transporting subunit alpha 1(ATP1A1),cause Charcot-Marie-Tooth disease type 2(CMT2)disease and refractory seizures.To develop in vivo models to study the role of Na^(+)/K^(+)-ATPase in these diseases,we modified the Drosophila gene homolog,Atpα,to mimic the human ATP1A1 gene mutations that cause CMT2.Mutations located within the helical linker region of human ATP1A1(I592T,A597T,P600T,and D601F)were simultaneously introduced into endogenous Drosophila Atpαby CRISPR/Cas9-mediated genome editing,generating the Atpα^(TTTF)model.In addition,the same strategy was used to generate the corresponding single point mutations in flies(Atpα^(I571T),Atpα^(A576T),Atpα^(P579T),and Atpα^(D580F)).Moreover,a deletion mutation(Atpα^(mut))that causes premature termination of translation was generated as a positive control.Of these alleles,we found two that could be maintained as homozygotes(Atpα^(I571T)and Atpα^(P579T)).Three alleles(Atpα^(A576T),Atpα^(P579)and Atpα^(D580F))can form heterozygotes with the Atpαmut allele.We found that the Atpαallele carrying these CMT2-associated mutations showed differential phenotypes in Drosophila.Flies heterozygous for Atpα^(TTTF)mutations have motor performance defects,a reduced lifespan,seizures,and an abnormal neuronal morphology.These Drosophila models will provide a new platform for studying the function and regulation of the sodium-potassium pump.

Mental retardation,seizures and language delay caused by new SETD1B mutations:Three case reports

BACKGROUND The SETD1B gene is instrumental in human intelligence and nerve development.Mutations in the SETD1B gene have been linked in recent studies to neurodevelopmental disorders,seizures,and language delay.CASE SUMMARY This study aimed to analyze the clinical manifestations and treatment of three patients suffering from mental retardation,epilepsy,and language delay resulting from a new mutation in the SETD1B gene.Three individuals with these symptoms were selected,and their clinical symptoms,gene test results,and treatment were analyzed.This article discusses the impact of the SETD1B gene mutation on patients and outlines the treatment approach.Among the three patients(two females and one male,aged 8,4,and 1,respectively),all exhibited psychomotor retardation,attention deficit,and hyperactivity disorder,and two had epilepsy.Antiepileptic treatment with sodium tripolyvalproate halted the seizures in the affected child,although mental development remained somewhat delayed.Whole exome sequencing revealed new mutations in the SETD1B gene for all patients,specifically with c.5473C>T(p.Arg1825trp),c.4120C>T(p.Gln1374*,593),c.14_15insC(p.His5Hisfs*33).CONCLUSION Possessing the SETD1B gene mutation may cause mental retardation accompanied by seizures and language delay.Although the exact mechanism is not fully understood,interventions such as drug therapy,rehabilitation training,and family support can assist patients in managing their symptoms and enhancing their quality of life.Furthermore,genetic testing supplies healthcare providers with more precise diagnostic and therapeutic guidance,informs families about genetic disease risks,and contributes to understanding disease pathogenesis and drug research and development.

Epidemiological, Diagnostic and Evolutionary Profile of Seizures in Young Infants at Albert Royer (Dakar/Senegal)

Introduction: Seizures are one of the most common neurological complications in the infant period. The aim of our study was to describe the epidemiological, clinical, therapeutic and prognostic features of seizures in infants at the Albert Royer Children’s Hospital (Senegal). Materials and Methods: This was a retrospective, descriptive study from 1 January 2012 to 30 September 2018 of infants aged 0 days to 2 months who presented with seizures. Results: The hospital rate was 8.5%. Almost all the mothers (99.1%) had undergone at least 3 antenatal visits. Urogenital infection, gestational arterial hypertension and funicular anomalies were the main pregnancy-related pathologies. Delivery was vaginal in the majority of cases (80.9%). Most infants (43.6%) had not cried at birth. The majority of infants (63%) were born at term. Trophicity was normal in 68% of cases. The average age of the infants was 6.7 days. The main causes of seizures were hypoxic-ischemic encephalopathy (48.7%), metabolic disturbances (48.1%) and central ոеrvοսѕ system infections (15.6%). Phenobarbital was the 1st-line anticonvulsant. The case fatality rate was 39.5%. The main sequela observed were delayed psychomotor development (20.6%). Conclusion: Optimal management of infant seizures requires early diagnosis and etiological treatment by improving the quality of perinatal care to ensure better management of risk factors, as well as increasing the availability of neuroimaging equipment.

Neuroimaging features in a patient with non-ketotic hyperglycaemic seizures: A case report

BACKGROUND Non-ketotic hyperglycaemic(NKH)seizures are a rare neurological complication of diabetes caused by hyperglycaemia in non-ketotic and non-hyperosmotic states.The clinical characteristics of NKH seizures are atypical and lack unified diagnostic criteria,leading to potential misdiagnoses in the early stages of the disease.CASE SUMMARY This report presents a rare case of NKH seizures in a 52-year-old male patient with a history of type 2 diabetes mellitus.We performed comprehensive magnetic resonance imaging(MRI)studies at admission,12 d post-admission,and 20 d post-discharge.The imaging techniques included contrast-enhanced head MRI,T2-weighted imaging(T2WI),fluid-attenuated inversion recovery(FLAIR),diffusion-weighted imaging,susceptibility-weighted imaging,magnetic reso-nance spectroscopy(MRS),and magnetic resonance venography.At the time of admission,T2WI and FLAIR of the cranial MRI showed that the left parieto-occipital cortex had gyrus-like swelling and high signal,and subcortical stripes had low signal.MRS showed a reduced N-acetylaspartate peak and increased creatine and choline peaks in the affected areas.A follow-up MRI 20 d later showed that the swelling and high signal of the left parieto-occipital cortex had disappeared,and the low signal of the subcortex had disappeared.CONCLUSION This case study provides valuable insights into the potential pathogenesis,diagnosis,and treatment of NKH seizures.The comprehensive MRI findings highlight the potential utility of various MRI sequences in diagnosing and characterizing NKH seizures.

In-hospital new-onset seizures in patients admitted to the medical intensive care unit:An observational study and algorithmic approach

BACKGROUND Seizures are one of the most common neurological complications encountered in the intensive care unit(ICU).They can occur in the background of exacerbation of a known neurological disease or secondary to non-neurological conditions such as sepsis and metabolic disturbances.However,there is a paucity of literature on the incidence and pattern of new-onset seizures in ICUs.AIM To study the incidence and patterns of new-onset seizures in patients admitted to the medical ICU.METHODS This was a prospective,multicenter,observational study performed in two tertiary care centers in Hyderabad,India over a period of 1 year.Patients upon ICU admission,who developed new-onset generalized tonic clonic seizures(GTCS),were enrolled.Those with a pre-existing seizure disorder,acute cerebrovascular accident,head injury,known structural brain lesions,or chronic liver disease were excluded as they have a higher likelihood of developing seizures.All enrolled patients were subjected to biochemical routines,radiological imaging of either computed tomography or magnetic resonance imaging,and other relevant laboratory tests as per clinical suspicion according to the protocol,and their data were recorded.Statistical analyses were conducted using descriptive statistics,χ^(2) tests,and linear regression.RESULTS A total of 61 of 2522 patients developed GTCS.Among all etiologies of seizures,metabolic causes were most frequent(35%)followed by infective causes(27%)and others(new-onset structural,drug withdrawal,druginduced,toxicology-related,and miscellaneous factors).Logistic regression analysis showed that increased sodium and calcium levels were associated with a lower likelihood of developing seizures.CONCLUSION This study identified the etiology of new-onset seizures developing in critically ill patients admitted to the ICU.These findings highlight the need for targeted monitoring of those at risk of developing seizures.

Changes of serum adrenocorticotropic hormone and cortisol levels during sleep seizures

Objective Measuring the serum concentrations of adrenocorticotropic hormone （ACTH） and cortisol in epileptic seizures during sleep to investigate their link to the EEG changes. Methods Pre-surgical evaluation was performed by videoEEG monitoring using 24 channel recording. Thirty six epilepsy patients could be attributed to two groups： 28 patients had spontaneous seizures, and the other 8 patients whose seizures were induced by bemegride. Another 11 persons with confirmed psychogenic non-epileptic seizures （PNES） served as control group. Blood samples were obtained at five points： wake （08：00 a.m.）, sleep （00：00 a.m.）, and shortly before, during and after an epileptic seizure. The serum ACTH and cortisol were measured and analyzed by chemiluminescent immunoassay. Results The levels of ACTH and cortisol in serum underwent significant changes： declining below the average sleep-level shortly before seizures, increasing during seizures, and far above the average wake-level after seizures （P 〈 0.001）. Such changes did not occur in the control group （P 〉 0.05）. The ACTH and cortisol levels had no significant difference between spontaneous group and bemegride-induced group （P 〉 0.05）. Conclusion The serum concentrations of ACTH and cortisol during sleep seizures are linked with pre-ictal and ictal EEG changes in epilepsy patients.

Glucocorticoid receptor expression in neonatal rat cortex following recurrent seizures The role in developing brain injury

BACKGROUND： Studies have explored changes in neonatal rat glucocorticoid receptor （GR） expression changes following mature brain injury. OBJECTIVE： To investigate the temporal and special changes of GR during brain development in rats with recurrent seizures. DESIGN, TIME AND SE＇n＇ING： A randomized, controlled animal experiment was performed at the Department of Pediatrics, Second Xiangya Hospital of Central South University, from February 2008 to March 2009. MATERIALS： Rabbit anti-rat GR monoclonal antibody was purchased from Santa Cruz Biotechnology, USA; goat anti-rabbit IgG was purchased from Zhongshan Goldenbridge Biotechnology, China. METHODS： A total of 48 Sprague-Dawley rats, 7 days old, were randomly assigned to control and seizure groups, with 24 animals in each group. Seizures were induced by inhalant flurothyl. MAIN OUTCOME MEASURES： Changes in GR protein expression in the rat cerebral cortex were detected by Western blotting analysis and immunohistochemistry. RESULTS： GR expression in the cerebral cortex of control rats significantly increased with aging （P 〈 0.05）, and varied in the frontal lobe, temporal lobe, and parietal lobe. GR was predominantly expressed in the cytoplasm early and rapidly increased in the nuclei. GR protein expression in the cerebral cortex after seizure was lower in the cytoplasm at 15 days and in nuclear protein at 19 days. CONCLUSION： GR expression displayed temporal and spatial changes in brain development. Recurrent seizures in neonatal rats cause abnormal GR expression and might play an important role in developing brain injury.

Diagnosis of neurocysticercosis among patients with seizures in northern coastal districts of Andhra Pradesh, India

Objective: To report cases of neurocysticercosis(NCC) from three neighboring districts of Andhra Pradesh state in India where NCC burden was never explored before.Methods: A total of 160 patients presenting with recent onset seizures were recruited from neurology, general medicine, and pediatric outpatient clinics of a local major tertiary care teaching hospital serving above districts during the period 2011–2014. Brain imaging was performed in all the above cases. A commercial immunoglobulin G-ELISA kit(sensitivity = 85%; specificity = 94%) was employed for the serological diagnosis of NCC.Results: The recruited patients presented with generalized, simple partial, and complex partial seizures(55%, 31.25% and 13.75% respectively). NCC was diagnosed in 44 of160(27.5%) seizure cases based on imaging characteristics, and a positive serum antibody ELISA. No association was detected between seropositivity with the number and location of the lesion(s) in the brain.Conclusions: The possible potentiality of NCC could be identified as an underlying cause of the recent onset of seizures in this region as explored in the present study. It is recommended that NCC should be suspected as one of the major differential in every recent onset seizure with or without a radio imaging supportive diagnosis, especially in areas endemic for taeniasis/cysticercosis.

Microglial displacement of GABAergic synapses has endogenous protective function in generation of complex febrile seizures

OBJECTIVE Microglia-mediated dis-placement of synapses has been reported in the setting of experimental neuroinflammation,but its role in neurological disorders is poorly understood.Complex febrile seizures(FS) are the most common infantile seizures,yet its pathological progress is largely unknown.METHODS Mice pups(postnatal 8-10 d) were posted to 43℃ hyperthermia condition to develop FS,and then the latency and threshold of seizures were determined.The displacement of synapses was observed through immunofluorescence staining.We researched whether microglial displacement of GABAergic synapses will influence complex FS-induced increase in GABAergic neurotransmission and neuronal excitability with patch-clamp electrophysiology.Moreover,we used the CD11 bD TR mice to selective ablation of microglia or pharmacological inhibition of microglia to observe their effects on susceptibility to FS and synaptic stripping.RESULTS GABAergic presynaptic terminals surrounding neuronal soma and GABAergic transmissions were increased in complex FS.Meanwhile,the activated microglia ensheathe glutamatergic neuronal soma to displace,but do not phagocytize,GABAergic presynaptic terminals.Patch-clamp electrophysiology established that the microglial displacement of GABAergic synapses reduced complex FS-induced increase in GABAergic neurotransmission and neuronal excitability,while GABA exerts excitatory action in this immature stage.Moreover,pharmacological inhibition of microglial displacement of GABAergic synapses or selective ablation of microglia in CD11 bDTR mice promoted the generation of complex FS.CONCLUSION Displacement of GABAergic synapses by microglia is a protective event in the pathological progress of complex FS.

An insulinoma with clinical and electroencephalographic features resembling complex partial seizures

We described a female patient with insulinoma who experienced recurrent episodes of automatism, confusion and convulsion. Furthermore, her electroencephalography （EEG） findings resembled the pattern in complex partial seizures with secondary generalization. The interictal EEG showed spikes and sharp waves, as well as focal slowing over the left temporal lobe, and the ictal EEG revealed generalized spikes and sharp waves associated with diffused slowing. She was initially misdiagnosed as pharmacoresistant epilepsy. After the insulinoma was found and surgically removed, her EEG turned normal and she was seizure-free during the 4-year follow-up. This report highlights the need for careful reassessment of all seizures refractory to medication, even for the oatients associated with eoileotiform discharges on EEG.

Models and detection of spontaneous recurrent seizures in laboratory rodents

Epilepsy, characterized by spontaneous recurrent seizures （SRS）, is a serious and common neurological disorder afflicting an estimated 1% of the population worldwide. Animal experiments, especially those utilizing small laboratory rodents, remain essential to understanding the fundamental mechanisms underlying epilepsy and to prevent, diagnose, and treat this disease. While much attention has been focused on epileptogenesis in animal models of epilepsy, there is little discussion on SRS, the hallmark of epilepsy. This is in part due to the technical difficulties of rigorous SRS detection. In this review, we comprehensively summarize both genetic and acquired models of SRS and discuss the methodology used to monitor and detect SRS in mice and rats.

Improving control effects of absence seizures using single-pulse alternately resetting stimulation (SARS) of corticothalamic circuit

Presently,we develop a simplified corticothalamic(SCT)model and propose a single-pulse alternately resetting stimulation(SARS)with sequentially applying anodic(A,“+”)or cathodic(C,“−”)phase pulses to the thalamic reticular(RE)nuclei,thalamus-cortex(TC)relay nuclei,and cortical excitatory(EX)neurons,respectively.Abatement effects of ACC-SARS of RE,TC,and EX for the 2 Hz-4 Hz spike and wave discharges(SWD)of absence seizures are then concerned.The m∶n on-off ACC-SARS protocol is shown to effectively reduce the SWD with the least current consumption.In particular,when its frequency is out of the 2 Hz-4 Hz SWD dominant rhythm,the desired seizure abatements can be obtained,which can be further improved by our proposed directional steering(DS)stimulation.The dynamical explanations for the SARS induced seizure abatements are lastly given by calculating the averaged mean firing rate(AMFR)of neurons and triggering averaged mean firing rates(TAMFRs)of 2 Hz-4 Hz SWD.

Immunohistochemical investigation of voltage-gated potassium channel-interacting protein 1 in normal rat brain and Pentylenettrazole-induced seizures

Objective To explore the possible role of voltage-gated potassium channel-interacting protein 1 (KChIP1) in the pathogenesis of epilepsy. Methods Sprague Dawley female adult rats were treated with pentylenettrazole (PTZ) to develop acute and chronic epilepsy models. The approximate coronal sections of normal and epilepsy rat brain were processed for immunohistochemistry. Double-labeling confocal microscopy was used to determine the coexistence of KChIP1 and gamma-aminobutyric acid (GABA). Results KChIP1 was expressed abundantly throughout adult rat brain. KChIP1 is highly co-localize with GABA transmitter in hippocampus and cerebral cortex. In the acute PTZ-induced convulsive rats, the number of KChIP1-postive cells was significantly increased especially in the regions of CA1 and CA3 (P < 0.05); whereas the chronic PTZ-induced convulsive rats were found no changes. The number of GABA-labeled and co-labeled neurons in the hippocampus appeared to have no significant alteration responding to the epilepsy-genesis treatments. Conclusion KChIP1 might be involved in the PTZ-induced epileptogenesis process as a regulator to neuronal excitability through influencing the properties of potassium channels. KChIP1 is preferentially expressed in GABAergic neurons, but its changes did not couple with GABA in the epileptic models.

The efficacy and tolerability of lamotrigine adjunctive/monotherapy in patients with partial seizures refractory to poly-AEDs

Objective： This study was designed as an open-label trial to assess the effects of changing the antiepileptic drugs （AEDs） regimen to lamotrigine （LTG） as adjunctive/monotherapy in patients with partial seizures who were dissatisfied with their drug regimen because of intractable seizures. Methods： The patients were recruited from mulficenters using the following criteria： age≥ 18 years; at least 3 seizures per month during the last 16 weeks; previous use of at least 3 AEDs. The study involved a baseline phase and 2 experimental phases： LTG was first added to the regimen, and then patients could gradually change to LTG monotherapy if their seizures were reduced by at least 50 percent/month. Tolerability, the primary end point, was assessed using the Liverpool Adverse Experience Profile （LAEP）. Secondary end points included quality of life, as measured with the Quality of Life in Epilepsy-31 inventory. Reductions in seizures from baseline throughout each phase were also analyzed. Results： One hundred and fourteen patients aged between 18 and 52 years （age 27.8___ 13.2 years; 71 men and 43 women） were enrolled. After adding LTG, 105 patients （92.11%） Completed adjunctive therapy. Upon completion of the adjunctive phase, mean improvement from baseline was 2.6 points on the LAEP （p=0.037）. The overall score on the QOLIE-31 improved by 8.49 points from baseline （p=0.023）. At the end of the trial, 26 （22.81%） of patients completed LTG monotherapy, and 65 patients （57.02%） experienced at least 50% reduction in seizure frequency compared to baseline, The mean improvement from baseline was 5.1 points on the LAEP （p=0.0059）, and the overall score on the QOLIE-31 score improved by 12,72 points from baseline（p=0,0071）. Twenty-two （19.30%） patients reported adverse effects and 9 patients discontinued participation in the trial because of adverse effects. Conclusion： For patients with partial seizures who were dissatisfied with their AED regimen because of intractable seizures, adding LTG to the drug regimen was well tolerated and effective in improving the quality of life and controlling seizures. Furthermore, switching to LTG monotherapy was associated with further improvement.

Pneumonia and seizures due to hypereosinophilic syndrome—organ damage and eosinophilia without synchronisation:A case report

BACKGROUND Hypereosinophilic syndrome(HES)is a condition characterized by increased eosinophil proliferation in the bone marrow,as well as tissue eosinophilia,often causing organ damage.The cause of the disease is unknown.Initial symptoms include fatigue,cough,shortness of breath,myalgia,angioedema,fever,and pneumonia.In addition to the respiratory symptoms,damage to the central nervous system can lead to severe seizures.Here,we report a case with pneumonia and complex partial seizures secondary to HES.CASE SUMMARY A 94-year-old woman was admitted to our hospital for heart failure and bloody stools.After admission,she also showed symptoms of pneumonia.Non-contrast computed tomography of the chest showed pleural effusion and infiltrative shadows.Lower gastrointestinal endoscopy showed multiple ulcers in the sigmoid colon.Blood analyses showed marked eosinophilia(eosinophils 1760/mm3,total leukocytes 6850/mm3).Initial treatment with furosemide 20 mg/d and prednisolone 25 mg/d relieved these symptoms.However,the patient subsequently experienced localised epileptic seizures characterized by bilateral eyelid twitching and eyes rolling upwards,without generalized convulsions,and respiratory arrest occurred.Electroencephalography showed spikes and waves.Non-contrast magnetic resonance imaging of the brain showed extensive periventricular hyperintensity.With administration of levetiracetam 1000 mg/d the epileptic seizures disappeared.However,the patient’s consciousness remained impaired,and her pneumonia worsened again.Two weeks later,she died of pneumonia.CONCLUSION HES symptoms are variable and atypical,and the level and timing of eosinophilia and organ damage are often discordant.

Response of levetiracetam in neonatal seizures

AIM: To review the clinical response to levetiracetam(LEV) in neonatal seizure management in intensive care unit.METHODS: Medical records of neonates who received LEV from January 2009 to August 2014 were reviewed. Their demographic data, clinical characteristics, etiology, seizures, electroencephalograms, response to treatment and outcome were noted. Literature review of use of LEV in neonates were also performed via Pub Med and EMBASE with keywords- "neonates", "seizures", "epilepsy" and "LEV" up to Sep 2014 and retrieved the publications. The response rate to LEV was compared.RESULTS: Twelve neonates were identified during the study period. All patients received phenobarbitone loading prior to consideration of LEV. Seven(58%) and nine(75%) achieved seizure freedom 24 h and 72 h after LEV was added, both clinically and electrographically. No serious adverse effects were associated with LEV use. From the literature, there are total 144 neonates reported to have used LEV. The overall results suggested that LEV could control up to 90% of neonatal seizures.CONCLUSION: LEV was found to be relatively safe and efficacious in treating neonatal seizures, but might not work well in the most severe hypoxic ischemic encephalopathy.

Elevated NKCC1 transporter expression facilitates early post-traumatic brain injury seizures

As a leading cause for morbidity and mortality in young adults,traumatic brain injury（TBI）,along with the poorly understood TBI-related seizures inducing their predispositions,pose a major health and socioeconomic problem in the world（Huang,2013）.

ACTA2 mutation is responsible for multisystemic smooth muscle dysfunction syndrome with seizures:A case report and review of literature

BACKGROUND ACTA2 gene is a specific gene that encodes actinα2.Multisystem smooth muscle dysfunction syndrome(MSMDS)is a multisystem disease characterized by aortic and cerebrovascular lesions caused by ACTA2 gene mutations.There have been many reports of cardiac,pulmonary and cerebrovascular lesions caused by MSMDS;however,few studies have focused on seizures caused by MSMDS.CASE SUMMARY Our patient was a girl aged 7 years and 8 mo with recurrent cough,asthma and seizures for 7 years.She was diagnosed with severe pneumonia,congenital heart disease,cardiac insufficiency,and malnutrition in the local hospital.Cardiac ultrasonography revealed congenital heart disease,patent ductus arteriosus(with a diameter of 0.68 cm),left coronary arteriectasis,patent oval foramen(0.12 cm),tricuspid and pulmonary regurgitation,and pulmonary hypertension.Cerebral magnetic resonance imaging and magnetic resonance angiography indicated stiffness in the brain vessels,together with multiple aberrant signaling shadows in bilateral paraventricular regions.A heterozygous mutation(c.536G>A)was identified in the ACTA2 gene,resulting in generation of p.R179H.Finally,the girl was diagnosed with MSMDS combined with epilepsy.The patient had 4 episodes of seizures before treatment,and no onset of seizure was reported after oral administration of sodium valproate for 1 year.CONCLUSION MSMDS has a variety of clinical manifestations and unique cranial imaging features.Cerebrovascular injury and white matter injury may lead to seizures.Gene detection can confirm the diagnosis and prevent missed diagnosis or misdiagnosis.

Pure Salivatory Seizures Secondary to a Subtle Malformation of the Right Parietal Cortex

Background: Salivatory seizures are a singularly rare condition, which can occur both in idiopathic and symptomatic epilepsies. Objectives: To describe and discuss the case of an adolescent patient with sleep-triggered “pure” salivatory seizures associated with a subtle cortical malformation of the right parietal cortex. Case report: Herein, we report a 17-year-old female who started to present salivatory paroxysms, which occasionally secondarily generalized, shortly after falling asleep, at the age of eight years. Video-electroencephalographic monitoring with scalp electrodes failed to show any epileptiform activity during the several recorded clinical events. Brain MRI and curvilinear reconstruction revealed, in the three orthogonal planes, a subtle cortical thickening, limited to a single gyrus in the right parietal cortex, suggestive of a focal cortical malformation. After antiepileptic drug therapy was optimized, the patient became seizure-free. Conclusion: An epilepsy diagnosis should be pursued in patients presenting isolated, paroxysmal hypersalivation, despite possible negative scalp EEG studies.

Classification of low-density EEG for epileptic seizures by energy and fractal features based on EMD

We are here to present a new method for the classification of epileptic seizures from electroencephalogram(EEG) signals.It consists of applying empirical mode decomposition(EMD) to extract the most relevant intrinsic mode functions(IMFs) and subsequent computation of the Teager and instantaneous energy,Higuchi and Petrosian fractal dimension,and detrended fluctuation analysis(DFA) for each IMF.We validated the method using a public dataset of 24 subjects with EEG signals from 22 channels and showed that it is possible to classify the epileptic seizures,even with segments of six seconds and a smaller number of channels(e.g.,an accuracy of0.93 using five channels).We were able to create a general machine-learning-based model to detect epileptic seizures of new subjects using epileptic-seizure data from various subjects,after reducing the number of instances,based on the k-means algorithm.