Epilepsy - Science topic
A disorder characterized by recurrent episodes of paroxysmal brain dysfunction due to a sudden, disorderly, and excessive neuronal discharge. Epilepsy classification systems are generally based upon: (1) clinical features of the seizure episodes (e.g., motor seizure), (2) etiology (e.g., post-traumatic), (3) anatomic site of seizure origin (e.g., frontal lobe seizure), (4) tendency to spread to other structures in the brain, and (5) temporal patterns (e.g., nocturnal epilepsy). (From Adams et al., Principles of Neurology, 6th ed, p313)
Questions related to Epilepsy
I am writing a manuscript on my clinical experience with positive results, want to know about published evidence, experiements or case reports.
I need to test the reaction to Pilocarpine of some mutant mice and need to know the exact maximum dose of Pilocarpine to which wild type animals do not respond.
We have been using the model for the last 3 years and it was reproducible enough: SE was observed in 70-80% male Wistar rats (160-180 g, P70).
But last experiments showed decrease in amount of rats that underwent SE to 10-20%.
The protocol is quite standart:
1. LiCl 127 mg/kg i.p. 18-24 hours prior to pilocarpine
2. Metscopolamine bromide 1 mg/kg s.c. 30 min prior to pilocarpine
3. Pilocarpine hydrochloride 25 mg/kg i.p. (all chemicals from Sigma)
Have anyone had such a problem?
Many brain insults, including TBI, stroke and encephalitis, may be associated with “early seizures” in the first week after the insult. These seizures are not spontaneous (unprovoked), but are directly caused by the initial insult. Late unprovoked (i.e., spontaneously recurrent seizures), may follow weeks, months or years later.
Our question is: May such early seizures also occur after a status epilepticus and is there literature on this (both for patients and SE models)?
We do typically observe early seizures in different SE models (e.g., pilocarpine, kainate) in rats. They occur with a peak frequency at 3-5 days following SE (if the SE was effectively interrupted after 60-120 min) and then subside. Late seizures occur earliest after about 7 days but often later.
There are some questions concerning video recording of spontaneous seizures in the lithium-pilocarpine model of epilepsy:
1. At what time of the day is it preferable to run the registration? (Or, if you register an individual behavior during 24 h, how do you avoid the social isolation?)
2. Is there any facility to speed up the analysis of video data obtained?
As there are two methods for the intrahippocampal injection for the establishment of SE.
Kainic acid and pilocarpine.
which one is better?
As far as I know, the kainic acid is a typical model for TLE, while the direct injection of kainic acid will trigger the excitoxicity which make me have some questions upon this model. Like, the theory of this model is that inducing the epilepsy then result in the degeneration or the excitoxicity triggers the epilepsy?
Hope anyone could discuss with me about that interesting question. THX.
In "Adenosine Dysfunction in Epilepsy and Associated Comorbidities" we cited two papers "Zhang Y, Wang X, Tang C, Guan Y, Chen F, Gao Q, et al. Genetic variations of adenosine kinase as predictable biomarkers of efficacy of vagus nerve stimulation in patients with pharmacoresistant epilepsy. Journal of Neurosurgery 2021; 1-10."
"Li T, Ren G, Kaplan DL, Boison D. Human mesenchymal stem cell grafts engineered to release adenosine reduce chronic seizures in a mouse model of CA3-selective epileptogenesis. Epilepsy Res 2009; 84(2-3): 238-41."
I am trying to tweaking my machine learning model optimizer, and i would love to test that in healthcare domain space, especially for rare illnesses.
Thus, do any one knows any deidentified electronic health records for Epilepsy, Parkinson , or other rare diseases patients (maybe those who are treated with warfarin) ?
Please guide me how to get these datasets.
I already spoke with many research authors, but yet no responses.
Nerve cells in the brain produce electrical impulses as soon as a temporary disorder or disorder occurs, convulsions and seizures occur. Microorganisms use the energy of electrical impulses, so when they listen to the nervous system, which weakens nerve signals.
Does the accumulation of fungal toxins in the body that are found in eating him cause epilepsy?
Colleagues, we need a general or multidisciplinary pharmacology or central nervous system journal
with an impact factor of 1 or highو free or reasonable fees for publication
3 years old child with uncontrolled seizure but he has spastic tetraplegia because of CP , he has also nail hypoplasia? what do you think doctors
Hello. I intend to simulate extracellular epileptogenesis-like conditions in microglia cultures. I concluded that the most well-fundamented and ready available way is to alter ionic concentrations. I decided to start with increasing extracellular potassium concentration to 10-12 mM.
For the in vitro model, I use RPMI 1640 glutamax medium, which already contains KCl 5.333 mM.
I intend to incubate the cells for a period with high K+ cocentration, incubate with normal medium once again and continue the experiment for a number of days more.
What would be the most correct way to increase the potassium concentration from 5.333 to 10-12 mM in this readymade medium?
Thank you for the attention
Seizures are fascinating intellectually, but they can be devastating for the person suffering from them. We have all heard stories of young people who seemingly have no genetic or other past medical history and present to the Neurological ICU in status epilepticus -- an entity known as NORSE. All our algorithms fail and we are left scrambling for effective approaches without any evidence. Often, despite our best interventions, these young healthy patients have >35% mortality rate. And those that survive rarely make it past the SNF.
We have one such patient in our Neurological ICU currently. So I wanted to ask what you guys do when the standard treatments have failed? Per the American Epilepsy Society guidelines, we initially treated her status with Ativan, Midazolam, Keppra loads, Vimpat loads, Fosphenytoin loads, Versed drips, and finally Pentobarbital coma. Currently she is on Keppra, Vimpat, Fosphenytoin, Felbamate, Epidiolex, and Fycompa. Thankfully the Pentobarbital is now off, but she continues to require continuous Versed drip.
In your experience, have you found anything effective in these situations?
Some PSG studies found patients with epilepsy had decreased REM sleep compared to healthy controls (TLE and JME). Furthermore, patients with refractory epilepsy had decreased percentage of REM sleep compared to those with medically controlled epilepsy.
Medications ( i.e, BZDs) are well known to decrease REM sleep. However, decreased REM sleep has also been observed among drug-naive patients with epilepsy.
-> Is the decrease of rapid eye movement sleep a cause or consequence of epilepsy?
I'm interested in ways other clinical researchers or centers quantify/calculate seizure burden for children and adolescents with epilepsy? Any standardized measures and/or clinical algorithms you've found helpful for research purposes?
Thanks in advance,
Despite being one of the world's oldest known medical conditions, public fear and misunderstanding about epilepsy persists, making many people reluctant to talk about it. That reluctance leads to lives lived in the shadows, lack of understanding about individual risk, discrimination in workplaces and communities, and a lack of funding for new therapies research. People with epilepsy die prematurely at a higher rate compared to the general population. The most common cause of death from epilepsy is sudden unexpected death in epilepsy, known as SUDEP. For many people living with epilepsy, the misconceptions and discrimination can be more difficult to overcome than the seizures themselves.
is there any way where scientists can reorient the molecular structures of present drugs used in the treatment of people with epilepsy ? and if so, would the drugs provide a different account that would help patients heal quickly from epilepsy
Periovulatory catamenial epilepsy- increased seizure frequency and severity on the days of ovulation due to the surge in the proconvulsant oestrogen. Oestrogen receptor GPER1 has an antagonist called G15. I want to induce epilepsy in mice to then add G15 when they ovulate to see the effects on seizure numbers.
I am trying to do a correlation between SO2 data obtained from satellite AURA OMI and SO2 data obtained from Ground Monitoring Stations.
Since both values show the level of concentration of SO2 in the atmosphere, though in different units, and one should increase if other is increasing but then why do they show a weak and negative correlation?
The study area is the Ahmedabad District. The correlation has been done for annual mean values for the years 2014-18.
Here is the screenshot of scatter plots generated from the regression analysis.
It is impossible to maintain social distancing between caretakers of epileptic patients during this COVID-19 pandemic. As result most of these patients are always in close proximity with the caretakers making them susceptible to COVID-19 infections.
We measured the number of epileptic crisis every 2 weeks for 42 days in patients using a placebo-controlled design. At different times of the experiment, some patients leave the clinical research protocol.
At the time of statistical analysis we did not find normality in neither Active group measurement, nor Sham ones, but we found homocedasticity.
We used Skillings-Mack test for intra-group analysis in Active group... We need a method to compare between groups.
Is there any non-parametric test like two-way repeated measures ANOVA for this case?
how to decrease the mortality of Lithium- Pilocarpine model?
Last few weeks, I tried the model of lithium pilocarpine model.
with 127mg/kg Lithium (24h before P)
1mg/kg Scopolamine methyl nitrate (30min before P)
and 30mg/kg P.
while the mortality is quite high. over 60%.
May I ask some sugguestion to decrease the mortality?
Besides, there is another question,
what is the difference between Scopolamine methyl nitrate and bromide? They are both used in papers.
« L’eau pour tous, est l’affaire de tous » Dicton Dr. Ahmed Kettab
Nous constatons que de plus en plus, il y a des personnes qui manquent d’eau dans le monde.
Près 25% de la population mondiale est en situation de « stress hydrique grave» ou pénurie d’eau grave.
Dix-sept (17) pays, sont concernés par cette pénurie d’eau.
75% des habitants des pays arabes vivent avec moins de 1000 m3 par an (le minimum étant de 1700m3/habitant/an).
La pénurie d'eau concernera 40 % de la population mondiale en 2030, et a l’horizon 2050? 2100?
Nous allons vers une vraie crise, s’il n’y aura pas une politique, une stratégie, une vision mondiale.
I am working on project epilepsy detector using EEG signal. But i failed to decompose EEG signal in EDF format.I will be thankful to him who provide MNE code or any suggestion.
Catamenial seizures are intractable seizures. However, with cluster formation, these acute repetitive seizures might become an emergency. It seems necessary to understand their neurophysiological mechanism of formation and occurrence. What you think about the proper care and effective treatment approach for catamenial seizure clusters or flurries?
I have read several reviews about poststroke epilepsy and in all of them it's written that the occurance of early post-stroke seizures increases risk of the occurance of late seizerus and post-stroke epilepsy. I followed to cited research articles and they are usually cohort-based. Since a more severe stroke increases the risk of early seizures and post-stroke epilepsy both, isn't it nessesary to perform a case-control (by stroke severity) study to prove the relation between early seizures and post-stroke epilepsy?
I searched for animal researches on this subject. It turned out that although repeated seizures increase infarct volume, a single seizure in some experimental conditions could even improve behavioral recovery.
I am new in this area and dont't understand why it is so commonly declarated early seizures increase risk of post-stroke epilepsy. Do people mostly have repeated early seizures? For example repeated partial seizures defined as single. Or human seizure have worse consequences than animal seizure-like activity due to brain complexity?
It is commonly known that some medicines are counter-indicated by sodium channelopathies. One of that medicines is Phenytoin (PH). But I know some patients, harboring truncating SCN1A mutations, for whom PH helped. Are there any studies about different types of medical treatment for nonsense- and missense-mutations of SCN1A gene?
Or can anyone suggest the biochemical causes of such medicine's behaviour?
I am writing a chapter on medico legal aspects of Epilepsy for a reference book.
I wish to collect your opinions and reasoning behind it to make a gentle reference while elaborating my point.
I am intending to elaborate my views on how epilepsy is a psychiatric disorder. Your opinions if befitting could be referred with due acknowledgement.
Please reinforce your opinions with sound reasoning or mentioning validating source of information.
Thanks to the US Government Comparative Toxicogenomics Database based in North Carolina, over 2000 Human genes impacted by Fluoride chronic poisoning are linked to Diseases resulting from the disruption of normal cellular and systemic processes.
Looking at just one of these genes, mTOR, Mammalian-homolog-Target-Of-Rapamycin, a known cause of Dental Fluorosis, we find the following diseases listed:
Cancer, features Hepatocellular Carcinoma, Adenocarcinoma, Ovarian Neoplasms, Mesothelioma, Mantle-Cell Lymphoma, Small Cell Carcinoma, Precursor T-Cell Lymphoblastic Leukemia - Lymphoma, Uterine Cervical Neoplasms, Renal Cell Carcinoma, Breast Neoplasms, Colonic Neoplasms, Non-Small-Cell Lung Carcinoma, Lymphatic Metastasis, Glioblastoma.
Damage to the Brain is listed under the general heading Neurotoxicity Syndromes, then Glioblastoma, Malformations of Cortical Development, Schizophrenia, Focal cortical dysplasia of Taylor (Epilepsy requiring surgery),
Other listed diseases include Congenital Capillary Malformations, Hypertension, Left Ventricular Hypertrophy.
Please let me know of any more Fluoride induced diseases you have found linked to mTOR.
Previously I worked with the attatched dataset in order to classify the normal and ictal EEG signals. Which is available at
- V. Bajaj and R. Pachori, “Classification of seizure and non-seizure EEG signals using empirical mode decomposition,” IEEE Trans. Inf. Technol. Biomed., vol. 16, no. 6, pp. 1135–1142, Nov. 2012.
- EEG Time Series Download Page 2012 [Online]. Available:http://epileptologie-bonn.de/cms/front_content.php?idcat=193&lang3
But in the following research paper I come to know about CHBMIT EEG dataset
- V. Geethu & S. Santhoshkumar (2018): An Efficient FPGA Realization of Seizure Detection from EEG Signal Using Wavelet Transform and Statistical Features, IETE Journal of Research.
The attatched file contains the information about normal (Z) and ictal (S) EEG signals. But in case of CHBMIT dataset I am getting confused which dataset is exactly containing almost same information like subset S and subset Z. because lots of information is given in the link of CHBMIT dataset. Can anybody, give me the clean dataset of CHBMIT that will contain only the normal and ictal EEG signals of length 2048 samples as found in the research paper V. Geethu et al..
My query is regarding identification of interical and preictal stages in CHB-MIT Scalp EEG Database of epileptic seizures collected at Children’s Hospital Boston , in which Seizure intervals are given in annotations. Generally most of the literature use only two classes of seizures in this database, viz. SEIZURE and NON-SEIZURE. My question is about identification of INTER-ICTAL, PREICTAL and ICTAL classes, so that appropriate Machine Learning/Deep Learning algorithm can be adopted for prediction of such seizure classes. Thanks in advance .
I recorded some abnormal EPSCs in my iPSC-derived neurons. Not like the individually separated EPSC signals, the ones appear in my Heterogeneous neurons which harbor the mutation associated with epilepsy, and these are some "Busting Like" EPSC events. It jumps to the maximum amplitude and stays there for quite some time and not going back (see attached pic). It only appears in my Het but not in control.
I am wondering how this happened, and any thoughts would be appreciated!
Subjects, who are planned to undergo TMS for therapeutic purpose are evaluated for history of epilepsy. Most of the RCTs that evaluated efficacy of TMS, exclude patients with history of epilepsy, considering the risks of seizure. However, evidences also support the beneficial role of TMS in epilepsy. Some interesting articles are here -
Should the recommendations for use of TMS need to be broadened?
Should the future researches evaluating role of TMS in various psychiatric disorders, also include those patients with co-morbid epilepsy?
Please tell me where can I get EEG data for Alzheimer's disease , because I am working on designing an automatic diagnosis system for detecting diseases.
I'm working on NrCAM gene mutation. I'm searching to know about any known mutations recorded in NrCAM gene. But I'm not getting any databases or articles regarding that. Can anyone suggest me any mutation database or links to know about the mutations of NrCAM gene in humans.
I am a newbie to M/EEG Source Localisation, I have a resting state Epileptic data through which I want to get a source time series (here condense sources to 68 ROIs-parcellations). However, I am unable to conceptualize which algorithm to choose.
I have read the literature and managed to understand about the differences clearly stated between dipole and distributed models but not (i might have missed literature here) between distributed and beamformers. So can someone help me in choosing the source localisation algorithms for resting state epileptic m/eeg signals. Can you also point me to good literature on differences between (advantages/disadvantages) distributed and beamformer methods. Many thanks in advance.
Does anyone know of any mouse line expressing either the flipase or the Dre recombinase or any other type of recombinase (except the Cre) under the control of the DAT promoter ?
Hi, I am currently working on epilepsy and I am searching for a epilepsy database that contains multiple channels. I have tried http://physionet.org/ dataset but for some reason there may have some problem with channels. Please share if anyone know about some other sources. Thanks.
in several studies focusing on Epilepsy they pretreat mice/rats 30min with scopolamine methyl bromide (1mg/kg) before trating the animal with Pilocarpine.
Most of them used intraperitoneal (IP) injections.
My question is:
why do they wait such a long time?
Normally drugs injected IP are adsorbed pretty fast, like 5min.
Is it just to be on the safe side before the application of the high dosage of Pilocarpine (to induce the seizures)?
Even if this is the case, wouldn't 10-15min be already more than enough?
So far I was not able to find an answer.
I am searching on topic for phd especially on: 1- epilepsy prediction using EEG signals or in 2- Emotional Intelligent with machine learning ,
kindly i want suggestions topics on those areas or if any one have another ideas please share it with me.
my question for epileptic seizure patient if there is ability to prevent the epilepsy to happen using medicines based on prediction
I want to connect EEG sensors with raspberry bi to make new wearable scalp for collect data from epilepsy patients and monitor them brain, then send the data to online database or wifi, also I want to know what are the types of EEG sensors that can connect with raspberry bi.
I am looking for the safest anti-emetic drug in children/pediatrics for my clinical assignment, I have searched but didn't get anything, please share the information.
Usually KD is recom as one of the last option in a child with drug resistent epilepsy (DRE): A new therapeutical point of view should be a new option in a infant?
Actually, We are doing Epilepsy Detection Project. Due to some reasons it is compulsory for us to convert .edf files into csv format. if anyone knows about the code please tell me. I didn't find any helping material from internet.
Individuals with MECP2 duplication syndrome have a wide variety of seizures (e.g., myoclonic, atonic, hypermotor, generalized tonic-clonic). Some also have episodes where muscle tone is lost for prolonged periods (often 10 -30 minutes) with clouded consciousness. Often, the loss of muscle tone only affects the neck so the head hangs limp, but sometimes the whole body seems to be limp as in flaccid paralysis. Have seizures like this been seen in others and have they been investigated? Are these Focal Atonic Seizures?
I am currently working on a paper, i have a population of patients with epilepsy and i would like to divide them according to the weight of seizure activity. every one underwent 10-20 stEEG, most of them did also a 24H eeg.
Many of these patients had 2-3 seizures in their life and are drug responders, thus it is hard to divide them in sub-groups according to seizure frequency.
I was wondering if there is a published reliable method to weight stEEG abnormalities (egs n spikes) in a semiquantitative way.
Hello, dear friends.
I have a patient (boy, 6 years old) with a severe epileptic syndrome, which leads to the seizures with tendency to status epilepticus. I observe him for a long time, and I've noticed one interesting phenomenon. After the severest seizures, which end in emergency service, his physical and mental development goes up exponentially.
For example. A week ago he tried to learn to write the cyrillic letter D (see the image 1; the uper inscriptions are the examples). Very poor. Then was the severe seizure, and he didn't try the exercises at all for a week, and today he has taken the paper and written the letter at his own initiative. Now it looks like very good inscription of prescholar (see the image 2).
Other example. A week ago he tried to read, but couldn't understand how to prononce syllables. And today he amazed his parents as he started to prononce good syllables of Consonant-Vowel pattern. It looks like the new grammatical rule arose in his neuronets.
And there are lots of other examples of such behaviour from the beginning of his illness. Not only this particular case. What could be the reason of this? Could you please give me some clues or link what to read on this theme? Thank you.
Patients with Arachnoid cysts or meningioma at the skull base display to some extent epilepsy; how many did observe this?
I'm looking for chemical or physiological parameters (which can be measured) that change minutes or seconds before an epilepsy crisis. In other terms, what are the chemical, biological and physiological changes that occur just before an epilepsy crisis ?
Perampanel or PER (noncompetitive α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor antagonist) is currently used for the treatment of primary generalized tonic-clonic seizures (pGTCS) in idiopathic generalized epilepsy (the term ‘idiopathic generalized epilepsy’ has been replaced by ‘electroclinical syndrome’). It has been noticed that pGTCS are reduced effectively by PER with good tolerability and without aggravating absence seizures/ or myoclonic seizures.
However, although animal model studies do not reveal teratogenic effects, why PER is not recommended for young childbearing age women without contraception?
i will work by EEG signal for diagnosis epilepsy disease and for it i need to collect EEG signal data base.please help me anyone that work in this field recently.
I m studying on experimental models of epilepsy especially chemical model with PTZ. I want to calculate seizure thresholds. Please give me clear information about it.
Do you know anything about possible interactions between proline and mGluR5 glutamate receptor ? I have found that proline interferes with other glutamate receptors, but nothing about mGluR5, but it is possible because I am moving in a field where I do not have sufficient confidence.
Eg... These results suggest that endogenous extracellular proline regulates the basal function of some glutamate synapses by maintaining them in a partially potentiated state... and more
However, do you think that "bona fide" can this also be possible for mGluR5 glutamate receptor ? It would be interesting to know if in mice, generated for this work, there is some anomaly in the proline and glutamate metabolism.
All this for the intriguing and elegant article reported here
If I would like to provide energy to a brain using dietary MCT's in humans, which MCT would be most efficient for doing that, the C8 or C10-containing MCT's? Are there any known biochemical or physiological differences at all between the two?
What are the current state-of-the-art techniques to detect and manage brain seizures (e.g. Epilepsy)? and what are their Pros and Cons?
I'm doing research to the influence of activities on epilepsie. I am working at a epilepsy centre in Holland. On a daily bases I am providing activities for people with a mental disability and epilepsy.
It is known that contraceptives (mainly estrogen part) increases the metabolism of certain AEDs and vice versa, and hence, there is an extreme need of more research for searching non-enzyme-inducing AEDs effective for women with epilepsy and intractable epilepsy in women related to menstrual cycle.
Would you suggest the adolescent and young women with epilepsy (WWE) for considering the option of non-enzyme-inducing AEDs as long-term antiepileptic treatment, where applicable?
Hi all! I have some MR spectroscopy data from epileptic patients and normal cases. I want to compare the metabolite rates in normal cases and 2 types of focal and generalized epilepsy. I need to be able to review the data and import the values into MATLAB. I'm not able to open data in MATLAB. Do you know of any toolbox or function to help with this?
Thanks in advance
In different literature it has been concluded that there is a significant inverse correlation between SUV_mean and ADC_mean.
I need to know about metabolic energy in different parts of tumor (qualitatively of semi-quantitatively) but I only have Average diffusion coefficient maps. Since FDG-SUV is related to metabolic energy somehow and since there is an inverse but significant correlation between SUV and ADC, I wonder if I can use ADC maps for mapping tumor's activity or not? (For example in parts with lower ADC, I assume higher SUV (activity) vice versa)
Any help would be appreciated.
Thanks in advance.