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1.
Braz. j. biol ; 83: e237412, 2023. tab, graf
Article in English | LILACS, VETINDEX | ID: biblio-1355854

ABSTRACT

Abstract Only few studies have focus on animals that received Pilocarpine (Pilo) and did not develop behavioral status epilepticus (SE) and, whether they may become epileptic in the model's chronic phase. Previews works observed mossy fiber sprouting in the hippocampus of Non-SE (NSE) rats, while others observed spontaneous and recurrent seizures (SRS) 6 - 8 months after animals received Pilo. It is known that neuronal excitability is influenced by female hormones, as well as, the occurrence of SE in castrated and non-castrated female rats. However, it is not known whether females that received Pilo and did not show SE, may have SRS. The aim of this work was to investigate whether castrated and non-castrated female rats that did not show behavioral SE after Pilo, will develop SRS in the following one-year. For that, animals received 360 mg/kg of Pilo and were video monitored for 12 months. SE females from castrated and non-castrated groups became epileptic since the first month after drug injection. Epileptic behaviors were identified watching video monitoring recordings in the fast speed. Castrated and Non-castrated NSE animals showed behaviors resembling seizures described by Racine Scale stages 1 - 3. Motor alterations showed by NSE groups could be observed only when recordings were analyzed in slow speed. In addition, behavioral manifestations as, rhythmic head movements, sudden head movements, whole body movements and immobility were also observed in both, SE and NSE groups. We concluded that NSE female rats may have become epileptic. Adding to it, slow speed analysis of motor alterations was essential for the observation of NSE findings, which suggests that possibly many motor alterations have been underestimated in epilepsy experimental research.


Resumo Poucos são os estudos com foco em animais que receberam Pilocarpina (Pilo) e não desenvolveram status epilepticus (SE) comportamental e, se os mesmos se tornarão epilépticos na fase crônica do modelo. Autores observaram o brotamento das fibras musgosas no hipocampo de ratos Não-SE (NSE), enquanto outros observaram crises espontâneas e recorrentes (CER) 6 - 8 meses após receberam a droga. A excitabilidade neuronal é influenciada pelos hormônios femininos e, da mesma forma, a ocorrência de SE em ratas castradas e não-castradas. Entretanto, não é sabido se as fêmeas que não apresentam SE terão CER. O objetivo deste trabalho foi investigar se fêmeas castradas e não castradas que não tiveram SE comportamental após a injeção de Pilo desenvolverão CER dentro de um ano. Para isto, os animais receberam 360 mg/kg de Pilo e foram videomonitorados por 12 meses. As fêmeas SE castradas e não-castradas se tornaram epilépticas desde o primeiro mês pós Pilo. O comportamento epiléptico foi identificado assistindo as gravações na velocidade rápida. As fêmeas NSE castradas e não-castradas apresentaram comportamentos similares aos estágios 1 - 3 da Escala de Racine. As alterações motoras nestes grupos (NSE) foram observadas apenas quando as videomonitoração foi analisada na velocidade lenta. Além destas, manifestações comportamentais como movimentos rítmicos da cabeça, movimentos súbitos da cabeça, movimentos de todo o corpo e imobilidade também foram observadas em ambos grupos, SE e NSE. Concluímos que as fêmeas NE podem ter se tornado epilépticas. Adicionado a isto, a análise das alterações motoras na velocidade lenta foi essencial para a observação dos achados das fêmeas NSE, o que sugere que possivelmente muitas alterações motoras têm sido subestimados na pesquisa em epilepsia experimental.


Subject(s)
Animals , Female , Rats , Pilocarpine/toxicity , Seizures/chemically induced , Status Epilepticus/chemically induced , Rats, Wistar , Muscarinic Agonists/toxicity , Models, Theoretical
2.
J Transl Med ; 20(1): 406, 2022 Sep 05.
Article in English | MEDLINE | ID: mdl-36064418

ABSTRACT

BACKGROUND: Glucocorticoid signalling is closely related to both epilepsy and associated cognitive impairment, possibly through mechanisms involving neuronal apoptosis. As a critical enzyme for glucocorticoid action, the role of 11ß-hydroxysteroid dehydrogenase 1 (11ß-HSD1) in epileptogenesis and associated cognitive impairment has not previously been studied. METHODS: We first investigated the expression of 11ß-HSD1 in the pentylenetetrazole (PTZ) kindling mouse model of epilepsy. We then observed the effect of overexpressing 11ß-HSD1 on the excitability of primary cultured neurons in vitro using whole-cell patch clamp recordings. Further, we assessed the effects of adeno-associated virus (AAV)-induced hippocampal 11ß-HSD1 knockdown in the PTZ model, conducting behavioural observations of seizures, assessment of spatial learning and memory using the Morris water maze, and biochemical and histopathological analyses. RESULTS: We found that 11ß-HSD1 was primarily expressed in neurons but not astrocytes, and its expression was significantly (p < 0.05) increased in the hippocampus of PTZ epilepsy mice compared to sham controls. Whole-cell patch clamp recordings showed that overexpression of 11ß-HSD1 significantly decreased the threshold voltage while increasing the frequency of action potential firing in cultured hippocampal neurons. Hippocampal knockdown of 11ß-HSD1 significantly reduced the severity score of PTZ seizures and increased the latent period required to reach the fully kindled state compared to control knockdown. Knockdown of 11ß-HSD1 also significantly mitigated the impairment of spatial learning and memory, attenuated hippocampal neuronal damage and increased the ratio of Bcl-2/Bax, while decreasing the expression of cleaved caspase-3. CONCLUSIONS: 11ß-HSD1 participates in the pathogenesis of both epilepsy and the associated cognitive impairment by elevating neuronal excitability and contributing to apoptosis and subsequent hippocampal neuronal damage. Inhibition of 11ß-HSD1, therefore, represents a promising strategy to treat epilepsy and cognitive comorbidity.


Subject(s)
Cognitive Dysfunction , Epilepsy , 11-beta-Hydroxysteroid Dehydrogenase Type 1/genetics , 11-beta-Hydroxysteroid Dehydrogenase Type 1/metabolism , Aging , Animals , Apoptosis , Cognitive Dysfunction/complications , Epilepsy/complications , Epilepsy/genetics , Glucocorticoids , Maze Learning/physiology , Mice , Seizures/genetics
3.
Yakugaku Zasshi ; 142(9): 1031-1035, 2022.
Article in Japanese | MEDLINE | ID: mdl-36047215

ABSTRACT

Lacosamide is a novel antiepileptic drug. Although many antiepileptic drugs reportedly pose a risk to fetuses, patients with epilepsy are advised to continue their medications during pregnancy. There have been few reports on lacosamide use during pregnancy, and its effects on the fetus remain unclear. Here, we report a case of lacosamide use during pregnancy. The 33-year-old patient was treated with oral lacosamide (400 mg/d) for symptomatic partial epilepsy. She was concomitantly treated with folic acid (5 mg/d) beginning 4 days before her last menstrual cycle. She was also concomitantly treated with oral perampanel (2 mg/d) at 5-7 weeks' gestation for seizure control but discontinued perampanel after the pregnancy was discovered. She progressed through her pregnancy with only mild seizures. Fetal growth was normal and ultrasonography revealed no external malformations. The patient had an elective cesarean section at 37 weeks and 2 days owing to a previous post-cesarean pregnancy. Her baby boy weighed 3025 g; his Apgar score was 8 and 9, 1 and 5 min, respectively, and his umbilical artery blood pH was 7.348. He had no congenital anomalies and no neonatal drug withdrawal symptoms. This suggests that lacosamide may have a low risk of teratogenicity and fetal toxicity. Thus, this case is valuable for clinicians who are considering the administration of antiepileptic drugs during pregnancy. In the future, more reports on the use of lacosamide during pregnancy should be collected.


Subject(s)
Anticonvulsants , Epilepsy , Adult , Anticonvulsants/adverse effects , Cesarean Section , Epilepsy/chemically induced , Epilepsy/drug therapy , Female , Humans , Infant , Lacosamide/adverse effects , Male , Pregnancy , Seizures/chemically induced , Treatment Outcome
4.
Front Neural Circuits ; 16: 901334, 2022.
Article in English | MEDLINE | ID: mdl-36051473

ABSTRACT

Objective: Sudden Unexpected Death in Epilepsy (SUDEP) accounts for 20% of mortality in those with recurrent seizures. While risk factors, monitoring systems, and standard practices are in place, the pathophysiology of SUDEP is still not well understood. Better knowledge of SUDEP and its potential mechanisms of action is crucial to reducing risk in this patient population and developing potential treatment options. Clinical studies and animal models of SUDEP suggest that diminished post-ictal respiratory control may be the dominant mechanism contributing to mortality. Recently, it was demonstrated that the depletion of the neuropeptide galanin in the amygdala occurs in human SUDEP. The amygdala plays a key role in the central integration of respiratory signaling; the depletion of galanin may represent a critical change that predisposes individuals to SUDEP. Materials and methods: To evaluate the impact of enhancing galaninergic signaling to potentially protect against SUDEP, we studied seizure-induced respiratory arrest (S-IRA) following central (intracerebroventricular, intra-amygdala) and systemic (intraperitoneal, subcutaneous) administration of galanin analogs. Seizure naïve and seizure experienced (fully kindled) mice were tested. Results: Central and systemically administered galanin analogs protect against S-IRA in naïve C57Bl/6J mice. Differential efficacy between receptor subtype-selective analogs varied based on the route of administration. Sub-chronic systemic administration at doses that reduced 6 Hz seizures also protected against S-IRA. Acute treatment benefits also extended to fully kindled mice experiencing tonic extension. Significance: These data demonstrate that galanin analogs may be protective against post-ictal respiratory collapse.


Subject(s)
Sudden Unexpected Death in Epilepsy , Animals , Death, Sudden/etiology , Death, Sudden/prevention & control , Galanin/pharmacology , Galanin/therapeutic use , Humans , Mice , Mice, Inbred C57BL , Seizures/drug therapy
5.
Medicina (B Aires) ; 82 Suppl 3: 7-12, 2022 Aug 30.
Article in Spanish | MEDLINE | ID: mdl-36054850

ABSTRACT

The prevalence of true drug-resistant epilepsy (DRE) in the general population is about 20%. The International League Against Epilepsy (ILAE) working group defined DRE as the failure of seizure control by adequate trials of two well-tolerated and appropriately selected drugs, either in monotherapy or in combination. DREs can be divided into two broad categories: pseudo drug-resistant (DR) and true DR. Pseudo DRE correspond to those that are incorrectly treated due to patient error, healthcare deficiencies, or physician error or omission. Errors on the part of the patient are irregular compliance with the intake of antiseizure medications (ASMs) such as inadequate time distribution of the ASMs and an unhealthy lifestyle. Healthcare deficiencies are related, for example, to the poor quality of some drugs in patients who stop receiving original drugs and switch to generic drugs. Regarding omissions or errors by physicians, it is important to note that a significant group of patients referred to the clinic as having DRE may have non-epileptic paroxysmal disorders, including functional seizures, errors in the recognition of the type of seizures and epileptic syndromes as well as etiology, and inadequate management of the ASMs and other treatments We consider it essential to systematically study patients with DRE in a multidisciplinary team and we believe that a considerable number of patients will benefit from an early correct diagnosis and adequate comprehensive treatment.


La prevalencia de las verdaderas epilepsias farmacorresistentes (EFR) en la población general es el 20% aproximadamente. El grupo de trabajo perteneciente a la International League Against Epilepsy definió a las EFR como la falla en el control de las crisis al tratamiento con dos fármacos bien tolerados y adecuadamente seleccionados, en monoterapia o en combinación. Las EFR pueden dividirse en dos grandes categorías: las pseudo resistentes a los fármacos (RF) y las verdaderamente RF. Las epilepsias pseudo RF corresponden a aquellas que son incorrectamente tratadas debido a errores por parte del paciente, por deficiencias sanitarias y por error u omisión del médico. Los errores por parte del paciente son el cumplimiento irregular de la toma de los fármacos anticonvulsivos (FACs) como la distribución horaria inadecuada y una vida desordenada. Las deficiencias sanitarias corresponden por ejemplo a una mala calidad en algunos fármacos en pacientes que dejan de recibir medicamentos originales y pasan a ingerir drogas genéricas. En relación a una omisión o error de los médicos, es importante destacar que un grupo importante de pacientes remitidos a la consulta como portadores de EFR, pueden presentar trastornos paroxísticos no epilépticos incluidas crisis funcionales, errores en el reconocimiento del tipo de crisis y síndromes epilépticos como la etiología y un manejo inadecuado de los FACs y otros tratamientos. Consideramos imprescindible el estudio sistemático de los pacientes con EFR a través de un equipo multidisciplinario, por lo cual creemos que un número considerable de pacientes se beneficiarán si se realiza un diagnóstico correcto temprano y un tratamiento integral adecuado.


Subject(s)
Drug Resistant Epilepsy , Epilepsy , Child , Drug Resistant Epilepsy/diagnosis , Drug Resistant Epilepsy/drug therapy , Epilepsy/drug therapy , Epilepsy/epidemiology , Humans , Prevalence , Seizures
6.
Medicina (B Aires) ; 82 Suppl 3: 13-18, 2022 Aug 30.
Article in Spanish | MEDLINE | ID: mdl-36054851

ABSTRACT

The International League Against Epilepsy (ILAE) recently socialized the proposed classification for epileptic syndromes of neonatal onset and up to the first 2 years of age, dividing them into self-limited epileptic syndromes and epileptic and developmental encephalopathies (DEEs). In this review we will focus on DEEs, defined as disorders in which there is developmental impairment related to both the underlying aetiology independent of epileptiform activity and epileptic encephalopathy. These include early infantile epileptic encephalopathy or Ohtahara syndrome and early myoclonic encephalopathy in the neonatal period, now grouped under the name of epileptic and early childhood developmental encephalopathies (EIDEE). Infantile epileptic spasms syndrome, childhood epilepsy with migratory crises and Dravet syndrome are part of the infant-onset encephalopathies. The importance of early recognition of epileptic encephalopathies lies not only in the control of epileptic seizures, but also in stopping deterioration by trying to change the course of the disease. It is essential to know the etiology, avoiding medications that can exacerbate seizures and worsen the course, applying precision m edicine as well as identifying candidate patients for early epilepsy surgery.


Recientemente la Liga Internacional contra la Epilepsia (ILAE) socializó la clasificación propuesta para síndromes epilépticos de inicio neonatal y hasta los primeros 2 años de edad, dividiéndolos en síndromes epilépticos autolimitados y las encefalopatías epilépticas y del desarrollo (DEEs). En esta revisión nos dedicaremos a las DEEs, definidas como trastornos donde existe deterioro del desarrollo relacionado tanto con la etiología subyacente independiente de la actividad epileptiforme como con la encefalopatía epiléptica. Estas incluyen en el período neonatal la encefalopatía epiléptica infantil temprana o síndrome de Ohtahara y la encefalopatía mioclónica temprana, ahora agrupadas bajo la denominación de encefalopatías epilépticas y del desarrollo infantil temprano (EIDEE). El síndrome de espamos epilépticos infantiles, la epilepsia de la infancia con crisis migratorias y el síndrome de Dravet forman parte de las encefalopatías de inicio en el lactante. La importancia del reconocimiento temprano de las encefalopatías epilépticas radica no solo en el control de las crisis epilépticas, sino en detener el deterioro intentando cambiar el curso de la enfermedad. Es fundamental conocer la etiología evitando medicamentos que puedan exacerbar las crisis y empeorar el curso, aplicando medicina de precisión así como identificando pacientes candidatos a cirugía temprana de epilepsia.


Subject(s)
Brain Diseases , Epilepsy , Epileptic Syndromes , Spasms, Infantile , Child, Preschool , Electroencephalography , Epilepsy/diagnosis , Epilepsy/etiology , Humans , Infant , Infant, Newborn , Seizures , Spasms, Infantile/diagnosis , Spasms, Infantile/etiology
7.
Medicina (B Aires) ; 82 Suppl 3: 19-24, 2022 Aug 30.
Article in Spanish | MEDLINE | ID: mdl-36054852

ABSTRACT

Non-epileptic paroxysmal events (NEPE) are defined as episodes of sudden onset and short duration that mimic an epileptic seizure, caused by a brain dysfunction of diverse origin and, unlike epilepsy, are not due to excessive neuronal discharge. Its incidence is much higher than epilepsy and can appear at any age, but are more frequent in the first years of life. The immaturity of the central nervous system in childhood favors that in this period the clinical manifestations are more spectacular and different from other ages. Normal and common phenomena in children can also be confused with epileptic seizures. The first step for a correct diagnosis is to establish whether this first episode corresponds to an epileptic seizure or could be a first episode of NEPE. It is important to follow a diagnostic protocol, assessing the personal and family history, without forgetting the physical examination, analyzing the possible triggering factors, the details of each episode, if it's possible a record of the episodes, applying common sense and experience and only carrying out basic complementary tests such as EEG recording or others in case of doubt or for diagnostic confirmation. In some cases, a genetic basis has been demonstrated. Therapeutic options are scarce and the majority of NEPE have a favorable evolution.


Los eventos paroxísticos no epilépticos (EPNE) 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 y 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, pero son más frecuentes en los primeros años de vida. La inmadurez del sistema nervioso central en la infancia favorece que en este período las manifestaciones clínicas sean muy floridas y diferentes de otras edades. Fenómenos normales y comunes en el niño pueden también confundirse con crisis epilépticas. El primer paso para un diagnóstico correcto es establecer si este primer episodio corresponde a una crisis epiléptica o puede tratarse de un primer episodio de EPNE. Es importante seguir un protocolo de diagnóstico, valorando los antecedentes personales y familiares, sin olvidar el examen físico, analizar los posibles factores desencadenantes, los pormenores de cada episodio, si es posible un registro de los episodios, aplicar el sentido común y la experiencia y solamente proceder a los exámenes complementarios básicos como el registro EEG u otras exploraciones en caso de duda o para confirmación diagnóstica. En algunos casos se ha demostrado una base genética. Las opciones terapéuticas son escasas y la mayoría de EPNE tienen una evolución favorable.


Subject(s)
Electroencephalography , Epilepsy , Child , Diagnosis, Differential , Epilepsy/diagnosis , Humans , Seizures/diagnosis
8.
J Law Med ; 29(3): 707-713, 2022 Aug.
Article in English | MEDLINE | ID: mdl-36056661

ABSTRACT

This column provides an overview of how courts have taken into account seizures and postictal states in terms of assigning criminal responsibility. In England, New Zealand and Australia, courts have generally treated evidence of epileptic seizures and postictal states as raising the defence of mental impairment which often results in indefinite detention. In comparison, there is a series of Canadian cases that have resulted in acquittals after evidence of seizures has been accepted as negating voluntariness or the fault element of the offence. It appears that policy issues have been influential in the Canadian cases, particularly a reluctance to equate epilepsy with "mental disorder".


Subject(s)
Criminals , Epilepsy , Psychotic Disorders , Canada , Humans , Seizures
9.
BMC Anesthesiol ; 22(1): 280, 2022 09 02.
Article in English | MEDLINE | ID: mdl-36056318

ABSTRACT

BACKGROUND: Dexmedetomidine was found to be protective against traumatic brain injury (TBI) in animal studies and safe for use in previous clinical studies, but whether it improves TBI patient survival remains to be determined. We sought to answer this question by analyzing data from the MIMIC clinical database. METHODS: Data for TBI patients from the MIMIC III and MIMIC IV databases were extracted and divided into a dexmedetomidine group and a control group. In the former group, dexmedetomidine was used for sedation, while in the latter, it was not used. Parameters including patient age, the Acute Physiology score III, the Glasgow Coma Scale, other sedatives used, and pupillary response within 24 h were employed in propensity score matching to achieve a balance between groups for further analysis. In-hospital survival and 6-month survival were analyzed by Kaplan-Meier survival analysis and compared by log-rank test. Cox regression was used repeatedly for the univariate analysis, the multivariate analysis, the propensity score-matched analysis, and the inverse probability of treatment weighted analysis of survival data. Meanwhile, the influences of hypotension, bradycardia, infection, and seizure on outcome were also analyzed. RESULTS: Different types of survival analyses demonstrated the same trend. Dexmedetomidine significantly improved TBI patient survival. It caused no more incidents of hypotension, infection, and seizure. Hypotension was not correlated with in-hospital mortality, but was significantly correlated with 6-month mortality. CONCLUSIONS: Dexmedetomidine may improve the survival of TBI patients. It should be used with careful avoidance of hypotension.


Subject(s)
Brain Injuries, Traumatic , Brain Injuries , Dexmedetomidine , Hypotension , Brain Injuries, Traumatic/drug therapy , Dexmedetomidine/therapeutic use , Glasgow Coma Scale , Humans , Hypotension/drug therapy , Propensity Score , Seizures
11.
Comput Biol Med ; 149: 106053, 2022 Oct.
Article in English | MEDLINE | ID: mdl-36108415

ABSTRACT

Epilepsy is a disorder of the brain denoted by frequent seizures. The symptoms of seizure include confusion, abnormal staring, and rapid, sudden, and uncontrollable hand movements. Epileptic seizure detection methods involve neurological exams, blood tests, neuropsychological tests, and neuroimaging modalities. Among these, neuroimaging modalities have received considerable attention from specialist physicians. One method to facilitate the accurate and fast diagnosis of epileptic seizures is to employ computer-aided diagnosis systems (CADS) based on deep learning (DL) and neuroimaging modalities. This paper has studied a comprehensive overview of DL methods employed for epileptic seizures detection and prediction using neuroimaging modalities. First, DL-based CADS for epileptic seizures detection and prediction using neuroimaging modalities are discussed. Also, descriptions of various datasets, preprocessing algorithms, and DL models which have been used for epileptic seizures detection and prediction have been included. Then, research on rehabilitation tools has been presented, which contains brain-computer interface (BCI), cloud computing, internet of things (IoT), hardware implementation of DL techniques on field-programmable gate array (FPGA), etc. In the discussion section, a comparison has been carried out between research on epileptic seizure detection and prediction. The challenges in epileptic seizures detection and prediction using neuroimaging modalities and DL models have been described. In addition, possible directions for future works in this field, specifically for solving challenges in datasets, DL, rehabilitation, and hardware models, have been proposed. The final section is dedicated to the conclusion which summarizes the significant findings of the paper.


Subject(s)
Deep Learning , Epilepsy , Algorithms , Electroencephalography/methods , Epilepsy/diagnostic imaging , Humans , Neuroimaging , Seizures/diagnostic imaging
12.
Behav Neurol ; 2022: 1142215, 2022.
Article in English | MEDLINE | ID: mdl-36134035

ABSTRACT

Acceptance of illness is regarded as an indicator of functioning and predictor of quality of life. However, quality of life of patients with epilepsy in sub-Saharan countries worsen because of low medication adherence, increased morbidity and mortality, and the stigmatization associated with the disease. This research is aimed at assessing the level of acceptance of illness of patients with epilepsy and associated quality of life in North-East Ethiopia. Methods. A cross-sectional study was conducted from January to June 2021 at the Debre Berhan Referral Hospital, North-East Ethiopia. A total of 78 patients with epilepsy aged more than 18 years were randomly selected and assessed using Quality of Life in Epilepsy Inventory 31 and acceptance of illness scale. In addition, authors owned questionnaire were used to evaluate the sociodemographic and clinical characteristics of the patients. P value < 0.05 at 95% confidence level was considered to be statistically significant in all the analysis. Result. The study participants' age varied between 18 and 67 years with the mean age of 28.9 years. Phenobarbital was the most used (73.9%) antiepileptic drug, and 68.7% (n = 66) of the patients seizure was controlled. 72.9% (n = 70) of the patients had medium acceptance of illness (scored 20-30), while 17.7% (n = 17) had low illness acceptance level (scored 8-19), and 9.4% (n = 9) had high acceptance of illness (scored 31-40). The mean of overall acceptance of illness among epileptic patients was 21.04 ± 7.21. The overall score of QOLIE-31 was 79.14 ± 25.46, and the highest mean score was for cognitive (83.5 ± 27.1), while the lowest mean score was that of medication effect (72.7 ± 28.7). Five of the seven QOLIE-31 components correlated significantly with level of acceptance of illness. Cognitive domain (r = 0.498, p < 0.001) demonstrated the highest correlation followed by overall quality of life (r = 0.489, p < 0.001), seizure worry (r = 0.433, p < 0.001), energy/fatigue (r = 0.342, p < 0.001), and emotional well-being (r = 0.278, p < 0.001). Conclusion. Patients with epilepsy in the study area had medium acceptance of illness, and nearly half of them had mean and more than the mean quality of life. The patients' acceptance of illness was significantly associated with overall quality of life, seizure worry, emotional well-being, and cognitive domain of the patients.


Subject(s)
Epilepsy , Quality of Life , Adult , Anticonvulsants/therapeutic use , Cross-Sectional Studies , Epilepsy/psychology , Ethiopia , Humans , Phenobarbital , Quality of Life/psychology , Seizures/drug therapy , Surveys and Questionnaires
14.
Orphanet J Rare Dis ; 17(1): 355, 2022 Sep 14.
Article in English | MEDLINE | ID: mdl-36104799

ABSTRACT

BACKGROUND: Facial angiofibroma is the most predominant cutaneous manifestation of tuberous sclerosis complex (TSC), a rare autosomal dominant genetic disorder impacting the mechanistic target of rapamycin (mTOR). Facial angiofibroma can bleed spontaneously, impair eyesight, and cause aesthetic disfiguration causing psychological and social stress. To date, there is little or no evidence on the demographics, and other TSC features associated with facial angiofibroma or the use of mTOR inhibitor for the management of facial angiofibroma. This is a retrospective study of TSC Alliance's Natural History Database aimed to characterize facial angiofibroma and to evaluate features associated with a higher risk of facial angiofibroma or the use of topical mTOR inhibitors for the management of facial angiofibroma. Data in the NHD was obtained from 18 clinical sites in the US since 2006. RESULTS: Of the 2240 patients, 2088 patients were enrolled in the US and data from 2057 patients were included in this analysis. The mean (median) age of overall TSC patients was 22.4 (19.0) years. A total of 69 patients were ≤ 5 years of age. Facial angiofibroma was noted in 1329 (64.6%) patients with TSC. Patients with facial angiofibroma were older on average (Mean: 25.9 [median, 23.0] vs. 16.0 [12.4 years] years, p < 0.0001). In patients with vs. without facial angiofibroma, TSC2 mutation (38.9% vs. 34.8%) was more common than TSC1 mutation (12.3% vs. 18.1%), and the incidence rate of most of the other TSC-related manifestations was significantly higher in patients with facial angiofibroma. Majority of patients had focal seizures (72.8% vs. 60.7%), followed by angiomyolipoma (63.7% vs. 21.8%) and renal cysts (59.4% vs. 33.5%). The age groups, 11-17 (odds ratio [OR], 2.53) and 18-45 years (5.98), TSC2 mutation (1.31), focal seizures (1.50), ADHD (1.47) angiomyolipoma (2.79), and renal cysts (2.63) were significantly associated with a higher risk of facial angiofibroma based on multivariate logistic regression. Abrasive or laser therapy was used by 17.1% and 2.6% patients, respectively. Topical mTOR inhibitor use was noted for 329 (24.8%) patients with facial angiofibroma. Overall systemic mTOR inhibitor use was observed in 399 (30.0%) patients for management of one or more TSC manifestations. Use of systemic mTOR inhibitor for facial angiofibroma was noted for 163 (12.3%) patients, among whom only 9 (0.7%) patients used exclusively for the management of facial angiofibroma. Of the patients with facial angiofibroma, 44.6% did not receive any treatment. Significantly higher use of topical mTOR inhibitor was associated with the 11-17 years age group (OR, 1.67), anxiety (1.57), angiomyolipoma (1.51), and renal cysts (1.33). CONCLUSIONS: The presence of TSC2 mutations and most other TSC-related manifestations was significantly higher in patients with facial angiofibroma. About one-fourth of patients with facial angiofibroma used a topical mTOR inhibitor and use of systemic mTOR inhibitor for the management of facial angiofibroma or for the other manifestations was noted for 30.0%. About 44.6% of patients did not receive any treatment for the management of facial angiofibroma.


Subject(s)
Angiomyolipoma , Kidney Diseases, Cystic , Kidney Neoplasms , Tuberous Sclerosis , Adult , Angiomyolipoma/drug therapy , Carotenoids , Humans , Immunosuppressive Agents/therapeutic use , Kidney Neoplasms/complications , MTOR Inhibitors , Retrospective Studies , Seizures/drug therapy , Sirolimus/therapeutic use , Tuberous Sclerosis/complications , Tuberous Sclerosis/drug therapy , Tuberous Sclerosis/genetics , United States , Vitamin A/analogs & derivatives , Young Adult
15.
FASEB J ; 36(10): e22554, 2022 Oct.
Article in English | MEDLINE | ID: mdl-36111973

ABSTRACT

Mesial temporal lobe epilepsy (MTLE) is one of the most common refractory epilepsies and is usually accompanied by a range of brain pathological changes, such as neuronal injury and astrocytosis. Naïve astrocytes are readily converted to cytotoxic reactive astrocytes (A1) in response to inflammatory stimulation, suppressing the polarization of A1 protects against neuronal death in early central nervous system injury. Our previous study found that pro-inflammatory cytokines and miR-132-3p (hereinafter referred to as "miR-132") expression were upregulated, but how miR-132 affected reactive astrocyte polarization and neuronal damage during epilepsy is not fully understood. Here, we aimed to explore the effect and mechanism of miR-132 on A1 polarization. Our results confirmed that A1 markers were significantly elevated in the hippocampus of MTLE rats and IL-1ß-treated primary astrocytes. In vivo, knockdown of miR-132 by lateral ventricular injection reduced A1 astrocytes, neuronal loss, mossy fiber sprouting, and remitted the severity of status epilepticus and the recurrence of spontaneous recurrent seizures. In vitro, the neuronal cell viability and axon length were reduced by additional treatment with A1 astrocyte conditioned media (ACM), and downregulation of astrocyte miR-132 rescued the inhibition of cell activity by A1 ACM, while the length of axons was further inhibited. The regulation of miR-132 on A1 astrocytes may be related to its target gene expression. Our results show that interfering with astrocyte polarization may be a breakthrough in the treatment of refractory epilepsy, which may extend to the research of other astrocyte polarization-mediated brain injuries.


Subject(s)
Epilepsy, Temporal Lobe , MicroRNAs , Status Epilepticus , Animals , Astrocytes/metabolism , Culture Media, Conditioned/pharmacology , Epilepsy, Temporal Lobe/chemically induced , Epilepsy, Temporal Lobe/genetics , Epilepsy, Temporal Lobe/metabolism , Hippocampus/metabolism , MicroRNAs/metabolism , Rats , Seizures/metabolism , Status Epilepticus/chemically induced , Status Epilepticus/genetics , Status Epilepticus/metabolism
16.
Article in English | MEDLINE | ID: mdl-36063519

ABSTRACT

Electroencephalogram (EEG) based seizure subtype classification is very important in clinical diagnostics. However, manual seizure subtype classification is expensive and time-consuming, whereas automatic classification usually needs a large number of labeled samples for model training. This paper proposes an EEGNet-based slim deep neural network, which relieves the labeled data requirement in EEG-based seizure subtype classification. A temporal information enhancement module with sinusoidal encoding is used to augment the first convolution layer of EEGNet. A training strategy for automatic hyper-parameter selection is also proposed. Experiments on the public TUSZ dataset and our own CHSZ dataset with infants and children demonstrated that our proposed TIE-EEGNet outperformed several traditional and deep learning models in cross-subject seizure subtype classification. Additionally, it also achieved the best performance in a challenging transfer learning scenario. Both our code and the CHSZ dataset are publicized.


Subject(s)
Seizures , Signal Processing, Computer-Assisted , Child , Electroencephalography , Humans , Neural Networks, Computer
17.
BMC Neurol ; 22(1): 352, 2022 Sep 16.
Article in English | MEDLINE | ID: mdl-36114472

ABSTRACT

BACKGROUND: The cerebellum plays an important role in motor control, however, its involvement in epilepsy has not been fully understood. Arterial spin labelling perfusion magnetic resonance image (ASL) is a noninvasive method to evaluate cerebral and cerebellar blood flow. We investigated cerebellar perfusion in patients with epileptic seizures using ASL. METHODS: Adult patients with epileptic seizures who underwent ASL in three post labeling delay (PLD) conditions (1525, 1800, and 2500 msec) and conventional electroencephalography (EEG) on the same day were investigated. Clinical and EEG characteristics of them were retrospectively analyzed. RESULTS: Six patients (6 women, age; 36.2 ± 17.9 years (mean ± SD)) showed hyperperfusion in selective areas in the cerebellar paravermis of lobule VIIb. One patient with generalized epilepsy (tentative diagnosis of juvenile myoclonic epilepsy or epilepsy with myoclonic absences) showed unilateral hypoperfusion in PLD 1525 msec and hyperperfusion in PLD 1800 and 2500 msec at the area while EEG showed generalized spike-wave complexes. After successful treatment, these perfusion abnormalities disappeared. In two patients with focal epilepsy manifesting with asymmetrical motor symptoms, cerebellar hyperperfusion was found on the opposite side to the seizure focus estimated by seizure semiology. Besides hyperperfusion of the VIIb lobule, hypoperfusion at the same area was detected in shorter PLD condition in four patients and in longer PLD condition in one patient. CONCLUSION: The cerebellar paravermis of lobule VIIb can be a component of motor circuit and participate in epileptic network in humans. Cerebellar perfusion abnormalities can be associated with neurovascular coupling via capillary bed.


Subject(s)
Epilepsy , Seizures , Adolescent , Adult , Cerebellum/blood supply , Cerebellum/diagnostic imaging , Epilepsy/diagnostic imaging , Female , Humans , Middle Aged , Retrospective Studies , Spin Labels , Young Adult
18.
Open Vet J ; 12(4): 508-510, 2022.
Article in English | MEDLINE | ID: mdl-36118720

ABSTRACT

Background: Antiparasitic drug toxicosis is commonly described in dogs and cats, but reports on the management of antiparasitic drug toxicities in pet rabbits are scarce. Here, we describe the successful clinical management of two pet rabbits with fipronil toxicosis. Cases Description: The first case was a 5-month-old, intact female, rabbit that presented with the acute onset of seizures, obtunded mentation, and in lateral recumbency, while the second rabbit was a 1-year-old, intact male, rabbit that presented with anorexia and lethargy. In both cases, the owners reported to have administered a 0.5 ml fipronil vial topically on the skin as an antiparasitic drug between 4 and 6 hours prior to presentation. Complete blood count and serum biochemistry were unremarkable and both rabbits tested negative on Encephalitozoon cuniculi serology. Both animals were decontaminated by bathing with tepid water and dishwashing soap. The rabbit with seizures received on admission intravenous midazolam. In both cases, overnight hospitalization, intravenous isotonic crystalloid fluids, and assisted-feeding by oral syringe were provided until voluntary feeding was resumed. Both rabbits rapidly improved approximately 12 hours of initiating supportive care. Complete resolution of clinical signs and return of normal appetite and defecation occurred within 24 hours of hospitalization in both animals. No recurrence of neurological signs was reported in the rabbit presenting with seizures on a follow-up period of 1 month. Conclusion: The outcome of these cases suggests that supportive treatment of fipronil toxicity in pet rabbits can be successful if administered promptly.


Subject(s)
Cat Diseases , Dog Diseases , Animals , Antiparasitic Agents/therapeutic use , Cat Diseases/drug therapy , Cats , Crystalloid Solutions/therapeutic use , Dog Diseases/drug therapy , Dogs , Female , Male , Midazolam/therapeutic use , Pyrazoles , Rabbits , Seizures/chemically induced , Seizures/drug therapy , Seizures/veterinary , Soaps/therapeutic use
19.
Open Vet J ; 12(4): 445-450, 2022.
Article in English | MEDLINE | ID: mdl-36118733

ABSTRACT

Background: Idiopathic or genetic epilepsy commonly affects dogs; affected dogs are often refractory to anti-seizure drug therapy. Felbamate is an anti-seizure drug with established pharmacokinetic and safety data for dogs, but little published evidence of efficacy for managing generalized seizures in this species. Aim: The purpose of this retrospective case series was to evaluate the clinical efficacy and tolerability of oral felbamate in six presumptive epileptic dogs experiencing generalized seizures. Methods: Medical records from six dogs with presumptive idiopathic/genetic epilepsy manifesting as generalized seizure activity, for which oral felbamate was used as an add-on treatment, were reviewed. The number of seizures recorded for the 3-month period immediately before instituting felbamate was recorded for each dog. Short-term (3 months) and long-term (6 months or greater) seizure frequency post-felbamate therapy was recorded for each dog and compared with baseline. Results: Overall, dogs experienced a reduction (82%) in seizures after adding felbamate in the short term, with 5/6 dogs (83%) classified as responders (50% or greater reduction in seizures) and 3/6 dogs (50%) attaining seizure-free status. Mean and median long-term follow-up times were 13 and 11 months, respectively (range: 6 to 23 months). Four of the 6 dogs (67%) remained drug responders at final follow-up, with an average seizure reduction of 98%, 2 of which remained seizure-free at 8 and 21 months. Two dogs (33%) experienced increased seizure activity during long-term follow-up (12 and 23 months) and were considered non-responders. The non-responder dogs had an average long-term seizure reduction of 33%. No dog experienced any obvious adverse effects associated with felbamate administration. However, one dog not included in the analysis because of insufficient (<3 month) post-felbamate follow-up, was weaned off felbamate because of suspected hepatotoxicity. Conclusion: Our small case series suggests that oral felbamate might show promise as an add-on drug for epileptic dogs experiencing generalized seizures resistant to drug therapy. These results warrant a more controlled, prospective investigation into felbamate as a therapeutic agent for canine epilepsy.


Subject(s)
Dog Diseases , Epilepsy , Animals , Anticonvulsants/therapeutic use , Dog Diseases/etiology , Dogs , Epilepsy/drug therapy , Epilepsy/etiology , Epilepsy/veterinary , Felbamate/therapeutic use , Prospective Studies , Retrospective Studies , Seizures/chemically induced , Seizures/drug therapy , Seizures/veterinary
20.
Neurosurg Rev ; 45(5): 3291-3298, 2022 Oct.
Article in English | MEDLINE | ID: mdl-36097085

ABSTRACT

Postoperative seizures are a frequently occurring yet not well-understood complication in patients undergoing surgical treatment of chronic subdural haematomas (cSDHs). Therefore, we investigated surgical and non-surgical risk factors that are commonly considered causal in provoking epileptic seizures, paying special attention to the intracranial course of the subdural drain (SDD) and the configuration of the haematoma. Data of patients with a cSDH, that were treated at our neurosurgical department between 2008 and 2014 were analysed. Patients suffering from severe pre-existing conditions and those who have been treated conservatively were excluded. Epidemiologic data as well as relevant clinical data were collected. Pre- and postoperative CT scans were analysed regarding morpho- and volumetric parameters. In order to objectify the influence of the SDD, its intracranial course and localisation (entering angle as well as the angle between drain and brain surface) were measured. For statistical analysis, univariate and multiple logistic regression models as well as Fisher's exact test were used. Two hundred eleven consecutive patients have been included. Mean age was 75.6 years, and 69% were male. Nineteen (9%) patients suffered from postsurgical seizures. Membranes within the haematoma were present in 81.5%. Pre- to postoperative haematoma reduction was significant (mean of difference - 12.76 mm/ - 9.47 mm in coronal/axial CT planes, p = 0.001/ < 0.001). In 77.9%, SDD showed cortical contact with eloquent regions and had an unfavourable course in 30 cases (14.2%). Surgical complications consisted of cortical bleeding in 2.5%, fresh subdural haematoma in 33.5% and wound infections in 1.4% of patients. Neither in univariate nor in multiple regression analyses any of the following independent variates was significantly correlated with postsurgical seizures: pre-existing epilepsy, alcohol abuse, right-sided haematomas, localization and thickness of haematoma, presence of septations, SDD-localization and to-brain angle, subdural air, and electrolyte levels. Instead, in multiple regression analyses, we found the risk of postsurgical seizures to be significantly correlated and increased with left-sided cSDH treated via craniotomy (p = 0.03) and an unfavourable course of the SDD in left-sided cSDH (p = 0.033). Burr hole trepanation should be preferred over craniotomy and care must be taken when placing a SDD to avoid irritating cortical tissue. The configuration of the haematoma does not appear to affect the postoperative seizure rate.


Subject(s)
Hematoma, Subdural, Chronic , Aged , Drainage/adverse effects , Electrolytes , Female , Hematoma , Hematoma, Subdural, Chronic/etiology , Hematoma, Subdural, Chronic/surgery , Humans , Male , Postoperative Complications/epidemiology , Postoperative Complications/etiology , Risk Factors , Seizures/epidemiology , Seizures/etiology
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