Manifestation Of Epilepsy Research Articles

Ictal asystole as a manifestation of pure insular epilepsy

Life-threatening cardiac asystole has been reported as a rare manifestation of insular epilepsy [1]. However, previously reported cases were considered to have insular-origin seizures without invasive intracerebral recordings and therefore lacked certainty regarding the anatomo-electro-clinical correlations. We herein describe the first observation of ictal asystole evoked by pure insular seizures, which was proved by intracerebral EEG.

Proteomic signature of the Dravet syndrome in the genetic Scn1a-A1783V mouse model

BackgroundDravet syndrome is a rare, severe pediatric epileptic encephalopathy associated with intellectual and motor disabilities. Proteomic profiling in a mouse model of Dravet syndrome can provide information about the molecular consequences of the genetic deficiency and about pathophysiological mechanisms developing during the disease course. MethodsA knock-in mouse model of Dravet syndrome with Scn1a haploinsufficiency was used for whole proteome, seizure, and behavioral analysis. Hippocampal tissue was dissected from two- (prior to epilepsy manifestation) and four- (following epilepsy manifestation) week-old male mice and analyzed using LC-MS/MS with label-free quantification. Proteomic data sets were subjected to bioinformatic analysis including pathway enrichment analysis. The differential expression of selected proteins was confirmed by immunohistochemical staining. ResultsThe findings confirmed an increased susceptibility to hyperthermia-associated seizures, the development of spontaneous seizures, and behavioral alterations in the novel Scn1a-A1873V mouse model of Dravet syndrome. As expected, proteomic analysis demonstrated more pronounced alterations following epilepsy manifestation. In particular, proteins involved in neurotransmitter dynamics, receptor and ion channel function, synaptic plasticity, astrogliosis, neoangiogenesis, and nitric oxide signaling showed a pronounced regulation in Dravet mice. Pathway enrichment analysis identified several significantly regulated pathways at the later time point, with pathways linked to synaptic transmission and glutamatergic signaling dominating the list. ConclusionIn conclusion, the whole proteome analysis in a mouse model of Dravet syndrome demonstrated complex molecular alterations in the hippocampus. Some of these alterations may have an impact on excitability or may serve a compensatory function, which, however, needs to be further confirmed by future investigations. The proteomic data indicate that, due to the molecular consequences of the genetic deficiency, the pathophysiological mechanisms may become more complex during the course of the disease. As a result, the management of Dravet syndrome may need to consider further molecular and cellular alterations. Ensuing functional follow-up studies, this data set may provide valuable guidance for the future development of novel therapeutic approaches.

Intracranial correlates of small sharp spikes

ObjectiveTo identify cortical correlates of scalp small sharp spikes (SSS) using simultaneous scalp and intracranial EEG recordings. MethodsPatients were retrospectively evaluated based on a database of intracranial long-term recordings at the Epilepsy Center Freiburg. Inclusion criteria were: simultaneous recordings with intracranial and scalp EEGs and the presence of at least five unequivocal SSS in the scalp EEG.Intracranial recordings were analyzed regarding the co-occurring intracranial potentials during scalp SSS. Results33 patients, aged 9-60y, 17 females, fulfilled the above-mentioned criteria. Almost all patients had intracranial SSS correlates in the form of spike/polyspike-waves in the temporal lobe, predominantly in the hippocampus (24/28), less frequently involving the amygdala (5/29), temporal basal (3/18), lateral neocortical (4/32), entorhinal cortices (1/12), and the parietal lobe (2/13). Amplitudes of intrahippocampal spikes or polyspikes co-occurring with SSS were significantly higher than intracranial discharges without scalp correlates. In 45% of patients, intracranial spikes accompanying SSS were located within the seizure onset zone (SOZ). ConclusionsOur results strongly support an epileptic origin of SSS and provide evidence about their heterogenous generators. SignificanceThis study suggests that SSS cannot with certainty be classified as “benign” but rather considered as one of the EEG manifestations of focal epilepsy.

Knowledge and attitudes toward epilepsy among Libyan people with and without epilepsy in a tertiary medical center

BackgroundAlthough patients with epilepsy (PWE) constitute a considerable sector of the population in Benghazi, there is no adequate knowledge about this disease. ObjectivesTo assess knowledge and attitudes toward epilepsy among Libyan people who live in Benghazi city. MethodsA cross-sectional prospective hospital-based study was conducted in the year 2020, from June to August. The participants were adults, PWE were included as well as people without epilepsy (NEP).Participants were interviewed through a twelve-item questionnaire related to knowledge which included definition, causes, manifestations, first aids, treatment options, and curability. In addition, attitudes toward epilepsy were tested by questions that include immediate actions when seeing a patient seizing, and whether or not PWE can drive, work, marry, and conceive). Data analysisData were processed by the statistical software (SPSS) version 18.0. Differences between categorical variables were tested by Chi square and P value at 0.05, which has been considered statistically significant. ResultsThe total number of the interviewees was 156. The mean age was 43 ± 14 SD years (18–76 years), 105 (67%) were males.Twenty-eight (18%) of the participants were PWE, while the remaining 128 (82%) were NEP. Ninety-nine (64%) and 145 (92%) of the participants answered correctly regarding definition and manifestations of epilepsy, respectively. The participants with Bachelor degree and post graduate level have shown a better understanding of definitions and treatments of epilepsy (P = 0.000). They also had better attitudes toward PWE in terms of their ability to conceive (P = 0.002).PWE had better knowledge about manifestations and first aids of epilepsy compared to NEP, though they did not have differences in attitude compared to NEP. Participants’ knowledge about epilepsy was mainly obtained from friends (41; 26%), patients (40; 26%), and media (37; 24%). A major portion of participants 94 (60%) did not feel satisfactory about their own information about epilepsy. ConclusionKnowledge and attitudes toward epilepsy were generally satisfactory. Participants with Bachelor degree or higher level of education had better knowledge and positive attitudes toward PWE. Patients and media are important tools to improve knowledge and attitudes about epilepsy.

Neuromuscular Problems in the Patients With COVID-19: A Review Study

Purpose: SARS-CoV-2 is a member of the betacoronavirus genus that primarily targets the human respiratory system and causes pneumonia-like symptoms. This article aims to review neuromuscular problems in patients with COVID-19 based on the available evidence and possible consequences. Methods: This narrative review study gathered the related and newest studies published (without time limitation) about the neurological impairment of the coronavirus. Results: The studies showed that the patients with COVID-19 show a variety of respiratory symptoms and neuromuscular and neurological symptoms. The neurological symptoms associated with the underlying disease include headache, dizziness, disturbance of consciousness, ataxia, manifestations of epilepsy, stroke, peripheral nerve injury (like hypoadomia, hyposemia, neuralgia). The findings of this review study also reveal that there are a variety of neuromuscular symptoms in the affected patients. Besides, some specific changes in these symptoms have occurred since the emergence of this epidemic. Conclusion: Neurologists should pay more attention to the possible signs of direct and indirect involvement of the nervous system and its lasting effects, which might have been ignored in the acute phase of the disease.

Unusual drug-resistant psychotic state with epilepsy manifestations, cognitive deterioration and muscular atrophy - case report

Introduction This article will focus on the case of patient whose disease manifested after episode of dehydration at 16 years of age and within 8 years led to his death. During the eight years of illness, the patient suffered from polymorfic psychotic states accompanied by various types of epileptic seizures, including absence and grand-mal seizures, resistant to drug therapy. In addition, he suffered from multiple motor disorders, skeletal and mimiс muscle atrophy, as well as progressive cognitive decline from very high level of cognitive functions to level of moderate deterioration. Despite repeated evaluations, there was no unequivocal diagnosis of his disorder.ObjectivesMale, born in 1994, without a known hereditary pathology in the field of neurology or psychiatry. Pregnancy and childbirth proceeded without features and the early stages of cognitive-motor development were marked as normative, with the exception of a single epileptic seizure at the age of 3 years (according to the description of the parents). Until the age of 16, the patient was not under the supervision of a neurologist or psychiatrist, developed on a par with his peers, successfully attended school with high marks in the exact sciences, and went in for sports.MethodsCase reportResultsCase reportConclusionsA patient is considered with a non-standard course of psychosis and epilepsy, which was accompanied by multiple neurological and psychiatric symptoms.In Israel there are only 13 patients with a resemble clinical picture and there is no diagnosis or group of diagnoses in ICD, DSM or any neulogical classificatin tha can describe his disease.

The syndrome of transient epileptic amnesia: a combined series of 115 cases and literature review.

The term transient epileptic amnesia was coined in 1990 to describe a form of epilepsy causing predominantly amnestic seizures which could be confused with episodes of Transient Global Amnesia. Subsequent descriptions have highlighted its association with ‘atypical’ forms of memory disturbance including accelerated long-term forgetting, disproportionate autobiographical amnesia and topographical amnesia. However, this highly treatment-responsive condition remains under-recognized and undertreated. We describe the clinical and neuropsychological features in 65 consecutive cases of transient epileptic amnesia referred to our study, comparing these to our previous cohort of 50 patients and to those reported in 102 literature cases described since our 2008 review. Findings in our two cohorts are substantially consistent: The onset of transient epileptic amnesia occurs at an average age of 62 years, giving rise to amnestic episodes at a frequency of around 1/month, typically lasting 15–30 min and often occurring on waking. Amnesia is the only manifestation of epilepsy in 24% of patients; olfactory hallucinations occur in 43%, motor automatisms in 41%, brief unresponsiveness in 39%. The majority of patients describe at least one of the atypical forms of memory disturbance mentioned above; easily provoked tearfulness is a common accompanying feature. There is a male predominance (85:30). Epileptiform changes were present in 35% of cases, while suspected causative magnetic resonance imaging abnormalities were detected in only 5%. Seizures ceased with anticonvulsant treatment in 93% of cases. Some clinical features were detected more commonly in the second series than the first, probably as a result of heightened awareness. Neuropsychological testing and comparison to two age and IQ-matched control groups (n = 24 and 22) revealed consistent findings across the two cohorts, namely elevated mean IQ, preserved executive function, mild impairment at the group level on standard measures of memory, with additional evidence for accelerated long-term forgetting and autobiographical amnesia, particularly affecting episodic recollection. Review of the literature cases revealed broadly consistent features except that topographical amnesia, olfactory hallucinations and emotionality have been reported rarely to date by other researchers. We conclude that transient epileptic amnesia is a distinctive syndrome of late-onset limbic epilepsy of unknown cause, typically occurring in late middle age. It is an important, treatable cause of memory loss in older people, often mistaken for dementia, cerebrovascular disease and functional amnesia. Its aetiology, the monthly occurrence of seizures in some patients and the mechanisms and interrelationships of the interictal features—amnestic and affective—all warrant further study.

Absence seizures and their relationship to depression and anxiety: Evidence for bidirectionality.

Absence seizures (AS), presenting as short losses of consciousness with staring spells, are a common manifestation of childhood epilepsy that is associated with behavioral, emotional, and social impairments. It has also been suggested that patients with AS are more likely to suffer from mood disorders such as depression and anxiety. This systematic review and meta-analysis synthesizes human and animal models that investigated mood disorders and AS. Of the 1019 scientific publications identified, 35 articles met the inclusion criteria for this review. We found that patients with AS had greater odds of developing depression and anxiety when compared to controls (odds ratio = 4.93, 95% confidence interval = 2.91-8.35, p<.01). The included studies further suggest a strong correlation between AS and depression and anxiety in the form of a bidirectional relationship. The current literature emphasizes that these conditions likely share underlying mechanisms, such as genetic predisposition, neurophysiology, and anatomical pathways. Further research will clarify this relationship and ensure more effective treatment for AS and mood disorders.

Resting-state hippocampal networks related to language processing reveal unique patterns in temporal lobe epilepsy

ObjectivePatients with temporal lobe epilepsy (TLE) commonly experience a broad range of language impairments. These deficits are thought to arise from repeated seizure activity that damages language regions. However, connectivity between the seizure onset region in the hippocampus and regions related to language processing has rarely been studied, and could also have a strong impact on language function. The purpose of this study was to use resting-state functional connectivity (FC) measures to assess hippocampal network patterns and their relation to language abilities in patients with right TLE (RLTE), left TLE (LTLE), and healthy controls. MethodsPresurgical resting-state 3T functional MRI data were acquired from 40 patients with mesial TLE (27 RTLE, 13 LTLE) and 54 controls. The regions of interest were the anterior and posterior bilateral hippocampi and eleven regions grouped by frontal or temporo-parietal locations, including large areas of language-related cortex. FC values were computed with the right/left anterior and posterior hippocampi as the seeds and frontal and temporo-parietal regions as targets. Resting-state lateralization indices were also calculated (LI-Rest), and all FC measures were correlated to neuropsychological language scores and measures related to manifestation of epilepsy including age of onset, duration of disease, monthly seizure frequency, and hippocampal volume. ResultsWe found significant group differences between the anterior hippocampi and temporo-parietal regions closest to the seizure focus, in which RTLE and LTLE showed stronger connectivity to their contralateral hippocampus, while controls showed similar connectivity to both hippocampi. In addition, LI-Rest demonstrated significantly more right lateralization in LTLE compared to RTLE for temporo-parietal regions only. In LTLE, we found significant associations between stronger hippocampal network resting-state FC and later age of onset and decreased left anterior hippocampal volume. SignificanceThe results of our study indicate that the presence of TLE impacts hippocampal-temporo-parietal networks relevant to language processing.

Deletion of the Na-K-2Cl cotransporter NKCC1 results in a more severe epileptic phenotype in the intrahippocampal kainate mouse model of temporal lobe epilepsy

Increased neuronal expression of the Na-K-2Cl cotransporter NKCC1 has been implicated in the generation of seizures and epilepsy. However, conclusions from studies on the NKCC1-specific inhibitor, bumetanide, are equivocal, which is a consequence of the multiple potential cellular targets and poor brain penetration of this drug. Here, we used Nkcc1 knockout (KO) and wildtype (WT) littermate control mice to study the ictogenic and epileptogenic effects of intrahippocampal injection of kainate. Kainate (0.23 μg in 50 nl) induced limbic status epilepticus (SE) in both KO and WT mice with similar incidence, latency to SE onset, and SE duration, but the number of intermittent generalized convulsive seizures during SE was significantly higher in Nkcc1 KO mice, indicating increased SE severity. Following SE, spontaneous recurrent seizures (SRS) were recorded by continuous (24/7) video/EEG monitoring at 0-1, 4-5, and 12-13 weeks after kainate, using depth electrodes in the ipsilateral hippocampus. Latency to onset of electrographic SRS and the incidence of electrographic SRS were similar in WT and KO mice. However, the frequency of electrographic seizures was lower whereas the frequency of electroclinical seizures was higher in Nkcc1 KO mice, indicating a facilitated progression from electrographic to electroclinical seizures during chronic epilepsy, and a more severe epileptic phenotype, in the absence of NKCC1. The present findings suggest that NKCC1 is dispensable for the induction, progression and manifestation of epilepsy, and they do not support the widely held notion that inhibition of NKCC1 in the brain is a useful strategy for preventing or modifying epilepsy.

Intricacies of GABAA Receptor Function: The Critical Role of the β3 Subunit in Norm and Pathology

Neuronal intracellular chloride ([Cl−]i) is a key determinant in γ-aminobutyric acid type A (GABA)ergic signaling. γ-Aminobutyric acid type A receptors (GABAARs) mediate both inhibitory and excitatory neurotransmission, as the passive fluxes of Cl− and HCO3− via pores can be reversed by changes in the transmembrane concentration gradient of Cl−. The cation–chloride co-transporters (CCCs) are the primary systems for maintaining [Cl−]i homeostasis. However, despite extensive electrophysiological data obtained in vitro that are supported by a wide range of molecular biological studies on the expression patterns and properties of CCCs, the presence of ontogenetic changes in [Cl−]i—along with the consequent shift in GABA reversal potential—remain a subject of debate. Recent studies showed that the β3 subunit possesses properties of the P-type ATPase that participates in the ATP-consuming movement of Cl− via the receptor. Moreover, row studies have demonstrated that the β3 subunit is a key player in GABAAR performance and in the appearance of serious neurological disorders. In this review, we discuss the properties and driving forces of CCCs and Cl−, HCO3−ATPase in the maintenance of [Cl−]i homeostasis after changes in upcoming GABAAR function. Moreover, we discuss the contribution of the β3 subunit in the manifestation of epilepsy, autism, and other syndromes.

Orbitofrontal syndrome and “goosebumps”—A new manifestation of autoimmune epilepsy in anti-LGI1 encephalitis

Anti–leucine-rich glioma-inactivated 1 (anti-LGI1) encephalitis is a rare autoimmune disorder that presents with a triad of cognitive and psychiatric disturbances, hyponatremia, and autoimmune epilepsy. Facial-brachial dystonic (FBD) seizures are considered a pathognomonic sign of this condition. However, more subtle seizure types can occur and should be recognized, allowing for timely diagnosis and treatment. We report a case of anti-LGI1 autoimmune encephalitis presenting as orbitofrontal syndrome with focal “goosebump” seizures.

A case report of ictal bradycardia and asystole: An uncommon manifestation of epilepsy

The ictal bradycardia syndrome occurs when epileptic discharges disrupt normal cardiac rhythms leading to a reduction of heart rate that is more than 10 beats/min below the baseline. Mostly documented ictal bradycardias are accompanied by complex partial seizures of temporal lobe origin. Sudden unexpected death in epilepsy is often assumed to be associated with a concomitant seizure, but it is almost impossible to prove conclusively. Here, we report the case of a 52-year-old female patient admitted with the complaints of two episodes of generalized tonic–clonic seizures and vomiting followed by presyncope and syncope. The patient was admitted in a drowsy disoriented state with hypotension and electrocardiogram (ECG) illustrating sinus tachycardia. Later during admission, the patient developed complex focal seizures with secondary generalization and cardiac arrest. During video electroencephalogram/ECG, she had another similar episode and cardiac arrest. ECG showed rapid progression to asystole and ventricular pause of 25 s followed by complete heart block with ventricular escape rhythm of 17 beats/min. She was implanted with a temporary pacemaker but later during the hospitalization, sudden unexpected death in epilepsy occurred in spite of cardiac pacing and optimum antiepileptic medication. Most documented pauses are of nonlife-threatening duration (range 3–20 s) with longer pauses being observed. Cardiac pacing may help to reduce the risk of falls, but in the absence of official practice guidelines, cardiac pacing should only be considered for patients in whom conventional antiepileptic therapy has failed to prevent ictal asystole. Early diagnosis, interventions, and optimum antiepileptic dose escalation with occasional epilepsy surgery are the mainstay to prevent mortality and severe prognosis of the ictal bradycardia syndrome.

V.A.Muratov. To pathological physiology and differential diagnosis of cortical epilepsy. Medical Review. 1896, n ° 1

The author cites the history of the illness of one patient with manifestations of cortical epilepsy: convulsions began on the face, then passed on to the arm and leg, for the most part the seizure was limited to one left side. Left n. facialis was paralyzed; in the left extremities - paresis with reduced rigidity and increased tendon reflexes, while in the arms paresis and rigidity were almost the same, and rigidity prevailed in the legs. After the seizure, the paralysis intensified sharply. Some seizures were preceded by a motor aura: clonic convulsions in the paralyzed limbs. Left side sensitivity was decreased; muscle feeling weakened, stronger in the arms, less in the legs. The patient died of tuberculous pneumonia. When opened, found in the right hemisphere softening, which occupied the lower third of the posterior central gyrus. Gyrus marginalis in the anterior part was destroyed. The softening into the depths did not extend equally. In the rear part, it went quite deep; the radiant end in the supramargi nalis area is softened, the system of long connecting paths, apparently, is not affected; small focus in the superior parietal gyrus In the middle of the focus, destruction is limited to the cortex. In the front part, the softening was located under the cortical layer and reached the inner capsule. Deep-lying gray masses, corpus callosum and cingulum have survived from destruction. Microscopic examination showed extensive degeneration in connective and adhesive pathways; the descending rebirth was barely expressed and was found only in Marchi.

Coffin-Siris syndrome and epilepsy.

Coffin-Siris syndrome is a rare genetic disorder defined by the presence of particular facial traits, congenital malformations, intellectual disability, and speech impairment. Epilepsy in Coffin-Siris syndrome has only occasionally been reported, and its features are poorly defined. We provide a detailed description of the clinical and instrumental findings of three patients with Coffin-Siris syndrome and epilepsy. The clinical diagnosis in our patients was confirmed by molecular analysis, which identified the presence of de novo mutations of ARID1B and SMARCB1 genes, in two patients and one patient, respectively. All the patients presented with epilepsy, with a mean age of seizure onset of 5.5years. Seizures were brief and had a focal onset with secondary generalization. Electroencephalographic recording documented a unilateral, and less commonly bilateral, paroxysmal activity in the temporal, parietal, and occipital regions. Clinical response to anticonvulsive therapy was satisfactory, with a low rate of seizure recurrence. Our case series contributes to delineate the phenotype of Coffin-Siris syndrome. We wish this report could pave the way for further studies that will better define the prevalence and clinical manifestations of epilepsy in this rare syndrome.

Secondary school students' knowledge, attitude, and practices towards epilepsy in Nsukka City, Enugu State

BackgroundEpilepsy is the most common noninfectious neurologic disease in Nigeria and other developing African countries. Epilepsy remains a stigmatized disease. The stigma stems from the traditional African belief, which views epilepsy as a spiritual disease. A lack of information and illiteracy has been blamed as the cause of the stigmatization. AimsThe aim of the present study was to assess the awareness, knowledge, and attitude towards epilepsy among secondary school students in Nsukka. MethodsThis was a cross-sectional survey using a validated, self-administered questionnaire comprising four sections: demographic characteristics, awareness, knowledge, and attitude towards people living with epilepsy (PLWE). Data were analyzed using the IBM SPSS Statistics 23. Descriptive analysis (frequencies, percentage, mean, and standard deviations) were used to summarize the data. The relationship between sociodemographic characteristics and knowledge score and attitude score was performed using chi-square analysis. Statistical significance was set as a p-value <0.05. ResultsThe majority of the students (87.4%) had heard of epilepsy as a disease. The most common source of information was the electronic media (21.5%). More than half (61.6%) had witnessed a convulsion in the past, and 36.9% knew someone with epilepsy. The majority of the students (66.7%) believed that epilepsy is caused by witchcraft. Jerking (77.3%) and loss of consciousness (82.4%) were identified as the commonest manifestation of epilepsy. Regarding treatment management of epilepsy, 81.3% of the students believe the use of orthodox medicine, while 85.4% would insert a spoon in the mouth when a seizure occurs as part of first-aid treatment. Nearly half of the students had good knowledge (48.1%) of epilepsy and a positive attitude (46.5%) towards the disease. The students' knowledge was associated with their school (X2 = 23.21, p = 0.001). However, students' attitude towards epilepsy was associated with their schools (X2 = 5.93, p = 0.015) and their guardians' level of education (X2 = 14.65, p = 0.012). ConclusionThe findings of this study suggest poor knowledge and attitude towards epilepsy among secondary school students in Nsukka, Enugu State, Nigeria.

Network Fragility for Seizure Genesis in an Acute in vivo Model of Epilepsy.

Epilepsy affects over 50 million people worldwide and 30% of patients' seizures are medically refractory. The process of localizing and removing the epileptogenic zone is error-prone and ill-posed in part because we do not understand how epilepsy manifests. It has recently been proposed that the epileptic cortex is fragile in the sense that seizures manifest through small perturbations in the synaptic connections that render the entire cortical network unstable. If the fragility of the cortical network could be computed over a period in which seizure genesis occurs, then it might elucidate network mechanisms correlated to the epileptogenic zone. In this study, we used local field potentials (LFP) from neocortex by implementing an acute model of epilepsy in mice. These recordings were used to develop a dynamical network model that quantifies the fragility of the nodes from LFP epochs of baseline activity, preictal and ictal states. Fragility was quantified by the generation of a linear time-varying model to which we then applied a perturbation to determine the sensitivity of nodes in the network. Spatiotemporal fragility maps showed clear quantifiable changes in the epileptogenic network's properties throughout different states of seizure genesis. We quantified this difference over a baseline, preictal and ictal periods to show that network fragility is modulated in the manifestation of epilepsy.

ELECTROCLINICAL ASPECTS OF OCCIPITAL EPILEPSY SEEN IN THE NEUROSCIENCES AND MENTAL HEALTH LABORATORY ANTSAKAVIRO

Introduction: Occipital epilepsy occurs when the initial site of epileptic discharge involves part or all of the occipital lobe. Occipital epilepsy is the least common of the other types of epilepsy and is rarely described in the literature. However, the manifestation located initially in the occipital cortex, which is a functional zone of vision, leads to its protean aspect. It can be a source of diagnostic wandering. The purpose of this study is to describe the electroencephalographic clinical characteristics of patients seen for occipital epilepsy at the Laboratory of Neurosciences and Mental Health, Antsakaviro, Madagascar. &#x0D; Methods: This is a retrospective and descriptive study that took place over a one-year period (January 2016 to December 2016). Included in this study were all patients diagnosed with clinically and EEG-confirmed occipital epilepsy. A correlation between clinical manifestations and electroclinical data is sought. &#x0D; Results: We retained 66 patients with male predominance (sex ratio: 1.4). The age of the patients ranged from 3 to 55 years with a mean age of 13.77 years. Patients reside in urban areas and the majority are of non-school age. The clinical manifestations of occipital epilepsy are mainly paroxysmal visual hallucinations lasting on average 3 minutes and of variable frequency. EEG signs are predominantly paroxysmal activities with a predominant or occipital starting point. &#x0D; Conclusion: The clinical and electroencephalographic manifestations of occipital epilepsy deserve special attention in order to make a proper diagnosis.

HMGB1/CXCL12-Mediated Immunity and Th17 Cells Might Underlie Highly Suspected Autoimmune Epilepsy in Elderly Individuals.

PurposeLate-onset epilepsy due to autoimmune dysfunction has been reported. However, definitive diagnosis requires positive antibody results. As a result, patients with negative antibody results, but presenting with classical manifestation of autoimmune epilepsy, may be managed as suspected cases. In this study, we aim to isolate and profile the concentration of cytokines/chemokines in the cerebrospinal fluid (CSF) and the serum to ascertain if they could act as alternative diagnostic biomarkers.Patients and MethodsTwenty patients aged ≥50 years were considered in this study. Ten patients were diagnosed with suspected autoimmune epilepsy (sAE) based on clinic manifestation, electroencephalogram, magnetic resonance imaging, and with negative antibody results of the serum and the CSF. The equivalent control group exhibited neurological disorders due to non-inflammatory pathologies. Serum and CSF were analyzed for cytokines/chemokines concentration, including interleukin (IL)-6, IL-10, IL-17, chemokine (C-X-C motif) ligand (CXCL)12 and CXCL13, as well as high-mobility group box protein 1 (HMGB1) and B cell activation factor (BAFF)).ResultsThe CSF levels of IL-6, IL-17, HMGB1, and CXCL12 were significantly higher in the sAE group than in the control group. There was no difference in the CSF levels of IL-10, CXCL13 and BAFF. The serum levels of HMGB1 and CXCL12 were elevated in the sAE group compared with the control group, and there was no statistical difference in the serum levels of IL-6, IL-10, IL-17, CXCL13, and BAFF between the two groups.ConclusionOur study shows that cytokines/chemokines may act as alternative biomarkers for diagnosis of sAE. The activation of both HMGB1/CXCL12-mediated immunity and T helper cells 17 (Th17) cells may be playing a central role in the pathogenesis of sAE. We suggest that cytokines/chemokines be treated as adjuvant biomarkers, instead of solely relying on antibody screening test. However, a larger cohort in a prospective approach is required to validate our findings.

Neurochemical Theory of Epilepsy Pathogenesis in It&amp;apos;s Neurological and Mental Manifestations

In the article, in light of the hypothesis about the pathogenesis of epilepsy the author considers certain clinical manifestations of epilepsy, touches upon the neurochemistry of behavior, as well as neurotransmitter hypothesis of schizophrenia. According to the hypothesis, in epileptic patients, epileptogenic substances are permanently accumulating in the brain, which in the course of epileptic activity in the brain undergo metabolic changes requiring their removal from the organism. When the concentration of epileptogenic substances in the brain reaches a threshold value, they cause a seizure, and in lower concentrations, they cause epileptic activity typical for the interictal period. In the context of this hypothesis, there are discussed the clinical signs of epilepsy such as forced normalization, reinforcement epilepsy activity during the sleep deprivation and one of the paradoxical effect of antiepileptic drugs such as phenomen when antiepileptic drugs prescribed cause an improvement of the electroencephalographic image but the clinical deterioration and increasing frequency of seizures, and the change of antiepileptic drugs give us the opposite results: improvement of the clinical picture and the deterioration of the electroencephalographic image. According to the supplemented hypothesis, epileptogenic substances, except that, during epileptic activity in the brain undergo metabolic transformations necessary for their removal from the body; there are also alternative transformation neurochemical pathways necessary for their further removal (elimination) from the organism. The hypothesis discusses the modern principles of epilepsy treatment. It was proposed to call the phenomenon “clinical-electroencephalographic dissociation” when the anti-epileptic drugs are associated with the improved electroencephalographic pattern, but with the deterioration of the clinic and frequent seizures, and the drug change leads to the opposite—the improvement of the clinical picture and the EEG deterioration. Forced normalization is considered as one of the manifestations of epilepsy aggravation and “clinical-electroencephalographic dissociation”. When reviewing biological antagonism of schizophrenia and epilepsy the author suggests a hypothesis that if an area of the brain producing epileptogenic substances and an area of the brain producing endogenic psychogenic substances causing psychopathology coexist simultaneously, then, in the event of a generalized convulsive seizure involving the brain in full, epileptogenic as well as psychogenic substances are released. At the same time epilepsy is demonstrated, while schizophrenia is not. The same could be the mechanism of therapeutic activity (effect) of electroconvulsive therapy.