Single Seizure Research Articles

Use of Head Computed Tomography (CT) in the Pediatric Emergency Department in Evaluation of Children With New-Onset Afebrile Seizure.

Cranial computed tomography (CT) is not recommended in the routine evaluation of children with first afebrile seizure due to its low yield. The objective was to assess the current practice in our pediatric emergency department regarding the use of head CT in children with first afebrile seizure and to identify the factors that lead to ordering a head CT. Medical records of patients between 1 month and 18 years old evaluated at our emergency department for presentation of first afebrile seizure between 2010 and 2014 were retrospectively reviewed. Data extracted include age, gender, seizure type, single or multiple seizures at presentation, seizure duration, predisposing conditions to seizures (ie, history of developmental delay), and whether a head CT was performed. Contingency tables with chi-square analyses were used to determine which variables were associated with increased use of head CT. Of 155 patients (88M/67F) included in the study, 72 (46.5%) underwent head CT and only 3 had clinically significant findings that did not require acute management. There were no differences in CT use by age, sex, seizure type, seizure number, seizure risk factors, or findings on physical examination. Head CT was performed more frequently in cases with seizures ≥5 minutes and unknown seizure duration ( P = .04). Despite existing evidence, the emergent head CT rate was high in our cohort. Children with seizure duration of ≥5 minutes or of unknown duration were more likely to undergo head CT in our emergency department.

Transient Morphological Alterations in the Hippocampus After Pentylenetetrazole-Induced Seizures in Rats.

The relationships between seizures, neuronal death, and epilepsy remain one of the most disputed questions in translational neuroscience. Although it is broadly accepted that prolonged and repeated seizures cause neuronal death and epileptogenesis, whether brief seizures can produce a mild but similar effect is controversial. In the present work, using a rat pentylenetetrazole (PTZ) model of seizures, we evaluated how a single episode of clonic-tonic seizures affected the viability of neurons in the hippocampus, the area of the brain most vulnerable to seizures, and morphological changes in the hippocampus up to 1week after PTZ treatment (recovery period). The main findings of the study were: (1) PTZ-induced seizures caused the transient appearance of massively shrunken, hyperbasophilic, and hyperelectrondense (dark) cells but did not lead to detectable neuronal cell loss. These dark neurons were alive, suggesting that they could cope with seizure-related dysfunction. (2) Neuronal and biochemical alterations following seizures were observed for at least 1week. The temporal dynamics of the appearance and disappearance of dark neurons differed in different zones of the hippocampus. (3) The numbers of cells with structural and functional abnormalities in the hippocampus after PTZ-induced seizures decreased in the following order: CA1 > CA3b,c > hilus > dentate gyrus. Neurons in the CA3a subarea were most resistant to PTZ-induced seizures. These results suggest that even a single seizure episode is a potent stressor of hippocampal neurons and that it can trigger complex neuroplastic changes in the hippocampus.

T57. Prediction of early tumor progression based on pre- and post-operative seizure frequency in low grade gliomas

Low-grade gliomas (LGG) are slow-growing tumors characterized by an infiltrative growth pattern and cortical predilection in the central nervous system (CNS). Up to 90% of LGG patients may have seizures as the initial presentation leading to tumor diagnosis, and up to 15% of them develop refractory epilepsy. Predicting which patient will evolve into refractory epilepsy versus have more benign disease course remains a challenge. Moreover, seizure recurrence following surgical resection may predict early tumor recurrence, especially in patients who have achieved long seizure-freedom period. This study analyzed 148 patients meeting inclusion criteria (age > 18 years, LGG diagnosis, at least one seizures event at some point of the disease process). All patients were treated by the Department of Neuro-Oncology and Neurosurgery at University of Texas MD Anderson Cancer Center (MDACC) from Jan/2000 and Dec/2015. Seizure frequency was divided in 4 categories: none, one, few (2–3 seizures) and several (>4 seizures). Perioperative seizures (up to 48 h from surgery) were excluded from this analysis. One hundred sixteen (78.4%) patients had seizures as the initial presentation. On average, the first seizure occurred 4.75 months prior to surgical resection (range 0.1–24.2). Pre-operatively, 54 (36.5%) patients had a single seizure, 23 (15.5%) patients had few seizures and 39 (26.4%) patients had several seizures. After initial event, most patients (74%) were started on antiepileptic drugs (AED). Ninety-two (63%) patients accomplished partial resection, whereas 54 (37%) patients accomplished gross total resection of the tumor. Univariate analysis of seizure frequency between the 6-month pre-op and post-op periods was significant in predicting recurrence-free survival in the following 2 (2-RFS) and 5 (5-RFS) years (p = 0.0379). Patients with no/one seizure pre-op who continued to have no/one seizure in the 6-month post-op period had the highest 2-RFS and 5-RFS (0.984 and 0.667 [CI 95%, 0.889–0.998 and 0.528–0.773], respectively); patients who had no/one seizure pre-op and developed few/several seizures in the 6-month post-op period had the lowest probability of being progression-free in the following 2 and 5 years (0.750 and 0.545 [CI95%, 0.463–0.898 and 0.274–0.753], respectively). Multicovariate cox-regression analysis on RFS based on the seizure frequency change between pre-op and post-op periods revealed that patients with no/one seizure pre-op who had increase in seizure frequency to few/several seizures on the 6-month post-op period had significantly more risk of progression compared to patients who initially had no/one seizure pre-op and continued to have no/one seizure in the 6-month post-op period (HR 2.431 [CI95% 1.318, 4.482], p = 0.0044). Seizure frequency following surgical resection of LGG and the seizure frequency change between the 6-month pre-op and post-op periods predict early tumor recurrence in LGG.

The seizure precipitating effect of alcohol: A prospective observational cross-over study

PurposeThe aim of this study was to investigate the association between alcohol use and seizures in acutely hospitalized patients. We wished to study the extent of the problem as well as the clinical characteristics of people with various forms of alcohol-related seizures, including their drinking pattern. MethodAfter admission, a semi-structured interview took place with 134 consecutive patients (epilepsy 92, single seizures 42). Alcohol use was assessed by the Alcohol Use Disorders Identification Test (AUDIT) and by the number of alcohol units consumed during 6 days prior to the seizure. Sleep time was recorded during the previous 3 days and nights. A follow-up telephone interview covering the same weekdays was performed on a seizure-free day at least 4 weeks later. Results28% of patients had AUDIT scores ≥8 (hazardous drinking); 22% in epilepsy, 43% in single seizures (p = .012). Non-focal seizures were increased in single seizures, suggesting a withdrawal mechanism. In the 58 epilepsy patients with social drinking (excluded hazardous drinking or excessive binging), the alcohol intake was not different prior to seizure compared to follow-up, downgrading the role of modest alcohol intake as a seizure precipitant in epilepsy. On the other hand, a high percentage of binge drinkers had epilepsy (57%), and in the subgroup of Idiopathic Generalized Epilepsy (IGE) even social drinking was associated with seizures. Seizures peaked on Sundays and Mondays. Less sleep prior to the seizure was associated with hazardous drinking. ConclusionAlcohol is a major seizure precipitant in the context of hazardous drinking and withdrawal. In people with epilepsy, occasional binge drinking is associated with loss of seizure control. Social drinking is an uncommon cause of seizure breakthrough in predominantly focal epilepsy, but caution is warranted in IGE. Alcohol intake prior to a seizure is often accompanied by other triggers, such as sleep loss. Alcohol alone should not always be blamed.

Anti-N-methyl-D-aspartate receptor encephalitis relapse in the brainstem

Anti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis is an autoimmune disorder involving IgG antibody reaction against NMDAR. It typically develops in women with ovarian teratoma, and its characteristic clinical symptoms include acute behavioural...

Risk of epilepsy after a single seizure in multiple sclerosis.

The 2014 International League Against Epilepsy clinical definition of epilepsy allows diagnosis after a single unprovoked seizure if the 10-year recurrence risk exceeds 60%. Multiple sclerosis (MS) carries an increased risk of epilepsy, but the risk after a first seizure is unknown. We aimed to investigate the risk of epilepsy in patients with MS who had suffered a first seizure. We cross-referenced data from the Swedish MS register with the national patient register for 15810 patients with MS and 43635 controls and included 289 patients with MS and 222 controls with a first diagnosis of seizure or status epilepticus (SE) without prior epilepsy or presumed symptomatic aetiology. Kaplan-Meier curves were used to estimate the risk of epilepsy. The 10-year risk of epilepsy was 51.4% [95% confidence interval (CI), 44.0-58.9] for patients with MS and 41.3% (95% CI, 33.5-49.1) for controls. The risk was 46.1% (95% CI, 35.3-56.9) for patients with relapsing-remitting MS and 60.7% (95% CI, 46.6-74.8) for patients with secondary progressive MS. For patients with MS with SE, the 10-year risk of epilepsy was 85.9% (95% CI, 67.9-100). Our data indicate that patients with relapsing-remitting MS have a similar risk as controls of developing epilepsy after a single seizure. Patients with secondary progressive MS could run a greater risk of subsequent epilepsy, but our data do not indicate a risk that, with certainty, exceeds the threshold specified by the International League Against Epilepsy. Patients with SE have a high risk of epilepsy, possibly motivating diagnosis and treatment.

Seizure characteristics and the use of anti-epileptic drugs in children and young people with brain tumours and epileptic seizures: Analysis of regional paediatric cancer service population

PurposeEpileptic seizures complicate the management of childhood brain tumours. There are no published standards for clinical practice concerning risk factors, treatment selection or strategies to withdraw treatment with antiepileptic drugs (AED). Methodwe undertook a case note review of 120 patients with newly diagnosed brain tumours, referred to a regional paediatric cancer service. Resultsdata was available on 117/120 (98%) children <18 years: median age at tumour presentation was 8.1 years (IQR 25°−75°: 3.6–12.7), median follow up was 33 months (IQR 25°−75°: 24–56), and 35/117 (29%) experienced seizures.A cortical tumour location was associated with the highest risk of seizures (OR: 7.1; CI 95% 2.9–17.3). At a median follow up of 24 months (IQR25°−75°: 15–48), 22/35 (63%) with seizures, had a single seizure episode, 15/35 (43%) were seizure free (SF) on AEDs, 13/35 (37%) were SF off AEDs, and 7/35 (20%) experienced continuing epileptic seizures. Overall 34/35 (97%) were treated with AEDs after a seizure, of whom 12/35 (35%) withdrew from AED medication, and although 4/35 (12%) had seizure relapse, all were after further acute events. The median duration of AED before withdrawal was 11 months (IQR25°−75° 5–14 months), and the median follow up after withdrawal was 15 months (IQR25°−75° 5–34 months). ConclusionsSeizures affect about 1/3rd of children and young people presenting with and being treated for brain tumours particularly when the tumour is in the cerebral cortex.The low risk of recurrent seizures after AED treatment justifies consideration of early withdrawal of AED after seizure control.

RNA Polymerase 1 Is Transiently Regulated by Seizures and Plays a Role in a Pharmacological Kindling Model of Epilepsy.

Ribosome biogenesis, including the RNA polymerase 1 (Pol1)-mediated transcription of rRNA, is regulated by the pro-epileptogenic mTOR pathway. Therefore, hippocampal Pol1 activity was examined in mouse models of epilepsy including kainic acid- and pilocarpine-induced status epilepticus (SE) as well as a single seizure in response to pentylenetetrazole (PTZ). Elevated 47S pre-rRNA levels were present acutely after induction of SE suggesting activation of Pol1. Conversely, after a single seizure, 47S pre-rRNA was transiently downregulated with increased levels of unprocessed 18S rRNA precursors in the cornu Ammonis (CA) region. At least in the dentate gyrus (DG), the pilocarpine SE-mediated transient activation of Pol1 did not translate into long-term changes of pre-rRNA levels or total ribosome content. Unaltered hippocampal ribosome content was also found after a 20-day PTZ kindling paradigm with increasing pro-convulsive effects of low dose PTZ that was injected every other day. However, after selectively deleting the essential Pol1 co-activator, transcription initiation factor-1A (Tif1a/Rrn3) from excitatory neurons, PTZ kindling was impaired while DG total ribosome content was moderately reduced and no major neurodegeneration was observed throughout the hippocampus. Therefore, Pol1 activity of excitatory neurons is required for PTZ kindling. As seizures affect ribosome biogenesis without long-term effects on the total ribosome content, such a requirement may be associated with a need to produce specialized ribosomes that promote pro-epileptic plasticity.

Feasibility of imaging epileptic seizure onset with EIT and depth electrodes

Imaging ictal and interictal activity with Electrical Impedance Tomography (EIT) using intracranial electrode mats has been demonstrated in animal models of epilepsy. In human epilepsy subjects undergoing presurgical evaluation, depth electrodes are often preferred. The purpose of this work was to evaluate the feasibility of using EIT to localise epileptogenic areas with intracranial electrodes in humans. The accuracy of localisation of the ictal onset zone was evaluated in computer simulations using 9M element FEM models derived from three subjects. 5 mm radius perturbations imitating a single seizure onset event were placed in several locations forming two groups: under depth electrode coverage and in the contralateral hemisphere. Simulations were made for impedance changes of 1% expected for neuronal depolarisation over milliseconds and 10% for cell swelling over seconds. Reconstructions were compared with EEG source modelling for a radially orientated dipole with respect to the closest EEG recording contact. The best accuracy of EIT was obtained using all depth and 32 scalp electrodes, greater than the equivalent accuracy with EEG inverse source modelling. The localisation error was 5.2 ± 1.8, 4.3 ± 0 and 46.2 ± 25.8 mm for perturbations within the volume enclosed by depth electrodes and 29.6 ± 38.7, 26.1 ± 36.2, 54.0 ± 26.2 mm for those without (EIT 1%, 10% change, EEG source modelling, n = 15 in 3 subjects, p < 0.01). As EIT was insensitive to source dipole orientation, all 15 perturbations within the volume enclosed by depth electrodes were localised, whereas the standard clinical method of visual inspection of EEG voltages, only localised 8 out of 15 cases. This suggests that adding EIT to SEEG measurements could be beneficial in localising the onset of seizures.

SOMATIC COMORBID ITY AND DE VELOPIN G EPILEPSY IN CHILDREN AFTER A SINGLE SEI ZURE

Aim – to study chronic somatic comorbidity as a possible predictor of epilepsy in children after a single seizure. Materials and methods. Based on the follow-up results, 279 cases were studied and compared: the study group – epilepsy – included 166 children with two or more seizures developed at least 24 hours after the first seizure; the control group – 113 children with a single seizure that remained isolated for the subsequent three years. Results. We found that at the time of the first (single) attack, the background of chronic ocular morbidity (myopia, hypermetropia, optic nerve atrophy, retinal dystrophy) was significantly more common among children in the control group as compared with the confirmed epilepsy group where cardiovascular disorders prevailed. Other concomitant diseases had no statistically significant correlations with the occurrence of epilepsy after a single seizure. Conclusion. Diagnosis of somatic comorbidity in children with a single seizure may be a prognostic factor of subsequent epilepsy.

LOCAL AND SYSTEMIC EFFECTS OF REPETITIVE SEIZURES

LOCAL AND SYSTEMIC EFFECTS OF REPETITIVE SEIZURES

EVALUATION OF SERUM SODIUM LEVEL IN SINGLE AND RECURRENT FEBRILE SEIZURES

Background &#x0D; Febrile seizures are the most common form of childhood seizures. Its either simple (when it is single attack within next 24 hours, plus other characters) or complex (when is recurrent within same period plus other characteristics).&#x0D; Objectives&#x0D; &#x0D; This study was conducted to determine the role of low serum sodium levels in predicting single or recurrent febrile seizures among children.&#x0D; Patients and Methods&#x0D; In this study, 100 patients aged 6-60 months old were enrolled. The patients were divided into two groups: those with single, and those with recurrent febrile seizures. Then 100 children with febrile illness, but no febrile convulsion, taken as a control. For those 3 groups serum sodium levels were studied.&#x0D; Results&#x0D; Among the patients, male gender was predominant. Among those with 12-24 months old, positive family history of febrile seizures was significant. The mean serum sodium of patients with single febrile seizure was (137.91), while the mean serum sodium level of patients with recurrent febrile seizures was (139), and the mean serum sodium of control group was (141.42). The P-value of comparison between control and those with single febrile seizure was significant (0.002), but the P-value of comparison between control and those with recurrent febrile seizures was not significant (0.813). There was no significant role of the serum sodium found during admission of the patients. &#x0D; Conclusion&#x0D; We found in present study: there was no significant role for the serum sodium during single or recurrent F.S.s. These findings reaffirm the recommendation of the American Academy of Pediatrics not to routinely obtain serum electrolytes in febrile seizures unless clinically indicated.

The production of IL-6 in acute epileptic seizure: A video-EEG study

Experimental and clinical reports highlight the role of cytokines in pathophysiological processes in underpinning epilepsy, but the clinical data remains somewhat limited. The levels of Interleukin (IL)-6 were measured in serum from 49 patients with refractory epilepsy [temporal lobe epilepsy (TLE, n=23), extratemporal lobe epilepsy (XLE, n=22), and idiopathic generalized epilepsy (IGE, n=4)] before and after the first verified seizure (IS; index seizure) during inpatient video-electroencephalographic (VEEG) monitoring. The levels of IL-6 increased significantly at all time points between 3h and 24h after the IS compared to the baseline. IL-6 concentrations were significantly higher at the 3h and 6h time point after tonic-clonic seizures (TCS) compared to the situation with simple partial and complex partial seizures. An IS duration longer than 100s, low baseline IL-6 level and <10 seizures/month in patients with TLE were associated with an increase in IL-6 concentrations during the 24h after the IS. In patients with TLE, the maximum change in IL-6 levels after IS was significantly higher than in XLE. If the baseline level of IL-6 was low (under 5pg/ml), seizures induced a significant elevation in both absolute and relative values in TLE patients but not in XLE. In patients with ≤10 seizures per month during the last year, the maximum change was higher than in patients with >10 seizures. If the total seizure burden during registration was ≥100s, the IL-6 increase was significantly higher than if it were under 100s. The results of this study highlight the complexity of factors involved in the seizure induced production of the inflammatory cytokine, IL-6. The major factor is the epilepsy type i.e. increased production of IL-6 in TLE compared to XLE. The response to a single seizure in TLE is dependent on the previous seizure frequency and the baseline IL-6 concentration.

Seizure outcomes in patients with anti‐NMDARencephalitis: A follow‐up study

To evaluate the long-term seizure outcome and potential factors associated with seizure outcome in patients with anti-N-methyl-d-aspartate receptor (anti-NMDAR) encephalitis. In the setting of a prospective, single-center, longitudinal cohort study, 109 patients were evaluated with ongoing follow-up. Patients underwent clinical evaluation every 3 months. Seizure outcomes and the potential risk factors were assessed with a median follow-up of 24 months (6-60 months). Of 109 patients (47 men; 62 women) with anti-NMDAR encephalitis, 88 patients (80.7%) had reported seizures at acute phase, including single seizure (17/88, 19.3%), repetitive seizures (27/88, 30.7%), nonrefractory status epilepticus (22/88, 25%), refractory status epilepticus (SE; 13/88, 14.8%), and super refractory status epilepticus (9/88, 10.2%). Seizure was more likely to recur in patients with tumor presence, status epilepticus (SE) development, coma, or intensive care unit (ICU) admission in the acute phase (p < 0.05). Seizure freedom was achieved within 2 years in all patients. More than 80% of the whole cohort with acute seizures had their last seizure within 6 months of disease onset. Seizure is a common feature in the acute stage of anti-NMDAR encephalitis but not thereafter. The presence of tumor, SE, coma, and/or ICU admission in the acute phase predicts early seizure occurrence after the acute phase. Seizure freedom was typically achieved in our follow-up, and long-term use of antiepileptic drugs may not be necessary.

Application of amplitude-integrated electroencephalography in neonates with acute hypoglycemic brain injury

Objective To explore the value of amplitude integrated electroencephalography (aEEG) in diagnosis and prognosis in neonates with acute hypoglycemic brain injury. Methods A total of 47 cases of neonatal hypoglycemic brain injury were prospectively enrolled in the study from January 2011 to July 2015.The aEEG traces were classified according to background activity (normal, moderate, or severely abnormal), presence of seizures and sleep-wake cycling (SWC). The neuromotor development of survivors with neonatal hypoglycemic brain injury was assessed by using the 0-6 years old children′s neurological and psychological development scale of China Capital Institute of Pediatrics.Clinical data were collected and compared with the result of aEEG. Results The characteristic of aEEG tracings in 47 infants showed continuous normal voltage (CNV)(n=9), discontinuous voltage(DC)(n=29), continuous low voltage(CLV)(n=3), burst-suppression(BS)(n=6); mature sleep-wake cycling(SWC)(n=9), immature SWC(n=17), no SWC (n=21); 39 infants(83.0%) had electrical seizures: single seizure(n=11), repetitive seizures(n=20), and status epilepticus (SE)(n=8). aEEG of 23 infants who had poor outcome showed CLV(n=3), BS/SE(n=4), BS/repetitive seizures(n=2), DC/SE(n=4), DC/repetitive seizures(n=10). By chi-square analysis and Spearman rank correlation analysis, the results of aEEG classification, background pattern and SWC were correlated with outcome of these infants with hypoglycemic brain injury. Conclusion Amplitude integrated electroencephalography can provide important information of the status of cerebral function in neonates with acute hypoglycemic brain injury and help to predict their outcome. Key words: Amplitude integrated electroencephalography; Brain injuries; Hypoglycemia; Neonate,

Méningo-encéphalite à Pasteurella multocida chez un enfant de 14 ans

Pasteurella multocida is generally responsible for local infections through animal bites. It can be a cause of meningitis, which tends to affect people at the extreme ages of life or suffering from immunodeficiency. A 14-year-old teenager was hospitalized with typical signs of bacterial meningitis. P.multocida was evidenced in the cerebrospinal fluid. Progression was marked by a degradation on the 4th day of treatment, despite intravenous antibiotic therapy with third-generation cephalosporin, followed by a single seizure on the 7th day of treatment. The CT scan and magnetic resonance imaging showed pansinusitis but no intracerebral complications. Later progression was favorable, without neurological sequelae. The mode of contamination was inoculation via the upper airways with sinusitis. P.multocida meningitis is rare. The contamination does not always involve animal trauma.

P.31 - A diagnostic challenge of late onset adult merosinopathy

A 51-year-old caucasian woman presented with a 6 year history of, initially exercise dependent, proximal leg weakness. Her brain MRI showed extensive, predominantly supratentorial white matter changes, that could not be attributed to her known hypertension. She had a single grand mal seizure as a teenager upon photostimulation and suffers from migraine with aura. Her mother was reported to suffer from epilepsy due to traumatic brain injury and her two sisters were said to have skeletal deformities due to use of analgetics during the pregnancies. Our patient's sisters, son and daughter report no neuromuscular complaints. Her serum CK was 200 - 500 U/l, CSF analysis and lab work-up for adult white matter disorders did not reveal abnormalities, but vastus muscle biopsy showed mildly dystrophic changes with an increased fibre size variation, fibre degeneration and regeneration, some fibrosis as well as rimmed vacuoles. Immunohistochemistry showed normal reactivities, including anti-laminin α2 (NCL-MEROSIN) and -α-dystroglycan, but for anti-p62 deposition along rimmed vacuoles. However, anti-laminin α2 western blot showed loss of the 80 kDa band (Millipore MAB1922). Genetic analysis for m.A3243G and m.A8344G point mutations as well as DNAJB6 and NOTCH3 genes gave normal results. In the LAMA2 gene two variants were found, c.2171_2172del and c.2173C > A, the former a known pathogenic mutation, however, in cis. We conclude that this is a case of late onset adult merosinopathy with an affection of the second LAMA2 allele escaping detection so far. In suspected laminin α2 disorders, both, the 300 kD and 80 kD subunit, need to be examined. We did not observe a selective reduction of the 300 kD isoform that has been suggested for milder forms, and hope to be able to examine further family members to ensure that their reported symptoms are indeed unrelated.

Long‐term applicability of the new ILAE definition of epilepsy. Results from the PRO‐LONG study

The new epilepsy definition adopted by the International League Against Epilepsy (ILAE) includes patients with one unprovoked seizure with a probability of further seizures, similar to the general recurrence risk after two unprovoked seizures, occurring in a 10-year period. Long-term follow-up of patients diagnosed after a single seizure is needed to assess the applicability of the new epilepsy definition in clinical practice. Patients with newly diagnosed epilepsy were recruited retrospectively with a minimum follow-up of 10years. Patients were stratified in two groups depending on the occurrence of one (new definition, ND) or two or more unprovoked seizures (traditional definition, TD) at the time of epilepsy diagnosis and compared for disease characteristics and factors predicting seizure recurrence. The primary outcome was the occurrence of a new unprovoked seizure during follow-up in the ND group. The secondary outcome was the achievement of an early remission in both groups. Among 1,006 patients with newly diagnosed epilepsy, 152 (15.1%) were diagnosed after a single seizure. Compared to patients diagnosed using the TD, patients diagnosed according to the ND showed a higher proportion of subjects with an abnormal neurologic examination (19.9% vs. 13.7%, p=0.0504) and with focal seizures (69.3% vs. 60.4%, p=0.0021). The two samples differed in the presence of at least one of the factors predicting seizure recurrence (focal seizures or abnormal findings in at least one among the following: neurologic examination, electroencephalography [EEG], and neuroimaging) (94.6% vs. 89.1%, p=0.0376). Long-term recurrence in patients diagnosed with the new definition was 83.6% at 10years and 89.1% at 15years. The probability of early remission did not differ between the two groups. Our results support the applicability of the new epilepsy definition in clinical practice. Individual patient characteristics and a personalized diagnostic approach can justify treatment after a single unprovoked seizure.

Medial septum modulates hippocampal gamma activity and prepulse inhibition in an N-methyl-d-aspartate receptor antagonist model of schizophrenia

We reviewed the participation of the septohippocampal system in an animal model of schizophrenia that was acutely induced by systemic injection of an N-methyl-d-aspartate (NMDA) receptor antagonist such as phencyclidine, MK-801 and ketamine. The NMDA receptor antagonist-induced model of schizophrenia is characterized by behavioral and electrophysiological disruptions, including a decrease in prepulse inhibition of the acoustic startle response (PPI), hyperlocomotion, decrease in gating of hippocampal auditory evoked potentials and robust increase in hippocampal gamma (30–100Hz) oscillations. Similar disruptions were also induced by a single electrographic seizure in the hippocampus. The behavioral and electrophysiological disruptions induced by an NMDA receptor antagonist can be reduced by inactivation or lesion of GABAergic neurons in the medial septum, deep brain stimulation of the medial septum or nucleus accumbens, or positive modulation of GABAB receptors. Our results suggest a close association between high-amplitude hippocampal gamma oscillations and psychosis-relevant behaviors including PPI loss, behavioral hyperactivity and loss in auditory gating. Abnormal electrophysiology suggests a disruption of somatic and apical dendritic inhibition in the hippocampus, resulting in distorted sensory integration, and impaired cognitive and memory processing. The hippocampus is suggested to be a hub in a brain network that participates in psychosis-relevant behaviors, through its direct projection to the nucleus accumbens, or through indirect connections via the entorhinal, cingulate and prefrontal cortices.

In this issue – July 2017

In this issue – July 2017