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OBJECTIVE: The aim of this article is to answer three relevant issues: i/What epileptic condition is referred to as subacute encephalopathy with seizures in alcoholics (SESA) syndrome; ii/ Why it can be important to distinguish SESA syndrome in clinical practice and iii/ What do we know about its pathophysiology. METHODS: We reviewed all cases published in the English language from the initial description of the syndrome to the present. All met the previously established criteria for SESA syndrome were included in our analysis. RESULTS: We found 34 patients diagnosed with SESA syndrome Fourteen (41.1%) out of 34 patients were over 60 years of age. In 12 (35.2 %), abstinence, and in 4 (11.7 %) excessive consumption of alcohol, were considered precipitating factors, respectively. Triggering causes were unknown in 18 cases (53.0 %). All cases (100 %) presented with altered mental status. Fourteen (41.1 %) subjects had a history of epileptic seizures in the context of alcohol withdrawal syndrome (AWS). Twenty (58.8 %) patients had focal motor seizures (FMSs), 24 (70.5 %) bilateral tonic-clonic seizures (BTCSs), and 15 (44.1 %) focal impaired awareness seizures (FIASs). In 8 (23.5 %), criteria for focal nonconvulsive status epilepticus (NCSE) were met. Twenty-eight (82.3 %) subjects had transient neurological deficits. In 29 (85.2 %) subjects, lateralized periodic discharges (LPDs) were observed on the EEG. Areas of signal hyperintensities and restricted diffusion in neuroimaging were mentioned in 22 subjects (64.7 %). Transfer to the intensive care unit was necessary in 8 (23.5 %) subjects. Thirteen (38.2 %) had recurrent episodes. Enduring brain damage was mentioned in 9 (26.4 %) cases. The most used anti-seizure medication (ASM) was levetiracetam, followed by phenytoin and lacosamide. CONCLUSIONS: SESA syndrome represents a well-defined subtype of focal NCSE in patients with chronic alcoholism. Its prompt recognition can facilitate the initiation of early ASM therapy and help design appropriate video-EEG evaluation and a treatment strategy.
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Absence status epilepticus (ASE) is a rare but treatable condition, and when present in older adults, it can be misinterpreted as encephalopathy or behavioral changes. Our case discusses a 63-year-old patient with myelofibrosis and allogeneic stem cell transplant with late-onset de novo status epilepticus. This case report adds to the rare body of literature discussing de novo ASE whose clinical presentation can be indistinguishable from other encephalopathic or behavioral conditions. Moreover, its occurrence during oncologic treatment warrants clinicians to be on the lookout for similar presentations and encourages future reports of this condition in association with similar therapies. This case report provides value to providers treating patients with similar oncologic therapies and highlights the need for ASE to be further studied as it is a possible rare complication of allogeneic transplantation of stem cells.
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A 24-year-old female patient with pre-existing refractory epilepsy caused by tuberous sclerosis (TSC) and electroclinical features of Lennox-Gastaut syndrome (LGS) was referred to our hospital from an external clinic. Upon arrival, she presented with super-refractory status epilepticus (SRSE) since anaesthetics had already been used in the referring clinic. Despite various changes in ASM-treatment and continuous administration of anaesthetics for more than two weeks, SRSE could not be terminated. On treatment day 24, we started Fenfluramin (FFA) which was soon titrated to a dose of 0,7 mg/kg/day. A few days after beginning the treatment with FFA, EEG and clinical situation improved dramatically. The following 6 weeks of treatment went without reported seizures. This case illustrates the successful use of FFA in SRSE in TSC and LGS and, to the best of our knowledge, represents the first report of FFA in this clinical context.
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OBJECTIVE: Timely treatment is one of the most relevant prognostic factors in patients with urgent epileptic seizures. Despite the available evidence, treatment times remain suboptimal. The aim of this study was to demonstrate the impact of the "seizure code" in an emergency department, focusing on both treatment times and hospital outcomes of patients with urgent epileptic seizures. METHODS: An ambispective cohort study was conducted in the emergency department of a public hospital in Bogotá, Colombia. Treatment times and hospital outcomes were evaluated both before and after the implementation of the seizure code. RESULTS: A total of 336 patients were included (94 in the pre-seizure code period and 242 in the post-seizure code period). Both cohorts were comparable in terms of clinical and demographic baseline characteristics. After the implementation of the seizure code, in-hospital treatment times improved among patients with status epilepticus and seizure cluster. For the group of patients with status epilepticus, the time from arrival to the first benzodiazepine decreased from a median of 100.5 min (IQR: 43-152.5) to a median of 20 min (IQR: 10-45) (p = .0063), and the time from arrival to the first non-benzodiazepine antiseizure medication decreased from a median of 155 min (IQR: 49-194) to a median of 39 min (IQR: 25-57) (p = .0071). For the group of patients with seizure cluster, the time from arrival to the first non-benzodiazepine antiseizure medication decreased from a median of 296 min (IQR: 112.5-409) to a median of 72 min (IQR: 46-111) (p < .001). The seizure code significantly decreased the risk of inappropriate benzodiazepine use (p = .0087), in-hospital seizure recurrence (p < .001), in-hospital mortality (p = .0074), and prolonged hospitalizations (more than 48 h) (p = .0475). SIGNIFICANCE: The seizure code shortens the time to treatment, reduces the length of hospital stay, decreases the risk of inappropriate benzodiazepine use, and lowers both the in-hospital seizure recurrence and in-hospital mortality among patients with urgent epileptic seizures.
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OBJECTIVE: Intravenous (IV) push (IVP) is an alternative administration method for levetiracetam, but evidence evaluating it compared to IV piggyback (IVPB) for loading doses in acutely seizing patients is limited, particularly in patients with status epilepticus (SE). This study aimed to compare the efficiency and safety of IVP versus IVPB levetiracetam loading doses. METHODS: This was a single-center sequential retrospective study conducted in adult (≥18 years) patients who received an IV levetiracetam loading dose (>2000 mg or ≥20 mg/kg) for acute or suspected seizure. The primary outcome was time to administration, compared between doses given as IVP versus IVPB. Secondary outcomes included rates of adverse events (AEs), rescue benzodiazepine or antiseizure medication administration, intubation, and intensive care unit (ICU) admission between groups. RESULTS: A total of 246 patients were included; 116 received IVP and 130 received IVPB loading doses. Median age was 56 years; most patients were male (62%) and White (60%) and had witnessed seizures (67%). Doses were administered for SE in 32 (27.5%) and 46 (35.4%) patients in the IVP and IVPB arms, respectively. Median time to administration was shorter in the IVP group (12 vs. 38 min, p < .001). Bradycardia (1.7% vs. 2.3%, p = .99), hypotension (7.8% vs. 12%, p = .30), sedation (6% vs. 12.3%, p = .09), intubation (10% vs. 8%, p = .37), ICU admission (32% vs. 39%, p = .31), and rescue medication administration (8.6% vs. 14.6% p = .10) were similar between groups. In SE patients, IVP was associated with shorter time to administration (12 vs. 44 min, p = .003) and lower odds of ICU admission after adjustment for age, dose, Status Epilepticus Severity Score, and seizure history (adjusted odds ratio = .23, 95% confidence interval = .06-.81). SIGNIFICANCE: IVP reduced time to levetiracetam administration versus IVPB and was not associated with more AEs. Rescue agent use, intubation, and ICU admission were similar between arms, but IVP may reduce ICU admissions in SE patients. Prospective studies should assess the effectiveness of IVP versus IVPB.
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BACKGROUND: Acute central nervous system (CNS) complications are common and well described among pediatric patients undergoing haematopoietic cell transplantation (HCT). However, their long-term outcomes are not known. The aim of this study is to describe the incidence, characteristics, and risk factors of long-term epilepsy in pediatric patients with acute CNS complications of HCT. METHODS: This retrospective study included pediatric patients who developed acute CNS complications from autologous or allogeneic HCT between 2000 and 2022. Clinical, therapeutic and prognostic data including long-term outcomes were analyzed. A diagnosis of epilepsy was provided if unprovoked seizures occurred during follow-up. RESULTS: Ninety-four patients (63 males, 31 females, median age 10 years, range 1-21 years) were included. The most common acute CNS complications were posterior reversible encephalopathy syndrome (n = 43, 46 %) and infections (n = 15, 16 %). Sixty-five patients (69 %) had acute symptomatic seizures, with 14 (16 %) having one or more episodes of status epilepticus (SE). Nine patients (9.6 %) were diagnosed with long-term focal epilepsy during the follow-up (5-year cumulative incidence from the acute complication, 13.3 %). Acute symptomatic SE during neurological complications of HCT was associated with an increased risk of long-term epilepsy (OR=14, 95 % CI 2.87-68.97). CONCLUSIONS: A higher occurrence of epilepsy has been observed in our cohort compared to the general population. Acute symptomatic SE during HCT was associated with a higher risk of long-term epilepsy. Pediatric patients with CNS complications during HCT could benefit from specific neurological follow-up. Further studies are needed to characterize mechanisms of epileptogenesis in pediatric patients undergoing HCT.
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INTRODUCTION: Status Epilepticus (SE) can occur in patients without a previous epilepsy diagnosis, a condition identified as "new-onset status epilepticus" (NOSE). Treatment with benzodiazepine may fail in NOSE termination, requiring anti-seizure medication (ASM) employment. The term "established NOSE" (eNOSE) is generally employed in this context. This study aims to describe the main clinical characteristics of a large sample of patients suffering from eNOSE, compare the ASM efficacy, and explore the risk factors associated with ASM treatment unresponsiveness and eNOSE-associated mortality. METHODS: Adult patients diagnosed with eNOSE were retrospectively selected between January 2016 and December 2022. We reviewed demographics, clinical data, diagnostic work-up, and treatment. We considered the last ASM introduced before the eNOSE termination as effective. RESULTS: 123 patients were included (age: 67.9 ± 17.3). eNOSE acute etiology was mostly reported. In the overall cohort, phenytoin showed the highest response rate (p = 0.01). In the pairwise comparisons, valproate was superior to levetiracetam (p = 0.02) but not to lacosamide (p = 0.50). Phenytoin had a significantly higher resolution rate than levetiracetam (p = 0.001) but not lacosamide (p = 0.14). Thirty patients were refractory to ASM treatment. No predictors of refractoriness were identified. Thirty-nine patients died. Age and GCS were identified as eNOSE-related mortality risk factors. CONCLUSION: eNOSE frequently has an acute etiology with several associated syndromes. Phenytoin is more effective in managing eNOSE, even though lacosamide, valproate, and levetiracetam can represent further therapeutic options. Age and GCS are the main risk factors for eNOSE-associated mortality.
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Traumatic brain injuries lead to post-traumatic seizures (PTS), with acute subdural hematomas (ASDH) posing a particularly elevated risk. The development of refractory nonconvulsive status epilepticus (NCSE) in such cases, especially in older patients, requires immediate and effective management. This case report highlights the improvement of refractory NCSE in an elderly patient with ASDH through endoscope-assisted evacuation. An 88-year-old woman was hospitalized for dysarthria and right hemiparesis 3 days after a fall. Computed tomography (CT) revealed a left hemispheric ASDH, 9 mm thick, along with minor traumatic subarachnoid bleeding in the interpeduncular cistern. The initial treatment was conservative, including the administration of lacosamide at 100 mg/day. However, her consciousness deteriorated 4 days after admission, and she experienced convulsions in the right face and arm on day 5. Although the convulsions stopped after the administration of diazepam 10 mg IV and her consciousness temporarily improved, it worsened again on day 6, leading to a diagnosis of NCSE on an electroencephalogram (EEG). Despite aggressive pharmacological interventions with fosphenytoin (750 mg initially followed by 262 mg/day) and phenobarbital (625 mg/day), the patient's cognitive state and EEG findings did not improve. Consequently, on the 13th day, she underwent an endoscopic procedure to remove the SDH, which alleviated her symptoms and ended the seizures. This case demonstrates that even the absence of a significant mass effect from ASDH can trigger NCSE, underscoring the necessity for swift diagnosis and consideration of surgical options when conventional treatment fails. Endoscope-assisted evacuation is a safe and effective treatment option, particularly in older patients.
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Background/Objectives: To determine the impact of psychiatric disorders on epilepsy treatment outcomes and healthcare utilization in children with epilepsy (CWE) based on the presence or timing of the onset of psychiatric disorders. Methods: This retrospective controlled study enrolled children (age < 18 years) with newly diagnosed epilepsy into four groups stratified by the presence and timing of the onset of psychiatric disorders (None: no psychiatric disorders; Before: psychiatric disorders only preceding the epilepsy diagnosis; After: new psychiatric disorders diagnosed only after the epilepsy diagnosis; Mixed: different psychiatric disorders diagnosed both before and after epilepsy diagnosis) and compared the intergroup differences in epilepsy treatment outcomes and healthcare utilization. Results: Among the CWE (n = 37,678), 13,285 (35.26%) had comorbid psychiatric disorders. The After (n = 7892), Mixed (n = 3105), and Before (n = 2288) groups had significantly longer treatment periods than those in the None group (p < 0.001). Compared with the None group, the remaining groups had significantly higher frequencies of outpatient visits, emergency room visits, and admissions and higher rates of status epilepticus and drug-resistant epilepsy (p < 0.001, respectively), with higher odds ratios [95% confidence interval] for status epilepticus (2.92 [2.68-3.18]) and drug-resistant epilepsy (3.01 [2.85-3.17]) in the After group. Conclusions: Psychiatric comorbidities, diagnosed before and after epilepsy diagnosis, negatively affected the treatment outcomes. CWE without prior psychiatric disorders that were newly diagnosed during epilepsy treatment had the worst outcomes and the highest healthcare utilization rates.
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New-onset refractory status epilepticus (NORSE) is a devastating clinical condition that often leads to severe disability. Intrathecal dexamethasone (IT-DEX) has been reported to improve refractory status epilepticus. We present an 11-year-old female with anti-GAD 65 encephalitis presenting as NORSE who had minimal response to standard anti-seizure medications and first-line immunotherapies. The patient received 6 doses of IT-DEX in conjunction with rituximab which correlated with subsequent decreased neuroinflammation, reduced seizure burden and aided in weaning anesthetic infusions. Our case with literature review suggests IT-DEX may be utilized as an early intervention in those with refractory status epilepticus from various etiologies.
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The triggers of status epilepticus (SE) in non-epileptic patients can vary widely, from idiopathic causes to exposure to chemoconvulsants. Regardless of its etiology, prolonged SE can cause significant brain damage, commonly resulting in the development of epilepsy, which is often accompanied by increased anxiety. GABAA receptor (GABAAR)-mediated inhibition has a central role among the mechanisms underlying brain damage and the ensuing epilepsy and anxiety. During SE, calcium influx primarily via ionotropic glutamate receptors activates signaling cascades which trigger a rapid internalization of synaptic GABAARs; this weakens inhibition, exacerbating seizures and excitotoxicity. GABAergic interneurons are more susceptible to excitotoxic death than principal neurons. During the latent period of epileptogenesis, the aberrant reorganization in synaptic interactions that follow interneuronal loss in injured brain regions, leads to the formation of hyperexcitable, seizurogenic neuronal circuits, along with disturbances in brain oscillatory rhythms. Reduction in the spontaneous, rhythmic "bursts" of IPSCs in basolateral amygdala neurons is likely to play a central role in anxiogenesis. Protecting interneurons during SE is key to preventing both epilepsy and anxiety. Antiglutamatergic treatments, including antagonism of calcium-permeable AMPA receptors, can be expected to control seizures and reduce excitotoxicity not only by directly suppressing hyperexcitation, but also by counteracting the internalization of synaptic GABAARs. Benzodiazepines, as delayed treatment of SE, have low efficacy due to the reduction and dispersion of their targets (the synaptic GABAARs), but also because themselves contribute to further reduction of available GABAARs at the synapse; furthermore, benzodiazepines may be completely ineffective in the immature brain.
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Collagen VI (Col-VI) is an extracellular matrix protein primarily known for its bridging role in connective tissues that has been suggested to play a neuroprotective role. In the present study we report increased mRNA and protein expression of Col-VI in the hippocampus and cortex at a late stage of epileptogenesis in a post-status epilepticus (SE) model of epilepsy and in brain tissue from patients with epilepsy. We further present a novel finding that exposure of mouse hippocampal slices to Col-VI augments paired-pulse facilitation in Schaffer collateral-CA1 excitatory synapses indicating decreased release probability of glutamate. In line with this finding, lack of Col-VI expression in the knock-out mice show paired-pulse depression in these synapses, suggesting increased release probability of glutamate. In addition, we observed dynamic changes in Col-VI blood plasma levels in rats after Kainate-induced SE, and increased levels of Col-VI mRNA and protein in autopsy or postmortem brain of humans suffering from epilepsy. Thus, our data indicate that elevated levels of ColVI following seizures leads to attenuated glutamatergic transmission, ultimately resulting in less overall network excitability. Presumably, increased Col-VI may act as part of endogenous compensatory mechanism against enhanced excitability during epileptogenic processes in the hippocampus, and could be further investigated as a potential functional biomarker of epileptogenesis, and/or a novel target for therapeutic intervention.
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Introduction: New onset refractory status epilepticus (NORSE) is a rare and devastating condition characterised by the sudden onset of refractory status epilepticus (RSE) without an identifiable acute or active structural, toxic, or metabolic cause in an individual without a pre-existing diagnosis of epilepsy. Febrile infection-related epilepsy syndrome (FIRES) is considered a subcategory of NORSE and presents following a febrile illness prior to seizure onset. NORSE/FIRES is associated with high morbidity and mortality in children and adults. Methods and results: In this review we first briefly summarise the reported clinical, paraclinical, treatment and outcome data in the literature. We then report on existing knowledge of the underlying pathophysiology in relation to in vitro and in vivo pre-clinical seizure and epilepsy models of potential relevance to NORSE/FIRES. Discussion: We highlight how pre-clinical models can enhance our understanding of FIRES/NORSE and propose future directions for research.
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BACKGROUND: Status epilepticus (SE) imposes a significant burden in terms of in-hospital mortality and costs, but the relationship between SE causes, patient comorbidities, mortality, and cost remains insufficiently understood. We determined the in-hospital mortality and cost-driving factors of SE using a large and comprehensive database. METHODS: We conducted a retrospective cohort study involving patients experiencing their first hospitalization with an ICD-10 code diagnosis of SE, spanning from January 1, 2015, to December 31, 2019, using the French health insurance database which covers 99% of population. Patient characteristics, SE causes, Intensive Care Unit (ICU) admissions, mechanical ventilation, discharge status, and health insurance costs were extracted for each hospitalization. RESULTS: We identified 52,487 patients hospitalized for a first SE. In-hospital mortality occurred in 11,464 patients (21.8%), with associated factors including age (Odds Ratio [OR], 10.3, 95% Confidence Interval [CI] 7.87-13.8 for ages over 80 compared to 10-19), acute causes (OR, 15.3, 95% CI 13.9-16.8 for hypoxic cause), tumors (OR, 1.75, 95% CI 1.63-1.8), comorbidities (OR, 3.00, 95% CI 2.79-3.24 for 3 or more comorbidities compared to 0), and prolonged mechanical ventilation (OR, 2.61, 95% CI 2.42-2.82). The median reimbursed cost for each SE hospitalization was 6517 (3364-13,354), with cost factors mirroring those of in-hospital mortality. CONCLUSION: Causes and co-morbidities are major determinants of mortality and hospital costs in status epilepticus, and factors associated with higher mortality are also often associated with higher costs. Further studies are needed to identify their long-term effects.
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STUDY OBJECTIVES: Seizures are rare in rapid eye movement sleep (REM). However; seizures sometimes occur in REM, and a small number of focal epilepsy patients display their maximum rate of interictal epileptiform discharges in REM. We sought to systematically identify and characterize seizures in REM. METHODS: We reviewed all admissions to the Epilepsy Monitoring Unit (EMU) at the Winnipeg Health Sciences Centre over 12-months in 2014-2015. American Academy of Sleep Medicine sleep-stage scoring was initially applied in the standard 30-second epochs. Then, to capture sudden changes in sleep-wake state on shorter timescales that are associated with seizure formation and propagation, we re-scored ictal and peri-ictal EEG epochs every 1 second. Patients found to have seizures in REM were subject to chart review spanning three years pre- and post-admission. RESULTS: REM seizures occurred in 3/63 EMU patients. Notably, one patient exhibited continuous epileptiform activity, consistent with focal nonconvulsive electrographic status epilepticus, throughout REM cycles for each night of her admission. Otherwise, discrete REM seizures constituted a small fraction of the other patients' total seizures (range 5.0-8.3%), occurred shortly after REM onset from non-REM 2, and were manifest as minor epileptic arousals. CONCLUSIONS: Our results confirm that REM seizures are rare, while highlighting outliers who widen the known spectrum of heterogeneous sleep effects on seizures/epilepsy. We also report the first case of paradoxical status epilepticus in REM.
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This case report presents a 38-year-old male patient who, after a febrile infection, developed super-refractory status epilepticus and multiorgan failure, and died in 2 weeks despite the best possible intensive care. Autopsy revealed findings suggestive of hemophagocytic lymphohistiocytosis (HLH). This case shows that a rare immunological cause such as HLH may cause febrile infection-related epilepsy syndrome (FIRES), and complications of intensive care can mask the physiological and laboratory changes in HLH. PLAIN LANGUAGE SUMMARY: This case report presents a 38-year-old man who, after a febrile infection, developed intractable epileptic activity requiring intensive care treatment. During the intensive care, the patient showed signs of multiple organ damage and died in 2 weeks despite the best possible treatment. Autopsy revealed findings suggestive of hemophagocytic lymphohistiocytosis (HLH), which is a rare immune system regulation disorder leading to persistent inflammatory state and organ damages. This case shows that an immunological disorder like HLH may underlie treatment resistant fever-related epileptic seizures.
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Stiripentol (STP, Diacomit©) is an antiseizure medication indicated for Dravet syndrome, a rare developmental and epileptic encephalopathy characterized by drug-resistant seizures, including status epilepticus (SE). SE is a life-threatening event that may lead to increased risk of morbidity and mortality. Here, we evaluated the effect of STP on SE and SE-associated mortality using a CBA mouse model induced by systemic administration of methionine sulfoximine (MSO), an irreversible inhibitor of glutamine synthetase. MSO induces convulsions, prolonged seizure (SE) and death, with an increase of blood ammonia level. A single acute intraperitoneal pretreatment with 200-300-400 mg/kg of STP significantly inhibited the number of seizures, SE occurrence and death in MSO-treated animals in a dose-dependent manner. Regarding blood ammonia level, STP significantly reduced by 41 % the hyperammonemia induced by MSO. In conclusion, our results show protective effects of STP to reduce and or suppress the occurrence of SE as well as its associated mortality in mice.
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Introduction: The pregnant state may cause or exacerbate existing neurological disease. Gliomas appear to be influenced by the physiological changes that occur during pregnancy. The pregnant state may also cause seizures, including status epilepticus. There are currently no defined treatment guidelines to direct clinical decision making, and many of the commonly employed therapies are contraindicated during pregnancy. Case Presentation: The current article describes the case of a 40-year-old G3P1101 female at 10 weeks' gestation, who sought medical care for recurrent left hemifacial twitching, eventually leading to nonconvulsive status epilepticus. Intubation and sedation were required to achieve seizure cessation. Imaging revealed a lobulated cystic mass in the right parietal lobe, suspicious for low-grade glioma. Despite thorough explanation of the potential risks, the patient adamantly wished to pursue surgical intervention. An uneventful craniotomy was performed for resection of a low-grade glioma. No patient or fetal complications were encountered, and the patient has not had any reported seizures since surgery. Discussion: Managing complex neurosurgical diseases in pregnant patients provides both clinical and ethical quandaries. We describe the successful management of a patient presenting with status epilepticus caused by an underlying glioma during pregnancy. Although challenging, favorable neurosurgical outcomes are possible during pregnancy.
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INTRODUCTION: We analyze the diagnostic utility of urgent EEG (electroencephalogram) performed in children under 16 years of age in our center. MATERIAL AND METHODS: Descriptive, retrospective, observational study of consecutive patients from 0 to 16 years of age, who underwent an urgent EEG for any reason, from January to December 2022. RESULTS: Of the 388 patients, 70 were children: 37 (52.85%) women, and 33 (47.14%) men. Average age: 6.27⯱â¯4.809. Of the 70 patients, 6 (8.57%) had previous epilepsy. Reasons for consultation: 17 febrile seizures, 10 first focal seizures, 10 first TCG seizures, 6 paroxysmal episodes, 6 absences, 3 myoclonus of extremities, 3 syncope, 2 SE, 2 visual alterations, 2 low level of consciousness, 2 cyanosis, 2 suspected meningitis or encephalitis, 1 choking, 1 atypical headache, 1 chorea, 1 presyncope, 1 language delay. Of the 70 patients, 47 had a normal EEG (67.14%). Of the 47 patients with a normal EEG, 10 were diagnosed with epilepsy, and 3 of them began receiving antiepileptic treatment upon discharge. None of the patients with suspected syncope or paroxysmal disorder (17 patients, 24.28%) had EEG abnormalities. Of the 17 patients with atypical febrile seizures, 3 had EEG abnormalities. CONCLUSIONS: A third of the EEG records performed in the Emergency Department showed alterations, probably due to the time taken. Almost half of the patients with suspected epilepsy or EE showed EEG abnormalities, which confirmed the diagnosis in these cases and encouraged the clinician to start drug treatment. No case with a high suspicion of epilepsy was dismissed due to the normality of the EEG recording in our series. No patient diagnosed with syncope or paroxysmal disorder had EEG abnormalities. Nearly a quarter of patients with atypical febrile seizures showed EEG abnormalities. We barely register cases of status epilepticus, probably due to the degree of complexity of our center.
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Cognitive impairment is a prevalent co-morbidity associated with epilepsy. Emerging studies indicate that neuroinflammation could be a possible link between epilepsy and its comorbidities, including cognitive impairment. In this context, the roles of glial activation, proinflammatory mediators, and neuronal death have been well studied and correlated with epilepsy-associated cognitive impairment in animal studies. While recent reports have demonstrated the anti-epileptogenic and anti-convulsant actions of metformin, its effect on epilepsy associated cognitive deficit remains unknown. Therefore, the current study investigated the effect of metformin treatment on neuroinflammation, neurodegeneration, and cognitive deficits after inducing status epilepticus (SE) with lithium-pilocarpine in rats. Metformin treatment improved the hippocampal-dependent spatial and recognition memory in Morris water maze and Novel object recognition tasks, respectively. Further, metformin treatment attenuated microglial and astroglial activation, accompanied by reduced IL-1ß, COX-2 and NF-Ä¸ß gene expression. Additionally, metformin conferred neuroprotection by inhibiting the neuronal death as assessed by Nissl staining and transmission electron microscopy. These findings suggest that metformin holds promise as a therapeutic intervention for cognitive impairment associated with epilepsy, possibly through its modulation of glial activation and neuronal survival. Further research is needed to elucidate the precise mechanisms and to assess the long-term effect of metformin in epilepsy-associated cognitive impairment.