Symptomatic Epileptic Seizures Research Articles

Pharmacological Investigation of Anticonvulsant Effect of Artemisia Vulgaris on Pentylenetetrazole-Induced Epileptic Seizures in Zebrafish Experimental Model

Background:: Epilepsy is the most common neurological disorder, characterized by abnormal, unpredictable, and recurrent seizures. In the alternative medicine system, Artemisia vulgaris has been used to treat epileptic symptoms since its inception. However, scientific evidence concerning its effect on the treatment of epileptic seizures is not available. Objective:: The objective of the study is to evaluate the anti-convulsant potential of Artemisia vulgaris in zebrafish experimental models. Methods:: Zebrafish larvae and adult zebrafish were used as experimental models. Briefly, larvae and adult zebrafish were exposed to 0.5% of the test medicine Artemisia vulgaris mother tincture (ϕ) and its potencies (6CH, 30CH), and valproic acid for 1 hour. After 1 hour of exposure, they were exposed to pentylenetetrazole to record different seizure scores from 1 to 5 using ANY maze video tracking software. Results:: Artemisia vulgaris 30CH in zebrafish larvae and Artemisia vulgaris 6CH and 30CH in adult zebrafish delayed the latency score from score 1 to score 5 and were found effective against PTZinduced locomotor activity and seizure duration and intensity. Conclusion:: In conclusion, Artemisia vulgaris (6CH and 30CH) has the potential to be a novel treatment for symptomatic epileptic seizures and could be a potential alternative drug candidate for symptomatic treatment of epilepsy.

Prognosis and management of acute symptomatic seizures: a prospective, multicenter, observational study

BackgroundAcute symptomatic epileptic seizures are frequently seen in neurocritical care. To prevent subsequent unprovoked seizures, long-term treatments with antiseizure medications are often initiated although supporting evidence is lacking. This study aimed at prospectively assessing the risk of unprovoked seizure relapse with respect to the use of antiseizure medications. It was hypothesized that after a first acute symptomatic seizure of structural etiology, the cumulative 12-month risk of unprovoked seizure relapse is ≤ 25%.MethodsInclusion criteria were age ≥ 18 and acute symptomatic first-ever epileptic seizure; patients with status epilepticus were excluded. Using telephone and mail interviews, participants were followed for 12 months after the acute symptomatic first seizure. Primary endpoint was the occurrence and timing of a first unprovoked seizure relapse. In addition, neuro-intensivists in Germany were interviewed about their antiseizure treatment strategies through an anonymous online survey.ResultsEleven of 122 participants with structural etiology had an unprovoked seizure relapse, resulting in a cumulative 12-month risk of 10.7% (95%CI, 4.7%–16.7%). None of 19 participants with a non-structural etiology had a subsequent unprovoked seizure. Compared to structural etiology alone, combined infectious and structural etiology was independently associated with unprovoked seizure relapse (OR 11.1; 95%CI, 1.8–69.7). Median duration of antiseizure treatment was 3.4 months (IQR 0–9.3). Seven out of 11 participants had their unprovoked seizure relapse while taking antiseizure medication; longer treatment durations were not associated with decreased risk of unprovoked seizure relapse. Following the non-representative online survey, most neuro-intensivists consider 3 months or less of antiseizure medication to be adequate.ConclusionsEven in case of structural etiology, acute symptomatic seizures bear a low risk of subsequent unprovoked seizures. There is still no evidence favoring long-term treatments with antiseizure medications. Hence, individual constellations with an increased risk of unprovoked seizure relapse should be identified, such as central nervous system infections causing structural brain damage. However, in the absence of high-risk features, antiseizure medications should be discontinued early to avoid overtreatment.

Epileptic seizures and epilepsy in children after stroke

Despite the low prevalence of cerebrovascular diseases in childhood, up to 60% of children realize acute symptomatic epileptic seizures and up to 30% of patients develop post-stroke epilepsy in the long-term period. The lack of a unified terminology and temporal criteria for both acute symptomatic epileptic seizures and post-stroke epilepsy complicates the analysis of the studied groups. Many studies are limited to small groups, proprietary terminology, different age medians, and inclusion criteria. Both clinical and instrumental risk factors for the development of post-stroke epilepsy in childhood have not been identified, which makes it difficult to identify risk groups and predict the outcome in the long term period. The only significant risk factor in most publications is «younger age», but its boundaries are blurred. Most studies are retrospective, which may affect the incidence and type of epileptic seizures in acute cerebrovascular accident. Electroencephalography is the most informative method for detecting subclinical changes and identifying risk groups. Continuous electroencephalography is effective primarily in the detection of non-convulsive status epilepticus. Currently, there are no unified protocols for examining stroke patients, both at the onset and in follow-up. The search for articles was carried out in the scientific platforms PubMed, Google Scholar, eLIBRARY.

Intracranial hemorrhage in a patient with depressive anxiety disorder about a case

IntroductionWe present the case of a 69-year-old patient who went to the emergency department due to an episode of aggressiveness and behavioral alteration, presenting irritability and nervousness, of about 2 days of evolution according to her family member. Given that the patient had previously presented chronic behavioral disorders and had previously been followed up in psychiatric consultations, psychiatry was notified after an initial evaluation by the emergency physician.ObjectivesSomatic personal history: NAMC. HTA. Not DM, not DL. Former smoker of 20 cigarettes/day. Recurrent intracranial hemorrhage secondary to amyloid angiopathy and suspected amyloid vasculitis. Last admission to the neurology service in June 2022, also presenting symptomatic epileptic seizures and secondary behavioral alterations. Mastocytosis. Post-traumatic vertebral fracture. Non-anticoagulated paroxysmal atrial fibrillation. Surgical: Left ear surgery. appendectomy. Hysterectomy + oophorectomy.Personal psychiatric history: In follow-up since May 2021 referred from neurology for emotional lability, episodes of anger and fear. Diagnosed with anxiety-depressive disorder secondary to a medical illness.Current psychiatric treatment: Oxcarbazepine 800mg 0-0-1, trazodone 100mg 0-0-1, aripiprazole 10mg 1-0-0.MethodsCurrent illness: The patient goes to the emergency room brought by her husband. During the interview she minimizes her aggressive behaviors or even does not remember them. She is disoriented in time, with very striking memory failures. Her husband comments verbal aggressiveness if he contradicts her in something, sometimes even presenting physical aggressiveness with her relatives. They report that in the last psychiatric consultation a little over 1 month ago, aripiprazole was withdrawn due to an increased risk of cardiovascular events.After the examination of the patient, she was referred back to the emergency department for a new assessment and to rule out the organicity of the current condition, given that the patient had cardiovascular risk factors, due to the suspicion of a new episode of intracranial hemorrhage.Resultssychopathological examination: Vigil, conscious, disoriented in time, partially in space. Collaborative, calm during the interview. Coherent, structured speech, with obvious memory failures. Labile, irritable mood. Verbal and physical heteroaggressiveness at home, not during the interview. No structured or planned autolytic ideation at this time. Appetite and sleep preserved.ConclusionsAn urgent head CT was requested, with the result of a small intraparenchymal bleeding in the left frontal location, and she was admitted to the neurology department, with a diagnosis at discharge of: small left frontal haematoma, suspected amyloid vasculitis, and secondary behavioral alteration (vascular dementia).Disclosure of InterestNone Declared

Acute symptomatic epileptic seizures and epilepsy after stroke

Acute symptomatic epileptic seizures occur within 7 days after the stroke onset. Acute symptomatic epileptic seizures occur in 6.3% of stroke cases: ischemic stroke 4.2%, cerebral infarction with hemorrhagic transformation 12.5%, intracerebral hemorrhage 16.2%. Cumulative risk of subsequent unprovoked epileptic seizure after the first acute symptomatic seizure at follow-up for 10 years is 18.7 %. In acute symptomatic epileptic seizure secondary prevention with antiepileptic drugs usually is not indicated. If antiepileptic drug treatment is initiated after a single acute symptomatic seizure, it should be discontinued after the acute period of the disease. The 10-years risk of subsequent unprovoked epileptic seizures after the single unprovoked epileptic seizure in stroke patients is 71.5%. In this situation the epilepsy diagnosis is reasonable and antiepileptic drug treatment should be initiated. The incidence of epilepsy after acute ischemic or hemorrhagic stroke is identical 1012%. The choice of the group of antiepileptic drugs should be based on clinical guidelines for patients with focal forms of epilepsy. Pharmacokinetic interactions between antiepileptic drugs and oral anticoagulants, antiplatelet agents, antihypertensive drugs, and other xenobiotics should be minimized. Thus antiepileptic drugs that induce or inhibit microsomal liver enzymes should also be avoided.

Treatment of COVID‐19‐induced refractory status epilepticus by tocilizumab

Background and purposeCOVID‐19 is a novel infectious disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) in which neurological complications have been increasingly recognized. Acute symptomatic epileptic seizures and status epilepticus are frequently reported neurological complications associated with this infection. The nervous system damage caused by SARS‐CoV‐2 may be mediated by the immune system. Interleukin 6 (IL‐6), an important component of the cytokine storm, is directly correlated with the severity of symptoms. Tocilizumab is an inhibitor of IL‐6 receptors, which blocks IL‐6‐mediated signal transduction and is used in the treatment of COVID‐19 and status epilepticus.Case reportA patient with the Unverricht–Lundborg disease is presented who had developed refractory recurrent status epilepticus during COVID‐19 infection, which was finally controlled by treatment with tocilizumab.DiscussionTocilizumab, an IL‐6 inhibitor, may be considered as a treatment option in patients with status epilepticus and refractory seizures.

Symptomatic Epileptic Seizures in Patients with Brain Gliomas

Introduction. Epileptic seizures are an important problem that significantly worsens the quality of patients’ life with both newly diagnosed and recurrent brain gliomas.Review. The analysis of domestic and foreign literature showed that low-grade gliomas, this symptom occurs on average in 76%, with high-grade gliomas – in 21% of patients. Despite the maximum allowable tumor resection, it is likely that epileptic seizures persist in 18-64% of patients, and in 5% of patients they first appear in the postoperative period. From 15 to 50% of epileptic seizures in cerebral gliomas are drug-resistant. In patients undergoing chemotherapy, it is better to use new antiepileptic drugs because their cross-effects are minimal.Conclusion. There is no generally accepted algorithm for prescribing and discontinuing antiepileptic drugs in patients with symptomatic epileptic seizures with cerebral gliomas. Further research is needed to determine the optimal combination and dosage regimen of antiepileptic drugs, especially during chemotherapy.

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Acute symptomatic seizures during haematopoietic stem cell transplantation

Acute symptomatic epileptic seizures are one of the complications of hematopoietic stem cell transplantation. The etiological factors leading to the development of this complication differ from those in the general population, while the significance of each of them is different depending on the time after transplantation. We analyze the literature data on the role of drugs, metabolic disorders and infectious complications, as well as the structural pathology of the brain substance in the development of acute symptomatic seizures in patients with oncohematological pathology. We also consider the clinical features of symptomatic epileptic seizures and the possible prognostic significance of their development in patients who underwent hematopoietic stem cell transplantation.

Acute symptomatic epileptic seizures in the early postoperative period

The article provides an overview of recent studies related to epidemiology, diagnosis and treatment of acute symptomatic epileptic seizures (ASES)in the early postoperative period after brain intervention. Themain points distinguishing ASES fromseizures in epilepsy are highlighted. The initial condition of the patient, the reason for which the surgery was performed and the volume of the intervention are the main criteria that must be taken into account when assessing risk factors for epileptic seizures. An algorithm for managing a patient with ASES is presented.

The study of sodium and potassium channel gene single-nucleotide variation significance in non-mechanical forms of epilepsy

BackgroundEpilepsy is one of the most common and heterogeneous neurological diseases. The main clinical signs of the disease are repeated symptomatic or idiopathic epileptic seizures of both convulsive and non-convulsive nature that develop against a background of lost or preserved consciousness. The genetic component plays a large role in the etiology of idiopathic forms of epilepsy. The study of the molecular genetic basis of neurological disorders has led to a rapidly growing number of gene mutations known to be involved in hereditary ion channel dysfunction. The aim of this research was to evaluate the involvement of single-nucleotide variants that modify the function of genes (SCN1A, KCNT1, KCNTС1, and KCNQ2) encoding sodium and potassium ion channel polypeptides in the development of epilepsy.ResultsDe novo mutations in the sodium channel gene SCN1A c.5347G>A (p. Ala1783Thr) were detected in two patients with Dravet syndrome, with a deletion in exon 26 found in one. Three de novo mutations in the potassium channel gene KCNT1 c.2800G>A (p. Ala934Thr), were observed in two patients with temporal lobe epilepsy (TLE) and one patient with residual encephalopathy. Moreover, a control cohort matched to the case cohort did not reveal any SNVs among conditionally healthy individuals, supporting the pathogenic significance of the studied SNVs.ConclusionOur results are supported by literature data showing that the sodium ion channel gene SCN1A c.5347G>A mutation may be involved in the pathogenesis of Dravet syndrome. We also note that the c.2800G>A mutation in the potassium channel gene KCNT1 can cause not only autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) but also other forms of epilepsy. To treat pathogenetic mutations that accelerate the function of sodium and potassium ion channels, we recommend ion channel blockade drug therapy.

Clinical Diagnosis and Perioperative Management of Glioma-Related Epilepsy.

Gliomas account for more than half of all adult primary brain tumors. Epilepsy is the most common initial clinical presentation in gliomas. Glioma related epilepsy (GRE) is defined as symptomatic epileptic seizures secondary to gliomas, occurring in nearly 50% in high-grade glioma (HGG) patients and up to 90% in patients with low-grade glioma (LGG). Uncontrolled seizures, which have major impact on patients’ quality of life, are caused by multiple factors. Although the anti-seizure medications (ASMs), chemotherapy and radiation therapy are also beneficial for seizure treatment, the overall seizure control for GRE continue to be unsatisfactory. Due to the close relationship between GRE and glioma, surgical resection is often the treatment of choice not only for the tumor treatment, but also for the seizure control. Despite aggressive surgical treatment, there are about 30% of patients continue to have poor seizure control postoperatively. Furthermore, the diagnostic criteria for GRE is not well established. In this review, we propose an algorithm for the diagnosis and perioperative management for GRE.

Analysis of the role of viral encephalitis in the development of epileptic seizures and epilepsy

The aim – to determine the role of viral lesions of the central nervous system (CNS) in the development of epileptic seizures and epilepsy.Materials and methods: analysis of scientific literature data. The review discusses the role of non-epidemic viral encephalitis and human immunodeficiency virus in the development of acute epileptic seizures and epilepsy; epidemiological data and risk factors.Results. Viral infections are often complicated by acute (early) epileptic seizures and causes the risk of further epilepsy. The mechanisms of development of early and late seizures differ. Except herpetic encephalitis, in which risk of epilepsy in early seizures is up to 60 %, the risk of late seizures in other viral encephalitis hasn't been determined. Timely treatment of viral infections and early seizures reduces the risk of epilepsy. Treatment of epilepsy with infectious lesions of the central nervous system and other types of symptomatic epilepsy is similar, and the antiepileptic drug is determined by the semiology of seizures. The interaction between it and anti-infective drugs can change the concentration in the blood of each of them, which will lead to reduced effectiveness or toxicity. This is especially important for individuals with human immunodeficiency virus infection in whom antiretroviral drugs have significant interactions with antiepileptic drugs. Since epileptic activity of the brain is associated with the severity and complications of the underlying infection, early aggressive therapy prevents the development of late seizures and epilepsy.Conclusions. CNS infections account for 15 % of all newly diagnosed symptomatic epileptic seizures. The 20-year risk of unprovoked seizures and epilepsy after CNS infections ranges from 2.4 % to 22 %. The risk depends on the etiology, location of the lesion and the severity; it is high in herpes-associated encephalitis

Correlation between Kir4.1 expression and barium-sensitive currents in rat and human glioma cell lines

Gliomas are the most common primary brain tumors and often become apparent through symptomatic epileptic seizures. Glial cells express the inwardly rectifying K+ channel Kir4.1 playing a major role in K+ buffering, and are presumably involved in facilitating epileptic hyperexcitability. We therefore aimed to investigate the molecular and functional expression of Kir4.1 channels in cultured rat and human glioma cells. Quantitative PCR showed reduced expression of Kir4.1 in rat C6 and F98 cells as compared to control. In human U-87MG cells and in patient-derived low-passage glioblastoma cultures, Kir4.1 expression was also reduced as compared to autopsy controls. Testing Kir4.1 function using whole-cell patch-clamp experiments on rat C6 and two human low-passage glioblastoma cell lines (HROG38 and HROG05), we found a significantly depolarized resting membrane potential (RMP) in HROG05 (-29 ± 2 mV, n = 11) compared to C6 (-71 ± 1 mV, n = 12, P < 0.05) and HROG38 (-60 ± 2 mV, n = 12, P < 0.05). Sustained K+ inward or outward currents were sensitive to Ba2+ added to the bath solution in HROG38 and C6 cells, but not in HROG05 cells, consistent with RMP depolarization. While immunocytochemistry confirmed Kir4.1 in all three cell lines including HROG05, we found that aquaporin-4 and Kir5.1 were also significantly reduced suggesting that the Ba2+-sensitive K+ current is generally impaired in glioma tissue. In summary, we demonstrated that glioma cells differentially express functional inwardly rectifying K+ channels suggesting that impaired K+ buffering in cells lacking functional Ba2+-sensitive K+ currents may be a risk factor for increased excitability and thereby contribute to the differential epileptogenicity of gliomas.

The Difference of Lymphocyte, hs-CRP, and Electroencephalogram with and without Simvastatin in Acute Ischemic Stroke

Mortality and morbidity due to stroke rank the highest in Indonesia (15.4%), and most types of stroke are ischemic (87%). Inflammation has a role in the pathophysiology of both ischemic stroke and also inhibits acute symptomatic epileptic seizures (3-6%) in the first 7 days after stroke. Statins have been used for the treatment of dyslipidemia in stroke patients. Some studies showed that statins reduced the inflammatory response after a stroke and prevented the recovery of epileptic seizures. This study aimed to determine the differences in lymphocytes, hs-CRP, Electroencephalogram (EEG) with and without Simvastatin in acute ischemic stroke. This research was an experimental study with a double-blind, randomized control trial design consisting of two groups, a group given Simvastatin 20 mg/day, and a group given a placebo for seven days. The difference in lymphocytes, hs-CRP, EEG, and epileptic seizures between the two groups were then analyzed. The sample was 26 people, consisting of 17 (65.4%) males and 9 (34.6%) females with an average age of 59±5.8 years. Chi-Square and Fisher's test showed a significant difference in hs-CRP (p=0.005) and epileptic seizures (p=0.015), but no significant difference in lymphocytes (p=0.336) and EEG (p=0.42) between groups given Simvastatin 20 mg/day and those given placebo. There was a significant difference in hs-CRP and epileptic seizures, but no significant difference in lymphocyte count and EEG between the two groups with and without Simvastatin administration.

Seizure-like events leading to hospital referrals in infants: A retrospective population-based study.

To identify the aetiology and outcome of seizure-like events leading to hospital referrals in infants and to identify early predictors of epilepsy and delayed neurodevelopment. This Norwegian population-based study focused on all children born in Sør-Trøndelag county, who were up to one year of age in 2014-2015. They were identified by diagnostic codes for seizure-like events and electroencephalography (EEG) examinations. Hospital records were examined up to 1.5years of age. The one-year prevalence of seizure-like events was 1.5% (114/7430). Epilepsy was diagnosed in 17%, 57% had non-epileptic paroxysmal events (NEPE), 16% had febrile seizures, and 10% had other acute symptomatic epileptic seizures. Neurodevelopmental delay occurred in 21%. The cumulative incidence was 0.22% for epilepsy and 0.79% for NEPE. Abnormal brain magnetic resonance imaging, abnormal first EEGs and neonatal care increased the likelihood of epilepsy and delayed development. Identifying situation-related factors decreased the epilepsy risk. Occurrence at a younger age increased the risk of delayed development. Absence of unambiguous motor symptoms was less common in epilepsy than in NEPE. Seizure-like events were common in infants and most were not caused by epilepsy. Specific anamnestic clues, and detailed descriptions of the entire event, helped to predict adverse outcomes.

Neurological Manifestations of Sanjad–Sakati Syndrome: New Three Reported Cases from Tunisia

AbstractSanjad–Sakati syndrome (SSS), or hypoparathyroidism–mental retardation dysmorphism syndrome, is a rare autosomal recessive congenital disorder characterized by congenital hypoparathyroidism, growth and neurodevelopmental delay, acute symptomatic seizures due to hypocalcemia, and dysmorphic features. The syndrome is underdiagnosed, and neurological manifestations are not previously described. We report three Tunisian patients with SSS revealed by acute symptomatic hypocalcemic epileptic seizures. Despite the well-controlled seizures, patients tend to continue having poor growth and neurological outcome. The diagnosis of SSS allowed for proper treatment of the patients, prevented associated comorbidities, and provided genetic counseling to their families.

Epileptic seizures and outcome in different subtypes of subarachnoid haemorrhage – Results of a single-center retrospective analysis

BackgroundSymptomatic epileptic seizures are an important complication in subarachnoid haemorrhage (SAH) with a frequency of 0.9–25% with importance for patient outcome. The majority of previous studies investigated the incidence of symptomatic epileptic seizures after aneurysmatic SAH. Here we compared the seizure incidence and its impact on the outcome between non-aneurysmatic and aneurysmatic SAH. MethodsWe analysed retrospectively 109 consecutive patients with spontaneous, non-traumatic SAH. Patients were divided in three groups (perimesencephalic, non-aneurysmatic and aneurysmatic SAH). All patients received standard-of-care treatment. The occurrence of acute (0–7 days after SAH) and remote symptomatic epileptic seizures (7 days or more after SAH), severity of SAH as well as clinical outcome parameters (modified Rankin scale [mRS]) at discharge and the frequency of in-house complications were assessed. mRS scores were dichotomized in 0–3 vs. 4–6 to stratify for good versus bad outcome. ResultsPerimesencephalic SAH patients did not experience acute seizures whereas non-aneurysmatic and aneurysmatic SAH patients showed acute seizures with similar frequency (9% and 11%, p = 0.23). The frequency of remote symptomatic seizures was similar in all subgroups (12% vs. 9% vs. 7%, p = 0.72). Seizure occurrence was not predictive for a poor outcome (mRS >4; acute seizures: OR 0.35 [95%CI: 0.02–6.96], p = 0.49; remote seizures: OR 1.72 [95%CI: 0.14–20.1], p = 0.67). ConclusionsSeizures are important neurologic complications of SAH of all etiologies. Nevertheless, acute as well as remote symptomatic seizures are unrelated to the short-term outcome. These results should be treated as hypothesis generating and require confirmation.

Clinical practice guidelines for the diagnosis and treatment of adult diffuse glioma-related epilepsy.

BackgroundGlioma‐related epilepsy (GRE) is defined as symptomatic epileptic seizures secondary to gliomas, it brings both heavy financial and psychosocial burdens to patients with diffuse glioma and significantly decreases their quality of life. To date, there have been no clinical guidelines that provide recommendations for the optimal diagnostic and therapeutic procedures for GRE patients.MethodsIn March 2017, the Joint Task Force for GRE of China Association Against Epilepsy and Society for Neuro‐Oncology of China launched the guideline committee for the diagnosis and treatment of GRE. The guideline committee conducted a comprehensive review of relevant domestic and international literatures that were evaluated and graded based on the Oxford Centre for Evidence‐Based Medicine Levels of Evidence, and then held three consensus meetings to discuss relevant recommendations. The recommendations were eventually given according to those relevant literatures, together with the experiences in the diagnosis and treatment of over 3000 GRE cases from 24 tertiary level hospitals that specialize in clinical research of epilepsy, glioma, and GRE in China.ResultsThe manuscript presented the current standard recommendations for the diagnostic and therapeutic procedures of GRE.ConclusionsThe current work will provide a framework and assurance for the diagnosis and treatment strategy of GRE to reduce complications and costs caused by unnecessary treatment. Additionally, it can serve as a reference for all professionals involved in the management of patients with GRE.

Serum magnesium in adult patients with idiopathic and symptomatic epilepsy in Maiduguri, Northeast Nigeria.

Alteration in the homeostasis of trace elements such as magnesium may play a role in the development of epileptic seizures. This study aims to investigate the levels of serum magnesium in people with idiopathic generalized epileptic (IGE) seizures and symptomatic seizures in Northeast Nigeria. Serum magnesium level was measured using atomic absorption spectrometry among 40 adults with IGE, 20 adults with symptomatic epileptic seizures, and 30 healthy controls. Serum calcium, potassium, phosphate, and albumin were also measured. The mean serum magnesium level was significantly lower among people with epilepsy compared with the controls [0.79 ± 0.18 mmol/L vs 0.90 mmol/L ± 0.17, P = 0.007, 95% confidence interval (CI): (-0.189 to -0.031)]. People with IGE had significantly lower levels of magnesium compared with those with symptomatic seizures [0.74 ± 0.17 mmol/L vs 0.9 ± 0.16 mmol/L, P < 0.001 95% CI: (-0.251 to -0.069)]. The mean magnesium level for all groups was in the reference range, but the lowest levels were observed in those with IGE. There is no significant correlation between the level of serum magnesium and the severity of seizure attacks. There was significantly lower level of calcium in people with IGE compared with those with symptomatic seizures [2.3 ± 0.13 mmol/L vs 2.4 ± 0.16 mmol/L, P = 0.012, 95% CI: (-0.177 to 0.023)] or controls [2.3 ± 0.13 mmol/L vs 2.4 ± 0.12 mmol/L, P < 0.01, 95% CI: (-0.156 to -0.044)]. No significant differences were observed in the levels of potassium, phosphate, and albumin. This study suggests that low serum magnesium and calcium may play a role in IGE, and supplementation may be useful in reducing seizures in Black patients with epilepsy.