Journal of epilepsy research最新文献

Background and purpose: There are no highly sensitive biomarkers for epilepsy to date. Recently, promising results regarding functional connectivity analysis have been obtained, which may improve epilepsy diagnosis even in the absence of visible abnormality in electroencephalography. We aimed to investigate the differences in functional connectivity after a first unprovoked seizure between patients diagnosed with epilepsy within 1 year due to subsequent seizures and those who were not.

Methods: We compared quantitative electroencephalography power spectra and functional connectivity between 12 patients who were diagnosed with epilepsy (two or more unprovoked seizures) within 1 year and 17 controls (those not diagnosed within 1 year) using iSyncBrain^® (iMediSync Inc., Suwon, Korea; https://isyncbrain.com/). In the source-level analysis, the current distribution across the brain was assessed using the standardized low-resolution brain electromagnetic tomography technique, to compare relative power values in 68 regions of interest and connectivity (the imaginary part of coherency) between regions of interest.

Results: In the epilepsy group, quantitative electroencephalography showed lower alpha2 band power in left frontal, central, superior temporal, and parietal regions and higher beta2 power in both frontal, central, temporal, occipital, and left parietal regions compared with the control group. Additionally, epilepsy patients had significantly lower connectivity in alpha2 and beta2 bands than the controls.

Conclusions: Patients experiencing their first unprovoked seizure presented different brain function according to whether they have subsequent seizures and future epilepsy. Our results propose the potential clinical ability to diagnose epilepsy after the first unprovoked seizure in the absence of interictal epileptiform discharges.

New-onset refractory status epilepticus (NORSE) is a condition defined as the occurrence of refractory status epilepticus in patients without active epilepsy and no other acute causes of seizure. Although there is evidence that immune-mediated pathogenesis has a pivotal role in the epileptogenesis of NORSE, the diagnosis of NORSE is usually made on the clinical observation because there is no established biological marker suggesting the diagnosis of NORSE. We recently encountered a NORSE patient who was successfully treated with immunotherapy including tocilizumab, an anti-interleukin-6 (IL-6) receptor monoclonal antibody, and the markedly increased levels of serum and cerebrospinal fluid IL-6 were the only laboratory abnormality during the early treatment of the patient.

Perampanel is a novel antiepileptic drug that has been used as an adjunctive treatment for focal-onset seizures. No reports to date have documented respiratory suppression as a side effect of perampanel in adults. Herein, we report a 51-year-old man with focal epilepsy presented with type 2 respiratory failure after accidently consuming of 66 mg of perampanel. Clinicians should consider the possibility of respiratory compromise whenever a high dose of perampanel needs to be administered to patients.

Background and purpose: De novo status epilepticus (SE) had worse outcome in comparison to the patients with SE who had previous history of epilepsy. The aim of the present study was to identify clinical features of de novo convulsive status epilepticus (CSE) and the predictors of in-hospital mortality.

Methods: Seventy-seven elderly (≥60 years of age) hospitalized patients with de novo CSE were evaluated for clinical profile, aetiologies and predictors of in-hospital mortality.

Results: The average age of the participants in the study was 65.96±6.72 years. In de novo CSE, the most common aetiologies were acute symptomatic in 68.8% of cases, followed by remote symptomatic in 24.7%. In-hospital mortality in the de novo CSE in the elderly was 30 (38.9%) in our series. Stroke was the leading cause of death among them (acute stroke in 23 cases and old infarct in 1 case), followed by post-traumatic (n=4) and CNS infection (n=2). On multivariate analysis, it was found that variables significantly related to mortality in de novo CSE were low Glasgow coma scale (GCS) (adjusted odds ratio [AOR], 53.5; 95% confidence interval [CI], 5.17-555.14; p=0.001) and lack of response to first line treatment (AOR, 0.06; 95% CI, 0.01-0.50; p=0.01).

Conclusions: In-hospital mortality in de novo CSE patients was linked to a low GCS and a lack of response to first-line therapy. The most efficient strategy to prevent in-hospital mortality in the elderly is to treat de novo CSE promptly and aggressively in the setting of stroke.

Cerebral salt wasting syndrome (CSWS) is defined as a renal loss of sodium in cerebral disorders causing hyponatremia and loss of extracellular fluid volume. Similar laboratory findings may be seen in other conditions such as syndrome of inappropriate antidiuretic hormone secretion (SIADH). A 58-year-old male visited our emergency department because of the sudden development of seizures during sleep. Magnetic resonance imaging revealed subtle high signal intensity in the right hippocampus on diffusion-weighted imaging. Ictal rhythmic discharges were observed in the concordant area. Altered metal status, polyuria and laboratory test findings including hyponatremia were compatible with CSWS. After hydration and salt replacement, his mental state and hyponatremia gradually recovered. For diagnosing CSWS, meticulous physical examinations including analysis of fluid balance are essential. CSWS should be considered in patients with hyponatremia and polyuria. Accurate diagnosis of CSWS and SIADH is crucial as the treatment plans for these two conditions are completely different.

Background and purpose: Status epilepticus (SE) results in permanent neuronal brain damage in the central nervous system. One of the complex etiologies underlying SE pathogenesis is neuroinflammation. Dapsone has been recently considered as a potential neuroprotective agent in neuroinflammatory conditions. Therefore, the present study aims to investigate effects of dapsone on lithium-pilocarpine-induced SE in rats and assess whether tumor necrosis factor-alpha (TNF-α) and nitric oxide (NO) pathway participate in this effect.

Methods: SE was established by injecting lithium chloride (127 mg/kg, intraperitoneally [i.p.]) and pilocarpine (60 mg/kg, i.p.). The animals received pre-treatment dapsone (2, 5, 10, and 20 mg/kg, oral gavage) and post-treatment dapsone (10 mg/kg). Subsequently, seizure score and mortality rate were documented. To assess the underlying signaling pathway, L-Nω-Nitro-L-arginine methyl ester hydrochloride (a non-specific NO synthase [NOS] inhibitor), 7-nitroindazole (a specific neuronal NOS inhibitor), and aminoguanidine (a specific inducible NOS inhibitor) were administered 15 minutes before dapsone (10 mg/kg) pre- or post-treatment. Hippocampal tissue TNF-α and NO concentrations were quantified using the enzyme-linked immunosorbent assay method.

Results: Dapsone (10 mg/kg) pre-and post-treatment significantly attenuated the increased seizure score and mortality rate due to lithium-pilocarpine-induced SE. The development of SE in animals was associated with higher TNF-α and NO metabolites levels, which notably decreased in the dapsone-treated rats. Moreover, co-administration of NOS inhibitors with dapsone markedly reversed the anti-epileptic effects of dapsone and caused an escalation in TNF-α level but a significant reduction in NO concentration level.

Conclusions: It seems that dapsone may exert an anti-epileptic effect on lithium-pilocarpine-induced SE through TNF-α inhibition and modulation of the nitrergic pathway.