Psychogenic non-epileptic seizures (PNES), which closely resemble epileptic seizures (ES), are typically triggered by psychological distress and represent the most prevalent form of conversion disorder encountered in clinical practice. Multiple physical conditions can both precipitate and sustain PNES episodes. Epilepsy, a common neurological disorder, imposes significant emotional and physical burdens, frequently resulting in elevated levels of anxiety and depression. This case report details the clinical course of a 19-year-old female whose PNES was exacerbated by the diagnosis and disease burden of epilepsy. The patient\'s background of childhood trauma, bullying, and sexual abuse likely predisposed her to the development of PNES. Upon receiving a diagnosis of epilepsy, characterized by focal seizures originating from the left parietal region, the patient experienced increased anxiety and required frequent hospitalizations. Despite adjustments to her treatment regimen, including the administration of levetiracetam (LEV) and lacosamide (LCM), her seizures persisted. Comprehensive evaluations, comprising electroencephalography (EEG) and single-photon emission computed tomography (SPECT), indicated the coexistence of epilepsy and PNES. Although surgical intervention was initially considered, it was ultimately deemed unnecessary, which subsequently alleviated the patient\'s anxiety. Psychoeducation highlighting the manageability of her epilepsy with ongoing pharmacotherapy significantly reduced her PNES episodes. This case emphasizes the critical role of addressing the psychosocial burden associated with an epilepsy diagnosis, as these factors may exacerbate PNES. It also underscores the importance of a holistic treatment approach that integrates psychological support with medical management.

UNASSIGNED: Electroconvulsive therapy (ECT) is widely recognized as one of the most effective treatments for various psychiatric disorders and is generally considered safe. However, a few reports have mentioned that multiple ECT sessions could induce electroencephalography (EEG) abnormalities and epileptic seizures, a serious side effect of ECT. We experienced a case with EEG abnormalities after multiple ECT sessions and aimed to share our insights on conducting ECT safely.
UNASSIGNED: We present the case of a 73-year-old female diagnosed with major depressive disorder. She underwent regular ECT sessions to alleviate her psychiatric symptoms. However, after more than 80 sessions, previously undetected EEG abnormalities were observed. Since the patient did not have clinical seizures, we were able to continue ECT at longer intervals without the use of antiepileptic drugs.
UNASSIGNED: Our case suggests the importance of routine EEG testing in patients undergoing prolonged ECT. While careful monitoring is necessary, continuing ECT without antiepileptic medication in patients with EEG abnormalities could be permissible.

A 4-year-old male neutered Boston Terrier was presented with status epilepticus. He was diagnosed with idiopathic epilepsy and hospitalized with supportive care. During hospitalization, the patient developed both supraventricular and ventricular arrhythmias as well as focal left ventricular dyskinesis. Cardiac troponin I was significantly increased, which was supportive of myocardial damage. Neurogenic stunned myocardium was suspected, and the patient was treated and responded to esmolol. Follow-up echocardiography demonstrated the resolution of the ventricular dyskinesia. This report describes the clinical presentation, diagnostic findings, treatment, management, and outcome of the first reported case of naturally occurring neurogenic stunned myocardium in a dog. Electrocardiogram monitoring, cardiac troponin I, and echocardiography should be considered in patients presenting with seizure activity, especially when exhibiting cluster seizures or in status epilepticus.

The vein of Galen aneurysmal malformation (VGAM) is a rare congenital arteriovenous fistula of the embryonic median prosencephalic vein of Markowski, resulting in its pathological dilation. If left untreated, it can lead to multiple severe complications in the neonatal period, among which obstructive hydrocephalus. We present a case report of a six-year-old male patient with severe status epilepticus and a clinical history of VGAM and obstructive hydrocephalus, diagnosed via an MRI and an MR-angiography. The hydrocephalus was treated via a ventriculostomy at the age of six months, while the VGAM underwent a partial transarterial endovascular embolization when the patient was four years old. The procedures were successful, and there were no significant post-operative complications observed. The epileptic seizures began at a later point and were successfully medicated with valproate. However, they resumed due to a lowering of the medication dosage by the patient\'s parents. The patient was given a new valproic acid regimen with an appropriate dosage, and his parents reported no further seizures. This case report emphasizes the use of appropriate prenatal and neonatal diagnostic methods for VGAM and explores the nature of the multi-procedural therapy approach towards the pathology and its complications in relation to a possibly idiopathic co-pathology, namely epilepsy.

Dyke-Davidoff-Masson syndrome (DDMS) is a rare entity. Few cases have been described in the literature. It can be symptomatic or asymptomatic. The clinical signs are very varied. Imaging is the key to diagnosis. Calvarial thickening, enlargement sinus, and cerebral hemiatrophy are suggestive signs. It is a cause of cerebral hemiatrophy and epilepsy. We report the clinical and radiological signs of this syndrome through a case of an 8-year-old male child treated for epilepsy. The importance of our article is to report a case diagnosed at an early age (8 years). Most studies report cases diagnosed in adults. MRI revealed pathognomonic signs of Dyke-Davidoff-Masson syndrome.

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The congenital disorder of glycosylation associated with ALG1 (ALG1-CDG) is a rare autosomal recessive disease. Due to the deficiency of β1,4 mannosyltransferase caused by pathogenic variants in ALG1 gene, the assembly and processing of glycans in the protein glycosylation pathway are impaired, resulting in a broad clinical spectrum with multi-organ involvement. To raise awareness of clinicians for its manifestations and genotype, we here reported a new patient with a novel variant in ALG1 gene and reviewed the literature to study the genotype-phenotype correlation.
Clinical characteristics were collected, and clinical exome sequencing was used to identify the causative variants. MutationTaster, PyMol, and FoldX were used to predict the pathogenicity, changes in 3D model molecular structure of protein, and changes of free energy caused by novel variants.
The proband was a 13-month-old Chinese Han male characterized by epileptic seizures, psychomotor development delay, muscular hypotonia, liver and cardiac involvement. Clinical exome sequencing revealed the biallelic compound heterozygosity variants, a previously reported variant c.434G>A (p.G145N, paternal) and a novel variant c.314T>A (p.V105N, maternal). The literature review found that in severe phenotypes, the incidences of clinical manifestations were significantly higher than that in mild phenotypes, including congenital nephrotic syndrome, agammaglobulinemia, and severe hydrops. Homozygous c.773C>T was a strongly pathogenic variant associated with a severe phenotype. When heterozygous for c.773C>T, patients with another variant leading to substitution in amino acids within the strongly conserved regions (c.866A>T, c.1025A>C, c.1182C>G) may cause a more severe phenotype than those within less-conserved regions (c.434G>A, c.450C>G, c.765G>A, c.1287T>A). c.1129A>G, c.1076C>T, and c.1287T>A were more likely to be associated with a mild phenotype. The assessment of disease phenotypes requires a combination of genotype and clinical manifestations.
The case reported herein adds to the mutations identified in ALG1-CDG and a review of this literature expands the study of the phenotypic and genotypic spectrum of this disorder.

The new coronavirus quickly spread throughout the world in late 2019 and became a pandemic in early 2020. The most common symptoms observed are fever, dry cough, loss of taste and smell, and respiratory distress. Other rarer complications can involve the cardiovascular, gastrointestinal, or neurological systems. Of the neurological complications, epileptic seizures are a subject of particular interest due to their relatively unknown and widespread etiologies. It is understood that the entry or production of pro-inflammatory cytokines during a COVID-19 infection can result in neurotransmitter modulation and ion channel dysfunction, leading to neuronal hyperexcitability, presenting as seizures. To the best of our knowledge, we present the first case in sub-Saharan Africa of a COVID-19 positive patient presenting to our institution with a reported seizure followed by confusion. Our case highlights the need to broaden our differential diagnosis to include COVID-19 infections in patients presenting with seizures.

Diffuse leptomeningeal glioneuronal tumors (DLGNTs) are a rare indolent neoplasm described in the 2016 WHO classification of tumors of the central nervous system (CNS). We describe a case of an 11 year old boy who initially presented intermittent headache, low back pain and communicating hydrocephalus, misdiagnosed as having tuberculous meningitis. Further clinical deterioration with seizures was observed and follow-up MRI showed further aggravation of leptomeningeal enhancement in the basal cisterns. Biopsy of the brain and leptomeninges revealed a diffuse leptomeningeal glioneuronal tumor. DLGNT should be considered in the differential diagnosis of conditions presenting as communicating hydrocephalus with nodular lesions and leptomeningeal enhancement. A timely histologic diagnosis through a biopsy of the brain is necessary to confirm the diagnosis.

OBJECTIVE: Despite a significant improvement in the number of studies on myelin oligodendrocyte glycoprotein (MOG)-immunoglobulin G (IgG)-associated disorder (MOGAD) over the past few years, MOG-IgG-associated cortical/brainstem encephalitis remains a relatively uncommon and less-reported presentation among the MOGAD spectrum. This study aimed to report the clinical course, imaging features, and therapeutic response of MOG-IgG-associated cortical/brainstem encephalitis.
METHODS: Data of four patients who suffered from cortical encephalitis with epileptic seizures and/or brainstem encephalitis during the course of the disease were retrospectively collected and analyzed.
RESULTS: In this study, three male patients and one female patient, with a median age of onset of 21 years (ranging 20-51 years) were enrolled. An epileptic seizure was the main symptom of cortical encephalitis in these patients, while the manifestations of brainstem encephalitis were diverse. Cranial MRI demonstrated abnormal signals in unilateral or bilateral cortical or brainstem. Cerebrospinal fluid studies showed normal or mildly elevated leukocyte counts and protein levels, and a cell-based assay detected positive MOG-IgG in the serum of all patients. Two patients were misdiagnosed at the first attack, and both experienced a relapse. All of them accepted the first-line immunotherapy after a confirmed diagnosis and had a good outcome.
CONCLUSIONS: Early suspicion of MOG-IgG-associated encephalitis is necessary for any patient with sudden onset of seizures or symptoms of brainstem damage, especially with lesions on unilateral/bilateral cortical or brainstem on brain MRI.