Aug 2026· The Egyptian Journal of Neurology Psychiatry and Neurosurgery· Vol 62· 0 citations· 15 references
TL;DR
The present case demonstrates that RSE with cortical involvement on MRI could be anatomically associated with CLN, which is accompanied by massive infiltration of plasma cells and T lymphocytes, which was seen in the overlying subarachnoid membrane and in the adjacent intact appearing parenchyma.
Abstract
Status epilepticus (SE) has been defined as a seizure that persists for more than 5 min. If SE persists despite benzodiazepine and appropriately dosed antiseizure medications, it could be regarded as refractory SE (RSE). New-onset refractory status epilepticus (NORSE) is a separate syndrome that occurs in individuals without active epilepsy or other preexisting relevant neurological disorders. A small number of neuropathology reports of patients who died of SE, RSE and NORSE are available, revealing hypoxic and ischemic neuronal damage and cortical laminar necrosis (CLN). CLN is a well-known sequela of SE, which has been often suspected radiologically, although its anatomical background is largely unknown. An 84-year-old man with a history of malignant lymphoma in complete remission presented with high fever and impaired consciousness. He developed tonic-clonic convulsions, which lapsed into SE. CSF revealed a normal cell count and elevated protein. MRI of the brain showed high signal intensities on diffusion-weighted and FLAIR images in the mid-temporal lobe bilaterally and left insular cortex. EEG showed epileptic discharges on the left side with an extreme delta brush pattern. He was diagnosed with possible autoimmune encephalitis. Despite treatments, he remained comatose and died of pneumonia, 24 days after the onset of seizures. A complete autopsy failed to reveal the presence of malignancy. Neuropathologically, the brain showed atrophic changes involving the insular cortex, orbitofrontal cortex and medial temporal lobe, predominantly on the left side. Histologically, the lesions corresponding to the abnormal MRI images revealed CLN involving the mid- cortical layers. Remarkably, this was associated with perivascular and intraparenchymal infiltration of plasma cells and T lymphocytes, which was also seen in the overlying subarachnoid membrane and in the adjacent intact appearing parenchyma. The present case demonstrates that RSE with cortical involvement on MRI could be anatomically associated with CLN, which is accompanied by massive infiltration of plasma cells and T lymphocytes. The novel association of CLN and lympho-plasmacytic infiltration requires further investigation.
Catatonia is a psychomotor syndrome that occurs in various psychiatric, neurological, and medical conditions. Differentiating malignant catatonia from neuroleptic malignant syndrome (NMS) and non-convulsive status epilepticus (NCSE) is particularly challenging in complex cases involving multiple contributing factors. Both catatonia and NCSE have been associated with dysfunction of the gamma-aminobutyric acid (GABA)-A receptor system, which may underlie overlapping clinical features. We report the case of a 43-year-old man with a long-standing history of schizophrenia who developed malignant catatonia following a suicide attempt that resulted in multiple traumatic injuries. Postoperatively, he exhibited autonomic instability, decreased consciousness, muscle rigidity, and catatonic signs. An electroencephalogram revealed generalized spike-and-wave activity consistent with NCSE, and levetiracetam was initiated. Despite the resolution of the epileptiform discharges, the catatonic symptoms persisted. A transient positive response to lorazepam supported the diagnosis of malignant catatonia. Modified electroconvulsive therapy (m-ECT) was introduced on day 40 of hospitalization. After four sessions, the patient showed marked improvement in both motor and autonomic symptoms. Thirteen sessions were completed, and the patient was discharged on day 81. He remained relapse-free for over five years. This case highlights the importance of considering malignant catatonia in patients with schizophrenia who present with persistent catatonic symptoms despite adequate treatment of NCSE. Although antiepileptic therapy suppressed epileptiform activity, resolution of catatonia required m-ECT, suggesting that seizure control alone may be insufficient. Clinicians should recognize that catatonia and NCSE may coexist and overlap in GABA-A-related pathophysiology, and that early GABA-A-targeted interventions, including m-ECT, may be critical for recovery.
Chihiro Iino, Rintaro Fujii, Shogo Kitagawa et al.· Journal of UOEH· 0 citations
Beyond the clinical severity of NORSE, the findings show that cohort composition is highly sensitive to the temporal operationalization of consensus criteria, and standardized application of diagnostic timing may therefore be essential for comparability across NORSE studies.
C. Jünemann, Meike Menche, Marc-Philipp Bergmann et al.· Neurological Research and Pr...· 0 citations
Focal epileptic seizures with sensory impairment can be difficult to recognize and are often mistaken for behavioral disorders. Electroencephalography (EEG) can provide important supportive evidence for their epileptic origin when interpreted in conjunction with clinical presentation. This article describes three cases of canine patients: a 2-year-old Border Terrier, a 1-year-old Poodle mix, and a 4-year-old mixed-breed dog. All three were presented with a history of recurrent episodes characterized by fear, restlessness, hyperactivity, hiding, staring into space or at the sky, lip licking, and hypersalivation. In two dogs, there were also signs of impaired consciousness. The frequency of the episodes varied, ranging from multiple episodes per day to one episode every 1–2 weeks. No pre-ictal or post-ictal signs were reported. Clinical and neurological examinations were unremarkable in all three cases. The diagnostic workup included EEG using a Natus Xltek system and magnetic resonance imaging (MRI) of the brain with a Siemens 1.5 T scanner. EEG monitoring lasting 1.5–4 h revealed epileptiform discharges predominantly in the parietal and temporal regions. This case series highlights the occurrence of behavioral and autonomic symptoms without typical motor manifestations as a presentation of presumed idiopathic epilepsy in dogs, supported by EEG findings in conjunction with the clinical presentation. All three dogs were treated with antiseizure medication, which resulted in a decrease in both the frequency and intensity of episodes, with complete seizure freedom achieved in two dogs.
Adriana Czerwik, Agnieszka Olszewska, Daniela Farke et al.· Frontiers in Veterinary Scie...· 0 citations
Basilar artery occlusion (BAO) is a catastrophic ischemic stroke with subtle initial manifestations. Although convulsive‐like movements are well recognized in brainstem ischemia, true status epilepticus (SE) as the presenting sign of BAO is exceedingly rare and frequently misdiagnosed. This study presents an illustrative case of SE with early posterior circulation ischemic changes highly suggestive of BAO, and a systematic review to identify confirmed cases of BAO presenting with SE, clarify diagnostic pitfalls, and outline bedside “red flags” prompting urgent posterior circulation imaging.
A PubMed/Scopus search (September 2025) was performed using predefined terms for basilar artery occlusion and status epilepticus. Inclusion required imaging‐confirmed BAO and SE; SE was defined according to ILAE/Salzburg definitions. Clinical, electroencephalographic, therapeutic, and outcome data were extracted and critically analyzed.
Six patients met the inclusion criteria, including focal motor, generalized convulsive, and non‐convulsive SE (two early, one established, two refractory, and one non‐convulsive SE). Benzodiazepine resistance occurred in half of the cases. Despite successful reperfusion in two patients, all survivors had poor outcomes.
True SE can herald BAO across multiple phenotypes, but it appears rare and is frequently confounded by mimics. Diagnostic “red flags” include new‐onset SE in adults without a history of epilepsy, early benzodiazepine resistance, brainstem signs, pupillary abnormalities, and the “looking away from the seizure” sign. Recognition of BAO‐related SE as a vascular stroke equivalent, often representing a Stage 1 Plus SE, may suggest early posterior circulation imaging to avoid fatal delays in reperfusion.
G. Magro· Neurology and Clinical Neuro...· 0 citations
Mild encephalitis/encephalopathy with a reversible splenial lesion (MERS) is a rare clinico-radiological syndrome characterized by transient encephalopathy associated with a reversible lesion in the splenium of the corpus callosum, most commonly occurring in the setting of infection or metabolic disturbance. We report the case of a 21-year-old male who presented with an acute generalized seizure following an influenza-like illness. Brain magnetic resonance imaging (MRI) demonstrated a well-defined ovoid lesion in the midline splenium of the corpus callosum, hyperintense on T2-weighted and FLAIR sequences, with marked diffusion restriction and corresponding low apparent diffusion coefficient (ADC) values, without contrast enhancement. Laboratory investigations, including serum studies and cerebrospinal fluid analysis, were within normal limits. The patient was managed with supportive care and antiepileptic therapy, with complete clinical recovery. Follow-up MRI performed after recovery demonstrated complete resolution of the splenial lesion, confirming its transient nature. This case highlights the importance of recognizing MERS in young patients presenting with post-infectious altered consciousness or new-onset seizures and underscores the central role of MRI in establishing the diagnosis and excluding other causes of splenial diffusion restriction.
S. Ben Elhend, R. Roukhssi, N. Hammoune et al.· Radiology Case Reports· 0 citations
Remission of the generalized epileptiform discharges correlates with ASM treatment and seizure outcome is excellent, despite persistence of centrotemporal spikes, suggesting that it reflects an EEG trait.
María Augusta Montenegro, Shifteh Sattar, M. Nespeca et al.· Epilepsy & Behavior· 0 citations
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