Hyperosmolar hyperglycaemic state causing atypical status epilepticus with hippocampal involvement

Diabetes mellitus may arise abruptly and decompensate suddenly, leading to a hyperglycaemic hyperosmolar state. Coma often ensues, although this usually reverses after the metabolic abnormalities have resolved. Acute symptomatic seizures can also occur in patients who are conscious, although these usually resolve after osmolarity and glycaemia have normalised. We describe an elderly woman who failed to regain vigilance despite prompt treatment; the cause was an unusual non-convulsive status epilepticus arising from the mesial temporal lobe and promoting a progressive and selective hippocampal involvement. During follow-up, her seizures recurred after stopping antiseizure medication and she developed hippocampal sclerosis, although she subsequently became seizure-free with antiseizure medications. Patients who are unresponsive in a hyperglycaemic hyperosmolar state may be having subclinical epileptiform discharges and risk developing permanent brain damage and long-term epilepsy.

Epilepsy and other seizure disorders in acute psychiatric inpatients

Background It is well known that patients with epilepsy have a high rate of psychiatric comorbidity. However, studies exploring epilepsy in psychiatric cohorts are scarce. The aim of this study was to examine the prevalence of seizure disorders in acute psychiatric inpatients. Methods This is a cross-sectional study performed in a catchment-area based acute psychiatric department. All patients (age > 18) admitted during September 2011 - March 2012 were eligible for inclusion. Consenting patients were screened for a life-time history of epilepsy or seizures using self-reported questionnaire data and diagnostic codes for epilepsy in hospital and National registries. Patients scoring positive to one or more of these screening criteria underwent a thorough diagnostic validation (chart review), and the seizure disorders were classified as epilepsy, acute symptomatic seizures and/or psychogenic non-epileptic seizures according to current definitions. Results A total of 380 out of 591 (64.3%) consecutively admitted patients consented to participate in the study. Eighty-nine patients (23.4%) scored positive to one or more screening criteria. Fifteen (3.9%) were classified with epilepsy, 21 (5.5%) with acute symptomatic seizures and 9 (2.4%) with psychogenic non-epileptic seizures. Conclusions This is the first study to report on the prevalence of seizure disorders in acute psychiatric inpatients. The life-time prevalence of epilepsy in this cohort of patients is five – six times as high as reports in the general population. These findings underscore the need for the clinical psychiatrist to have comprehensive knowledge on the interface between epileptology and psychiatry. Trials registration ClinicalTrials.gov identifier NCT01415323.

Clinical Heterogeneity in Acute Symptomatic Seizures due to Autoimmune Encephalitis Related to GAD65 Antibodies

<b><i>Introduction:</i></b> This study aimed to explore the diversity and clinical features of acute symptomatic seizures due to autoimmune encephalitis related to anti-glutamate decarboxylase (GAD) 65 antibodies. <b><i>Methods:</i></b> Clinical data of a series of 6 patients positive for anti-GAD65 antibodies were retrospectively analyzed. <b><i>Results:</i></b> Five of the patients were male and 1 was a female, with a median age of 44.1 years (range 18–70 years). Seizure forms were varied in 6 patients when they were admitted to the hospital: 3 cases of seizures only and 3 accompanied by other symptoms, such as mental disorder, cognitive impairment, cerebellar ataxia, and ocular movement disorder. Three patients (50%) had coexisting systemic autoimmune diseases, including diabetes mellitus, vitiligo, and hyperthyroidism. Five patients (83%) had abnormal brain MRI findings. They were all treated by immunotherapy, 5 of 6 patients improved significantly but relapsed after withdrawing methylprednisolone, and 1 patient got deteriorated. None of them were diagnosed with tumors. <b><i>Conclusions:</i></b> Clinical features of acute symptomatic seizures related to GAD65 antibodies are diverse, and early and continuous immunotherapy is necessary for patients.

Epidemiology and Pathophysiology of Epilepsy

About 10% of people in the United States have 1 seizure in their lifetime; less than 4% have recurrent seizures or epilepsy. Currently, more than 3.4 million people in the United States have active epilepsy, making it one of the most common neurologic disorders. Seizures can develop at any age, but the most common times are during childhood and after age 60 years. The greatest incidence is in elderly patients. Acute symptomatic seizures (also called provoked seizures or reactive seizures) result from new and active insults to the central nervous system.

Evaluation and Management of First-Time Seizure in Adults

First seizures are often perceived as devastating events by patients and their families due to the fear of having a life-long disease. One in 10 people experiences one or more seizures during their lifetime, while 1 in 26 people develops epilepsy. Acute symptomatic seizures are often related to a provoking factor or an acute brain insult and typically do not recur. Careful history and clinical examination should guide clinicians' management plans. Electroencephalography and brain imaging, preferably with epilepsy-specific magnetic resonance imaging, may help characterize both etiology and risk of seizure recurrence. Antiepileptic drugs should be initiated in patients with newly diagnosed epilepsy. In patients without an epilepsy diagnosis, the decision to prescribe drugs depends on individual risk factors for seizure recurrence and possible complications from seizures, which should be discussed with the patient. Counseling about driving and lifestyle modifications should be provided early, often at the first seizure encounter.

Risk of Post-stroke Epilepsy Following Stroke-Associated Acute Symptomatic Seizures

Objective: Post-stroke epilepsy (PSE) is associated with increased morbidity and mortality. Stroke-associated acute symptomatic seizures are an important risk factor: 20.8–34.3% of these patients will go on to develop PSE. Identifying these “high risk” individuals may result in earlier PSE diagnosis, treatment, and avoidance of seizure-related morbidity. This study was to identify predictors of PSE development in patients with stroke-associated acute symptomatic seizures.Participants and Methods: This was a retrospective cohort study of 167 patients with stroke-associated acute symptomatic seizures admitted to the Neurology Department of a tertiary Hospital of China, from 1 May 2006 to 30 January 2020. Both those with primary ischemic stroke and intracerebral hemorrhage were included in the study. Patient demographics, medical history, stroke-associated, and seizure-related variables were evaluated with univariable analysis and multivariable Cox regression analysis. PSE was defined as unprovoked seizures occurring &gt; 7 days post-stroke. Data points were extracted from medical records and supplemented by tele-interview.Results: Of the 167 patients with stroke-associated acute symptomatic seizures, 49 (29.3%) developed PSE. NIHSS score &gt; 14 [hazard ratio (HR) 2.98, 95% CI 1.57–5.67], longer interval from stroke to acute symptomatic seizures (days 4–7 post-stroke) (HR 2.51, 95% CI 1.37–4.59) and multiple acute symptomatic seizures (HR 5.08, 95% CI 2.58–9.99) were independently associated with PSE development. This association remained in the sub-analysis within the ischemic stroke cohort. In the sub-analysis of the hemorrhagic stroke cohort, multilobar involvement (HR 4.80, 95% CI 1.49–15.39) was also independently associated with development of PSE. Further, we developed a nomogram to predict individual risk of developing PSE following stroke-associated acute symptomatic seizures. The nomogram showed a C-index of 0.73.Conclusion: More severe neurofunctional deficits (NIHSS score &gt; 14), longer interval from stroke to acute symptomatic seizures (days 4–7 post-stroke), and multiple acute symptomatic seizures were independently associated with development of PSE in patients with stroke-associated acute symptomatic seizures. This knowledge may increase clinical vigilance for development of PSE, facilitating rapid diagnosis and treatment initiation, and subsequently reduce seizure-related morbidity.

Early postoperative seizures in liver and kidney recipients

Background. Transplantation is presently the only treatment for end-stage liver and kidney failure. Up to 42% of liver transplant recipients and up to 30% of kidney transplant recipients have neurological complications from the transplantation. Acute symptomatic seizures (ACS) occupy an important place in the structure of early postoperative neurological complications. Verification of the causes of seizures and management of the risk of relapse is presently a critical task.Objective: to review recent advances in ACS assessment, prevalence, and treatment approaches in liver and kidney transplant recipients.Materials and methods. The causes of ACS after liver and kidney transplant are diverse. Nonspecific causes of seizures such as dysmetabolic and volemic changes associated with transplantation are widely known. There are also specific syndromes associated with seizures in liver and kidney recipients, such as posterior reversible leukoencephalopathy syndrome, neurotoxicity of calcineurin inhibitors, hyponatremia in the final stage of liver failure, hypocalcemia in kidney recipients, etc. Diagnosis is made based on general rules, and treatment depends on the identified causes of seizures. Management of acute symptomatic seizures involves prescribing anticonvulsants according to the risk of seizure recurrence; immunosuppression is converted when neurotoxicity is identified. Results. The diagnostic algorithm, and often the treatment strategies, in ACS cases in liver and kidney recipients, are not clearly defined.Conclusion. Due to the multiple causes of ACS, there are differences in treatment tactics. Further accumulation and generalization of ACS outcome data will help in creating a convenient algorithm for rapid identification of the cause and the most effective treatment tactics.

Seizures and Interictal Epileptiform Activity in the Rat Collagenase Model for Intracerebral Hemorrhage

AimsIntracerebral hemorrhage (ICH) is a known risk factor for the development of acute symptomatic as well as late unprovoked seizures. The underlying pathophysiology of post-ICH seizures is incompletely understood and there are no reliable predictive biomarkers. An animal model to study post-ICH seizures is currently lacking. The aim of this study was to investigate (1) the occurrence of seizures and interictal epileptiform activity in the ICH rat collagenase model using long-term video-EEG monitoring (VEM) and (2) whether seizure occurrence was associated with interictal epileptiform activity and histological features.MethodsMale Sprague-Dawley rats were implanted with epidural electrodes. After 1 week of baseline VEM, collagenase was injected in left striatum to induce an ICH. VEM was continued for 180 days to assess the occurrence of post-ICH seizures and interictal epileptiform activity (spikes and epileptiform discharges). At the end of the experiment, animals were euthanized for histological characterization of the hemorrhagic lesion, using cresyl violet, Prussian blue and immunofluorescence staining.ResultsAcute symptomatic seizures occurred in 4/12 animals between 46 and 80 h after ICH induction. Late unprovoked seizures were present in 2/12 animals and started at 90 and 103 days post-ICH. Animals with late unprovoked seizures did not have acute symptomatic seizures. All electrographic seizures were accompanied by clear behavioral changes. Interictal spikes and epileptiform discharges were observed in all animals but occurred more frequently in rats with late seizures (p = 0.019 and p &lt; 0.001, respectively). Animals with acute symptomatic seizures had more extended hemorrhagic lesions and hemosiderin deposits in the piriform cortex.ConclusionBoth acute symptomatic and late unprovoked seizures were observed in the rat collagenase model. Interictal epileptiform activity was more frequently seen in animals with late seizures. Rats with acute symptomatic seizures showed more extensive lesions and hemosiderin deposits in the piriform cortex. This model could be used to further explore possible biomarkers for epileptogenesis.