Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Status epilepticus is a common and under-recognized cause of unconsciousness among hospitalized patients. It can clinically mimic delirium and other causes of acute mental status change, especially when clinically relevant seizure activity is not appreciated on physical examination. While the successful treatment of status epilepticus may require anesthetic dosing of antiepileptics such as barbiturates, these seemingly drastic therapeutic measures are justified when goals of care are life prolonging as they may allow a patient to regain consciousness and meaningfully interact with loved ones. However, medical burden from electroencephalogram (EEG) monitoring and other care associated with its diagnosis and treatment can contribute to distress for patients who may be dying from a comorbid illness. Furthermore, when goals of care transition to comfort, care challenges can result regarding the ongoing management of barbiturates or other sedatives, previously prescribed to treat the status epilepticus. In this case study, the lack of clinically significant seizure activity led us to conclude that the discontinuation of a barbiturate infusion and the EEG monitoring was the clinically appropriate approach for a dying patient with comfort goals of care and nonconvulsive status epilepticus.
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PMID:Treat the Patient, Not the Test When a Hospitalized Patient in Status Epilepticus Transitions to Comfort-Focused Goals of Care. 2995 33

BACKGROUND Central nervous system complications after transplantation occur in up to 40% of recipients and these complications are associated with increased length of hospital stay and mortality. Catatonia is a neuropsychiatric clinical syndrome which has been described in case reports and in a small case series as occurring in the immediate post-solid organ transplantation (SOT) period, and it has been attributed to calcineurin inhibitor neurotoxicity, psychological vulnerability, and depression. Among transplant recipients, the incidence of catatonia is unknown; it may be under diagnosed in part due to a broad differential diagnosis in the post-transplantation setting, which includes hypoactive delirium, non-convulsive status epilepticus, drug toxicity, conversion disorder, and volitional uncooperativeness. CASE REPORT We present 2 cases of catatonia diagnosed in liver allograft recipients. We also reviewed current literature for cases of catatonia among SOT recipients. We provide provisional evaluation and management strategies of recipients with clinical concern for catatonia. Catatonia generally occurs within the few first days after liver transplantation, and presents with staring, immobility, or mutism, but is also associated with other neurological and psychiatric symptoms. Catatonia can be successfully treated with intravenous lorazepam, and thus, modifying immunosuppressive regimens may be avoidable. Medications to treat catatonia are generally tapered over weeks to months, and psychiatric follow-up is indicated. The early post-liver transplantation period may be a state of relative deficiency in GABA (gamma-aminobutyric acid) signaling, predisposing liver transplant recipients in particular to post-transplantation catatonia. CONCLUSIONS Despite difficulties in establishing the diagnosis, catatonia after liver transplantation was rapidly responsive to intravenous lorazepam, indicating that changing immunosuppressants may be avoidable.
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PMID:Catatonia After Liver Transplantation. 3015 Jun 6

Background/Objectives: Delirium occurs in up to 50 % of hospitalized old patients and is associated with increased morbidity and mortality. Acute medical conditions favor delirium, but the pathophysiology is unclear. Preliminary evidence from retrospective and prospective studies suggests that a substantial minority of old patients with unexplained delirium have non-convulsive seizures or status epilepticus (NCSE). Yet, seeking epileptic activity only in unexplained cases of delirium might result in misinterpretation of its actual prevalence. We aimed to systematically investigate the role of epileptic activity in all older patients with delirium regardless of the underlying etiology. Design, Setting: Prospective observational study in a tertiary medical center. Adults >65 years with delirium underwent at least 24 h of continuous electro-encephalographic monitoring (cEEG). Background patterns and ictal and interictal epileptic discharges were identified, as well as clinical and biological characteristics. Participants: Fifty patients were included in the study. Results: NCSE was found in 6 (12%) patients and interictal discharges in 15 (30%). There was no difference in the prevalence of epileptic activity rates between delirium associated with an acute medical condition and delirium of unknown etiology. Conclusion: Epileptic activity may play a substantial role in the pathophysiology of delirium by altering brain functioning and neuronal metabolism. No clinical or biological marker was found to distinguish delirious patients with or without epileptic activity, underlining the importance of cEEG in this context.
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PMID:Role of Epileptic Activity in Older Adults With Delirium, a Prospective Continuous EEG Study. 3094 Oct 98

The 2018 Paris Intensive Care symposium entitled "Update in Neurocritical Care" was organized in Paris, June 21-22, 2018, under the auspices of the French Intensive Care Society. This 2-day post-graduate educational symposium comprised several chapters, aiming first to provide all-board intensivists with current standards for the clinical assessment of altered consciousness states (including coma and delirium) and peripheral nervous system in critically ill patients, monitoring of brain function (specifically, electro-encephalography) and best practices for sedation-analgesia-delirium management. An update on the treatment of specific severe brain pathologies-including ischaemic/haemorrhagic stroke, cerebral venous thrombosis, hypoxic-ischaemic brain injury, immune-mediated and infectious encephalitis and refractory status epilepticus-was also provided. Finally, we discuss how to approach some difficult decisions, namely the role of decompressive craniectomy and prognostication models in patients with head injury. For each chapter, the scope of the present review was to provide important issues and key messages, provide most recent and relevant literature in the field, and briefly describe new developments in the field.
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PMID:Update in Neurocritical Care: a summary of the 2018 Paris international conference of the French Society of Intensive Care. 3099 50

Refractory seizures or status epilepticus (RS/SE) continues to be a challenge in the inpatient setting. Failure to abort a seizure with antiepileptic drugs (AEDs) may lead to intubation and treatment with general anesthesia exposing patients to complications, extending hospitalization, and increasing the cost of care. Studies have shown a key role of inflammatory mediators in seizure generation and termination. We describe 4 patients with RS/SE that was aborted when dexamethasone was added to conventional AEDs: a 61-year-old female with temporal lobe epilepsy who presented with delirium, nonconvulsive status epilepticus, and oculomyoclonic status; a 56-year-old female with history of traumatic left frontal lobe hemorrhage who developed right face and hand epilepsia partialis continua followed by refractory focal clonic seizures; a 51-year-old male with history of traumatic intracranial hemorrhage who exhibited left-sided epilepsia partialis continua; and a 75-year-old female with history of breast cancer who manifested nonconvulsive status epilepticus and refractory focal clonic seizures. All patients continued experiencing RS/SE despite first- and second-line therapy, and one patient continued to experience RS/SE despite third-line therapy. Failure to abort RS/SE with conventional therapy motivated us to administer intravenous dexamethasone. A 10-mg load was given (except in one patient) followed by 4.0- 5.2 mg q6h. All clinical and electrographic seizures stopped 3-4 days after starting dexamethasone. When dexamethasone was discontinued 1-3 days after seizures stopped, all patients remained seizure-free on 2-3 AEDs. The cessation of RS/SE when dexamethasone was added to conventional antiseizure therapy suggests that inflammatory processes are involved in the pathogenesis of RS/SE.
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PMID:Dexamethasone as Abortive Treatment for Refractory Seizures or Status Epilepticus in the Inpatient Setting. 3110 35

Benzodiazepine withdrawal symptoms vary from mild anxiety to life-threatening delirium or seizures. In susceptible individuals, such as those with mood disorders, benzodiazepine withdrawal may also precipitate catatonia. A 26-year-old man with schizoaffective disorder (depressed type with catatonia) ran out of lorazepam and presented with catatonia, delirium, and seizures. He was taking olanzapine, venlafaxine, and trazodone for schizoaffective disorder. Lorazepam 2 mg twice daily kept him free of catatonia for 6 months. Besides catatonia and delirium, lorazepam withdrawal also triggered convulsive seizures and nonconvulsive status epilepticus. He was admitted to the intensive care unit where he underwent continuous video-EEG monitoring. Catatonia resolved with lorazepam on day 2. Seizures stopped with levetiracetam, lacosamide, and propofol on day 4. His mental status was normal when he was discharged on day 6. If not immediately recognized and treated, catatonia and delirium can lead to significant morbidity or mortality. Unfortunately, physicians tend to overlook catatonia and delirium, especially if both syndromes are present. At first, we suspected that our patient had ictal catatonia, but video-EEG showed no clear-cut correlation between catatonia, seizures, and epileptiform activity. As with prior observations, the patient's catatonia was more sensitive to benzodiazepine withdrawal and treatment than his seizures. The efficacy of benzodiazepines in aborting catatonia, seizures, and mixed delirium-catatonia syndromes suggests a key pathogenetic role of abnormal GABA neurotransmission in these brain disorders.
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PMID:Benzodiazepine Withdrawal Catatonia, Delirium, and Seizures in a Patient With Schizoaffective Disorder. 3313 43

Introduction: Neurological manifestations are emerging as relatively frequent complications of corona virus disease 2019 (COVID-19), including stroke and encephalopathy. Clinical characteristics of the latter are heterogeneous and not yet fully elucidated, while the pathogenesis appears related to neuroinflammation in a subset of patients. Case: A middle-aged man presented with acute language disturbance at the emergency department. Examination revealed expressive aphasia, mild ideomotor slowing, and severe hypocapnic hypoxemia. Multimodal CT assessment and electroencephalogram (EEG) did not reveal any abnormalities. COVID-19 was diagnosed based on chest CT findings and positive severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) reverse transcription PCR (RT-PCR) on nasopharyngeal swab. The following day, neurological symptoms progressed to agitated delirium and respiratory status worsened, requiring admission to the ICU and mechanical ventilation. Brain MRI and cerebrospinal fluid (CSF) studies were unremarkable. RT-PCR for SARS-CoV-2 on CSF was negative. He received supportive treatment and intravenous low-dose steroids. His neurological and respiratory status resolved completely within 2 weeks. Conclusions: We report a patient with reversible COVID-19-related encephalopathy presenting as acute aphasia, mimicking stroke or status epilepticus, eventually evolving into delirium. Although large-vessel stroke is frequently encountered in COVID-19, our case suggests that focal neurological deficits may occur as the earliest feature of encephalopathy. Neurological status reversibility and the absence of abnormalities on brain MRI are consistent with a functional rather than a structural neuronal network impairment.
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PMID:Encephalopathy in COVID-19 Presenting With Acute Aphasia Mimicking Stroke. 3319 51


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