Seizures, Epilepsy and Infectious Diseases of the Nervous System
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Status Epilepticus Clinical Pathway
JOHNS HOPKINS ALL CHILDREN’S HOSPITAL Status Epilepticus Clinical Pathway 1 Johns Hopkins All Children's Hospital Status Epilepticus Clinical Pathway Table of Contents 1. Rationale 2. Background 3. Diagnosis 4. Labs 5. Radiologic Studies 6. General Management 7. Status Epilepticus Pathway 8. Pharmacologic Management 9. Therapeutic Drug Monitoring 10. Inpatient Status Admission Criteria a. Admission Pathway 11. Outcome Measures 12. References Last updated: July 7, 2019 Owners: Danielle Hirsch, MD, Emergency Medicine; Jennifer Avallone, DO, Neurology This pathway is intended as a guide for physicians, physician assistants, nurse practitioners and other healthcare providers. It should be adapted to the care of specific patient based on the patient’s individualized circumstances and the practitioner’s professional judgment. 2 Johns Hopkins All Children's Hospital Status Epilepticus Clinical Pathway Rationale This clinical pathway was developed by a consensus group of JHACH neurologists/epileptologists, emergency physicians, advanced practice providers, hospitalists, intensivists, nurses, and pharmacists to standardize the management of children treated for status epilepticus. The following clinical issues are addressed: ● When to evaluate for status epilepticus ● When to consider admission for further evaluation and treatment of status epilepticus ● When to consult Neurology, Hospitalists, or Critical Care Team for further management of status epilepticus ● When to obtain further neuroimaging for status epilepticus ● What ongoing therapy patients should receive for status epilepticus Background: Status epilepticus (SE) is the most common neurological emergency in children1 and has the potential to cause substantial morbidity and mortality. Incidence among children ranges from 17 to 23 per 100,000 annually.2 Prevalence is highest in pediatric patients from zero to four years of age.3 Ng3 acknowledges the most current definition of SE as a continuous seizure lasting more than five minutes or two or more distinct seizures without regaining awareness in between. -
Myalgic Encephalomyelitis/Chronic Fatigue
2019 Science & Discovery Webinar Series ME/CFS in the Era of the Human Microbiome: Persistent Pathogens Drive Chronic Symptoms by Interfering With Host Metabolism, Gene Expression, and Immunity with Amy Proal, Ph.D. November 14, 2019 | 1:00 PM Eastern www.SolveME.org About Our Webinars • Welcome to the 2019 Webinar Series! • The audience is muted; use the question box to send us questions. Dr. Proal will address as many questions as time permits at the end of the webinar • Webinars are recorded and the recording is made available on our YouTube channel http://youtube.com/SolveCFS • The Solve ME/CFS Initiative does not provide medical advice www.SolveCFS.org 2019 Science & Discovery Webinar Series ME/CFS in the Era of the Human Microbiome: Persistent Pathogens Drive Chronic Symptoms by Interfering With Host Metabolism, Gene Expression, and Immunity with Amy Proal, Ph.D. November 14, 2019 | 1:00 PM Eastern www.SolveME.org Myalgic Encephalomyelitis/Chronic Fatigue Syndrome in the Era of the Human Microbiome: Persistent Pathogens Drive Chronic Symptoms by Interfering With Host Metabolism, Gene Expression, and Immunity Amy Proal, Autoimmunity Research Foundation/PolyBio Millions of patients across the globe are suffering with myalgic encephalomyelitis (ME/CFS) Currently there is no one disease-specific biomarker and severely ill patients are often wheelchair dependent, bedridden and unable to perform basic tasks of work or daily living. #millionsmissing Myalgic Encephalomeylitis (ME) = swelling of the brain • Unrelenting fatigue that does -
African Meningitis Belt
WHO/EMC/BAC/98.3 Control of epidemic meningococcal disease. WHO practical guidelines. 2nd edition World Health Organization Emerging and other Communicable Diseases, Surveillance and Control This document has been downloaded from the WHO/EMC Web site. The original cover pages and lists of participants are not included. See http://www.who.int/emc for more information. © World Health Organization This document is not a formal publication of the World Health Organization (WHO), and all rights are reserved by the Organization. The document may, however, be freely reviewed, abstracted, reproduced and translated, in part or in whole, but not for sale nor for use in conjunction with commercial purposes. The views expressed in documents by named authors are solely the responsibility of those authors. The mention of specific companies or specific manufacturers' products does no imply that they are endorsed or recommended by the World Health Organization in preference to others of a similar nature that are not mentioned. CONTENTS CONTENTS ................................................................................... i PREFACE ..................................................................................... vii INTRODUCTION ......................................................................... 1 1. MAGNITUDE OF THE PROBLEM ........................................................3 1.1 REVIEW OF EPIDEMICS SINCE THE 1970S .......................................................................................... 3 Geographical distribution -
Meningitis/Encephalitis Pathogen Panel
Meningitis/Encephalitis Pathogen Panel The list of pathogens which can potentially cause meningitis, encephalitis, and meningoencephalitis is broad. Early effective therapy for both bacterial and certain viral pathogens has been associated with improved outcomes. Patients whose history, exam, and/or imaging suggests one of these conditions should have a lumber puncture performed with appropriate diagnostic testing including a cell count with differential, protein, and glucose. Additional tests to consider include bacterial culture, cryptococcal antigen testing, fungal cultures, cultures for acid fast bacilli and/or the new Meningitis/Encephalitis Pathogen Panel. Nebraska Medicine has recently introduced a new FDA-approved test called the Meningitis/Encephalitis Pathogen Panel (MEPP). This test uses a nested multiplex PCR-approach to amplify DNA targets directly from cerebrospinal fluid (CSF) in patients with signs and symptoms of meningitis or encephalitis. It is able to detect a variety of common bacterial, viral, and fungal pathogens (Table 1). Table 1: Pathogens Detected by Meningitis/Encephalitis Pathogen Panel Bacteria Viruses Yeast Gram-negative Cytomegalovirus Cryptococcus Escherichia coli K1 Enterovirus neoformans/gattii Haemophilus influenzae Herpes simplex virus 1 Neisseria meningitidis Herpes simplex virus 2 Gram-positive Human herpesvirus 6 Listeria monocytogenes Human parechovirus Streptococcus agalactiae (Group B Strep) Varicella zoster virus (VZV) Streptococcus pneumoniae This test is sensitive and very specific (see Supplementary Table 1 for complete detail), and should only be performed in patients where CNS infection is being seriously considered. Previous studies have shown that using clinical and CSF criteria to determine when to perform PCR testing is unlikely to miss clinically significant results and is highly cost-effective.1-3 For example Wilen, et al.3 restricted herpes virus and enterovirus PCR testing to patients who were: age <2 years, immunosuppressed, or who had >10 WBCs/µl. -
Myoclonic Atonic Epilepsy Another Generalized Epilepsy Syndrome That Is “Not So” Generalized
EDITORIAL Myoclonic atonic epilepsy Another generalized epilepsy syndrome that is “not so” generalized John M. Zempel, MD, Myoclonic atonic/astatic epilepsy (MAE), first described have shown predominant thalamic activation PhD well by Doose1 (pronounced dough sah: http://www. and default mode network deactivation.6–8 Even Tadaaki Mano, MD, PhD youtube.com/watch?v5hNNiWXV2wF0), is a general- Lennox-Gastaut syndrome, a devastating epileptic ized electroclinical syndrome with early onset charac- encephalopathy with EEG findings of runs of slow terized by myoclonic, atonic/astatic, generalized spike and wave and paroxysmal higher frequency Correspondence to tonic-clonic, and absence seizures (but not tonic activity, has fMRI correlates that are more focal than Dr. Zempel: [email protected] seizures) in association with generalized spike-wave expected in a syndrome with widespread EEG (GSW) discharges. Thought to have a genetic com- abnormalities.9,10 Neurology® 2014;82:1486–1487 ponent that has proven to be complicated,2 MAE EEG-fMRI is maturing as a research and clinical sometimes occurs in children who have otherwise technique. Recording scalp EEG in an electrically been developing normally and has variable outcome. hostile environment is not an easy task. Substantial MAE is typically treated with antiseizure medications technical artifacts, such as changing imaging gradients that are used for generalized epilepsy syndromes, with and ballistocardiogram (ECG-linked artifact observed perhaps a best response to valproate, felbamate, or the in the scalp electrodes), contaminate the EEG signal. ketogenic diet.3,4 However, the relatively distinctive EEG discharges in In this issue of Neurology®, Moeller et al.5 report patients with epilepsy have partially circumvented on the fMRI correlates of GSW discharges as mea- this problem. -