Migraine Triggered Seizures and Epilepsy Triggered Headache and Migraine Attacks: a Need for Re-Assessment
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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. -
The Migraine-Epilepsy Syndrome
medigraphic Artemisaen línea Arch Neurocien (Mex) Vol 11, No. 4: 282-287, 2006 The Migraine- Epilepsy Syndrome Arch Neurocien (Mex) Vol. 11, No. 4: 282-287, 2006 Artículo de revisión ©INNN, 2006 de caso The migraine-epilepsy syndrome Enrique Otero Siliceo†, Fernando Zermeño EL SINDROME MIGRAÑA-EPILEPSIA represent a neural exitation. Since that the glutamate has in important rol in both patologys depending of the part of the brain more affected the symptoms might RESUMEN vary from visual to abdominal phemomena. La migraña y la epilepsia tienen varios puntos en común Key words: migraine epilepsy, EEG abnormalities, sintomática clínica y genéticamente lo que ha sido glutamate, diagnosis. postulado por más de cien años. El fenómeno referido como migraña-epilepsia sugiere que exista una he first steps of a practical, approach by patofisiología común. El síndrome de migraña o physicians in recognizing and treating neuro- epilepsia tiene fenómenos comunes de dolor adominal T logic diseases are to recognithat there are jaqueca anormalidades del EE y respuesta a droga various overlaps between migraine and epilepsy. antiepilépticas. En ocasiones el paciente puede tener Epileptic seizures and classic migraine episodes may un ataque migrañoso o una convulsión o en otras occur in the same patient. Migraine and epilepsy share ambas. La comorbilidad puede explicarse por estados several genetic, clinical, evolutive and neurophysio- de hiperrexcitabilidad neural. Alteraciones electroen- logic features. A relationship between epilepsy and cefalográficas son comunes en estos estados. En migraine has been postulated for over a hundred years apariencia el glutamato tiene un papel importante tanto and the syndrome of Migraine-Epilepsy illustrates this en la migraña como en la epilepsia. -
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REVIEW OF OPTOMETRY EARN 2 CE CREDITS: Positive Visual Phenomena—Etiologies Beyond the Eye, PAGE 58 ■ VOL. 155 NO. 1 January 15, 2018 www.reviewofoptometry.comwww.reviewofoptometry.com ■ ANNUAL CORNEA REPORT JANUARY 15, 2018 ■ CXL ■ EPITHELIAL DEFECTS How to Heal Persistent Epithelial Defects PAGE 38 ■ TRANSPLANTS Corneal Transplants: The OD’s Role PAGE 44 ■ INFILTRATES Diagnosing Corneal Infiltrative Disease PAGE 50 ■ POSITIVE VISUAL PHENOMENA CXL: Your Top 12 Questions —Answered! PAGE 30 001_ro0118_fc.indd 1 1/5/18 4:34 PM ĊčĞĉėĆęĊĉĆĒēĎĔęĎĈĒĊĒćėĆēĊċĔėĎēǦĔċċĎĈĊĕėĔĈĊĉĚėĊĘ ĊđĎĊċĎēĘĎČčę ċċĊĈęĎěĊ Ȉ 1 Ȉ 1 ĊđđǦęĔđĊėĆęĊĉ Ȉ Ȉ ĎĒĕđĊĎēǦĔċċĎĈĊĕėĔĈĊĉĚėĊ Ȉ Ȉ ĔēěĊēĎĊēę Ȉ͝ Ȉ Ȉ Ƭ 1 ǡ ǡǡǤ͚͙͘͜Ǥ Ȁ Ǥ ͚͙͘͜ǣ͘͘ǣ͘͘͘Ǧ͘͘͘ ĕĕđĎĈĆęĎĔēĘ Ȉ Ȉ Ȉ Ȉ Ȉ čĊĚėĎĔē̾ėĔĈĊĘĘ Ȉ Ȉ Katena — Your completecomplete resource forfor amniotic membrane pprocedurerocedure pproducts:roducts: Single use speculums Single use spears ͙͘͘ǡ͘͘͘ήĊĞĊĘęėĊĆęĊĉ Forceps ® ,#"EWB3FW XXXLBUFOBDPNr RO0118_Katena.indd 1 1/2/18 10:34 AM News Review VOL. 155 NO. 1 ■ JANUARY 15, 2018 IN THE NEWS Accelerated CXL Shows The FDA recently approved Luxturna (voretigene neparvovec-rzyl, Spark Promise—and Caution Therapeutics), a directly administered gene therapy that targets biallelic This new technology is already advancing, but not without RPE65 mutation-associated retinal dystrophy. The therapy is designed to some bumps in the road. deliver a normal copy of the gene to By Rebecca Hepp, Managing Editor retinal cells to restore vision loss. While the approval provides hope for patients, wo new studies highlight the resulted in infection—while tradi- the $425,000 per eye price tag stands as pros and cons of accelerated tional C-CXL has a reported inci- a signifi cant hurdle. -
Elementary Visual Hallucinations, Blindness, and Headache in Idiopathic Occipital Epilepsy: Diverentiation from Migraine
536 J Neurol Neurosurg Psychiatry 1999;66:536–540 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.66.4.536 on 1 April 1999. Downloaded from SHORT REPORT Elementary visual hallucinations, blindness, and headache in idiopathic occipital epilepsy: diVerentiation from migraine C P Panayiotopoulos Abstract also fundamental symptoms often with the This is a qualitative and chronological same sequence of events in occipital seizures.1−9 analysis of ictal and postictal symptoms, This is a systematic prospective qualitative frequency of seizures, family history, study of the characteristics of elementary visual response to treatment, and prognosis in hallucinations, blindness, and headache in nine patients with idiopathic occipital epi- idiopathic occipital epilepsy. lepsy and visual seizures. Ictal elementary visual hallucinations are stereotyped for Methods each patient, usually lasting for seconds. These are detailed elsewhere.910 Patients with They consist of mainly multiple, bright occipital seizures were prospectively evaluated coloured, small circular spots, circles, or and followed up from 1973. Nine patients with balls. Mostly, they appear in a temporal idiopathic occipital epilepsy with visual halluci- hemifield often moving contralaterally or nations (IOEVH) had: in the centre where they may be flashing. (a) Incontrovertible clinical evidence of oc- They may multiply and increase in size in cipital seizures with or without secondarily the course of the seizure and may progress generalisation. to other non-visual occipital seizure (b) Normal physical, neurological, and men- symptoms and more rarely to extra- tal states and high resolution MRI. They all had detailed interviews, seven com- occipital manifestations and convulsions. 9 Blindness occurs usually from the begin- pleted a purposely designed questionnaire, ning and postictal headache, often indis- and eight provided drawings of their visual hal- tinguishable from migraine, is common. -
Myoclonic Status Epilepticus in Juvenile Myoclonic Epilepsy
Original article Epileptic Disord 2009; 11 (4): 309-14 Myoclonic status epilepticus in juvenile myoclonic epilepsy Julia Larch, Iris Unterberger, Gerhard Bauer, Johannes Reichsoellner, Giorgi Kuchukhidze, Eugen Trinka Department of Neurology, Medical University of Innsbruck, Austria Received April 9, 2009; Accepted November 18, 2009 ABSTRACT – Background. Myoclonic status epilepticus (MSE) is rarely found in juvenile myoclonic epilepsy (JME) and its clinical features are not well described. We aimed to analyze MSE incidence, precipitating factors and clini- cal course by studying patients with JME from a large outpatient epilepsy clinic. Methods. We retrospectively screened all patients with JME treated at the Department of Neurology, Medical University of Innsbruck, Austria between 1970 and 2007 for a history of MSE. We analyzed age, sex, age at seizure onset, seizure types, EEG, MRI/CT findings and response to antiepileptic drugs. Results. Seven patients (five women, two men; median age at time of MSE 31 years; range 17-73) with MSE out of a total of 247 patients with JME were identi- fied. The median follow-up time was seven years (range 0-35), the incidence was 3.2/1,000 patient years. Median duration of epilepsy before MSE was 26 years (range 10-58). We identified three subtypes: 1) MSE with myoclonic seizures only in two patients, 2) MSE with generalized tonic clonic seizures in three, and 3) generalized tonic clonic seizures with myoclonic absence status in two patients. All patients responded promptly to benzodiazepines. One patient had repeated episodes of MSE. Precipitating events were identified in all but one patient. Drug withdrawal was identified in four patients, one of whom had additional sleep deprivation and alcohol intake. -
Emergency Department Management of Neuroleptic Malignant Syndrome
The Journal of Emergency Medicine, Vol. -, No. -, pp. 1–4, 2016 Ó 2016 Elsevier Inc. All rights reserved. 0736-4679/$ - see front matter http://dx.doi.org/10.1016/j.jemermed.2015.10.042 Selected Topics: Psychiatric Emergencies PSYCHIATRIC EMERGENCIES FOR CLINICIANS: EMERGENCY DEPARTMENT MANAGEMENT OF NEUROLEPTIC MALIGNANT SYNDROME Michael P. Wilson, MD, PHD,*† Gary M. Vilke, MD,*† Stephen R. Hayden, MD,* and Kimberly Nordstrom, MD, JD‡§ *University of California at San Diego Medical Center, San Diego, California, †Department of Emergency Medicine Behavioral Emergencies Research (DEMBER) Laboratory, University of California San Diego, San Diego, California, ‡Denver Health Medical Center, Department of Behavioral Health, Psychiatric Emergency Service, Denver, Colorado, and §University of Colorado Denver, School of Medicine, Aurora, Colorado Reprint Address: Michael P. Wilson, MD, PHD, Department of Emergency Medicine, University of California at San Diego Medical Center, 200 West Arbor Drive, Mail Code #8676, San Diego, CA, 92103 , Keywords—altered mental status; neuroleptic malig- What Do You Think is Going on with This Patient? nant syndrome; dystonia; catatonia; rigidity The clinical presentation suggests neuroleptic malignant syndrome (NMS). Although first described more than 50 years ago, the diagnosis of NMS is primarily CLINICAL SCENARIO clinical (1). A 25-year-old man presents with a recent diagnosis of schizophrenia. He was discharged 1 week earlier from What Key Findings Lead to the Diagnosis? an inpatient psychiatric unit. His mother states that he has been acting ‘‘differently’’ for the past 2 days. He Clues to an NMS diagnosis include a recent diagnosis of a has not been ‘‘making any sense,’’ has felt warm to the psychotic disorder and inpatient psychiatric hospitaliza- touch, and today has been stiff and moving rigidly like tion. -
ILAE Classification and Definition of Epilepsy Syndromes with Onset in Childhood: Position Paper by the ILAE Task Force on Nosology and Definitions
ILAE Classification and Definition of Epilepsy Syndromes with Onset in Childhood: Position Paper by the ILAE Task Force on Nosology and Definitions N Specchio1, EC Wirrell2*, IE Scheffer3, R Nabbout4, K Riney5, P Samia6, SM Zuberi7, JM Wilmshurst8, E Yozawitz9, R Pressler10, E Hirsch11, S Wiebe12, JH Cross13, P Tinuper14, S Auvin15 1. Rare and Complex Epilepsy Unit, Department of Neuroscience, Bambino Gesu’ Children’s Hospital, IRCCS, Member of European Reference Network EpiCARE, Rome, Italy 2. Divisions of Child and Adolescent Neurology and Epilepsy, Department of Neurology, Mayo Clinic, Rochester MN, USA. 3. University of Melbourne, Austin Health and Royal Children’s Hospital, Florey Institute, Murdoch Children’s Research Institute, Melbourne, Australia. 4. Reference Centre for Rare Epilepsies, Department of Pediatric Neurology, Necker–Enfants Malades Hospital, APHP, Member of European Reference Network EpiCARE, Institut Imagine, INSERM, UMR 1163, Université de Paris, Paris, France. 5. Neurosciences Unit, Queensland Children's Hospital, South Brisbane, Queensland, Australia. Faculty of Medicine, University of Queensland, Queensland, Australia. 6. Department of Paediatrics and Child Health, Aga Khan University, East Africa. 7. Paediatric Neurosciences Research Group, Royal Hospital for Children & Institute of Health & Wellbeing, University of Glasgow, Member of European Refence Network EpiCARE, Glasgow, UK. 8. Department of Paediatric Neurology, Red Cross War Memorial Children’s Hospital, Neuroscience Institute, University of Cape Town, South Africa. 9. Isabelle Rapin Division of Child Neurology of the Saul R Korey Department of Neurology, Montefiore Medical Center, Bronx, NY USA. 10. Programme of Developmental Neurosciences, UCL NIHR BRC Great Ormond Street Institute of Child Health, Department of Clinical Neurophysiology, Great Ormond Street Hospital for Children, London, UK 11. -
Lafora Disease Masquerading As Hepatic Dysfunction
Thomas Jefferson University Jefferson Digital Commons Abington Jefferson Health Papers Abington Jefferson Health 8-24-2018 Lafora Disease Masquerading as Hepatic Dysfunction Faisal Inayat Allama Iqbal Medical College Waqas Ullah Abington Jefferson Health Hanan T. Lodhi University of Nebraska at Omaha Zarak H. Khan St. Mary Mercy Hospital Livonia Ghulam Ilyas SUNY Downstate Medical Center Follow this and additional works at: https://jdc.jefferson.edu/abingtonfp See next page for additional authors Part of the Gastroenterology Commons, and the Medical Genetics Commons Let us know how access to this document benefits ouy Recommended Citation Inayat, Faisal; Ullah, Waqas; Lodhi, Hanan T.; Khan, Zarak H.; Ilyas, Ghulam; Ali, Nouman Safdar; and Abdullah, Hafez Mohammad A., "Lafora Disease Masquerading as Hepatic Dysfunction" (2018). Abington Jefferson Health Papers. Paper 7. https://jdc.jefferson.edu/abingtonfp/7 This Article is brought to you for free and open access by the Jefferson Digital Commons. The Jefferson Digital Commons is a service of Thomas Jefferson University's Center for Teaching and Learning (CTL). The Commons is a showcase for Jefferson books and journals, peer-reviewed scholarly publications, unique historical collections from the University archives, and teaching tools. The Jefferson Digital Commons allows researchers and interested readers anywhere in the world to learn about and keep up to date with Jefferson scholarship. This article has been accepted for inclusion in Abington Jefferson Health Papers by an authorized administrator of the Jefferson Digital Commons. For more information, please contact: [email protected]. Authors Faisal Inayat, Waqas Ullah, Hanan T. Lodhi, Zarak H. Khan, Ghulam Ilyas, Nouman Safdar Ali, and Hafez Mohammad A. -
RLS), a Clinical Diagnosis
Liza Ashbrook, MD February 10, 2017 Recent Advances in Neurology Patient 1 This 70-year-old man has restless leg syndrome (RLS), a clinical diagnosis. RLS affects 5-10% of the adult population of European ancestry, though likely only 2-3% come to clinical attention. The cause of RLS is not clear but it is associated with low central iron stores. This is supported by evidence from autopsy studies, CSF analysis, gradient echo MRI and transcranial ultrasound. A family history of RLS is reported in 63-92% of individuals suggesting a strong genetic component as well. RLS is typically separated into intermittent symptoms, defined by fewer than twice/week over a year and chronic symptoms. When symptoms are only bothersome intermittently, such as a long plane flight, medications such as carbidopa/levodopa 25/100 can be very effective, however use more than twice weekly can lead to augmentation. Benzodiazepines and hypnotics are also recommended only for as needed use. Periodic limb movements (PLMs) occur in up to 80% of patients with RLS and are diagnosed by polysomnography. These are stereotyped kicking movements and patients are usually unaware of their presence though bed partners may complain. A small subset of those with PLMs are thought to have periodic leg movement disorder (PLMD), defined by PLMs causing either night time or daytime impairment. Other causes of insomnia and hypersomnia must be ruled out and those with RLS cannot have a diagnosis of PLMD. PLMs are of unclear clinical significance and may be a part of normal aging or an epiphenomenon. RLS and PLMs are commonly confused. -
Neuroleptic Malignant Syndrome in a Patient
Psychiatria Danubina, 2018; Vol. 30, Suppl. 7, pp 415-417 Conference paper © Medicinska naklada - Zagreb, Croatia NEUROLEPTIC MALIGNANT SYNDROME IN A PATIENT TREATED WITH CLOTIAPINE Clémentine Lantin, Miriam Franco, François-Xavier Dekeuleneer, Didier Chamart & Juan Martin Tecco Mental Health Unit, Centre Hospitalier Universitaire et Psychiatrique de Mons-Borinage (CHUP-MB), Mons, Belgium SUMMARY Background: Neuroleptic malignant syndrome (NMS), which is linked to the use of antipsychotic medication, is a potentially lethal neurological emergency. The interest of our study is that NMS induced by the use of clotiapine has never previously been described. Subjects and methods: We present the case of a 61-year old man whose sleep disorders were treated with clotiapine 40 mg/day. After 7 days of taking 40 mg clotiapine, the patient presented with a deterioration of his general health which had gradually taken hold, with altered consciousness accompanied by generalised muscle rigidity and hypersalivation. Laboratory blood tests revealed elevated levels of Creatine Phosphokinase (CPK) at 812 U/l. The patient was diagnosed with NMS and treated accordingly. Results: The mechanism that underlies the appearance of NMS remains largely unknown. Clotiapine is a second-generation antipsychotic, first released onto the market in the 1970s, and is available in a few countries, including Belgium. NMS is treated as a medical emergency due to the possibility of morbidity and death. The first step in the treatment of NMS consists in withholding the agent suspected of provoking the symptoms. Conclusions: NMS is difficult to diagnose due to a great variability in clinical presentations and the absence of specific tests and laboratory results. -
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Ziprasidone Associated Neuroleptic KANSAS JOURNAL of MEDICINE Malignant Syndrome Jeffrey D. Bell, M.D.1, Chancen Hall, D.O.2, Justin Sandall, D.O.2 1Beaver Medical Group, Redland, CA NMS, serotonin syndrome (SS), non-convulsive status epilepticus, 2University of Kansas School of Medicine-Wichita, Wichita, KS or other central nervous system (CNS) pathology. Blood, urine, and Department of Anesthesiology sputum cultures were obtained, and she was considered for a lumbar Received Oct. 7, 2019; Accepted for publication Dec. 21, 2020; Published online March 19, 2021 puncture to evaluate for meningitis. In addition, medical records were https://doi.org/10.17161/kjm.vol1411970 obtained from the outside facility and showed she had been receiving INTRODUCTION increasing doses of ziprasidone along with haloperidol, lithium, dulox- Neuroleptic malignant syndrome (NMS) is a severe and potentially etine, oxybutynin, and baclofen. lethal disorder due to an adverse reaction to dopamine receptor antag- Once this information was received and in consultation with our 1 onism or the rapid withdrawal of dopaminergic medications. While neurology and psychiatry colleagues, the patient was treated for a pre- 1 2 incidence is estimated to be 0.02% generally and 0.2% among neu- sumptive diagnosis of NMS with IV bromocriptine 10 mg every six roleptic users, NMS continues to be an unpredictable and potentially hours and a one-time dose of IV dantrolene 2.5 mg/kg, discontinuation life-threatening condition of which case reports continue to be a main of possible causative agents, a cooling blanket and antipyretics, and IV 3 source of information for clinicians. fluids. Despite the advent of second-generation antipsychotics (SGA), SS, which presents with dysautonomia and hyperreflexia in the NMS continues to be a rare yet severe adverse reaction to neurolep- setting of serotonergic medications, was considered for this patient, 4 tics. -
A Comparison of Four Treatments for Generalized Convulsive Status Epilepticus
The New England Journal of Medicine A COMPARISON OF FOUR TREATMENTS FOR GENERALIZED CONVULSIVE STATUS EPILEPTICUS DAVID M. TREIMAN, M.D., PATTI D. MEYERS, M.P.A., NANCY Y. WALTON, PH.D., JOSEPH F. COLLINS, SC.D., CINDY COLLING, R.PH., M.S., A. JAMES ROWAN, M.D., ADRIAN HANDFORTH, M.D., EDWARD FAUGHT, M.D., VINCENT P. CALABRESE, M.D., BASIM M. UTHMAN, M.D., R. EUGENE RAMSAY, M.D., AND MEENAL B. MAMDANI, M.D., FOR THE VETERANS AFFAIRS STATUS EPILEPTICUS COOPERATIVE STUDY GROUP* ABSTRACT TATUS epilepticus is a life-threatening emer- Background and Methods Although generalized gency that affects 65,0001 to 150,0002 peo- convulsive status epilepticus is a life-threatening ple in the United States each year. General- emergency, the best initial drug treatment is uncer- ized convulsive status epilepticus is the most tain. We conducted a five-year randomized, double- Scommon and most dangerous type. blind, multicenter trial of four intravenous regimens: Phenobarbital,3-5 phenytoin,6-14 diazepam plus phen- diazepam (0.15 mg per kilogram of body weight) fol- ytoin,15,16 and lorazepam17-28 have been advocated for lowed by phenytoin (18 mg per kilogram), lorazepam the initial treatment of generalized convulsive status (0.1 mg per kilogram), phenobarbital (15 mg per kil- epilepticus, and each is used by a substantial number ogram), and phenytoin (18 mg per kilogram). Pa- 3 tients were classified as having either overt general- of physicians. There are few data from controlled ized status epilepticus (defined as easily visible trials, however, to document the efficacy of these generalized convulsions) or subtle status epilepticus treatments, and they have not been directly com- (indicated by coma and ictal discharges on the elec- pared.