Status Epilepticus

Total Page:16

File Type:pdf, Size:1020Kb

Status Epilepticus Status Epilepticus Ednea Simon, MD Swedish Pediatric Neuroscience Center 1 Status Epilepticus • Status epilepticus (SE) is a condition resulting either from failure of the mechanisms responsible for seizure termination or form the initiation of mechanisms which lead to abnormally prolonged seizures. • It can have long-term consequences, including neuronal death, neuronal injury, and alteration of neuronal networks, depending on the type and duration of seizures • Prolonged seizures lasting over 30 minutes or repeated frequently enough that recover between seizures does not occur. • Important considerations in treatment – T1 when a seizure is likely to be prolonged leading to continuous seizure activity and treatment should be established after 5-minute mark for convulsive seizure and 10 minute mark for focal seizure – T2 marks the time at which neuronal damage or self perpetuating alteration of neuronal networks may begin if seizure is not controlled Trinka E, Cock H, Hesdorffer D at al, Epilepsia 56(10): 1515-23, 2015 Lowenstein et al. Epilepsia 40:120-122, 1999 2 Status Epilepticus • Goal of therapy: rapid cessation of seizure activity before 30-minute mark when seizure-associated neurologic injury can occur • Incidence of up to 10-41 cases per 100,000 per year and overall mortality of 20% – Risk factors • Etiology • Higher incidence in ages less than 12 months and over 60 years • Long duration SE Betjemann JP & Lowenstein DH. Lancet Neurology (6): 615-24, 2015 Kantanen AM et al. Epilepsy Behav, 49 (Aug): 131-4, 2015 Trinka et al., Seizure 44: 65-73, 2017 3 Age-specific incidence of SE Mortality of SE DeLorenzo et al. Epidemiology of Status Epilepticus, J Clin Neurophys; 12(4):316-25, 1995 4 CLASSIFICATION OF STATUS EPILEPTICUS • With prominent motor symptoms – Convulsive type comprises 37-70% of all forms of status – Myoclonic – Focal motor – Tonic – Hyperkinectic • Nonconvulsive status epilepticus: enduring epileptic condition with reduced or altered consciousness, behavioral, and vegetative abnormalities, or merely subjective symptoms without major convulsive movements lasting more than 30 minutes with ictal epileptiform discharges on EEG. – 8-34% of patient with altered mental status in ICU presents NCSE – With associated coma represents a life threatening condition that requires urgent treatment – Without coma • Focal • Generalized Trinka E et al. Epilepsia 53(suppl 4): 127-138, 2012 5 ETIOLOGY OF STATUS EPILEPTICUS • Symptomatic – Acute symptomatic – Remote symptomatic – Progressive symptomatic • Unknown • Most frequent causes – Acute symptomatic 48-63% of cases with stroke present in 14-22% – Preexisting epilepsy -> low level of AED (25% of cases) that has good prognosis with mortality of 4-8.6% – Remote stroke • Approximately 12% of patients with epilepsy have had at least 1 episode of SE in their lifetime • Acute symptomatic etiology may account for 40-50% of cases Trinka E et al. Epilepsia 53(suppl 4): 127-138, 2012 DeLorenzo RJ et al. J Clin Neurophysiol 12:316-25, 1995 Towne AR et at. Epilepsia 35:27-34, 1994 6 ETIOLOGY OF STATUS EPILEPTICUS Trinka E et al. Epilepsia 53(suppl 4): 127-138, 2012 7 ETIOLOGY OF STATUS EPILEPTICUS • Hypoxic ischemic encephalopathy • Cerebrovascular diseases • Withdrawal or low AEDs levels • Metabolic • Intracranial tumors • CNS infections • Neurodegenerative diseases • Cortical dysplasia • Head trauma • Intoxication • Autoimmune • Mitochondrial cytopathy • Genetic • Neurocutaneous syndromes • NORSE – New onset refractory status epilepticus (adults) • FIRES – Febrile infection related epilepsy syndrome Trinka E et al. Epilepsia 56(10): 1515-23, 2015 8 NORSE NEW ONSET REFRACTORY STATUS EPILEPTICUS • Condition characterized by the sudden onset of continuous seizures or a flurry of very frequent seizures that can not be controlled with seizure medications • In many cases there is report of a cold or flu like illness days to weeks prior to the start of seizures • Affects otherwise healthy young adults, although it can affect people of any age. • Super-refractory status epilepticus with patients often treated with IV anesthetics for weeks in an intensive care unit • NORSE is a life-threatening condition, with a death rate of around 30%. Survivors often have lasting brain damage and epilepsy. A minority of people fully recover and return to a normal lifestyle 9 FIRES FEBRILE INFECTION-RELATED EPILEPSY SYNDROME • Rare epilepsy syndrome of unclear etiology in which children, usually of school age, suddenly develop very frequent seizures (up to hundreds per day) within two weeks after a mild febrile illness. • Super-refractory status epilepticus despite use of IV anesthetics that can last months • Immune treatment and the ketogenic diet may help. • Outcome is poor with cognitive disability and refractory epilepsy. 10 TIME IS BRAIN! CLINICAL COURSE Early phase 5-10 Impending SE MIN 10-30 Established SE MIN 30-60 Refractory SE MIN Super >24 H Refractory SE PROGNOSIS OF STATUS EPILEPTICUS WORSENS WITH INCREASING DURATION OF SEIZURE ACTIVITY Trinka et al., Seizure 44: 65-73, 2017 11 Treatment Algorithm of Status Epilepticus • Stabilization phase (0-5 minutes of seizure activity) including standard initial first aid for seizures and initial assessments and monitoring. Maintain airway, respiration, and circulation EARLY TREATMENT SHOULD BE EMPHASIZED SINCE TREATMENT BECOMES LESS EFFECTIVE THE LONGER THE EPISODE OF STATUS EPILEPTICUS LASTS • Initial therapy phase (5-20 minutes) when it is clear the seizure requires medical intervention. • Second therapy phase (20-40 minutes) when response (or lack of response) to the initial therapy should be apparent. • Third therapy phase (+40 minutes) if second therapy fails to stop the seizures, treatment consideration should include repeating second line therapy or IV anesthetic drugs that require continuous video-EEG monitoring. Trinka et al., Seizure 44: 65-73, 2017 12 Treatment Algorithm of Status Epilepticus Stabilization phase • Intubation for airway protection if unconscious • Monitor blood pressure, pulse, cardiac rhythm, and oxygen saturation • Intravenous access • Initial labs: toxic screen, ethanol level, complete blood count, comprehensive metabolic panel, antiepileptic drug levels • Neuroimaging investigation • CSF studies, if indicated • Electroencephalogram 13 TREATMENT OF EARLY PHASE SE FIRST LINE TREATMENT: BENZODIAZEPINE Benzodiazepine is recommended IM or IN midazolam, IV lorazepam, IV diazepam with demonstrated efficacy, safety, and tolerability • Lorazepam IV – 0.07-0.1 mg/kg at rate 2 mg/min • Diazepam IV or rectal – 0.2 mg/kg at rate 5 mg/min – 5-10 mg up to 20 mg • Midazolam IM or IN or buccal – 0.2 mg/kg, dose 10 mg Benzodiazepine increases channel opening frequency of GABA-A receptors with increased chloride conductance and neuronal hyperpolarization, with increased inhibition Trinka et al., Seizure 44: 65-73, 2017 14 TREATMENT OF EARLY PHASE SE FIRST LINE TREATMENT: BENZODIAZEPINE • VA cooperative study using IV lorazepam vs IV phenytoin as first line treatment for SE – 64.9% controlled with IV lorazepam – 43.5 % controlled with IV phenytoin 15 IM Midazolam vs IV Lorazepam as first line for treatment of status epilepticus Double blind study including 893 children and adults treated by paramedics IM Midazolam IV Lorazepam Seizure control 73.4% 63.4% Time administration 1.2 min 4.8 min Clinical seizure cessation 3.3 min 1.6 min RAMPART- rapid anticonvulsant medications prior to arrival trial Silbergleit R et al., N Engl J Med 2012; 366 February (7): 591-600 16 INTRAVENOUS LORAZEPAM VS DIAZEPAM • Meta analysis of 5 randomized controlled trial including 656 patients – 320 treated with LZP – 336 with DZP • No statistically significant differences were found between IV LZP and IV DZP regarding – Clinical seizure cessation – Continuation of SE requiring a different drug – Seizure cessation after a single dose of medication – Ventilatory support – Clinically relevant hypotension Brigo et al., Epilepsy Behav 64 (Oct): 29-36, 2016 17 BENZODIAZEPINES AND ROUTES OF ADMINISTRATION Meta-analysis of 19 studies for efficacy and safety in children and adults using non-intravenous midazolam and rectal or intravenous diazepam. Study included 1,933 seizures in 1,602 patients • For seizure cessation, non-IV midazolam was as effective as IV or rectal diazepam • Time interval between arrival and seizure cessation was shorter with non-IV midazolam • Time from time interval from drug administration to clinical seizure cessation as shorter for diazepam by any route • Non difference in side effects found with midazolam or with any route of diazepam • Non-intravenous midazolam routes represents a practical, rapid, reasonably safe and effective alternative as first-line treatment in out of hospital setting Brigo et al., Epilepsy Behav 2015; 49(August): 325-36; Brigo et al., CNS drugs 2015 A(August) 18 TREATMENT OF ESTABLISHED SE SECOND THERAPY PHASE Approximately 40% of patients with generalized convulsive SE are refractory to benzodiazepine treatment Options: • Fosphenytoin/Phenytoin • Valproic acid • Levetiracetam • Phenobarbital • Lacosamide There is no class I evidence for choosing one AED over the other. Drug choice should take into consideration comorbidities and side effect profile Trinka et al., Seizure 44: 65-73, 2017 19 TREATMENT OF ESTABLISHED SE SECOND THERAPY PHASE • Fosphenytoin/Phenytoin – Fosphenytoin: 20 mg/kg IV at 150 mg PE/min – Phenytoin: 20 mg/kg IV at 50 mg /min – Effect noted within 20 minutes of administration – If seizure persist
Recommended publications
  • Forensic Medicine
    YEREVAN STATE MEDICAL UNIVERSITY AFTER M. HERATSI DEPARTMENT OF Sh. Vardanyan K. Avagyan S. Hakobyan FORENSIC MEDICINE Handout for foreign students YEREVAN 2007 This handbook is adopted by the Methodical Council of Foreign Students of the University DEATH AND ITS CAUSES Thanatology deals with death in all its aspects. Death is of two types: (1) somatic, systemic or clinical, and (2) molecular or cellular. Somatic Death: It is the complete and irreversible stoppage of the circulation, respiration and brain functions, but there is no legal definition of death. THE MOMENT OF DEATH: Historically (medically and legally), the concept of death was that of "heart and respiration death", i.e. stoppage of spontaneous heart and breathing functions. Heart-lung bypass machines, mechanical respirators, and other devices, however have changed this medically in favor of a new concept "brain death", that is, irreversible loss of Cerebral function. Brain death is of three types: (1) Cortical or cerebral death with an intact brain stem. This produces a vegetative state in which respiration continues, but there is total loss of power of perception by the senses. This state of deep coma can be produced by cerebral hypoxia, toxic conditions or widespread brain injury. (2) Brain stem death, where the cerebrum may be intact, though cut off functionally by the stem lesion. The loss of the vital centers that control respiration, and of the ascending reticular activating system that sustains consciousness, cause the victim to be irreversibly comatose and incapable of spontaneous breathing. This can be produced by raised intracranial pressure, cerebral oedema, intracranial haemorrhage, etc.(3) Whole brain death (combination of 1 and 2).
    [Show full text]
  • 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.
    [Show full text]
  • Coma Stimulation: Suggested Activities
    Coma stimulation: suggested activities Headway’s publications are all available to freely download from the information library on the charity’s website, while individuals and families can request hard copies of the booklets via the helpline. As a charity, we rely on donations from people like you to continue providing free information to people affected by brain injury. Donate today: www.headway.org.uk/donate. Introduction It is quite common for family members to feel ‘useless’ when a relative is in a coma, and to be desperate to do something to help. A coma stimulation programme (sometimes called a coma arousal programme) is an approach based on stimulating the unconscious person’s senses of hearing, touch, smell, taste and vision individually in order to help their recovery. There is still controversy over how effective it is to try to stimulate a person in coma. However, most would say that such programmes have some beneficial effect, even if only to provide something constructive for the family to do. It is very important that the activities used would have been enjoyable for the patient before the injury. For example, only play music they like and talk to them about subjects they are interested in. Try not to do anything for too long in order to avoid tiring the person out. A stimulation programme must only be started after discussion with the clinical staff, who will advise you what might be appropriate at any particular stage in the recovery process. Activity suggestions Here are some examples of activities that could form part of a coma stimulation programme: • Make sure that a few friends and family members visit regularly, rather than in large groups at a time.
    [Show full text]
  • Phenobarbital Brand Name: Phenobarb
    Generic Name: Phenobarbital Brand Name: Phenobarb What Is It Used For? Decreasing seizure activity in various types of seizures. Especially useful for controlling seizures in neonates and infants Given intravenously in the emergency department for status epilepticus. How Long Does The Oral Medicine Take to Work? 10-30 days What Are The Important Safety Concerns? When first starting the medicine, your child may be slightly drowsy and/or dizzy. Only adjust the dosage as recommended by your health care provider. They will usually increase this medication slowly to avoid side effects. Never increase the dosage more than once per week unless directed otherwise. Once you have started with one brand of the medication stay with it. Avoid switching between different brands. Check with your pharmacist before taking herbal medications and/or over-the- counter medications. They may have adverse effects if taken with anti-seizure medications. Do not stop taking this medication suddenly because this could result in seizures. It is important to keep a record of your child’s seizures and side effects to determine how well they are responding to the medication. Does My Child Need Bloodwork With This Medication? Routine blood work may be done to help determine the best dosage for your child, and also if they have side effects to the medication. If your child is required to have blood work it must be done BEFORE they get the medication. This is called a trough level. This level usually falls between 65 and 170. A blood test may be done before starting this medication to check your child’s liver function and blood counts.
    [Show full text]
  • CDHO Factsheet Epilepsy
    Disease/Medical Condition EPILEPSY Date of Publication: August 7, 2014 (also known as “seizure disorder”) Is the initiation of non-invasive dental hygiene procedures* contra-indicated? No Is medical consult advised? ...................................... No (assuming patient/client is already under medical care for epilepsy, which is well controlled) Is the initiation of invasive dental hygiene procedures contra-indicated?** No Is medical consult advised? ....................................... Possibly (e.g., if there is medication non-compliance) Is medical clearance required? .................................. Possibly (e.g., if there is significant risk of seizure; patient/ client should be seizure-free for several months to be considered controlled) Is antibiotic prophylaxis required? .............................. No Is postponing treatment advised? ............................... No (assuming patient/client is already under medical care for epilepsy, which is well controlled and for which there are no anticipated exacerbating factors in the office setting) Oral management implications Important considerations in the management of epileptic patients/clients are prevention of seizures in the dental chair and preparation for managing seizures if they occur. When a patient/client responds positively to questions about seizures/ epilepsy during health history taking, further information should be obtained. Based on the patient/client’s responses, the dental hygienist may choose to postpone treatment to avoid triggering a seizure in the dental chair. It is valuable for the dental hygienist to know what factors have the potential to exacerbate epileptic seizures in a particular patient/client in order that trigger stimuli can be avoided. The dental hygienist can reduce stress and anxiety by explaining procedures before starting. Bright light should be kept out of the patient/client’s eyes, and dark glasses may assist with this.
    [Show full text]
  • Evaluation and Management in an Urgent Care Setting
    Syncope Evaluation and Management in an Urgent Care Setting Urgent message: When a patient presents to urgent care after a syncopal event, the clinician’s charge is to determine whether the episode was of benign or potentially life-threatening etiology and whether the patient should be transferred for further evaluation. Kenneth V. Iserson, MD, MBA, FACEP, FAAEM, Professor of Emergency Medicine, The University of Arizona, Tucson, AZ Introduction yncope is a sudden, transient loss of consciousness with a loss of postural tone (typically, falling). It results from an abrupt, transient, and diffuse cerebral Smalfunction and is quickly followed by sponta- neous recovery. The term syncope excludes seizures, coma, shock, or other states of altered consciousness. Many patients will ascribe their syncopal episode to a sit- uationally mediated vasovagal episode. Despite this, the goals in the urgent care setting include the following: Ⅲ Determining whether the patient’s episode was actually a syncopal or presyncopal event, and if it could have a life-threatening etiology Ⅲ Stabilizing the patient Ⅲ Transferring those patients who need further diag- nostic studies or therapeutic interventions © John Bolesky, Artville © John Bolesky, Epidemiology Syncope accounts for up to 3% of emergency depart- common in young adults, while cardiac syncope ment (ED) visits and up to 6% of hospital admissions becomes increasingly more frequent with advancing each year in the United States.1,2 At some time in their age.4 The chance of having at least one syncopal episode lives, up to about half the population (12% to 48%) of in childhood is between 15% and 50%.5 Though a people may experience syncope.3 benign cause is usually found, syncope in children war- Syncope occurs in all age groups, but it is most com- rants prompt detailed evaluation.6 mon in adults.
    [Show full text]
  • EEG in the Diagnosis, Classification, and Management of Patients With
    EEG IN THE DIAGNOSIS, J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.2005.069245 on 16 June 2005. Downloaded from CLASSIFICATION, AND MANAGEMENT ii2 OF PATIENTS WITH EPILEPSY SJMSmith J Neurol Neurosurg Psychiatry 2005;76(Suppl II):ii2–ii7. doi: 10.1136/jnnp.2005.069245 he human electroencephalogram (EEG) was discovered by the German psychiatrist, Hans Berger, in 1929. Its potential applications in epilepsy rapidly became clear, when Gibbs and Tcolleagues in Boston demonstrated 3 per second spike wave discharge in what was then termed petit mal epilepsy. EEG continues to play a central role in diagnosis and management of patients with seizure disorders—in conjunction with the now remarkable variety of other diagnostic techniques developed over the last 30 or so years—because it is a convenient and relatively inexpensive way to demonstrate the physiological manifestations of abnormal cortical excitability that underlie epilepsy. However, the EEG has a number of limitations. Electrical activity recorded by electrodes placed on the scalp or surface of the brain mostly reflects summation of excitatory and inhibitory postsynaptic potentials in apical dendrites of pyramidal neurons in the more superficial layers of the cortex. Quite large areas of cortex—in the order of a few square centimetres—have to be activated synchronously to generate enough potential for changes to be registered at electrodes placed on the scalp. Propagation of electrical activity along physiological pathways or through volume conduction in extracellular spaces may give a misleading impression as to location of the source of the electrical activity. Cortical generators of the many normal and abnormal cortical activities recorded in the EEG are still largely unknown.
    [Show full text]
  • Pentobarbital Sodium
    PENTobarbital Sodium Brand names Nembutal Sodium Medication error Look-alike, sound-alike drug names. Tall man letters (not FDA approved) are recommended potential to decrease confusion between PENTobarbital and PHENobarbital.(1,2) ISMP recommends the following tall man letters (not FDA approved): PENTobarbital.(30) Contraindications Contraindications: In patients with known hypersensitivity to barbiturates or any com- and warnings ponent of the formulation.(2) If an allergic or hypersensitivity reaction or a life-threatening adverse event occurs, rapid substitution of an alternative agent may be necessary. If pentobarbital is discontinued due to development of a rash, an anticonvulsant that is structurally dissimilar should be used (i.e., nonaromatic). (See Rare Adverse Effects in the Comments section.) Also contraindicated in patients with a history of manifest or latent porphyria.(2) Warnings: Rapid administration may cause respiratory depression, apnea, laryngospasm, or vasodilation with hypotension.(2) Should be withdrawn gradually if large doses have been used for prolonged periods.(2) Paradoxical excitement may occur or important symptoms could be masked when given to patients with acute or chronic pain.(2) May be habit forming. Infusion-related Respiratory depression and arrest requiring mechanical ventilation may occur. Monitor cautions oxygen saturation. If hypotension occurs, the infusion rate should be decreased and/or the patient should be treated with IV fluids and/or vasopressors. Pentobarbital is an alkaline solution (pH = 9–10.5); therefore, extravasation may cause tissue necrosis.(2) (See Appendix E for management.) Gangrene may occur following inadvertent intra-arterial injection.(2) Dosage Medically induced coma (for persistently elevated intracranial pressure (ICP) or refractory status epilepticus): Patient should be intubated and mechanically ventilated.
    [Show full text]
  • 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.
    [Show full text]
  • Migraine Triggered Seizures and Epilepsy Triggered Headache and Migraine Attacks: a Need for Re-Assessment
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by PubMed Central J Headache Pain (2011) 12:287–288 DOI 10.1007/s10194-011-0344-2 COMMENTARY Migraine triggered seizures and epilepsy triggered headache and migraine attacks: a need for re-assessment Paul T. G. Davies • C. P. Panayiotopoulos Received: 5 April 2011 / Accepted: 8 April 2011 / Published online: 24 April 2011 Ó The Author(s) 2011. This article is published with open access at Springerlink.com In this issue of the Journal, Belcastro and associates review Migralepsy terminology and classification issues for migralepsy, hem- icrania epileptica, post-ictal and ictal headache [1]. They According to the ICHD-II 1.5.5, ‘‘migraine-triggered sei- raise key points such as ictal headache and visual seizures zure (sometimes referred to as migralepsy)’’ denotes an are often misdiagnosed as migraine, ‘‘migralepsy’’ is unli- epileptic seizure that occurs ‘‘during or within one hour kely to exist and an ‘‘epilepsy-migraine sequence’’ is much after a migraine aura’’ [3]. However, the evidence of this more common and well documented than the dominant ‘‘migraine-seizure’’ sequence is weak and the proposed view of a ‘‘migraine-epilepsy sequence’’. Their relevant criterion of 1 h gap between the end of the ‘‘aura’’ and the proposals need appropriate attention by the committee of start of an epileptic seizure is entirely arbitrary the international classification of headache disorders Migralepsy is an old term derived from migra(ine) and (ICHD) as well as the physicians in their clinical practice (epi)lepsy, coined by Dr Douglas Davidson, but mainly because of the consequences that misdiagnosis may have on attributed to Lennox and Lennox, which we quote, ‘‘a patients.
    [Show full text]
  • 1,1,1-Trichloroethane (CASRN 71-55-6) | IRIS
    Integrated Risk Information System (IRIS) U.S. Environmental Protection Agency Chemical Assessment Summary National Center for Environmental Assessment 1,1,1-Trichloroethane; CASRN 71-55-6 Human health assessment information on a chemical substance is included in the IRIS database only after a comprehensive review of toxicity data, as outlined in the IRIS assessment development process. Sections I (Health Hazard Assessments for Noncarcinogenic Effects) and II (Carcinogenicity Assessment for Lifetime Exposure) present the conclusions that were reached during the assessment development process. Supporting information and explanations of the methods used to derive the values given in IRIS are provided in the guidance documents located on the IRIS website. STATUS OF DATA FOR 1,1,1-Trichloroethane File First On-Line 03/31/1987 Category (section) Assessment Available? Last Revised Oral RfD (I.A.) Acute Oral RfD (I.A.1.) qualitative discussion 09/28/2007 Short-term Oral RfD (I.A.2.) qualitative discussion 09/28/2007 Subchronic Oral RfD (I.A.3.) yes 09/28/2007 Chronic Oral RfD (I.A.4.) yes 09/28/2007 Inhalation RfC (I.B.) Acute Inhalation RfC (I.B.1.) yes 09/28/2007 Short-term Inhalation RfC (I.B.2.) yes 09/28/2007 Subchronic Inhalation RfC (I.B.3.) yes 09/28/2007 1 Integrated Risk Information System (IRIS) U.S. Environmental Protection Agency Chemical Assessment Summary National Center for Environmental Assessment Category (section) Assessment Available? Last Revised Chronic Inhalation RfC (I.B.4.) yes 09/28/2007 Carcinogenicity Assessment (II.) yes 09/28/2007 I. Health Hazard Assessments for Noncarcinogenic Effects I.A.
    [Show full text]
  • 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.
    [Show full text]