European Headache Federation Guideline on Idiopathic Intracranial
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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. -
Stand up to Chronic Migraine with Botox®
#1 PRESCRIBED BRANDED TREATMENT FOR CHRONIC MIGRAINE* Chronic Migraine DON’T LIE DOWN BOTOX ® STAND UP TO Prevention CHRONIC MIGRAINE® WITH BOTOX Treatment Experience Treatment *Truven Health MarketScan Data, October 2010-April 2017. Prevent Headaches and Migraines Before They Even Start BOTOX ® BOTOX® prevents on average 8 to 9 headache days and migraine/probable migraine days a month (vs 6 to 7 for placebo) Savings Program For adults with Chronic Migraine, 15 or more headache days a month, each lasting 4 hours or more. BOTOX® is not approved for adults with migraine who have 14 or fewer headache days a month. Indication • Spread of toxin effects. The effect of botulinum toxin may affect areas BOTOX® is a prescription medicine that is injected to prevent headaches in adults away from the injection site and cause serious symptoms including: loss of with chronic migraine who have 15 or more days each month with headache strength and all-over muscle weakness, double vision, blurred vision and lasting 4 or more hours each day in people 18 years or older. drooping eyelids, hoarseness or change or loss of voice, trouble saying words It is not known whether BOTOX® is safe or effective to prevent headaches clearly, loss of bladder control, trouble breathing, trouble swallowing. in patients with migraine who have 14 or fewer headache days each month There has not been a confirmed serious case of spread of toxin effect away from (episodic migraine). the injection site when BOTOX® has been used at the recommended dose to IMPORTANT SAFETY INFORMATION treat chronic migraine. Resources BOTOX® may cause serious side effects that can be life threatening. -
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. -
Journal of Neurological Disorders DOI: 10.4172/2329-6895.1000275 ISSN: 2329-6895
olog eur ica N l D f i o s l o a r n d r e u r s o J Derakhshan, J Neurol Disord 2016, 4:4 Journal of Neurological Disorders DOI: 10.4172/2329-6895.1000275 ISSN: 2329-6895 Research Article Open Access Successful Opioid Monotherapy in Migralepsy: A Case Series Iraj Derakhshan* Department of Neurology, Case Western Reserve and Cincinnati Universities, Ohio, USA *Corresponding author: Iraj Derakhshan, Associate Professor, Department of Neurology, Case Western Reserve and Cincinnati Universities, Ohio, 205 Cyrus Drive, Charleston West Virginia, 25314, USA, Tel: 304 345 5174; E-mail: [email protected] Rec date: June 10, 2016; Acc date: July 06, 2016; Pub date: July 10, 2016 Copyright: © 2016 Derakhshan I. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract Background: There is a consensus that migraine and epilepsy are comorbid conditions. The novel concept explored and developed in this case series is that of the primacy of headaches in generating seizures in those patients suffering from migraine-triggered epilepsy (i.e., migralepsy). As demonstrated in the five cases descried here, much like the effect of ketogenic-diet on migraine-triggered epilepsy, once the migraine headaches were completely suppressed after adopting daily scheduled opioid therapy the seizures stopped from occurring, but they returned with the recurrence of the migraines once the patients had stopped their daily opiate regimen for any reason. Clinical implications: The above pharmacological scenario is reminiscent of a similar but naturalistic course of events as described in reports concerning the salutary effects of ketogenic diet, or restoration of sleep, in cases of migraine-triggered epilepsy. -
Migraine Mimics
ISSN 0017-8748 Headache doi: 10.1111/head.12518 © 2015 American Headache Society Published by Wiley Periodicals, Inc. Expert Opinion Migraine Mimics Randolph W. Evans, MD The symptoms of migraine are non-specific and can be present in many other primary and secondary headache disorders, which are reviewed. Even experienced headache specialists may be challenged at times when diagnosing what appears to be first or worst, new type, migraine status, and chronic migraine. Key words: migraine, migraine mimic, symptomatic migraine, hemicrania continua (Headache 2015;55:313-322) The symptoms of migraine are non-specific and She had seen 2 headache specialists previously. can be present in many other primary and secondary She had been tried on sumatriptan p.o. and subcuta- headache disorders.1,2 Even experienced headache neously, diclofenac powder, ketorolac oral and intra- specialists may be challenged at times when diagnos- muscular, dihydroergotamine nasal spray, and had an ing what appears to be first or worst, new type, occipital nerve block without benefit. Gabapentin migraine status, and chronic migraine. Another diag- and pregabalin did not help. She was placed on indo- nosis may be responsible when physicians use the term methacin 75 mg sustained release once a day for 8 “atypical migraine.” days without benefit. Prednisone 60 mg daily for 10 days did not help.An intravenous dihydroergotamine CASE HISTORIES regimen for 5 days did not help. Case 1.—This 48-year-old woman was seen for a A magnetic resonance imaging (MRI) and mag- third opinion with a 20-year history of only menstrual netic resonance angiogram (MRA) of the brain and headaches always preceded by a visual aura followed cervical spine and magnetic resonance venogram by a generalized throbbing with an intensity of 5–6/10 (MRV) of the brain were negative. -
DIAGNOSTICS and THERAPY of INCREASED INTRACRANIAL PRESSURE in ISCHEMIC STROKE
DIAGNOSTICS and THERAPY of INCREASED INTRACRANIAL PRESSURE in ISCHEMIC STROKE Erich Schmutzhard INNSBRUCK, AUSTRIA e - mail: erich.schmutzhard@i - med.ac.at Neuro - ICU Innsbruck Conflict of interest : Speaker‘s honoraria from ZOLL Medical and Honoraria for manuscripts from Pfizer Neuro - ICU Innsbruck OUTLINE Introduction Definition: ICP, CPP, PbtiO2, metabolic monitoring, lactate , pyruvate , brain temperature etc Epidemiology of ischemic stroke and ICP elevation in ischemic stroke ACM infarction and the role of collaterals and/ or lack of collaterals for ICP etc Hydrocephalus in posterioir fossa ( mainly cerebellar ) infarction Diagnosis of ICP etc Monitoring of ICP etc Therapeutic management : decompressive craniectomy – meta - analysis of DESTINY HAMLET und co deepening of analgosedation , ventilation , hyperventilation , osmotherapy , CPP - oriented th , MAP management , hypothermia , prophylactic normothermia , external ventricular drainage Neuro - ICU Innsbruck Introduction - Malignant cerebral edema following ischemic stroke is life threatening. - The pathophysiology of brain edema involves failure of the sodium - potassium adenosine triphosphatase pump and disruption of the blood - brain barrier, leading to cytotoxic edema and cellular death. - The Monro - Kellie doctrine clearlc states that - since the brain is encased in a finite space - increased intracranial pressure (ICP) due to cerebral edema can result in herniation through the foramen magnum and openings formed by the falx and tentorium. - Moreover, elevated ICP can cause secondary brain ischemia through decreased cerebral perfusion and blood flow, brain tissue hypoxia, and metabolic crisis. - Direct cerebrovascular compression caused by brain tissue shifting can lead to secondary infarction, especially in the territories of the anterior and posterior cerebral artery. - Tissue shifts can also stretch and tear cerebral vessels, causing intracranial hemorrhage such as Duret’s hemorrhage of the brainstem. -
Decreased Risk of Dementia in Migraine Patients with Traditional Chinese Medicine Use: a Population-Based Cohort Study
www.impactjournals.com/oncotarget/ Oncotarget, 2017, Vol. 8, (No. 45), pp: 79680-79692 Clinical Research Paper Decreased risk of dementia in migraine patients with traditional Chinese medicine use: a population-based cohort study Chun-Ting Liu1,*, Bei-Yu Wu1,*, Yu-Chiang Hung1,2,*, Lin-Yi Wang3, Yan-Yuh Lee3, Tsu-Kung Lin4, Pao-Yen Lin5, Wu-Fu Chen6, Jen-Huai Chiang7,8, Sheng-Feng Hsu9,10 and Wen-Long Hu1,11,12,* 1Department of Chinese Medicine, Kaohsiung Chang Gung Memorial Hospital and School of Traditional Chinese Medicine, Chang Gung University College of Medicine, Kaohsiung, Taiwan 2School of Chinese Medicine for Post Baccalaureate, I-Shou University, Kaohsiung, Taiwan 3Department of Physical Medicine and Rehabilitation, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan 4Department of Neurology, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan 5Department of Psychiatry, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan 6Department of Neurosurgery, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan 7Management Office for Health Data, China Medical University Hospital, Taichung, Taiwan 8College of Medicine, China Medical University, Taichung, Taiwan 9Graduate Institute of Acupuncture Science, China Medical University, Taichung, Taiwan 10Department of Chinese Medicine, China Medical University Hospital, Taipei Branch, Taipei, Taiwan 11Kaohsiung Medical University College of Medicine, Kaohsiung, Taiwan 12Fooyin University College of Nursing, Kaohsiung, Taiwan *These authors contributed equally to this work Correspondence to: Wen-Long Hu, email: [email protected] Keywords: dementia, migraine, pharmaco-epidemiology, national health insurance research database, Chinese herbal product Received: February 27, 2017 Accepted: June 28, 2017 Published: July 08, 2017 Copyright: Liu et al. -
Episodic Visual Snow Associated with Migraine Attacks
Letters RESEARCH LETTER Discussion | Three patients report episodes of VS exclusively at the beginning or during migraine attacks. The description was Episodic Visual Snow Associated identical and matched the definition of VS in VSS except for With Migraine Attacks not being continuous.1,2 In the syndrome-defining study,1 only Visual snow syndrome (VSS) is a debilitating disorder charac- patients with continuous VS were included, impeding the iden- terized by continuous visual snow (VS), ie, tiny flickering dots tification of an episodic form. Based on the present case se- in the entire visual field resembling the view of a badly tuned ries, we propose to distinguish between VSS, a debilitating dis- analog television (Figure), plus additional visual symptoms, order characterized by continuous VS and additional visual such as photophobia and palinopsia. There is a high comor- symptoms persisting over years, and eVS, an uncommon self- 1 bidity with migraine and migraine aura. To our knowledge, limiting symptom during migraine attacks. this is the first report of patients with an episodic form of VS The relationship between migraine and VSS is still (eVS), strictly co-occurring with migraine attacks. unresolved.3 Although the severity of VS in VSS does not fluc- tuate in parallel to the migraine cycle,1 the strict co-occurrence Methods | Between January 2016 and December 2017, we saw of eVS and migraine reported here epitomizes a close proxim- 3 patients with eVS and 1934 patients with migraine at our ter- ity.This is in agreement with the clinical picture of migraine being tiary outpatient headache center. -
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. -
Stroke Intracranial Hypertension Cerebral Edema Roman Gardlík, MD, Phd
Stroke Intracranial hypertension Cerebral edema Roman Gardlík, MD, PhD. Institute of Pathological Physiology Institute of Molecular Biomedicine [email protected] Books • Silbernagl 356 • Other book 667 Brain • The most complex structure in the body • Anatomically • Functionally • Signals to and from various part of the body are controlled by very specific areas within the brain • Brain is more vulnerable to focal lesions than other organs • Renal infarct does not have a significant effect on kidney function • Brain infarct of the same size can produce complete paralysis on one side of the body Brain • 2% of body weight • Receives 1/6 of resting cardiac output • 20% of oxygen consumption Blood-brain barrier Mechanisms of brain injury • Various causes: • trauma • tumors • stroke • metabolic dysbalance • Common pathways of injury: • Hypoxia • Ischemia • Cerebral edema • Increased intracranial pressure Hypoxia • Deprivation of oxygen with maintained blood flow • Causes: • Exposure to reduced atmospheric pressure • Carbon monoxide poisoning • Severe anemia • Failure to ogygenate blood • Well tolerated, particularly if chronic • Neurons capable of anaerobic metabolism • Euphoria, listlessness, drowsiness, impaired problem solving • Acute and severe hypoxia – unconsciousness and convulsions • Brain anoxia can result to cardiac arrest Ischemia • Reduced blood flow • Focal / global ischemia • Energy sources (glucose and glycogen) are exhausted in 2 to 4 minutes • Cellular ATP stores are depleted in 4 to 5 minutes • 50% - 75% of energy is -
Idiopathic Intracranial Hypertension
IDIOPATHIC INTRACRANIAL HYPERTENSION William L Hills, MD Neuro-ophthalmology Oregon Neurology Associates Affiliated Assistant Professor Ophthalmology and Neurology Casey Eye Institute, OHSU No disclosures CASE - 19 YO WOMAN WITH HEADACHES X 3 MONTHS Headaches frontal PMHx: obesity Worse lying down Meds: takes ibuprofen for headaches Wake from sleep Pulsatile tinnitus x 1 month. Vision blacks out transiently when she bends over or sits down EXAMINATION Vision: 20/20 R eye, 20/25 L eye. Neuro: PERRL, no APD, EOMI, VF full to confrontation. Dilated fundoscopic exam: 360 degree blurring of disc margins in both eyes, absent SVP. Formal visual field testing: Enlargement of the blind spot, generalized constriction both eyes. MRI brain: Lumbar puncture: Posterior flattening of Opening pressure 39 the globes cm H20 Empty sella Normal CSF studies otherwise normal Headache improved after LP IDIOPATHIC INTRACRANIAL HYPERTENSION SYNDROME: Increased intracranial pressure without ventriculomegaly or mass lesion Normal CSF composition NOMENCLATURE Idiopathic intracranial hypertension (IIH) Benign intracranial hypertension Pseudotumor cerebri Intracranial hypertension secondary to… DIAGNOSTIC CRITERIA Original criteria have been updated to reflect new imaging modalities: 1492 Friedman and Jacobsen. Neurology 2002; 59: Symptoms and signs reflect only those of - increased ICP or papilledema 1495 Documented increased ICP during LP in lateral decubitus position Normal CSF composition No evidence of mass, hydrocephalus, structural -