“Seizures (Epilepsy)” a Seizure: Partial – Start in a Specific Part of the Brain, Not in the Whole Is a Symptom of an Electrical Disturbance in the Brain Brain
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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. -
Prognostic Utility of Hypsarrhythmia Scoring in Children with West
Clinical Neurology and Neurosurgery 184 (2019) 105402 Contents lists available at ScienceDirect Clinical Neurology and Neurosurgery journal homepage: www.elsevier.com/locate/clineuro Prognostic utility of hypsarrhythmia scoring in children with West syndrome T after ketogenic diet ⁎ Yunjian Zhang1, Lifei Yu1, Yuanfeng Zhou, Linmei Zhang, Yi Wang, Shuizhen Zhou Department of Pediatric Neurology, Children’s Hospital of Fudan University, China ARTICLE INFO ABSTRACT Keywords: Objective: The aim of this study was to evaluate the clinical efficacy and electroencephalographic (EEG) changes West syndrome of West syndrome after ketogenic diet (KD) therapy and to explore the correlation of EEG features and clinical Ketogenic diet efficacy. EEG Patients and methods: We retrospectively studied 39 patients with West syndrome who accepted KD therapy from Hypsarrhythmia May 2011 to October 2017. Outcomes including clinical efficacy and EEG features with hypsarrhythmia severity scores were analyzed. Results: After 3 months of treatment, 20 patients (51.3%) had ≥50% seizure reduction, including 4 patients (10.3%) who became seizure-free. After 6 months of treatment, 4 patients remained seizure free, 12 (30.8%) had 90–99% seizure reduction, 8 (20.5%) had a reduction of 50–89%, and 15 (38.5%) had < 50% reduction. Hypsarrhythmia scores were significantly decreased at 3 months of KD. They were associated with seizure outcomes at 6 months independent of gender, the course of disease and etiologies. Patients with a hypsar- rhythmia score ≥8 at 3 months of therapy may not be benefited from KD. Conclusion: Our findings suggest a potential benefit of KD for patients with drug-resistant West syndrome. Early change of EEG after KD may be a predictor of a patient’s response to the therapy. -
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. -
Managing Children with Epilepsy School Nurse Guide
MANAGING CHILDREN WITH EPILEPSY SCHOOL NURSE GUIDE ACKNOWLEDGEMENTS TO THOSE WHO HAVE CONTRIBUTED TO THE NOTEBOOK Children’s Hospital of Orange County Melodie Balsbaugh, RN Sue Nagel, RN Giana Nguyen, CHOC Institutes Fullerton School District Jane Bockhacker, RN Orange Unified School District Andrea Bautista, RN Martha Boughen, RN Karen Hanson, RN TABLE OF CONTENTS I. EPILEPSY What is epilepsy? Facts about epilepsy Basic neuroanatomy overview Classification of epileptic seizures Diagnostic Tests II. TREATMENT Medications Vagus Nerve Stimulation Ketogenic Diet Surgery III. SAFETY First Aid IV. SPECIAL CONCERNS MedicAlert Helmets Driving Employment and the law V. EPILEPSY AT SCHOOL School epilepsy assessment tool Seizure record Teaching children about epilepsy lesson plan Creating your own individualized health care plan VI. RESOURCES/SUPPORT GROUPS VII. ACCESS TO HEALTHCARE CHOC Epilepsy Center After-Hours Care After Hours Health Care Advice Healthy Families California Kids MediCal CHOC Clinics Healthy Tomorrows VIII. REFERENCES EPILEPSY WHAT IS EPILEPSY? Epilepsy is a neurological disorder. The brain contains millions of nerve cells called neurons that send electrical charges to each other. A seizure occurs when there is a sudden and brief excess surge of electrical activity in the brain between nerve cells. This results in an alteration in sensation, behavior, and consciousness. Seizures may be caused by developmental problems before birth, trauma at birth, head injury, tumor, structural problems, vascular problems (i.e. stroke, abnormal blood vessels), metabolic conditions (i.e. low blood sugar, low calcium), infections (i.e. meningitis, encephalitis) and idiopathic causes. Children who have idiopathic seizures are most likely to respond to medications and outgrow seizures. -
Operational Classification of Seizure Types by the International League Against Epilepsy: Position Paper of the ILAE Commission
ILAE POSITION PAPER Operational classification of seizure types by the International League Against Epilepsy: Position Paper of the ILAE Commission for Classification and Terminology *Robert S. Fisher, †J. Helen Cross, ‡Jacqueline A. French, §Norimichi Higurashi, ¶Edouard Hirsch, #Floor E. Jansen, **Lieven Lagae, ††Solomon L. Moshe, ‡‡Jukka Peltola, §§Eliane Roulet Perez, ¶¶Ingrid E. Scheffer, and ##***Sameer M. Zuberi Epilepsia, 58(4):522–530, 2017 doi: 10.1111/epi.13670 SUMMARY The International League Against Epilepsy (ILAE) presents a revised operational clas- sification of seizure types. The purpose of such a revision is to recognize that some sei- zure types can have either a focal or generalized onset, to allow classification when the onset is unobserved, to include some missing seizure types, and to adopt more trans- parent names. Because current knowledge is insufficient to form a scientifically based classification, the 2017 Classification is operational (practical) and based on the 1981 Classification, extended in 2010. Changes include the following: (1) “partial” becomes “focal”; (2) awareness is used as a classifier of focal seizures; (3) the terms dyscognitive, simple partial, complex partial, psychic, and secondarily generalized are eliminated; Dr. Robert S. Fisher, (4) new focal seizure types include automatisms, behavior arrest, hyperkinetic, auto- past president of nomic, cognitive, and emotional; (5) atonic, clonic, epileptic spasms, myoclonic, and American Epilepsy tonic seizures can be of either focal or generalized onset; (6) focal to bilateral tonic– Society and editor of clonic seizure replaces secondarily generalized seizure; (7) new generalized seizure Epilepsia and types are absence with eyelid myoclonia, myoclonic absence, myoclonic–atonic, epilepsy.com, led the myoclonic–tonic–clonic; and (8) seizures of unknown onset may have features that can Seizure Classification still be classified. -
Evaluation of Behavior and Cognitive Function in Children with Myoclonic
& The ics ra tr pe ia u Niimi et al., Pediat Therapeut 2013, 3:3 t i d c e s P DOI: 10.4172/2161-0665.1000159 Pediatrics & Therapeutics ISSN: 2161-0665 Case Report Open Access Evaluation of Behavior and Cognitive Function in Children with Myoclonic Astatic Epilepsy Taemi Niimi1, Yuji Inaba1, Mitsuo Motobayashi1, Takafumi Nishimura1, Naoko Shiba1, Tetsuhiro Fukuyama2, Tsukasa Higuchi3, and Kenichi Koike1 1Department of Pediatrics, Shinshu University School of Medicine, Matsumoto, Japan 2Department of Pediatric Neurology, Nagano Children’s Hospital, Azumino, Japan 3Department of General Pediatrics, Nagano Children’s Hospital, Azumino, Japan Abstract Background: Myoclonic astatic epilepsy (MAE) is an idiopathic and generalized childhood epileptic syndrome. Although several studies have reported on cognitive function and intellectual outcome in MAE, little is known about the behavioral problems associated with this disease. The aim of this study was to clarify behavior and cognitive function in children with MAE. Methods: Four children who were diagnosed as having MAE using the proposed criteria of the International Classification of Epilepsies were retrospectively analyzed using patient records with regard to clinical and neuropsychological findings such as age of seizure onset, semiology and severity of seizures, treatment course, behavioral problems, EEG findings, and WISC-III and Pervasive Developmental Disorders Autism Society Japan Rating Scale (PARS) scores that indicate the tendency of autistic behaviors. Results: Disease onset in our cohort ranged from 9 to 35 months of age. Seizures were controlled within 3-8 months over a follow-up period of 4-12 years. All patients had borderline normal intelligence (mean IQ: 75.8 at 5-7 years of age) and exhibited impaired coordination, clumsiness, hyperactivity or impulsivity, and impaired social interaction after improvement of seizures. -
Understanding Seizures and Epilepsy
Understanding Sei zures & Epilepsy Selim R. Benbadis, MD Leanne Heriaud, RN Comprehensive Epilepsy Program Table of Contents * What is a seizure and what is epilepsy?....................................... 3 * Who is affected by epilepsy? ......................................................... 3 * Types of seizures ............................................................................. 3 * Types of epilepsy ............................................................................. 6 * How is epilepsy diagnosed? .......................................................... 9 * How is epilepsy treated? .............................................................. 10 Drug therapy ......................................................................... 10 How medication is prescribed ............................................ 12 Will treatment work?............................................................ 12 How long will treatment last?............................................. 12 Other treatment options....................................................... 13 * First aid for a person having a seizure ....................................... 13 * Safety and epilepsy ....................................................................... 14 * Epilepsy and driving..................................................................... 15 * Epilepsy and pregnancy ............................................................... 15 * More Information .......................................................................... 16 Comprehensive -
Juvenile Myoclonic Epilepsy: Under-Appreciated and Under-Diagnosed R Renganathan, N Delanty
78 Postgrad Med J: first published as 10.1136/pmj.79.928.78 on 1 February 2003. Downloaded from REVIEW Juvenile myoclonic epilepsy: under-appreciated and under-diagnosed R Renganathan, N Delanty ............................................................................................................................. Postgrad Med J 2003;79:78–80 Juvenile myoclonic epilepsy (JME) is a hereditary, AETIOPATHOGENESIS idiopathic, generalised epilepsy and is found in JME is an inherited disorder, but the exact mode of inheritance is not clear. There is a positive fam- 5%–11% of patients with epilepsy. It is characterised by ily history in 50% of cases or less. One study has myoclonic jerks, occasional generalised tonic-clonic confirmed a causative role of EJM1 in the patho- seizures, and sometimes absence seizures. JME genesis of idiopathic generalised seizures in the majority of German families of JME patients. This continues to be under-appreciated and study has refined a candidate region of 10.1 cM in under-diagnosed. Accurate diagnosis is important as it the chromosomal region 6p21 between the flank- usually responds well to treatment with appropriate ing loci HLA-DQ and D6s1019.3 However, some studies have revealed controversial results and anticonvulsants and misdiagnosis often results in genetic heterogeneity is suspected. Linkage to unnecessary morbidity. In addition lifelong therapy is chromosome 15 has at most a minor role in usually indicated as the natural history is one of relapse JME.4 Few studies have focused on pathological find- -
Idiopathic Intracranial Hypertension: Consensus Guidelines On
General Neurology J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp-2017-317440 on 14 June 2018. Downloaded from REVIEW Idiopathic intracranial hypertension: consensus guidelines on management Susan P Mollan,1,2 Brendan Davies,3 Nick C Silver,4 Simon Shaw,5 Conor L Mallucci,6,7 Benjamin R Wakerley,8,9 Anita Krishnan,4 Swarupsinh V Chavda,10 Satheesh Ramalingam,10 Julie Edwards,11,12 Krystal Hemmings,13 Michelle Williamson,13 Michael A Burdon,2 Ghaniah Hassan-Smith,1,12 Kathleen Digre,14 Grant T Liu,15 Rigmor Højland Jensen,16 Alexandra J Sinclair1,2,12,17 ► Additional material is ABSTRact contains information that will be of interest to those published online only. To view The aim was to capture interdisciplinary expertise from a in primary care and other healthcare professionals. please visit the journal online large group of clinicians, reflecting practice from across The increasing economic burden of IIH has been (http:// dx. doi. org/ 10. 1136/ 1 2 jnnp- 2017- 317440). the UK and further, to inform subsequent development of highlighted by a number of groups. Clear guid- a national consensus guidance for optimal management ance will help educate the attending doctors to For numbered affiliations see of idiopathic intracranial hypertension (IIH). manage these patients appropriately. This will help end of article. Methods Between September 2015 and October reduce the repeat unsolicited emergency hospital 2017, a specialist interest group including neurology, attendances and reduce IIH-related disability. Correspondence to There are a number of ongoing clinical trials in IIH Dr Alexandra J Sinclair, neurosurgery, neuroradiology, ophthalmology, nursing, Metabolic Neurology, Institute primary care doctors and patient representatives (https://www. -
Occipital and Parietal Lobe Epilepsies
Chapter 15 Occipital and parietal lobe epilepsies JOHN S. DUNCAN UCL Institute of Neurology, National Hospital for Neurology and Neurosurgery, Queen Square, London Epileptic seizures of parietal and occipital origin are heterogeneous and mainly characterised by the presenting auras, although the most dramatic clinical manifestations may reflect spread, and overshadow the focal origin. The two lobes serve mainly sensory functions, and the characteristic seizure phenomena are therefore subjective sensations. The incidence of these seizures is not well known, but they are generally considered rare. Occipital seizures have been reported to constitute 8% and parietal seizures 1.4% of total seizures in the prevalent population with epilepsy1,2. The pattern of seizures is most commonly focal seizures without impairment of awareness, with occasional secondary generalisation. Focal seizures with impairment of awareness are rare and usually indicate spread of the seizure into the temporal lobe. Seizures with somatosensory symptomatology1-3 Somatosensory seizures may arise from any of the three sensory areas of the parietal lobe, but the post-central gyrus is most commonly involved. Seizures present with contralateral, or rarely ipsilateral, or bilateral sensations. All sensory modalities may be represented, most commonly tingling and numbness, alone or together. There may be prickling, tickling or crawling sensations, or a feeling of electric shock in the affected body part. The arms and the face are the most common sites, but any segment or region may be affected. The paraesthesia may spread in a Jacksonian manner, and when this occurs motor activity in the affected body member follows the sensations in about 50% of cases. -
European Headache Federation Guideline on Idiopathic Intracranial
Hoffmann et al. The Journal of Headache and Pain (2018) 19:93 The Journal of Headache https://doi.org/10.1186/s10194-018-0919-2 and Pain CONSENSUSARTICLE Open Access European Headache Federation guideline on idiopathic intracranial hypertension Jan Hoffmann1* , Susan P Mollan2, Koen Paemeleire3, Christian Lampl4, Rigmor H Jensen5 and Alexandra J Sinclair6 Abstract Background: Idiopathic Intracranial Hypertension (IIH) is characterized by an elevation of intracranial pressure (ICP no identifiable cause. The aetiology remains largely unknown, however observations made in a number of recent clinical studies are increasing the understanding of the disease and now provide the basis for evidence-based treatment strategies. Methods: The Embase, CDSR, CENTRAL, DARE and MEDLINE databases were searched up to 1st June 2018. We analyzed randomized controlled trials and systematic reviews that investigate IIH. Results: Diagnostic uncertainty, headache morbidity and visual loss are among the highest concerns of clinicians and patients in this disease area. Research in this field is infrequent due to the rarity of the disease and the lack of understanding of the underlying pathology. Conclusions: This European Headache Federation consensus paper provides evidence-based recommendations and practical advice on the investigation and management of IIH. Objective Headache Society (IHS) [3] (Table 1). The term ‘pseudo- Idiopathic Intracranial Hypertension (IIH) is character- tumor cerebri’, in the past commonly used as a synonym ized by an elevation of intracranial pressure (ICP) with for IIH, is now used as an umbrella term that describes no identifiable cause [1]. Despite the fact that its aeti- the chronic elevation of ICP regardless of its aetiology ology remains largely unknown, the observations made and further subdivides in the primary (IIH) and second- in a significant number of recent clinical studies and the ary forms [2]. -
Epileptic Seizures in Neurodegenerative Dementia Syndromes
2010 iMedPub Journals JOURNAL OF NEUROLOGY AND NEUROSCIENCE Vol.1 No. 1:3 doi: 10:3823/302 Epileptic seizures in neurodegenerative dementia syndromes AJ Larner Consultant Neurologist. Cognitive Function Clinic, Walton Centre for Neurology and Neurosurgery, Liverpool, United Kingdom Correspondence: AJ Larner, Cognitive Function Clinic, Walton Centre for Neurology and Neurosurgery, Lower Lane, Fazakerley, Liverpool, UK Tel: (44) 151 529 5727 FAX: (44) 151 529 8552 e-mail: [email protected] Summary Epileptic seizures may be a feature of some neurodegenerative dementia syndromes. There is an increased incidence of seizures in Alzheimer’s disease compared to age-matched controls. Seizures also occur in prion disorders and some frontotemporal lobar degenera- tion syndromes, whereas parkinsonian dementia disorders seem relatively seizure free. Seizure pathogenesis in these conditions is uncer- tain, but may relate to neocortical and hippocampal hyperexcitability and synchronised activity, possibly as a consequence of dysfunctio- nal protein metabolism, neuronal structural changes, and concurrent cerebrovascular disease. Alzheimer’s disease may be a neuronal network disorder, characterised by both cognitive decline and epileptic activity, in which seizures are an integral part of disease phenotype rather than epiphenomena. Treatment of seizures in dementia syndromes currently remains empirical. Greater understanding of demen- tia pathogenesis may shed light on mechanisms of epileptogenesis and facilitate more rational approaches