Migraine and Stroke
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Pathophysiology of Migraine
PathophysiologyPathophysiology ofof MigraineMigraine 1 MIGRAINEMIGRAINE PATHOPHYSIOLOGY:PATHOPHYSIOLOGY: AA NEUROVASCULARNEUROVASCULAR HEADACHEHEADACHE Objectives Review the neurobiology of migraine - Features of acute attack - neuroanatomical substrates Discuss the current understanding of migraine, vulnerability, initiation and activation of the trigeminocervical pain system Describe the modulation of head pain in the CNS 2 WHATWHAT ISIS MIGRAINE?MIGRAINE? Neurobiologically based, common clinical syndrome characterized by recurrent episodic attacks of head pain which serve no protective purpose The headache is accompanied by associated symptoms such as nausea, sensitivity to light, sound, or head movement The vulnerability to migraine if for many, an inherited tendency Migraine is a complex neurobiological disorder that has been recognized since antiquity. Many current books cover the subject in great detail. The core features of migraine are headache, which is usually throbbing and often unilateral, and associated features of nausea, sensitivity to light, sound, and exacerbation with head movement. Migraine has long been regarded as a vascular disorder because of the throbbing nature of the pain. However, as we shall explore here, vascular changes do not provide sufficient explanation of the pathophysiology of migraine. Up to one-third of patients do not have throbbing pain. Modern imaging has demonstrated that vascular changes are not linked to pain and diameter changes are not linked with treatment. This presentation aims to demonstrate that: • Migraine should be regarded as neurovascular headache. • Understanding the anatomy and physiology of migraine can enrich clinical practice. Lance JW, Goadsby PJ. Mechanism and Management of Headache. London, England: Butterworth-Heinemann; 1998. Silberstein SD, Lipton RB, Goadsby PJ. Headache in Clinical Practice. 2nd ed. -
Prolonged Hemiplegic Migraine Associated with Irreversible Neurological Defcit and Cortical Laminar Necrosis in a Patient with Patent Foramen Ovale :A Case Report
Prolonged Hemiplegic Migraine Associated with Irreversible Neurological Decit and Cortical Laminar Necrosis in a Patient with Patent Foramen Ovale A case report Yacen Hu Xiangya Hospital Central South University https://orcid.org/0000-0002-1199-4659 Zhiqin Wang Xiangya Hospital Central South University Lin Zhou Xiangya Hospital Central South University Qiying Sun ( [email protected] ) Xiangya Hospital, Central South University https://orcid.org/0000-0002-2031-8345 Case report Keywords: Hemiplegic migraine, irreversible neurological decit, cortical laminar necrosis, patent foramen ovale, case report Posted Date: April 30th, 2021 DOI: https://doi.org/10.21203/rs.3.rs-439782/v1 License: This work is licensed under a Creative Commons Attribution 4.0 International License. Read Full License Page 1/7 Abstract Background: Aura symptoms of hemiplegic migraine (HM) usually resolve completely, permanent attack-related decit and radiographic change are rare. Case presentation: We reported a HM case presented with progressively aggravated hemiplegic migraine episodes refractory to medication. He experienced two prolonged hemiplegic migraine attacks that led to irreversible visual impairment and cortical laminar necrosis (CLN) on brain MRI. Patent foramen ovale (PFO) was found on the patient. PFO closure resulted in a signicant reduction of HM attacks. Conclusions: Prolonged hemiplegic migraine attack could result in irreversible neurological decit with neuroimaging changes manifested as CLN. We recommend screening for PFO in patients with prolonged or intractable hemiplegic migraine, for that closure of PFO might alleviate the attacks thus preventing patient from disabling sequelae. Background Hemiplegic migraine (HM) is characterized by aura of motor weakness accompanied by visual, sensory, and/or speech symptoms followed by migraine headache[1]. -
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. -
Fullness, and Tinni- Tus
Neurology® Clinical Practice The evaluation of a patient with dizziness Kevin A. Kerber, MD Robert W. Baloh, MD Summary Dizziness is the quintessential symptom presenta- tion in all of clinical medicine. It can stem from a disturbance in nearly any system of the body. Pa- tient descriptions of the symptom are often vague and inconsistent, so careful probing is essential. The physical examination is performed by observ- ing the patient at rest and following simple move- ments or bedside tests. In general, no special tools are required. The causes of dizziness range from benign to life-threatening disorders, and features that distinguish among these may be subtle. When diagnostic testing is considered, parsimony should be the rule. Identifying common peripheral vestibu- lar disorders is a priority. Picking this “low hanging fruit” can be the key component to excluding more serious central causes of dizziness. eurologists play an important role in the evaluation and management of pa- tients with dizziness. The possibility of a serious neurologic disorder is un- Nnerving to front-line physicians who have ranked decision support for identifying central causes of vertigo as a top priority.1 Although dangerous cen- tral disorders do not commonly present as isolated dizziness, stroke and other neurologic disorders can occur in this manner. The history and physical examination are the critical elements in determining the management of these patients. In this article, we review the approach to the evaluation and management of patients with dizziness. History The first step in assessing a patient presenting with dizziness is to define the symptom (table 1). -
Vertebral Artery Dissection Presenting As Transient Global Amnesia: a Case Report and Review of Literature
Dementia and Neurocognitive Disorders 2014; 13: 46-49 CASE REPORT http://dx.doi.org/10.12779/dnd.2014.13.2.46 Vertebral Artery Dissection Presenting as Transient Global Amnesia: A Case Report and Review of Literature , Yeonsil Moon*, Seol-Heui Han* † Vertebral artery dissection is one of the most common causes of stroke in young adults. The course of the vertebral artery dissection is usually benign, and pure transient amnesia as an initial symptom has Department of Neurology*, Konkuk University Medical Center, Seoul; Center for Geriatric been rarely reported. We describe a patient with vertebral artery dissection who presented with acute Neuroscience Research, Institute of transient amnesia, and review the medical literatures about the pathophysiological mechanism of tran- Biomedical Science†, Konkuk University, sient global amenesia (TGA). This case could be a one of evidence which supports the cerebrovascular Seoul, Korea mechanism of TGA. Received: May 19, 2014 Revision received: June 26, 2014 Accepted: June 26, 2014 Address for correspondence Seol-Heui Han, M.D. Department of Neurology, Konkuk University School of Medicine, 120-1 Neungdong-ro, Gwangjin-gu, Seoul 143-729, Korea Tel: +82-2-2030-7561 Fax: +82-2-2030-7469 E-mail: [email protected] Key Words: Transient global amnesia, Vertebral artery dissection, Cerebrovascular Vertebral artery dissection is one of the most common longed cognitive decline and review the medical literatures causes of stroke in young adults [1]. The course of the verte- about the pathophysiological mechanism of transient global bral artery dissection is usually benign, but seldom reaches to amenesia (TGA). severe complication, such as brainstem infarction, subarach- noid hemorrhage (SAH) or death [2]. -
SOS – Save Our Shoulders: a Guide for Polio Survivors
1 • Save Our Shoulders: A Guide for Polio Survivors A Guide for Polio Survivors S.O.S. Save Our Shoulders: A Guide for Polio Survivors by Jennifer Kuehl, MPT Roberta Costello, MSN, RN Janet Wechsler, PT Funding for the production of this manual was made possible by: The National Institute for Disability and Rehabilitation Research Grant #H133A000101 and The U.S. Department of the Army Grant #DAMD17-00-1-0533 Investigators: Mary Klein, PhD Mary Ann Keenan, MD Alberto Esquenazi, MD Acknowledgements We gratefully acknowledge the contributions and input provided from all of those who participated in our research. The time and effort of our participants was instrumental in the creation of this manual. Jennifer Kuehl, MPT Moss Rehabilitation Research Institute, Philadelphia Roberta Costello, MSN, RN Moss Rehabilitation Research Institute, Philadelphia Janet Wechsler, PT Moss Rehabilitation Research Institute, Philadelphia Mary Klein, PhD Moss Rehabilitation Research Institute, Philadelphia Mary Ann Keenan, MD University of Pennsylvania, Philadelphia Alberto Esquenazi, MD MossRehab Hospital, Philadelphia Cover and manual design by Ron Kalstein, MEd Albert Einstein Medical Center, Philadelphia Table of Contents 1. Introduction . .5 2. General Information About the Shoulder . .6 3. Facts About Shoulder Problems . .8 4. Treatment Options . .13 5. About Exercise . .16 6. Stretching Exercises . .19 7. Cane Stretches . .22 8. Strengthening Exercises . .25 9. Tips to Avoid Shoulder Problems . .29 10. Conclusion . .31 11. Resources . .31 The information contained within this manual is for reference only and is not a substitute for professional medical advice. Before beginning any exercise program consult your physician. Save Our Shoulders: A Guide for Polio Survivors • 4 Introduction Many polio survivors report new symptoms as they age. -
Second Edition
COVID-19 Evidence Update COVID-19 Update from SAHMRI, Health Translation SA and the Commission on Excellence and Innovation in Health Updated 4 May 2020 – 2nd Edition “What is the prevalence, positive predictive value, negative predictive value, sensitivity and specificity of anosmia in the diagnosis of COVID-19?” Executive Summary There is widespread reporting of a potential link between anosmia (loss of smell) and ageusia (loss of taste) and SARS-COV-2 infection, as an early sign and with sudden onset predominantly without nasal obstruction. There are calls for anosmia and ageusia to be recognised as symptoms for COVID-19. Since the 1st edition of this briefing (25 March 2020), there has been a significant expansion of literature on this topic, including 3 systematic reviews. Predictive value: The reported prevalence of anosmia/hyposmia and ageusia/hypogeusia in SARS-COV-2 positive patients are in the order of 36-68% and 33-71% respectively. There are reports of anosmia as the first symptom in some patients. Estimates from one study for hyposmia and hypogeusia: • Positive likelihood ratios: 4.5 and 5.8 • Sensitivity: 46% and 62% • Specificity: 90% and 89% The US Centres for Disease Control and Prevention (CDC) has added new loss or taste or smell to its list of recognised symptoms for SARS-COV-2 infection. To date, the World Health Organization has not. Conclusion: There is sufficient evidence to warrant adding loss of taste and smell to the list of symptoms for COVID-19 and promoting this information to the public. Context • Early detection of COVID-19 is key to the ongoing management of the pandemic. -
COVID-19 Vaccines: Update on Allergic Reactions, Contraindications, and Precautions
Centers for Disease Control and Prevention Center for Preparedness and Response COVID-19 Vaccines: Update on Allergic Reactions, Contraindications, and Precautions Clinician Outreach and Communication Activity (COCA) Webinar Wednesday, December 30, 2020 Continuing Education Continuing education will not be offered for this COCA Call. To Ask a Question ▪ All participants joining us today are in listen-only mode. ▪ Using the Webinar System – Click the “Q&A” button. – Type your question in the “Q&A” box. – Submit your question. ▪ The video recording of this COCA Call will be posted at https://emergency.cdc.gov/coca/calls/2020/callinfo_123020.asp and available to view on-demand a few hours after the call ends. ▪ If you are a patient, please refer your questions to your healthcare provider. ▪ For media questions, please contact CDC Media Relations at 404-639-3286, or send an email to [email protected]. Centers for Disease Control and Prevention Center for Preparedness and Response Today’s First Presenter Tom Shimabukuro, MD, MPH, MBA CAPT, U.S. Public Health Service Vaccine Safety Team Lead COVID-19 Response Centers for Disease Control and Prevention Centers for Disease Control and Prevention Center for Preparedness and Response Today’s Second Presenter Sarah Mbaeyi, MD, MPH CDR, U.S. Public Health Service Clinical Guidelines Team COVID-19 Response Centers for Disease Control and Prevention National Center for Immunization & Respiratory Diseases Anaphylaxis following mRNA COVID-19 vaccination Tom Shimabukuro, MD, MPH, MBA CDC COVID-19 Vaccine -
Damages for Pain and Suffering
DAMAGES FOR PAIN AND SUFFERING MARCUS L. PLANT* THE SHAPE OF THE LAw GENERALLY It does not require any lengthy exposition to set forth the basic principles relating to the recovery of damages for pain and suffering in personal injury actions in tort. Such damages are a recognized element of the successful plaintiff's award.1 The pain and suffering for which recovery may be had includes that incidental to the injury itself and also 2 such as may be attributable to subsequent surgical or medical treatment. It is not essential that plaintiff specifically allege that he endured pain and suffering as a result of the injuries specified in the pleading, if his injuries stated are of such nature that pain and suffering would normally be a consequence of them.' It would be a rare case, however, in which plaintiff's counsel failed to allege pain and suffering and claim damages therefor. Difficult pleading problems do not seem to be involved. The recovery for pain and suffering is a peculiarly personal element of plaintiff's damages. For this reason it was held in the older cases, in which the husband recovered much of the damages for injury to his wife, that the injured married woman could recover for her own pain and suffering.4 Similarly a minor is permitted to recover for his pain 5 and suffering. No particular amount of pain and suffering or term of duration is required as a basis for recovery. It is only necessary that the sufferer be conscious.6 Accordingly, recovery for pain and suffering is not usually permitted in cases involving instantaneous death." Aside from this, how- ever,. -
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. -
Fatigue After Stroke
SPECIAL REPORT Fatigue after stroke PJ Tyrrell Fatigue is a common symptom after stroke. It is not invariably related to stroke severity & DG Smithard† and can occur in the absence of depression. It is one of the most troublesome symptoms for †Author for correspondence many patients and yet nothing is known of its causation. There are no specific treatments. William Harvey Hospital, Richard Steven’s Ward, This article assesses the available literature in the context of what is known about fatigue Ashford, Kent, in other disorders. Post-stroke fatigue may be a manifestation of sickness behavior, TN24 0LZ, UK mediated through the central effects of the cytokine interleukin-1, perhaps via effects on Tel.: +44 123 361 6214 Fax: +44 123 361 6662 glutamate neurotransmission. Possible therapeutic strategies are discussed which might be [email protected] a logical basis from which to plan randomized control trials. Following stroke, approximately a third of common and disabling symptom of Parkinson’s patients die, a third recover and a third remain disease [7,8] and of systemic lupus [9]. More than significantly disabled. Even those who recover 90% of patients with poliomyelitis develop a physically may be left with significant emotional delayed syndrome of post-myelitis fatigue [10]. and psychologic dysfunction – including anxi- Fatigue is the most prevalent symptom of ety, readjustment reactions and depression. One patients with cancer who receive radiation, cyto- common but often overlooked symptom is toxic or other therapies [11], and it may persist fatigue. This may occur soon or late after stroke, for years after the cessation of treatment [12]. -
Common Myths About the Joint Commission Pain Standards
T H S Y M Common myths about The Joint Commission pain standards Myth No. 1: The Joint Commission endorses pain as a vital sign. The Joint Commission never endorsed pain as a vital sign. Joint Commission standards never stated that pain needs to be treated like a vital sign. The roots of this misconception go back to 1990 (more than a decade before Joint Commission pain standards were released), when pain experts called for pain to be “made visible.” Some organizations tried to achieve this by making pain a vital sign. The only time the standards referenced the fifth vital sign was when examples were provided of how some organizations were assessing patient pain. In 2002, The Joint Commission addressed the problems of the fifth vital sign concept by describing the unintended consequences of this approach to pain management, and described how organizations subsequently modified their processes. Myth No. 2: The Joint Commission requires pain assessment for all patients. The original pain standards, which were applicable to all accreditation programs, stated “Pain is assessed in all patients.” This requirement was eliminated in 2009 from all programs except Behavioral Health Care. It was The Joint Commission thought that these patients were less able to bring up the fact that they were in pain and, therefore, required a more pain standards aggressive approach. The current Behavioral Health Care standard states, “The organization screens all patients • The hospital educates for physical pain.” The current standard for the hospital and other programs states, “The organization assesses and all licensed independent practitioners on assessing manages the patient’s pain.” This allows organizations to set their own policies regarding which patients should and managing pain.