Alcohol Related Brain Impairment
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Approach to Acute Ataxia in Childhood: Diagnosis and Evaluation Lalitha Sivaswamy, MD
FEATURE Approach to Acute Ataxia in Childhood: Diagnosis and Evaluation Lalitha Sivaswamy, MD opsoclonus myoclonus ataxia syndrome, must receive special mention because the underlying disease process may be ame- nable to surgical intervention. In the tod- dler- and school-age groups, certain condi- tions (such as stroke and acute cerebellitis) require immediate recognition and imag- ing, whereas others (such as post-infec- tious ataxia and concussion) require close follow-up. Finally, mention must be made of diseases outside of the central nervous system that can present with ataxia, such as Guillain-Barré syndrome. he word ataxia is derived from the Greek word ataktos, which T means “lack of order.” Ataxia is characterized by disturbances in the voluntary coordination of posture and movement. In children, it is most prominent during walking (the sine qua non being a staggering gait with impaired tandem), but it can also be present during sitting or standing, or © Shutterstock when the child is performing move- Abstract Lalitha Sivaswamy, MD, is Associate Profes- ments of the arms, legs, or eyes. sor of Pediatrics and Neurology, Department Ataxia refers to motor incoordination that is This review focuses on the etiol- of Neurology, Wayne State University School of usually most prominent during movement ogy and diagnostic considerations for Medicine; and Medical Director, Headache Clinic, or when a child is attempting to maintain a acute ataxia, which for the purposes of Children’s Hospital of Michigan. sitting posture. The first part of the review this discussion refers to ataxia with a Address correspondence to: Lalitha Sivas- focuses on the anatomic localization of symptom evolution time of less than wamy, MD, Department of Neurology, Wayne ataxia — both within the nervous system 72 hours.1 State University School of Medicine, Children’s and without — using a combination of his- Motor coordination requires sensory Hospital of Michigan, 3901 Beaubien, Detroit, MI torical features and physical findings. -
Scientific Opinion
SCIENTIFIC OPINION ADOPTED: DD Month YEAR doi:10.2903/j.efsa.20YY.NNNN 1 Evaluation of the health risks related to the 2 presence of cyanogenic glycosides in foods other than raw 3 apricot kernels 4 5 EFSA Panel on Contaminants in the Food Chain (CONTAM), 6 Margherita Bignami, Laurent Bodin, James Kevin Chipman, Jesús del Mazo, Bettina Grasl- 7 Kraupp, Christer Hogstrand, Laurentius (Ron) Hoogenboom, Jean-Charles Leblanc, Carlo 8 Stefano Nebbia, Elsa Nielsen, Evangelia Ntzani, Annette Petersen, Salomon Sand, Dieter 9 Schrenk, Christiane Vleminckx, Heather Wallace, Diane Benford, Leon Brimer, Francesca 10 Romana Mancini, Manfred Metzler, Barbara Viviani, Andrea Altieri, Davide Arcella, Hans 11 Steinkellner and Tanja Schwerdtle 12 Abstract 13 In 2016, the EFSA CONTAM Panel published a scientific opinion on the acute health risks related to 14 the presence of cyanogenic glycosides (CNGs) in raw apricot kernels in which an acute reference dose 15 (ARfD) of 20 µg/kg bw was established for cyanide (CN). In the present opinion, the CONTAM Panel 16 concluded that this ARfD is applicable for acute effects of CN regardless the dietary source. Estimated 17 mean acute dietary exposures to cyanide from foods containing CNGs did not exceed the ARfD in any 18 age group. At the 95th percentile, the ARfD was exceeded up to about 2.5-fold in some surveys for 19 children and adolescent age groups. The main contributors to exposures were biscuits, juice or nectar 20 and pastries and cakes that could potentially contain CNGs. Taking into account the conservatism in 21 the exposure assessment and in derivation of the ARfD, it is unlikely that this estimated exceedance 22 would result in adverse effects. -
Alcohol Sensitivity As an Endophenotype of Alcohol Use Disorder: Exploring Its Translational Utility Between Rodents and Humans
brain sciences Review Alcohol Sensitivity as an Endophenotype of Alcohol Use Disorder: Exploring Its Translational Utility between Rodents and Humans Clarissa C. Parker 1,*, Ryan Lusk 2 and Laura M. Saba 2,* 1 Department of Psychology and Program in Neuroscience, Middlebury College, Middlebury, VT 05753, USA 2 Department of Pharmaceutical Sciences, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA; [email protected] * Correspondence: [email protected] (C.C.P.); [email protected] (L.M.S.) Received: 3 September 2020; Accepted: 9 October 2020; Published: 13 October 2020 Abstract: Alcohol use disorder (AUD) is a complex, chronic, relapsing disorder with multiple interacting genetic and environmental influences. Numerous studies have verified the influence of genetics on AUD, yet the underlying biological pathways remain unknown. One strategy to interrogate complex diseases is the use of endophenotypes, which deconstruct current diagnostic categories into component traits that may be more amenable to genetic research. In this review, we explore how an endophenotype such as sensitivity to alcohol can be used in conjunction with rodent models to provide mechanistic insights into AUD. We evaluate three alcohol sensitivity endophenotypes (stimulation, intoxication, and aversion) for their translatability across human and rodent research by examining the underlying neurobiology and its relationship to consumption and AUD. We show examples in which results gleaned from rodents are successfully integrated with information from human studies to gain insight in the genetic underpinnings of AUD and AUD-related endophenotypes. Finally, we identify areas for future translational research that could greatly expand our knowledge of the biological and molecular aspects of the transition to AUD with the broad hope of finding better ways to treat this devastating disorder. -
Mechanisms of Ethanol-Induced Cerebellar Ataxia: Underpinnings of Neuronal Death in the Cerebellum
International Journal of Environmental Research and Public Health Review Mechanisms of Ethanol-Induced Cerebellar Ataxia: Underpinnings of Neuronal Death in the Cerebellum Hiroshi Mitoma 1,* , Mario Manto 2,3 and Aasef G. Shaikh 4 1 Medical Education Promotion Center, Tokyo Medical University, Tokyo 160-0023, Japan 2 Unité des Ataxies Cérébelleuses, Service de Neurologie, CHU-Charleroi, 6000 Charleroi, Belgium; [email protected] 3 Service des Neurosciences, University of Mons, 7000 Mons, Belgium 4 Louis Stokes Cleveland VA Medical Center, University Hospitals Cleveland Medical Center, Cleveland, OH 44022, USA; [email protected] * Correspondence: [email protected] Abstract: Ethanol consumption remains a major concern at a world scale in terms of transient or irreversible neurological consequences, with motor, cognitive, or social consequences. Cerebellum is particularly vulnerable to ethanol, both during development and at the adult stage. In adults, chronic alcoholism elicits, in particular, cerebellar vermis atrophy, the anterior lobe of the cerebellum being highly vulnerable. Alcohol-dependent patients develop gait ataxia and lower limb postural tremor. Prenatal exposure to ethanol causes fetal alcohol spectrum disorder (FASD), characterized by permanent congenital disabilities in both motor and cognitive domains, including deficits in general intelligence, attention, executive function, language, memory, visual perception, and commu- nication/social skills. Children with FASD show volume deficits in the anterior lobules related to sensorimotor functions (Lobules I, II, IV, V, and VI), and lobules related to cognitive functions (Crus II and Lobule VIIB). Various mechanisms underlie ethanol-induced cell death, with oxidative stress and Citation: Mitoma, H.; Manto, M.; Shaikh, A.G. Mechanisms of endoplasmic reticulum (ER) stress being the main pro-apoptotic mechanisms in alcohol abuse and Ethanol-Induced Cerebellar Ataxia: FASD. -
Binge Drinking and the Risk of Liver Events: a Population-Based Cohort Study
Received: 10 January 2017 | Accepted: 26 February 2017 DOI: 10.1111/liv.13408 GENETIC AND METABOLIC LIVER DISEASE Binge drinking and the risk of liver events: A population- based cohort study Fredrik Åberg1 | Jaana Helenius-Hietala2 | Pauli Puukka3 | Antti Jula3 1Transplantation and Liver Surgery Clinic, Helsinki University Hospital, Helsinki Abstract University, Helsinki, Finland Background & Aims: Binge drinking or heavy episodic drinking is increasingly preva- 2 Department of Oral and Maxillofacial lent, but the health effects are incompletely understood. We investigated whether Diseases, Helsinki University Hospital, Helsinki University, Helsinki, Finland binge drinking increases the risk for liver disease above and beyond the risk due to 3Department of Health, National Institute for average alcohol consumption. Health and Welfare, Turku, Finland Methods: 6366 subjects without baseline liver disease who participated in the Finnish Correspondence population- based Health 2000 Study (2000- 2001), a nationally representative cohort. Fredrik Åberg, MD, PhD, Transplantation Follow- up data from national registers until 2013 were analysed for liver- related ad- and Liver Surgery Clinic, Helsinki University Hospital, Helsinki University, Helsinki, Finland. missions, mortality and liver cancer. Binge drinking (≥5 drinks per occasion, standard Email: [email protected] drink 12 g ethanol) was categorised as weekly, monthly, or as less often or none. Funding information Multiple confounders were considered. FÅ received research grants from Wilhelm and Else Stockmanns Foundation, Liv och Hälsa, Results: Eighty- four subjects developed decompensated liver disease. Binge drinking and Finska Läkaresällskapet. frequency showed a direct association with liver- disease risk after adjustment for aver- Handling Editor: Helena Cortez-Pinto age daily alcohol intake and age. -
Management of Alcohol Use Disorders: a Pocket Reference for Primary Care Providers
Management of alcohol use disorders: A pocket reference for primary care providers Meldon Kahan, MD Edited by Kate Hardy, MSW and Sarah Clarke, PhD Acknowledgments Mentoring, Education, and Clinical Tools for Addiction: Primary Care–Hospital Integration (META:PHI) is an ongoing initiative to improve the experience of addiction care for both patients and providers. The purpose of this initiative is to set up and implement care pathways for addiction, foster mentoring relationships between addiction physicians and other health care providers, and create and disseminate educational materials for addiction care. This pocket guide is excerpted from Safe prescribing practices for addictive medications and management of substance use disorders in primary care: A pocket reference for primary care providers, a quick-reference tool for primary care providers to assist them in implementing best practices for prescribing potentially addictive medications and managing substance use disorders in primary care, endorsed by the College of Family Physicians of Canada. This excerpt is a guide to talking to patients about their alcohol use and managing at-risk drinking and alcohol use disorders. We thank those who have given feedback on this document: Dr. Mark Ben-Aron, Dr. Peter Butt, Dr. Delmar Donald, Dr. Mike Franklyn, Dr. Melissa Holowaty, Dr. Anita Srivastava, and three anonymous CFPC reviewers. We gratefully acknowledge funding and support from the following organizations: Adopting Research to Improve Care (Health Quality Ontario & Council of Academic Hospitals of Ontario) The College of Family Physicians of Canada Toronto Central Local Health Integration Network Women’s College Hospital Version date: December 19, 2017 © 2017 Women’s College Hospital All rights reserved. -
Ataxia Digest
Ataxia Digest 2015 Vol. 2 News from the Johns Hopkins Ataxia Center 2016 What is Ataxia? Ataxia is typically defined as the presence of Regardless of the type of ataxia a person may have, it abnormal, uncoordinated movements. This term is is important for all individuals with ataxia to seek proper most often, but not always, used to describe a medical attention. For the vast majority of ataxias, a neurological symptom caused by dysfunction of the treatment or cure for the disease is not yet available, so cerebellum. The cerebellum is responsible for many the focus is on identifying symptoms related to or motor functions, including the coordination of caused by the ataxia. By identifying the symptoms of voluntary movements and the maintenance of balance ataxia it becomes possible to treat those symptoms and posture. through medication, physical therapy, exercise, other therapies and sometimes medications. Those with cerebellar ataxia often have an “ataxic” gait, which is walking The Johns Hopkins Ataxia Center has a that appears unsteady, uncoordinated multidisciplinary clinical team that is dedicated to and staggered. Other activities that helping those affected by ataxia. The center has trained require fine motor control like writing, specialist ranging from neurologists, nurses, reading, picking up objects, speaking rehabilitation specialists, genetic counselors, and many clearly and swallowing may be others. This edition of the Ataxia Digest will provide abnormal. Symptoms vary depending you with information on living with ataxia and the on the cause of the ataxia and are multidisciplinary center at Johns Hopkins. specific to each person. Letter from the Director Welcome to the second edition of the Ataxia Digest. -
Medication Use and Driving Risks by Tammie Lee Demler, BS Pharm, Pharmd
CONTINUING EDUCATION Medication Use and Driving Risks by Tammie Lee Demler, BS Pharm, PharmD pon successful completion of this ar- the influence of alcohol has Useful Websites ticle, pharmacists should be able to: long been accepted as one 1. Identify the key functional ele- of the most important causes ■ www.dot.gov/ or http://www.dot.gov/ ments that are required to ensure of traffic accidents and driv- odapc/ competent, safe driving. ing fatalities. Driving under Website of the U.S. Department of 2. Identify the side effects associated with pre- the influence of alcohol has Transportation, which contains trends Uscription, over-the-counter and herbal medi- been studied not only in ex- and law updates. It also contains an cations that can pose risks to drivers. perimental research, but also excellent search engine. 3. Describe the potential impact of certain medi- in epidemiological road side ■ www.mayoclinic.com/health/herbal- cation classes on driving competence. studies. The effort that society supplements/SA00044 4. Describe the pharmacist’s duty to warn re- has made to take serious le- Website for the Mayo Clinic, with garding medications that have the potential to gal action against those who information about herbal supplements. impair a patient’s driving competence. choose to drink and drive It offers an expert blog for further exploration about specific therapies and 5. Provide counseling points to support safe driv- has resulted in the significant to receive/share insight about personal ing in all patients who are receiving medication. deterrents of negative social driving impairment with herbal drugs. stigma and incarceration. -
The Dentate Nucleus in Friedreich's Ataxia
Gen_0701:Gen_0701.qxd 07 04 17 4:27 PM Page 1 Ge neratio ns The Official Publication of the National Ataxia Foundation Volume 35, Number 1 Spring 2007 The Dentate Nucleus in F riedre ich’ s Ataxia By Arnulf H. Koeppen, MD Research and Neurology Services, V. A. Medical Center, Albany, NY 12208 Friedreich’s ataxia (F RDA) affects several the small power packs that provide energy to organs, including heart, insulin-producing cells the cell in the form of adenosine triphosphate, of the pancreas, bones, peripheral nerves, spinal and the work by Dr. Lamarche and his collabo - cord, ganglia of the dorsal spinal roots, and a rators in Sherbrooke received renewed atten - specific area of the brain called the dentate tion. Indeed, the disease of the heart in FRDA nucleus. can be attributed, in some measure, to iron in Since the first description of this autosomal mitochondria. recessive ataxia by Nicholaus Friedreich in the At this time, there is no evidence that a simi - 19th century, most neurologists have consid - lar accumulation of iron occurs in the spinal ered FRDA a disease of the spinal cord. cord or its dorsal root ganglia. The normal Friedreich was aware of heart disease in his dentate nucleus of the cerebellum ( f ig. 1 on patients but thought that it was due to high page 2) contains abundant iron, possibly typhoid-like fever. making it especially vulnerable to frataxin In 1980, Dr. Jacques B. Lamarche and associ - deficiency in FRDA. The dentate nucleus is ates in Sherbrooke, Québec, Canada, discov - the main way-station for impulses leaving the ered minute iron-rich granules in heart muscle cerebellum. -
Alcohol Withdrawal
Alcohol withdrawal TERMINOLOGY CLINICAL CLARIFICATION • Alcohol withdrawal may occur after cessation or reduction of heavy and prolonged alcohol use; manifestations are characterized by autonomic hyperactivity and central nervous system excitation 1, 2 • Severe symptom manifestations (eg, seizures, delirium tremens) may develop in up to 5% of patients 3 CLASSIFICATION • Based on severity ○ Minor alcohol withdrawal syndrome 4, 5 – Manifestations occur early, within the first 48 hours after last drink or decrease in consumption 6 □ Manifestations develop about 6 hours after last drink or decrease in consumption and usually peak about 24 to 36 hours; resolution occurs in 2 to 7 days 7 if withdrawal does not progress to major alcohol withdrawal syndrome 4 – Characterized by mild autonomic hyperactivity (eg, tachycardia, hypertension, diaphoresis, hyperreflexia), mild tremor, anxiety, irritability, sleep disturbances (eg, insomnia, vivid dreams), gastrointestinal symptoms (eg, anorexia, nausea, vomiting), headache, and craving alcohol 4 ○ Major alcohol withdrawal syndrome 5, 4 – Progression and worsening of withdrawal manifestations, usually after about 24 hours from the onset of initial manifestations 4 □ Manifestations often peak around 50 hours before gradual resolution or may continue to progress to severe (complicated) withdrawal, particularly without treatment 4 – Characterized by moderate to severe autonomic hyperactivity (eg, tachycardia, hypertension, diaphoresis, hyperreflexia, fever); marked tremor; pronounced anxiety, insomnia, -
Binge Drinking Research
WTAG binge-drinking research Report of research and consultation conducted by MCM Research Ltd for Wine Intelligence September 2004 MCM Research Limited 27/28 St Clements, Oxford OX4 1AB Tel: 01865 204211 Fax: 01865 793137 Email: [email protected] WTAG Binge Drinking Research Introduction The term ‘binge-drinking’ has, in recent years, come to replace earlier epithets such as ‘lager louts’ in discussions of alcohol-related antisocial behaviour. The use of such a new term is taken by many commentators to imply that the phenomenon to which it relates is also quite novel. But in the way that aggressive outbursts from motorists were common long before the descriptor ‘road rage’ was coined, the patterns of behaviour that fall within the loose boundaries of binge-drinking also have a long ancestry in Britain. One only has to read The Pub and the People, written by Tom Harrisson and his Mass Observation colleagues in the late 1930s, to be reminded of this. He refers us, for example, to the annual report of the Worktown (Bolton) Temperance Society annual report of 1854 which commented1: “That drunkenness is painfully prevalent in the Borough a thousand facts bear most painful testimony. Men and women staggering along the public streets, fights brawls of the most barbarous character …” The contemporary observations made by Harrisson and co in Bolton and Blackpool were, in many substantial ways, consistent with what we have seen in our research over the past 20 years and with the present-day patterns of activity in towns and cities all over the country. For example: “At closing time back and front streets crowded, some people dancing, men and women doing foxtrots and a group of women trying to do a fling. -
Not to Be Disclosed to the Registrants of Hydrogen Cyanamide Formulations
FORM HS1 Application for Reassessment of a Hazardous Substance under section 63 of the Hazardous Substances and New Organisms Act 1996 Name of Substance: Soluble concentrates containing Hydrogen Cyanamide (520 to 540 g/L) APPENDICES 2 to 11 Applicant: Chief Executive ERMA New Zealand Contents Appendix 2 – Class 1 to 8 Hazardous Properties Classification ............................................... 3 Appendix 3 - Class 9 - Hazardous Properties of Hydrogen Cyanamide and its Formulations 33 Appendix 4 - Overseas Case Studies on Human Exposure to Hydrogen Cyanamide ............. 46 Appendix 5 - NZKGI 0800 complaints for 2003 and 2004 ..................................................... 51 Appendix 6a - National Poisons Centre calls 1998-2001 ........................................................ 52 Appendix 6b - National Poisons Centre calls 2002-2005 ........................................................ 53 Appendix 7 - Toi Te Ora Public Health records of hydrogen cyanamide complaints 1998- 2004 ......................................................................................................................................... 64 Appendix 8 – Qualitative scales for describing effects ........................................................... 65 Appendix 9 – Human Health Exposure Modelling ................................................................. 68 Appendix 10 - Environmental Exposure Modelling ................................................................ 74 Application for Reassessment of Hydrogen Cyanamide: Appendices