The Role of Secondary Brain Insults in Status Epilepticus: a Systematic Review
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What to Expect After Having a Subarachnoid Hemorrhage (SAH) Information for Patients and Families Table of Contents
What to expect after having a subarachnoid hemorrhage (SAH) Information for patients and families Table of contents What is a subarachnoid hemorrhage (SAH)? .......................................... 3 What are the signs that I may have had an SAH? .................................. 4 How did I get this aneurysm? ..................................................................... 4 Why do aneurysms need to be treated?.................................................... 4 What is an angiogram? .................................................................................. 5 How are aneurysms repaired? ..................................................................... 6 What are common complications after having an SAH? ..................... 8 What is vasospasm? ...................................................................................... 8 What is hydrocephalus? ............................................................................... 10 What is hyponatremia? ................................................................................ 12 What happens as I begin to get better? .................................................... 13 What can I expect after I leave the hospital? .......................................... 13 How will the SAH change my health? ........................................................ 14 Will the SAH cause any long-term effects? ............................................. 14 How will my emotions be affected? .......................................................... 15 When should -
What%Is%Epilepsy?%
What%is%Epilepsy?% Epilepsy(is(a(brain(disorder(in(which(a(person(has(repeated(seizures((convulsions)(over(time.(Seizures(are( episodes(of(disturbed(brain(activity(that(cause(changes(in(attention(or(behavior.( Causes( Epilepsy(occurs(when(permanent(changes(in(brain(tissue(cause(the(brain(to(be(too(excitable(or(jumpy.( The(brain(sends(out(abnormal(signals.(This(results(in(repeated,(unpredictable(seizures.((A(single(seizure( that(does(not(happen(again(is(not(epilepsy.)( Epilepsy(may(be(due(to(a(medical(condition(or(injury(that(affects(the(brain,(or(the(cause(may(be( unknown((idiopathic).( Common(causes(of(epilepsy(include:( •Stroke(or(transient(ischemic(attack((TIA)( •Dementia,(such(as(Alzheimer's(disease( •Traumatic(brain(injury( •Infections,(including(brain(abscess,(meningitis,(encephalitis,(and(AIDS( •Brain(problems(that(are(present(at(birth((congenital(brain(defect)( •Brain(injury(that(occurs(during(or(near(birth( •Metabolism(disorders(present(at(birth((such(as(phenylketonuria)( •Brain(tumor( •Abnormal(blood(vessels(in(the(brain( •Other(illness(that(damage(or(destroy(brain(tissue( •Use(of(certain(medications,(including(antidepressants,(tramadol,(cocaine,(and(amphetamines( Epilepsy(seizures(usually(begin(between(ages(5(and(20,(but(they(can(happen(at(any(age.(There(may(be(a( family(history(of(seizures(or(epilepsy.( Symptoms( Symptoms(vary(from(person(to(person.(Some(people(may(have(simple(staring(spells,(while(others(have( violent(shaking(and(loss(of(alertness.(The(type(of(seizure(depends(on(the(part(of(the(brain(affected(and( cause(of(epilepsy.( -
Brain Injury and Opioid Overdose
Brain Injury and Opioid Overdose: Acquired Brain Injury is damage to the brain 2.8 million brain injury related occurring after birth and is not related to congenital or degenerative disease. This includes anoxia and hospital stays/deaths in 2013 hypoxia, impairment (lack of oxygen), a condition consistent with drug overdose. 70-80% of hospitalized patients are discharged with an opioid Rx Opioid Use Disorder, as defined in DSM 5, is a problematic pattern of opioid use leading to clinically significant impairment, manifested by meaningful risk 63,000+ drug overdose-related factors occurring within a 12-month period. deaths in 2016 Overdose is injury to the body (poisoning) that happens when a drug is taken in excessive amounts “As the number of drug overdoses continues to rise, and can be fatal. Opioid overdose induces respiratory doctors are struggling to cope with the increasing number depression that can lead to anoxic or hypoxic brain of patients facing irreversible brain damage and other long injury. term health issues.” Substance Use and Misuse is: The frontal lobe is • Often a contributing factor to brain injury. History of highly susceptible abuse/misuse is common among individuals who to brain oxygen have sustained a brain injury. loss, and damage • Likely to increase for individuals who have misused leads to potential substances prior to and post-injury. loss of executive Acute or chronic pain is a common result after brain function. injury due to: • Headaches, back or neck pain and other musculo- Sources: Stojanovic et al 2016; Melton, C. Nov. 15,2017; Devi E. skeletal conditions commonly reported by veterans Nampiaparampil, M.D., 2008; Seal K.H., Bertenthal D., Barnes D.E., et al 2017; with a history of brain injury. -
Traumatic Brain Injury and Domestic Violence
TRAUMATIC BRAIN INJURY AND DOMESTIC VIOLENCE Women who are abused often suffer injury to their head, neck, and face. The high potential for women who are abused to have mild to severe Traumatic Brain Injury (TBI) is a growing concern, since the effects can cause irreversible psychological and physical harm. Women who are abused are more likely to have repeated injuries to the head. As injuries accumulate, likelihood of recovery dramatically decreases. In addition, sustaining another head trauma prior to the complete healing of the initial injury may be fatal. Severe, obvious trauma does not have to occur for brain injury to exist. A woman can sustain a blow to the head without any loss of consciousness or apparent reason to seek medical assistance, yet display symptoms of TBI. (NOTE: While loss of consciousness can be significant in helping to determine the extent of the injury, people with minor TBI often do not lose consciousness, yet still have difficulties as a result of their injury). Many women suffer from a TBI unknowingly and misdiagnosis is common since symptoms may not be immediately apparent and may mirror those of mental health diagnoses. In addition, subtle injuries that are not identifiable through MRIs or CT scans may still lead to cognitive symptoms. What is Traumatic Brain Injury? Traumatic brain injury (TBI) is defined as an injury to the brain that is caused by external physical force and is not present at birth or degenerative. TBI can be caused by: • A blow to the head, o e.g., being hit on the head forcefully with object or fist, having one’s head smashed against object/wall, falling and hitting head, gunshot to head. -
Traumatic Brain Injury (TBI)
Traumatic Brain Injury (TBI) Carol A. Waldmann, MD raumatic brain injury (TBI), caused either by blunt force or acceleration/ deceleration forces, is common in the general population. Homeless persons Tare at particularly high risk of head trauma and adverse outcomes to TBI. Even mild traumatic brain injury can lead to persistent symptoms including cognitive, physical, and behavioral problems. It is important to understand brain injury in the homeless population so that appropriate referrals to specialists and supportive services can be made. Understanding the symptoms and syndromes caused by brain injury sheds light on some of the difficult behavior observed in some homeless persons. This understanding can help clinicians facilitate and guide the care of these individuals. Prevalence and Distribution recover fully, but up to 15% of patients diagnosed TBI and Mood Every year in the USA, approximately 1.5 with MTBI by a physician experience persistent Swings. million people sustain traumatic brain injury disabling problems. Up to 75% of brain injuries This man suffered (TBI), 230,000 people are hospitalized due to TBI are classified as MTBI. These injuries cost the US a gunshot wound and survive, over 50,000 people die from TBI, and almost $17 billion per year. The groups most at risk to the head and many subsequent more than 1 million people are treated in emergency for TBI are those aged 15-24 years and those aged traumatic brain rooms for TBI. In persons under the age of 45 years, 65 years and older. Men are twice as likely to sustain injuries while TBI is the leading cause of death. -
Rapidly Progressive Tetraplegia and Cognitive Deterioration During Rehabilitation: a Case of Neurodegenerative Disease
J Surg Med. 2019;3(1):100-102. Case report DOI: 10.28982/josam.454181 Olgu sunumu Rapidly progressive tetraplegia and cognitive deterioration during rehabilitation: A case of neurodegenerative disease Rehabilitasyon sırasında hızlı ilerleyen tetrapleji ve bilişsel bozulma: Bir nörodejeneratif hastalık olgusu Sevgi İkbali Afşar 1, Oya Ümit Yemişçi 1 1 Department of Physical Medicine and Abstract Rehabilitation, Baskent University, Human prion diseases are fatal, progressive neurodegenerative disorders caused by neurolytic pathogen proteins, called Faculty of Medicine, Ankara, Turkey prions. The most common human prion disease is sporadic Creutzfeldt-Jakob disease, with an approximate annual prevalence of 0.5-1 per million. The symptoms and signs include rapidly progressive dementia, ataxia, myoclonic ORCID ID of the authors SİA: 0000-0002-4003-3646 seizures, akinetic mutism and other neurological and neurobehavioral disorders. The clinical spectrum of Creutzfeldt- OÜY: 0000-0002-0501-5127 Jakob disease is highly variable; therefore it can be difficult to diagnose premortem. This article describes a 78-year- old woman who initially presented with difficulty walking and balance disorder. As a result of the evaluation, the patient was transferred to rehabilitation clinic, with a diagnosis of cervical spinal stenosis. During hospitalization, she showed progressive decline in gait and balance and deteriorated rapidly. The patient was considered to be probable sporadic Creutzfeldt-Jakob disease after further investigations. Keywords: Neurodegenerative disease, Creutzfeldt-Jakob disease, Rehabilitation Öz Corresponding author / Sorumlu yazar: İnsan prion hastalıkları, prionlar olarak adlandırılan nörolitik patojen proteinlerin neden olduğu ilerleyici Sevgi İkbali Afşar Address / Adres: Fevzi Cakmak Cad. 5. Sokak nörodejeneratif hastalıklardır. En yaygın insan prion hastalığı sporadik Creutzfeldt-Jakob hastalığı olup, yıllık No: 48, 06490, Ankara, Türkiye prevalansı yaklaşık milyonda 0.5-1'dir. -
Case Report of Hyperacute Edema and Cavitation Following Deep Brain Stimulation Lead Implantation Albert J
www.surgicalneurologyint.com Surgical Neurology International Editor-in-Chief: Nancy E. Epstein, MD, Clinical Professor of Neurological Surgery, School of Medicine, State U. of NY at Stony Brook. SNI: Stereotactic Editor Veronica Lok-Sea Chiang, MD Yale School of Medicine, New Haven, CT, USA Open Access Case Report Case report of hyperacute edema and cavitation following deep brain stimulation lead implantation Albert J. Fenoy1,2, Christopher R. Conner2, Joseph S. Withrow2, Aaron W. Hocher2 Movement Disorders and Neurodegenerative Disease Program, Departments of 1Neurology, 2Neurosurgery, McGovern Medical School, Houston, Texas, United States. E-mail: *Albert J. Fenoy - [email protected]; Christopher R. Conner - [email protected]; Joseph S. Withrow - joseph.s.withrow@ uth.tmc.edu; Aaron W. Hocher - [email protected] ABSTRACT Background: Postoperative cerebral edema around a deep brain stimulation (DBS) electrode is an uncommonly reported complication of DBS surgery. e etiology of this remains unknown, and the presentation is highly variable; however, the patients generally report a good outcome. Case Description: Here, we report an unusual presentation of postoperative edema in a 66-year-old female *Corresponding author: who has bilateral dentatorubrothalamic tract (specifically, the ventral intermediate nucleus) DBS for a mixed Albert J. Fenoy, type tremor disorder. Initial postoperative computed tomography (CT) was unremarkable and the patient was Department of Neurosurgery, admitted for observation. She declined later on postoperative day (POD) 1 and became lethargic. Stat head CT McGovern Medical School, scan performed revealed marked left-sided peri-lead edema extending into the centrum semiovale with cystic 6431 Fannin St., Houston, Texas cavitation, and trace right-sided edema. -
Guidelines for the Management of Severe Traumatic Brain Injury 4Th Edition
Guidelines for the Management of Severe Traumatic Brain Injury 4th Edition Nancy Carney, PhD Oregon Health & Science University, Portland, OR Annette M. Totten, PhD Oregon Health & Science University, Portland, OR Cindy O'Reilly, BS Oregon Health & Science University, Portland, OR Jamie S. Ullman, MD Hofstra North Shore-LIJ School of Medicine, Hempstead, NY Gregory W. J. Hawryluk, MD, PhD University of Utah, Salt Lake City, UT Michael J. Bell, MD University of Pittsburgh, Pittsburgh, PA Susan L. Bratton, MD University of Utah, Salt Lake City, UT Randall Chesnut, MD University of Washington, Seattle, WA Odette A. Harris, MD, MPH Stanford University, Stanford, CA Niranjan Kissoon, MD University of British Columbia, Vancouver, BC Andres M. Rubiano, MD El Bosque University, Bogota, Colombia; MEDITECH Foundation, Neiva, Colombia Lori Shutter, MD University of Pittsburgh, Pittsburgh, PA Robert C. Tasker, MBBS, MD Harvard Medical School & Boston Children’s Hospital, Boston, MA Monica S. Vavilala, MD University of Washington, Seattle, WA Jack Wilberger, MD Drexel University, Pittsburgh, PA David W. Wright, MD Emory University, Atlanta, GA Jamshid Ghajar, MD, PhD Stanford University, Stanford, CA Reviewed for evidence-based integrity and endorsed by the American Association of Neurological Surgeons and the Congress of Neurological Surgeons. September 2016 TABLE OF CONTENTS PREFACE ...................................................................................................................................... 5 ACKNOWLEDGEMENTS ............................................................................................................................................. -
Influence of Mild Hypothermia on Hypoxic- Ischemic Brain Damage in the Immature Rat
003 I-399X/s 113404-0525$03.00/0 PEDIATRIC RESEARCH Vol. 34. No. 4. 1993 Copyright fc 1993 lnternat~onalPedlatnc Research Foundat~on.Inc. Prrt~rc~drn Lr.S..4. Influence of Mild Hypothermia on Hypoxic- Ischemic Brain Damage in the Immature Rat J. YAGER. J. TOWFIGHI. AND R. C. VANNUCCl Di,puritno~ic~l'Pi~cliciirii~.s /J. Y/. Roj.ul L'nivcrsii! IIo.spiiul. L'ni~~c,r.sii!*c~f'Su.sX.uic~lrc~~~~ut~, Su.skuioot~. Su.sku~chc~c~ut~,C'ut~udu. S7N 0x0: and D(~purrtnenrc~f'Purhol~~s.!~ (Nnrroputllok~g~ /J. T.1 und Pc~diuiricA'~,r~ro/ox~~ /R.('. I,./. 7%i, .l/iliot~S. Ilcr.sl~c,!~hI(~dicu1 ('cwrc~r. Tlli. Pi~t~n.s~-l~~unicrSiurc Crni~~c,r.vit!~. IIi~r.s/rc~~~.Pc~t~t~.s~~/vut~iu 17033 ABSTRACT. Recent studies in adult animals have shown mia also is protective (8. 9). Conversely. hyperthermia either that even small decreases in brain or core temperature during or after an hypoxic-ischemic insult worsens ultimate brain ameliorate the damage resulting from hypoxic-ischemic damage (lo, l I). insults. To determine the effect of minor reductions in In contrast to the adult. the human term infant. under physi- ambient temperature either during or after an hypoxic- ologic circumstances can maintain thermal neutrality only over ischemic insult on the brain of the immature rat, 7-d- a severely restricted range of environmental temperatures ( 12- postnatal rat pups underwent unilateral common carotid 15). Infants, who are frequently exposed to a variety of "stresses" artery ligation followed by exposure to hypoxia in 8% (birth asphyxia. -
Pathophysiology and Treatment of Stroke: Present Status and Future Perspectives
International Journal of Molecular Sciences Review Pathophysiology and Treatment of Stroke: Present Status and Future Perspectives Diji Kuriakose and Zhicheng Xiao * Development and Stem Cells Program, Monash Biomedicine Discovery Institute and Department of Anatomy and Developmental Biology, Monash University, Melbourne, VIC 3800, Australia; [email protected] * Correspondence: [email protected] Received: 29 September 2020; Accepted: 13 October 2020; Published: 15 October 2020 Abstract: Stroke is the second leading cause of death and a major contributor to disability worldwide. The prevalence of stroke is highest in developing countries, with ischemic stroke being the most common type. Considerable progress has been made in our understanding of the pathophysiology of stroke and the underlying mechanisms leading to ischemic insult. Stroke therapy primarily focuses on restoring blood flow to the brain and treating stroke-induced neurological damage. Lack of success in recent clinical trials has led to significant refinement of animal models, focus-driven study design and use of new technologies in stroke research. Simultaneously, despite progress in stroke management, post-stroke care exerts a substantial impact on families, the healthcare system and the economy. Improvements in pre-clinical and clinical care are likely to underpin successful stroke treatment, recovery, rehabilitation and prevention. In this review, we focus on the pathophysiology of stroke, major advances in the identification of therapeutic targets and recent trends in stroke research. Keywords: stroke; pathophysiology; treatment; neurological deficit; recovery; rehabilitation 1. Introduction Stroke is a neurological disorder characterized by blockage of blood vessels. Clots form in the brain and interrupt blood flow, clogging arteries and causing blood vessels to break, leading to bleeding. -
Suarez, JI: Hypertonic Saline for Cerebral Edema
Hypertonic saline for cerebral edema and elevated intracranial pressure JOSE´ I. SUAREZ, MD erebral edema and elevated intracranial movements. Because transport through the BBB is a pressure (ICP) are important and frequent selective process, the osmotic gradient that a particle problems in the neurocritically ill patient. can create is also dependent on how restricted its They can both result from various insults permeability through the barrier is. This restriction is C expressed in the osmotic reflection coefficient, which to the brain. Improving cerebral edema and decreas- ing ICP has been associated with improved out- ranges from 0 (for particles that can diffuse freely) to come.1 However, all current treatment modalities 1.0 (for particles that are excluded the most effec- are far from perfect and are associated with serious tively and therefore are osmotically the most active). adverse events:1–4 indiscriminate hyperventilation The reflection coefficient for sodium chloride is can lead to brain ischemia; mannitol can cause 1.0 (mannitol’s is 0.9), and under normal conditions intravascular volume depletion, renal insufficiency, sodium (Na+) has to be transported actively into the and rebound ICP elevation; barbiturates are associat- CSF.5,6 Animal studies have shown that in condi- ed with cardiovascular and respiratory depression tions of an intact BBB, CSF Na+ concentrations and prolonged coma; and cerebrospinal fluid (CSF) increase when an osmotic gradient exists but lag drainage via intraventricular catheter insertion may behind plasma concentrations for 1 to 4 hours.5 result in intracranial bleeding and infection. Thus, elevations in serum Na+ will create an effec- Other treatment modalities have been explored, tive osmotic gradient and draw water from brain into and hypertonic saline (HS) solutions particularly the intravascular space. -
Neurologic Complications of Electrolyte Disturbances and Acid–Base Balance
Handbook of Clinical Neurology, Vol. 119 (3rd series) Neurologic Aspects of Systemic Disease Part I Jose Biller and Jose M. Ferro, Editors © 2014 Elsevier B.V. All rights reserved Chapter 23 Neurologic complications of electrolyte disturbances and acid–base balance ALBERTO J. ESPAY* James J. and Joan A. Gardner Center for Parkinson’s Disease and Movement Disorders, Department of Neurology, UC Neuroscience Institute, University of Cincinnati, Cincinnati, OH, USA INTRODUCTION hyperglycemia or mannitol intake, when plasma osmolal- ity is high (hypertonic) due to the presence of either of The complex interplay between respiratory and renal these osmotically active substances (Weisberg, 1989; function is at the center of the electrolytic and acid-based Lippi and Aloe, 2010). True or hypotonic hyponatremia environment in which the central and peripheral nervous is always due to a relative excess of water compared to systems function. Neurological manifestations are sodium, and can occur in the setting of hypovolemia, accompaniments of all electrolytic and acid–base distur- euvolemia, and hypervolemia (Table 23.2), invariably bances once certain thresholds are reached (Riggs, reflecting an abnormal relationship between water and 2002). This chapter reviews the major changes resulting sodium, whereby the former is retained at a rate faster alterations in the plasma concentration of sodium, from than the latter (Milionis et al., 2002). Homeostatic mech- potassium, calcium, magnesium, and phosphorus as well anisms protecting against changes in volume and sodium as from acidemia and alkalemia (Table 23.1). concentration include sympathetic activity, the renin– angiotensin–aldosterone system, which cause resorption HYPONATREMIA of sodium by the kidneys, and the hypothalamic arginine vasopressin, also known as antidiuretic hormone (ADH), History and terminology which prompts resorption of water (Eiskjaer et al., 1991).