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Acute Stroke Management in the First 24 Hours
2
A Practical Guide for Clinicians
EDITED BY
MAXIM MOKIN, MD, PHD
ASSISTANT PROFESSOR OF NEUROLOGY AND NEUROSURGERY UNIVERSITY OF SOUTH
FLORIDA MEDICAL DIRECTOR OF NEUROINTERVENTIONAL SERVICES TAMPA GENERAL
HOSPITAL TAMPA, FL
EDWARD C. JAUCH, MD, MS

PROFESSOR, CHAIR, DEPARTMENT OF EMERGENCY MEDICINE PROFESSOR, DEPARTMENT OF
NEUROLOGY MEDICAL UNIVERSITY OF SOUTH CAROLINA CHARLESTON, SC ADJUNCT
PROFESSOR, DEPARTMENT OF BIOENGINEERING CLEMSON UNIVERSITY CLEMSON, SC
ITALO LINFANTE, MD, FAHA
MEDICAL DIRECTOR OF INTERVENTIONAL NEURORADIOLOGY AND ENDOVASCULAR

NEUROSURGERY MIAMI CARDIAC AND VASCULAR INSTITUTE AND BAPTIST NEUROSCIENCE
INSTITUTE CLINICAL PROFESSOR OF RADIOLOGY AND NEUROSCIENCE HERBERT WERTHEIM
COLLEGE OF MEDICINE FLORIDA INTERNATIONAL UNIVERSITY MIAMI, FL
ADNAN SIDDIQUI, MD, PHD, FAHA

VICE-CHAIRMAN AND PROFESSOR OF NEUROSURGERY AND RADIOLOGY DIRECTOR OF
NEUROENDOVASCULAR FELLOWSHIP PROGRAM JACOBS SCHOOL OF MEDICINE AND
BIOMEDICAL SCIENCES THE STATE UNIVERSITY OF NEW YORK AT BUFFALO DIRECTOR OF
THE NEUROSURGICAL STROKE SERVICE KALEIDA HEALTH BUFFALO, NY
ELAD LEVY, MD, MBA, FACS, FAHA

CHAIRMAN OF NEUROLOGICAL SURGERY PROFESSOR OF NEUROSURGERY AND RADIOLOGY
JACOBS SCHOOL OF MEDICINE AND BIOMEDICAL SCIENCES THE STATE UNIVERSITY OF NEW
YORK AT BUFFALO MEDICAL DIRECTOR OF NEUROENDOVASCULAR SERVICES GATES
VASCULAR INSTITUTE BUFFALO, NY
3
Oxford University Press is a department of the University of Oxford. It furthers the University’s objective of excellence in research, scholarship,
and education by publishing worldwide. Oxford is a registered trade mark of Oxford University Press in the UK and certain other countries.
Published in the United States of America by Oxford University Press

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© Oxford University Press 2018
All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means,
without the prior permission in writing of Oxford University Press, or as expressly permitted by law, by license, or under terms agreed with the
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Department, Oxford University Press, at the address above.
You must not circulate this work in any other form and you must impose this same condition on any acquirer.
Library of Congress Cataloging-in-Publication Data

Names: Mokin, Maxim, editor. | Jauch, Edward C., editor. |
Linfante, Italo, editor. | Siddiqui, Adnan, editor. | Levy, Elad, editor.
Title: Acute stroke management in the first 24 hours: a practical guide for clinicians /
edited by Maxim Mokin, Edward C. Jauch, Italo Linfante, Adnan Siddiqui, Elad Levy.
Description: Oxford; New York: Oxford University Press, [2018] |
Includes bibliographical references.
Identifiers: LCCN 2017054218 | ISBN 9780190856519 (pbk.: alk. paper) | ISBN 9780190856533 (epub)
Subjects: | MESH: Stroke–diagnosis | Stroke–therapy | Critical Care–methods |
Emergency Treatment–methods
Classification: LCC RC388.5 | NLM WL 356 | DDC 616.8/1–dc23
LC record available at https://lccn.loc.gov/2017054218
This material is not intended to be, and should not be considered, a substitute for medical or other professional advice. Treatment for the
conditions described in this material is highly dependent on the individual circumstances. And, while this material is designed to offer accurate
information with respect to the subject matter covered and to be current as of the time it was written, research and knowledge about medical
and health issues is constantly evolving and dose schedules for medications are being revised continually, with new side effects recognized and
accounted for regularly. Readers must therefore always check the product information and clinical procedures with the most up-to-date
published product information and data sheets provided by the manufacturers and the most recent codes of conduct and safety regulation. The
publisher and the authors make no representations or warranties to readers, express or implied, as to the accuracy or completeness of this
material. Without limiting the foregoing, the publisher and the authors make no representations or warranties as to the accuracy or efficacy of
the drug dosages mentioned in the material. The authors and the publisher do not accept, and expressly disclaim, any responsibility for any
liability, loss or risk that may be claimed or incurred as a consequence of the use and/or application of any of the contents of this material.
4
CONTENTS
Foreword
Preface
Contributors
1. Basic Clinical Syndromes and Definitions

Aparna Pendurthi and Maxim Mokin
2. Stroke Systems of Care

Casey Frey, Laura Bishop, Stacey Q. Wolfe, and Kyle M. Fargen
3. Prehospital Triage of Stroke: Clinical Evaluation

Vera Sharashidze, Clara Barreira, Diogo Hauseen, and Raul G. Nogueira
4. Prehospital Assessment of Stroke: Mobile Stroke Units

Andrew Blake Buletko, Jason Mathew, Tapan Thacker, Lila Sheikhi, Andrew Russman, and M. Shazam
Hussain
5. Evaluation of Stroke in the Emergency Department

Robert Sawyer and Edward C. Jauch
6. Imaging of Acute Stroke

Maxim Mokin
7. Telemedicine for Evaluation of Stroke Patients

Kaustubh Limaye and Lawrence R. Wechsler
8. Intravenous Thrombolysis in Acute Ischemic Stroke

Waldo R. Guerrero, Edgar A. Samaniego, and Santiago Ortega-Gutierrez
9. Endovascular Treatment of Stroke

Mandy J. Binning and Daniel R. Felbaum
10. Care of Stroke Patients Post Intravenous Alteplase and Endovascular Thrombectomy
Violiza Inoa and Lucas Elijovich
11. In-Hospital Stroke

Noella J. Cypress West and Maxim Mokin
12. Medical Management of Ischemic Stroke

Maxim Mokin and Juan Ramos-Canseco
13. Medical Management of Hemorrhagic Stroke

Shashank Shekhar, Shreyas Gangadhara, and Rebecca Sugg
14. Surgical Treatment of Hemorrhagic Stroke
5
Vladimir Ljubimov, Travis Dailey, and Siviero Agazzi
15. Cerebral Venous Thrombosis

Juan Ramos-Canseco and Maxim Mokin
Index
6
FOREWORD
TUDOR G. JOVIN ■
The dream of being able to reverse a stroke by opening the occluded cerebral artery from within started in the
early days of neuroendovascular therapies pioneered by the neurologist Egaz Moniz and has become reality in
the era of modern mechanical thrombectomy. After years of stagnation that followed publication of the
landmark NINDS iv t-PA trial in 1995, which led to the implementation of intravenous t-PA as the standard
and only proven treatment for acute ischemic stroke, the past years have witnessed disruptive changes in the
delivery of acute stroke care. Remarkable technological advances, spearheaded by physicians and industry
along with a maturation process on the part of stroke care providers with regards to patient selection,
workflow, and peri- and intra-procedural care culminated in no less than eight completed and strongly
positive randomized trials of thrombectomy for acute stroke due to large vessel occlusion. These studies,
which together have enrolled over 2,000 patients, have not only demonstrated a treatment effect only a
handful of other procedural based therapies can claim in medicine but have also widened the therapeutic time
window to a previously unimaginable 24 hours. Highly effective as these interventions are, favorable outcomes
are still observed in only about half of the patients treated. Furthermore, a substantial proportion of patients
potentially eligible for this procedure remain untreated. Much work remains ahead to establish more effective
approaches that will not only lead to more patients treated but also result in higher rates of favorable outcomes
Not unlike ischemic stroke prior to the recent developments, intracerebral hemorrhage has been plagued by
decades of therapeutic nihilism. And while this area of vascular neuroscience has not yet achieved a
breakthrough similar to that observed with ischemic stroke, there are exciting new minimally invasive
approaches that hold great promise for the future.
Considering the exquisite time-sensitive benefit of thrombectomy, dramatic paradigm shift implementation
required at both individual and system levels for the care of patients with acute stroke represents a formidable
challenge. Among the many interventions necessary for an effective change in the delivery of acute stroke care,
healthcare provider education is of paramount importance.
From that standpoint, Acute Stroke Management in the First 24 Hours is a much needed and timely
contribution that fills a real void in knowledge as it represents a comprehensive overview of most aspects
related to the care of the acute ischemic and hemorrhagic stroke patient. Furthermore, as a novel and
refreshing approach, it follows the logical progression of care from evaluation and management in the pre-
hospital setting to the in-hospital hyperacute intervention (when indicated) and through to the critical stage of
early post-admission care. This practical yet well-grounded in science material represents the result of a
collaborative work by a multispecialty group of widely acknowledged experts in the field of cerebrovascular
diseases. Given the complexity of acute stroke care and the fact that knowledge included and easily accessible
in this book can be life (or brain) saving, every physician and healthcare provider involved in the care of
patients with acute stroke could benefit from adding a copy of Acute Stroke Management in the First 24 Hours
to their library.
Tudor G. Jovin, MD
7
Professor of Neurology and Neurosurgery
Director, University of Pittsburgh Medical Center (UPMC) Stroke Institute
Director, UPMC Center for Neuroendovascular Therapy
Pittsburgh, PA
8
PREFACE
The last two decades have ushered a dramatic evolution in management of acute stroke patients through
promising advances in medical, endovascular, and open surgical procedures. Physicians who are at the
vanguard of treating the acute stroke patient are faced with ever increasing challenges and race against time to
achieve the best possible clinical outcomes. Navigating the complexities of the stroke system of care starts with
time-sensitive identification of the acute stroke patient in the prehospital setting, followed by appropriate
hospital triage, and continues in hospital with selection of a suitable and individualized treatment.
The treatment of acute ischemic stroke has become considerably more complex now that endovascular
thrombectomy has proved its high safety and efficacy as treatment option. While some patients are candidates
for only one particular type of revascularization therapy (either intravenous thrombolysis or endovascular
thrombectomy), others may benefit from both therapies combined; making proper patient selection and triage
more challenging. Randomized trials focusing on medical and surgical management of intracerebral and
subarachnoid hemorrhage have expanded our understanding of patients with cerebrovascular diseases.
Although promising, these results have further confounded clinical decision making for hemorrhagic stroke
patients. Furthermore, the evaluation and treatment protocols for acute stroke frequently exclude patients
whose clinical presentation does not fall within the established guidelines.
Aware of these challenges, neurologists, neurosurgeons, interventionalists, and emergency medicine
specialists who traditionally practice within a narrow scope now find themselves assuming new roles to achieve
optimal patient outcomes. Clinician collaboration within a multidisciplinary team that includes first
responders and hospital administration is vital to the establishment of stroke outreach programs and updated,
progressive triage protocols. Acute Stroke Management in the First 24 Hours is a practical, collaborative road
map for a broad audience of health-care providers involved in the initial evaluation and management of acute
stroke patients. It benefits from the experience of its authors who expertly understand the burgeoning need of
a cooperative approach to acute stroke treatment.
9
CONTRIBUTORS
Siviero Agazzi, MD, MBA, FCAS

Professor, College of Medicine Neurosurgery
Director, Division of Cranial Surgery
Department of Neurosurgery and Brain Repair
University of South Florida
Tampa, FL
Clara Barreira, MD
Clinical Research Fellow
Department of Neurology
Emory University School of Medicine
Atlanta, GA
Mandy J. Binning, MD
Assistant Professor
Stroke Director
Department of Neurosurgery
Drexel University
Philadelphia, PA
Laura Bishop, MD
Assistant Professor, Neurology
Wake Forest University
Winston-Salem, NC
Andrew Blake Buletko, MD

Vascular Neurology Fellow
Cerebrovascular Center, Neurological Institute
Cleveland Clinic
Cleveland, OH
Noella J. Cypress West, ARNP

Vascular Neurology Nurse Practitioner
Tampa General Hospital
Tampa, FL
Travis Dailey, MD
PGY-3 Resident
10
Tampa, FL
Lucas Elijovich, MD, FAHA

Associate Professor
Departments of Neurology and Neurosurgery
Semmes-Murphey Neurologic Institute
University of Tennessee Health Sciences Center
Memphis, TN
Kyle M. Fargen, MD, MPH

Assistant Professor, Neurosurgery
Department of Neurological Surgery
Winston-Salem, NC
Daniel R. Felbaum, MD
Department of Neurosurgery
Drexel University
Philadelphia, PA
Casey Frey, MS
Winston-Salem, NC
Shreyas Gangadhara, MD
University of Mississippi Medical Center
Jackson, MS
Waldo R. Guerrero, MD
Neuroendovascular Surgery Fellow Associate
Department of Neurology, Stroke Division
University of Iowa Carver College of Medicine
Iowa City, IA
Diogo Hauseen, MD
Assistant Professor
Grady Memorial Hospital
Atlanta, GA
11
M. Shazam Hussain, MD
Associate Professor, Cleveland Clinic Lerner College of Medicine
Director, Cerebrovascular Center Neurological Institute
Cleveland Clinic
Cleveland, OH
Violiza Inoa, MD
Assistant Professor
Departments of Neurology and Neurosurgery
Semmes-Murphey Neurologic Institute
University of Tennessee Health Sciences Center
Memphis, TN
Kaustubh Limaye, MD
Clinical Assistant Professor of Neurology, Cerebrovascular Diseases
Iowa City, IA
Vladimir Ljubimov, MD
PGY-2 Resident
Tampa, FL
Jason Mathew, DO
Cerebrovascular Center, Neurological Institute
Cleveland Clinic
Cleveland, OH
Raul G. Nogueira, MD
Director, Neuroendovascular Division
Marcus Stroke & Neuroscience Center
Grady Memorial Hospital
Atlanta, GA
Santiago Ortega-Gutierrez, MD, MSC

Clinical Assistant Professor
Director of the Neurointerventional Surgery in Neurology
Associate Program Director of the Neuroendovascular Surgery Fellowship Program
Department of Neurology, Stroke Division
12
Iowa City, IA
Aparna Pendurthi, MD
Instructor
University of Kansas Medical Center
Kansas City, KS
Juan Ramos-Canseco, MD
Vascular Neurology
Palm Beach Neuroscience Institute
West Palm Beach, FL
Andrew Russman, DO
Head, Cleveland Clinic Stroke Program
Cerebrovascular Center
Neurological Institute
Cleveland Clinic
Cleveland, OH
Edgar A. Samaniego, MD
Clinical Assistant Professor
Department of Neurology Stroke Division
Iowa City, IA
Robert Sawyer, MD
Associate Professor
University at Buffalo, the State University of New York
New York, NY
Vera Sharashidze, MD
Resident
Atlanta, GA
Lila Sheikhi, MD
13
Cleveland Clinic
Cleveland, OH
Shashank Shekhar, MD, MSc

Jackson, MS
Rebecca Sugg, MD, FAHA

Associate Professor, Vice Chair, and Director
Jackson, MS
Tapan Thacker, MD
Cleveland Clinic
Cleveland, OH
Lawrence R. Wechsler, MD
Henry B. Higman Professor and Chair
Vice President of Telemedicine Services
Physician Services Division
University of Pittsburgh Schools of the Health Sciences
Pittsburgh, PA
Stacey Q. Wolfe, MD
Program Director and Associate Professor
Winston-Salem, NC
14
15
1
Basic Clinical Syndromes and Definitions
APARNA PENDURTHI AND MAXIM MOKIN ■
CONTENTS
1. Introduction
2. Classification
2.1 Transient ischemic attack
2.2 Stroke
3. Ischemic stroke
3.1 Lacunar stroke syndromes
3.1.1 Pure motor hemiparesis
3.1.2 Pure sensory stroke
3.1.3 Sensorimotor stroke
3.1.4 Ataxic hemiparesis
3.1.5 Dysarthria-clumsy hand syndrome
3.2 Large vessel stroke syndromes
3.2.1 Anterior circulation strokes
3.2.1.1 Middle cerebral artery stroke
3.2.1.2 Anterior cerebral artery stroke
3.2.2 Posterior circulation strokes
3.2.2.1 Basilar artery stroke
3.2.2.2 Posterior cerebral artery stroke
3.3 Stroke syndromes—medium size vessels
3.3.1 Anterior choroidal artery stroke
3.3.2 Superior cerebellar artery stroke
3.3.3 Anterior inferior cerebellar artery stroke
3.3.4 Posterior inferior cerebellar artery stroke
3.3.5 Anterior spinal artery stroke
3.4 Embolic stroke
4. Hemorrhagic stroke
5. Clinical cases
Case 1.1 Transient ischemic attack
Case 1.2 MCA stroke
Case 1.3 Top of the basilar artery stroke
References
16
1 INTRODUCTION
Stroke remains the single leading cause of long-term care disability in the United States and the fifth leading
cause of death, killing nearly 133,000 people a year.1 The goal for neurological evaluation in the Emergency
Department (ED) is to appropriately route potential acute ischemic or hemorrhagic stroke patients toward
medical intervention in the most expedient manner possible. Emergency medical services are the primary
access point for stroke evaluations, with providers performing the initial diagnostic workup and care. Patients
aged 75 and over had the highest rate of emergency room visits from 2001 to 2011 for stroke and transient
ischemic attacks (TIAs), with nearly a 10% increase in admissions/transfer from EDs in that time.2
Even before radiographic scans, quick and thorough neurological evaluations can establish the likelihood of
acute stroke syndromes and mobilize providers toward appropriate therapies. This chapter focuses on
familiarizing the reader with stroke subtypes and clinical manifestations associated with specific syndromes.
This information can assist in rapid identification of common stroke presentations.
2 CLASSIFICATION
Acute neurologic episodes being evaluated in the emergent setting for stroke workup can be divided into
broad categories based on duration of symptoms and findings from basic imaging. Box 1.1 and Figure 1.1
describe the common types of cerebral infrarctions that are freqeuntly encountered in an acute setting.
Box 1.1
TYPES OF CEREBRAL INFARCTIONS BASED ON CLINICAL AND RADIOGRAPHIC CHARACTERISTICS
Ischemic stroke
• Imaging or pathological evidence of cerebral, retinal, or spinal cord focal ischemic injury in a defined
vascular distribution
• OR focal ischemic injury based on symptoms lasting ≥24 hours
Silent infarction
• Imaging (such as MRI or CT) or pathological evidence of CNS infarction without a corresponding
clinical deficit
TIA
• Transient episode of neurological dysfunction
• AND no acute infarction on brain, retinal, or spinal cord imaging
ICH
• A focal collection of blood within the brain parenchyma
Intraventricular hemorrhage
• A type of intarcerebral hemorrhage with blood present in the ventricular system
Subarachnoid hemorrhage
• Focal or diffuse collection of blood within the subarachnoid space
17
Subdural and epidural hematomas
• Bleeding external to the brain and subarachnoid space. Mostly as a result of trauma but can be
spontaneous.
• Are not considered strokes by the 2013 American Heart Association statement, given the differences
in mechanisms and pathology
Cerebral venous thrombosis

• Ischemic infarction and/or hemorrhage caused by thrombosis of draining veins and venous sinuses
Adapted from the 2013 Statement for Healthcare Professionals from the American Heart Association4
Figure 1.1 Types of cerebral infarctions based on clinical and radiographic characteristics.
SOURCE: Adapted from the 2013 Statement for Healthcare Professionals from the American Heart Association.
Question 1.1: How often does magnetic resonance imaging (MRI) detect acute stroke in patients with
transient episodes of neurologic dysfunction?
Answer: It is critical that all patients with suspected TIAs receive a brain MRI. Research shows that
between 9% and 67% of patients fitting the clinical definition of TIAs have evidence of acute stroke on
MRI.
2.1 Transient ischemic attack

TIAs are episodes of focal neurologic dysfunction caused by disruption in cerebral blood flow without
complete obstruction. TIAs present with the same symptoms associated with stroke, such as acute onset
hemibody weakness or numbness, aphasia (inability to speak), dysarthria (slurred speech), and visual deficits
that correspond to specific vascular regions. However, these events do not lead to permanent neuronal cell
damage seen on radiographic imaging and typically last less than one hour.3
In the past, before the widespread use of MRI, TIAs used to be defined as neurologic events lasting less
than 24 hours. The 24-hour mark was chosen arbitrarily, and studies subsequently proved that many of these
18
patients would have evidence of acute ischemia detected with MRI imaging. The modern definition of a TIA
therefore includes both clinical and radiographic criteria. A TIA is a transient episode of neurological
dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction (Case 1.1).4,5
TIAs secondary to periods of interrupted blood flow do not cause persistent clinical impairment but are
considered to be events that increase long-term stroke risk and, as such, require thorough evaluation. These
episodes contribute to between 200,000 and 500,000 neurologic evaluations in the United States yearly in the
ED and outpatient setting.6 There are various potential underlying causes for transient flow reductions,
including atherosclerosis of intra- or extra-cranial arteries, cardioembolic sources, inflammation of the arteries,
sympathomimetic drugs, or hypercoaguable conditions.
As TIA symptoms often resolve prior to physician evaluation, the goals of assessment are to uncover any
subtle, persistent neurological deficits and risk stratify for future ischemic events. Adequate history and review
of previous medical records is vital, as alternate diagnoses, including focal seizures, arrythmia, or migraine
headaches, can often be mistaken for TIAs. Initial diagnostic evaluation can be achieved by obtaining basic
vital signs, including blood pressure, heart rate and rhythm evaluation, laboratory workup, and imaging in the
ED. Hypoglycemia, blood pressure abnormalities, electrolyte derangements, and cardiac and vestibular
etiologies are all non-neurologic sources of transient mentation changes that can quickly be elucidated by
providers.
Once the likelihood of transient ischemia has been determined, further assessment can assist with
estimation of short-term stroke risk. The ABCD2 score, first introduced in 2007, has aided medical providers
with a numerical scale to assess benefits of hosptialization and further diagnostic workup. Originally
developed for outpatient evaluation of TIA, it has since been shown that as the ABCD2 score increases, the
risk of subsequent stroke also increases across multiple settings.7,8 The score is based on various stroke risk
factors including age, blood pressure values, clinical featues, duration, and pre-existing diabetes. It is used to
gauge the risk of stroke within 2, 7, 30, and 90 days after a TIA and has become a mainstay of ED evaluations
(Box 1.2).9
Box 1.2
ABCD2 SCORE TO PREDICT STROKE RISK AFTER A TRANSIENT ISCHEMIC ATTACK EPISODE AND ITS
RECOMMENDED INTERPRETATION BY THE AMERICAN HEART ASSOCIATION
ABCD2 score calculation (0–7 points)

• Age ≥ 60 years = 1 point
• Blood pressure ≥140/90 mm Hg on first evaluation = 1 point
• Symptoms of focal weakness or speech impairment lasting ≥ 60 minutes = 2 points OR
• Symptoms of focal weakness or speech impairment lasting 10–59 minutes = 1 point
• Diabetes mellitus = 1 point
The 2-day risk of stroke

• 0% for score of 0 or 1
• 1.3% for score 2 or 3,
19
• 4.1% for score 4 or 5
• 8.1% for score 6 or 7
Patients with a recent (within 72 hours of symptoms occurrence) TIA should be hospitalized when
• Total score ≥3
• OR total score is 0–2 but unable to compete diagnostic workup within 2 days
Adapted from the 2009 Statement for Healthcare Professionals from the American Heart Association on evaluation of TIAs5
For patients deemed low risk via the ABCD2 criteria (score 0–3), an outpatient workup including further
vascular imaging, antithrombotic therapy, cardiac event monitoring, and statin therapy may be most
appropriate; the details of such further management are discussed in subsequent chapters. For patients
considered high risk (ABCD2 score >3), hospital admission may be advisable to expedite such interventions.
2.2 Stroke
Stroke, in comparison to TIAs, is an acute, persistent neurological deficit with associated central nervous
system (CNS) injury from interrupted blood supply. Brain injury associated with vascular deficiencies is often
focal and localizes to specific cerebral regions, producing characteristic clinical deficits. Similar to TIAs, acute
stroke can present with acute weakness, numbness, and verbal or visual deficits; however, the impairment does
not resolve and is usually present at the time of assessment by medical providers. Physiologically, neuronal
tissue undergoes irreversible damage and death in the absence of oxygen, with the average patient losing
approximately 120 million neurons each hour (equivalent to 3.6 years of normal aging).10
Nearly 800,000 people in the United States suffer strokes yearly, with three-fourths of these events being
first-time occurrences. The majority of these represent ischemic strokes, which occur in the absence of blood
flow to the cerebral tissue, and account for 85% of all strokes. Hemorrhagic strokes, caused by arterial leakage
into brain parenchyma, comprise the remaining 15%.
Further clinical differentiation can be made into cortical versus subcortical infarcts, which broadly specify
the location of the infarcted territory. As their name implies, cortical strokes affect regions of the cerebral
cortex such as the frontal, parietal, temporal, and occipital lobes. Cortical strokes may disrupt higher cognitive
functioning, producing symptoms like aphasia (the inability to produce or express language), alexia (inability
to read), agraphia (inability to write), and hemibody neglect. Subcortical strokes, by comparison, affect regions
below the cortex, such as the internal capsule, thalamus, basal ganglia, brainstem, and cerebellum. Subcortical
strokes do not classically affect higher cognitive functioning. While all subtypes of acute stroke are associated
with permanent neuronal damage, the etiology and management vary significantly with respect to
thrombolytic use, supportive parameters, medication recommendations, and need for neurosurgical
evaluations.
3 ISCHEMIC STROKE
Ischemic stroke results from obstruction within a blood vessel, prohibiting flow to a portion of the CNS. This
originates from atherosclerotic plaque buildup within the arteries, blood clot (thrombus) formed at the site of
occlusion, or an embolism that travels from another portion of the circulatory system to distally occlude
20
cerebral vasculature. Small vessel, or lacunar strokes, are the most common type of ischemic stroke; they can
occur from closing off small arteries that supply deep brain structures including the internal capsule, basal
ganglia, thalamus, and paramedian regions of the brain.11 These are often considered the end-organ effects of
systemic hypertension and atheromatous disease. Artery-to-artery embolism refers to infarcts that arise from
atherosclerotic lesions in proximal arteries that fragment and travel to distal vessels, occluding them. Large
artery thrombosis often occurs as atherosclerotic plaque builds up to create progressive stenosis, with final
artery occlusion resulting from thrombosis of the narrowed lumen. Embolic material can originate from a
variety of sources, including mural thrombi/platelet aggregates from extracranial vasculature, cardiac
thrombus, or less frequently, calcific plaques and fat embolism.12,13 Determining the source of embolic
material often requires multiple vascular imaging modalities; however, despite extensive evaluation and the use
of various techniques (discussed in future chapters), the sources of 17% of all presumed embolic strokes have
not been identified.14
Question 1.2: Are lacunar strokes common?
Answer: Lacunar infarcts are common, accounting for 25–40% of all ischemic strokes. Some studies
indicate that lacunar stroke is the most common type of ischemic stroke in general population.
3.1 Lacunar stroke syndromes

Lacunar strokes are considered small (≤15 mm in diameter) subcortical strokes associated with the occlusion
of a penetrating branch of one artery.11 These strokes are thought to occur from small vessel disease, likely
related to end-organ effects of systemic hypertension, lipohylanosis, or microatheromas.15 Uncontrolled
stroke-associated risk factors, such as aging, hypertension, diabetes, hyperlipidemia, and smoking, are
considered the most significant factors for the development of lacunar infarcts. They are estimated to
represent 15–25% of all ischemic strokes in the United States. Ischemic stroke outcomes are variable
depending on size, co-morbidities, and interventions available. Lacunar stroke outcomes are better than for
other stroke subtypes, with 96% having a 30-day survival rate and 70–80% of patients having functional
independence at one year.16 Over 20 lacunar syndromes have been described, including the classic 5 lacunar
syndromes first established by Dr. Charles Miller Fisher in the 1960s, which continue to be used today.
Detailed in the following discussion, they have been validated for predictive value between physical
examination findings and radiographic stroke correlation.17
3.1.1 PURE MOTOR HEMIPARESIS
Pure motor stroke is the most common lacunar syndrome, comprising 45–57% of lacunar syndromes.18 This
syndrome primarily affects the posterior limb of the internal capsule, which carries descending corticospinal
and corticobulbar tracts, thus interrupting descending motor relay signals. Lesions can also be seen in the
pons. Clinically, the patient presents with hemiparesis (weakness) or hemiplegia (paralysis) of the face, arm,
and leg contralateral to the infarcted region; it is not typically associated with sensory, vocal, or visual deficits.
3.1.2 PURE SENSORY STROKE
Pure sensory stroke is estimated to encompass 7–18% of lacunar strokes19 and most consistently localizes to
21
the ventral posterolateral nucleus of the thalamus. This stroke presents as a contralateral numbness of the face,
arm, and leg and in the absence of motor, verbal, or visual deficits. The sensory loss associated with this
syndrome is usually noted to cease at the midline, which is characteristic of lesions to the thalamus.
3.1.3 SENSORIMOTOR STROKE
This lacunar syndrome is an infarct that affects both thalamus and the adjacent portion of the internal
capsule’s posterior limb, effectively causing both sensory and motor symptoms. Patients with this pattern
describe contralateral hemibody weakness and sensory impairment of the face, arm, and leg.
3.1.4 ATAXIC HEMIPARESIS
Ataxic hemiparesis, the second most frequent lacunar stroke, has been shown to have a 95% positive predictive
value for corresponding radiologic lesions.16 This syndrome results from damage to the corticospinal and
cerebellar pathways by infarction of the pons or internal capsule. Ataxic hemiparesis features both cerebellar
and motor symptoms, including weakness and clumsiness on the ipsilateral side of the body, with the lower
extremities typically more involved than the upper extremities. A combination of pyramidal signs
(hemiparesis, hyperreflexia, Babinski sign) and cerebellar ataxia may be present on the affected side.
3.1.5 DYSARTHRIA-CLUMSY HAND SYNDROME
Dysarthria-clumsy hand syndrome is the least common of all lacunar syndromes, accounting for 2–6% of
lacunar strokes in a case series review.17 It is sometimes considered a variant of ataxic hemiparesis, as it also
involves infarction of the pons or internal capsule. However, this syndrome differs in its characteristic
dysarthria and contralateral hand weakness, which is often best provoked by testing the patient’s handwriting.
With a pontine lesion, facial, and tongue weakness may also be seen.
Question 1.3: What is the most common occlusion site in large vessel occlusion strokes?
Answer: Proximal (M1 segment) middle cerebral artery (MCA).
3.2 Large vessel stroke syndromes

In contrast to small lacunar infarctions, thrombosis of higher diameter vessels can produce infarct in large
arteries supplying significant neuronal tissue. As previously described, thrombotic ischemic events are
associated with elevated blood pressure, hyperlipidemia, diabetes, tobacco use, and age. Progressive
atherosclerosis acts to impede blood flow to cerebral vascular territories, with thrombosis ultimately
terminating blood supply to distal cerebral structures. Large vessel thrombotic disease can encompass
extracranial (common carotid and internal carotid arteries), posterior cerebral circulation (vertebral arteries),
and intracranial artery (Circle of Willis and its more proximal divisions) territories. Figures 1.2 and 1.3
illustrate the normal cranial and cervical anatomy of major arteries supplying the brain. As stenosis impedes
blood flow, fragments from these obstructed arteries can break off as emboli to travel distally; like embolic
strokes from elsewhere in the circulatory system, stroke occurs as the emboli reach arteries too small to
transverse. While atherosclerosis is the most common cause of thrombotic ischemic strokes, other pathologies
affecting these vessels, including dissection, arteritis, fibromuscular dysplasia, and vasculopathies, can similarly
produce infarction.19
22
Figure 1.2 Intracranial arterial circulation.
(A) Axial and (B) coronal views of the MR angiography of the head showing normal vascular anatomy.
ABBREVIATIONS: ACA, anterior cerebral artery; BA, basilar artery, ICA, internal carotid artery; MCA, middle cerebral artery; PCA, posterior
cerebral artery; VA, vertebral artery.
Figure 1.3 Cervical arterial circulation.

(A) Coronal and (B) oblique lateral views of the magnetic resonance angiography of the neck showing normal vascular anatomy.
ABBREVIATIONS: CCA, common carotid artery; ICA, internal carotid artery; SA, subclavian artery; VA, vertebral artery.
Acute ischemic strokes affecting large arteries produce characteristic neurologic deficits based on the area of
neuronal tissue impacted. Once familiarized with the clinical characteristics of large vessel occlusion
syndromes, a clinical provider can easily and reliably localize the likely area of at risk neuronal tissue prior to
radiographic findings. In scenarios when imaging availability is limited or delayed, such knowledge can assist
in rapidly mobilizing medical and surgical interventions.
3.2.1 ANTERIOR CIRCULATION STROKES
23
The blood supply comprising the anterior portion of the cerebral hemispheres is derived from the common
carotid arteries, which further divides into internal and external division at the level of the fourth cervical
vertebra. The internal carotid divisions travel into the cranium to supply the brain, while the external carotid
branches travel superficially to supply the neck and face. Within the skull, the left and right internal carotid
arteries further divide into corresponding cerebral branches, comprised of left and right anterior cerebral and
middle cerebral arteries. These arteries supply large areas of eloquent tissue over the frontal, parietal, and
temporal lobes.
3.2.1.1 Middle cerebral artery stroke
Acute occlusion of the internal carotid and left MCA produces characteristic clinical deficits, with the MCA
being the artery most often occluded in stroke.20 The MCAs are the primary blood supply for the motor and
sensory cortices involving the head, neck, trunk, and arm; the basal ganglia; and the anterior portion of the
internal capsule. In over 90% of the population, the left cerebral hemisphere is also the dominant hemisphere
conferring language comprehension and fluency.21
The MCA then further bifurcates into two main branches: the superior and inferior divisions. Often, the
MCA is classified into four segments based on nearby anatomic landmarks.22 The sphenoidal segment (M1)
is the origin of the MCA to the bifurcation. The second M2 segment, also known as the insular segment,
encompasses the bifurcation to the insula. The more distal M3 segment (opercular branches) lay within the
Sylvian fissure, and the M4 region describes the branches over the outer convexity of the brain. Infarction to
any branch of the MCA can produce clinically evident stroke syndromes.
A large stroke affecting the main trunk of the MCA prior to its bifurcation will produce contralateral
hemiplegia, deviation of the head and eyes toward the side of the infarct, contralateral sensory loss, and
hemianopia (partial visual loss secondary to visual radiation tract involvement) (Case 1.2).23 In addition, if the
stroke is located in the dominant hemisphere, global aphasia will also occur as speech and language centers
become impaired. In the non-dominant hemisphere, neglect and impaired awareness of the stroke is expected.
When the infarct is large with significant brain tissue involvement, there is risk for decline and herniation
secondary to development of cytotoxic edema in the region, known as malignant infarction.24 Malignant
infarctions usually require an escalation in acute management, either with medical or neurosurgical
management.
MCA strokes distal to the superior/inferior branch bifurcation will produce symptoms similar to those of a
complete artery occlusion, though likely less severe. A superior division MCA occlusion in the dominant
hemisphere will produce weakness and sensory deficits to the contralateral hemibody and is likely to produce
expressive (Broca’s) aphasia.25,26 This type of aphasia, which occurs with damage to the inferior frontal gyrus,
affects the ability to speak fluently but spares comprehension. In a non-dominant stroke to the superior
division, weakness and sensory loss may be present with some degree of visual/spatial neglect; language is not
usually impaired.27
An inferior division MCA stroke often spares the motor and sensory regions but does involve verbal and
visual areas. In a left dominant hemisphere stroke of the inferior MCA, the primary examination findings may
be contralateral homonymous hemianopia (visual field loss on the right side of the vertical midline) and
receptive (Wernicke’s) aphasia.23,24
24
3.2.1.2 Anterior cerebral artery stroke
The anterior cerebral artery (ACA) occlusion represents between 0.6% and 3% of all ischemic strokes.28,29
The ACA extends upwards from the internal carotid artery and supplies the frontal lobes, the parts of the
brain that control personality, logical thought, and lower extremity movement. Stroke within the ACA
territory produces ischemia within the paracentral lobule, usually resulting in sensory loss and weakness in the
contralateral leg. Weakness is usually greater in the distal lower extremity than proximally. Lesions within the
ACA can also produce symptoms of anomia (the inability to recall the names of everyday objects), agraphia
(the inability to write), and abulia (lack of will or initiative), as well as emotional and personality changes.
3.2.2 POSTERIOR CIRCULATION STROKES
The vertebral arteries originate from the subclavian arteries and travel upward. Inside the skull, the two
vertebral arteries join at the junction between the medulla oblongata and pons to form the basilar artery. The
basilar artery contributes to the main blood supply for the brainstem. Several accompanying arteries branch off
the basilar artery, including the posterior cerebral arteries, superior cerebellar arteries, and anterior inferior
cerebellar arteries, as well as multiple minor paramedian perforating arteries. Strokes involving the posterior
circulation account for approximately 20% of all ischemic strokes.30
3.2.2.1 Basilar artery stroke
Acute occlusion of the basilar artery has dramatic effects on circulation to the brainstem. They account for 1–
4% of all ischemic strokes but are associated with a mortality rate of greater than 85% without intervention.31
The most common presenting symptoms association with this stroke type is often imprecise on initial
evaluation. Prodromal symptoms include nausea, vomiting, headache, and neck pain. If occlusion is located in
the mid-basilar region, patients may progress to locked-in syndrome, where bilateral ventral pontine ischemia
produces full body paralysis, lateral gaze weakness, and aphasia; however, these individuals remain cognitively
intact and vertical eye and blink movements are preserved. Occlusion of the distal tip of the basilar artery
results in top of the basilar syndrome, causing ischemia of the midbrain, thalami, inferior temporal lobes, and
occipital lobes (Case 1.3). This can result in decreased alertness, loss of voluntary vertical eye movements,
upper eyelid retraction, delayed or absent pupillary reaction to light, or visual hallucinations. In contrast to
other syndromes, sensory and motor abnormalities are often absent. Most occlusions of the rostral brainstem
are associated with embolic phenomenon and require urgent neurological and neurosurgical evaluation and
treatment, given the poor prognosis associated with infarcts in this region.
3.2.2.2 Posterior cerebral artery stroke
Common symptoms of a posterior cerebral artery stroke include dizziness, imbalance, visual deficits
(contralateral hemianopia with macular sparing), nausea, and sensory loss affecting the contralateral face and
limb. Weakness may be variably present, as the posterior aspect of the internal capsule receives some blood
supply from the proximal portions of the posterior cerebral artery.
3.3 Stroke syndromes—medium size vessels
25
3.3.1 ANTERIOR CHOROIDAL ARTERY STROKE
The anterior choroidal artery originates from the internal carotid artery and travels intracranially to supply
portions of the optic tract, thalamus, midbrain, and internal capsule. This rather small-size vessel can
nevertheless result in a number of neurological deficits. Infarction of the anterior choroidal artery can produce
hemiplegia, sensory deficits of the contralateral body, and homonymous heminanopsia as a result of internal
capsule, thalamus, and optic tract impairment. Symptoms are often variable given the presence of adjacent
blood supply from lenticulostriate arteries of the MCA.32
3.3.2 SUPERIOR CEREBELLAR ARTERY STROKE
The superior cerebellar artery, derived as a branch of the basilar artery, travels posteriorly around the cerebellar
peduncle to the surface of the cerebellum, thereby supplying part of the midbrain, cerebellar vermis, and the
superior half of the cerebellum. While stroke affecting the cerebellum accounts for less than 2% of all acute
ischemic infarcts, nearly half of them involve the superior cerebellar artery.33 Symptoms associated with
cerebellar infarcts are often vague, presenting as poorly defined headache, dizziness, nausea, and vomiting.
Signs localizing to the midbrain such as dysarthria, nystagmus, and Horner’s syndrome or to the cerebellum
(ipsilateral ataxia, intention tremor) may be of diagnostic assistance.
3.3.3 ANTERIOR INFERIOR CEREBELLAR ARTERY STROKE
The anterior inferior cerebellar arteries travel from their origins in the basilar artery posteriorly to the
cerebellum, where it supplies the anterior inferior surface of the cerebellum, the middle cerebellar peduncle,
and lateral pons. Stroke in this region is somewhat uncommon given anastomoses among the superior
cerebellar arteries and posterior inferior cerebellar arteries.34 When it does occur, multiple nuclei and tracts are
affected, producing lateral pontine syndrome (Marie-Foix Syndrome). Symptoms associated with this
includes contralateral loss of pain and temperature from the trunk and extremities from spinothalamic tract
involvement, contralateral weakness of the upper and lower extremities from corticospinal tract involvement,
ipsilateral paralysis of the face secondary to facial nucleus and nerve involvement, and ipsilateral cerebellar
ataxia from affected cerebellar peduncles. Descending sympathetic tracts may also be subject to ischemia and
result in ipsilateral Horner’s syndrome.
3.3.4 POSTERIOR INFERIOR CEREBELLAR ARTERY STROKE
The posterior inferior cerebellar artery is the largest branch of each vertebral artery prior to their confluence to
form the basilar artery. This artery travels past the medulla oblongata, over the cerebellar peduncle to the
inferior surface of the cerebellum. Occlusion of the posterior inferior cerebellar artery results in a well
described syndrome known as Wallenberg syndrome (lateral medullary syndrome). This syndrome classically
produces crossed sensory findings of loss of pain and temperature sensation on the contralateral side of the
body and ipsilateral side of the face. Multiple cranial nuclei reside in this region and contribute to the other
symptomatic findings of this infarction, including gait dysphasia, nystagmus, vertigo, ataxia, and ipsilateral
Horner’s syndrome (ptosis, miosis, and anihdrosis).
3.3.5 ANTERIOR SPINAL ARTERY STROKE
Infarction of the anterior spinal artery, which branches from each vertebral artery and joins at the level of the
26
medulla oblongata, can result in Dejerine syndrome (medial medullary syndrome). Though extremely
infrequent, less than 1% of all vertebrobasilar strokes, it is easily identified with classical clinical characteristics.
The presentation usually consists of deviation of the tongue toward the side of the lesion secondary to
hypoglossal nerve involvement, contralateral hemiparesis or hemiplegia, and contralateral sensory loss.
3.4 Embolic stroke

Acute ischemia from embolic sources can cause any of the previously mentioned stroke syndromes or a
combination of neurological symptoms if emboli travel to multiple vascular territories. Of emboli to the brain,
approximately 80% involve the anterior circulation, with the remaining 20% involving the posterior cerebral
blood supply.
Cardiogenic embolism accounts for approximately 20% of ischemic strokes in the United States, and nearly
50% of those are related to non-valvular atrial fibrillation.35,36 Other cardiac sources of emboli include
ventricular thrombus, prosthetic valves, acute myocardial infarction, rheumatic heart disease, cardiac tumors,
and paradoxical emboli via atrial septal defects such as patent foramen ovale. Atrial fibrillation is present in
approximately 1% of the US population and increases in prevalence with age. This arrhythmia is associated
with a fivefold increased risk of stroke and often requires extended cardiac workup and electrocardiogram
monitoring to uncover.
4 HEMORRHAGIC STROKE
Here we focus our description mainly on intracerebral hemorrhage (ICH), which results from vascular rupture
and bleeding directly into brain parenchyma, with possible extension into the ventricles (known as
intraventricular extension). Subarachnoid hemorrhage is discussed in the chapters on medical and surgical
management of hemorrhagic stroke. Cerebral venous thrombosis shares some features of both ischemic and
hemorrhagic stroke. However, given its unique mechanisms and course, cerebral venous thrombosis is a
separate category and is reviewed in a separate chapter.
While less frequent than ischemic stroke, ICH encompasses between 10–15%41 of all strokes, comprising
approximately 40,000 to 67,000 cases each year in the United States. The extent of appreciable neurological
dysfunction is dependent on several factors, including size and location of the bleed, degree of edema in the
surrounding tissue, and compression of surrounding intracranial structures.
The most important risk factor for the development of ICH is hypertension. African Americans, who have
a higher frequency of hypertension, have in tandem been noted to have a higher frequency of ICH.37
Incidence has also been noted to be higher in Asian and Hispanic populations.38,39 Other risk factors that
have been correlated, in varying degrees, with ICH include increasing age, sympathomimetic drug use
(cocaine, amphetamines), and high alcohol use. While hypertensive vasculopathy persists as a principal cause
of non-traumatic hemorrhages, other etiologies include cerebral amyloid angiopathy, vascular malformations
such as arteriovenous malformations and aneurysms, venous sinus thrombosis, vasculitis, coagulopathy, use of
anticoagulation medications, and cerebral tumors.
Clinical presentation of ICH is variable but often occurs as an acutely progressive alteration in
consciousness, nausea, vomiting, and headache; seizures occur in approximately 6–7% of presenting scenarios.
27
Hemorrhage into a specific cerebral region will likely cause dysfunction of that eloquent tissue and may
present as aphasia, hemiplegia, vertigo, diplopia (double vision), or sensory deficits. Hypertension-related
ICH occurs predominately in the basal ganglia, thalamus, pons, and cerebellum, whereas hemorrhage
associated with cerebral amyloid angiopathy or cerebral arteriovenous malformations typically appears in a
lobar distribution. Large intracranial bleeds may be evident with patients who are comatose at initial
presentation, along with markedly high blood pressures >220/170 mm Hg. Rapid computerized tomography
(CT) scan and vascular imaging aides significantly in the detection and treatment of these patients, with
radiographic variations discussed in the chapter on imaging of acute stroke.
Mortality associated with ICH is significant, with a review from 30 centers reporting a 34% mortality rate
at 3 months.40 Other reviews reported mortality rates of 31% at 7 days, 59% at 1 year, 82% at 10 years, and
more than 90% at 16 years.41,42 To aide in prognostic assessment, an ICH score calculation was developed by
JC Hemphill et al. in 2001; it is still an efficient computational tool for all providers. The components of the
ICH score are derived from the patient’s age, presenting Glasgow Coma Scale, the degree of ICH volume,
the presence of intraventricular hemorrhage, and the location of the hemorrhage (infratentorial vs.
supratentorial). The corresponding ICH score for these values (between 0–6 points) provides mortality risk at
30 days.
Early assessment and management of intracranial hemorrhage focuses on maintaining hemodynamic
stability, airway protection, and correction of any underlying coagulopathy. These patients invariably require
intensive care monitoring and often neurosurgical evaluation in the acute phase, given the risk of progression
of bleeding, swelling, or herniation syndromes that could necessitate urgent surgical intervention. Diligent
correction of fever, hyperglycemia, treatment of seizures with antiepileptic medications, maintenance of
systolic blood pressure <18043 and frequent neurological examinations are vital to the management of ICH in
the first few days.
5 CLINICAL CASES
CASE 1.1 Transient ischemic attack

CASE DESCRIPTION
A patient in her 70s with past medical history significant for coronary artery disease and diabetes presented to
the ED with a transient episode of word-finding difficulty early in the day, which resolved spontaneously after
30 minutes. The patient’s family witnessed the episode and stated that the patient could only answer simple
questions with “yes” or “no” answers, but was able to understand most commands. Blood pressure in the ED
was 172/95 mm Hg. The patient’s neurologic exam, upon evaluation by the emergency room physician, was
unremarkable. MRI brain showed no evidence of acute infarction (Figure 1.4).
28
Figure 1.4 Case of a transient ischemic attack. Magnetic resonance imaging brain shows no acute ischemia on the diffusion weighted image
sequence, supporting the diagnosis of transient ischemic attack.
(A) Cortical and (B) subcortical regions are shown. The anterior cerebral artery (ACA), middle cerebral artery (MCA), and posterior cerebral
artery (PCA) territories are separated by the dotted white lines.
PRACTICAL POINTS
• This patient’s history and presentation are highly suspicious for an episode of TIA. The deficit is best
characterized as expressive or Broca’s aphasia. Alternative diagnosis, such as complex migraine or a focal
seizure, is less likely.
• “Negative” MRI brain imaging helps confirm the diagnosis of a TIA, and the ABCD2 score can guide
the emergency room physician about whether an inpatient admission is indicated. Some hospitals have
designated TIA observation units where the minimum required diagnostic TIA workup (such as
telemetry, carotid ultrasound, and cardiac echocardiogram) can all be completed within 24 to 48 hours.
CASE 1.2 MCA stroke

CASE DESCRIPTION
A patient was brought to the hospital by the paramedics after a 911 call made by a bystander who witnessed
the patient collapsing at the mall. The patient was noted to have deviation of the head and eyes to the right,
left-sided hemiplegia (paralysis), and sensory loss. Blood pressure on arrival was 221/112 mm Hg.
PRACTICAL POINTS
• Emergent imaging is required to differentiate between ischemic versus hemorrhagic stroke. This
patient’s exam fits the description of the right hemispheric syndrome. If intracranial hemorrhage is ruled
out, additional imaging is needed to determine if large vessel occlusion is responsible for this patient’s
neurologic deficits (such as of the proximal right MCA; Figure 1.5).
29
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OCTOBER 1946, VOLUME 15 ***
TRIAL
OF
THE MAJOR WAR CRIMINALS

BEFORE
THE INTERNATIONAL
MILITARY TRIBUNAL
NUREMBERG
14 NOVEMBER 1945—1 OCTOBER 1946
P U B L I S H E D AT N U R E M B E R G , G E R M A N Y
1948
This volume is published in accordance with the
direction of the International Military Tribunal by
the Secretariat of the Tribunal, under the jurisdiction
of the Allied Control Authority for Germany.
VOLUME XV
OFFICIAL TEXT
IN THE
ENGLISH LANGUAGE
PROCEEDINGS
29 May 1946-10 June 1946

CONTENTS
One Hundred and Forty-first Day, Wednesday, 29 May 1946,

Morning Session 1
Afternoon Session 36
One Hundred and Forty-second Day, Thursday, 30 May 1946,

Morning Session 63
One Hundred and Forty-third Day, Friday, 31 May 1946,

Morning Session 132
One Hundred and Forty-fourth Day, Saturday, 1 June 1946,

Morning Session 212
One Hundred and Forty-fifth Day, Monday, 3 June 1946,

Morning Session 253
One Hundred and Forty-sixth Day, Tuesday, 4 June 1946,

Morning Session 311
One Hundred and Forty-seventh Day, Wednesday, 5 June 1946,

Morning Session 370
One Hundred and Forty-eighth Day, Thursday, 6 June 1946,

Morning Session 435
One Hundred and Forty-ninth Day, Friday, 7 June 1946,

Morning Session 512
One Hundred and Fiftieth Day, Saturday, 8 June 1946,
Morning Session 574
One Hundred and Fifty-first Day, Monday, 10 June 1946,

Morning Session 610
ONE HUNDRED AND FORTY-FIRST DAY
Wednesday, 29 May 1946
Morning Session
THE PRESIDENT (Lord Justice Sir Geoffrey Lawrence): The
Tribunal will adjourn this afternoon at 4 o’clock in order to sit in
closed session.
MR. THOMAS J. DODD (Executive Trial Counsel for the United
States): Mr. President, the day before yesterday the Tribunal asked if
we would ascertain whether or not Document Number D-880 had
been offered in evidence. It consists of extracts from the testimony of
Admiral Raeder, and we have ascertained that it was offered, and it
is Exhibit Number GB-483. It was put to a witness by Mr. Elwyn
Jones in the course of cross-examination, and it has been offered in
evidence.
THE PRESIDENT: Thank you.
MR. DODD: Also, with respect to the Court’s inquiry concerning
the status of other defendants and their documents, we are able to
say this morning that with respect to the Defendant Jodl the
documents are now being translated and mimeographed, and there
is no need for any hearing before the Tribunal.
The Seyss-Inquart documents have been heard and are now
being translated and mimeographed.
The Von Papen documents are settled; there is no
disagreement between the Prosecution and the Defendant Von
Papen, and they are in the process of being mimeographed and
translated.
With respect to the Defendant Speer, we think there will be no
need for any hearing, and I expect that by the end of today they will
be sent to the translating and mimeographing departments.
The documents for the Defendant Von Neurath have not yet
been submitted by the defendant to the Prosecution.
And with respect to the Defendant Fritzsche, our Russian
colleagues will be in a position to advise us more exactly in the
course of the day. I expect that I shall be able to advise the Tribunal
as to the Defendant Fritzsche before the session ends today.
THE PRESIDENT: Does that conclude all questions of
witnesses?
MR. DODD: Yes, I believe—at least, we have no objection to
any of the witnesses.
THE PRESIDENT: Very well, then; there need not be any further
hearing in open court on the cases of the Defendants Jodl, Seyss-
Inquart, Von Papen, and Speer until their actual cases are
presented.
MR. DODD: Yes, Sir.
THE PRESIDENT: Thank you.
DR. ROBERT SERVATIUS (Counsel for the Defendant
Sauckel): Mr. President, I have a technical question to bring up.
Yesterday the witness Hildebrandt arrived, but again it was the
wrong Hildebrandt. This is the third witness who has appeared here
in this comedy of errors. It was the wrong one for Mende, the wrong
one for Stothfang, and the wrong one for Hildebrandt. But this
witness knows where the right ones are.
The witnesses had received information in their camp that they
were to appear here and they were then taken to the collecting
center for Ministerial Directors in Berlin-Lichterfelde. Perhaps it will
still be possible to bring these two witnesses here. Especially the
witness Hildebrandt, who can testify about the French matters, would
be of importance if we could still get him.
THE PRESIDENT: Was the name given accurately to the
General Secretary?
DR. SERVATIUS: The name was given accurately. The other
man’s name was also Hildebrandt, only not Hubert but Heinrich. He
was also a Ministerial Director...
THE PRESIDENT: I do not mean only the surname but all his
Christian names.
DR. SERVATIUS: Yes, one name was Heinrich and the other
Hubert, and abbreviated it was “H” for both, Dr. H. Hildebrandt, which
apparently caused the confusion.
THE PRESIDENT: Well, I say the names of all witnesses had
better be given in full; really in full, not merely with initials.
DR. SERVATIUS: I had given the name in full. As to the
physician, the Witness Dr. Jäger, I received his private address this
morning. He is not under arrest. He was at first a witness for the
Prosecution. His private address is in Essen, in the Viehhof Platz,
and he is there now.
THE PRESIDENT: I think you had better take up all these details
with the General Secretary, and he will give you every assistance.
DR. SERVATIUS: Concerning the case of Sauckel, I should like
to make one more remark to the Tribunal.
There are about 150 documents which have been submitted by
the Prosecution, and some of them are only remotely connected with
Sauckel. No trial brief and no special charges were presented here
orally against Sauckel, so that I cannot see in detail to what extent
Sauckel is held responsible. The case was dealt with only under the
heading of “Slave Labor,” and so the ground of the defense is
somewhat unsteady.
I do not intend to discuss every one of these 150 documents,
but I should like to reserve the right to deal with some of them later if
that should appear necessary. I want to point out only the most
important ones, and then return to them in the course of the
proceedings. At any rate, may I ask you not to construe it as an
admission if I do not raise objections against any of these documents
now.
THE PRESIDENT: No admission will be inferred from that. Dr.
Servatius, I have before me here a document presented by the
French Prosecution against the Defendant Sauckel. I suppose what
you mean is that that document, that trial brief entitled
Responsabilité Individuelle, does not refer to each of these 150
documents.
DR. SERVATIUS: There was, first of all, a document book,
“Slave Labor,” submitted by the American Prosecution, which is not
headed “Sauckel” but “Slave Labor”; and I cannot say, therefore,
which parts concern Sauckel in particular.
THE PRESIDENT: Well, it does say, “...and the special
responsibility of the Defendants Sauckel and Speer therefore...” That
is the American document book. It does name Sauckel.
DR. SERVATIUS: Yes.
THE PRESIDENT: And there is this other trial brief presented by
Mr. Mounier on behalf of the French Delegation, which is definitely
against Sauckel. But no doubt that does not specify all these 150
documents that you are referring to.
DR. SERVATIUS: Yes.
[The Defendant Sauckel resumed the stand.]
Witness, yesterday near the end of the session we spoke about
a manifesto—that memorandum which was intended to impress
upon the various offices their duty to carry out your directives and to
remove the resistance that existed. Now, you yourself have made
statements which are hardly compatible with your directives, it
seems. I submit to you Document Number R-124. That concerns a
meeting of the Central Planning Board of 1 March 1944. There, with
regard to recruitment, you said that, in order to get the workers, one
ought to resort to “shanghai,” as was the custom in earlier days. You
said:
“I have even resorted to the method of training staffs of
French men and women agents ... who go out on man
hunts and stupefy victims with drink and persuasive
arguments in order to get them to Germany.”
Have you found that?
FRITZ SAUCKEL (Defendant): I have found it.
THE PRESIDENT: Whereabouts in 124 is it?
DR. SERVATIUS: That is Document R-124.
THE PRESIDENT: Yes, but it is a very long document.
DR. SERVATIUS: It is in the document itself, Page 1770.
THE PRESIDENT: Yes, I have got it.
SAUCKEL: That is, as I can see, the report or record of a
meeting of the Central Planning Board of the spring of 1944. During
that year it had become extremely difficult for me to meet the
demands of the various employers of labor represented in the
Central Planning Board. At no time did I issue directives or even
recommendations to “shanghai.” In this conference I merely used
that word as reminiscent of my days as a seaman, in order to defend
myself against those who demanded workers of me, and in order to
make it clear to the gentlemen how difficult my task had become,
particularly in 1944. Actually, a very simple situation is at the root of
this. According to German labor laws and according to my own
convictions, the “Arbeitsvermittlung” (procurement of labor)—the old
word for “Arbeitseinsatz” (allocation of labor)—was a right of the
State; and we, myself included, scorned private methods of
recruitment. In 1944 Premier Laval, the head of the French
government, told me that he was also having great difficulties in
carrying out the labor laws where his own workers were concerned.
In view of that, and in agreement with one of my collaborators,
Dr. Didier, conferences were held in the German Embassy—the
witness Hildebrandt, I believe, is better able to give information about
that—with the head of the collaborationist associations, that is to say,
associations among the French population which advocated
collaboration with Germany. During these conferences at the
German Embassy these associations stated that in their opinion
official recruitment in France had become very difficult. They said
that they would like to take charge of that and would like to provide
recruiting agents from their own ranks and also provide people from
among their members who would go to Germany voluntarily.
Recruitment was not to take place through official agencies but in
cafés. In these cafés, of course, certain expenses would be
necessary which would have to be met; and the recruiting agents
would have to be paid a bonus, or be compensated by a glass of
wine or some gin. That way of doing things, naturally, did not appeal
to me personally; but I was in such difficulties in view of the demands
put to me that I agreed, without intending, of course, that the idea of
“shanghai” with its overseas suggestions and so forth should be
seriously considered.
DR. SERVATIUS: Did this suggestion come from the
Frenchmen, or was it your suggestion?
SAUCKEL: As I have said already, the suggestion was made by
the French leaders of these associations.
DR. SERVATIUS: If you read on a few lines in the document,
you will find that mention is made of special executive powers which
you wanted to create for the allocation of labor; it says there:
“Beyond that, I have charged a few capable men with the
establishment of a special executive force for the Allocation
of Labor. Under the leadership of the Higher SS and Police
Leader a number of indigenous units have been trained and
armed, and I now have to ask the Ministry of Munitions for
weapons for these people.”
How do you explain that?
SAUCKEL: That, also, can be explained clearly only in
connection with the events that I have just described. At that time
there had been many attacks on German offices and mixed German-
French labor offices. The Director of the Department for the
Allocation of Labor in the office of the military commander in France,
President Dr. Ritter, had been murdered. A number of recruiting
offices had been raided and destroyed. For that reason these
associations who were in favor of collaboration had suggested, for
the protection of their own members, that a sort of bodyguard for the
recruiting organization should be set up. Of course I could not do
that myself because I had neither the authority nor the machinery for
it. In accordance with the orders of the military commander, it had to
be done by the Higher SS and Police Leader; that is, under his
supervision. This was carried out in conjunction with the French
Minister of the Interior at that time, Darnand; so as to be able to
stand my ground against the censure of the Central Planning Board,
I used an example in this drastic form. As far as I know, these
hypothetical suggestions were not put into practice.
DR. SERVATIUS: Who actually carried out the recruitment of the
foreign workers?
SAUCKEL: The actual recruitment of foreign workers was the
task of the German offices established in the various regions, the
offices of the military commanders or similar civilian German
institutions.
DR. SERVATIUS: You ordered recruitment to be voluntary. What
was the success of that voluntary recruitment?
SAUCKEL: Several million foreign workers came to Germany
voluntarily, as voluntary recruitment was the underlying principle.
DR. SERVATIUS: Now, at the meeting of the Central Planning
Board—the same meeting which we have just discussed—you made
a remark which contradicts that. It is on Page 67 of the German
photostat, Page 1827 of the English text. I shall read the sentence to
you. Kehrl is speaking. He says, “During that entire period, you
brought a large number of Frenchmen to the Reich by voluntary
recruitment.”
Then an interruption by Sauckel: “Also by forced recruitment.”
The speaker continues, “Forced recruitment started when
voluntary recruitment no longer yielded sufficient numbers.”
Now comes the remark on which I want you to comment. You
answered, “Of the 5 million foreign workers who came to Germany,
less than 200,000 came voluntarily.”
Please explain that contradiction.
SAUCKEL: I see that this is another interruption which I made.
All I wanted to say by it was that Herr Kehrl’s opinion that all workers
had come voluntarily was not quite correct. This proportion, which is
put down here by the stenographer or the man writing the records, is
quite impossible. How that error occurred, I do not know. I never saw
the record; but the witness Timm, or others, can give information on
that.
DR. SERVATIUS: I refer now to Exhibit Sauckel-15. That is
Directive Number 4, which has been quoted already and which lays
down specific regulations with regard to recruiting measures. It has
already been submitted as Document Number 3044-PS. Why did
you now abandon the principle of voluntary recruitment?
SAUCKEL: In the course of the war our opponents also carried
out very considerable and widespread countermeasures. The need
for manpower in Germany, on the other hand, had become
tremendous. During that period a request was also put to me by
French, Belgian, and Dutch circles to bring about a better balance in
the economy of these territories and even to introduce what we
called a labor draft law, so that the pressure of enemy propaganda
would be reduced and the Dutch, Belgians, and French themselves
could say that they were not going to Germany voluntarily but that
they had to go because of a compulsory labor service and because
of laws.
DR. SERVATIUS: Did the proximity of the front have any
influence on the fact that people no longer wanted to come
voluntarily?
SAUCKEL: Of course I came to feel that; and it is
understandable that the chances of victory and defeat caused great
agitation among the workers; and the way things looked at the front
certainly played an important part.
DR. SERVATIUS: Did purely military considerations also cause
the introduction...
THE TRIBUNAL (Mr. Francis Biddle, Member for the United
States): Dr. Servatius, will you ask the witness what he means by a
labor draft law. Does he mean a law of Germany or a law of the
occupied countries?
DR. SERVATIUS: Witness, you heard the question, whether you
mean a German law or a law of the administration of the occupied
countries?
SAUCKEL: That varied. The Reich Government in some of the
territories introduced laws which corresponded to the laws that were
valid for the German people themselves. Those laws could not be
issued by me, but they were issued by the chiefs of the regional
administrations or the government of the country concerned on the
order of the German Government.
In France these laws were issued by the Laval Government, in
agreement with Marshal Pétain; in Belgium, in agreement with the
Belgian general secretaries or general directors still in office or with
the ministries.
THE PRESIDENT: Do you mean, in the other countries, by the
German Government or the German Government’s representatives?
You have only spoken of...
SAUCKEL: The order to introduce German labor laws in the
occupied territories was given by the Führer. They were proclaimed
and introduced by the chiefs who had been appointed by the Führer
for these territories, for I myself was not in a position to issue any
directives, laws, or regulations there.
THE PRESIDENT: Go on.
DR. SERVATIUS: How were these laws carried out?
SAUCKEL: The laws were published in the official publications
and legal gazettes, as well as being made known through the press
and by posters in those territories.
DR. SERVATIUS: I mean the practical execution. How were the
people brought to Germany?
SAUCKEL: They were summoned to the local labor office, which
was mostly administered by local authorities. Cases had to be
examined individually, according to my directives, which have been
submitted here as documents. Cases of hardship to the family, or
other such cases, were given special consideration. Then, in the
normal manner—as was done in Germany also—the individual
workers or conscripted persons were brought to Germany.
DR. SERVATIUS: Were you present—did you ever witness this
procedure?
SAUCKEL: I observed this procedure personally in a number of
cities in Russia, France, and Belgium; and I made sure that it was
carried out in accordance with orders.
DR. SERVATIUS: If compulsion was necessary, what coercive
measures were taken?
SAUCKEL: At first, such compulsory measures were taken as
are justified and necessary in every normal civil administration.
DR. SERVATIUS: And if they were not sufficient?
SAUCKEL: Then proceedings were proposed.
DR. SERVATIUS: These were legal measures, were they?
SAUCKEL: According to my conviction, they were legal
measures.
DR. SERVATIUS: You have stated repeatedly in documents,
which are available here, that a certain amount of pressure was to
be used. What did you mean by that?
SAUCKEL: I consider that every administrative measure taken
on the basis of laws or duties imposed by the state, on one’s own
nation, or in any other way, constitutes some form of stress, duty,
pressure.
DR. SERVATIUS: Were not measures used which brought about
some sort of collective pressure?
SAUCKEL: I rejected every kind of collective pressure. The
refusal to employ collective pressure is also evident from decrees
issued by other German offices in the Reich.
DR. SERVATIUS: Is it not true that in the East the villages were
called upon to provide a certain number of people?
SAUCKEL: In the East, of course, administrative procedure was
rendered difficult on account of the great distances. In the lower
grades, as far as I know, native mayors were in office in every case.
It is possible that a mayor was requested to select a number of
workers from his village or town for work in Germany.
DR. SERVATIUS: Is that the same as that form of collective
pressure, where, if nobody came, the entire village was to be
punished?
SAUCKEL: Measures of that kind I rejected entirely in my field
of activity, because I could not and would not bring to the German
economy workers who had been taken to Germany in such a
manner that they would hate their life and their work in Germany
from the very outset.
DR. SERVATIUS: What police facilities were at your disposal?
SAUCKEL: I had no police facilities at my disposal.
DR. SERVATIUS: Who exercised the police pressure?
SAUCKEL: Police pressure in the occupied territories could be
exerted on order or application of the respective chief of the territory,
or of the Higher SS and Police Leader, if authorized.
DR. SERVATIUS: Then it was not within your competence to
exert direct pressure?
SAUCKEL: No.
DR. SERVATIUS: Did you exert indirect pressure by your
directives, by cutting off food supplies, or similar measures?
SAUCKEL: After the fall of Stalingrad and the proclamation of
the state of total war, Reich Minister Dr. Goebbels in Berlin interfered
considerably in all these problems. He ordered that in cases of
persistent refusal or signs of resistance compulsion was to be used
by means of refusing additional food rations, or even by withdrawal
of ration cards. I personally rejected measures of that kind
energetically, because I knew very well that in the western territories
the so-called food ration card played a subordinate role and that
supplies were provided for the resistance movement and its
members on such a large scale that such measures would have
been quite ineffective. I did not order or suggest them.
DR. SERVATIUS: At the meeting of the Central Planning Board
on 1 March 1944 you also stated that, if the French executive
agencies were unable to get results, then one might have to put a
prefect up against a wall. Do you still consider this to be legally
justified pressure?
SAUCKEL: That is a similarly drastic remark of mine in the
Central Planning Board which was never actually followed by an
official order and not even by any prompting on my part. It was
simply that I had been informed that in several departments in
France the prefects or responsible chiefs supported the resistance
movement wholeheartedly. Railroad tracks had been blown up;
bridges had been blown up; and that remark was a verbal reaction
on my part. I believe, however, I was then only thinking of a legal
measure, because there did, in fact, exist a French law which made
sabotage an offense punishable by death.
DR. SERVATIUS: May I refer to the document in this
connection?
THE PRESIDENT: Is it in Document Number R-124?
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ADNAN SIDDIQUI, MD, PHD, FAHA

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Published in the United States of America by Oxford University Press

© Oxford University Press 2018

Library of Congress Cataloging-in-Publication Data

1. Basic Clinical Syndromes and Definitions

2. Stroke Systems of Care

3. Prehospital Triage of Stroke: Clinical Evaluation

4. Prehospital Assessment of Stroke: Mobile Stroke Units

5. Evaluation of Stroke in the Emergency Department

6. Imaging of Acute Stroke

7. Telemedicine for Evaluation of Stroke Patients

8. Intravenous Thrombolysis in Acute Ischemic Stroke

9. Endovascular Treatment of Stroke

11. In-Hospital Stroke

12. Medical Management of Ischemic Stroke

13. Medical Management of Hemorrhagic Stroke

14. Surgical Treatment of Hemorrhagic Stroke

15. Cerebral Venous Thrombosis

Siviero Agazzi, MD, MBA, FCAS

Andrew Blake Buletko, MD

Noella J. Cypress West, ARNP

Lucas Elijovich, MD, FAHA

Kyle M. Fargen, MD, MPH

Santiago Ortega-Gutierrez, MD, MSC

Shashank Shekhar, MD, MSc

Rebecca Sugg, MD, FAHA

Cerebral venous thrombosis

2.1 Transient ischemic attack

ABCD2 score calculation (0–7 points)

The 2-day risk of stroke

Question 1.2: Are lacunar strokes common?

3.1 Lacunar stroke syndromes

3.1.1 PURE MOTOR HEMIPARESIS

3.1.2 PURE SENSORY STROKE

3.1.3 SENSORIMOTOR STROKE

3.1.4 ATAXIC HEMIPARESIS

3.1.5 DYSARTHRIA-CLUMSY HAND SYNDROME

3.2 Large vessel stroke syndromes

Figure 1.3 Cervical arterial circulation.

3.2.1 ANTERIOR CIRCULATION STROKES

3.2.1.1 Middle cerebral artery stroke

3.2.2 POSTERIOR CIRCULATION STROKES

3.2.2.1 Basilar artery stroke

3.2.2.2 Posterior cerebral artery stroke

3.3 Stroke syndromes—medium size vessels