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Description

Practical Management of Pediatric and Adult Brachial Plexus Palsies covers in-depth surgical techniques for managing disorders of this crucial nerve complex so that you can most effectively treat injuries in patients of any age. Drs. Kevin Chung, Lynda Yan, and John McGillicuddy present a multidisciplinary approach to pediatric brachial plexus injury treatment and rehabilitation, obstetric considerations, and other hot topics in the field. With access to the full text and surgical videos online at expertconsult.com, you’ll have the dynamic, visual guidance you need to manage injuries to the brachial plexus.

  • Access the fully searchable text online at www.expertconsult.com, along with surgical videos demonstrating how to perform key procedures.
  • See cases as they present in practice through color illustrations, photos, and diagrams that highlight key anatomical structures and relationships.
  • Apply multidisciplinary best practices with advice from internationally respected authorities in neurosurgery, orthopaedics, plastic surgery, and other relevant fields.
  • Hone your technique with coverage that emphasizes optimizing outcomes with pearls and discussions of common pitfalls.
  • Prepare for collaborating with other physicians thanks to a multidisciplinary approach that covers medical and legal aspects in addition to surgery.
  • Find information quickly and easily with a full-color layout.

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Publié par
Date de parution 22 août 2011
Nombre de lectures 5
EAN13 9781437736236
Langue English
Poids de l'ouvrage 3 Mo

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Exrait

Practical Management of Pediatric and Adult Brachial Plexus Palsies

Kevin C. Chung, MD, MS
Professor of Surgery, Section of Plastic Surgery, Department of Surgery, Assistant Dean for Faculty Affairs, University of Michigan Medical School, Ann Arbor, MI, USA

Lynda J.-S. Yang, MD, PhD
Associate Professor, Department of Neurosurgery, University of Michigan Medical School, Ann Arbor, MI, USA

John E. McGillicuddy, MD
Emeritus Professor of Neurosurgery and Orthopedic Surgery, Department of Neurosurgery, University of Michigan Health System, Ann Arbor, MI, USA
Clinical Professor of Neurosurgery, Division of Neurosurgery, Department of Neurosciences, Medical University of South Carolina, Charleston, SC, USA
Saunders
Front Matter

Practical Management of Pediatric and Adult Brachial Plexus Palsies
Kevin C. Chung, MD, MS
Professor of Surgery
Section of Plastic Surgery
Department of Surgery
Assistant Dean for Faculty Affairs
University of Michigan Medical School
Ann Arbor, MI, USA
Lynda J.-S. Yang, MD, PhD
Associate Professor
Department of Neurosurgery
University of Michigan Medical School
Ann Arbor, MI, USA
John E. McGillicuddy, MD
Emeritus Professor of Neurosurgery and Orthopedic Surgery
Department of Neurosurgery
University of Michigan Health System
Ann Arbor, MI, USA
Clinical Professor of Neurosurgery
Division of Neurosurgery
Department of Neurosciences
Medical University of South Carolina
Charleston, SC, USA

Edinburgh London New York Oxford Philadelphia St Louis Sydney Toronto 2012
Copyright

© 2012, Elsevier Inc. All rights reserved.
No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Details on how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions .
This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein).


Notices
Knowledge and best practice in this field are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary. Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility.
With respect to any drug or pharmaceutical products identified, readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions.
To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors, assume any liability for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein.
ISBN-13: 9781437705751
British Library Cataloguing in Publication Data
Practical management of pediatric and adult brachial plexus palsies.
1.  Brachial plexus – Wounds and injuries – Treatment.
I.  Chung, Kevin. II.  Yang, Lynda J-S. III.  McGillicuddy, John.
617.4′83044 – dc22
A catalogue record for this book is available from the British Library
Library of Congress Cataloging in Publication Data
A catalog record for this book is available from the Library of Congress
Printed in the United States of America
Last digit is the print number: 9 8 7 6 5 4 3 2 1
Preface
On behalf of my co-editors Drs. Yang and McGillicuddy, it is my distinct pleasure to introduce this comprehensive brachial plexus textbook to you. This textbook is a combination of an extensive amount of effort by our colleagues from around the world who have produced the most updated and inclusive chapters to help you take care of your patients with this devastating condition. The uniqueness of this textbook is the collaborative effort among all of the relevant specialties involved in the treatment of this condition, which includes Neurosurgery, Plastic/Hand Surgery, Orthopaedic Surgery, Physical Medicine and Rehabilitation, Obstetrics and Gynecology, Occupational Physical Therapy and the Legal Profession. Patients with this condition are not simply the territory of a particular specialty, but rather require the input and support of multiple specialties in order to help the patients integrate into society. We included a chapter that discusses the predisposing factors for the neonatal brachial plexus condition that is mired in controversy with regard to the exact cause of this condition. Furthermore, brachial plexus conditions often have legal ramifications; we are privileged to incorporate the expertise of our legal experts who give practical instructions on how the legal system views these conditions and how physicians should approach these conditions in order to give an objective assessment.
The genesis of this textbook is derived from the concept of the Comprehensive Interdisciplinary Brachial Plexus Program at the University of Michigan with clinics that occur on a regular basis to evaluate complex pediatric and adult brachial plexus conditions. This clinic enjoys participation by representatives from all the specialties in a single clinic setting. The interchange of ideas to a consensus on a treatment course is particularly rewarding for us as well as for our patients. There are no egos on this team, and each shares his/her opinions openly to reach the best consensus treatment plan for our patients. It is only through this collaborative approach that we can continue to advance the treatment of complex brachial plexus conditions by incorporating not only expertise from various specialties, but also solicit contributions from various regions of the world. As you can see from the author list, all the contributing authors are noted experts who shared their knowledge from a life-long interest in the care of brachial plexus conditions. Additionally, this textbook contains carefully organized videos, ranging from a detailed description of the anatomy of the brachial plexus to a comprehensive physical examination of muscle deficits associated with this condition. This is a richly illustrated textbook that should be the authoritative textbook in this discipline.
I would be remiss without acknowledging certain people who have been critical in the success in this textbook. I would like to acknowledge Dr. Lynda Yang for her foresight in initiating the Comprehensive Brachial Plexus Program at the University of Michigan and for her invaluable assistance in organizing all the chapters by meticulously checking every single detail from the inception of this textbook to its full production. I am certain that her dedication to this effort is the main reason that this textbook will be the pride of this specialty. We are indebted to Dr. McGillicuddy for his implicit support and dedication to the Program’s efforts. Additionally, I would also like to acknowledge our staff, Phil Clapham, Pouya Entezami, Lilly Bellfi, Holly Wagner and Connie McGovern for their help and our Elsevier development editor, Alex Mortimer, whose patience has overcome many of the difficulties and obstacles in this multi-author, international collaborative effort.
My most important acknowledgement is to our contributing authors who are all our closest colleagues in putting aside a certain portion of their practice and family life to share their expertise for the advancement of this specialty. They have put their heart and soul into every word in this volume, and we are certainly appreciative of their generous contributions.
I hope that you will cherish this book in your care of patients with brachial plexus conditions. I am certain that we will continue to update this textbook by keeping up with the advancement in surgical techniques and nerve research.

Kevin C. Chung, MD, MS, Professor of Surgery Section of Plastic Surgery Assistant Dean for Faculty Affairs University of Michigan Medical School
List of Contributors

Nasser I. Alhodaib, MBBS, FRCSC, Consultant Plastic and Reconstructive Microsurgeon Department of Surgery King Abdulaziz Medical City Riyadh, Saudi Arabia
13 Outcomes of Treatment for Neonatal Brachial Plexus Palsy

Allan J. Belzberg, MD, FRCSC, Department of Neurosurgery Johns Hopkins School of Medicine Baltimore, MD, USA
23 Strategies for Treating Pain

Allen T. Bishop, MD, Professor of Orthopedic Surgery Mayo Clinic College of Medicine, Consultant, Division of Hand Surgery Department of Orthopedic Surgery Mayo Clinic Rochester, MN, USA
19 Reconstructive Procedures for the Upper Extremity

Richard C. Boothman, JD, Chief Risk Officer Adjunct Assistant Professor Department of Surgery University of Michigan Medical School Ann Arbor, MI, USA
6 Guidelines for attorney-physician interactions about brachial plexus palsy patients

Neal Chen, MD, Medsport Department of Orthopaedic Surgery University of Michigan Health System Ann Arbor, MI, USA
1 Anatomy of the Brachial Plexus

Wilson Chimbira, MBChB, FRCA, Pediatric Anesthesiologist Department of Anesthesia University of Michigan Ann Arbor, MI, USA
4 Clinical Presentation and Considerations of Neonatal Brachial Plexus Palsy

Kevin C. Chung, MD, MS, Professor of Surgery Section of Plastic Surgery Department of Surgery Assistant Dean for Faculty Affairs University of Michigan Medical School Ann Arbor, MI, USA
1 Anatomy of the Brachial Plexus
2 Physiology of Nerve Injury and Regeneration
11 Reconstructive Strategies for Recovery of Hand Function
20 Surgical Procedures for Recovery of Hand Function

Howard M. Clarke, PhD, MD, FRCSC, FACS, FAAP, Professor of Surgery Department of Surgery University of Toronto Active Staff Surgeon Division of Plastic Surgery The Hospital for Sick Children Toronto, Ontario, Canada
13 Outcomes of Treatment for Neonatal Brachial Plexus Palsy

Michael J. Dorsi, MD, Chief Resident Department of Neurosurgery Johns Hopkins School of Medicine Baltimore, MD, USA
23 Strategies for Treating Pain

Stefano Ferraresi, MD, Chief of Neurosurgery Unit Director of the Department of Neurological Sciences Ospedale Santa Maria della Misericordia Rovigo, Italy
18 Radiographic Assessment of Adult Brachial Plexus Injuries

Debora Garozzo, MD, Neurosurgery Unit Department of Neurological Sciences Ospedale Santa Maria della Misericordia Rovigo, Italy
18 Radiographic Assessment of Adult Brachial Plexus Injuries

Roberto Gasparotti, MD, Associate Professor of Neuroradiology University of Brescia School of Medicine Director of Neuroradiology Unit Department of Diagnostic Imaging Spedali Civili di Brescia Brescia, Italy
18 Radiographic Assessment of Adult Brachial Plexus Injuries

Bernard Gonik, MD, Professor and Fann Srere Chair of Perinatal Medicine Department of Obstetrics and Gynecology Wayne State University School of Medicine Detroit, MI, USA
5 Neonatal Brachial Plexus Palsy: Antecedent Obstetrical Factors

Marie-Noëlle Hébert-Blouin, MD, Mayo Clinic Departments of Neurologic Surgery Rochester, MN, USA
19 Reconstructive Procedures for the Upper Extremity

Denise Justice, OTR, Department of Neurosurgery University of Michigan Health System Ann Arbor, MI, USA
12 Rehabilitation Concepts for Pediatric Brachial Plexus Palsies

Brian M. Kelly, DO, Associate Professor Department of Physical Medicine and Rehabilitation University of Michigan Ann Arbor, MI, USA
21 Rehabilitation Concepts for Adult Brachial Plexus Injuries

David G. Kline, MD, Retired Boyd Professor and Emeritus Chair of Neurosurgery Louisiana State University New Orleans, LA, USA
16 Operative Neurophysiology of the Brachial Plexus Intraoperative Electrodiagnostic Studie s
24 Outcomes of treatment for adult brachial plexus injuries

Scott H. Kozin, MD, Professor Department of Orthopaedic Surgery Temple University Philadelphia, PA, USA Director, Hand and Upper Extremity Surgery Shriners Hospital for Children, Philadelphia, PA, USA
10 Shoulder Sequelae in Children with Brachial Plexus Palsy

James A. Leonard, Jr., MD, Professor & Medical Director Physical Medicine and Rehabilitation Division of Orthotics and Prosthetics Department of Physical Medicine and Rehabilitation University of Michigan Ann Arbor, MI, USA
7 The Role of Electrodiagnosis in Infants with Brachial Plexus Palsies
17 Practical Application of Electrodiagnostic Studies to Evaluate Adult Brachial Plexus Lesions
21 Rehabilitation Concepts for Adult Brachial Plexus Injuries

Aymeric Y.T. Lim, FRCS (Glas), Associate Professor Department of Orthopaedic Surgery National University of Singapore Senior Consultant Department of Hand & Reconstructive Microsurgery National University Hospital Singapore
14 Clinical Examination and Diagnosis

Martijn J.A. Malessy, MD, PhD, Professor of Nerve Surgery Department of Neurosurgery Leiden University Medical Center Leiden, The Netherlands
9 Nerve Repair/Reconstruction Strategies for Neonatal Brachial Plexus Palsies

John E. McGillicuddy, MD, Emeritus Professor of Neurosurgery and Orthopedic Surgery Department of Neurosurgery University of Michigan Health System Ann Arbor, MI, USA Clinical Professor of Neurosurgery Division of Neurosurgery Department of Neurosciences Medical University of South Carolina Charleston, SC, USA
3 Clinical Examination of the Patient with Brachial Plexus Palsy
4 Clinical Presentation and Considerations of Neonatal Brachial Plexus Palsy
22 Thoracic Outlet Syndrome

Rajiv Midha, MD, MSc, FRCS(C), Professor and Head Division of Neurosurgery Department of Clinical Neurosciences Faculty of Medicine University of Calgary Calgary, Alberta, Canada
15 Nerve Repair/Nerve Transfer Strategies for Adult Brachial Plexus Palsies

Virginia S. Nelson, MD, MPH, Professor Department of Physical Medicine and Rehabilitation University of Michigan Medical School Ann Arbor, MI, USA
12 Rehabilitation Concepts for Pediatric Brachial Plexus Palsies

W.J.R. van Ouwerkerk, MD, PhD, Department of Neurosurgery Postadres Vrije Universiteit Medical Center Amsterdam, The Netherlands
8 Radiographic Assessment in Pediatric Brachial Plexus Palsies

Miriana G. Popadich, RN, MSN, FNP, Department of Neurosurgery University of Michigan Health System Ann Arbor, MI, USA
12 Rehabilitation Concepts for Pediatric Brachial Plexus Palsies

Willem Pondaag, MD, Department of Neurosurgery Leiden University Medical Center Leiden, The Netherlands
9 Nerve Repair/Reconstruction Strategies for Neonatal Brachial Plexus Palsies

Lynnette Rasmussen, OTR, Department of Neurosurgery University of Michigan Health System Ann Arbor, MI, USA
12 Rehabilitation Concepts for Pediatric Brachial Plexus Palsies

Edward C. Reynolds, Jr., JD, Assistant General Counsel Office of the General Counsel University of Michigan Ann Arbor, MI, USA
6 Guidelines for attorney-physician interactions about brachial plexus palsy patients

Stephen M. Russell, MD, Assistant Professor of Neurosurgery New York University School of Medicine New York, NY, USA
3 Clinical Examination of the Patient with Brachial Plexus Palsy

Sandeep J. Sebastin, MCh (Plast), Associate Consultant Department of Hand and Reconstructive Microsurgery National University Health System Singapore
11 Reconstructive Strategies for Recovery of Hand Function
14 Clinical Examination and Diagnosis

Alexander Y. Shin, MD, Professor and Consultant of Orthopaedic Surgery Department of Orthopaedic Surgery Division of Hand Surgery Mayo Clinic Rochester, MN, USA
19 Reconstructive Procedures for the Upper Extremity

J.A. van der Sluijs, MD, PhD, Consultant Pediatric Orthopaedic Surgery Department of Orthopaedic Surgery Vrije Universiteit Medical Center Amsterdam, The Netherlands
8 Radiographic Assessment in Pediatric Brachial Plexus Palsies

M. Catherine Spires, MD, Professor Department of Physical Medicine and Rehabilitation University of Michigan Ann Arbor, MI, USA
7 The Role of Electrodiagnosis in Infants with Brachial Plexus Palsies
17 Practical Application of Electrodiagnostic Studies to Evaluate Adult Brachial Plexus Lesions

Robert J. Spinner, MD, Professor Departments of Neurologic Surgery and Orthopedic Surgery Mayo Clinic Rochester, MN, USA
19 Reconstructive Procedures for the Upper Extremity

Olawale A.R. Sulaiman, MD, PhD, FRCS (C), Associate Professor of Neurosurgery Tulane School of Medicine Medical Director Ochsner Spine Center Chairman Department of Neurosurgery Ochsner Health System New Orleans, LA, USA
24 Outcomes of treatment for adult brachial plexus injuries

Yuan-Kun Tu, MD, Professor Superintendent Department of Orthopaedic Surgery E-DA Hospital I-Shou University Kaohsiung, Taiwan
20 Surgical Procedures for Recovery of Hand Function

Kelly L. Vander Have, MD, Associate Professor Department of Orthopaedic Surgery Division of Pediatric Orthopaedics University of Michigan Ann Arbor, MI, USA
10 Shoulder Sequelae in Children with Brachial Plexus Palsy

Jacob D. de Villiers Alant, MBChB, MMed, FRCS(C), Division of NeurosurgeryDepartment of Clinical Neurosciences University of Calgary Calgary, Alberta, Canada
15 Nerve Repair/Nerve Transfer Strategies for Adult Brachial Plexus Palsies

James Wolfe, RNCST, Nerve Conduction Technologist Electroneuromyography Laboratory University of Michigan Health System Ann Arbor, MI, USA
7 The Role of Electrodiagnosis in Infants with Brachial Plexus Palsies
17 Practical Application of Electrodiagnostic Studies to Evaluate Adult Brachial Plexus Lesions

Lynda J.-S. Yang, MD, PhD, Associate Professor Department of Neurosurgery University of Michigan Ann Arbor, MI, USA
1 Anatomy of the Brachial Plexus
2 Physiology of Nerve Injury and Regeneration
4 Clinical Presentation and Considerations of Neonatal Brachial Plexus Palsy
AcknowledgementS
To Chin-yin and William

Kevin C. Chung
To Lucie, Y-C Lin, and Sam

Lynda J.-S. Yang
To John and Theresa, to Jim Stemple, and especially to Bridget

John E. McGillicuddy
Table of Contents
Instructions for online access
Front Matter
Copyright
Preface
List of Contributors
AcknowledgementS
Section One: The Basics
Chapter 1: Anatomy of the brachial plexus
Chapter 2: Physiology of nerve injury and regeneration
Chapter 3: Clinical examination of the patient with brachial plexus palsy
Section Two: Pediatric Brachial Plexus Palsies
Chapter 4: Clinical presentation and considerations of neonatal brachial plexus palsy
Chapter 5: Neonatal brachial plexus palsy: Antecedent obstetrical factors
Chapter 6: Guidelines for attorney–physician interactions about brachial plexus palsy patients
Chapter 7: The role of electrodiagnosis in infants with brachial plexus palsies
Chapter 8: Radiographic assessment in pediatric brachial plexus palsies
Chapter 9: Nerve repair/reconstruction strategies for neonatal brachial plexus palsies
Chapter 10: Shoulder sequelae in children with brachial plexus palsy
Chapter 11: Reconstructive strategies for recovery of hand function
Chapter 12: Rehabilitation concepts for pediatric brachial plexus palsies
Chapter 13: Outcomes of treatment for neonatal brachial plexus palsy
Section Three: Adult Brachial Plexus Palsies
Chapter 14: Clinical examination and diagnosis
Chapter 15: Nerve repair/nerve transfer strategies for adult brachial plexus palsies
Chapter 16: Operative neurophysiology of the brachial plexus intraoperative electrodiagnostic studies
Chapter 17: Practical application of electrodiagnostic studies to evaluate adult brachial plexus lesions
Chapter 18: Radiographic assessment of adult brachial plexus injuries
Chapter 19: Reconstructive procedures for the upper extremity
Chapter 20: Surgical procedures for recovery of hand function
Chapter 21: Rehabilitation concepts for adult brachial plexus injuries
Chapter 22: Thoracic outlet syndrome
Chapter 23: Strategies for treating pain
Chapter 24: Outcomes of treatment for adult brachial plexus injuries
Index
Section One
The Basics
CHAPTER 1 Anatomy of the brachial plexus

Neal Chen, MD, Lynda J.-S. Yang, MD, PhD, Kevin C. Chung, MD, MS


Summary box

1 The brachial plexus can be organized into 5 zones: spinal nerve roots, trunks, divisions, cords and terminal branches.
2 C5-6 nerve roots form the upper trunk, C7 nerve root forms the middle trunk and C8-T1 nerve roots form the lower trunk.
3 The anterior divisions of the upper and middle trunks form the lateral cord, the posterior divisions of all the trunks form the posterior cord, and the anterior division of the lower trunk forms the medial cord.
4 The lateral cord and the medial cord forms the median nerve.
5 The lateral cord terminates into the musculocutaneous nerve, and the medial cord terminates into the ulnar nerve.
6 The posterior cord terminates into the axillary nerve and the radial nerve.
7 The omohyoid muscle separates the posterior triangle into a superior, omotrapezial triangle and an inferior, omoclavicular triangle.
8 The upper and middle trunks and their divisions generally lie in the omotrapezial triangle, whereas the lower trunk lies in the omoclavicular triangle
9 The upper, middle, and lower trunks ramify into their respective divisions posterior to the clavicle.
10 The divisions form cords around the axillary artery, and each cord is named based on its relationship to the artery.

Introduction
The brachial plexus is a beautiful, intricate, and complex structure that comprises connections of the spinal nerves to their terminal branches in the upper extremity. There are multiple descriptions through which this neurological conduit can be decoded: (1) schematic anatomy, (2) surgical anatomy and its relationships with surrounding tissues, and (3) descriptions of its anatomical variations.
Each of these 3 descriptions has advantages and shortcomings. Surgical anatomy is helpful in describing the relationships with nearby structures and can serve as a guide to approaching the brachial plexus, but this description does not address intraplexal anatomy directly and can overlook important internal variations. Schematic anatomy provides a framework with which function of the plexus can be understood and lesions within the plexus can be identified. However, schematic anatomy can be misleading, especially when there are anatomic variations. Finally, the description of anatomic variability is comprehensive, but unwieldy. The goal of this chapter is to capitalize on the advantages of each of these approaches to provide an understandable yet thorough treatment of brachial plexus anatomy.

Historical perspective
At the end of the 19th century, understanding of the brachial plexus relied on large treatises describing collections of anatomic dissections. 1 The strength of these descriptions was fortified by the number of dissections available; however, the quality of these dissections remains uncertain. A number of the anatomic specimens were dissected by medical students, and the accuracy, especially of anatomic variations, is debatable. Many of these descriptions describe copious variations in how the trunks of the plexus coalesce, either into one solid cord, 2 cords, or multiple cords. Many of these early descriptions have not withstood the test of time.
During the same period, a number of works began to codify what was believed to be a “true form” of the plexus. Kerr, Walsh, and Harris 2 - 4 described a series of personally performed or scrutinized dissections that suggested there was far less anatomic variation than previously believed. Convergence of these descriptions of the brachial plexus has allowed a more schematic presentation from which a general foundation can be constructed.
As the understanding of the brachial plexus became more complete, what remained unclear was which cervical roots contributed to it. Some authors believed the plexus was pre-fixed (the plexus originated more cranially than normal and included the C4 nerve root) or that the plexus was post-fixed (the plexus originated more caudally to include the T2 nerve root). 1 Other authors believed that instead of having a more cranial or caudal origin, the brachial plexus had a broader or a less broad origin. An even more complex problem was the topographic mapping of nerves within the brachial plexus. A number of authors have pursued microscopic, fascicular dissection of the plexus in order to advance our understanding of the connections within this complex structure. 5
Advances in developmental biology have yielded some insights into how the plexus is formed and why contributions to the plexus are not entirely consistent. Molecular events result in vertebrate segmentation, and from these vertebrate segments, neural crest cells migrate from the axis to the periphery. Although these processes are not fully understood, evidence is accumulating that these molecular events ultimately dictate the final morphology of the brachial plexus.
Primate anatomy also provides some insight into the human brachial plexus. Comparative anatomy suggests an increasing pattern of progressive organization. In lower primates, the artery lies superficial to the brachial plexus and has a larger degree of variation. In higher primates, the artery also lies superficial to the brachial plexus, but there is a tendency toward a more organized, consistent brachial plexus. In humans, the axillary artery lies deep to the anterior divisions to become intimate with the cords (which are named by their relationship to the axillary artery), and the brachial plexus maintains a highly organized and consistent structure throughout its course.

Schematic anatomy
The standard schematic diagram used to describe the brachial plexus uses 5 zones: (1) spinal nerve roots, (2) trunks, (3) divisions, (4) cords, and (5) terminal branches. 6 The C5 to T1 nerve roots typically contribute to the brachial plexus. The C5 and C6 roots coalesce to form the upper trunk, the C7 root forms the middle trunk, and the C8 and T1 roots coalesce to form the lower trunk. Each trunk divides into an anterior and posterior division. All 3 posterior divisions join to form the posterior cord. The anterior divisions from the upper and middle trunk form the lateral cord, and the anterior division from the lower trunk forms the medial cord. The posterior cord ultimately branches into the terminal branches of the axillary and radial nerves. The lateral cord and medial cord each produce a branch that contributes to form the median nerve. In addition to its contribution to the median nerve, the lateral cord terminates in the musculocutaneous nerve, and the medial cord terminates in the ulnar nerve ( Figure 1.1 ).

Figure 1.1 Schematic diagram of the brachial plexus.
A number of terminal branches (nerves) arise from various zones of the basic structure; knowing these branches and their function facilitates localization of a potential lesion. For instance, the dorsal scapular nerve arises quite proximally from C5, and the long thoracic nerve arises from the nerve roots of C5 to C7; lack of function of either nerve implies a proximal injury of the brachial plexus at the level of the nerve roots. Similarly, the phrenic nerve arises from C3, C4, and C5; diaphragmatic paralysis is also consistent with a proximal lesion of the brachial plexus. The upper trunk gives origin to the suprascapular nerve; lack of supraspinatus and infraspinatus function in the context of deltoid and biceps weakness implies a lesion affecting the upper trunk. More distally, the lateral cord gives rise to the lateral pectoral nerve; the posterior cord gives rise to the upper subscapular nerve, the thoracodorsal nerve, and the lower subscapular nerve; the medial cord gives rise to the medial pectoral nerve, the medial brachial cutaneous nerve, and the medial antebrachial cutaneous nerve ( Figure 1.1 ). Similar logic can be applied to these nerves to determine the site of injury within the brachial plexus.
This basic schematic anatomy provides a crucial foundation from which to understand surgical anatomic relationships, and provides a benchmark against which to measure anatomic variations.

Surgical anatomy (relationship of the brachial plexus to surrounding structures)
As described above, the brachial plexus has 5 roots (C5-T1), 3 trunks (upper, middle, and lower), 6 divisions (2 divisions, anterior and posterior, per trunk), 3 cords (lateral, posterior, and medial) and 5 main terminal nerve branches (musculocutaneous, radial, axillary, median, and ulnar). Grossly, the brachial plexus emerges in the posterior triangle of the neck (bordered by the sternocleidomastoid and trapezius muscles, clavicle, and occiput). The neck is commonly conceptualized as a set of triangles bounded by identifiable structures. The sternocleidomastoid muscle divides the neck into an anterior and posterior triangle. The omohyoid muscle separates the posterior triangle into a superior, omotrapezial triangle and an inferior, omoclavicular triangle. The upper and middle trunks and their divisions generally lie in the omotrapezial triangle, whereas the lower trunk lies in the omoclavicular triangle ( Figure 1.2 ).

Figure 1.2 Triangles of the neck.
Note that the spinal accessory nerve emerges posterior to the sternocleidomastoid muscle, 2/3 of the way up from the sternum to the mastoid, and travels relatively superficially toward the trapezius. More specifically, the trunks of the brachial plexus emerge within the interscalene triangle bordered by the anterior scalene, middle scalene, and the clavicle.
The subclavian artery also travels through the interscalene triangle, whereas the subclavian vein travels anterior to the anterior scalene. The anterior scalene attaches to the anterior tubercle of the transverse process of the vertebrae and the clavicle, and the middle scalene attaches to the posterior tubercle of the transverse process; the anterior tubercle of C6 is particularly bulbous (Chassaignac’s tubercle) and can be used as an intraoperative marker.

Proximal anatomical relationships
The dorsal rootlet (sensory) and ventral rootlet (motor) converge to form a spinal nerve root. These 2 structures converge approximately at the level of neural foramen ( Figure 1.3 ). The cell bodies of the axons of the sensory rootlet reside in the dorsal root ganglion (outside of the spinal cord), whereas cell bodies of the motor rootlet lie within the anterior horn of the spinal cord. Knowledge of this anatomy not only facilitates intraoperative surgical planning but also the understanding of preoperative electrodiagnostic studies.

Figure 1.3 Axial representation of the spinal column demonstrating the ventral and dorsal rootlets converging into spinal nerve roots and their relationship to the sympathetic ganglia.
The nerve root is enveloped by the epineurium, which is confluent with the dura. The nerve roots contributing to the trunks exit from their neural foramina and run along the bony groove between the anterior and posterior tubercles of the vertebrae. These bony “chutes” are well-formed for the nerves comprising the upper trunk (C5, C6), and more abbreviated for the nerves comprising the lower trunk. In addition, there is less connective tissue binding the lower nerve roots to the bony chutes when compared to the upper nerve roots. Consequently, the lower nerve roots (C8, T1) are prone to preganglionic (avulsion) injury, whereas nerves comprising the upper trunk tend to sustain postganglionic injury.
As the spinal nerves emerge from the neural foramina, they receive rami from the sympathetic ganglia ( Figure 1.3 ). Typically, the C5 and C6 nerves receive contributions from the middle cervical ganglion, C7 and C8 nerves receive contributions from the inferior cervical ganglion, and the first thoracic nerve receives a contribution from its associated ganglion. These contributions occur distal to the dorsal root ganglion. Understanding the relationship of the brachial plexus with the sympathetic ganglia allows the examiner to deduct the presence of a proximal C8, T1 lesion in the presence of Horner’s sign (ptosis, meiosis, and anhydrosis).
The nerve roots of C5 through C7 emerge from the vertebral foramina and separate into anterior (innervates the upper extremity) and posterior primary rami (innervates the paraspinal muscles and posterior vertebral elements). The anterior rami lie in a groove in the transverse process that is posterior to the vertebral artery ( Figure 1.4 ). The anterior rami usually emerge between the anterior and middle scalene muscles to form the upper trunk.

Figure 1.4 Relationship of the spinal nerve roots to the vertebral artery at the level of the neural foramen.
The nerve roots of C8 and T1 are retroclavicular. The 1st and 2nd rib lie posteriorly and the pleura lies inferior to these roots. C8 traverses superiorly, and T1 passes inferior to the 1st rib. Proceeding distally, the nerve roots coalesce to form the lower trunk on the superior surface of the 1st rib. The lower trunk then emerges between the anterior and middle scalene muscles.
Furthermore, the brachial plexus is comprised of the nerve structures by which the central nervous system communicates with the upper extremity. The brachial plexus is intimately associated with prominent vasculature. In the supraclavicular region, the subclavian vessels are in close proximity with the lower roots/lower trunk. In the infraclavicular region, the cords surround the axillary artery, and in the arm, the median nerve travels with the brachial artery.

Distal anatomical relationships
The upper, middle, and lower trunks ramify into their respective divisions posterior to the clavicle. The divisions form cords around the axillary artery. Each cord is named based on its relationship to the artery. The space around the plexus is in the form of a pyramid: the posterior wall around the distal plexus is formed by the subscapularis, teres major, and latissimus dorsi muscles; the anterior wall is formed by the pectoralis major, pectoralis minor, and the clavipectoral fascia; and the medial wall is formed by the upper ribs and the serratus anterior. The anterior and posterior walls converge along the medial humerus.

Surgical approaches to the brachial plexus

Anterior approach

Supraclavicular exposure
The supraclavicular brachial plexus is exposed in the posterior triangle of the neck. The patient is supine with a roll under the scapulae, and the head turned toward the opposite direction with the neck in gentle extension. If there is a need to acquire a sural nerve graft, a roll is also placed under the buttock to internally rotate and flex the ipsilateral leg. The lower part of the face, neck, shoulder, entire chest, and leg are prepped for surgery.
A curvilinear incision extending from the sternocleidomastoid muscle to the trapezius muscle is made approximately 1.5 cm above the clavicle. 7 The platysma is incised perpendicular to its fibers, and a generous subplatysmal dissection is performed. The external jugular vein is often encountered and must be retracted or ligated when necessary. The position of the spinal accessory nerve is relatively superficial as it courses from the posterior aspect of the sternocleidomastoid muscle (2/3 of the distance from the sternum to the mastoid) toward its insertion into the trapezius muscle ( Figures 1.5 , 1.6 ). Identification of the spinal accessory nerve along its course is crucial to preserve trapezius function and to use its branches as potential donors for nerve transfer. An intraoperative nerve stimulator can be used to identify and confirm this nerve.

Figure 1.5 Supraclavicular exposure of the brachial plexus/posterior triangle of the neck.

Figure 1.6 Exposure of the posterior triangle of the neck demonstrating the omohyoid and supraclavicular nerves.
The lateral margin of the sternocleidomastoid muscle is identified, with its sternal and clavicular heads. The lateral aspect of the clavicular head is released to facilitate exposure ( Figure 1.7 ). The supraclavicular nerves (sensory nerves branches of the ansa cervicalis, C2-C4) are identified along their superficial cranial-caudal course. These nerves are likewise preserved for anatomical landmarks and as potential donors for nerve graft material. The supraclavicular nerves are followed proximally until the C4 spinal nerve root is identified. From the C4 spinal nerve root, a branch from this nerve can be followed to the phrenic nerve, which is derived from C3, C4 and C5. The phrenic nerve is dissected along its length on the anterior aspect of the anterior scalene muscle. One should carefully mobilize the phrenic nerve to preserve function of the diaphragm. Periodic stimulation of the nerve with an intraoperative nerve stimulator will confirm intraoperative integrity of the nerve.

Figure 1.7 Supraclavicular exposure of the posterior triangle of the neck demonstrating a supraclavicular nerve and the phrenic nerve.
The lateral edge of the anterior scalene muscle is identified. The scalene fat pad is released from this border in a cranial-to-caudal direction, then in a medial-to-lateral direction to reflect the fat pad laterally. When releasing the fat pad deep in this region during exposure of the left supraclavicular brachial plexus, one should preserve or ligate the thoracic duct to avoid chyle leakage. The omohyoid muscle is identified along its course toward the suprascapular notch, and it can be tagged and divided. Note that preserving this muscle to identify the suprascapular notch can facilitate identification of the suprascapular nerve (see below), especially in patients whose anatomy is distorted by trauma.
The phrenic nerve courses lateral-to-medial toward the diaphragm, whereas the contents of the plexus and surrounding nerves course from medial-to-lateral. As the phrenic nerve approaches the lateral edge of the anterior scalene, the C5 spinal nerve root emerges ( Figure 1.8 ). Following the C5 root distally leads to the upper trunk, and following the upper trunk proximally will lead to the C6 spinal nerve root. The C6 spinal nerve root is located caudal and dorsal to the C5 spinal nerve root. The anterior tubercle of C6 is very prominent (Chassaignac’s tubercle). The C7, C8, and T1 spinal nerve roots are sequentially more caudal and dorsal. The transverse cervical artery and vein cross the C7 spinal nerve root and can be ligated. Following the C7 spinal nerve distally will reveal the middle trunk. The C8 and T1 spinal nerves combine quickly to form the lower trunk, which is adjacent to the subclavian vessels ( Figure 1.8 ). Roots of the lower trunk surround the first rib; therefore, care should be taken to avoid injury to the pleura. Should more proximal exposure of the nerve roots be necessary, the lateral edge of the anterior scalene muscle and the bony “chutes” conducting the spinal nerve roots can be resected. Occasionally, clear fluid may be observed during proximal exposure of the spinal nerve roots, indicating the presence of a pseudomeningocele and a likely avulsed root.

Figure 1.8 Supraclavicular exposure of the brachial plexus and its relationship to the subclavian artery.
The next step is to identify the suprascapular nerve and the divisions of the upper trunk. The upper trunk can be seen to “split” into 3 separate structures (lateral to medial): the suprascapular nerve, the posterior division, and the anterior division. Exposure of divisions of the brachial plexus can often be accomplished with downward retraction of the clavicle. Distally, the dorsal scapular artery and the suprascapular artery and vein lie at the level of the divisions of the plexus, which may be ligated as necessary for exposure. The clavicle can either be preserved and mobilized with traction or is cut. If an osteotomy is preferred, a clavicle plate should be applied initially and removed, and then the bone is cut to facilitate closure.

Infraclavicular exposure
The infraclavicular brachial plexus is exposed through the deltopectoral groove. The patient is placed in the supine position, and a linear incision is made from the clavicle toward the axilla, in line with the deltopectoral groove. The cephalic vein is visualized within the groove, and it can be retracted laterally or ligated. If needed, a portion of the pectoralis muscle can be detached from the inferior surface of the clavicle and from the humerus. The cuff of tendon from the humerus is tagged to facilitate later repair.
Once the interval is opened, the conjoint tendon can be identified originating from the coracoid, which consists of the short head of the biceps and coracobrachialis. Attachment of the pectoralis minor can be identified with the muscle proceeding medially; blunt dissection will separate the pectoralis minor from the surrounding tissues. This can be either transected and released or tagged for later repair. It is convenient to place sutures into the tendon on either side of the divided tendon for retraction and reapproximation.
Division of the pectoralis minor will reveal the infraclavicular brachial plexus lying immediately underneath ( Figure 1.9 ). When the arm is at or lower than the plane of the shoulder, the most superficial structures are the lateral cord with its lateral branch leading to the musculocutaneous nerve and its medial branch leading to the median nerve. The medial cord may be identified medial and slightly posterior to the axillary artery, and the lateral branch of the medial cord will lead to the median nerve (the medial branch continues down the arm as the ulnar nerve) ( Figure 1.10 ). Exposure of the posterior cord and its axillary and radial nerve branches is best accomplished in the region lateral to the axillary artery.

Figure 1.9 Infraclavicular exposure of the brachial plexus.

Posterior approach
The posterior approach is rarely used but can be applied to resection of proximal lower brachial plexus tumors or revision brachial plexus surgery. 8 The patient is positioned prone with the shoulder flexed and adducted to maximize scapular protraction. The head is turned toward the operative side to maximize access to the intervertebral foramina.
A curvilinear incision approximately 2 fingerbreadths medial to the medial border of the scapula is made, extending from the superior to inferior angle. The trapezius is released, then the medial musculature— rhomboid major, rhomboid minor, and levator scapulae—is transected trans-tendinously. If possible, a cuff of distal tendon should be preserved for repair. Care should be taken to preserve the dorsal scapular nerve and circumflex scapular artery.
The posterior and middle scalenes are released. If needed, a portion or the entire first rib can be resected extraperiosteally and the facets can be partially resected to gain access to the nerve roots.

Approach to the medial arm
The approach to the medial arm can be performed through an incision along the medial border of the biceps tendon. The axillary artery, median nerve, and ulnar nerve, as well as the medial brachial and medial antebrachial nerves, lie relatively superficially in the arm. In the mid-arm, the median nerve lies anterior to the artery and the ulnar nerve lies medial to the artery. In the distal humerus, the ulnar nerve pierces the intermuscular septum to proceed into the posterior compartment; whereas in the anterior compartment, the artery proceeds radial to the median nerve. When dissected more deeply, one will find the musculocutaneous nerve supplies the biceps and half of the brachialis, and the median nerve supplies the other half of the brachialis. The musculocutaneous nerve lies in the interval between the biceps and brachialis, terminating into the lateral antebrachial cutaneous nerve ( Figure 1.10 ).

Figure 1.10 Exposure of the nervous anatomy in the medial aspect of the arm.

Anatomic variability

Brachial plexus variations
The greatest anatomic variation of the plexus occurs with regard to the actual spinal roots that contribute to the brachial plexus. The typical schematic anatomy describes the brachial plexus as originating from C5 to T1; however, the brachial plexus may receive contributions from C4 or T2. Some authors have defined a “pre-fixed” plexus as one that receives a substantive contribution from C4 and a “post-fixed” plexus as one that receives a substantive contribution from T2 ( Figures 1.11 , 1.12 ). The occurrence rate for these aberrant contributions remains unclear. Estimates range from 15% to 75% and defining the exact prevalence requires further study.

Figure 1.11 Schematic diagram of the Pre-fixed brachial plexus.

Figure 1.12 Schematic diagram of the Post-fixed brachial plexus.
A relatively common variation occurs when the lateral cord contributes to the ulnar nerve. This variation has been reported in up to 43% of cases. A second variation may occur when contribution of the lateral cord to the median nerve is insignificant. Oftentimes when this occurs, there is a distal contribution of the musculocutaneous nerve to the median nerve.
There is some debate whether the posterior cord is in fact a true structure or whether it is just the radial and axillary nerves arising proximally and independently in the plexus and running together posterior to the axillary artery. Some dissections have noted an entirely independent course of the 2 nerves in 20% of specimens.

Brachial plexus/axillary artery variability
The relationship of the brachial plexus to the axillary artery varies widely as well. Miller 9 extensively studied 480 specimens and found 8% of cases demonstrating aberrant anatomy. She described 5 types of aberrant findings:
1 The brachial artery or a branch of the brachial artery is superficial to the median nerve.
2 The median nerve is divided by a branch of the artery.
3 A structure of the plexus is modified by an aberrant axillary artery.
4 A cord of the plexus is divided by an arterial branch.
5 The nerves communicate around the axillary artery or its branches.
Ultimately, these types of aberrant findings are variations of the axillary artery or a portion of the axillary artery traversing the brachial plexus more superficially.

Terminal branch variability
There is significant variation from the standard diagram used to describe the origin of terminal branches of the brachial plexus. In approximately 65% of cases, Ballesteros et al. 10 found aberrant origins of the long thoracic, upper subscapular, and inferior subscapular nerves. Dorsal subscapular nerves varied in 50% of cases, and the suprascapular and thoracodorsal had variant origin in approximately 20% of cases.

Conclusions
Brachial plexus injuries can be devastating to the patient’s normal functional status, and the long-term implications of these injuries are often not immediately understood by the patients or their families. The challenging achievement of optimal functional outcomes relies upon the basic schematic and functional anatomic knowledge. The treating practitioner must apply anatomical knowledge to the clinical presentation and the appropriate use of ancillary radiographic and electrodiagnostic studies to determine the proper course and timing of surgical treatment. With increased awareness of the condition and its anatomical basis, the outlook for patients suffering severe brachial plexus injures will continue to improve.

References

1 Leffert RD. Brachial plexus injuries . New York: Churchill Livingstone; 1985. p. ix
2 Kerr AT. The brachial plexus of nerves in man, the variations in its formation and branches. Am J Anat . 1918;23:285-395.
3 Harris W. The true form of the brachial plexus and its distribution. J Anat Physiol . 1904;33:399-422.
4 Walsh JF. The anatomy of the brachial plexus. Am J Med Sci . 1877;74:387-399.
5 Herzberg G, Narakas A, Comtet JJ, et al. Microsurgical relations of the roots of the brachial plexus. Practical applications. Ann Chir Main . 1985;4:120-133.
6 Hollinshead WH. Anatomy for surgeons . Philadelphia: Harper & Row; 1982.
7 Shin AY, Spinner RJ. Clinically relevant surgical anatomy and exposures of the brachial plexus. Hand Clin . 2005;21:1-11.
8 Biggs MT. Posterior subscapular approach for specific brachial plexus lesions. J Clin Neurosci . 2001;8:340-342.
9 Miller RA. Observations upon the arrangement of the axillary artery and brachial plexus. Am J Anat . 1939;64:143-163.
10 Ballesteros LE, Ramirez LM. Variations of the origin of collateral branches emerging from the posterior aspect of the brachial plexus. J Brachial Plex Peripher Nerve Inj . 2007;2:14.
CHAPTER 2 Physiology of nerve injury and regeneration

Lynda J.-S. Yang, MD, PhD, Kevin C. Chung, MD, MS


Summary box

1 Worldwide prevalence of brachial plexus/peripheral nerve injuries continues to increase as the rates of motor vehicle collisions and “extreme sporting” accidents increase.
2 Brachial plexus injuries can be classified in several ways: supra - versus infraclavicular; pre- versus postganglionic; closed versus open; neurapraxia, axonotmesis, or neurotmesis.
3 Lower elements of the brachial plexus are more susceptible to preganglionic (avulsion) injuries than upper elements.
4 After nerve injury, the proximal portion undergoes apoptosis with neuronal cell death, and if the neuronal cell body survives, it undergoes chromatolysis prior to regeneration.
5 After nerve injury, the distal portion undergoes Wallerian degeneration.
6 Denervation leads to a series of structural and electrical changes resulting in atrophy of the muscle if neural regeneration does not occur.
7 Fibrillations result from the acquired supersensitivity of muscle fibers to acetylcholine, which manifests clinically as spontaneous uncoordinated muscle activity.
8 Restoration of function after nerve injury comprises several arbitrarily divided processes: (a) survival of the neuronal cell, (b) axonal elongation, (c) axonal extension through the area of injury, (d) proper targeting to re-establish the neuromuscular junction, and (e) preservation of the integrity of the end organ muscle.
9 Following axonal regeneration, remyelination must occur for optimal functional recovery.
10 Functional recovery relies upon regenerating axons that can grow to reach their target muscle before the denervated muscle degenerates. Unfortunately, the rate of axon growth is only approximately 1 mm/day, so much research is underway to expedite nerve regeneration.

Introduction
In this chapter, we review the key physiological concepts underlying nerve injury and regeneration relevant to the clinical treatment of complex peripheral nerve disorders, such as brachial plexus palsies that manifest as paresis or paralysis of the upper extremity. Motor vehicle accidents cause approximately 70% of adult brachial plexus palsies (BPP). 1 Young adult males comprise a significant proportion of patients suffering traumatic palsies, and they encounter substantial socioeconomic difficulty as a result of their disability. 2 - 4 As the number of “extreme” sporting events and high-speed motor vehicle collisions increase, so does the worldwide prevalence of BPP. 3, 5 - 9 For countries such as Thailand, Vietnam, and India that rely on motorcycles as the main mode of transportation, the incidence of BPP is remarkably high. As the medical and surgical treatment of patients with BPP continues to improve, outcomes will be enhanced by increasing our knowledge of nerve and muscle pathophysiology after nerve injury and during neural regeneration.

Classifications of nerve injury
Injuries leading to brachial plexus palsies can be classified in several ways. They can be open or closed, sharp or ragged, clean or dirty. Consideration of the pathophysiology of these injury types led Dubuisson and Kline 10 to propose an algorithm for the timing of nerve repair ( Figure 2.1 ). Nerve injury can occur in either or all of the supraclavicular (roots, trunks), retroclavicular (divisions), and/or infraclavicular (cords, terminal branches) regions. Most injuries affect the nerve roots and trunks in the supraclavicular region. Supraclavicular injuries can be classified as preganglionic or postganglionic ( Figure 2.2 ), but this seemingly simple classification has profound implications. In preganglionic lesions, the nerve roots are avulsed from the spinal cord, making nerve repair essentially impossible. In contrast, postganglionic lesions imply that the cell body is anatomically preserved so the nerve can be repaired with expectation of nerve regeneration.

Figure 2.1 Algorithm for the timing of nerve surgery.
(Redrawn from Dubuisson A, Kline DG: Indications for peripheral nerve and brachial plexus surgery, Neurol Clin 10:935–951, 1992.)

Figure 2.2 Illustration of supraclavicular brachial plexus injury. Panels A and B represent lower nerve roots of the brachial plexus, which are mechanically more likely to sustain preganglionic injury. In contrast, panels C and D represent upper nerve roots of the brachial plexus, which are mechanically more likely to sustain postganglionic injury.
The nerve roots contributing to the trunks exit from their neural foramina and run along the bony groove between the anterior and posterior tubercles of the vertebrae. These bony “chutes” are well-formed and underlie the nerves comprising the upper trunk (C5, C6); however, these “chutes” are less well-defined for nerves comprising the lower trunk. In addition, there is less connective tissue binding the lower nerve roots to the bony chutes when compared to the upper nerve roots. Consequently, the lower nerve roots (C8, T1) are prone to preganglionic (avulsion) injury, whereas the nerves comprising the upper trunk tend to sustain postganglionic injury. A preganglionic injury results in permanent paralysis of the muscles innervated by the avulsed roots and complete sensory loss of the corresponding dermatomes. Spontaneous nerve regeneration is unlikely. A postganglionic injury allows potential retention of function of the cell body within the ventral horn of the spinal cord, and these neurons may regenerate axons under appropriate conditions.
At the microscopic level, Seddon proposed a system for classifying nerve injury in 1943 that is still useful today. 11 This classification system consists of neurapraxia, axonotmesis, and neurotmesis ( Figure 2.3 ). Neurapraxia refers to segmental interruption of the myelin sheath, which leaves the axons and surrounding connective tissues intact; this type of injury recovers spontaneously within a few weeks. Axonotmesis refers to interruption of both the myelin sheath and the axons, but with sparing of the surrounding connective tissues (intact Schwann cell basal lamina); this injury may recover spontaneously within months to years if axonal regeneration is able to progress across the injury zone. Neurotmesis refers to interruption of all elements including the axons, myelin sheaths, and surrounding connective tissues; spontaneous recovery does not occur.

Figure 2.3 Seddon’s classification of nerve injury: neurapraxia, axonotmesis, and neurotmesis.

Reaction to nerve injury

Nerve cell response to nerve injury
After a peripheral nerve is injured, a coordinated sequence of events occurs to remove the damaged tissue that ultimately initiates the regenerative process. When the nerve is disrupted, the severed ends retract due to the elasticity of the endoneurium. Trauma to the vasa nervorum occurs, which leads to robust inflammation triggering fibroblasts to proliferate to form the basis for a dense scar at the injury site. The scar may involve both adjacent elements and intrafascicular tissue, leading to significant inhibition of regeneration. In the most severe cases, the nerve ends become markedly disorganized, with fibroblasts, macrophages, capillaries, Schwann cells, and collagen fibers within which the regenerating axons form disorganized masses known as neuromas.
The proximal segment is generally reduced in diameter due to loss of functional connectivity to the end-organ muscle and ensheathing Schwann cells. Consequently, the conduction velocity of the injured nerve is reduced. Microscopically, the degree of damage sustained by the proximal segment and neuronal cell body depends on the distance of the zone of injury from the cell body. If the zone of injury is far from the neuronal cell body, the Schwann cells degrade and the axonal degradation may extend just to the adjacent node of Ranvier. However, if the zone of injury is near or adjacent to the neuronal cell body, neuronal degeneration may extend all the way to the cell body to cause neuronal cell death. For example, apoptosis-related cell death in dorsal root ganglion neurons following axonotmesis can reach 50%. 12 If the nerve cell body survives, stereotyped changes occur. The nucleus migrates to the periphery of the cell and select cytoplasmic elements (eg, Nissl granules, endoplasmic reticulum) undergo chromatolysis ( Figure 2.4 ). Cell survival has been shown to rely upon the Schwann cells and trophic molecules present in the immediate environment. 13, 14

Figure 2.4 Morphological changes in the injured neuron: (I) normal nerve cell; (II) after injury, the Nissl substance degenerates; (III) swollen cell body with eccentric nucleus/chromatolysis; (IVa) cell death; (IVb) cell recovery.
Conversely, the distal portion of the axon, which is disconnected from the cell body, undergoes granular disintegration of the cytoskeleton and axoplasm over several days to weeks. This degradative process, known as Wallerian degeneration, must be recognized in order to select the appropriate timing for diagnostic electrophysiologic studies. Early after injury, until the distal axons are totally degenerated, motor conductivity and/or sensory nerve potentials still can be observed in the distal segment. Therefore, electrodiagnostic studies used to predict severity of the lesion and to guide treatment recommendations should not be performed within the first several weeks after injury.
Wallerian degeneration involves both the neuron and the ensheathing myelin and begins hours after injury. The internal disarray of the microtubules and neurofilaments disrupts the axonal structure ( Figure 2.5 A and B ). Disintegration of myelin follows shortly thereafter. Within hours after injury, Schwann cells multiply to accommodate the amount of degenerated neural material to process and shuttle the debris to circulating macrophages; migration of these macrophages to the zone of injury is facilitated by serotonin and histamine released by endoneural mast cells ( Figure 2.5 C ). This complex sequence of degeneration is generally completed by 2 months, and endoneurial tubes and Schwann cells are all that remain ( Figure 2.5 D ).

Figure 2.5 Peripheral nerve degeneration and regeneration.
Without axons present, the endoneurial tubes shrink, and the endoneurial sheath progressively thickens due to collagen deposition along the Schwann cell basement membrane, ultimately obliterating the internal diameter of the tube unless a regenerating axon preserves the space ( Figure 2.5 E and F ). 15 The stacks of Schwann cell processes and collapsed endoneurial tubes are known as bands of Büngner.

Muscle response to denervation
When a peripheral nerve is injured, the accompanying muscle is denervated. Denervation leads to a series of structural changes and atrophy of the muscle if neural regeneration does not occur. A few days after nerve sectioning, the functional properties of denervated muscles change drastically. Atrophy is seen as a mean 70% reduction in the cross-sectional area after 2 months. 16 Changes in muscle activation are exemplified by fast muscle fibers that show a slowing of dynamic properties by prolonged contraction and relaxation times and decreased tension development rates and velocities. 17 These changes precede the more permanent morphological alterations that include proliferation of sarcoplasmic reticulum and shifts in myofibrillar isoforms in laboratory models. 18, 19 Sodium channels regress toward embryonic forms with altered biochemical properties, 20 - 22 and acetylcholine receptors redistribute to cover the entire muscle surface. 23, 24 This supersensitivity to acetylcholine manifests clinically as spontaneous uncoordin ated muscle activity, otherwise known as fibrillation.
The morphology and function of denervated muscles can be preserved through electrical stimulation, which supports the necessary role of neural stimulation in maintaining muscle physiology. 25 In addition, deficiency of neurotrophins at the neuromuscular junction is accompanied by muscle denervation. Ciliary neurotrophic factor has been implicated as a possible agent that could mediate the trophic action of nerve on muscle. 26, 27
Tissue reaction to nerve injury is evidenced by a vast proliferation of fibroblasts and deposition of new collagen in the peri- and endomysium. The space between the atrophied fibers is filled by thickened connective tissue, but the overall internal muscle structure is retained. Death of muscle fibers generally does not occur, but when it does, dropout occurs between 6 and 12 months after denervation. 16

Nerve regeneration
Nerve regeneration processes vary according to severity of the injury. For neurapraxic injuries, morphological and physiological changes are fully reversible with repair and restoration of function to the cell membranes of the axon and surrounding Schwann cells. Reversal of the conduction block restores normal axonal conduction. For axonotmetic injuries, the process is slower and relies upon the integrity of axonal regeneration. Although functional recovery is expected, it implies that the regenerating axons remain confined to the endoneurial sheath and encounter minimal scar tissue formation.
In neurotmesis, tissues surrounding the axon and the axon itself are disrupted, and regenerating axons are no longer within the guidance of the original endoneurial sheath. They digress toward surrounding tissues or enter adjacent endoneurial tubes resulting in failed restoration of the original neuromuscular connections. Functional recovery is ultimately compromised and reflective of the degree of the nerve injury.
Regeneration of the interrupted axon toward its correct muscular target depends on guidance by the basal Schwann cell lamina (axonotmesis) or grafted basal lamina (neurotmesis). Axons of the proximal stump will sprout, and a growth cone leads each sprout. The distal stump degenerates, and axonal and myelin debris will be cleared away by macrophages (Wallerian degeneration) to prepare the distal stump for reception of the outgrowing axonal sprouts. The “growing point” of the regenerating axons can produce paresthesias when tapped (Tinel’s sign). A neuroma is formed where the outgrowing stump of axonal growth cones is stymied by scar tissue at the injury site.
Restoration of function after nerve injury comprises several arbitrarily divided processes: (1) survival of the neuronal cell, (2) axonal elongation, (3) axonal extension through the area of injury, (4) proper targeting to re-establish the neuromuscular junction, and (5) preservation of the integrity of the end-organ muscle. Failure of any of these sequential processes will contribute to unsuccessful restoration of muscle function.
The timing of nerve regeneration lasts for months to years. If the neuronal cell body survives, reversal of chromatolysis is shown by morphological and metabolic changes in the cell body. The nucleus returns to the center of the cell, and Nissl granules are restored. Ribonucleic acid synthesis increases and neurotransmitter synthesis decreases, indicating the shift in cell function from synaptic transmission to cellular repair. Axoplasmic transport increases to supply adequate proteins and lipids from the cell body to the site of axonal regeneration. This regenerative response can persist for at least one year after injury.
Elongation of the axon likewise depends on the severity of the injury. Retrograde degradation determines the distance between the regenerating axon tip and the injury site as well as the latency time prior to initiation of elongation. The rate of elongation is affected not only by the condition of the neuronal cell body and of the regenerating axon, but also the extent of inhibition of axonal outgrowth by the injured tissue environment. The rate of axonal elongation is generally accepted to be approximately 1 mm per day, although regeneration after surgical nerve repair is thought to be slower. 16 Other encouraging factors include short distance to the elongating axon from the neuronal cell body, and younger patient age.
As the axon regenerates, targeting of the axon through the original endoneurial sheath is ideal, but no specific factor has been found to direct the elongating fiber. Surgical repair to bypass the injury site likewise provides no assurance of orientation or proper targeting. However, if an axon is successful in entering the endoneurial tube, it generally reaches the end organ muscle when an appropriate amount of time has elapsed. These endoneurial tubes are potential spaces rather than actual empty tubes into which axons extend. The newly proliferating Schwann cells organize themselves into columns. As the multiple filopodia comprising the regenerating axon growth cone sprout, they associate themselves with these Schwann cells and regenerate between the layers of basal lamina of the Schwann cell processes ( Figure 2.5 ). If the regenerating sprouts enter or travel along inappropriate tubes, misdirection of axonal growth occurs and the resultant motor/sensory function is not ideal. Optimal functional result depends on the number of axon sprouts that associate themselves with the appropriate Schwann cell columns to reinnervate suitable end organs. The remaining bands of Büngner in the distal nerve segment are interpreted to be endoneurial tubes that have not been re-innervated.
Reformation of the neuromuscular junction does not occur until the regenerating axon reaches the motor endplates; the synaptic folds of the motor endplates remain intact for >1 year after denervation. Collateral sprouting can occur, resulting in groups of reinnervated muscle fibers showing the electrodiagnostic phenomenon of polyphasic waves. This finding is characteristic of reinnervated muscle and is not seen in nascent musculature. Like the obstacles to neuronal regeneration, several factors can negatively affect functional muscle reinnervation. Intramuscular fibrosis will decrease the efficiency of a nerve impulse. The number of axons that successfully reconnect with the muscle affects functional recovery, but the integrity of reinnervation is also important. For example, if axons previously innervating slow fibers establish new connections with fast fibers, inefficient muscle contraction results. Likewise, failure to reinnervate sensory receptors can result in proprioceptive losses, ultimately limiting the usefulness of the return of motor function. Denervated sensory receptors can still recover useful functional connections after one year. 16
Following axonal regeneration, remyelination must occur for optimal functional recovery. Within 2 weeks of the initiation of axon regeneration, Schwann cells encircle the axon to reform the multi-lamellated sheath. Maturation of intercellular communications must occur with the aid of neurotrophic factors such as brain-derived neurotrophic factors, ciliary neurotrophic factor, and nerve growth factor. 14, 28 These molecules are involved in neuronal cell survival, maintenance, and repair by binding to specific cell surface receptors to ultimately regulate gene activation appropriate for the injury state of the neuron.

Conclusions/future improvements
Functional recovery relies upon regenerating axons that can grow to reach their target muscle before the denervated muscle degenerates. Unfortunately, the rate of axon regeneration is approximately 1 mm/day, so axonotmetic injury to the supraclavicular brachial plexus may require months to years before the recovering axons reach the distal musculature. After long periods of denervation, the distal musculature will have degenerated and the joints may develop contractures. Research for expediting nerve regeneration is underway and includes understanding the immunology of nerve transplantation, the use of novel nerve conduits and scaffolds, the use of electrical stimulation, the signals to encourage specific motor reinnervation, and overcoming the inhibitory environment to facilitate axon regeneration. 29, 30 However, adjunctive pharmacologic agents to enhance nerve regeneration are not currently ready for clinical use.

References

1 Narakas AO. The treatment of brachial plexus injuries. Int Orthop . 1985;9:29-36.
2 Allieu Y. Evolution of our indications for neurotization. Our concept of functional restoration of the upper limb after brachial plexus injuries. Chir Main . 1999;18:165-166.
3 Doi K, Muramatsu K, Hattori Y, et al. Restoration of prehension with the double free muscle technique following complete avulsion of the brachial plexus. Indications and long-term results. J Bone Joint Surg Am . 2000;82:652-666.
4 Malone JM, Leal JM, Underwood J, et al. Brachial plexus injury management through upper extremity amputation with immediate postoperative prostheses. Arch Phys Med Rehabil . 1982;63:89-91.
5 Allieu Y, Cenac P. Is surgical intervention justifiable for total paralysis secondary to multiple avulsion injuries of the brachial plexus? Hand Clin . 1988;4:609-618.
6 Azze RJ, Mattar Jenior J, Ferreira MC, et al. Extraplexual neurotization of brachial plexus. Microsurgery . 1994;15:28-32.
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CHAPTER 3 Clinical examination of the patient with brachial plexus palsy

Stephen M. Russell, MD, John E. McGillicuddy, MD


Summary box

1 Brachial plexus and upper extremity musculoskeletal anatomy must be thoroughly understood in order to properly examine, diagnose, and localize brachial plexus injuries.
2 The clinical examination of a patient with a brachial plexus injury requires practice, and should be performed in a comprehensive, step-wise fashion for each patient.
3 Proximal brachial plexus injuries may be localized based on the deficits observed with palsies affecting one or more spinal nerves.
4 Distal brachial plexus injuries may be localized based on the deficits observed with palsies affecting one or more terminal branches of the plexus (ie, musculocutaneous, median, ulnar, radial, and axillary nerves).
5 Sensory testing and the motor examination of smaller, direct branches off the brachial plexus (eg, dorsal scapular nerve) further localize the lesion within the plexus and help confirm the diagnosis.
6 Serial examinations over time, as well as corroboration with electrophysiological and imaging results, improve diagnostic accuracy.
7 Consistent, reproducible, and comprehensible documentation of clinical examination results are required for optimal patient care.

Introduction
The complex regional anatomy, along with the nuance and range of upper extremity function, can make physical examination and lesion localization within the brachial plexus a daunting task for the clinician. Nevertheless, once brachial plexus anatomy is mastered, the components of this structure can be considered separately during the examination, making lesion localization more straightforward. As with any injury affecting the musculoskeletal system, physical examination begins with a visual inspection and palpation of the affected limb, assessment of passive joint range of motion, inspection of joint/bone integrity, as well as a thorough neurological evaluation. Examining a patient over time (i.e., serial examinations) is a very important but often forgotten component of the diagnostic process.
In this chapter, the physical examination of brachial plexus injury will be described, along with comments on how to integrate abnormal findings into one’s thought process regarding lesion localization and diagnosis. The technique for examining muscles innervated by direct branches of the brachial plexus will be discussed in the text and photo-illustrated. Examination techniques for muscles innervated by the major terminal branches of the brachial plexus (ie, median, ulnar, musculocutaneous, and radial nerves) will not be reviewed in the text, but will be described in the video presentation associated with this chapter. Other sources may be reviewed for additional detail regarding upper extremity motor testing. 1, 2, 3

Visual inspection and general assessment
The patient should disrobe above the waist. Women are instructed to wear a sports bra so that they do not have to wear a gown during the examination, as a gown limits global comparison of the affected versus non-affected sides ( Figure 3.1 ). Shoulder position in relation to the normal shoulder may indicate a trapezius palsy. Scapular winging at rest should be documented. Any atrophy is noted, both from an anterior and posterior view. Previous surgical scars and penetrating wounds, healed and unhealed, are examined. Trophic skin changes can result from nerve injury; they can present as ulcers or wounds on the hand and often heal very poorly. The paraspinal muscles, supraclavicular space, infraclavicular space, axilla, and upper arm are all inspected and palpated. Palpation begins in a gentle manner and progresses to a more deep assessment of the soft tissues. The course of the brachial plexus is tapped by a reflex hammer or the examiner’s fingers to check for Hoffman-Tinel’s sign. The pupils should be examined to exclude Horner’s syndrome, which would indicate a very proximal injury to the T1 spinal nerve, usually its avulsion from the spinal cord. Pulses in the extremities are assessed, and auscultation and percussion of the lungs to exclude paralysis of a hemidiaphragm secondary to a phrenic nerve palsy.

Figure 3.1 This patient has severe atrophy affecting his left shoulder girdle secondary to a brachial plexus injury.

Passive range of motion of joints
Passive range of joint motion should be tested, including the cervical spine, shoulder, scapula, elbow, wrist, and hand. Contractures and pathological signs (e.g., simian hand, muscle atrophy) are documented. Any subluxation of the shoulder, including partial dislocation at rest secondary to rotator cuff muscle paralysis, should be carefully assessed. Point tenderness, marked joint trauma and contractures, or significant pain on passive movement may be signs of musculoskeletal injury preventing limb motion, and not neurological injury per se.

Muscle examination techniques TENTTMuscle (see video)
Documentation of motor strength requires an easy to remember and readily applicable grading scale. Use of a standardized scale is paramount for documenting a patient’s examination over time, as well as for comparing different individuals before and after treatment. The Medical Research Council published the classic motor function grading scale (MRC grading scale) shortly after World War II. 1 This grading scale is presented in Table 3.1 , and ranges from 5 (full strength) to 0 (no muscle contraction). The MRC grading scale is the best known and most utilized throughout the world. The simplicity of the MRC grading scale no doubt has contributed to its popularity; however, it has certain limitations that should be recognized. For example, it does not take into consideration range of motion, tends to be weighted toward weaker contractions, and is poorly applicable to certain muscles (e.g., rhomboids). In response to these deficiencies, other grading scales have been described. The Louisiana State University (LSU) motor function grading scales are popular amongst peripheral nerve surgeons and are specific for each major peripheral nerve or element of the brachial plexus. 4
Table 3.1 Medical Research Council motor function grading scale Grade Function 5 Full strength 4 Movement against resistance 3 Movement against gravity only 2 Movement with gravity eliminated 1 Muscle contraction but no movement 0 No muscle contraction
This section presents the examination technique for muscles innervated by direct branches of the brachial plexus. Examination techniques for other distal upper extremity musculature are well-known, are presented elsewhere in detail, 1, 3, 4 and are illustrated in the video supplement to this chapter.
The long thoracic nerve is a proximal branch of the brachial plexus, arising from the proximal C5, C6, and C7 spinal nerves, that innervates the serratus anterior muscle. This muscle originates on the lateral surfaces of the upper 8 ribs and inserts on the entire medial border of the scapula. It pulls the scapula away from the midline and forward around the thorax (scapular abduction). It also rotates the lateral angle of the scapula upward. Most importantly, however, this muscle fixes and stabilizes the scapula so that muscles originating from it can function properly. Furthermore, anterior arm flexion is stabilized by the serratus anterior, with flexion above 90 degrees mostly due to upward rotation of the scapula. Injury to the long thoracic nerve causes winging of the scapula. Winging may occur at rest, is most noticeable at the inferomedial angle, and is classically worsened when the patient pushes forward against resistance. Winging continues when the upper extremity is locked in extension with the shoulder girdle protracted forward (anteriorly). To test this muscle, instruct patients to reach for a point on the wall in front of them, and then apply resistance at the hand or wrist while stabilizing the thorax with the other hand ( Figure 3.2 ). A common mistake is to not have patients displace their shoulder girdle far enough forward, because without doing so, scapular winging due to trapezius or rhomboid weakness may be misdiagnosed as a long thoracic palsy. It is important to note that all 3 causes of scapular winging cause winging when the arm is pushed against resistance across the chest with the arm bent. Only serratus anterior weakness will show severe winging when pushing the fully extended arm forward (protracting) against resistance ( Figure 3.3 ).

Figure 3.2 Testing serratus anterior.

Figure 3.3 Scapular winging is present on the patient’s right side secondary to a spinal accessory palsy.
The dorsal scapular nerve is a very proximal branch from the C5 spinal root. This nerve innervates both the major and minor rhomboid muscles. The rhomboids connect the medial edge of the scapulae to the spinal column. When contracted, the rhomboids pull the scapula toward the midline (scapular adduction and retraction) and superiorly (downward rotation of the lateral angle). The rhomboids move the scapula in the opposite direction to that of the serratus anterior muscles. With chronic denervation, wasting of this muscle deep to the trapezius is evident. With rhomboid weakness, there may be mild scapular winging at rest, especially at the inferior medial edge. The scapula may also be displaced laterally and inferiorly and rotated laterally. To test the rhomboids, have patients place their palm facing outward on their lower back. Instruct them to push the palm away from the lower back as the examiner applies resistance to the hand as well as to the arm (the arm is pushed anterolaterally around the thorax) ( Figure 3.4 ). The rhomboids are observed and palpated along the medial scapular border during this maneuver. If the rhomboids are weak, only resist at the hand. An alternate method to examine the rhomboids is to have patients bring their shoulders and scapulae together posteriorly. In this position, the contracted rhomboids can be palpated between the lower aspects of the scapulae. The dorsal scapular nerve can also provide partial innervation to the levator scapulae as it passes underneath this muscle. This muscle assists the upper trapezius in shrugging the shoulders.

Figure 3.4 Testing rhomboids. Note palpation along the medial border of the scapula.
The suprascapular nerve (C5, C6) originates from the upper trunk of the brachial plexus and passes the inferior belly of the omohyoid to the suprascapular notch through which it passes to the posterior surface of the scapula. The suprascapular nerve innervates the supraspinatus and infraspinatus muscles. The supraspinatus attaches to the superior aspect of the humeral head and mediates the initial 20-30 degrees of arm abduction. The infraspinatus attaches to the posterior lateral aspect of the humeral head and is the primary external rotator of the arm. Test the supraspinatus muscle by having patients abduct a straight arm from their side against resistance ( Figure 3.5 ). Test the infraspinatus muscle by having patients flex their forearm to 90 degrees, and while stabilizing their elbow against their side, instruct them to externally rotate their arm against resistance, like a tennis swing ( Figure 3.6 ). Contraction can be observed and palpated over the scapula while testing these muscles. With chronic denervation, atrophy above (supraspinatus) or below (infraspinatus) the scapular spine is readily appreciated.

Figure 3.5 Testing supraspinatus.

Figure 3.6 Testing infraspinatus. It is important to keep the patient’s arm firmly against his side to prevent abduction mimicking external rotation.
The axillary nerve (C5, C6) arises from the posterior cord deep to the axillary artery and divides into an anterior and posterior division near the humeral neck as it passes medially and posteriorly to it. The anterior division innervates the anterior and lateral deltoid. The posterior division gives a branch to the teres minor, innervates the posterior portion of the deltoid, and gives a sensory branch to the lateral shoulder region. The teres minor assists the infraspinatus in externally rotating the arm. It also weakly assists the teres major in adducting an extended arm. It is not possible to test this muscle in complete isolation, but one may observe and palpate it if the patient is thin. The deltoid is the prime abductor, as well as flexor (lifting the arm in front of the body) of the arm. The initial 30 degrees of abduction is primarily controlled by the supraspinatus, whereas abduction above 90 degrees has an important trapezius and serratus component that tilts the shoulder girdle upward. Therefore, test the deltoid by having patients abduct their arm between 30 and 90 degrees against resistance ( Figure 3.7 ). The deltoid has 3 separate heads: the anterior, lateral, and posterior. Abducting the arm to the side and slightly in front of the body tests the anterior and lateral heads of the deltoid. To assess the posterior head, have patients place a straightened arm at almost 90 degrees abducted, and then ask them to move the arm posteriorly and superiorly against resistance ( Figure 3.8 ).

Figure 3.7 Testing deltoid.

Figure 3.8 Testing posterior deltoid. The patient should be instructed to both raise his arm and move it posteriorly in the same movement.
The lateral pectoral nerve (C5, C6) is a branch from the lateral cord. It often communicates with the medial pectoral nerve (C6-T1) and predominantly innervates the clavicular head of the pectoralis major. To test the clavicular head, and therefore the lateral pectoral nerve, have patients abduct their arm to 90 degrees with their forearm in flexion. Then, against resistance at the medial elbow, have them swing their arm toward midline ( Figure 3.9 ). The medial pectoral nerve originates from the medial cord and innervates the pectoralis minor and then pierces the clavipectoral fascia to innervate the sternal head of the pectoralis major. This nerve almost always communicates with the lateral pectoral nerve. To test the sternal head of the pectoralis major, patients should begin with their forearm flexed 90 degrees and their arm abducted about 30 degrees. Instruct the patient to adduct the arm against resistance ( Figure 3.10 ). The pectoralis minor cannot be adequately isolated from the pectoralis major and, therefore, cannot be tested in isolation.

Figure 3.9 Testing the clavicular head of pectoralis major. The muscle can be palpated immediately below the clavicle.

Figure 3.10 Testing the sternal head of the pectoralis major. The muscle can be palpated in the anterior axillary fold.
The upper and lower subscapular nerves (C5, C6) originate from the posterior cord. The upper subscapular nerve is not very long and enters and innervates the subscapularis muscle. The subscapularis muscle, along with the teres major (and latissimus dorsi and pectoralis major), internally rotates the arm. The subscapularis muscle cannot be completely isolated, but one can test internal arm rotation as a composite test ( Figure 3.11 ). The lower subscapular nerve innervates the lower half of the subscapularis muscle, as well as the teres major. To test the teres major, begin by having the patients abduct their arm to 90 degrees with the palm down. Instruct them to adduct their extended arm against resistance while you inspect the teres major ( Figure 3.12 ). Contraction of the teres major can be felt between the humerus and the lateral border of the scapula just below the shoulder joint.

Figure 3.11 Testing internal rotation of the arm, a composite of subscapularis, teres major, and pectoralis major. Difficult to sort out, but pectoralis and teres can be seen and felt during this test and weakness may be apparent in one. There is no way to solely evaluate the subscapularis.

Figure 3.12 Testing teres major. The muscle can be felt in the posterior axillary fold along the lateral margin of the scapula.
Another branch off the posterior cord is the thoracodorsal nerve (C7, C8), which innervates the latissimus dorsi muscle. To assess the latissimus dorsi, have patients adduct their arm when the forearm is flexed 90 degrees with the palm facing forward ( Figure 3.13 ). Muscle contraction can be palpated along the posterolateral chest wall. Latissimus dorsi contraction can also always be felt during a deep cough. In summary, all the branches from the posterior cord act to adduct and internally rotate the arm, a point worth remembering.

Figure 3.13 Testing latissimus dorsi. The muscle can be seen and felt on the lateral chest wall below the level of the scapula.
Although the spinal accessory nerve (cranial nerve XI) is not a branch of the brachial plexus, it is important to evaluate this nerve’s function because it is often used as a donor nerve during brachial plexus reconstruction, and it plays a major role in scapular and shoulder function. It stabilizes the scapula, thus allowing other shoulder girdle muscles to move the arm. Spinal accessory nerve palsy causes trapezius weakness. A patient with a weak trapezius reports trouble abducting the arm above the head (laterally), as well as major shoulder girdle discomfort. At rest, the affected shoulder often lies lower than the unaffected one. Even with a complete trapezius palsy, shoulder shrug weakness seldom occurs. This is because the levator scapulae muscle also shrugs the shoulders (innervated by the C3 and C4 ventral rami, via the cervical plexus). Weakness of the sternocleidomastoid muscle is rare, not only because its motor branches from the spinal accessory nerve branch quite proximally, but also because this muscle receives innervation from the cervical plexus. Secondary to the trapezius weakness, a spinal accessory palsy also causes scapular winging. Trapezius winging is mild at rest and usually involves the upper border of the scapula, although this is variable. Trapezius winging may be brought out by abducting the fully extended arm to 90 degrees. All types of winging (serratus anterior, trapezius, and rhomboid) are worse when an arm (partially flexed at the elbow) is pushed across the chest or in front of the body against resistance. However, only serratus anterior weakness causes winging when an extended, protracted arm is resisted. The presence of rhomboid weakness helps differentiate rhomboid versus trapezius winging.

Spinal myotomes as a template for the proximal brachial plexus
Spinal nerve myotomes (the muscles innervated by axons from a specific spinal nerve) remain useful for clinical evaluation of patients with proximal brachial plexus lesions. By matching the pattern of neurological deficit to each or a combination of spinal myotomes, lesions may be localized to the spinal nerve or trunk level. The C5 to T1 spinal nerve myotomes are subsequently reviewed.
Muscular innervation of the C5 spinal nerve includes arm abduction and external rotation. These 2 arm movements are very important for upper extremity function and are classically lost with upper brachial plexus injuries, including neonatal palsy (i.e., Erb’s palsy). The terminal branches mediating these movements include the axillary nerve to the deltoid muscle, and the suprascapular nerve to the supra- and infraspinatus muscles. A composite movement involving all 3 of these muscles, and therefore predominantly mediated by the C5 nerve root, is abduction of the arm. Beginning with the arms straight along the side of the body, the patient abducts them to 90 degrees while simultaneously externally rotating them so that the undersurface of the upper arm faces forward. The C5 dermatome covers the lateral portion of the shoulder and arm down to the elbow.
Muscular innervation of the C6 spinal nerve includes forearm supination and flexion, as well as arm extension/adduction. The radial nerve carries C6 innervation to the supinator (supination) and brachioradialis (forearm flexion with arm partially supinated), and the musculocutaneous nerve carries fibers to the biceps brachii (forearm flexion and supination) and brachialis (forearm flexion). The latissimus dorsi extends and adducts the arm via the thoracodorsal nerve, which is primarily C6 mediated (C7 can also provide major innervation to this muscle). A composite C6 body movement would be a classic underhand chin-up. For this movement, the supinated forearm flexes and latissimus dorsi contracts, pulling the chin over the bar. Lateral volar forearm and thumb are the sensory territory of the C6 spinal nerve.
With an upper trunk lesion, as expected, the C5 and C6 innervated muscles are weak. Therefore, the limb assumes a characteristic position at rest secondary to the unopposed action of the remaining musculature. Patients characteristically have their affected arm adducted and internally rotated (unopposed pull of pectoralis major), forearm extended and pronated (unopposed pull of the triceps and pronator teres), and the wrist and fingers flexed (from weak finger and wrist extensors [C6 co-innervated]). This position is also called a waiter’s tip hand. Weakness involving the rhomboids (dorsal scapular nerve), serratus anterior (long thoracic nerve), and/or diaphragm (phrenic nerve), helps localize the injury more proximally to the C5 and C6 spinal nerves where these branches originate, rather than the upper trunk per se. A lesion involving the upper trunk, or alternatively both the C5 and C6 spinal nerves, yields a sensory loss involving the lateral one-half of the arm and forearm, as well as the whole thumb.
Because the middle trunk is only comprised of fibers from the C7 spinal nerve, they will be considered together. Muscular control of the C7 nerve root includes the triceps (radial nerve), flexor carpi radialis (median nerve), flexor carpi ulnaris (ulnar nerve), and pronator teres (median nerve). The C7 also provides innervation to the wrist extensors, finger extensors, and finger flexors. However, innervation to these latter muscles is either variable or strongly shared with other nerve roots (ie, C6, C8), and therefore will not be considered an autonomous innervation of C7. Therefore, the composite movement of the C7 spinal nerve and middle trunk is the triceps pushdown. This movement is made when you push down on a tabletop when getting up from being seated at a table. For this to occur, one places the forearms in pronation (pronator teres), flexes the wrists (flexor carpi radialis and ulnaris), and contracts the triceps to extend the forearms. A person with a middle trunk palsy cannot do this. The volar and dorsal aspects of the long (middle) finger are almost exclusively within the C7 dermatome. Lesions of the middle trunk, comprised solely of C7 fibers, logically causes the same pattern of sensory loss as does a pure C7 palsy.
The C8 spinal nerve provides motor input to many of the long finger flexors (and extensors), as well as to the hand intrinsic muscles, sharing this latter innervation with T1. Some of the most common muscles to become weak with a C8 palsy include the flexor profundi to the index and long finger (distal interphalangeal joint flexion), thenar intrinsics including abductor pollicis brevis and opponens pollicis, and extensors to the thumb, index, and long finger. Therefore, a quick and easy way to assess C8 function would be to have the patient grasp and release your fingers, with attention paid especially to the first 3 digits. A patient with a C8 palsy will have trouble doing this smoothly, strongly, and repetitively. The C8 dermatome covers the medial, or ulnar, one-third of the hand, including the little finger and lateral hypothenar eminence.
The T1 spinal nerve is best tested in near isolation by having patients spread their fingers. This movement is mediated by the dorsal interossei muscles, which are predominantly T1 innervated. Atrophy of the first dorsal interosseus muscle, when present, is readily observed. The T1 sensory dermatome mainly covers the medial half of the forearm.
Because the lower trunk is comprised of the C8 and T1 nerve roots, injuries affecting this element cause marked hand weakness, including both hand grasp and finger spreading, as well as severe atrophy and trophic changes ( Figure 3.14 ). Injury to both the C8 and T1 spinal nerves is called a Klumpke’s palsy. When a Horner’s sign is present, T1 rootlet avulsion from the spinal cord is likely.

Figure 3.14 This patient has a “simian” hand deformity on the right, secondary to a complete lower trunk brachial plexus palsy.

“Plus” palsies as a template for the distal brachial plexus
To assess the distal brachial plexus, one needs to be familiar with patterns of neurological deficits that may occur following injury to the terminal branches of the plexus: musculocutaneous, median, ulnar, radial, and axillary nerves. With this prerequisite knowledge, diagnosis of injury localized to the brachial plexus cords is straightforward, being more or less a variation or combination of one or more of these major branches. Analogous to the proximal brachial plexus injury being assessed using its spinal nerve components, the distal plexus is evaluated in the context of its major terminal branches.
The lateral cord is formed by the anterior divisions of both upper and middle trunks, and therefore, contains fibers from C5, C6, and C7. This cord terminates by providing the median nerve’s lateral component (C5-C7), and then continuing distally as the musculocutaneous nerve. As expected, an isolated lesion to the lateral cord consists of a musculocutaneous nerve palsy, plus a partial median nerve deficit; that is, one only involving the median nerve’s C5 to C7 portion. This deficit pattern may be termed a musculocutaneous “plus” palsy.
The classic musculocutaneous palsy causes forearm flexion weakness secondary to biceps brachii, coracobrachialis, and brachialis weakness, and sensory loss in the lateral forearm (lateral antebrachial cutaneous nerve). As alluded to earlier, median nerve function can be divided into lateral (C5-C7; lateral cord) and medial (C8-T1; medial cord) components. The lateral cord provides all the median nerve’s sensory fibers (the medial cord does not provide any cutaneous sensation to the median nerve). Therefore, sensory loss in the lateral palm and first 3 digits occurs with a lateral cord injury. Although the lateral cord component is primarily sensory, it also controls the more proximal median innervated muscles (pronator teres and flexor carpi radialis) so that weakness in pronation and wrist flexion will be seen. Any wrist flexion will be from flexor carpi ulnaris (medial cord) and will show ulnar deviation as well. Furthermore, weakness of the clavicular head of the pectoralis major should also occur, considering that the medial pectoral nerve, which innervates this muscle, originates from the lateral cord.
The medial cord is a continuation of the lower trunk’s anterior division, containing C8 and T1 nerve fibers. The medial cord provides the medial contribution of the median nerve, containing C8 and T1 fibers, and then continues as the ulnar nerve into the arm. Therefore, an isolated medial cord lesion consists of an ulnar nerve palsy, plus loss of the C8 and T1 components of the median nerve. An ulnar palsy would cause weakness in wrist flexion (flexor carpi ulnaris), distal interphalangeal joint flexion weakness involving the ring and little fingers (flexor digitorum profundi), little finger movements (opponens, flexor, and abductor digiti minimi), and finger abduction and adduction (interossei). Medial cord sensory loss involves the medial one-third of the hand. As mentioned, the medial component of the median nerve controls median innervated hand intrinsics, including the opponens pollicis, flexor pollicis brevis (superficial head), abductor pollicis brevis, and the first 2 lumbricals. Therefore, a medial cord lesion, or ulnar “plus” palsy, would, in addition to causing ulnar motor loss, cause median innervated thumb weakness and trouble extending the proximal interphalangeal joints of the first 2 fingers (lumbricals). The medial cord also has a few side branches that can be utilized to confirm medial cord involvement. The medial brachial and antebrachial cutaneous nerves originate from the distal medial cord and mediate sensation over the medial aspect of the arm and forearm, respectively. The medial pectoral nerve originates from the proximal medial cord, and if damaged, leads to weakness in the sternal head of the pectoralis major.
The posterior cord comprises the posterior division of all 3 trunks and contains input from C5 to C8. Because the 2 terminal branches of the posterior cord are the radial and axillary nerves, a combination palsy of these 2 nerves is the hallmark of a posterior cord injury. Therefore, a posterior cord injury may also be called a radial axillary palsy. A radial palsy causes weakness in forearm extension (triceps), forearm supination (supinator), wrist extension (extensor carpi radialis longus and brevis, extensor carpi ulnaris), and finger/thumb extension (superficial and deep finger extensors). Radial nerve sensory loss involves the posterior arm (posterior brachial cutaneous nerve) and forearm (posterior antebrachial cutaneous nerve), the lower lateral aspect of the arm (lower lateral brachial cutaneous nerve), and lateral dorsal hand (superficial sensory radial nerve). An axillary nerve palsy causes arm abduction weakness secondary to deltoid paralysis. An axillary nerve lesion can also cause sensory loss in the upper lateral arm (upper lateral brachial cutaneous nerve), especially if the patient is examined soon after injury. Furthermore, arm adduction and internal rotation weakness helps confirm posterior cord damage, because these muscles are controlled by the minor branches off the posterior cord (upper and lower subscapular, and thoracodorsal nerves).

Divisional injuries to the brachial plexus
Unfortunately, isolated injury to one of the brachial plexus divisions can be difficult to clinically differentiate from cord or trunk level lesions. Nevertheless, an isolated injury to one or more divisions yields neurological deficits which are the same, or less severe, than a cord level injury. For example, an injury to the anterior division of the lower trunk (C8/T1) should involve nearly all fibers in the medial cord. A divisional injury involving the lateral cord can affect either the anterior division of either the upper (C5/C6) or middle trunks (C7). With an ability to readily diagnose proximal and distal brachial plexus lesions, one can perform a mental deduction to account for a divisional injury. Fortunately, injuries only involving the divisions are infrequently encountered.

Sensibility testing in patients with brachial plexus injuries
The C5 dermatome covers the lateral portion of the shoulder and arm down to the elbow ( Figure 3.15 ). Sensation from this area is carried in part by the upper lateral cutaneous nerve from the axillary nerve, as well as the lower lateral brachial cutaneous nerve from the proximal radial nerve. Lateral forearm and thumb are the sensory territory of the C6 spinal nerve. This sensation is carried in part by the lateral antebrachial cutaneous nerve off the musculocutaneous nerve, and for the thumb, by the terminal sensory branches of both the median (volar surface) and radial (dorsal surface) nerves. A lesion involving the upper trunk, or alternatively both the C5 and C6 spinal nerves, yields a sensory loss involving the lateral one-half of the arm and forearm, as well as the whole thumb.

Figure 3.15 Upper extremity dermatome schematic.
The volar and dorsal aspects of the long finger are almost exclusively within the C7 dermatome. The sensory division of the median nerve (volar aspect of the finger and nail bed) and the superficial sensory radial nerve (dorsal aspect of the finger) carry this sensation. Lesions of the middle trunk, comprised solely of C7 fibers, logically cause the same pattern of sensory loss as does a pure C7 palsy.
The C8 dermatome covers the medial, or ulnar, one-third of the hand, including the little finger and lateral hypothenar eminence. The dorsal ulnar cutaneous and palmar ulnar cutaneous nerves, along with the superficial sensory division of the ulnar nerve, carry sensation from this area. The T1 sensory dermatome mainly covers the medial half of the forearm, with its sensory fibers being carried by the medial antebrachial cutaneous nerve, a distal branch of the medial cord. A lower trunk, or combination C8 and T1 spinal nerve lesion, causes a sensory loss in the medial portion of the forearm and hand, including the little finger. Of note, the medial arm is mostly covered by the T2 dermatome, with the axilla (and some proximal medial arm) covered by T3.

Step-by-step examination of the brachial plexus (see video)
Despite localization being based on spinal myotomes and “plus” palsies, for simplicity, one should proceed proximal to distal when examining muscles of the shoulder girdle, arm, and hand ( Table 3.2 ).
Table 3.2 Step-by-step brachial plexus examination Anatomic area Examination targets Back     Observation   Rhomboids   Latissimus dorsi   Trapezius   Scapular winging Shoulder     Supraspinatus   Deltoid   Posterior deltoid   Teres major   Pectoralis major   Infraspinatus Arm     Triceps   Biceps   Brachioradialis Forearm     Supinator   Pronators   Wrist flexion   Wrist extension   Finger extension Hand     Observation   Finger flexion   Thenar intrinsics   Hypothenar intrinsics   Interossei   Lumbricals Skin     Sensation   Horner’s syndrome   Hoffman-Tinel’s sign
Start with the back. Examination begins with the patient facing away from the examiner. The presence of scapular winging, muscle atrophy, and asymmetry of the shoulders and scapulae at rest are noted. Next, the patient shrugs their shoulders upward to assess trapezius and levator scapulae function. Having the patient bring the scapulae together assesses the rhomboids. The latissimus dorsi is palpated bilaterally and the patient is asked to cough. The patient is instructed to raise his arms above his head to check trapezius function. Next, the patient should reach toward the wall with the affected arm. Scapular winging is assessed, with the upper extremity extended straight and protracted (long thoracic palsy), then partially flexed at the elbow (all types of winging).
Next, examine the shoulder. Beginning with the arm straight along his side, the patient is instructed to abduct the arm. In doing so, the supraspinatus and deltoids are assessed. With the arm horizontal to the floor, the posterior head of the deltoid (posterior movement) and teres major (downward movement) are tested. The patient then flexes the arm 90 degrees at the elbow and both the clavicular head of the pectoralis major (lateral pectoral nerve) followed by the sternal head (medial pectoral nerve) are assessed. Facing the patient’s flank, external arm rotation is tested (infraspinatus).
Proceed to test the arm, then forearm. The triceps are examined with the arm flexed at the shoulder, bringing it parallel to the floor in order to eliminate the effect of gravity. Forearm flexion at the elbow is tested with the forearm fully supinated (biceps brachii) and half supinated (brachioradialis). Supination and pronation are tested with the elbow straight to isolate supinator and pronator teres function. Next, wrist movement is assessed. The patient flexes the wrist (flexor carpi radialis and ulnaris), and then the arm is pronated and the forearm extensors are tested (extensor carpi radialis longus and brevis and extensor carpi ulnaris). With the arm placed on a flat surface, the long forearm finger extensors (extensor digitorum communis, extensor indicis, extensor digiti minimi, and extensors pollicis longus and brevis) are also evaluated.
Next, examine the hand. The hand is first observed at rest for signs of atrophy. The patient should open and close the hand so an ulnar claw hand or “benediction” (median nerve) sign can be observed, if present. Next, the thumb is evaluated further, including abduction, adduction, opposition, and flexion. Check for OK and Froment’s signs. Flexion at the proximal (flexor digitorum superficialis) and distal (flexor digitorum profundus) interphalangeal joints is assessed. Abduction and opposition of the little finger are evaluated, as well as Wartenburg’s and palmaris brevis signs. Finger abduction (dorsal interossei), adduction (palmar interossei), and extension at the interphalangeal joints is tested (lumbricals).
Finally, evaluate the skin. Sensation with light touch and pinprick is tested from the shoulder down to the hand. Testing is performed circumferentially on the arm, forearm, and hand. The fingertips are also tested, which is especially important. Any abnormality or asymmetry between the upper extremities is further evaluated, including assessment of 2-point discrimination and localization (patients close their eyes). Lack of sweating on the fingertips may be observed with an ophthalmoscope. The neck and axilla are palpated and observed for scars and masses. Pulses and biceps and triceps reflexes (C6, C7) are also tested.

Brachial plexus examination in infants
For infants and toddlers, the brachial plexus examination is based more on observation than on muscular testing based on examiner command. Therefore, additional time should be taken during a consultation with an infant so that all functional deficiencies may be observed. It is suggested that the mother be present and intermittently hold and/or interact with the child to pacify them as needed. Furthermore, if possible, a pediatric physical therapist should be present during the preoperative consultation, both to help note deficits as well as to document the patient’s baseline neuromuscular evaluation.
The following signs should be noted. Presence of a Horner’s syndrome that would indicate a lower plexus avulsion or proximal lower plexus injury should be documented. Limb atrophy and length discrepancies should be noted. The shoulder, arm, and hand range of motion, including internal and external rotation, should be passively tested. Any shoulder crepitus, marked discomfort, or incongruities along the clavicle on palpation are documented and may indicate a fracture or dislocation. Skin breakdown, infections, or repetitive biting or sucking of the hand or fingers may indicate neuropathic pain. The resting position of the arm and hand may reveal a classic Erb-Duchenne (upper plexus) or Dejerine-Klumpke (lower plexus) palsy. Spontaneous use of each arm is observed. Arm usage and range of motion is viewed when the child interacts with the mother or with toys. The normal arm may be gently immobilized to provoke movement in the affected arm in response to toys, keys, or food. For example, can the child bring a cookie to the mouth with the affected hand? The child can be placed prone to observe lifting of the torso by one or both arms, as well as arm symmetry during crawling or rolling. The neuromuscular examination may be supplemented with an MRI (or CT myelogram) of the cervical spine to document pseudomeningoceles, chest radiograph to check for clavicular fractures and paralysis of the hemidiaphragm, MRI of the shoulder to evaluate dysplastic changes involving the glenohumeral joint, and serial electromyography. Because these tests may be invasive or require sedation, they are applied on a case-by-case basis.

Summary
Once brachial plexus anatomy is understood and muscular examination techniques are mastered, the physical examination of brachial plexus injuries can be broken down into anatomical components, which makes diagnosis and localization readily achievable. With experience, the examination becomes routine and may be customized based on each individual’s clinical history.

Acknowledgments
The authors thank Dr. Anthony Wang and Ms. Amy Yamasaki for their assistance with creating the video associated with this chapter.

References

1 O’Brien MD. Aids to the examination of the peripheral nervous system , 4th ed. Philadelphia: W.B. Saunders Company; 2000.
2 Hislop HJ, Montgomery J. Daniels and Worthington’s muscle testing: techniques of manual examination , 7th ed. Philadelphia: W.B. Saunders Company; 2002.
3 Russell SM. Examination of peripheral nerve injury: an anatomical approach . New York: Thieme; 2006.
4 Kim DH, Midha R, Murovic JA, et al. Kline and Hudson’s nerve injuries: operative results for major nerve injuries, entrapments, and tumors , 2nd ed. Philadelphia: Saunders; 2007.
Section Two
Pediatric Brachial Plexus Palsies
CHAPTER 4 Clinical presentation and considerations of neonatal brachial plexus palsy

Lynda J.-S. Yang, MD, PhD, John E. McGillicuddy, MD, Wilson Chimbira, MBChB, FRCA


Summary box

1 Neonatal brachial plexus palsy (NBPP) can be defined as a flaccid paresis of an upper extremity due to traumatic stretching of the brachial plexus, with the passive range of motion greater than the active.
2 The incidence of this condition varies somewhat with different factors including geography and baby size, but published values range from 0.10 to 5.1 cases per 1000 live births.
3 High birth weight, maternal diabetes during pregnancy, and shoulder dystocia are risk factors that have been associated with NBPP.
4 Various classification schemes have been reported for NBPP, each with its own merit.
5 The natural history of NBPP remains controversial: some investigators provide an encouraging view with over 80% occurrence of a favorable outcome or complete recovery whereas other authors provide a contrasting view with less than 50% good recovery with persisting disabilities.
6 Earlier recovery presages more favorable recovery.
7 A thorough maternal, obstetric, and perinatal history is crucial for providing relevant information that helps to direct the physical examination.
8 Neonates are unable to comply with voluntary maneuvers of the physical examination; therefore, different strategies must be used to assess NBPP patients, although the basic anatomical principles remain constant. Once the diagnosis is made, the parents / caretakers must be counseled appropriately.
9 Commonly used assessment scales in NBPP have primarily focused upon joint angles or muscle activation.
10 Global functional/disablement scales must be developed in the future for determining the optimal treatment and for evaluating treatment efficacy.

Introduction
Neonatal brachial plexus palsy (NBPP) can be defined as a flaccid paresis of an upper extremity due to traumatic stretching of the brachial plexus, with the passive range of motion greater than the active. 1 The first description of NBPP was reported in the 18th century, and the noticeably shortened weak arm of Kaiser Wilhelm II of Germany has been attributed to NBPP. 2 Approximately 1200 reports regarding NBPP exist in Medline from 1948 to the present, with nearly 100 of those reports within the last year. Increased interest in this condition has paralleled the improvement in outcomes that is attributed to increased recognition of this condition, improved care, and expanding research via interdisciplinary collaborations.

Incidence
The incidence of this condition varies based on geography of the reported regions and baby size, but published values range from 0.10 to 5.1 cases per 1000 live births. 3 - 12 For instance, in the United States, analysis of data from the Kids’ Inpatient Database of over 11 million recorded births over 3 non-consecutive years yielded a mean +/− standard error of 1.51 +/− 0.02 cases per 1000 live births. 13 Bilateral brachial plexus palsies occur in 8.3–23% of cases, primarily occurring with breech presentation. 14 - 17 Advancements in modern neonatal and obstetric care, including more frequent use of Caesarian sections, were purported to decrease the incidence of NBPP, 18, 19 but recent published reports have not supported this idea. 20 - 22

Risk factors
NBPP has been associated with several maternal characteristics including advanced age (>35 yrs), 23 pelvic anatomy 24 high body mass indices (BMI), 25, 26 diabetes, 27 and primiparity. 28 Diabetes was present in 21% (vs 3–5% in the normal population) and hypertension was present in 17% (vs 2–3%) of women whose babies had NBPP (unpublished data). The most significant characteristic of the baby is high birth weight (>4 kg) 7, 8, 18, 27, 29 although the relationship between increasing birth weight and increasing severity of NBPP remains uncertain. Approximately 14% of babies with NBPP had 5-minute Apgar scores of less than 7 (vs 3.8%); 30 similarly, others report 49% of babies had an Apgar score of < or = to 7 at one minute. 23, 30 Labor and delivery factors include breech position, 31 shoulder dystocia, 32 forceps delivery, 7, 22 vacuum extraction, 7 clavicle fracture, 22, 23 precipitous delivery, prolonged labor (second stage), 28 and mode of delivery. These factors are addressed in detail in Chapter 5 .

Classification of clinical presentation
The most useful classification scheme was proposed by Gilbert and Tassin, 33 refined by Narakas ( Table 4.1 ), 34, 35 and supported by Birch. 36 The brachial plexus comprises the C5 through T1 nerve roots, and Group I represents the clinical findings resulting from nerve injury of C5 and C6, hallmarked by paresis of the deltoid and biceps but active function in limb extensors, wrist and hand. The clinical findings in Group II are related to injury of C5, C6 and C7. In addition to paresis of the deltoid and biceps, paresis of triceps and wrist extensors is also obvious; however, the long flexors and intrinsic muscles of the hand are relatively unaffected. Group III represents paresis of the entire arm consistent with injury of C5, C6, C7, C8, and T1. Group IV manifests as a paralyzed limb with the additional presence of Horner’s syndrome (ptosis, meiosis, anhydrosis) that implies injury to the all the nerve roots of the brachial plexus with a very severe proximal injury to the lower nerve roots. This Gilbert and Tassin/Narakas classification of NBPP was proposed following a prospective study of the natural history of the condition, discussed further in the next section. As such, when used between 2 and 4 weeks after birth (when neurapraxic lesions would be recovering), this system permits definition of the extent of injury and, more importantly, may guide prognosis.
Table 4.1 Gilbert and Tassin/Narakas classification scheme used for grading the severity of NBPP and for prognosis Group Affected nerve roots Rate of full spontaneous recovery I C5, C6 ~ 90% II C5, C6, C7 ~ 65% III C5, C6, C7, C8, T1 < 50% IV C5, C6, C7, C8, T1 with Horner’s syndrome ~ 0%
Other classification schemes are based on the anatomy and physiology of nerve injury. Sunderland reported a physiologic scheme comprising four types of injuries in increasing severity (neurapraxia, neuroma, rupture, and avulsion) 37 . He and others use an anatomical scheme comprising four categories based on anatomical location: upper, intermediate, lower and total plexus palsy. 38, 39 The concept of an upper plexus palsy involving C5, C6 and sometimes C7 was initially defined anatomically by Erb in 1874 40 after Duchenne in 1872 described four cases of complete paralysis involving loss of shoulder control and elbow flexion. 41 The upper palsy, also called Erb’s palsy is the most common type of NBPP. 36, 42 Erb’s palsy is visually recognized by the stereotyped “waiter’s tip posture” with the arm adducted, shoulder internally rotated, wrist flexed, fingers extended. Intermediate palsy was described by Jolly in 1896 43 and Thomas in 1905, 44 and this condition was thought to involve C7, C8 and Tl roots with the arms abducted, the elbows flexed, and the fingers/hands flaccid. Subsequently the muscles supplied by C8 and Tl spontaneously recovered to some extent but not those supplied by C7. A majority of these cases were bilateral and thought to be related to an obscure obstetric practice. Lower plexus palsy was described by Dejerine-Klumpke. 45, 46 This type of NBPP is rare 9, 47 but can be recognized by a flaccid hand in an otherwise active arm. Total plexus palsy is essentially the condition as described for Narakas Grades III and IV, and it is a devastating condition with total loss of function of the arm.

Natural history
The natural history of NBPP, around which the determination of optimal treatment revolves, remains the subject of speculation and is debated in many published reports. The evolution of NBPP is difficult to define because of the various combinations of lesions within the elements of the brachial plexus. Further difficulties include the interpretation of what constitutes recovery and the potential bias introduced by the referral patterns of reporting physicians, 48, 49 as many patients with Erb’s palsy recover spontaneously and are not referred to the specialists who publish most reports. With these caveats in mind, many authors provide an encouraging view of the natural history of NBPP with over 80% occurrence of a favorable outcome or complete recovery 14, 15, 50 - 53 whereas other authors provide a contrasting view with less than 50% good recovery or persisting disabilities. 49, 54 - 58 Regardless of the neurologic recovery, functional recovery can yet be compromised by musculoskeletal defects, (e.g. contractures, joint subluxation) even with appropriate therapy management. 59
Most practitioners agree that as the extent and severity of NBPP increase, the potential for recovery decreases. 15, 60, 61 A detailed prospective study by Gilbert and Tassin 33 reported that 32% made a complete recovery. These patients were characterized by early rapid improvements in arm function with recovery of deltoid and biceps before 2 months of age. Forty-three percent made far less than full recovery. This group of patients was characterized by slow progress, with no evidence of biceps recovery until after 6 months of age. Their study led to the following prognostic conclusions: 90% of patients with Group I NBPP progressed to full spontaneous recovery if there were clinical signs of recovery before 2 months of age. Approximately 65% of patients with Group II palsy recovered fully, but the remainder had persisting defects in shoulder and elbow movement. The timing of recovery of this group of patients is delayed with clinical signs of recovery not evident until 3 to 6 months of age. For Group III patients, less than 50% recover fully spontaneously, with the majority of patients disabled by significant deficits of movement throughout the arm; in approximately 25% of patients, even wrist and finger extension remain functionally compromised. Patients with Group IV NBPP have little if any chance for a full spontaneous recovery; the stark reality is the expectation of a complete neurologic deficit of motor and sensory function in the affected arm. This classification/prognostication system attributed to Gilbert and Tassin, and Narakas remains a popular classification system not only for describing the severity of the pathology but also as a strong predictor of outcomes. 22
Similarly, most practitioners agree that early recovery is associated with favorable outcomes. 62 The Collaborative Perinatal Study reported that 93% of patients who went on to full spontaneous recovery had done so by 4 months of age. 15 Metaizeau et al. reported that patients who showed no signs of clinical improvement by 3 months did not recover function adequately, and those who continued not to show improvement by 6 months had essentially no chance of adequate functional recovery. 63 Bennet and Harrold reported that their patients who recovered fully began to show clinical signs of improvement by 2 weeks of age. 14 Yet other authors contend that all patients who recover satisfactorily achieve biceps and deltoid function by 3 months of age, 64, 65 and failure of recovery of anti-gravity power in the proximal muscle groups by 6 months of age essentially presages future moderate to severe weakness in the affected extremity. 66, 67 Note, however, that early elbow flexion alone is likely not a sufficient criterion to recommend for or against nerve repair reconstruction. 68
The predictors of recovery described above use simple clinical muscle assessments, but some authors have constructed paradigms based of more complicated statistical analyses of multiple independent clinical variables, 50, 69 but these models show only modest improvement in predicting recovery.

Assessment of the NBPP patient

Physical examination
The basic premises of the brachial plexus examination can be found in Chapter 3 . However, many of these maneuvers require voluntary cooperation of the patient that the neonates are unable to provide. Therefore, different strategies must be used to assess NBPP patients, although the basic anatomical principles remain constant. Once the diagnosis is made, the parents/caretakers must be counseled appropriately.
Prior to the physical examination, a thorough maternal, obstetric, and perinatal history (detailed in Chapter 12 ) is crucial for providing relevant information that helps to direct the physical examination. In the early days after birth, skeletal injuries/fractures should be detected by clinical and radiographic examination and treated accordingly after performing a standard neonatal medical examination. Spontaneous movements and normal reflexes should be observed, and deficits may indicate other associated disorders such as cerebral palsy or cortical dysplasia. 70 Gentle handling of the neck and affected limb is appropriate, but no immobilization is recommended for NBPP that is not associated with skeletal injuries. Asymmetric expansion of the chest cavity and difficulty with oxygenation or feeding may indicate phrenic nerve palsy that can be confirmed with plain radiographs or ultrasound; this can be a dangerous condition resulting in early failure to thrive and should be addressed promptly. 71 Observation of ptosis and meiosis are consistent with Horner’s syndrome that may indicate severe NBPP. Likewise, observation of classic postures (e.g. waiter’s tip) implies particular NBPP lesions.
Passive range of motion should be assessed. Generally contractures and joint subluxations do not develop for several months after birth, and early limitations of passive range of motion may indicate other musculoskeletal abnormalities. 72, 73 Active range of motion and muscle power can be difficult to assess, but engaging the neonate or child in play with toys or with irritating stimuli can be instructive: much can be gleaned from responses such as reaching out to grasp keys on a key ring, placing a cracker into the mouth, and assuming weight-bearing postures such as side sitting or crawling. As the baby grows, measurements of the circumference and length of the arm should be tracked as indicators of musculoskeletal dysfunction. 74 Sensory function is similarly difficult to assess in detail, but a gestalt determination can be made by judging the baby’s response to particular stimuli (e.g. pinprick, pinch, heat or cold). Indications of chewing or biting of the arm / hand imply sensory alterations in the affected area. 75 The presence of skin rashes in dermatomal distributions can also indicate sensory alterations.
Supplementing the physical examination with radiographic and electrodiagnostic findings is helpful to decide whether nerve repair reconstruction will be beneficial, and detailed discussions regarding these topics are beyond the scope of this chapter and are found in Chapters 7 , 8 and 9 .

Peri-operative/anesthetic assessment
In the patient who requires surgical nerve repair/reconstruction, a necessary pre-operative assessment regards the neonate’s tolerance for anesthesia. For relatively short procedures such as CT-myelogram, the anesthesiologist must assess the patient for intravenous access and control of oxygenation during prone positioning. After placement of standard American Society of Anesthesiologists (ASA) monitors, anesthesia is induced using oxygen, nitrous oxide, and sevofluorane. Intravenous access is acquired and secured without using the unaffected upper extremity, thereby reserving the vessels in the unaffected upper extremity for easier intravenous access on the day of surgery which may be as early as a few days after the radiographic study. Because the positioning of the patient changes during the procedure, control of the airway is imperative: the airway must be firmly secured with an appropriately sized cuffed endotracheal tube that can be quite small, then the patient is turned prone with all pressure points padded. At the end of the procedure the patient is extubated awake and discharged home from the post anesthesia care unit once the discharge criteria are met.
For the longer procedures including surgical nerve repair reconstruction, the anesthesiologist’s concerns increase because anesthetic complications are a leading cause of intraoperative morbidity. 76 Pre-operative assessment of the neonate broadens to account for (i) the length of the procedure (over 6 hours), (ii) the availability of only one extremity for intravenous access and monitoring (both legs are prepared for potential harvesting of the sural nerves), (iii) the inability to use chemical paralytic agents because neurophysiological studies are used during surgery. Pre-operatively, midazolam 0.5 mg/kg orally can be used if separation anxiety is obvious. Anesthesia is then induced with oxygen, nitrous oxide, and sevoflurane. A peripheral intravenous catheter is placed and secured carefully in the unaffected upper extremity by the most experienced member of the anesthesia team (this is not a case for inexperienced personnel because there is only one limb to work with and very few veins that are readily accessible.) Propofol 1 mg/kg is given to facilitate endotracheal intubation and avoidance of muscle relaxants because of neurophysiologic assessment that will be used during surgery. The proper securing of the endotracheal tube to the contralateral side cannot be overemphasized. La Scala et al. found the most significant intraoperative complication in their series of patients undergoing brachial plexus surgery was inadvertent extubation that was resolved by suturing the endotracheal tube. 76 An alternative solution is to insert and maintain the endotracheal tube slightly deeper during surgery. A radial arterial line is placed in the same limb as the intravenous catheter for hemodynamic monitoring as well as for regular intraoperative assessment of hematocrit and blood glucose.
Due to the need for neurophysiologic assessment during surgery, maintenance of anesthesia involves a combination of remifentanil (0.05-0.5 mcg/kg/min) and isoflurane (1 MAC or less titrated to effect). Dexmedetomidine 0.1-0.5 mcg/kg/hr can be added to supplement the anesthesia with minimal effect on monitoring while allowing a reduction in the amount of volatile agent being administered. 77 Intraoperative neurophysiologic assessment may necessitate temporary muscle paralysis to reduce artifacts and can be achieved for approximately 30 minutes with cisatracurium (0.1 mg/kg). Perioperative fluid overload should be minimized by restricting intraoperative fluids to 4 ml/kg/hr. Assessment of fluid overload includes the monitoring of oxygen saturation to avoid pulmonary edema. The duration of surgery necessitates the tracking of blood glucose and hematocrit hourly. Continued postoperative vigilance of oxygen saturation and fluid status is necessary, especially if the baby is immobilized in a restrictive brace.

Assessment scales
Commonly used assessment scales in NBPP are used preoperatively but are more often used postoperatively to assess recovery. These scales primarily focus upon joint angles or muscle activation. For example, muscle power is generally expressed via the UK Medical Research Council Scale for muscle movement (MRC scale) ( Table 4.2 ). This provides structured grading of individual muscle groups, but does not provide any information about overall function of the limb or child. Because the MRC scale requires voluntary cooperation, it is difficult to apply in newborns. To overcome these difficulties in assessing the motor function in newborns, Curtis et al. proposed the Active Movement Scale (AMS) ( Table 4.3 ). 78 In 2 complementary studies, the AMS was reported to be a reliable tool for evaluating infants with upper-extremity paresis and its inter-rater variability was independent of the rater experience. Moving more towards function of the whole limb, the Mallet scale provides a quantifiable assessment for shoulder function ( Figure 4.1 ). 79 The inter-observer reliability of the Mallet score has been reported for the various movements, with the mean weighted kappa ranging from 0.53 for hand to mouth to 0.75 for abduction. 80 The Mallet scale can be used in conjunction with Gilbert’s classification of shoulder paralysis ( Table 4.4 ) with some consistency reported between the two systems. 36 The movements assessed in the Mallet scale use the shoulder and elbow. It primarily addresses upper plexus function after 3 years of age because it requires cooperation of the child. Likewise, limitations in passive range of motion, apraxia or neglect can alter the interpretation of the results. 81 The interobserver reliability and internal consistency for the Mallet score and the AMS were reported as reliable instruments for addressing upper extremity function in patients with NBPP. 82 For elbow function, an elbow recovery scale has been suggested by Gilbert and Raimondi ( Table 4.5 ). 83 Similarly, Raimondi has proposed a hand evaluation scale ( Table 4.6 ) 84 which has been used to assess hand function after nerve repair reconstruction and found to correlate with the pre-operative Gilbert and Tassin/Narakas grade. 85
Table 4.2 UK Medical Research Council Scale for muscle movement (MRC scale) for muscle power M1 Palpable muscle contraction without movement M2 Movement in a horizontal plane M3 Movement overcoming the pull of gravity M4 Movement overcoming resistance beyond the pull of gravity M5 Normal strength
Table 4.3 The Active Movement Scale (AMS) for assessing motor function in newborns Observation Muscle grade Gravity eliminated   No contraction 0 Contraction, no motion 1 Motion ≤ 1/2 range 2 Motion > 1/2 range 3 Full motion 4 Against gravity   Motion ≤ 1/2 range 5 Motion > 1/2 range 6 Full motion 7

Figure 4.1 The Mallet test for assessing shoulder function.
Table 4.4 Gilbert scale for staging shoulder function Shoulder function Stage Flail shoulder 0 Abduction or flexion to 45°; no active external I Abduction < 90°; external rotation to neutral II Abduction = 90°; weak external rotation III Abduction < 120°; incomplete external rotation IV Abduction > 120°; active external rotation V Normal VI
Table 4.5 Gilbert and Raimondi scale for evaluating elbow recovery Elbow function Score Flexion:   Nil or some contraction 1 Incomplete flexion 2 Complete flexion 3 Extension:   No extension 0 Weak extension 1 Good extension 2 Extension deficit:   0–30° 0 30–50° −1 >50° −2
Table 4.6 Raimondi scale for evaluating hand function Description Grade Complete paralysis or slight finger flexion of no use; useless thumb – no pinch; some or no sensation 0 Limited active flexion of fingers; no extension of wrist or fingers; possibility of thumb lateral pinch I Active flexion of wrist, with passive flexion of fingers (tenodesis); passive lateral pinch of thumb II Active complete flexion of wrist and fingers; mobile thumb with partial abduction – opposition. Intrinsic balance; no active supination; good possibilities for palliative surgery III Active complete flexion of wrist and fingers; active wrist extension; weak or absent finger extension. Good thumb opposition, with active ulnaris intrinsics; partial pronation/supination IV Hand IV, with finger extension and almost complete pronation/supination V
These assessment scales attempt to address the function of a particular muscle, joint, or limb. They have been the mainstay of preoperative evaluation and of postoperative outcomes recording as a measure of success, 65, 86 - 88 but they do little to address the overall function of the child. 89 A scheme based on five dimensions of disablement was proposed by the National Center for Medical Rehabilitation Research, 90 comprised of pathophysiology, impairment, functional limitation (activity), disability (participation), and societal limitation: it well demonstrates the shortcomings of the assessment scales described above especially regarding the functional limitation (activity), disability (participation), and societal limitation in patients with NBPP. Likewise, the International Classification Functioning, Disability, and Health defines function as body functions, activities, and participation. 91 Towards this end, Bellew et al. reported developmental and behavioral problems that were independent of Apgar scores in children with NBPP. 11 Boeschoten et al. reported a defined set of activities that were scored by videotape which shows potential for assessing the functional activities of children with NBPP, but a number of difficulties remain in observing and scoring by this method. 92 Speech dominance 93 and limb preference 94 have also been studied in the context of NBPP. Sundholm et al. contend that NBPP should be described in terms of impairment and disability and reported that most children had difficulty with activities of daily living. 95
Another step toward the assessment of the more global function of the child with NBPP used the Pediatric Outcomes Data Collection Instrument (PODCI). 96 This assessment obtains semi-quantitative, patient- and parent-reported measures of function and quality of life with respect to several domains: mobility and transfers, upper extremity (UE) function, ability to participate in sports, comfort or pain, and happiness. Except for the happiness domain, the instrument has been validated, 97, 98 and normative values for children without musculoskeletal limitations have been published. 99 With regard to NBPP, the PODCI was shown to reliably differentiate children who were potential candidates for reconstructive surgery from children without a musculoskeletal disorder. 96 Similarly, the PODCI has been applied to evaluating the results of tendon transfers for shoulder external rotation in children with NBPP. 100 Further characterization of the use of the PODCI in NBPP focused upon its correlation with other known measures of active movement. 101 Mean PODCI scores ranged from 35.1–100 (mean = 82.4) in NBPP patients versus the published value of 93.3 in normal children. Significant correlations existed between the PODCI scores and the other instruments for active movement, and the level of correlation with each of the other instruments varied by age. An encouraging report showed that despite lower PODCI scores, children with NBPP safely participated in a variety of sports at levels similar to their peers. 102
With further regard to self-care and activities of daily living, the Pediatric Evaluation of Disability Inventory (PEDI) was not shown to discriminate between the self-care ability of children with NBPP versus their peers but was effective in distinguishing between the different levels of NBPP severity. 103 The PEDI is a tool used to determine a child’s ability to perform their self-care activities in relation to their developmental age-expected performance. 104 Application of PODCI and PEDI are important steps toward functional assessments that can be used for determining optimal treatment as well as for evaluations of treatment efficacy in patients with NBPP.

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CHAPTER 5 Neonatal brachial plexus palsy
Antecedent obstetrical factors

Bernard Gonik, MD


Summary box

1 Neonatal brachial plexus palsy (NBPP) is identified in the immediate neonatal period and is due to trauma to the fetal brachial plexus at some point prior to completion of delivery.
2 The incidence of NBPP is reported to be approximately 1.5 per 1000 live births.
3 The majority of NBPP events are transient, eventually resulting in full return of function.
4 Compression, traction, vascular disruption, and inflammation have all been identified as pathologic mechanisms.
5 Upper trunk, lower trunk, complete (total), and bilateral brachial plexus injuries have been described.
6 A number of common obstetrical conditions have been reported to be associated with the occurrence of NBPP, including shoulder dystocia.
7 Recent data have highlighted the contribution of both endogenous and exogenous delivery forces on brachial plexus integrity. Threshold limits for brachial plexus disruption in the clinical arena have not been defined and likely vary based on a number of factors including fetal acid/base status, surrounding muscle tone, and the anatomic relationships of the fetal head to the aftercoming shoulders.
8 Laboratory modeling data have shown that currently established clinician-applied maneuvers at the time of shoulder dystocia identification reduces extraction forces and brachial plexus stretch.
9 General concepts on shoulder dystocia management include early identification of the obstruction, call for assistance, delaying further efforts at fetal delivery until attempts have been made to alleviate the obstruction, maintaining axial positioning of the fetal head, application of established shoulder dystocia maneuvers, and limiting the amount of extraction forces applied.
10 Given the infrequent occurrence of shoulder dystocia, no clinician can be guaranteed expertise in the management of this condition solely based on personal clinical experience. Therefore, recent attention has been focused on the need for high-fidelity simulation training models to improve clinician perception and management of this acute obstetric emergency.

Introduction
Neonatal brachial plexus palsy (NBPP) is typically defined as a finding identified in the immediate neonatal period due to trauma to the fetal brachial plexus at some point prior to completion of delivery. Although many times it is empirically assumed that the inciting pathophysiologic event occurs during the second stage of labor (specifically with extraction of the fetal shoulders), in fact, the exact timing of this event is poorly understood. There have been arguments presented in the literature that support an in utero occurrence prior to the labor process, an intrapartum event prior to the identification and delivery of an impacted fetal shoulder, or during the disimpaction process related to endogenously and exogenously applied forces to the fetus.
The incidence of NBPP is reported to be approximately 1.5/1000 live births, and has not decreased in recent years. 1, 2 According to the majority of reports, most injuries are transient with full return of function in 70–92% of cases, whereas in selected cases, permanent injuries after the identification of neonatal brachial plexopathy have been reported to occur with an incidence of 25-78%. 2 Chauhan and colleagues 3 described some common obstetric conditions associated with the occurrence of neonatal brachial plexus palsy in their tertiary care center over a 23-year time period. These have been summarized in Table 5.1 .
Table 5.1 Common obstetrical conditions associated with neonatal brachial plexus palsy Median gestational age 39 weeks Mean birth weight 3752 grams Diabetes (gestational and pre-gestational) 11% Neonatal weight > 4000 grams 37% Labor induction 13% Labor augmentation 40% Epidural usage 32% Spontaneous vaginal delivery 52%
Total number of deliveries = 89,978
Total number of cases with brachial plexus palsy = 185
Modified from Chauhan SP, Rose CH, Gherman RB, et al: Brachial plexus injury: a 23-year experience from a tertiary center. Am J Obstet Gynecol 192:1795-1802, 2005
NBPP can be divided into six clinical presentations: 1) complete (total) brachial plexus palsy; 2) Duchenne-Erb palsy; 3) upper-middle trunk brachial plexus palsy; 4) Klumpke palsy; 5) fascicular brachial plexus palsy; 6) bilateral brachial plexus palsy. 4 The two most common presentations of NBPP encountered in obstetrical practice are Duchenne-Erb and Klumpke palsies. The former occurs due to involvement of fifth and sixth cervical nerve roots, resulting in weakness of shoulder abduction, external rotation, elbow flexion, and forearm supination. There is minimal, if any, weakness in wrist and finger extension, and winging of the scapula may be present. Klumpke palsy results from involvement of the eighth cervical and first thoracic nerve roots, causing occasional weakness of elbow flexion, forearm supination, or wrist extension, but always with weakness of the hand, which may result in a claw-like deformity of the hand. 4 The prognosis for injuries isolated to the upper nerve trunk is significantly more favorable than those that include the lower components of the brachial plexus. Sjoberg and colleagues 5 reported that 66% of palsies involving both the upper and lower trunks were permanent as compared to only 21% of Duchenne-Erb’s palsy cases.

Risk factors for NBPP
It is difficult to tease out individual risk factors for brachial plexus palsy in the neonate, in that many overlap. Some, such as vaginal breech delivery with hyperabduction of the fetal arms, are primarily of historical interest because of the sharp decline in this route of delivery. Most authorities agree that the occurrence of injury in the clinical arena cannot be accurately predicted based on epidemiologically derived risk factors reported in the literature. In fact, there are a number of reports that describe brachial plexus palsies in newborn infants without any identifiable risk factors being present. 6, 7 Obstetrical factors and the risk for brachial plexus palsy in the delivering neonate are listed in Table 5.2 . 8
Table 5.2 Obstetrical risk factors for neonatal brachial plexus palsy Risk factor Odds ratio 95% Confidence interval Maternal weight > 90 kg 1.3 0.2-62.6 Postdate pregnancy 1.8 0.9-3.9 Diabetes 3.2 1.6-6.3 Fetal macrosomia     4000–4500 9.6 6.2-14.9 >4500 17.9 10.3-31.3 >5000 45.2 15.8-128.8 Assisted delivery     Low-forceps 3.7 2.0-7.0 Mid-forceps 3.7 5.7-59.3 Vacuum extractor 17.2 5.1-58.2 Cesarean delivery 0.5 0.1-1.9 Prolonged second stage of labor 8.3 4.0-17.3 Epidural anesthesia 2.0 1.2-3.5 Use of Oxytocin 3.7 1.1-2.6 Shoulder dystocia 340.5 46.9-897.3 Application of fundal pressure 27.5 4.0-1163.4
Modified from Gherman RB, Ouzounian JG, Goodwin TM: Brachial plexus palsy: an in utero injury? Am J Obstet Gynecol 180:1303–1307, 1999
Shoulder dystocia appears prominently in this table, and in most investigations related to NBPP. Shoulder dystocia is the initial failure to deliver the fetal shoulder after the head has been delivered. The anterior, posterior, or both shoulders can be involved and the delivery route can be vaginal or by cesarean delivery. The majority of times, shoulder dystocia is a subjectively determined event, with the attending clinician assessing the degree of difficulty associated with extraction of the fetal shoulders. Sometimes utilization of specific maternal or fetal maneuvers is used to establish the occurrence of a shoulder dystocia event, as is recommended by both the Royal and American Colleges of Obstetricians and Gynecologists. 9, 10 An objective definition based on prolongation of the head-to-body delivery interval greater than 60 seconds, with or without ancillary obstetric maneuvers, has been suggested but is not commonly employed in clinical practice. 11 The incidence of shoulder dystocia deliveries has been reported to be 0.2–2.1 percent of live births. 11, 12
Of interest, although a shoulder dystocia event has the highest odds ratio of NBPP as shown in Table 5.2 , 8 nearly half of all brachial plexus injuries occur without the identification of this obstetrical complication. In the largest series to date, 57% of NBPP were not associated with the occurrence of shoulder dystocia. 12 Although one may argue that this is because of under-reporting, in fact, multiple studies consistently support this finding. A confounding variable – neonatal weight – influences this relationship. In cases of NBPP, the finding of a shoulder dystocia event increases from 22% to 74% when birth weight goes from <3.5 kg to >4.5 kg, respectively. Some investigators have postulated that non-shoulder dystocia cases associated with NBP likely occur due to different mechanistic processes in labor 8, 13 and there is controversy as to whether these non-shoulder dystocia cases have a better 13 or worse 8 prognosis for full recovery.

Pathophysiologic mechanisms of NBPP
Compression, traction (with or without shoulder-neck angle widening), vascular disruption, and inflammation are identified pathologic mechanisms by which the newborn’s brachial plexus can be transiently or permanently affected. Intrauterine compressive brachial palsy is usually associated with an observed deformity of the upper limb, and may be caused by compression from a uterine anomaly and uterine or pelvic mass during gestation. 14, 15 Gonik and colleagues 16 have also recently described a mathematical model that hypothesizes the occurrence of brachial plexus compression underneath the symphysis pubis at the time of vaginal delivery. This compression of the brachial plexus is thought to be the result of either exogenous force generated by the delivering clinician with extraction of the anterior fetal shoulder or related to maternal endogenous forces with attempts to expulse the obstructed fetus.
Inflammation-induced disruption of the brachial plexus due to in utero viral 17 or bacterial 18 infection has been reported. In these cases, other associated findings are typically seen, such as muscular atrophy of the affected arm or humeral osteomyelitis. Other less common causes of in utero NBPP include hemangiomas, exostosis of the first rib, and neoplasms in the region of the brachial plexus.
Traction/stretching as an etiology for brachial plexus palsy in the newborn has received the most attention, particularly related to the occurrence of shoulder dystocia at the time of delivery. For many years the naïve explanation for NBPP associated with shoulder dystocia was that too much traction was applied by the clinician in an attempt to clear (usually) the anterior fetal shoulder from underneath the maternal symphysis pubis. As an aside, this “excessive” force has been the battle cry of the medicolegal community, as plaintiff and defense attempt to justify or explain why the injury took place. Of critical importance, one needs to first define excessive compared to what. Clearly from the obstetrician’s perspective, whatever force is applied to complete the delivery process is necessary, because without this assistance the fetus might suffer hypoxic injury or death by remaining in situ . The term “excessive” must therefore mean the force that is in excess to the inherent strength of the structure in question, here being the fetal brachial plexus. Germane to this discussion, these threshold forces have yet to be defined in the clinical setting and more importantly, may vary considerably depending on other factors such as the fetal acid/base status, muscle tone of the surrounding neck muscles, the anatomic relationship of the fetal head to the aftercoming shoulders, and the direction of any force that is applied. An additional factor needs to be mentioned, and that is the delivering clinician has a difficult time accurately perceiving the force that is being applied, regardless of the clinician’s years of experience, gender, or body mass index. 19, 20 With the use of a recently developed high-fidelity shoulder dystocia simulation mannequin, Crofts et al. 21 demonstrated a very wide range of “diagnostic traction” peak forces (6-250 Newtons) being applied before the implementation of shoulder dystocia maneuvers.

Delivery forces and their effect on the brachial plexus
In an attempt to better define the forces at play in the delivery process, bioengineering models have been developed to simulate vaginal delivery, specifically with obstruction of the anterior fetal shoulder, as is the case with shoulder dystocia. All of these modeling efforts have as an inherent limitation, the artificial nature of the construct, and therefore can be used to study process but not establish absolutes with regard to thresholds within the clinical setting. Allen and colleagues 22 examined shoulder extraction forces using force-sensing devices implanted in the fingertips of the clinician’s gloved hand. The results demonstrated a wide range of applied forces (25–100 Newtons). In this same series of experiments, objective engineering parameters could be retrospectively used to define the degree of difficulty in shoulder extraction. Acknowledging that the clinician’s perception of force is suboptimal under these circumstances, the investigators helped to define in situ extraction force parameters for the first time, the importance of counterintuitive behavior such as slow and steady application of force and, most importantly, the critical need for the development of teaching models to improve clinician perception and skills.
This same group of investigators designed and tested a laboratory maternal/fetal model for shoulder extraction in an attempt to study the fetal effects of clinician-applied forces. 23 As the fetal model was made “larger,” the anterior shoulder obstruction behind the maternal symphysis pubis became more pronounced and led to rapidly increasing extraction forces. In comparison to the axial fetal neck extension measurements, as the total applied force increased, extension (or stretching) within the fetal brachial plexus increased in a divergent fashion, suggesting a concentration of force within this region. Of particular interest was the finding that by rotating the maternal pelvis cephalad (McRoberts maneuver), overall extraction forces decreased as did brachial plexus extension and clavicular fracture. These latter data objectively supported clinically derived experiences with the use of McRoberts maneuver for shoulder dystocia events. 24 Several years later, another group of investigators utilizing a similar laboratory model examined another shoulder dystocia maneuver (manual rotation of the fetal shoulders anteriorly or posteriorly to 30 degrees), again objectively demonstrating significant reduction in anterior shoulder extraction forces. 25
To specifically examine in situ brachial plexus strain, a commercially available computer simulation software package (MADYMO, version 5.4, TNO Automotive, Delft, The Netherlands) was modified to study these biomechanics during a simulated obstructed vaginal delivery. 26, 27 Robustness of the model allowed for examination of maternally derived endogenous force, clinician-applied exogenous force, and various maneuvers and positions used clinically during shoulder dystocia. The results demonstrated that with the mother in the lithotomy position, brachial plexus stretching was observed with both endogenous and exogenous forces. Downward lateral displacement of the fetal head with extraction efforts led to a 30% increase in brachial plexus stretch compared to axially applied traction by the clinician. Application of maneuvers, including McRoberts rotation of the maternal pelvis, suprapubic pressure, oblique positioning of the fetal shoulders, and delivery of the posterior arm, all reduced brachial plexus strain. An interesting finding in the above study was that some of the largest amounts of brachial plexus stretching occurred when endogenous force was applied, but the delivery was not accomplished. This is perhaps analogous to the initial clinical occurrence of a shoulder dystocia event prior to any clinician attempts at delivery of the fetus. Allen and colleagues 28 using a different bioengineering laboratory model, similarly recorded brachial plexus strain during simulated routine and shoulder dystocia deliveries, suggesting all second-stage labors involve some degree of brachial plexus stretch during pelvic descent, crowning, and head restitution of the fetus.
As mentioned previously, thresholds for brachial plexus nerve injury have not been defined clinically, despite some in the field erroneously labeling 100 Newtons as an “injury-defining force.” Several tangential experimental studies have attempted to better define this issue. Caulfield et al. 29 using finite element idealization of the newborn spine and brachial plexus, applied loads ranging from 25 to 140 Newtons along the axis of the spine. They demonstrated that nerve stress increased linearly as load increased with a concentration of stress in the upper cervical roots and along the posterior nerve groups. At 140 Newtons, the nerves became stretched to a point in which they could no longer extend. Not specific to the brachial plexus, de Medinaceli and colleagues 30 noted that in their experimental model of isolated nerve stretch, a damaged or crushed nerve requires less stretch to result in functional deficit (perhaps can be extrapolated to a combination of compression and traction during a shoulder dystocia occurrence). Also, fixing the nerve in place (as might occur with pinning the brachial plexus against the symphysis pubis) results in a functional shortening of the nerve segment and therefore theoretically requires less traction force to induce injury.
Using infant cadavers, Metaizeau and associates 31 attempted to simulate traction to the fetal head being applied during shoulder dystocia, and demonstrated a wide range of forces (200–400 Newtons) that were associated with brachial plexus palsy. Many variables contributed to this wide scatter of injurious forces, including axis of traction, joint laxity, tissue thickness, infant weight, and collar bone fracture. They also acknowledged that because of their study design, which included dissection of the sternocleidomastoid muscle, direct quantitative comparisons could not be made with the clinical environment. They reported a chronology of lesions, first starting with the upper C5 and C6 levels, and progressing to the lower C7 and C8 levels. Of note, Jennett and colleagues 32 contradict these conclusions based on clinical observations, suggesting a different mechanism of injury when the lower plexus is involved.

Timing of the brachial plexus insult
The actual timing of when an injury occurs to the brachial plexus of the neonate is less important from a management standpoint as it is from the medicolegal perspective. Those injuries that occurred early as an in utero event may have other physical findings such as muscle atrophy or bone demineralization in the affected extremity. Later onset events may have no other associated findings. Likewise, injury to the brachial plexus that occurs during the labor process cannot be timed accurately to reflect an injury before or after the clinician has intervened to accomplish the delivery. This is despite (usually medicolegal) attempts to correlate neonatal sites of bruising with such associations.
Of interest, a medical malpractice case in 1989 reported the use of electromyography (EMG) in a 5-day-old newborn infant to define a brachial plexus palsy as an in utero event, based on the fact that muscle fibrillations were identified suggesting denervation. Unfortunately, this was extrapolated from adult-derived data that define EMG observed denervation as occurring 10–14 days after the acute injury. Gonik and colleagues 33 examined this relationship in the newborn piglet model and showed that after complete transection of the brachial plexus, denervation was detected by EMG beginning at 24 hours after the injury was induced. This refutes the use of EMG as previously described to establish an in utero occurrence for the injury. It also prompts the need to re-evaluate previously reported clinical observations of in utero injuries that were based on such EMG studies to time the event. 34 In the future, early EMG testing (and other diagnostic studies such as MRI) may have a place in therapeutic interventions, such as when immediate nerve repair/reconstruction may be a consideration.

Obstetrical management
The primary focus of this discussion centers on the management of shoulder dystocia because this is where the major impact might be seen. As previously noted, the incidence of brachial plexus palsy in the newborn has remained at the same level or higher despite significant attention to this obstetrical problem. 1, 2 This topic has extensively been reviewed elsewhere by Gherman et al. 35 In general terms, the lack of predictability based on historical or clinical features limits clinician intervention until the event has occurred. Screening for these “risk factors” can still be justified, in that it allows for proactive patient counseling and possible prophylactic preparation. The American College of Obstetricians and Gynecologists advocates offering gravidas with fetuses having an estimated fetal weight of >5000 grams (or >4500 grams in the diabetic patient) the option of elective cesarean delivery. This approach is empiric and has never been tested for effectiveness. With regard to interventions at the time of shoulder dystocia recognition, no prospective, randomized studies have been conducted to assess the impact of obstetrical maneuvers on neonatal morbidity. Most have been anecdotally derived, some have been studied using various engineering models as discussed earlier in this chapter, and most authorities say that no technique has proven clinical superiority over others with respect to neonatal injury. Gherman et al. 36 demonstrated that regardless of maneuvers utilized, brachial plexus injuries occurred, and there was no difference whether fetal maneuvers or maternal manipulations were used preferentially. McFarland et al. 37 did note that the number of maneuvers employed might predict severity of the event. In their study, when 1–2 maneuvers were needed, the incidence of Erb’s palsy was 7.7% and increased to 25% when 3 or more maneuvers were required. These latter scientific observations are contrary to the commonly articulated supposition that if different or additional maneuvers were utilized during a shoulder dystocia event, brachial plexus palsy could have been averted.
Some general concepts can be extrapolated from the scientific and clinical literature related to shoulder dystocia management. When possible (perhaps in part related to the presence of risk factors), anticipate and prepare for a shoulder dystocia event. Preemptive patient counseling and awareness is always encouraged. For both individuals and institutions, it is recommended to periodically review the topic, advocate for the development of training programs, and establish shoulder dystocia guidelines or protocols.
At the time of delivery, identify the obstruction early; think counter-intuitively and stop pulling and pushing efforts until the obstruction is thought to be cleared. In this regard, there is a certain amount of “diagnostic force” inherent in the identification of the shoulder dystocia condition. Call for assistance early in the intervention. Despite currently recognized limitations in clinician perception of force, be cognizant of the amount of traction being applied; use the least amount necessary to accomplish delivery. Use established shoulder dystocia maneuvers as per your training experience. In general, avoid uterine fundal pressure or justify its use. This is based on very limited evidence that fundal pressure is associated with an increased risk of brachial plexus palsy. 38 In the referenced study, fundal pressure may have only been a surrogate marker for severity of the obstruction encountered, thus confounding this association. Of interest, some shoulder dystocia maneuvers as originally described specifically advocated for fundal pressure as a component of the intervention (Woods Manuever). 39 Axial positioning of the fetal head when traction is applied has gained significant scientific support. Slow/steady traction should also be a part of the counter-intuitive approach to the application of exogenous clinician-applied forces. Careful documentation of the delivery event should be standard practice.
Given the infrequent occurrence of shoulder dystocia, no clinician can be guaranteed expertise in the management of this condition based on personal clinical experience. Therefore, recent attention has been focused on developing training models for shoulder dystocia management. Crofts and colleagues 40 in the United Kingdom tested high-fidelity mannequins to simulate shoulder dystocia events in the clinical setting. They demonstrated that training resulted in improved performance, a higher rate of successful deliveries, and a reduction in total applied extraction forces. In a follow-up study, this same group concluded that training resulted in a sustained improvement in performance, but that repetitive proficiency training is likely to be needed, based on initial competency. 41 When mandatory shoulder dystocia simulation training was introduced, utilization of shoulder dystocia maneuvers increased and there was a significant reduction in neonatal injury in births complicated by shoulder dystocia when compared to a historical patient cohort. 42

Conclusions
NBPP is identified in the immediate neonatal period and is due to trauma to the fetal brachial plexus at some point prior to completion of the delivery. The timing and etiology for this injury is not always easy to define. The incidence of NBPP is reported to be approximately 1.5 per 1000 live births. Fortunately, the majority of NBPP events are transient with eventual full return of function. Compression, traction, vascular disruption, and inflammation have all been identified as pathologic mechanisms. A number of common obstetrical conditions have been reported to be associated with the occurrence of NBPP. Because shoulder dystocia, an event caused by obstruction of the aftercoming shoulders following delivery of the fetal head, appears prominently in this list of obstetrical conditions, substantial empiric and scientific discussions have been generated. In this regard, recent data highlight the contribution of both endogenous and exogenous delivery forces on brachial plexus integrity. Also germane to this discussion is that threshold limits for brachial plexus disruption have not been defined, and likely vary based on a number of factors including fetal acid/base status, surrounding muscle tone, and the anatomic relationship of the fetal head to the aftercoming shoulders. Laboratory modeling data have shown that currently established clinician-applied maneuvers at the time of shoulder dystocia identification reduces extraction forces and brachial plexus stretch. Given the infrequent occurrence of shoulder dystocia, no clinician can be guaranteed expertise in the management of this condition solely based on personal clinical experience. Therefore, recent attention has been focused on the need for high-fidelity simulation training models to improve clinician perception and management of this acute obstetric emergency.

References

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2 Mollberg M, Hagberg H, Bager B, et al. High birthweight and shoulder dystocia: The strongest risk factors for obstetrical brachial plexus palsy in a Swedish population-based study. Acta Obstet Gynecol Scand . 2005;84:654-659.
3 Chauhan SP, Rose CH, Gherman RB, et al. Brachial plexus injury: a 23-year experience from a tertiary center. Am J Obstet Gynecol . 2005;192:1795-1802.
4 Alfonso I, Alfonso DT, Papazian O. Focal upper extremity neuropathy in neonates. Semin Pediatr Neurol . 2000;7:4-14.
5 Sjoberg I, Erichs K, Bjerre I. Cause and effect of obstetric (neonatal) brachial plexus palsy. Acta Paediatr Scand . 1988;77:357-364.
6 Ouzounian JG, Korst LM, Phelan JP. Permanent Erb palsy: a traction-related injury? Obstet Gynecol . 1997;89:139-141.
7 Peleg D, Hasnin J, Shalev E. Fractured clavicle and Erb’s palsy unrelated to birth trauma. Am J Obstet Gynecol . 1997;177:1038-1040.
8 Gherman RB, Ouzounian JG, Goodwin TM. Brachial plexus palsy: an in utero injury? Am J Obstet Gynecol . 1999;180:1303-1307.
9 American College of Obstetricians and Gynecologists. Shoulder dystocia. Practice Bulletin #40. Washington D.C., 2002. 4b.
10 Royal College of Obstetricians and Gynaecologists. Shoulder dystocia. No. 42, London, UK, 2005.
11 Gherman RB, Ouzounian JG, Goodwin TM. Obstetric maneuvers for shoulder dystocia and associated fetal morbidity. Am J Obstet Gynecol . 1998;178:1126-1130.
12 Gilbert WM, Nesbitt TS, Danielsen B. Associated factors in 1611 cases of brachial plexus injury. Obstet Gynecol . 1999;93:536-540.
13 Gurewitsch ED, Johnson E, Hamzehzadeh S, et al. Risk factors for brachial plexus injury with and without shoulder dystocia. Am J Obstet Gynecol . 2006;194:486-492.
14 Dunn DW, Engle WA. Brachial plexus palsy: intrauterine onset. Pediatr Neurol . 1985;1:367-369.
15 Alfonso I, Papazian O, Shuhaiber H, et al. Intrauterine shoulder weakness and obstetric brachial plexus palsy. Pediatr Neurol . 2004;31:225-227.
16 Gonik B, Zhang N, Grimm MJ. Defining forces that are associated with shoulder dystocia: the use of a mathematic dynamic computer model. Am J Obstet Gynecol . 2003;188:1068-1072.
17 Alfonso I, Papazian O, Altman N. Obstetric brachial plexopathy. Int Pediatr . 1991;6:229-232.
18 Sadleir LG, Connolly MB. Acquired brachial-plexus neuropathy in the neonate: a rare presentation of late-onset group-B streptococcal osteomyelitis. Dev Med Child Neurol . 1998;40:496-499.
19 Gonik B Allen RH. Establishing an engineering model to define shoulder dystocia: a preliminary report of applied forces. Proceeding of the Society of Perinatal Obstetricians #151 (Abstract), 1987.
20 Allen RH, Bankoski BR, Butzin CA, et al. Comparing clinician-applied loads for routine, difficult, and shoulder dystocia deliveries. Am J Obstet Gynecol . 1994;171:1621-1627.
21 Crofts JF, Ellis D, James M, et al. Pattern and degree of forces applied during simulation of shoulder dystocia. Am J Obstet Gynecol . 2007;197:156.e1-156.e6.
22 Allen R, Sorab J, Gonik B. Risk factors for shoulder dystocia: an engineering study of clinician-applied forces. Obstet Gynecol . 1991;77:352-355.
23 Gonik B, Allen R, Sorab J. Objective evaluation of the shoulder dystocia phenomenon: effect of maternal pelvic orientation on force reduction. Obstet Gynecol. . 1989;74:44-48.
24 Gherman RB, Goodwin TM, Souter I, et al. The McRoberts’ maneuver for the alleviation of shoulder dystocia: How successful is it? Am J Obstet Gynecol . 1997;176:656-661.
25 Gurewitsch ED, Kim EJ, Yang JH, et al. Comparing McRoberts’ and Rubin’s maneuvers for initial management of shoulder dystocia: an objective evaluation. Am J Obstet Gynecol . 2005;192:153-160.
26 Gonik B, Zhang N, Grimm MJ. Prediction of brachial plexus stretching during shoulder dystocia using a computer simulation model. Am J Obstet Gynecol . 2003;189:1168-1172.
27 Costello R, Gonik B, Grimm M. The use of a MADYMO model to evaluate clinician maneuvers applied in the management of shoulder dystocia. Proceedings of the Summer Bioengineering Conference. June 2005.
28 Allen RH, Cha SL, Kranker LM, et al. Comparing mechanical fetal response during descent, crowning, and restitution among deliveries with and without shoulder dystocia. Am J Obstet Gynecol . 2007;196:539.e1-539.e5.
29 Caulfield JN, Allen RH, Miller F. A finite element idealization of the newborn spine and brachial plexus nerves. Proceedings of the A. I. Dupont Orthopedic Research Symposium. June 1995:58–59.
30 de Medinaceli L, Leblanc AL, Merle M. Functional consequences of isolated nerve stretch: Experimental long-term static loading. J Reconstr Microsurg . 1997;13:185-192.
31 Metaizeau JP, Gayet C, Plenat F. Les lesions obstetricales du plexus brachial. Chir Pediatr . 1979;20:159-163.
32 Jennett RJ, Tarby TJ, Krauss RL. Erb’s palsy contrasted with Klumpke’s and total palsy: different mechanisms are involved. Am J Obstet Gynecol . 2002;186:1216-1220.
33 Gonik B, McCormick EM, Verweij BH, et al. The timing of congenital brachial plexus injury: a study of electromyography findings in the newborn piglet. Am J Obstet Gynecol . 1998;178:688-695.
34 Koenigsberger MR. Brachial plexus at birth: intrauterine or due to delivery trauma. Ann Neurol . 1980;8:228.
35 Gherman RB, Chauhan S, Ouzounian JG, et al. Shoulder dystocia: the unpreventable obstetric emergency with empiric management guidelines. Am J Obstet Gynecol . 2006;195:657-672.
36 Gherman RB, Goodwin TM. Shoulder dystocia. Curr Opin Obstet Gynecol . 1998;10:459-463.
37 McFarland MB, Langer O, Piper JM, et al. Perinatal outcome and the type and number of maneuvers in shoulder dystocia. Int J Gynaecol Obstet . 1996;55:219-224.
38 Gross SJ, Shime J, Farine D. Shoulder dystocia: predictors and outcome. Am J Obstet Gynecol . 1987;156:334-336.
39 Woods CE, Westbury NY. A principle of physics as applicable to shoulder dystocia. Am J Obstet Gynecol . 1943;45:796-804.
40 Crofts JF, Bartlett C, Ellis D, et al. Training for shoulder dystocia: a trial of simulation using low-fidelity and high-fidelity mannequins. Obstet Gynecol . 2006;108:1477-1485.
41 Crofts JF, Bartlett C, Ellis D, et al. Management of shoulder dystocia: skill retention 6 and 12 months after training. Obstet Gynecol . 2007;110:1069-1074.
42 Draycott TJ, Crofts JF, Ash JP, et al. Improving neonatal outcome through practical shoulder dystocia training. Obstet Gynecol . 2008;112:14-20.
CHAPTER 6 Guidelines for attorney–physician interactions about brachial plexus palsy patients

Edward C. Reynolds, Jr., JD, Richard C. Boothman, JD


Summary box

1 Establish all the terms and conditions of proposed expert witness work before agreeing to take on the case.
2 An expert witness should be an advocate only for his/her expertise as a physician and for the truth of his/her opinions.
3 Competent, experienced, and fair-minded physiatrists should be willing to act as expert witnesses for patients/plaintiffs as well as for physiatrists/defendants.
4 Require a HIPAA-compliant authorization for release of the patient’s medical information before discussing the patient with any attorney, even the attorney for the patient.
5 Always consider whether you should have your attorney present for any meeting with an attorney representing a party to a lawsuit or claim.
6 Don’t hesitate to charge attorneys who request your time and professional skills.
7 Know when you can say “No” to attorney requests for meetings and deposition proposals.
8 Know the difference between service as a fact witness and an expert opinion witness.
9 Prepare thoroughly and commit. Prepare thoroughly and insist on as much time with your own lawyer as you need to be and feel ready to testify.
10 Understand your rights and know the rules for witnesses.
11 Don’t hesitate to look to your attorney for advice and counsel for all contacts by attorneys seeking time with you.

Introduction
Current treatment of brachial plexus palsy (BPP) is often a multi-disciplinary team approach, bringing to bear the skills of physical medicine and rehabilitation, neurosurgery, orthopedic surgery, plastic surgery, occupational and physical therapies, social work, and psychology. BPP patients often have another kind of team focused on BPP: an attorney and his/her support staff, which may consist of assistant attorneys, legal assistants, nurses and rehabilitation specialists, and even physicians. To do his/her job properly, the patient’s attorney will require evidence from one or more members of the BPP treatment team; sometimes the same is true of the defense attorney on the other side of the case. Attorneys need the knowledge of the treaters to support their theories of the case. It is inevitable that attorneys will contact one or more members of the treatment team. This chapter is about the ways in which that contact can occur and what you, the BPP specialists can do or not do in response.
BPP issues may arise in many types of civil litigation: e.g., medical malpractice, social security disability claims, Americans With Disabilities Act and other employment claims, workers’ compensation, and divorce/child custody. Severity of the individual patient’s BPP is always an issue, because it is the focus of the question of how well your patient can function for the rest of his/her life. What is the impact of the injury on the patient’s ability to perform activities of normal daily living? Is the patient employable? If so, what kind of work can the patient do? What kinds of workplace accommodations or home modifications are reasonable and necessary for the level of severity of BPP? These questions lead to economic considerations, such as whether there is need for surgery; or continuing therapies, and for what period of time; costs of care and support; and loss of earning capacity.
The following are types of cases in which you, as a member of a BPP treatment team, may be particularly qualified to assess in a patient with brachial plexus palsy, to describe the anatomy of the injury, and to offer opinions about the extent of physical limitations or disability.

Medical malpractice
BPP is most frequently the subject of medical malpractice suits, in which the defining issues are the applicable standards of care (usually for obstetrics, maternal-fetal medicine, family medicine, and/or labor and delivery nursing), whether the care provider violated a standard of care, what injuries resulted, and whether there was a foreseeable causal connection between the standard of care violation and the injuries. The physician’s expertise in brachial plexus surgery may also involve him or her in issues regarding adult surgery, particularly lateral neck and shoulder operations, with regard to the same issues of causation and standards of care.

Workers’ compensation and social security disability claims
The focus for BPP specialists in disability and workers’ compensation claims is most often the degree of injury and resulting physical limitations. Can the patient work, and if so, to what extent? Workers’ compensation claims may also deal with the issue of whether the BPP is work-related.

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