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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.
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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
S a u n d e r sFront 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 2012Copyright
© 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
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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 . eld 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 identi. ed, 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
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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 e ort 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 e ort 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 rami- cations;
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 a8
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comprehensive physical examination of muscle de- cits 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 e ort 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
e orts. Additionally, I would also like to acknowledge our sta , Phil Clapham,
Pouya Entezami, Lilly Bell- , Holly Wagner and Connie McGovern for their help
and our Elsevier development editor, Alex Mortimer, whose patience has overcome
many of the di culties 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 SchoolList 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 SurgeryUniversity 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 MedicineBaltimore, 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 ExtremityDenise 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 Studies
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 Lesions21 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 CalgaryCalgary, 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 MichiganAnn 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 MichiganAnn 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 ClinicalNeurosciences
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
PalsyAcknowledgementS
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. McGillicuddyTable 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
palsiesChapter 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
IndexSection One
The BasicsCHAPTER 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
C8T1 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 ishelpful 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 identi. ed. 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
1treatises describing collections of anatomic dissections. The strength of these
descriptions was forti. ed 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
2-4“true form” of the plexus. Kerr, Walsh, and Harris 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-. xed (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
1T2 nerve root). 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
5our understanding of the connections within this complex structure.
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 . nal
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. Inlower primates, the artery lies super. cial to the brachial plexus and has a larger degree of
variation. In higher primates, the artery also lies super. cial 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)
6spinal nerve roots, (2) trunks, (3) divisions, (4) cords, and (5) terminal branches. 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 a ecting 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
identi. able 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
super. cially toward the trapezius. More speci. cally, 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 conCuent 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 . rst 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 Cex the ipsilateral
leg. The lower part of the face, neck, shoulder, entire chest, and leg are prepped forsurgery.
A curvilinear incision extending from the sternocleidomastoid muscle to the trapezius
7muscle is made approximately 1.5 cm above the clavicle. The platysma is incised
perpendicular to its . bers, 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 super. cial 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).
Identi. cation 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 omohyoidand supraclavicular nerves.
The lateral margin of the sternocleidomastoid muscle is identi. ed, 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 identi. ed along their super. cial 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 identi. ed. 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 con. rm
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 identi. ed. The scalene fat pad is
released from this border in a cranial-to-caudal direction, then in a medial-to-lateral
direction to reCect 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 identi. ed 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 identi. cation 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, andfollowing 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 . rst 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 Cuid 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 identi. ed originating from the
coracoid, which consists of the short head of the biceps and coracobrachialis. Attachment
of the pectoralis minor can be identi. ed 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 super. cial 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 identi. ed 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>
8brachial plexus tumors or revision brachial plexus surgery. The patient is positioned
prone with the shoulder Cexed 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 . ngerbreadths 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 cu 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 . rst
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 super. cially 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
. nd 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 de. ned a “pre-. xed” plexus as one that
receives a substantive contribution from C4 and a “post-. xed” 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 de. ning
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 insigni. cant.
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
9The relationship of the brachial plexus to the axillary artery varies widely as well. Miller
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 . ndings are variations of the axillary artery or a
portion of the axillary artery traversing the brachial plexus more superficially.
Terminal branch variability
There is signi. cant variation from the standard diagram used to describe the origin of
terminal branches of the brachial plexus. In approximately 65% of cases, Ballesteros et
10al. 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 su ering 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<
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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
1brachial plexus palsies (BPP). Young adult males comprise a signi cant
proportion of patients su ering traumatic palsies, and they encounter substantial
2-4socioeconomic di>culty as a result of their disability. As the number of
“extreme” sporting events and high-speed motor vehicle collisions increase, so does
3,5-9the worldwide prevalence of BPP. 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 classi ed in several ways. They
can be open or closed, sharp or ragged, clean or dirty. Consideration of the
10pathophysiology of these injury types led Dubuisson and Kline 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 a ect the
nerve roots and trunks in the supraclavicular region. Supraclavicular injuries can
be classi ed as preganglionic or postganglionic (Figure 2.2), but this seemingly
simple classi cation 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<
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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-de ned 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
111943 that is still useful today. This classi cation 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 classi cation of nerve injury: neurapraxia, axonotmesis, and
neurotmesis.
Reaction to nerve injury<
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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
inGammation triggering broblasts 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 signi cant inhibition of regeneration. In the most severe cases, the
nerve ends become markedly disorganized, with broblasts, macrophages,
capillaries, Schwann cells, and collagen bers 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
12ganglion neurons following axonotmesis can reach 50%. 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
13,14Schwann cells and trophic molecules present in the immediate environment.<
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
neuro laments 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).<
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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
15regenerating axon preserves the space (Figure 2.5 E and F). 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
16mean 70% reduction in the cross-sectional area after 2 months. Changes in
muscle activation are exempli ed by fast muscle bers that show a slowing of
dynamic properties by prolonged contraction and relaxation times and decreased
17tension development rates and velocities. These changes precede the more
permanent morphological alterations that include proliferation of sarcoplasmic
18,19reticulum and shifts in myo brillar isoforms in laboratory models. Sodium
20-22channels regress toward embryonic forms with altered biochemical properties,
23,24and acetylcholine receptors redistribute to cover the entire muscle surface.<
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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
25maintaining muscle physiology. In addition, de ciency 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
26,27trophic action of nerve on muscle.
Tissue reaction to nerve injury is evidenced by a vast proliferation of broblasts
and deposition of new collagen in the peri- and endomysium. The space between
the atrophied bers is lled by thickened connective tissue, but the overall internal
muscle structure is retained. Death of muscle bers generally does not occur, but
16when it does, dropout occurs between 6 and 12 months after denervation.
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 con ned 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 reGective 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<
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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
16is thought to be slower. 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 speci c factor has been found to direct the elongating ber.
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 lopodia
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<
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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 bers showing the electrodiagnostic phenomenon of
polyphasic waves. This nding is characteristic of reinnervated muscle and is not
seen in nascent musculature. Like the obstacles to neuronal regeneration, several
factors can negatively a ect functional muscle reinnervation. Intramuscular
brosis will decrease the e>ciency of a nerve impulse. The number of axons that
successfully reconnect with the muscle a ects functional recovery, but the integrity
of reinnervation is also important. For example, if axons previously innervating
slow bers establish new connections with fast bers, ine>cient 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
16connections after one year.
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
brainderived neurotrophic factors, ciliary neurotrophic factor, and nerve growth
14,28factor. These molecules are involved in neuronal cell survival, maintenance,
and repair by binding to speci c 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 sca olds, the use of electrical stimulation, the signals to encourage
speci c motor reinnervation, and overcoming the inhibitory environment to
29,30facilitate axon regeneration. However, adjunctive pharmacologic agents to
enhance nerve regeneration are not currently ready for clinical use.
References
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2 Allieu Y. Evolution of our indications for neurotization. Our concept of functionalrestoration of the upper limb after brachial plexus injuries. Chir Main.
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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
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4 Malone JM, Leal JM, Underwood J, et al. Brachial plexus injury management
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5 Allieu Y, Cenac P. Is surgical intervention justifiable for total paralysis secondary to
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plexus. Microsurgery. 1994;15:28-32.
7 Brandt KE, Mackinnon SE. A technique for maximizing biceps recovery in brachial
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8 Brunelli G, Monini L. Direct muscular neurotization. J Hand Surg Am. 1985;10(6 Pt
2):993-997.
9 Doi K, Kuwata N, Muramatsu K, et al. Double muscle transfer for upper extremity
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10 Dubuisson A, Kline DG. Indications for peripheral nerve and brachial plexus
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13 Varon SS, Bunge RP. Trophic mechanisms in the peripheral nervous system. Annu
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1990;13:771-784.
16 Burnett MG, Zager EL. Pathophysiology of peripheral nerve injury: a brief review.
Neurosurg Focus. 2004;16:E1.
17 Midrio M. The denervated muscle: facts and hypotheses. A historical review. Eur J
Appl Physiol. 2006;98:1-21.
18 Takekura H, Kasuga N, Kitada K, et al. Morphological changes in the triads and
sarcoplasmic reticulum of rat slow and fast muscle fibres following denervation
and immobilization. J Muscle Res Cell Motil. 1996;17:391-400.
19 Sakakima H, Kawamata S, Kai S, et al. Effects of short-term denervation andsubsequent reinnervation on motor endplates and the soleus muscle in the rat.
Arch Histol Cytol. 2000;63:495-506.
20 Pappone PA. Voltage-clamp experiments in normal and denervated mammalian
skeletal muscle fibres. J Physiol. 1980;306:377-410.
21 Kallen RG, Sheng ZH, Yang J, et al. Primary structure and expression of a sodium
channel characteristic of denervated and immature rat skeletal muscle. Neuron.
1990;4:233-242.
22 Lupa MT, Krzemien DM, Schaller KL, et al. Expression and distribution of sodium
channels in short- and long-term denervated rodent skeletal muscles. J Physiol.
1995;483(Pt 1):109-118.
23 Schuetze SM, Role LW. Developmental regulation of nicotinic acetylcholine
receptors. Annu Rev Neurosci. 1987;10:403-457.
24 Witzemann V, Brenner HR, Sakmann B. Neural factors regulate AChR subunit
mRNAs at rat neuromuscular synapses. J Cell Biol. 1991;114:125-141.
25 Salmons S, et al. Functional electrical stimulation of denervated muscles: basic
issues. Artif Organs. 2005;29:199-202.
26 Helgren ME, Squinto SP, Davis HL, et al. Trophic effect of ciliary neurotrophic
factor on denervated skeletal muscle. Cell. 1994;76:493-504.
27 Huang S, Wang F, Hong G, et al. Protective effects of ciliary neurotrophic factor on
denervated skeletal muscle. J Huazhong Univ Sci Technolog Med Sci.
2002;22:148151.
28 Yan Q, Elliott J, Snider WD. Brain-derived neurotrophic factor rescues spinal motor
neurons from axotomy-induced cell death. Nature. 1992;360:753-755.
29 Song JW, Yang LJ, Russell SM. Peripheral nerve: what’s new in basic science
laboratories. Neurosurg Clin N Am. 2009;20:121-131.
30 Yang LJ, Schnaar RL. Axon regeneration inhibitors. Neurol Res. 2008;30:1047-1052.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 a0ecting the musculoskeletal system, physicalexamination begins with a visual inspection and palpation of the a0ected 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 4ndings 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
1,2,3testing.
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 a0ected versus non-a0ected 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 re: ex hammer or the examiner’s 4ngers to check for
Ho0man-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 a0ecting 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 cu0 muscle
paralysis, should be carefully assessed. Point tenderness, marked joint trauma and
contractures, or signi4cant 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 di0erent individuals
before and after treatment. The Medical Research Council published the classic
1motor function grading scale (MRC grading scale) shortly after World War II. 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 de4ciencies, other grading scales
have been described. The Louisiana State University (LSU) motor function grading
scales are popular amongst peripheral nerve surgeons and are speci4c for each
4major peripheral nerve or element of the brachial plexus.
Table 3.1 Medical Research Council motor function grading scaleGrade 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
1,3,4extremity musculature are well-known, are presented elsewhere in detail, 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 4xes
and stabilizes the scapula so that muscles originating from it can function properly.
Furthermore, anterior arm : exion is stabilized by the serratus anterior, with : exion
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 partialinnervation 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
: ex 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 4rmly
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 extendedarm. 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
: exor (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 : exion. Then, against resistance at the medial elbow,
have them swing their arm toward midline (Figure 3.9). The medial pectoral nerveoriginates 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 : exed 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. DiD cult 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 o0 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 : exed 90 degrees with the palm facing
forward (Figure 3.13). Muscle contraction can be palpated along the posterolateralchest 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 a0ected shoulder often lies lower than the una0ected 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 : exed at the elbow) is pushed across the chest or in front of the bodyagainst 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 speci4c spinal
nerve) remain useful for clinical evaluation of patients with proximal brachial
plexus lesions. By matching the pattern of neurological de4cit 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
supraand 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
: exion, as well as arm extension/adduction. The radial nerve carries C6
innervation to the supinator (supination) and brachioradialis (forearm : exion with
arm partially supinated), and the musculocutaneous nerve carries 4bers to the
biceps brachii (forearm : exion and supination) and brachialis (forearm : exion).
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 : exes 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 a0ected 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 4ngers : exed (from weak 4nger 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 (longthoracic 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
onehalf of the arm and forearm, as well as the whole thumb.
Because the middle trunk is only comprised of 4bers from the C7 spinal nerve,
they will be considered together. Muscular control of the C7 nerve root includes the
triceps (radial nerve), : exor carpi radialis (median nerve), : exor carpi ulnaris
(ulnar nerve), and pronator teres (median nerve). The C7 also provides innervation
to the wrist extensors, 4nger extensors, and 4nger : exors. 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), : exes the wrists (: exor 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) 4nger
are almost exclusively within the C7 dermatome. Lesions of the middle trunk,
comprised solely of C7 4bers, 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 4nger : exors (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 : exor profundi to the index and long 4nger (distal interphalangeal
joint : exion), thenar intrinsics including abductor pollicis brevis and opponens
pollicis, and extensors to the thumb, index, and long 4nger. Therefore, a quick and
easy way to assess C8 function would be to have the patient grasp and release your
4ngers, with attention paid especially to the 4rst 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 4ngers. This movement is mediated by the dorsal interossei muscles, which
are predominantly T1 innervated. Atrophy of the 4rst 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
a0ecting this element cause marked hand weakness, including both hand grasp
and 4nger 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 de4cits 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 4bers 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 de4cit; 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 : exion 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 4bers (the medial cord does not provide any cutaneous sensation to the
median nerve). Therefore, sensory loss in the lateral palm and 4rst 3 digits occurs
with a lateral cord injury. Although the lateral cord component is primarilysensory, it also controls the more proximal median innervated muscles (pronator
teres and : exor carpi radialis) so that weakness in pronation and wrist : exion will
be seen. Any wrist : exion will be from : exor 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 4bers. The medial cord provides the medial
contribution of the median nerve, containing C8 and T1 4bers, 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 : exion (: exor carpi ulnaris),
distal interphalangeal joint : exion weakness involving the ring and little 4ngers
(: exor digitorum profundi), little 4nger movements (opponens, : exor, and
abductor digiti minimi), and 4nger 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, : exor pollicis brevis (super4cial head), abductor
pollicis brevis, and the 4rst 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 4rst 2 4ngers (lumbricals). The medial cord also has a few side
branches that can be utilized to con4rm 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 4nger/thumb extension (super4cial and deep
4nger 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 con4rm posterior
cord damage, because these muscles are controlled by the minor branches o0 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
diD cult to clinically di0erentiate from cord or trunk level lesions. Nevertheless, an
isolated injury to one or more divisions yields neurological de4cits 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 4bers in the medial
cord. A divisional injury involving the lateral cord can a0ect 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 o0 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
onehalf of the arm and forearm, as well as the whole thumb.