Peripheral Nerve Entrapments Clinical

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Peripheral Nerve
Entrapments

Clinical Diagnosis
and Management

123
Peripheral Nerve Entrapments
Andrea M. Trescot
Editor

Peripheral Nerve Entrapments

Clinical Diagnosis and Management
Editor
Andrea M. Trescot, MD, ABIPP, FIPP
Medical Director - Pain and Headache Center
Anchorage
AK
USA

Videos to this book can be accessed at

http://link.springer.com/book/10.1007/978-3-319-27482-9.

ISBN 978-3-319-27480-5 ISBN 978-3-319-27482-9 (eBook)

DOI 10.1007/978-3-319-27482-9

Library of Congress Control Number: 2016939017

© Springer International Publishing Switzerland 2016

This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is
concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction
on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation,
computer software, or by similar or dissimilar methodology now known or hereafter developed.
The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not
imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and
regulations and therefore free for general use.
The publisher, the authors and the editors are safe to assume that the advice and information in this book are
believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give
a warranty, express or implied, with respect to the material contained herein or for any errors or omissions that may
have been made.

Printed on acid-free paper

This Springer imprint is published by Springer Nature

The registered company is Springer International Publishing AG Switzerland
This book is dedicated to my family, friends, and students, without whom
I would never have had the strength to finish this work, and to my patients,
who keep me motivated to find answers for their pain.

Andrea M. Trescot
Foreword

The contribution of Dr. Andrea M. Trescot and the multiple authors in the entrapment neuropa-
thy field is very significant. These are topics that often are not covered at conferences, as the
time limitations and program limitations exclude what appear to be minor areas. Ultimately,
patients suffering from entrapment neuropathies are treated with inappropriate, alternative,
excessive technological implants and/or heavy medications such as opioids and others. All
these occur because the explanation of the problem, if you do not know it, does not exist.
There are multiple very significant and successful treatment recommendations covered in
this book, including, for example, occipital neuralgia. Releasing the compression in the
suboccipital compartment by the suboccipital decompression technique can very successfully
treat migraine headache-type problems. Previously published and presently released results
show that injecting the multiple nerves involved in the production of headache usually gives
2 weeks pain relief whereas the suboccipital decompression gives 24 weeks pain relief. Studies
include a multitude of accurate and inaccurate diagnoses, but certain patients can experience
years without recurrence of the occipital pain after a single suboccipital decompression from
the inferior oblique muscle between C1 and C2, which is a considerable distance away from
the superficial injections. In other words, if you know the mechanism of causation, then you
are more likely to get long-term success.
The explanation for lower quadrant abdominal hypersensitivity is the entrapment of the
iliohypogastric and ilioinguinal nerves going through three muscle layers (the external oblique,
the internal oblique, and the transversus abdominis), before becoming cutaneous below the
umbilicus. This condition often occurs in the second trimester of pregnancy, especially in
muscular young mothers, where the growth of the baby stretches the abdominal musculature.
This pain raises significant differential diagnostic problems, such as a misdiagnosis of acute
appendicitis where surgical intervention may be hazardous and unnecessary at the same time.
The treatment is simple, injecting along the iliac crest, popping through the external oblique
aponeurosis and there is usually immediate pain relief; however, it may not last long enough.
One can repeat the procedure or, alternatively, choose a longer-lasting solution such as
cryoneurolysis in the same location, locating the nerve with the nerve stimulator at the tip of
the cryo probe and freezing the nerve. The pain relief can be from 2 days to 1,000 days. Here,
you see the diagnosis being made and appropriate treatment being carried out by short- and
long-lasting therapeutic methods such as cryoneurolysis.
Another form of entrapment neuropathy that is often missed is saphenous nerve entrapment.
The physician has to remember that the saphenous nerve comes off the femoral nerve and not
only carries a sensory nerve to the inside ankle (medial malleolus) and the knee, but also it has
significant sympathetic fibers. A saphenous block in Hunter’s Canal, 4 in. above the knee, with
a safe blunted Stealth™ needle, can relieve knee pain. This often helps regain mobility of knee
joints, reduce swelling and discoloration of the foot and lower leg following long duration
splinting and immobilization of ankle and knee joint. Here, the entrapment neuropathy comes
from the extended disuse of the knee or ankle joint following immobilization after surgery or
fractures. The resolution of the swelling comes from the lysis of the autonomic sympathetic
fibers.

vii
viii Foreword

After upper extremity shoulder surgery and fractures, because of immobilization, one may
see entrapment of the brachial plexus between the anterior and middle scalene muscles. Simple
interscalene injection, however, can be performed with an occluded tip needle so that intraneural
or intra-arterial injection should be less likely; even ultrasound guidance does not assure safety
if open-ended sharp needles are used. There have been a considerable number of brachiopathies
and cord injuries resulting in significant medical legal costs from the use of sharp needle
injections in vascular regions where nerve and arteries travel together at the same injection site.
Using needles of too small a gauge can also be dangerous. Pneumothorax is one of the most
common medical legal consequences of injections around the lungs; with small gauge needles,
the needle can penetrating the lung multiple times, since small gauge needles have a mind of
their own and do not go where the doctors wish they would go. The medical legal cost for a
pneumothorax can be from zero to multiple six figures. In medicine, the principle must always
be: primum non nocere, first do no harm.
Nerve entrapments can be caused by scarring anywhere along the path of the nerve, and the
“lysis of adhesions” concept extends to scar tissues, where tendons may be limited by scarring
and bleeding. Scarring also causes severe neuropathy in the spinal canal. Solving one source
of neuropathic pain does not necessarily solve all pains and the doctor needs to remain vigilant
by not just asking the question, “How is your pain?” but also examining the patient. It is
surprising how many times the patient does not know where the pain is coming from.
I believe Dr. Trescot’s recognition for the need to collect the subject matter in this book and
subsequent assemblage of its contents is truly remarkable. It has been my pleasure to know and
respect the work of Dr. Trescot; my reverence for her work originates in her realization of the
need to expand our horizon and treat the patients appropriately rather than excessively. I feel
the examples that I listed served to emphasize that not only does one need to recognize
problems, but also solve problems with long-term results in mind. Alternatively, the short-term
pain pill that may appear to work for hours will become a long-term issue by leading to
addiction, chronic pain, and loss of work. All of this starts with the premise, “If you don’t
know it, it doesn’t exist,” which is not in the best interest of the patient or doctor. In conclusion,
Dr. Trescot deserves all the accolades for exercising a tremendous effort to bring such valuable
and extensive information to all of us.

Dallas, TX, USA Gabor Racz, MD, FIPP

Preface

Peripheral nerve entrapments are a commonly overlooked cause of painful conditions, resulting
in pain literally from the head to the toe. Even the astute clinician may not be aware of these
syndromes, and entrapment of these often small nerves can lead to debilitating pain, mimicking
“migraines,” cardiac disease, intra-abdominal pathology, “endometriosis,” complex regional
pain syndrome (CRPS), and “plantar fasciitis.” Knowledge of these entrapments can prevent
expensive ineffective testing and treatment and can ideally avoid unnecessary pain and
suffering.
This book is a culmination of many years of my personal clinical observations as well as
collaboration between many providers. Over the years, when I would lecture on peripheral
nerve entrapments, I would be met with blank stares, or worse, derision. However, this lack of
knowledge is slowly changing. Fifteen years ago, when I would ask the audience to raise their
hand if they had ever even heard of the cluneal nerve, perhaps two or three hands would go up.
Now, with the same question, sometimes a majority of the room will raise their hands.
There is suddenly a plethora of articles in the literature regarding peripheral nerve
entrapment diagnosis and treatment, and the emergence of ultrasound-guided injections in
pain medicine has confirmed some of the mechanisms, while at the same time elucidated new
mechanisms of entrapment. One of the hardest parts of writing this book has been the decision
to stop adding new information to the chapters, since every time that I would find a new
reference, my developmental editor (Connie Walsh) would have to reformat the chapter.
This book has been designed to be a guide as well as a reference. We chose pain pattern
images that will hopefully trigger the clinician to think about peripheral nerve entrapment as a
cause of their patient’s pain, while at the same time providing the scholarly anatomic
descriptions of the nerve. We hope that this book will help you diagnose as well as treat your
patients, using physical exam, differential diagnosis, medications, injections (landmark-
guided, fluoroscopic-guided, and ultrasound-guided), neurolytics, neuromodulation, and
surgery. Videos showing the physical exam and landmark-guided injections are included for
most of the described nerves. We have also created an Index of Symptoms, so that a patient
who is complaining of an “ice pick in my eye” should lead you to consider the greater occipital
nerve as a possible etiology.
I hope that you will find this book useful to help the patient who is asking “who will stop
the pain?”

Anchorage, AK, USA Andrea M. Trescot, MD, ABIPP, FIPP

ix
Acknowledgements

A book of this size and scope is never created in isolation. Many thanks (and perhaps blame)
go to Dr. Peter Staats, who 3 years ago sent Springer Publishing to talk to me about doing this
book. Thanks also go to Connie Walsh (my developmental editor) and especially Joanna Perry
(my original supervising editor), who talked me out of my panic half way through this project.
When Joanna left Springer to pursue an MBA, she handed me over to Becky Amos, who shep-
herded this book to its final form.
I would like to thank my dear friend and collaborator, Dr. Helen (Ellie) Karl, who saw effi-
cacy of these treatments and has become a “true believer.” She has been the engine and orga-
nizer of this monumental project, and this book would have faltered and failed without her
help. She checked and challenged every statement and image, so that this book would be as
accurate as possible.
To my section editors, I give special thanks for their flexibility and trust, as the format and
even the selection of nerves changed over the course of the development of this book. Each
chapter author is a friend (or a friend of a friend), a fellow pain provider, and an advocate for
recognition of these clinical syndromes. Many are mentees who were taught by me and who
are now becoming the experts. Although each nerve chapter has an author’s name attached, we
have used a collaborative approach, with contributions by multiple authors, most unnamed,
along the lines of Wikipedia. A few, however, deserve special recognition.
Drs. Dan Krashin and Natalia Murinova, an extraordinary husband/wife team (he is a psy-
chiatrist and interventional pain physician, and she is a well-respected neurologist and migraine
specialist), not only wrote their own chapters, but also wrote and rewrote many of the other
chapters, some of which have their names on them and others that do not. In the same way, Dr.
Michael Brown (interventional physiatrist) and Dr. Beth Pearce (podiatrist) provided a special
expertise regarding pathologies of the lower extremities.
Dr. Thais Vanetti of Brazil and Dr. Tiffany Zhang of Seattle both did a wonderful job of
editing many of my “problem” chapters, all the more amazing because English is their second
language. Dr. Terri Dallas Prunskis jumped in to help me finish chapters as the final deadline
approached and painted her family and staff to provide many of the nerve pattern pictures. Dr.
Eric Wilson from South Africa helped to create the index of symptoms. My sister Leigh Trescot
Tobias spent hours helping me to reformat the book when I had the “bright idea” to change the
entire format after the book was three-quarters of the way done.
Dr. Agnes Stogicza, my “daughter” and (according to my husband) “mini-me,” spent hours
helping me by dissecting cadavers as well as creating US images of nerves as we traced nerves
to their site of entrapment. Many of these US techniques have never been described in the lit-
erature, so expect a flurry of articles to follow the publishing of this book. She arranged for
access to fresh cadavers in Hungary, as well as a wonderful anatomist, Gabor Balsa, who
patiently and skillfully helped us to isolate nerves. We ultrasounded each other to trace nerves,
and Agi always asked the tough questions of “why?” and “how?” and “what about this?” Her
enthusiasm for pain treatment and new knowledge has kept me motivated.

xi
xii Acknowledgements

Drs. Thiago Nouer Frederico and Fernando Mauad, from Brazil, and Drs. Michael Brown
and Brian Shilpe, from the United States, generously provided many ultrasound pictures of the
nerves. Thiago patiently traced nerves for me with ultrasound, showing potential entrapment
sites not yet well described. Dr. Michael (“Micha”) Sommer from the Netherlands reviewed
nearly every image and provided valuable insight regarding the ultrasound and non-ultrasound
images as well reviewing the “readability” of the language. Dr. Christ Declerck from Belgium
also shared a variety of intriguing images. David Spinner, DO, contributed his ultrasound
images of the supraorbital, infraorbital, and mental nerves, while Drs. Gladstone McDowell
and Porter McRoberts donated several peripheral stimulator images. Holly Long, editor of the
journal Pain Physician, graciously provided pictures and permissions from the American
Society of Interventional Pain Physicians (ASIPP) textbooks and articles.
Accuracy is critical in a book such as this, and I had help from Dr. J. David Prologo (an
interventional radiologist) who reviewed the MR images that I created and from Dr. Micha
Sommer who reviewed the US images. Dr. Rubina Ahmad also helped to review images.
Over a dinner conversation during a conference in Poland, Ben Zylicz, MD, provided
insight into the use of peripheral nerve injections in the treatment of cancer pain and agreed to
put these thoughts down in a chapter. Heather Tick, MD, provided a balanced, integrated view
of the non-interventional approach to these entrapments.
Edit Debreczeni, daughter of my friend Dr. Edit Racz of Hungary, volunteered on short
notice to be my model for the videos of examination and injection that accompanies this book.
Tamara Brothers, PA-C, Dr. Thais Vanetti, Dr. Joshua Balch, and my sister Caroline Kirkland
also served as willing models. And my brother, David Trescot, volunteered his skills as a pho-
tographer and videographer/video editor to create almost every image in this book and to edit
the raw video into the educational clips available here.
I would like to give special thanks to my children, Nicole and Joseph Gear, who were indis-
pensible assistants, serving as models as well as copy editors. They allowed me to draw on and
poke and scan their bodies to create just the right image, and then corrected my grammar and
syntax. Nicole, especially, spent multiple sessions posing for images, and the images of her (I
hope) have helped to unify the book; she also spend countless hours reviewing every word of
the book to make sure that the information made sense. And this book would never have been
possible without my loving, supportive, and long-suffering husband, Harold Gear, who even
offered to let me inject him, just so I could get a better image for the book.
A final thanks goes to the support and encouragement over the years from students and col-
leagues, who would come up to me after my lecture to ask – “Where can I find a book with all
this information?” Hopefully, this book will now answer that question.

Andrea M. Trescot, MD
St. Augustine Beach, Florida, USA

The plastinated human specimens shown in this book were produced by Prof. Dr. Hong-Jin
Sui, Director of Dalian Medical University, China and Dalian Hoffen Bio-Technique Co,. Ltd,
China, and are used here with their permission. The author wishes to thank Dr. Sui and Dalian
Hoffen Bio-Technique Co., Ltd., for permission to use the photographs of these specimens.
Contents

Part I Peripheral Nerve Entrapments: General Principles

Andrea M. Trescot, Section Editor, and Daniel Krashin

1 Epidemiology and Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3

Andrea M. Trescot, Daniel Krashin, and Helen W. Karl
2 History and Physical Exam . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11
Andrea M. Trescot and Daniel Krashin
3 Consequences of Peripheral Nerve Entrapment . . . . . . . . . . . . . . . . . . . . . . . . . . . 15
Andrea M. Trescot and Daniel Krashin
4 Pharmacological Treatment of Painful Nerve Entrapment Syndrome . . . . . . . . . 19
Tiffany Zhang
5 Non-pharmacologic Treatment of Peripheral Nerve Entrapment . . . . . . . . . . . . . 27
Helen W. Karl, Heather Tick, and Kris A. Sasaki
6 Diagnostic Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 35
Daniel Krashin and Andrea M. Trescot
7 Peripheral Nerve Entrapment: Injection Techniques . . . . . . . . . . . . . . . . . . . . . . . 37
Andrea M. Trescot and Natalia Murinova
8 Neurolytic Techniques. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45
Brett Lockman, Andrea M. Trescot, and Daniel Krashin
9 Neuromodulation for Treatment of Nerve Entrapment Syndromes . . . . . . . . . . . 59
Amitabh Gulati, Helen W. Karl, Tiffany Zhang, and Andrea M. Trescot
10 Surgical Treatment of Nerve Entrapment Syndromes . . . . . . . . . . . . . . . . . . . . . . 71
Amitabh Gulati, Daniel Krashin, and Helen W. Karl
11 The Why and What of Integrative Pain Medicine . . . . . . . . . . . . . . . . . . . . . . . . . . 75
Heather Tick
12 Peripheral Nerve Blocks in Palliative Care for Cancer Patients . . . . . . . . . . . . . . 79
Zbigniew (Ben) Zylicz
13 Complications of Nerve Entrapment Injection . . . . . . . . . . . . . . . . . . . . . . . . . . . . 85
Daniel Krashin and Natalia Murinova

xiii
xiv Contents

Part II Headache
Esther Rawner, Section Editor, and Matthew P. Rupert

14 Supraorbital Nerve Entrapment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 95

Rafael Justiz and Andrea M. Trescot
15 Auriculotemporal Nerve Entrapment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 105
Andrea M. Trescot and Esther Rawner
16 Great Auricular/Posterior Auricular Nerve Entrapment . . . . . . . . . . . . . . . . . . . 117
Leonard Benton and Andrea M. Trescot
17 Greater Occipital Nerve Entrapment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 127
Andrea M. Trescot, Esther Rawner, and David M. Irwin
18 Lesser Occipital Nerve Entrapment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 149
Esther Rawner, David M. Irwin, and Andrea M. Trescot
19 Third Occipital Nerve Entrapment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 159
Esther Rawner and Andrea M. Trescot
20 Suboccipital Neuralgia and Decompression . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 171
Andrea M. Trescot, Esther Rawner, Matthew P. Rupert, Rafael Justiz,
and Gabor Racz

Part III Facial and Cervical Nerve Entrapments

Agnes R. Stogicza, Section Editor

21 Supraorbital Nerve Entrapment: Face . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 185

Rafael Justiz
22 Infraorbital Nerve Entrapment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 197
Rafael Justiz and Eugene D. Kaplan
23 Maxillary Nerve Entrapment. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 205
Ava Yoon and Vinay Puttanniah
24 Mandibular Nerve Entrapment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 217
Ava Yoon and Vinay Puttanniah
25 Mental Nerve Entrapment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 229
Sydney E. Rose and Amitabh Gulati
26 Glossopharyngeal Nerve Entrapment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 241
Agnes R. Stogicza and Andrea M. Trescot

Part IV Chest Wall Peripheral Nerve Entrapment Syndromes

Amitabh Gulati, Section Editor

27 Spinal Accessory Nerve Entrapment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 253

Agnes R. Stogicza
28 Suprascapular Nerve Entrapment: Shoulder. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 267
Christopher J. Burnett and Helen W. Karl
29 Intercostal Nerve Entrapment: Chest Wall . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 279
Sola Olamikan, Amitabh Gulati, and Andrea M. Trescot
30 Long Thoracic Nerve Entrapment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 291
Sola Olamikan and Helen W. Karl
Contents xv

31 Axillary Nerve Entrapment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 305

Christopher J. Burnett and Helen W. Karl
32 Dorsal Scapular Nerve Entrapment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 315
Andrea M. Trescot

Part V Upper Extremity Peripheral Nerve Entrapments

Virtaj Singh, Section Editor

33 Thoracic Outlet Syndrome (Neurogenic) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 327

Virtaj Singh, Christopher J. Burnett, and Richard E. Seroussi
34 Suprascapular Nerve Entrapment: Upper Extremity . . . . . . . . . . . . . . . . . . . . . . 339
Christopher J. Burnett and Helen W. Karl
35 Deep Branch of the Radial Nerve Entrapment . . . . . . . . . . . . . . . . . . . . . . . . . . . 349
Richard E. Seroussi, Virtaj Singh, and Helen W. Karl
36 Superficial Radial Nerve Entrapment. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 359
Andrea M. Trescot and Helen W. Karl
37 Median Nerve Entrapments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 369
Virtaj Singh and William B. Ericson Jr.
38 Ulnar Nerve Entrapment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 383
Virtaj Singh and Andrea M. Trescot

Part VI Abdominal Wall Pain

Tiffany Zhang, Section Editor

39 Intercostal Nerve Entrapment: Abdomen . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 399

Sola Olamikan, Amitabh Gulati, and Andrea M. Trescot
40 Ilioinguinal and Iliohypogastric Nerve Entrapment: Abdominal . . . . . . . . . . . . 413
Neel Amin, Daniel Krashin, and Andrea M. Trescot
41 Genitofemoral Nerve Entrapment: Abdominal . . . . . . . . . . . . . . . . . . . . . . . . . . . 425
Thais Khouri Vanetti, Alexandra Tavares Raffaini Luba, Fabrício Dias Assis,
and Charles Amaral de Oliveira
42 Abdominal Cutaneous Nerve Entrapment Syndrome . . . . . . . . . . . . . . . . . . . . . . 437
Eugene D. Kaplan and Helen W. Karl
43 Lumbar Plexus Entrapment: Abdominal . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 451
Susan R. Anderson-Jones and Tiffany Zhang

Part VII Pelvic Pain

Daniel Krashin, Section Editor

44 Ilioinguinal Nerve Entrapment: Pelvic . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 467

Natalia Murinova, Daniel Krashin, and Andrea M. Trescot
45 Genitofemoral Nerve Entrapment: Pelvic . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 479
Thais Khouri Vanetti, Alexandra Tavares Raffaini Luba, Fabrício Dias Assis,
and Charles Amaral de Oliveira
46 Posterior Femoral Cutaneous Nerve Entrapment: Pelvic . . . . . . . . . . . . . . . . . . . 491
Natalia Murinova, Daniel Krashin, and Andrea M. Trescot
xvi Contents

47 Pudendal Nerve Entrapment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 499

Susanti K. Chowdhury and Andrea M. Trescot
48 Obturator Nerve Entrapment: Pelvic . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 515
Andrea M. Trescot
49 Lumbar Plexus Entrapment: Pelvic . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 527
Susan R. Anderson-Jones, Tiffany Zhang, and Andrea M. Trescot
50 Inferior Cluneal Nerve Entrapment: Pelvic . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 545
Terri Dallas-Prunskis

Part VIII Low Back Pain

Terri Dallas-Prunskis, Section Editor

51 Superior Cluneal Nerve Entrapment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 555

Terri Dallas-Prunskis
52 Inferior Cluneal Nerve Entrapment: Low Back . . . . . . . . . . . . . . . . . . . . . . . . . . 565
Terri Dallas-Prunskis
53 Superior Gluteal Nerve Entrapment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 571
Andrea M. Trescot
54 Inferior Gluteal Nerve Entrapment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 581
Andrea M. Trescot
55 Proximal Sciatic Nerve Entrapment: Low Back . . . . . . . . . . . . . . . . . . . . . . . . . . 589
Annemarie E. Gallagher, Amitabh Gulati, and Terri Dallas-Prunskis
56 Posterior Femoral Cutaneous Nerve Entrapment: Low Back . . . . . . . . . . . . . . . 605
Natalia Murinova, Daniel Krashin, and Andrea M. Trescot

Part IX Lower Extremity

Susan R. Anderson-Jones, Section Editor

57 Femoral Nerve Entrapment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 617

Christopher J. Burnett
58 Proximal Saphenous Nerve Entrapment: Thigh and Knee. . . . . . . . . . . . . . . . . . 627
Andrea M. Trescot, Helen W. Karl, Michael N. Brown, and Beth S. Pearce
59 Distal Saphenous Nerve Entrapment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 645
Michael N. Brown, Beth S. Pearce, Helen W. Karl, and Andrea M. Trescot
60 Genitofemoral Nerve Entrapment: Lower Extremity . . . . . . . . . . . . . . . . . . . . . . 655
Thais Khouri Vanetti, Alexandra Tavares Raffaini Luba, Fabrício Dias Assis, and
Charles Amaral de Oliveira
61 Lateral Femoral Cutaneous Nerve Entrapment . . . . . . . . . . . . . . . . . . . . . . . . . . 667
Lisa Rochelle Witkin, Amitabh Gulati, Tiffany Zhang, and Helen W. Karl
62 Posterior Femoral Cutaneous Nerve Entrapment: Pelvic . . . . . . . . . . . . . . . . . . . 683
Natalia Murinova, Daniel Krashin, and Andrea M. Trescot
63 Inferior Cluneal Nerve Entrapment: Lower Extremity . . . . . . . . . . . . . . . . . . . . 691
Terri Dallas-Prunskis
64 Obturator Nerve Entrapment: Lower Extremity . . . . . . . . . . . . . . . . . . . . . . . . . 699
Andrea M. Trescot and Helen W. Karl
Contents xvii

65 Proximal Sciatic Nerve Entrapment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 713

Annemarie E. Gallagher, Amitabh Gulati, and Terri Dallas-Prunskis
66 Lumbar Plexus Entrapment: Lower Extremity. . . . . . . . . . . . . . . . . . . . . . . . . . . 727
Susan R. Anderson-Jones, Tiffany Zhang, and Andrea M. Trescot
67 Common Peroneal Nerve Entrapment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 745
Natalia Murinova, Sheila C. Chiu, Daniel Krashin, and Helen W. Karl
68 Superficial Peroneal Nerve Entrapment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 759
Natalia Murinova, Sheila C. Chiu, Daniel Krashin, and Helen W. Karl
69 Deep Peroneal Nerve Entrapment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 769
Beth S. Pearce, Michael N. Brown, and Helen W. Karl
70 Interdigital Nerve Entrapment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 781
Beth S. Pearce, Michael N. Brown, and Thais Khouri Vanetti
71 Sural Nerve Entrapment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 795
Michael N. Brown, Beth S. Pearce, and Thais Khouri Vanetti
72 Lateral Sural Cutaneous Nerve Entrapment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 811
Heath McAnally
73 Tibial Nerve Entrapment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 819
Michael N. Brown, Beth S. Pearce, Andrea M. Trescot, and Helen W. Karl
74 Lateral Plantar Nerve Entrapment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 833
Michael N. Brown, Beth S. Pearce, Thais Khouri Vanetti, Andrea M. Trescot,
and Helen W. Karl
75 Medial Plantar Nerve Entrapment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 845
Michael N. Brown, Beth S. Pearce, Andrea M. Trescot, and Helen W. Karl
76 Inferior Calcaneal Nerve Entrapment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 859
Michael N. Brown, Beth S. Pearce, and Helen W. Karl
77 Medial Calcaneal Nerve Entrapment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 871
Michael N. Brown, Beth S. Pearce, Thais Khouri Vanetti, Andrea M. Trescot,
and Helen W. Karl
Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 883

Index of Symptoms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 901

Contributors

Neel Amin, MD Anesthesiology and Pain Medicine, American Pain Experts, Ft. Lauderdale,
FL, USA
Susan R. Anderson-Jones, MD Pain Management Clinic, Liberty Hospital, Liberty,
MO, USA
Fabrício Dias Assis, MD, FIPP Medical Director, Singular – Centro de Controle da Dor,
Campinas, São Paulo, Brazil
Leonard Benton, MD, FIPP Private Practice, Ft. Myers, FL, USA
Michael N. Brown, DC, MD Interventional Regenerative Orthopedic Medicine Institute,
Seattle, WA, USA
Christopher J. Burnett, MD Pain Management Division, Department of Anesthesiology,
Baylor Scott and White Memorial Hospital, Temple, TX, USA
Sheila C. Chiu, DO Department of Anesthesiology and Pain Medicine, University of
Washington, Seattle, WA, USA
Susanti K. Chowdhury, MD Advanced Interventional Spine Consultants, Largo, FL, USA
Terri Dallas-Prunskis, MD Illinois Pain Institute, Elgin, IL, USA
Charles Amaral de Oliveira, MD, FIPP Singular Pain Center, Campinas, São Paulo, Brazil
William B. Ericson Jr., MD, FACS, FAAOS Ericson Hand and Nerve Center,
Mountlake Terrace, WA, USA
Annemarie E. Gallagher, MD Interventional Pain and Spine Institute, Las Vegas, NV, USA
Amitabh Gulati, MD Director of Chronic Pain, Anesthesiology and Critical Care,
Memorial Sloan Kettering Cancer Center, New York, NY, USA
David M. Irwin, DO Pain and Interventional Medicine, Neurosurgery, UPMC Hamot
Medical Center, Erie, PA, USA
Rafael Justiz, MD, MS, DABA/PM, FIPP, DABIPP Department of Anesthesiology,
Oklahoma Pain Physicians, University of Oklahoma Health Sciences Center,
Oklahoma City, OK, USA
Eugene D. Kaplan, MD, MPH, DABNP, DABIPP, FIPP Optimum Health Medical Group,
PLLC, Clifton Park, NY, USA
Helen W. Karl, MD Department of Anesthesiology and Pain Medicine, University of
Washington, Seattle Children’s Hospital, Seattle, WA, USA
Daniel Krashin, MD Pain and Anesthesia and Psychiatry Departments, Chronic Fatigue
Clinic, University of Washington, Seattle, WA, USA
Brett Lockman, DO Advanced Wellness Sports and Spine, Davenport, IA, USA

xix
xx Contributors

Heath McAnally, MD, MSPH Interventional Pain Medicine, Northern Anesthesia and Pain
Medicine, LLC, Eagle River, AK, USA
Natalia Murinova, MD Department of Neurology, Headache Clinic, University
of Washington, Seattle, WA, USA
Sola Olamikan, MD Assistant Professor, Department of Anesthesiology and Pain Medicine,
University of Texas, Southwestern Medical Center, Dallas, TX, USA
Attending Pediatric Anesthesiologist and Pediatric Pain Specialist,
Children’s Health Medical Center, Dallas, TX, USA
Beth S. Pearce, DPM, BA (Biology) Orthopaedic Associates of St. Augustine,
St. Augustine, FL, USA
Vinay Puttanniah, MD Regional Anesthesia, Anesthesiology and Critical Care Medicine,
Memorial Sloan Kettering Cancer Center, New York, NY, USA
Gabor Racz, MD, DABIPP, FIPP Professor Emeritus, Department of Anesthesiology,
Texas Tech University Health Sciences Center, Lubbock, TX, USA
Alexandra Tavares Raffaini Luba, MD Singular – Centro de Controle da Dor, Campinas,
São Paulo, Brazil
Instituto do Cãncer do Estado de São Paulo, São Paulo, SP, Brazil
Santa Casa de São Paulo, Campinas, São Paulo, Brazil
Esther Rawner, MD Department of Neurology, Northwest Hospital, Seattle, WA, USA
Sydney E. Rose, MD Anesthesiology and Pain Medicine, New York – Presbyterian
Hospital, New York, NY, USA
Matthew P. Rupert, MD, MS, FIPP VERTEX Spine and Pain, Franklin, TN, USA
Kris A. Sasaki, DC, CCSP Vida Integrated Health, Seattle, WA, USA
Richard E. Seroussi, MD, MSc Department of Rehabilitation Medicine, Courtesy Clinical
Faculty, University of Washington, Seattle, WA, USA
Seattle Spine and Sports Medicine, Seattle, WA, USA
Virtaj Singh, MD Clinical Faculty, Department of Rehabilitation Medicine, University of
Washington, Seattle Spine and Sports Medicine, Seattle, WA, USA
Agnes R. Stogicza, MD, FIPP Department of Anesthesiology and Pain Medicine,
University of Washington, Seattle, WA, USA
Heather Tick, MA, MD Family Medicine and Anesthesiology and Pain Medicine,
University of Washington, Seattle, WA, USA
Andrea M. Trescot, MD, ABIPP, FIPP Pain and Headache Center, Anchorage, AK, USA
Thais Khouri Vanetti, MD, FIPP Singular – Centro de Controle da Dor, Campinas,
São Paulo, Brazil
Instituto do Cãncer do Estado de São Paulo, São Paulo, SP, Brazil
Lisa Rochelle Witkin, MD Division of Pain Medicine, Department of Anesthesiology,
New York-Presbyterian/Weill Cornell Medical Center, New York, NY, USA
Ava Yoon, MD Department of Anesthesiology, Kaiser Downey Medical Center, Downey,
CA, USA
Tiffany Zhang, MD, PhD Department of Anesthesiology and Pain Medicine, University of
Washington Medical Center, Seattle, WA, USA
Zbigniew (Ben) Zylicz, MD, PhD Oeitender Arzt, Palliative Care Team, University Hospital,
Basel, Switzerland
 Part I
Peripheral Nerve Entrapments: General Principles

Andrea M. Trescot and Daniel Krashin

Introduction

An entrapment neuropathy is defined as a pressure-induced injury to a peripheral nerve in a

segment of its course due to anatomic structures or pathologic processes [1]. Entrapment neu-
ropathies for many conditions have been known for years. For instance, Paget [2] described
entrapment of the ulnar nerve at the elbow in 1864, Learmonth [3] described carpal tunnel
syndrome in 1933, tarsal tunnel syndrome [4, 5] was described in 1962, and radial nerve
entrapment at the elbow in 1972 [6]. However, these are still often misunderstood, and there
are many other poorly recognized or misrecognized peripheral nerve entrapments associated
with clinical pain syndromes. Even for the astute clinician, these conditions may be difficult to
diagnose without a high clinical index of suspicion. Knowledge of the syndromes and recogni-
tion of the patterns and symptoms will help the clinician to make the right diagnosis.
Kopell and Thompson [7] stated that peripheral nerve entrapment occurs at anatomic sites
where the nerve changes direction to enter a fibrous or osseofibrous tunnel, or where the nerve
passes over a fibrous or muscular band, and that entrapment occurs at these sites because
mechanically induced irritation is most likely to occur at these locations. Trauma, such as sur-
gery or constriction, and peripheral swelling, such as seen perimenstrually or with dietary
indiscretions, can induce or perpetuate these entrapments, causing direct injury to the nerve or
compromising its blood flow. Peripheral nerve injections (peripheral nerve blocks) are inter-
ventional pain management techniques used to treat patients with nerve entrapments present-
ing as a variety of painful conditions. By delivering local anesthetic and deposteroid directly
onto the injured nerve, these injections can provide diagnostic as well as therapeutic benefit for
patients suffering from pain anywhere from the head to the toes. Recognition of these condi-
tions will lead to quicker diagnosis and treatment as well as decrease the inappropriate use of
expensive (and for these conditions, useless) imaging and painful surgeries [8].
Peripheral nerve entrapments can cause a variety of painful conditions as diverse as head-
ache, backache, “sciatica,” “endometriosis,” and foot pain. In addition, painful conditions with
well-described pathology such as chronic regional pain syndrome (CRPS) or postherpetic neu-
ralgia (PHN) may have a component of nerve entrapment, either as the initiating event (CRPS)
or as a consequence of the pathology (PHN).
Nerve entrapments may occur in varying degrees, leading to a variety of clinical presenta-
tions. Somatic neuropathic pain originating from these nerves can have multiple etiologies.
Nerve injury [2] has been reported from:

• Stretching
• Blunt trauma
• Compression with hypoxia
• Fibrosis with entrapment
• Suture ligature
2 Part I Peripheral Nerve Entrapments: General Principles

The pain will often have a burning, shooting, or lancinating quality. Although initially the pain may be
intermittent, the pain will usually become constant and more intense with time. If postsurgical, the pain can
occur immediately after surgery, or it may start weeks to years after the surgery, as the scar cicatrix gradu-
ally tightens around the nerve. Pain is usually aggravated by activity, menstruation (due to perineural edema,
hormone-induced increased neurotransmitters, and dorsal horn transmission cell sensitivity), or activity.
Clinical diagnosis is dependent on a high index of suspicion and physical exam, but peripheral nerve blocks
that provide complete relief, albeit temporary, are the sine qua non for establishing this diagnosis [9].
The injectate consists of a long-lasting local anesthetic (usually bupivicaine) and a depo-steroid. Because
entrapment of the nerve is usually the underlying pathology, care must be used to avoid further entrapment
with large volumes of injectate. Methylprednisolone (Depomedrol®) may be the steroid of choice, because
of its high lipophilic nature (to enter the myelin sheath) and its high concentration (80 mg/cc). Total dose of
steroid would normally be limited to 80 mg methylprednisolone (or equivalent), with no more than 40 mg
at any one site (less if the skin is thin or the injection superficial, because of the risk of steroid-induced skin
atrophy).
In this book, we hope to introduce the clinician to the myriad of pain conditions caused by peripheral
nerve entrapment that may be diagnosed and treated with peripheral nerve injections. This book is divided
into sections: the first is an overview of the history taking, physical exam, and diagnostic injection tech-
niques. This is followed by sections on headaches, face and neck pain, chest wall pain, upper extremity pain,
abdominal pain, low back pain, pelvic pain, and lower extremity pain. Each nerve has its own chapter, and
each chapter is designed to stand alone, describing the clinical presentation, the anatomy and entrapment, the
physical exam, the injection technique (blind, fluoroscopic, or ultrasound) and then the treatment modalities,
such as neurolysis or surgery. The chapter concludes with a review of the literature and references. We have
added an index of symptoms to aid the clinician in narrowing down the search for a specific nerve.
There have been many books written on regional anesthesia, and many pain practitioners come from this
arena, but we want to emphasize that these entrapments cause pain syndromes, and, unlike regional anes-
thesia, require low-volume precise injections for diagnosis and treatment.

References
1. Toussaint CP, Perry 3rd EC, Pisansky MT, Anderson DE. What’s new in the diagnosis and treatment of peripheral nerve
entrapment neuropathies. Neurol Clin. 2010;28(4):979–1004.
2. Paget J. Clinical lecture on some cases of local paralysis. Med Times Gazette, London. 1864;1:331.
3. Learmonth JR. The principle of decompression in the treatment of certain diseases of peripheral nerves. Surg Clin North
Am. 1933;13:905–13.
4. Keck C. The tarsal-tunnel syndrome. J Bone Joint Surg Am. 1962;44A:180–2.
5. Lam SJS. A tarsal-tunnel syndrome. Lancet. 1962;2:1354–5.
6. Roles NC, Maudsley RH. Radial tunnel syndrome. J Bone Joint Surg Am. 1972;4B:784–90.
7. Kopell HP, Thompson WA. Peripheral entrapment neuropathies. Baltimore: Williams and Wilkins; 1976.
8. Bora Jr FW, Osterman AL. Compression neuropathy. Clin Orthop Relat Res. 1982;163:20–32.
9. Kline DG, Hudson AR. Nerve injuries: operative results for major nerve injuries, entrapments, and tumors. Philadelphia:
W.B. Saunders; 1995.
 Epidemiology and Pathophysiology
1
Andrea M. Trescot, Daniel Krashin, and Helen W. Karl

there. Upon discharge from the ED, 45 % of patients reported

Epidemiology
an NRS of 4–7/10, and 29 % still had a pain score of 8–10/10.
A recent examination of the UK General Practice
More than 80 million people in the United States suffer
Research Database (which contains 1.8 million patient years
annually from serious pain, leading to disability, suffering,
of data), looking for new peripheral nerve entrapments,
drug addiction, depression, and suicide [1].
reported that they are relatively common [3] (Table 1.1). In
Although diagnostic tools such as MRI and endoscopic
another recent survey [4], 30 of 998 patients (3 %) referred
techniques have become more sophisticated, there are a sig-
to a gastroenterologist were diagnosed as having chronic
nificant number of patients who have been told that “it is all
abdominal wall pain (CAWP), presumably caused by myo-
in your head,” “you just want pain medication,” “there is
fascial spasm or peripheral nerve entrapment (see ACNES
nothing on the MRI,” or “the surgery looks perfect, so I don’t
syndrome – Chap. 42).
know why you are hurting.” Pain management clinics have
Post-traumatic neuropathy is nerve pain that has been trig-
been viewed as the place of last resort – “if all else fails, send
gered after an injury or as a consequence of medical interven-
them to pain management.” As such, the patient arrives on
tions such as surgery, injections, or radiotherapy. A recent
our doorstep, traumatized by ineffective surgeries, hyperal-
evaluation of more than 2,500 soldiers returning from Iraq and
gesic because of high-dose opioids, depressed because of the
Afghanistan revealed that 44 % had chronic pain, with 48.3 %
multiple failed treatments, and hostile because once more
of them having been in pain for more than a year. More than
they have to tell their story, only to watch the physician shrug
half (55.6 %) of the soldiers with chronic pain described it as
and say “I don’t know.”
constant; it was moderate to severe in 51.2 % [5].
Pain is a problem throughout the entire medical field. In
Acute postoperative pain can develop into chronic
fact, the most common reason that patients present in the
postsurgical pain (CPSP), which affects daily life in 10–50 %
emergency department (ED) is pain. Todd et al. [2] noted
of patients after surgery; this pain can be severe in 2–10 % of
that the median pain scores of patients on arrival in the ED
them [6]. A prospective study of approximately 5,000
were 8/10 on a number rating scale (NRS), and only half of
surgical patients identified acute neuropathic pain in 1–3 %;
them had a decrease in their pain by 2 or more points while
56 % of these had persistent chronic pain 1 year later [7]. The
incidence varies widely with the kind of surgical procedure
[8]. Simanski et al. confirmed these findings: more than 500
of 911 (57 %) patients had pain scores of greater than 3/10
A.M. Trescot, MD, ABIPP, FIPP (*)
Pain and Headache Center, Anchorage, AK, USA for a mean of 29 months after orthopedic, abdominal, and/or
e-mail: DrTrescot@gmail.com vascular surgery. Almost 15 % of these patients reported
D. Krashin, MD severe pain [9].
Chronic Fatigue Clinic, Pain and Anesthesia and Psychiatry Pain after inguinal hernia repair has been reported to range
Departments, University of Washington, Seattle, WA, USA from 0 % to 60 %. A 2007 systematic review of pain after
e-mail: krashind@uw.edu
mesh hernia repair showed that 11 % of patients had persistent
H.W. Karl, MD groin pain. More than a quarter of them had severe pain, and
Department of Anesthesiology and Pain Medicine,
more than a third had limitations of daily activities [10]. Post-
University of Washington, Seattle Children’s Hospital,
4800 Sand Point Way NE, Seattle, WA, USA herniorrhaphy pain is likely due to ilioinguinal (Chap. 40)
e-mail: helen.karl@seattlechildrens.org and/or genitofemoral (Chap. 41) nerve injury. Similar

© Springer International Publishing Switzerland 2016 3

A.M. Trescot (ed.), Peripheral Nerve Entrapments: Clinical Diagnosis and Management, DOI 10.1007/978-3-319-27482-9_1
4 A.M. Trescot et al.
Table 1.1 Incidence of peripheral nerve entrapments in UK primary
care in 2000 [3]
Men Women
Carpal tunnel syndrome 87.8a 192.8
Morton’s metatarsalgia 50.2 87.5
Ulnar neuropathy 25.2 18.9
Meralgia paresthetica 10.7 13.2
Radial neuropathy 2.97 1.42
a
Per 100,000 European standard population
outcomes were reported in 690 consecutive patients surveyed
2 years after a Pfannenstiel incision for cesarean delivery or
abdominal hysterectomy. One third still had incisional pain,
and nearly 10 % described pain that interfered with their lives.
Over half of the patients with moderate to severe pain (17 of
32) were found to have peripheral nerve entrapments [11].
Saphenous vein harvesting is performed in up to 27 % of
patients undergoing coronary artery bypass grafting
(CABG). In a survey of more than 1,000 CABG patients,
130 had chronic chest pain, 100 had leg pain, and 194
reported both. Although leg pain after vein harvest is usually
described as mild, in about a third of the patients with pain,
the prevalence of moderate to severe pain at a mean of
28 months after CABG was about 40 % [12].
Hicks and Simpson state that about 10–15 % of patients
with cancer-related pain could benefit from peripheral nerve
blocks (see Palliative Care – Chap. 12) [13].
We propose that many of these pain conditions are the
result of peripheral nerve entrapments.
Pathophysiology
An entrapment neuropathy is defined as a pressure-induced
segmental injury to a peripheral nerve due to an anatomic
structure or pathologic process [14–16]. The defining criteria
of an entrapment, according to Kashuk [17], include altered
transmission as a result of mechanical irritation from
impingement of an anatomic neighbor. Most of the nerve
entrapments discussed in this book occur at areas where
the nerve travels through a canal, channel, or tunnel.
The nerve has its own blood flow (vasa nervorum) as well as
accompanying vascular structures. Compression at these
sites, whether intrinsic or extrinsic, can cause damage to the
neurovascular structures running in the common course.
Multiple approaches have been used to try to categorize
these entrapment phenomena, and the naming is therefore
not consistent. The name of the condition can come from:
• The compressed nerve (e.g., lateral femoral cutaneous
neuralgia)
• The classic Greek or Latin name (e.g., meralgia
paresthetica)
• The anatomic area affected (e.g., metatarsalgia)
• The anatomic tunnel (e.g., carpal tunnel syndrome, tarsal
tunnel syndrome)
• The motion that causes the compression (e.g.,
hyperabduction syndrome)
• The names of the describing authors (e.g., Kiloh-Nevin’s
syndrome)
Some people are susceptible to a particular entrapment
neuropathy from congenital narrowing of a tunnel or thick-
ening of an overlying fascial structure, while others with a
systemic disorder such as diabetes mellitus (DM) show
entrapment signs and symptoms much more frequently than
nondiabetics [18–20].
Nerve injuries can result in clinical symptoms extending
from mild discomfort to numbness, paralysis, or incapacitat-
ing pain. These changes parallel the histologic changes that
occur in the implicated nerve (Fig. 1.1) [21]. In order to pro-
vide a common language for clinicians and researchers,
some generally accepted classifications have evolved [16,
22, 23] (Table 1.2). Most peripheral nerve entrapments result
in Grade 1 or Grade 2 injury. The most common mechanism
of nerve injury is mechanical, but thermal or chemical injury
may also occur (Table 1.3).
Mechanical injury may involve compressing,
overstretching, or partially or totally cutting a nerve.
Compression usually occurs at a site of direction change in
a relatively noncompliant corridor, such as a fibro-osseous
tunnel or fascial opening. Inflammation or edema of adjacent
structures (e.g., tendons) can reduce the size of the passage-
way. Graded experimental compression results in profound
short- and long-term effects on in vivo blood flow. Mild
compression (20–30 mmHg) decreases venous flow; moder-
ate compression decreases capillary and arterial flow; and
pressures of 60–80 mmHg cause frank ischemia [24]. These
pressures correspond to those measured clinically in the tar-
sal tunnel [25], carpal tunnel [26], and cubital tunnel [27].
Axonal transport is blocked by pressures of 50 mmHg [28],
and nerve impulse conduction is blocked after less than an
hour of compression of 70 mmHg in a peripheral nerve [29].
Other animal models of compression neuropathy sur-
round a large nerve with a Silastic tube and evaluate histol-
ogy and nerve conduction [21, 30]. Histologically, prolonged
compression leads to neural edema, which, in the absence of
relief, can progress to epineurial fibrosis and scarring, further
thickening the nerve and worsening the entrapment. Damage
to the myelin sheath and axonal disruption are end stages of
chronic compression, resulting in irreversible damage [21]
(Fig. 1.2).
Upton and McComas observed that 81/115 (70 %)
patients with carpal or cubital tunnel syndrome also had
electrophysiological evidence of a nerve injury in the neck
[31]. They named the phenomenon the “double crush
1 Epidemiology and Pathophysiology 5

Histopathology

Breakdown Connective tissue thickening

B.N.B

Localized
Fiber
Wallerian demyelination
degeneration Diffuse

Clinical findings Symptoms

Positive
Pressure
provocative
position
tests Intermittent
paresthesia /
weakness

Threshold tests / Persistent

weakness paresthesia /
weakness
Abnormal 2 pd / Numbness /
muscle atrophy paralysis

Fig. 1.1 The relationship between nerve histopathology, the patient’s symptoms, and the clinical findings (From Mackinnon [21]. Reprinted with
permission from Thieme Publishers). BNB blood nerve barrier

Table 1.2 Seddon and Sunderland classifications of nerve injury [16] Table 1.3 Causes of nerve injury
Seddon Sunderland Injury Mechanical
Neurapraxia Grade I Focal segmental Compression and/or Intraoperative retraction, suture material,
demyelination stretch scar [8]
Axonotmesis Grade II Axon damaged with Joint hypermobility [42]
intact endoneurium Expanding tumor or cyst
Axonotmesis Grade III Axon and endoneurium Dental work
damaged with intact
Infection
perineurium
Edema [60]
Axonotmesis Grade IV Axon, endoneurium,
and perineurium Congenital anomalies (e.g., muscle bands)
damaged with intact Blunt trauma with or without fracture
epineurium Systemic Diabetes mellitus [18, 20]
Neurotmesis Grade V Complete nerve susceptibility Chemotherapy [61]
transection Thyroid disease [62]
Grade VI Mixed levels of injury Chemical Dental care [52]
(MacKinnon and along the nerve
Infection
Dellon)
Leaking intervertebral disk
From Menorca et al. [16]. Reprinted with permission from Elsevier
Limited Thermal Total joint replacement [50]

syndrome” (DCS), where the presence of a more proximal
lesion renders the distal nerve trunk particularly vulnerable to
compression, with a degree of pain and dysfunction greater
than that expected from either entrapment alone. They postu-
lated that this was due to the effect of compression on
anterograde axoplasmic flow, as later confirmed by other
investigators [28, 32]. However, other mechanisms, and indeed
whether this phenomenon actually exists, are also under dis-
cussion [33]. Lundborg’s observation that patients with symp-
toms of ulnar compression in the wrist subsequently developed
compressive symptoms of the same nerve at the elbow led to
the concept of “reverse DCS,” thought to be due to disturbed
6 A.M. Trescot et al.

Nerve fibre Connective tissue

Myelin Perineurium

Axon
Endoneurium

Internal epineurium

External epineurium

Mesoneurium

Normal nerve

Microvessels

Perineurium

Blood nerve barrier changes Connective tissue changes

Myelinated fibres Normal

myelinated fibres

Unmyelinated fibres
Focal nerve fibre changes

Severe diffuse fibre changes with wallerian degeneration

1 Epidemiology and Pathophysiology 7

retrograde axoplasmic flow [34]. DCS has been observed at
several common locations, clinically [21, 35, 36], upon elec-
trodiagnostic investigation [37] (Table 1.4), and experimen-
tally [32]. The surgical outcome of carpal tunnel release is
poorer in those patients, suggesting that both entrapments
likely require treatment for optimal results [21].
The role of overstretching a nerve is sometimes over-
looked, but it is especially important with respect to nerves
that cross over joints, where changes in position are known
to change the amount of stretch [38, 39]. Stretch injury may
have a significant role in the pain after joint injuries, suggest-
ing that pain from degenerative joint disease (DJD) may not
be purely due to intra-articular pathology [40], as evidenced
by the pain relief seen with injection and denervation of the
infrapatellar saphenous nerve [41] (see Chap. 58). Also,
patients with joint hypermobility from Ehlers-Danlos syn-
drome have a much higher incidence of ulnar nerve sublux-
ation and potential entrapment at the elbow than patients
without Ehlers-Danlos [42] (see Chap. 37). Animal models
that investigate the underlying pathophysiologic mecha-
nisms support these clinical observations [38, 43]. High
degrees of stretch result in decreased blood flow, but electro-
physiologic changes are measurable at levels well below
those that cause ischemia [38]; as little as 6 % stretch of a
nerve can cause permanent injury [44].
Diabetes mellitus predisposes patients to not only entrap-
ment neuropathies but also to inflammatory ones [18, 45],
thereby acting like the first “crush.” This often results in the
classic stocking and glove symptom patterns in diabetic
patients [20, 46]. Entrapment susceptibility in diabetes is
thought to be the result of three factors: increased sorbitol con-
centration leading to neural swelling, abnormal axoplasmic
transport, and the presence of intraneural collagen-glucose
complexes that make the nerve less compliant [20].
Dellon has advocated early surgical decompression of
nerves to prevent and treat diabetic tissue loss. In the foot,
combined neurolysis of the common peroneal nerve at the
knee (Chap. 67), the superficial peroneal nerve above the
ankle (Chap. 68), and the posterior tibial nerve at the tarsal
tunnel (Chap. 73) has improved symptoms in the “stock-
ing” distribution. A recent multicenter prospective study
of tibial nerve neurolysis alone in 628 diabetic patients
with well-documented tibial nerve entrapment documented
improved foot ulceration [47], and a randomized clinical
trial in 42 patients showed that a four-site decompression
significantly improved foot pain [48]. In the upper extrem-
ity, combined neurolysis of the median nerve at the wrist
(Chap. 37) and the ulnar nerve at the elbow (Chap. 38),
with or without release of the radial sensory nerve in the
forearm (Chap. 36), improved symptoms in the “glove”
distribution [49].
Other causes of nerve compression and entrapment
include hematomas, especially with the increased use of pro-
phylactic anticoagulation postoperatively [44]. These
patients will present with swelling and increasing pain post-
operatively, and nerve testing is not helpful in this acute set-
ting. Hematoma-induced entrapment requires prompt
decompression to avoid permanent compromise. In addition,
there can be intraoperative nerve injury.
Thermal injury and chemical injury are less common,
but may occur after total joint replacement (because of the
exothermic reaction of the methyl methacrylate cement)
[50] or with leaking intervertebral disks (which contain a
“soup” of inflammatory cytokines) [51]. Dental materials

Table 1.4 Double crush syndromes

Median (Chap. 37) [21, 36] CTS and cervical radiculopathy
CTS and TOS (Chap. 33)
CTS and median nerve compression at the elbow (pronator syndrome)
Ulnar (Chap. 38) [21, 36] CuTS and cervical radiculopathy
CuTS and TOS
CuTS and ulnar nerve compression at the wrist (Guyon’s canal syndrome)
Radial (Chap. 35) [21, 36] RTS and cervical radiculopathy
Deep peroneal (Chap. 69) [37] ATTS and LBP
Posterior tibial (Chap. 72) [37] TTS and LBP
CTS carpal tunnel syndrome, median nerve entrapment at the wrist; TOS thoracic outlet syndrome; CuTS cubital tunnel syndrome, ulnar nerve
entrapment at the elbow; RTS radial tunnel syndrome, radial nerve entrapment near the elbow; ATTS anterior tarsal tunnel syndrome, peroneal
nerve entrapment; TTS tarsal tunnel syndrome, tibial nerve entrapment; LBP low back pain

Fig. 1.2 Histopathology of chronic nerve compression. The initial
changes occur at the level of the blood-nerve barrier. These changes are
followed by connective tissue changes and then focal nerve fiber
changes. The large myelinated fibers undergo segmental demyelination.
The small, unmyelinated fibers demonstrate evidence of degeneration
and regeneration with the presence of a new population of very small
unmyelinated fibers. With progression of the compression, diffuse
Wallerian degeneration is noted (From Mackinnon [21]. Reprinted with
permission from Thieme Publishers)
8 A.M. Trescot et al.
Fig. 1.3 MRI image of a large sciatic nerve neuroma after a leg ampu-
tation – white arrow (Image courtesy of Andrea Trescot, MD)
(such as those used for a root canal) can also create chemi-
cal injury. Chemical damage to a nerve can occur locally
from toxic materials such as paraformaldehyde for end-
odontic filling. Dental irrigation chemicals like sodium
hypochlorite can also be culprits. Additionally, chemical
injury can be caused internally by the body’s own local
inflammatory markers and cytokines, including those
released by cells fighting infection [52] or from a damaged
intervertebral disk [51].
When nerves are injured and try to regenerate, the
proximal segment may curl up on itself, causing an
ectopic-firing “knot” of nerve fibers called a neuroma
(Fig. 1.3). Neuromas are mostly composed of sprouting
axons, with a significant degree of sympathetic innervation,
and can cause pain spontaneously or with stimulation.
They can mimic entrapments or they can be caused by the
entrapments or the treatment for that entrapment (such as
surgery or neurolytics).
Results of Peripheral Nerve Entrapment
Peripheral nerve entrapment can lead or contribute to a wide
variety of disorders (Table 1.5). In addition, painful
conditions with well-described pathology such as complex
regional pain syndrome (CRPS) (as described below) or
postherpetic neuralgia (PHN) likely have a component of
nerve entrapment, either as the initiating event (CRPS) or as
a consequence of the pathology (PHN).
Table 1.5 Conditions that may be caused by entrapment of a peripheral
nerve
Headaches, including “Endometriosis”
“migraines”
Atypical face pain Postherpetic neuralgia
Chest wall pain CRPS (previously known as
RSD)
Carpal tunnel syndrome Low back syndrome
Abdominal wall pain “Sciatica”
Pelvic pain Foot pain
Recent histological [53] and animal [54] data show that
some form of initial nerve trauma is “an important trigger for
the cascade of events leading to CRPS” [55]. The distinction
between the pathogenesis of CRPS-I and that of CRPS-II is
a matter of degree and not mechanism [56].
Therefore, patients presenting with CRPS symptoms
should be carefully questioned as to where the pain started
and where it is most intense. If this is in the distribution of
a peripheral nerve, targeting that nerve for diagnostic block
and cryoneuroablation (see Chap. 8) can have beneficial
effects on the overall CRPS clinical picture. Identification
of entrapment neuropathy as the initiating event to CRPS
could provide a method for definitive treatment.
Interestingly, CRPS has been identified 4–6 months before
the diagnosis of a malignancy, perhaps from peripheral
nerve entrapment [57].
Recovery with a resolution of the symptoms of nerve
injury depends on the inciting event, the severity of the
nerve injury, and the patient’s ability to heal; it is often dif-
ficult to predict. Factors that influence healing include the
severity, duration, and location of the injury, the integrity
of any involved muscle, the patient’s age, underlying
genetics, and other diseases (e.g., diabetes) influencing the
health of the nerves. Since the blood flow and nutrients for
the nerve come from its origin in the spinal column [58],
distal nerves tend to be at more risk for injury, due to lim-
ited “resources”; however, because of the length of regen-
eration needed, proximal peripheral nerve injuries take
longer than more distal ones to resolve. Spontaneous
recovery is often incomplete and may require up to 2 years
or longer [59].
Conclusion
Chronic pain, occurring after surgery, after injury, and
occasionally spontaneously, may be caused and perpetu-
ated by peripheral nerve entrapments. The recognition that
“every chronic pain was once acute” [8] suggests that accu-
rate diagnosis coupled with early treatment may decrease
the number of acute pain “failures” and perhaps decrease
the risk of chronic pain. Knowing the clinical features and
treatment of these peripheral nerve disorders can provide
relief for patients who have often suffered for many years.
Another random document with
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superabundance of song which had only worldly associations and
was linked with the lower pleasures made them put superfine value
on the Hebrew Psalms as being most fit for the soul’s utterance
before the Infinite.
 CHAPTER XII
SCOTLAND’S ISLAND WORLD: IONA AND
STAFFA

While Scotland is, by its definition, a “pene-insula,” or

“peninsula,” that is, “almost an island,” it has, out in the Atlantic
Ocean, an archipelago of five hundred islands. Of these about one
fifth are inhabited, and of these one third have each a population of
only ten or even fewer souls. This great group lies wholly to the
westward, for the east coast of Scotland is singularly free from
islands, the number on this side being very much like that of angels’
visits, which are spoken of as few and far between.
These islands are all situated within three degrees of latitude.
Another name for them is the “Hebrides,” which term was formerly
held to embrace all the Scottish western islands, including also the
peninsula of Kintyre and islets in the Firth of Clyde, as well as the
Isle of Man and the Isle of Rathlin.
In discriminating between the Outer and the Inner Hebrides as
many do, this differentiation has a geological basis, for the Outer
Hebrides have a foundation of gneiss, while the more northerly at
least of the Inner Hebrides are of trap rock. Broadly speaking, in
popular usage the term is “Western Islands,” while in literature
“Hebrides” is used. This seems all the more appropriate, because it
was the accident of a misplaced or added letter that gave the islands
their literary cognomen.
As in the case of our own country, which has profited so richly
through Scottish emigration from those islands, some of the most
delightfully sounding names, in their present form, have come to us
through the mistake of a transcriber; as, for example, the romantic
name, Horicon, with which tourists on Lake George as well as
readers of Cooper’s novels are familiar. The real word intended for
the map is “Iroquois,” but as a Frenchman wrote it “Horicou,” which
was further altered by a misprint, which made it “Horicon,” it has so
remained. So also the “Hebudes” of Pliny, spelled by a misprint
“Hebrides,” has held its own. Sir Walter Scott adheres to the form
“Hebudes.” “Grampian,” which sounds so pleasant to the ear, is
another instance of a false reading or misprint, which improves the
original form and sound.
The total area of these Western Islands is 2812 square miles, or
a fourth larger than Delaware. Only one ninth of the soil is cultivated,
for most of the surface consists of moors and mountains. This region
being at the terminal of the Gulf Stream, the climate is mild, though
so humid that mists are almost perpetual. The drizzling rains are so
common that the mountains are hidden from view or shrouded in fog
or cloud most of the time. The rainfall is heavy. In one place forty-two
inches is the average. Potatoes and turnips, barley and oats form the
staple crops, though with sheep-farming, cattle-raising, fishing,
distilling, slate-quarrying, and the making of tweeds, tartans, and
woollen cloth, with assistance from the patronage of summer
tourists, the people are able to get a living. In religious “persuasion”
most of the inhabitants belong to the United Free Church, though on
some of the islands the people adhere to the forms of religion
cherished in the Roman Catholic Church.
From the earliest centuries the Scandinavian pagans poured into
the islands and among the Celts, to rob and burn, but also to settle
down and be decent. When satiated with robbery and slaughter, they
became peaceful, married the daughters of the land, and adopted
the language and faith of the islanders. The vikings and the
immigrants multiplied in the Hebrides, especially when tyrants in
Norway became unusually active and severe. Battles and fighting
between the islanders and the Norwegians kept the region in turmoil
for centuries. Not a few attempts were made by the Scottish kings to
displace the Norsemen. One of these, John Macdonald, adopted the
title of “Lord of the Isles.” He married the daughter of the earl, who
afterwards became Robert II. Battles, treaties, and alliances
followed, but insular sovereignty was abolished in the reign of James
V. Bloody feuds continued, through the sixteenth and seventeenth
centuries, among the rival clans and their dependent tribes.
Even the subsidies granted by William III to the chiefs could not
preserve order. Peace dawned only when the tribal system was
broken up. Then, through the abolition of hereditary jurisdiction,
through inheritance, and the appointments in the different districts of
sheriffs who held the writ of the king, peace was secured.
Nevertheless, in the new system of management the rents being
made too high, there began an emigration to America that continued
for many years, threatening at one time to depopulate the islands.
Dr. Johnson, who, with Boswell, made what was virtually an
exploration and published the classic, entitled “A Journey to the
Western Islands of Scotland,” in 1773, tells of the ships waiting in the
harbors ready to take on their human cargo for the continent of
promise. Thousands crossed the ocean to Canada or into those
Atlantic colonies which became the United States.
Following the loss of so many able-bodied men and women, the
standard of civilization in these islands began to sink, even though
the population, which subsisted almost wholly on potatoes and
herring, kept multiplying. When in 1846 the potato blight reduced the
masses, both in Ireland and in western Scotland, to the verge of
starvation, another large emigration of thousands to Australia and
America took place. Had Carlyle’s advice been followed, Canada
would have forty million and South Africa ten million loyal British
subjects. This sage wanted the Government to turn men-of-war into
emigrant ships, in order to give free transport of people to waste
lands beyond sea. A royal commission, appointed by Parliament,
later secured legislation which has made life for the crofters in the
island more tolerable.
Steering south from Oban, we passed some rocky isles, one of
which is called, from its shape, the Dutchman’s Cap. When in front of
Fingal’s Cave, we are awed by its imposing entrance which is
formed by a series of basaltic columns from twenty to forty feet high,
which sustain an arch sixty feet above the sea. We land in a boat
amid the fuming waves and climb into the cave, which for a distance
of about two hundred feet has a sort of rather rough natural sidewalk
made of fallen columns. The waves beneath us are continually
surging and the thunderous echoes resound continually. The island,
of volcanic origin, is nothing more or less than the fragment of an
ancient stream of lava. In Fingal’s Cave there is first a basement of
tufa, from which rise colonnades of basalt in pillars which form the
walls and faces of the grotto, the roof of which consists of
amorphous basalt.
Fingal’s Cave was first noted and described by Sir Joseph Banks
in 1773. The grotto is two hundred and twenty-seven feet long, forty-
two feet wide, and sixty-six feet high. But the height of the pillars is
irregular, being thirty-six feet on one side and but eighteen on the
other. Its waters are the haunts of seals and of sea-birds.
Happily for us, instead of seeing nothing but the sombre gray, in
an atmosphere of fog or cloud, or storm-tossed waves, which on
occasions do not allow passengers to disembark, the bursts of
sunlight made unique beauty, both in atmospheric conditions and in
an exquisite play of colors. The basalt appeared to combine every
tint of warm red, brown, and rich maroon, while the seaweed and
lichen of green and gold seemed like the upholstery of a palace.
Through the percolation of the limestone water, the walls were in
places of a snow-white tint. Looking upward we could see yellow,
crimson, and white stalactites. When we examined the columns they
appeared to possess a regularity so perfect as to suggest the work
of a Greek sculptor rather than the play of Nature’s forces in her
moods of agony. The Gaelic form of the name is taken from the
murmuring of the sea, meaning the “Cave of Music.” In times of
storm the compressed air rushes out producing a sound as of
thunder.
“Fingal” is the name of the hero in the poems of Ossian, which
are based on the ancient traditions of the Gaelic people of Scotland
and Ireland, still known and told among the people, so many of
whom in the outer islands use this ancient tongue. The Finn in these
old stories was the Rig or King of the Fenians of Leinster, Ireland,
who lived at a “du” or fort in the County of Kildare, and who was
killed on the Boyne by a fisherman, a.d. 283. As for the name
“Fingal,” it is thought to mean a “fair foreigner,” or Norwegian; the
word “Dubgal,” meaning a “dark foreigner” or invader; the blond
pirates or intruders being the Norwegians and the swarthy ones
coming from Denmark. Both varieties of these unscientific
marauders ravaged Ireland in the ninth century.
Only the chief caves have names. On the south-east coast is the
Clam Shell, or Scallop Cave. It is thirty feet high, eighteen feet wide,
and about one hundred and thirty feet long, one side of it consisting
of ridges of basalt which stand out like the ribs of a ship. Near by is
the Rock of the Herdsmen, from a supposed likeness to a
shepherd’s cap. The Isle of Columns can be fully seen only at low
water.
No human habitations were noted on the Island of Staffa by us,
during our short stay. We got on board the steamer again and
proceeded to Iona, that is, “the island”; for Columkill, or the Island of
Columba, from time unrecorded has had a fertile soil. This fertility,
supposed to be in the dark ages miraculous, led probably to its early
occupation.
Iona’s history begins in the year 563 when St. Columba, from
Ireland, landed on its shores with twelve apostles. By his life and
work he rendered the place so rich in holy associations that to-day
the hosts of divided Christendom, Roman Catholic, Protestant
Episcopal, and Presbyterian, claim Iona as the cradle of their faith,
and on different days—never together in holy union—visit the sacred
isle. Sweethearts and wives must not meet. Which is which?
Iona’s scenery was ever attractive, with its precipitous cliffs, its
dazzling stretches of white shells and sand, its fertile fields, and its
grassy hollows. Its natural charms drew visitors from afar and made
those dwelling upon its acres content. Even before the name of
Christ was uttered, it had been, as the Highlanders called it in their
Gaelic tongue, the “Island of the Druids.” It was therefore famous,
before it became the centre of Celtic Christianity, and the mother
community, whose children were the depositories of the human
spirit. From its numerous monastic houses, hundreds of alumni went
out as missionaries to convert all northern Britain. In a word, the
story of humanity in all the earth is told here. The strata of religions,
the deposits of the human soul, are almost as discernible on Iona as
are the layers of geology, or the floors of successive cities revealed
by the spade, in Egypt or Palestine, in the terpen of Holland or the
mounds of Babylon.
Even the humorous side of religion is here discernible to sharp
eyes. Some of the carvings in the choir stalls and chisellings of the
marble aloft show the joker in stone. The demons are represented as
having their fun—and this is equally true in the art of Buddhism in
Japan and of mediævalism in Iona. The tower of the church of St.
Mary, on this island, has one bit of sculpture representing an angel
weighing souls in a pair of scales, one of which is kept down by a
demon’s paw. It reminded us of Dr. Franklin’s Yankee
characterization of the Dutchman’s trade with the Indians.
Iona was at times so sacred a place, with its scores of
monasteries and nunneries, with its small forest of crosses, and with
architecture that enthralled by its beauty, that it was for centuries a
spot to which pilgrims came from all lands, and in its holy soil kings
and nobles longed to be buried; yet it was not free from the robber
pagan and the bloody spoiler. The North Sea rovers, from Sweden,
Norway, and Denmark, descended in the eighth century to plunder,
to burn, and to kill. For two hundred years Iona lay desolate, until
Queen Margaret restored the desecrated monastery, building the
chapel over the site of St. Columba’s grave. Later came the
Benedictine monks, who expelled or absorbed the Celtic community.
Intermittently the island was the seat of the bishopric of the Western
Isles, but at the Reformation the monastic buildings were dismantled
by order of the legal authorities. When Dr. Johnson visited Iona in
1773, only two persons on the island could speak English. None
could read or write.
Of Iona’s political fortunes the story is brief, the most interesting
point to an American being that, when oppression and the severe
conditions made life here undesirable or scarcely possible, the
people emigrated. From the hardy race, inhabiting this and other of
the Western Isles, the United States received a noble contingent, to
enrich its grand composite of humanity.
 We spent some time in the cemetery called “the Burial Place of
Kings,” which is reputed to contain the dust of forty-eight Scottish,
four Irish, and eight Danish and Norwegian monarchs, besides many
monumental stones. The number of crosses set up on Iona was
nearly equal to that of the days of the year. These were standing, up
to Reformation times, when most of them were thrown into the sea
by order of the Synod of Argyl. Yet a few still remain. The finest are
the Maclean’s cross and St. Martin’s cross, both being almost perfect
in form, despite centuries of weathering. Both are richly carved with
runic inscriptions, emblematic devices, and fanciful scroll-work.

THE KINGS’ GRAVES, IONA

It was certainly a brain stimulant and a heart-warmer to ramble
among these ruins. Imagination re-created the scenes in those
ancient days when the light of the gospel was brought by a saintly
man filled with the spirit of Jesus. We realized, in measure at least,
how great was his work and how far-reaching was his influence in
winning men to Christ, before Latin and Germanic disputes for
mastery had divided the Christian Church. Columba’s coming quickly
changed the landscape of pagan Scotland. First in the cities and
then in almost every village, the cross, symbol of the sacrificial death
of Him who came to give life more abundantly, arose, first in wood
and then in enduring stone. The savage people, whose passions and
appetites had so closely allied them to the brutes, were transformed
and uplifted.
In time the children of the first hearers of the gospel message
were converted, not only outwardly to the acceptance of creeds,—
which in their scholastic form they could not at first understand,—not
only to symbols, which are ever but the shadows of eternal truths,
but were inwardly transformed in the renewing of their minds.
Gradually they became so changed in heart and life that we, after
having seen Christianity in very many of its varied ethnic forms, and
met its exemplars in lands not a few, cannot but feel that in the
home, the school, and the church, there is no land on earth in which
Christianity is more genuine than in Scotland. Between Columba’s
homilies and “The Cotter’s Saturday Night” long centuries were to
pass slowly away. Nothing in literature, or art, or history, or statistics,
furnishes so true a picture of the leavening of a whole nation, or
illustrates more finely the truth that among believers, even the
common people may be “kings and priests unto God,” than this
poem of Burns. It is a revelation of “Old Scotia’s grandeur.”
 CHAPTER XIII
THE CALEDONIAN CANAL—SCOTTISH
SPORTS

The long inland waterway, of which the “Caledonian Canal” is the

main portion, unites the waters of the German Ocean, at Moray Firth,
with those of the Atlantic, which wash the shores of the Island of
Mull. Considered as one highway, this trough, which forms also the
eastern boundary of “the Highlands,” was made in part by nature and
in part by art. In easy and safe passage, it saves the shipmasters
about four hundred miles of coasting voyage around the north of
Great Britain, through the stormy Pentland Firth which divides
Caithness from the Orkney Islands. The total length of the canal
proper is about sixty miles; the part made by man’s work covering
twenty-two miles. A chain of fresh-water lakes, four in number, on
various levels, stretching along the line of the great glen of Scotland,
has been united by water ladders, up which ships are lifted and by
which time is saved.
The route of the canal was surveyed in 1773 by James Watt, the
famous engineer, better known in the annals of steam. Following an
Act of Parliament in 1803, the canal, constructed under the
supervision of Thomas Telford, was opened to navigation in 1822.
There are twenty-eight locks, each having the standard dimension of
one hundred and sixty feet length, so that steamers of comfortable
length can go through. It was on one of these, the Fusileer, that we
travelled from Oban to Inverness, on another we moved in reverse
order, and great were these days. One was sunny and warm. The
other was so cloudy and cold that a grate fire at the hotel at Fort
William felt thoroughly delightful.
 On the second of these inland voyages we were on the steamer
Gondolier. From Oban we cross Loch Linnhe, which forms the
southern end of the great canal, and call at Ardgour. At the head of
the loch we stop at Fort William, formerly called “the Key of the
Highlands.” It is now a town consisting chiefly of a long, narrow
street, full of hotels. The fort was originally erected in 1655 by
Cromwell’s General Monk and called “Kilmallie.” Under the reign of
King William, in 1690, General Hugh McKay enlarged the work and
named it after the Dutch king, the town being called “Maryburgh,” in
honor of the queen. It was to this place that the perpetrators of the
massacre at Glencoe came to divide their spoil.
In 1715 and again in 1746, the followers of “Bonnie Prince
Charlie,” the Jacobites, besieged the place, but unsuccessfully. No
remnants of the fort, which was dismantled in 1860, now remain, for
in 1890 the ruins were wholly removed to provide room for the iron
rails and railway station; for, since the hills come down close
together, there is not much level real-estate room. It illustrates the
sadness of things to find here great distilleries which are large
enough to mar the landscape.
The town produced a poet, and near the railway station is an
obelisk to the memory of Ewen MacLachlin, who wrote verses in
Gaelic. Four miles away is Ben Nevis, 4406 feet high, the loftiest
mountain in the British Islands. Later, at Inverness, I met a Scottish
artist who had painted the mountain from many points of view, but he
seemed more impressed with its ugliness and shaggy character than
with its beauty. In fact, in comparing the artistic work of this painter
with that of Mr. Robert Allan, who transfers to canvas the ideal
loveliness of the ocean,—both Scottish and both masterly,—we
recalled that inimitable passage of Ruskin, contrasting the form and
functions of the mountains and the sea, which furnishes so
illuminating a commentary on the passage written by an ancient
admirer of nature and its Creator,—“Thy righteousness is like the
great mountains; thy judgments are a great deep.”
We noted, in our summer travels, not a few men of the easel. A
mile and a half from the town is the grand old ruin of Inverlochie, to
which many landscape painters resort. Other places of interest are
the site of the battlefield of 1645 and the castle of Lord Abinger, built
in the Scottish baronial style.
Yet at all these attractions we did not much more than glance,
despite the importunities of local guides, who sounded their praises
unremittingly. The reason for which we stopped for a day or two in
this mountain stronghold was not to study military fortification, or to
see the town, which, apart from its summer life, has little allurement
for the tourist who values time. We were there to see the Highland
games, for this day in August was the date set for “the gathering of
the clans” of the shire. They came not for battle as in the old times,
but for the Lochaber Highland games, such as the hammer-throwing,
putting the stone, pole-vaulting, leaping, and jumping; besides the
various Scottish dances, such as prancing and stepping over swords
and the Highland fling.
Heavy rain came down in the early part of the morning, and
during the whole day there was a drizzle, making the air heavy with
dampness and the ground meadows miry. We supposed of course
that there would be no exhibition.
Vain thought! What does a Highlander care about moisture? To
him rain is but an old friend, whom he would no more think of
speaking against than of reviling his mother. Indeed, it is his native
element. So in the afternoon, our lady, donning her mackintosh,
which she had just purchased at Oban, and I with umbrella and
overcoat splashed over the fields to the hillside and meadows, where
thousands of people were gathered together. There may have been
other umbrellas in use, but they were not conspicuous, and certainly
not numerous. Some of the athletic performances were admirable
and the achievements of manly strength were worthy of the applause
which they so generously received.
Yet an alien, one not of the heather, cannot be rapturous in
honest praise of the dances, at least those which were prolonged to
the full and apparently appropriate time, and which the spectators
seemed greatly to enjoy. It was something, no doubt, to behold an
able-bodied man in a dress that quite equalled that of the peacock,
jumping about among the crossed lines of naked steel without
getting his toes cut off. There was undoubtedly some grace also in
the way he curved his arms above his head. Doubtless the very
swish of his kilts and the sight of his bare and hairy legs filled some
bosoms with emotions of envy, accompanied, as they were, with
what seemed blood-curdling cries, the relics of old savagery.
Probably my education had been neglected, for I should not wish to
attend these exhibitions too frequently, unless paid handsomely for
the labor incurred.
Indeed, my feelings of appreciation were very much on the same
par with those experiences when, in Japan, we were expected to sit
on the mats with our lower limbs doubled up, or tied in a knot, during
hours of personal agony. These classic performances were
manifestly full of delight to the cultured admirers of pose and motion,
in the “No” dances, though insufferably tedious to those whose legs
had fallen asleep. Even in later times, when chairs were provided
and the accessories were suggestive of comfort, there was not
enough in the dancing of the “No” operatic performers or in the
antics of the geisha, to serve as magnets.
It was easy to explain, however, why and wherefore Scottish
cheeks are so suggestive of rose gardens, and also why
consumption is so common. The rain did indeed redden the
complexions, but as to the number of cases of pneumonia, or
tuberculosis, which ensued after exposure on this chilly day, we
cannot inform our readers, not having the statistics at hand. To this,
however, we can testify, that when we got back to Room No. 6, of
the Waverley Hotel, we were the subjects of a sort of telepathy that
enabled us to feel profound sympathy with Peary when in search of
the North Pole. Never did a grate full of live coals seem more
welcome. We almost literally hung up ourselves, or at least what had
been our outward semblance, to dry. When properly desiccated, we
retired early, in order the more to enjoy the glorious island voyage
among the Highlands which we knew awaited us next morning.
It was genuine Scotch weather when we woke up and looked out
upon a landscape dominated by Ben Nevis, of whose towering form
we could catch glimpses now and then through the cloud rifts, while
on the hills around us lay patches and lines of snow. At times we
were in that “Scotch mist,” in which, as hostile critics declare, the
metaphysicians who live north of the Tweed do at times get lost. Just
when it began or left off raining might have puzzled a weather
bureau man to tell. As for ourselves, we could have taken oath as to
our own inability if we had been called upon in court. If a jury had
been empanelled, then and there, to determine whether it was or
was not raining, the verdict in either case would undoubtedly have
been, as became the country, “Not proven.”
Nevertheless, after we had crossed the gangway of the boat, a
sister ship to the Gondolier of yesterday, and looked over the
landscape, from both starboard and port side, we began to think it
was true, as Professor Blaikie once said, that “Scotland is like a
pebble, it requires rain to bring out its colors.” It is certain that many
spots in this charming glen did look like the water lines, waves, and
layers of varied tints which we have seen on the surfaces of
chalcedony.
When at the lapidary’s I used to watch the process of cutting in
half a stone, rolled for many ages mayhap and ground daily on the
outside by glacial or stream action, it seemed for a few seconds as if
the diamond saw, revolving with its irresistible edge, was to cut in
vain and reveal nothing. From an outward view all beauty was
hidden and the pebble seemed thoroughly ugly and uninteresting.
Nor could I guess that treasures were hidden in the interior; but
when the hemispheres were in our hands, emerging from their
baptism in clean water, there was revealed, if the stone were hollow,
a grotto of crystals, rich in Nature’s heraldry of color, telling the story
of its fiery past. It seemed a more wonderful story, in fact, than that
of Ali Baba and Open Sesame in fiction. Or, if solid, and, like Venus,
born from water, and formed in slow deposit of liquid instead of from
the cosmic flames, the curvilinear strata white, ruby red, black,
yellow, and brown, seemed to excel in splendor.
Even so, to-day Scotland revealed herself as a new wonderland.
The Caledonian pebble seemed a sapphire. For when, toward noon,
something like dry weather arrived and sunbursts were occasional,
Scotland looked as fresh as her maidens and almost as beautiful.
We passed cataracts in full activity. One, which we did not see,
ninety feet high and probably the finest on the great island, was near
Fort Augustus. Beyond this, called “Foyers,” was another fall thirty
feet high. To one, however, who has seen Niagara a hundred times,
and who dwells near Taughannock Falls, which are thirty feet higher,
and near Lake Cayuga, with two hundred waterfalls within a radius of
twenty miles, a cataract must be out of the ordinary to be visited at
the expenditure of time and money, when both these assets are
limited and things more novel are to be seen. In our home town of
Ithaca, as we two Americans mused, in that conceit and love of
business peculiar to our nationals, we have a “local Niagara” over
eighty feet high. Why visit Foyers?
At one of the lochs, we saw an Irishman, with the popular and
traditional face, shape, and garb; that is, of the kind we read about in
novels and see on the stage. He had on brogans, short breeches
split in the end at the knees, woollen stockings, a small and short-
tailed coat, a stumpy shillaly, a narrow-brimmed high hat, with pipe
stuck in the front band and a shamrock set in another place. Besides
bog-trotters’ capers and the dancing of an Irish jig, he sang songs
which recalled boyhood’s memories in Philadelphia. After the potato
famine in Ireland, the Emerald Isle was semi-depopulated, and the
emigrant ships, despite the Know-Nothings, set their prows in fleets
to the Land of Hope. I often saw seven ships a day bringing over the
raw material of citizenship. Some of the girls, as we learned from our
household experience in employing domestics, had never gone up—
though on ship and with us, at first, they came backwards down—a
pair of stairs. Such green but promising maids had never dwelt in a
house built with more than one story, or touched a faucet, or lighted
a gas jet. The Irishman’s song, in which his mention of Philadelphia
was mnemonic, was delightful to hear. Another song, which as a
child I heard my father’s coal-drivers and coal-heavers sing, told of
travels nearer home, and of this I caught the words. They ran thus:—

“I cut my stick and greased my brogues—

’T was in the month of May, sir:
And off to England I did go
To mow the corn and hay, sir.”
 With this son of Erin was a dirty and very skinny Highland lad, in
kilts and other checkered woollen garments much the worse for
wear. He also danced what was probably a Highland fling, though an
almost vicious desire possessed some of us to fling him into the
bathtub.
It is a good sign for the future of a noble race that the
manufacture of soap occupies many people in Scotland. Though the
glens are full of distilleries, which are sure to create poverty and dirt,
perhaps we must consider soap-boiling as a very honorable
occupation and the manufacture of this cleansing material as an
antidote to some of the mischief done by John Barleycorn. How
terrible is the scourge of alcohol in Great Britain was revealed, as
never before, during the war crisis of 1915, when even an appeal to
patriotism could not make the sodden workmen give up their cups.
My kinsman, the United States Consul at Dundee, showed me the
statistics of the liquor traffic in Scotland alone, which were appalling.
Even Christians, supposed to be devout in worship and genuine in
faith, invest their money, and some of them exclusively, in the
distilleries, thus upsetting at one end what the gospel agencies are
doing at the other. The British Empire is thus handicapped in the
race for progress. Yet who from the glorious Yankee nation can
throw a stone, especially when he sees the “American bar,”
“American long drinks,” and “American mixed drinks” flauntingly
advertised in Europe? We have heard, however, that the “long
drinks” are soft and harmless.
While propelled along Loch Ness, an earth-cleft, narrow, deep,
and twenty-four miles in length, we are again reminded of our home
near Lake Cayuga, fairest in the Iroquois chain of “finger lakes” in
the Empire State, and one of the deepest; for on either side of the
Caledonian Canal are metamorphic rocks rising out of crystal clear
water, and beneath, in the Byronic profundity of “a thousand feet in
depth below,” the rocky bottom. Grander and more rugged, however,
is the scenery, for the mountains are here higher, even as the water
is deeper, than in Iroquois land. The Scottish Highlands are the
fragments of the earliest land that emerged above the prehistoric
oceans. For centuries they formed a boundary in ethnology, politics,
and religion, even as in the æons of geology they form a frontier of
chronology.
When our voyage ends, we find that it is some distance between
the stopping-place of the steamer at Muirtown and Inverness. Since
names and sounds are continually playing tricks, summoning from
the privacy of memory forms long ago forgotten and ever retreating
in the perspective of the past, I recall my old Scotch professor at the
Central High School in Philadelphia. That good man MacMurtrie—
with a name meaning, I suppose, of, or from, or son of the Muirtrie,
or Moor-tree clan—first introduced thousands of youth, through his
lexicon, his fascinating lectures, and his choice cabinets, to the great
world of nature and science, and to the rapturous joy of discovery of
order and beauty in the mathematics of the universe.
From Muirtown, we take the hotel omnibus and soon enter
“Rose-red Inverness,” the bright and lively town, which in August
bursts into the full bloom of its summer activities.
 CHAPTER XIV
INVERNESS: THE CAPITAL OF THE
HIGHLANDS

One of the first things we noticed in this summer capital of the

Highlands was a male being, whom Thackeray would have liked to
cage for his “Book of Snobs.” From the monocle, or window in his
eye, and from certain physical peculiarities, and even pronunciation
in his speech, which he was helpless to conceal, I should imagine
that he was really a London cockney masquerading in a
Highlander’s costume. According to the fad or fashion of vacation
time, and appropriate for hot weather, he was encased in the
complete pavonine dress of the old days of clans and claymores, but
the motor within hardly suited the machine. With his buckled shoes,
checkered leggings,—in the side of one of which was stuck a long
dirk, having a silver handle holding a Cairngorm stone set in the top,
—with considerable public exposure of the cuticle around and above
his skinny knees, with gay kilts, decorated pouch, shoulder-brooch of
silver, coat, plaid, bonnet, and feather, the pageant of costume
seemed vastly more imposing than the man within.
This creature seemed a walking museum of Scottish antiquities.
All his unwonted paraphernalia, however, did not cure his gawkiness
or prevent impending disaster to his pride. In trying to pass by some
baskets belonging to a huckster, and full, if I remember aright, of
turnips, his dirk-handle caught in the end of a loose hoop. “Oh, what
a fall was there, my countrymen!” In a moment one would have
taken him for a measuring-rod. At least six feet of the gawk, more or
less, lay on the soil of what may have been his beloved native land.
Nevertheless, in all Christian charity, we tried our best to appear
blind, and resisted the temptation to laugh.
 I am bound to say, however, that I saw some solid-looking
citizens of Inverness wear the kilt and Highland coat most gracefully.
Moreover, in the evening, when some of the Gordon Highlanders,—I
believe they were,—whose barracks were not far away, rambled
through the streets, they certainly showed that the man and the
clothes had grown together.
One could easily see how well adapted was such a dress to a
rough campaign in a mountainous country. One scarcely wondered
why, when fighting in hilly regions, the Highlander was usually the
superior of the average infantryman. Nevertheless, some comical
chapters in eighteenth-century American history come into mind.
When we remembered that modern footgear was strange to men
who had been used to the ancient brogues and to whom the proverb
“as easy as an old shoe” was a novelty, the story is quite credible
that, in the repulse by the French of the attack made by the British
army under Abercrombie at Ticonderoga, in 1758, when the
Highlanders were forced to retreat from Fort Carillon, there were
thousands of shoes left stuck in the mud when the British ran to their
boats.
We could see at a glance that Inverness was the centre of traffic
and travel during the summer months, when tourists made the
northeast and west of cool Scotland very lively for a few weeks. We
looked in at the Town Hall, near which stands the old town cross. At
the foot of this is the lozenge-shaped stone, called the “Stone of the
Tubs,” reverenced as the palladium of Inverness. It was anciently
useful from its having served as a resting-place for women carrying
water from the river.
It is a sight for a stranger in the Highlands to see the
washerwomen in their fullest muscular activity on summer days,
when they renovate the linen of the tourists. Why men should want
to pay money to see the Salome and other dances popular in
Christian countries is a mystery to some of us, when among the
laundry-women the limits of cuticular exposure are reached. They
leap in frenzy upon the masses of linen in the suds which fill the
deep tubs, but the results justify the use of these primitive washing-
machines.
 Curiously enough, this part of Scotland is not wholly free from
earthquakes, for which the geologists give reasons. In the seismic
disturbances of 1816, the spire of the old jail, one hundred and fifty
feet high, was curiously twisted. Now this spire serves as a belfry for
the town clock. Westward from the Ness is the higher ground, called
the “Hill of the Fairies,” where lies the beautiful city of the dead—one
of the most attractively situated cemeteries in the whole of Britain.
On the athletic grounds near the town, at the end of September, are
held the Scottish games and athletic contests, the most important in
the country. Four bridges span the river. Altogether, our impressions
of the town were very pleasing.
But Inverness has a history also. It is believed to have been one
of those primitive strongholds—in this case, of the Picts—which were
so often to be found at the junction of waters. To this place came St.
Columba, in the year 565. Here, too, was the castle of Macbeth, in
which he murdered Duncan, which stood until it was demolished by
Malcolm Canmore, who built on its site a larger one. William the
Lion, in 1214, granted the town a charter, by which it became a royal
burgh. Of the Dominican abbey, founded in 1233, nothing remains.
The town was burned in 1411, by Donald of the Isles, and when
fifteen years later, James I held a parliament in the castle, Scottish
statecraft was still in a primitive stage of evolution, for three of the
northern chieftains summoned to the council were executed for
daring to assert their independence. In 1652, Queen Mary was
denied admittance into the castle, but she remembered the slight
and caused the governor to be hanged afterwards. Cromwell came
hither also and built a great fort. In Inverness gathered the Jacobites
who followed both the Old and the Young Pretender. Inverness has
had its ups and downs, and, as a Western orator once declared of
his district, has, besides raising much ham, raised also much more
of what General Sherman named as the synonym for war.
To come to Inverness without visiting Culloden would be like
going to Rome without seeing St. Peters; for at Culloden, where was
fought one of the decisive battles of the world, the death-blow was
given to Scottish feudalism. There the clan system was knocked to
pieces. Then, also, for the benefit and blessing of the whole world,