Introduction
Many non-pharmacologic treatments for pain, such as
manipulation [
1
], massage therapy [
2
], and acupuncture,
date back thousands of years. With the rise of “Western” bio-
medicine and increasingly powerful drug companies in the
last century, these methods were often sidelined as quackery
[
3
]. The diffi
culty of evaluating many of these therapies with
the gold-standard randomized clinical trials, which are well
suited to medication trials, contributed to their marginaliza-
tion [
4
]. Because of their effi
cacy in many situations, how-
ever, patients continue to use a variety of non- pharmacologic
therapies. Currently, increasingly sophisticated visualization
[
5

10
], anatomic [
11

16
], biochemical [
17

21
], and system-
atic data evaluation [
22

30
] techniques are able to show
objective tissue characteristics and response to therapies.
Myofascial
pain syndrome
(MFPS) symptoms may mimic
other conditions commonly thought to require invasive inter-
ventions, such as carpal tunnel syndrome, herniated discs
with sciatica, and thoracic outlet syndrome, among others. If
the myofascial component is recognized and treated, symp-
toms often abate, leading to less need for analgesic and anti-
infl
ammatory medication, invasive procedures, and surgery.
Unfortunately, many primary care practitioners and pain
practitioners have not been taught about this cause of mor-
bidity [
31
].
Patients with severe acute injuries may initially need pas-
sive modalities (see below) and traditional pharmacologic
intervention to allow suffi
cient reduction of excess infl
am-
mation before beginning more intensive manual therapies
(Table
5.1
). Those with less severe acute injuries should be
encouraged to start manipulative intervention early, while
those with chronic pain will benefi
t from the addition of the
non-pharmacologic therapies with effects synergistic to
those achieved with traditional pharmacology.
Myofascial Pain Syndromes
MFPS are characterized by diffusely aching pain and tender-
ness in one or more taut and shortened muscles, as well as
hypersensitive areas known as
myofascial trigger points
(MTrPs) [
32
]. The pain is often referred, rarely in the distri-
bution of a peripheral nerve or spinal segment [
33
], but rather
in the predictable pattern mapped by Travell and Simons
[
32
]. Unless palpation of the painful site evokes signs of
acute tenderness, the source is likely a MTrP somewhere
H. W. Karl , MD
Department of Anesthesiology and Pain Medicine ,
University of Washington, Seattle Children’s Hospital ,
Seattle , WA , USA
e-mail:
helen.karl@seattlechildrens.org
H. Tick , MA, MD (
*
)
Family Medicine and Anesthesiology & Pain Medicine ,
University of Washington , Seattle , WA , USA
e-mail:
htick@uw.edu
K. A. Sasaki , DC, CCSP
Director , Vida Integrated Health , Seattle , WA , USA
e-mail:
drsasaki@vidaintegratedhealth.com
5
Table 5.1
Therapeutic approaches to MFPS, in order of intensity
Manual therapies Needle therapies
Patient education on postural
habits and activity modifi
cation
Acupuncture (acupressure,
traditional and
electroacupuncture)
Therapeutic exercise Direct or remote intramuscular
stimulation (dry needling)
Myofascial mobilization Local anesthetic injection
Massage (including Swedish,
shiatsu, self-massage, structural
integration (Rolfi
ng),
craniosacral)
Instrument assisted (Astym®,
Graston®)
Neural mobilization (neural
fl
ossing)
Joint manipulation or
mobilization
drtrescot@gmail.com
28
else. Pressure on the most tender area often reproduces the
pain pattern, and massage or injection of local anesthetic into
that site relieves the pain for a period of time, usually much
greater than the duration of the drug [
32
]. The onset of MFPS
is usually a muscle injury that activates an MTrP; this can be
due to acute trauma, cumulative repetitive overload, or a
peripheral nerve injury. The intensity of the symptoms
refl
ects the degree of irritability of the MTrP rather than the
size of the muscle.
In addition to taut and shortened painful muscles, patients
with MFPS may have localized weakness and autonomic
changes, such as abnormal pilomotor, sudomotor, and vaso-
motor phenomena. Tendons can become thickened or enthe-
sopathic, with traction on tendon attachments and the
potential for compression of other structures, particularly
peripheral nerves. Symptoms presenting in a specifi
c indi-
vidual depend on the surrounding anatomical structures; for
example, if myofascial dysfunction causes nerve entrapment,
it is likely to result in localized neuropathic pain with radia-
tion and dysesthesias.
Clinical characteristics of the MTrPs in these muscles
have been well described [
32
]. These extremely tender nod-
ules, associated with taut muscle bands, cause local and
referred pain, and they produce a spinal cord refl
ex known as
a
local twitch response (LTR)
when stimulated by snapping
palpation or needle penetration. Travell and Simons pro-
posed a theory of the etiology of myofascial abnormalities
known as the integrated trigger point hypothesis [
32
]. MTrPs
are thought to result from excess acetylcholine at the neuro-
muscular junction, leading to persistent muscle contraction
and an “energy crisis” in this localized area with increased
demand and decreased supply. Gunn’s postulate that muscle
dysfunction is caused by subtle compression of the nerve
roots, which creates nerve dysfunction equivalent to partial
denervation, remains controversial [
34
], although nerve root
compression likely contributes to the “double crush” phe-
nomenon [
35
] (see Chap.
1
).
The advent of technologies to assess the functional
derangements of these anatomic muscle disorders allows
more to be learned about their properties. In a selective
review of animal studies, Mense described the ways that
algesic (pain-causing) agents, most commonly ATP and
low tissue pH, excite muscle nociceptors. Muscle spasm
and other causes of chronic ischemia, abnormal posture,
infl
ammation, and MTrPs are all associated with low tissue
pH. Chronic activation of muscle nociceptors can lead to
central sensitization [
9
,
36
]. Sikdar et al. have demon-
strated hypoechoic areas on ultrasound that correspond to
MTrPs and have used elastography to show that MTrPs are
stiffer than normal muscle [
7
]. Shah et al. have microdial-
ysed the interstitial fl
uid at MTrPs and found an infl
amma-
tory milieu in the trigger points, but not in an unaffected
muscle [
17
].
Investigations at the tissue and cellular level have also
been useful to identify mechanisms underlying
fascial dys-
function
. Fascia is a three-dimensional continuous network of
cells (mostly fi
broblasts) and intercellular fi
bers which envel-
ops and divides all the other components of the body [
37

40
].
It supplies structural support, transmits forces between mus-
cles [
41
,
42
], is highly innervated with
mechanoreceptors
and
autonomic fi
bers
[
43
], and has
piezoelectric
properties [
44
,
45
]. Fascia may become shortened by acute injuries such as
trauma or infl
ammation and by chronically abnormal posture
or repetitive use [
44
], but it has a remarkable ability to reform
[
43
,
46
]. Any kind of mechanical loading affects the extracel-
lular matrix and increases the number and function of embed-
ded fi
broblasts. Application of acute or chronic mechanical
loads at higher “doses,” as seen in acute trauma or repetitive
motion strain, leads to the release of the infl
ammatory media-
tors described above. In contrast, lower loads, as seen in
cyclic mechanical stretch or massage, release anti-infl
amma-
tory compounds and stimulate collagen metabolism [
47
,
48
].
Clinically, muscle and fascia are usually injured and treated
in concert; fi
broblasts appear to provide important connec-
tions between them at a subcellular level [
48
,
49
].
Taken together, these and many more objective examina-
tions of muscle and fascial dysfunction provide insight into the
complex etiology of MFPS and an evidence base for the success
of a variety of clinical approaches to its relief. Manual medical
therapies and needle therapies are the two broad approaches
found to be effective for the relief of myofascial pain.
Manual Medical Treatments
( Table
5.2
)
Numerous manipulative techniques have developed over the
last two centuries and have been practiced by often compet-
ing professionals [
1
,
20
]. Modern scientifi
c publication on
manipulative methods began with Travell [
50
] and quickly
progressed to include the benefi
ts of combined therapies,
such as manipulation and local anesthetic infi
ltration [
51
].
The results of subsequent work have been published by
Table 5.2
Manual therapies
Treatment Practitioners
Physical modalities Physical therapist, chiropractor
Patient education Physical therapist, movement
therapist, chiropractor
Massage, self-massage Massage therapist, structural
integration practitioner (Rolfer)
Active release techniques,
myofascial release
Physical therapist, chiropractor
Neural mobilization (neural
fl
ossing)
Physical therapist, chiropractor,
osteopathic physician
Joint manipulation or
mobilization
Chiropractor, osteopathic
physician, physical therapist
H.W. Karl et al.
drtrescot@gmail.com
29
investigators in multiple disciplines, often using different
terms for essentially the same maneuvers [
52
]. This is one
reason it has been diffi
cult to demonstrate the short- and
long-term benefi
ts of these techniques [
53
]. As the evidence
base increases, it is hoped that practitioners will use the
strengths of their particular backgrounds to cooperate at all
levels, from diagnosis and treatment of individual patients to
research and teaching [
22
,
39
,
52
,
53
].
Physical Modalities
Application of ice, heat,
contrast baths
(for complex regional
pain syndrome (CRPS) symptoms), splinting, compression
stockings, and/or electrical stimulation can help decrease
pain and infl
ammation. Application of
low-level laser ligh
t
has also been shown to be helpful [
54
,
55
]. The routine use
of
ice
to reduce infl
ammation in acute injuries has recently
come into question; its use does temporarily decrease dis-
comfort, but normal infl
ammation is a constructive part of
healing [
56

58
]. These passive interventions should be used
to facilitate active stretching and strengthening exercises to
correct biomechanics [
59
].
Patient Education on Postural Habits,
Ergonomics, and Activity Modifi
cation
Identifi
cation of work-related or lifestyle habits that cause or
contribute to MFPS is key to treatment. For long-term relief to
be successful, the patient must understand the
ergonomics
of
their diagnosis and actively participate in rehabilitation [
59
].
Body awareness therapies to address postural habits such as
Feldenkrais
and the
Alexander technique
naturally complement
education, self-massage, and active therapeutic exercises [
60
].
Structural Integration (Rolfi
ng)
Dr. Ida Rolf developed in the 1920s a combination of move-
ment training and massage designed to maximize the body’s
vertical alignment [
61

63
]. In theory, when the body is not
aligned with gravity, additional energy must be used for any
task, and affected fascia will shorten and thicken. For example,
if the head is shifted forward, its effective weight can more than
double, causing pain and fatigue. One study showed improve-
ment of neck pain and range of motion after ten sessions [
62
].
Massage
Massage therapy
has been defi
ned as “soft tissue manipulation
by trained therapists for therapeutic purposes” [
2
]. It encom-
passes hundreds of different techniques and may be performed
with hands alone or with instruments [
64
]. Skilled practitioners
can identify taut muscle bands and MTrPs, improve local blood
fl
ow, and reduce pain and disability. A recent meta-analysis of
its effectiveness for diverse chronic pain conditions has shown
massage alone to be effective for low back pain and progres-
sively less effective for shoulder and headache pain (moderate
support), with only modest support to treat fi
bromyalgia, mixed
chronic pain, neck pain, and carpal tunnel syndrome [
2
]. One
area of debate is the optimal location at which to apply pressure
or friction. Stecco et al. addressed this question by developing
a biomechanical model of the myofascial system (Fascial
Manipulation©), dividing this continuous structure into seg-
ments, each served by myofascial units defi
ned by specifi
c
movements [
12
,
13
,
65

68
]. Analysis of abnormal motion
allows identifi
cation of areas requiring treatment [
69
].
Therapeutic Mechanical Load
Employing instruments to amplify and concentrate the
hands’ ability to affect the muscle and fascia have been used
for centuries [
44
,
70
]. The Astym® [
71
] and Graston
Technique® are two contemporary, instrument-assisted soft-
tissue mobilization methods [
64
].
Neural Mobilization (NM, Colloquially Termed
“Neural Flossing”)
NM consists of active or passive exercises to improve the
movement of peripheral nerves with respect to the other tis-
sues that surround them. In clinical studies, there is level 3
evidence of effectiveness for the upper quadrant (cervical
spine, shoulder, arm) with less conclusive evidence in the
lower quadrant (lumbar spine, pelvis, leg) [
72
]. Authors have
reported particular success treating median nerve entrapment
at the carpal tunnel (Chap.
37
) [
73

75
], neck and arm pain
[
76
,
77
], and the pain of lateral epicondylitis and neurogenic
cervicobrachial disorders [
78
]. Dr. Gabor Racz has also
encouraged this type of nerve mobilization after cervical and
lumbar epidural adhesiolysis [
79
,
80
]. Recent studies in ani-
mals have provided evidence for the mechanisms underlying
this practice [
18
,
19
].
Joint Manipulation or Mobilization
Removing restrictions on almost any joint limited in its range of
motion can improve joint function and reduce the stress on
nearby myofascial structures. Broadly speaking, this can be
achieved with manipulation using low-amplitude, high- velocity
movements or with mobilization using higher- amplitude, low-
5 Non-pharmacologic Treatment of Peripheral Nerve Entrapment
drtrescot@gmail.com

 Introduction An entrapment neuropathy is defi ned as a pressure-induced injury to a peripheral nerve in a segment of its course due to anatomic structures or pathologic processes [ 1 ]. Entrapment neuropathies 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 diffi cult to diagnose without a high clinical index of suspicion. Knowledge of the syndromes and recognition 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 fi brous or osseofi brous tunnel, or where the nerve passes over a fi brous 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 surgery 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 fl ow. Peripheral nerve injections (peripheral nerve blocks) are interventional pain management techniques used to treat patients with nerve entrapments presenting 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 benefi t for patients suffering from pain anywhere from the head to the toes. Recognition of these conditions 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 headache, backache, “sciatica,” “endometriosis,” and foot pain. In addition, painful conditions with well-described pathology such as chronic regional pain syndrome (CRPS) or postherpetic neuralgia (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 presentations. 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 Part I Peripheral Nerve Entrapments: General Principles Andrea M. Trescot and Daniel Krashin drtrescot@gmail.com 2 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 gradually 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 superfi cial, 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 fi rst is an overview of the history taking, physical exam, and diagnostic injection techniques. 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, fl uoroscopic, 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 specifi c 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 anesthesia, 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. Part I Peripheral Nerve Entrapments: General Principles drtrescot@gmail.com © 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 Epidemiology and Pathophysiology An

Dr. Trescot, Peripheral Nerves

 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 confi rmed 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 fi nd 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 (landmarkguided, fl uoroscopic-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 fi nd this book useful to help the patient who is asking “who will stop the pain?” Anchorage , AK , USA Andrea M . Trescot , MD, ABIPP, FIPP

Epidemiology More than 80 million people in the United States suffer annually from serious pain, leading to disability, suffering, drug addiction, depression, and suicide [ 1 ]. Although diagnostic tools such as MRI and endoscopic techniques have become more sophisticated, there are a signifi cant number of patients who have been told that “it is all in your head,” “you just want pain medication,” “there is nothing on the MRI,” or “the surgery looks perfect, so I don’t know why you are hurting.” Pain management clinics have been viewed as the place of last resort – “if all else fails, send them to pain management.” As such, the patient arrives on our doorstep, traumatized by ineffective surgeries, hyperalgesic because of high-dose opioids, depressed because of the multiple failed treatments, and hostile because once more they have to tell their story, only to watch the physician shrug and say “I don’t know.” Pain is a problem throughout the entire medical fi eld. In fact, the most common reason that patients present in the emergency department (ED) is pain. Todd et al. [ 2 ] noted that the median pain scores of patients on arrival in the ED were 8/10 on a number rating scale (NRS), and only half of them had a decrease in their pain by 2 or more points while there. Upon discharge from the ED, 45 % of patients reported 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 Research Database (which contains 1.8 million patient years of data), looking for new peripheral nerve entrapments, reported that they are relatively common [ 3 ] (Table 1.1 ). In another recent survey [ 4 ], 30 of 998 patients (3 %) referred to a gastroenterologist were diagnosed as having chronic abdominal wall pain (CAWP), presumably caused by myofascial spasm or peripheral nerve entrapment (see ACNES syndrome – Chap. 42). Post - traumatic neuropathy is nerve pain that has been triggered after an injury or as a consequence of medical interventions such as surgery, injections, or radiotherapy. A recent evaluation of more than 2,500 soldiers returning from Iraq and Afghanistan revealed that 44 % had chronic pain, with 48.3 % of them having been in pain for more than a year. More than half (55.6 %) of the soldiers with chronic pain described it as constant; it was moderate to severe in 51.2 % [ 5 ]. Acute postoperative pain can develop into chronic postsurgical pain ( CPSP ), which affects daily life in 10–50 % of patients after surgery; this pain can be severe in 2–10 % of them [ 6 ]. A prospective study of approximately 5,000 surgical patients identifi ed acute neuropathic pain in 1–3 %; 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. confi rmed these fi ndings: more than 500 of 911 (57 %) patients had pain scores of greater than 3/10 for a mean of 29 months after orthopedic, abdominal, and/or vascular surgery. Almost 15 % of these patients reported severe pain [ 9 ]. Pain after inguinal hernia repair has been reported to range from 0 % to 60 %. A 2007 systematic review of pain after mesh hernia repair showed that 11 % of patients had persistent groin pain. More than a quarter of them had severe pain, and more than a third had limitations of daily activities [ 10 ]. Postherniorrhaphy pain is likely due to ilioinguinal (Chap. 40) and/or genitofemoral (Chap. 41) nerve injury. Similar A. M. Trescot , MD, ABIPP, FIPP (*) Pain and Headache Center , Anchorage , AK , USA e-mail: DrTrescot@gmail.com D. Krashin , MD Chronic Fatigue Clinic, Pain and Anesthesia and Psychiatry Departments , University of Washington , Seattle , WA , USA e-mail: krashind@uw.edu H. W. Karl , MD Department of Anesthesiology and Pain Medicine , University of Washington, Seattle Children’s Hospital , 4800 Sand Point Way NE , Seattle , WA , USA e-mail: helen.karl@seattlechildrens.org 1 drtrescot@gmail.com 4 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 benefi t 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. 

 Table 1.1 Incidence of peripheral nerve entrapments in UK primary care in 2000 [ 3 ] Men Women Carpal tunnel syndrome 87.8 a 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

 Pathophysiology An entrapment neuropathy is defi ned as a pressure-induced segmental injury to a peripheral nerve due to an anatomic structure or pathologic process [ 14 – 16 ]. The defi ning 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 fl ow ( 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 thickening 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 incapacitating pain. These changes parallel the histologic changes that occur in the implicated nerve (Fig. 1.1 ) [ 21 ]. In order to provide a common language for clinicians and researchers, some generally accepted classifi cations 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 fi bro-osseous tunnel or fascial opening. Infl ammation or edema of adjacent structures (e.g., tendons) can reduce the size of the passageway. Graded experimental compression results in profound short- and long-term effects on in vivo blood fl ow. Mild compression (20–30 mmHg) decreases venous fl ow; moderate compression decreases capillary and arterial fl ow; and pressures of 60–80 mmHg cause frank ischemia [ 24 ]. These pressures correspond to those measured clinically in the tarsal 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 surround a large nerve with a Silastic tube and evaluate histology and nerve conduction [ 21 , 30 ]. Histologically, prolonged compression leads to neural edema, which, in the absence of relief, can progress to epineurial fi brosis 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 Table 1.1 Incidence of peripheral nerve entrapments in UK primary 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 postulated that this was due to the effect of compression on anterograde axoplasmic fl ow, as later confi rmed by other investigators [ 28 , 32 ]. However, other mechanisms, and indeed whether this phenomenon actually exists, are also under discussion [ 33 ]. Lundborg’s observation that patients with symptoms 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 retrograde axoplasmic fl ow [ 34 ]. DCS has been observed at several common locations, clinically [ 21 , 35 , 36 ], upon electrodiagnostic investigation [ 37 ] (Table 1.4 ), and experimentally [ 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 overlooked, 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 signifi cant role in the pain after joint injuries, suggesting 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 syndrome have a much higher incidence of ulnar nerve subluxation and potential entrapment at the elbow than patients without Ehlers-Danlos [ 42 ] (see Chap. 37). Animal models that investigate the underlying pathophysiologic mechanisms support these clinical observations [ 38 , 43 ]. High degrees of stretch result in decreased blood fl ow, but electrophysiologic 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 entrapment neuropathies but also to infl ammatory ones [ 18 , 45 ], thereby acting like the fi rst “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 concentration 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 superfi cial peroneal nerve above the ankle (Chap. 68), and the posterior tibial nerve at the tarsal tunnel (Chap. 73) has improved symptoms in the “stocking” 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 signifi cantly improved foot pain [ 48 ]. In the upper extremity, 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 prophylactic anticoagulation postoperatively [ 44 ]. These patients will present with swelling and increasing pain postoperatively, and nerve testing is not helpful in this acute setting. 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 infl ammatory cytokines) [ 51 ]. Dental materials (such as those used for a root canal) can also create chemical injury. Chemical damage to a nerve can occur locally from toxic materials such as paraformaldehyde for endodontic fi lling. Dental irrigation chemicals like sodium hypochlorite can also be culprits. Additionally, chemical injury can be caused internally by the body’s own local infl ammatory markers and cytokines, including those released by cells fi ghting 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- fi ring “knot” of nerve fi bers called a neuroma (Fig. 1.3 ). Neuromas are mostly composed of sprouting axons, with a signifi cant 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). 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 benefi cial effects on the overall CRPS clinical picture. Identifi cation of entrapment neuropathy as the initiating event to CRPS could provide a method for defi nitive treatment. Interestingly, CRPS has been identifi ed 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- fi cult to predict. Factors that infl uence 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) infl uencing the health of the nerves. Since the blood fl ow 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 limited “resources”; however, because of the length of regeneration 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 perpetuated by peripheral nerve entrapments. The recognition that “every chronic pain was once acute” [ 8 ] suggests that accurate 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. Fig. 1.3 MRI image of a large sciatic nerve neuroma after a leg amputation – white arrow (Image courtesy of Andrea Trescot, MD) Table 1.5 Conditions that may be caused by entrapment of a peripheral nerve Headaches, including “migraines” “Endometriosis” 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 A.M. Trescot et al. d

 References 1. Rasor J, Harris G. Using opioids for patients with moderate to severe pain. J Am Osteopath Assoc. 2007;107(9 Suppl 5):Es4–10. 2. Todd KH, Ducharme J, Choiniere M, Crandall CS, Fosnocht DE, Homel P, et al. Pain in the emergency department: results of the pain and emergency medicine initiative (PEMI) multicenter study. J Pain Off J Am Pain Soc. 2007;8(6):460–6. 3. Latinovic R, Gulliford MC, Hughes RA. Incidence of common compressive neuropathies in primary care. J Neurol Neurosurg Psychiatry. 2006;77(2):263–5. 4. Adibi P, Toghiani A. Chronic abdominal wall pain: prevalence in out-patients. J Pak Med Assoc. 2012;62(3 Suppl 2):S17–20. 5. Toblin RL, Quartana PJ, Riviere LA, Walper KC, Hoge CW. Chronic pain and opioid use in US soldiers after combat deployment. JAMA Intern Med. 2014;174(8):1400–1. 6. Kehlet H, Jensen TS, Woolf CJ. Persistent postsurgical pain: risk factors and prevention. Lancet. 2006;367(9522):1618–25. 7. Hayes C, Browne S, Lantry G, Burstal R. Neuropathic pain in the acute pain service: a prospective survey. Acute Pain. 2002;4:45–8. 8. Katz J, Seltzer Z. Transition from acute to chronic postsurgical pain: risk factors and protective factors. Expert Rev Neurother. 2009;9(5):723–44. 9. Simanski CJ, Althaus A, Hoederath S, Kreutz KW, Hoederath P, Lefering R, et al. Incidence of chronic postsurgical pain (CPSP) after general surgery. Pain Med. 2014;15(7):1222–9. 10. Nienhuijs S, Staal E, Strobbe L, Rosman C, Groenewoud H, Bleichrodt R. Chronic pain after mesh repair of inguinal hernia: a systematic review. Am J Surg. 2007;194(3):394–400. 11. Loos MJ, Scheltinga MR, Mulders LG, Roumen RM. The Pfannenstiel incision as a source of chronic pain. Obstet Gynecol. 2008;111(4):839–46. 12. Bruce J, Drury N, Poobalan AS, Jeffrey RR, Smith WC, Chambers WA. The prevalence of chronic chest and leg pain following cardiac surgery: a historical cohort study. Pain. 2003;104(1–2):265–73. 13. Hicks F, Simpson KH. Nerve blocks in palliative care. Oxford: Oxford University Press; 2004. 129 p. 14. Kopell HP, Thompson WAL. Peripheral entrapment neuropathies. 2nd ed. Huntington: R. E. Krieger Pub. Co; 1976. 15. 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. 16. Menorca RM, Fussell TS, Elfar JC. Nerve physiology: mechanisms of injury and recovery. Hand Clin. 2013;29(3):317–30. 17. Kashuk K. Proximal peripheral nerve entrapment syndromes in the lower extremity. J Am Podiatry Assoc. 1977;67(8):529–44. 18. Vinik A, Mehrabyan A, Colen L, Boulton A. Focal entrapment neuropathies in diabetes. Diabetes Care. 2004;27(7):1783–8. 19. Dellon AL. Diabetic neuropathy: medical and surgical approaches. Clin Podiatr Med Surg. 2007;24(3):425–48, viii. 20. Dellon AL. Susceptibility of nerve in diabetes to compression: implications for pain treatment. Plast Reconstr Surg. 2014;134(4 Suppl 2):142S–50S. 21. Mackinnon SE. Double and multiple “crush” syndromes. Double and multiple entrapment neuropathies. Hand Clin. 1992;8(2):369–90. 22. Maggi SP, Lowe JB, Mackinnon SE. Pathophysiology of nerve injury. Clin Plast Surg. 2003;30(2):109–26. 23. Dellon AL. Clinical grading of peripheral nerve problems. Neurosurg Clin N Am. 2001;12(2):229–40. 24. Rydevik B, Lundborg G, Bagge U. Effects of graded compression on intraneural blood blow. An in vivo study on rabbit tibial nerve. J Hand Surg Am. 1981;6(1):3–12. 25. Dellon AL. The four medial ankle tunnels: a critical review of perceptions of tarsal tunnel syndrome and neuropathy. Neurosurg Clin N Am. 2008;19(4):629–48, vii. 26. Smith EM, Sonstegard DA, Anderson WH. Carpal tunnel syndrome: contribution of fl exor tendons. Arch Phys Med Rehabil. 1977;58(9):379–85. 27. Pechan J, Julis I. The pressure measurement in the ulnar nerve. A contribution to the pathophysiology of the cubital tunnel syndrome. J Biomech. 1975;8(1):75–9. 28. Rydevik B, McLean WG, Sjöstrand J, Lundborg G. Blockage of axonal transport induced by acute, graded compression of the rabbit vagus nerve. J Neurol Neurosurg Psychiatry. 1980;43(8):690–8. 29. Fern R, Harrison PJ. The effects of compression upon conduction in myelinated axons of the isolated frog sciatic nerve. J Physiol. 1991;432:111–22. 30. Mackinnon SE, Dellon AL, Hudson AR, Hunter DA. Chronic nerve compression – an experimental model in the rat. Ann Plast Surg. 1984;13(2):112–20. 31. Upton AR, McComas AJ. The double crush in nerve entrapment syndromes. Lancet. 1973;2(7825):359–62. 32. Dellon AL, Mackinnon SE. Chronic nerve compression model for the double crush hypothesis. Ann Plast Surg. 1991;26(3):259–64. 33. Schmid AB, Coppieters MW. The double crush syndrome revisited – a Delphi study to reveal current expert views on mechanisms underlying dual nerve disorders. Man Ther. 2011;16(6):557–62. 34. Lundborg G. The reversed double crush lesion. Am Soc Surg Hand Correspondence Newsletter. 1986. 35. Moghtaderi A, Izadi S. Double crush syndrome: an analysis of age, gender and body mass index. Clin Neurol Neurosurg. 2008;110(1):25–9. 36. Osterman AL. The double crush syndrome. Orthop Clin North Am. 1988;19(1):147–55. 37. Golovchinsky V. Double crush syndrome in lower extremities. Electromyogr Clin Neurophysiol. 1998;38(2):115–20. 38. Wall EJ, Massie JB, Kwan MK, Rydevik BL, Myers RR, Garfi n SR. Experimental stretch neuropathy. Changes in nerve conduction under tension. J Bone Joint Surg Br. 1992;74(1):126–9. 39. Walker FO, Cartwright MS, Wiesler ER, Caress J. Ultrasound of nerve and muscle. Clin Neurophysiol. 2004;115(3):495–507. 40. Ikeuchi M, Izumi M, Aso K, Sugimura N, Tani T. Clinical characteristics of pain originating from intra-articular structures of the knee joint in patients with medial knee osteoarthritis. SpringerPlus. 2013;2:628. 41. Kachar SM, Williams KM, Finn HA. Neuroma of the infrapatellar branch of the saphenous nerve a cause of reversible knee stiffness after total knee arthroplasty. J Arthroplasty. 2008;23(6):927–30. 42. Granata G, Padua L, Celletti C, Castori M, Saraceni VM, Camerota F. Entrapment neuropathies and polyneuropathies in joint hypermobility syndrome/Ehlers-Danlos syndrome. Clin Neurophysiol. 2013;124(8):1689–94. 43. Love JM, Chuang TH, Lieber RL, Shah SB. Nerve strain correlates with structural changes quantifi ed by Fourier analysis. Muscle Nerve. 2013;48(3):433–5. 44. Unwin A, Scott J. Nerve palsy after hip replacement: medico-legal implications. Int Orthop. 1999;23(3):133–7. 45. Perkins BA, Olaleye D, Bril V. Carpal tunnel syndrome in patients with diabetic polyneuropathy. Diabetes Care. 2002;25(3):565–9. 46. Dellon AL. A cause for optimism in diabetic neuropathy. Ann Plast Surg. 1988;20(2):103–5. 47. Dellon AL, Muse VL, Nickerson DS, Akre T, Anderson SR, Barrett SL, et al. Prevention of ulceration, amputation, and reduction of hospitalization: outcomes of a prospective multicenter trial of tibial neurolysis in patients with diabetic neuropathy. J Reconstr Microsurg. 2012;28(4):241–6. 48. van Maurik JFMM, van Hal M, van Eijk RPA, Kon M, Peters EJG. Value of surgical decompression of compressed nerves in the lower extremity in patients with painful diabetic neuropathy: a randomized controlled trial. Plast Reconstr Surg. 2014;134(2):325–32. 1 Epidemiology and Pathophysiology drtresc 49. Aszmann OC, Kress KM, Dellon AL. Results of decompression of peripheral nerves in diabetics: a prospective, blinded study. Plast Reconstr Surg. 2000;106(4):816–22. 50. Deramond H, Wright NT, Belkoff SM. Temperature elevation caused by bone cement polymerization during vertebroplasty. Bone. 1999;25(2 Suppl):17s–21s. 51. Raj PP. Intervertebral disc: anatomy-physiology-pathophysiologytreatment. Pain Pract. 2008;8(1):18–44. 52. Morse DR. Endodontic-related inferior alveolar nerve and mental foramen paresthesia. Compend Contin Educ Dent. 1997;18(10):963– 8, 70-3, 76-8 passim; quiz 98. 53. Albrecht PJ, Hines S, Eisenberg E, Pud D, Finlay DR, Connolly MK, et al. Pathologic alterations of cutaneous innervation and vasculature in affected limbs from patients with complex regional pain syndrome. Pain. 2006;120(3):244–66. 54. Oaklander AL, Fields HL. Is refl ex sympathetic dystrophy/complex regional pain syndrome type I a small-fi ber neuropathy? Ann Neurol. 2009;65(6):629–38. 55. Bruehl S. An update on the pathophysiology of complex regional pain syndrome. Anesthesiology. 2010;113(3):713–25. 56. Oaklander AL. Development of CRPS after shingles: it’s all about location. Pain. 2012;153(12):2309–10. 57. Goldberg E, Dobransky R, Gill R. Refl ex sympathetic dystrophy associated with malignancy. Arthritis Rheum. 1985;28(9):1079–80. 58. Ishibe K, Tamatsu Y, Miura M, Shimada K. Morphological study of the vasa nervorum in the peripheral branch of human facial nerve. Okajimas Folia Anat Jpn. 2011;88(3):111–9. 59. Kim DH, Kline DG. Management and results of peroneal nerve lesions. Neurosurgery. 1996;39(2):312–9; discussion 9–20. 60. Flanigan RM, DiGiovanni BF. Peripheral nerve entrapments of the lower leg, ankle, and foot. Foot Ankle Clin. 2011;16(2):255–74. 61. Peltier AC, Russell JW. Advances in understanding drug-induced neuropathies. Drug Saf. 2006;29(1):23–30. 62. Briemberg HR. Peripheral nerve complications of medical disease. Semin Neurol. 2009;29(2):124–35. 

 History and Physical Exam                     
     Andrea     M.     Trescot       and     Daniel     Krashin    
          History
T   he diagnosis is hidden in the patient’s history, and the cause is elicited by the physical exam. – J. Bart Staal
T   he history given by the patient, in the patient’s own words, is key to making the diagnosis of a peripheral nerve entrapment. Multiple patients use the same words to describe their pain perception (“My testicles are in a vise”). There are reproducible, recognizable patterns of pain that provide clues to the cause of the pain. Unfortunately, many patients with nerve entrapments present with poorly localized or widespread pain. By the time the patient has reached a pain specialist, the pain may have spread beyond its original site “like a forest fi re raging out of control,” so a careful history of the mechanism of injury, the initial site of pain, and the initial referral pattern are key clues to the etiology of a painful nerve entrapment.  The history of trauma can vary from mild to severe and, at the time of presentation, can be acute, subacute, or chronic. This trauma may have occurred as a result of surgery or fracture, or it may have originally been regarded as “trivial.” There may have been abnormal limb positioning, repetitive activity, or recent change in body habitus [ 1] . The patient often describes the pain as burning, shooting, or lancinating, and there may be associated numbness or tingling. There may also be a history of “clumsiness” and inadvertent injuries [ 1] . Symptoms are often worse at night, especially when the limb is in the same position for a prolonged period of time. 
T here are certain symptoms that point toward a compressive nerve pathology. Peripheral nerves are especially prone to compression, and activities that decrease the entrapment, such as changing position or “shaking it off,” will temporarily help. Although initially the pain may be intermittent, the pain usually becomes constant and more intense over time. If postsurgical, the pain can occur immediately after surgery, or it may start weeks to years after the surgery, as the scar cicatrix gradually tightens around the nerve. Pain is usually aggravated by activity or menstrual periods (due to perineural edema, hormone changes, induced modulation of levels of pain neurotransmitters, and increased dorsal horn transmission cell sensitivity). A history of trauma, operations, previous fractures, abnormal limb positioning, repetitive activities, and recent change in body habitus are also clues in the history [ 1 ].  However, it is important to remember that many nerve entrapments may present with nonspecifi c or poorly localized pain or even a false sense of numbness  (“nulliness”),  according to Dorman [ 2 ]. In this case, the mechanism of injury becomes even more important. C oncomitant symptoms, such as back pain when there is leg pain or neck pain with arm pain, may be signifi cant clues to the diagnosis. The history also gives a clue about potentially more serious conditions; for instance, loss of sphincter tone might represent a spinal cord injury.  Specifi c questions that should be asked while eliciting the patient’s history include:
• W   here does it hurt? (Attempting to localize the initial site of the injury, as well as patterns of pain radiation)  •   Where and when did it start to hurt?  •   What makes it worse? What makes it better? (It is important to ask these questions in this order, since patients will often respond “nothing” to “what makes it better?” if asked that question fi rst.)  •   Are there associated weakness or sensory disturbances?  •   Are there any changes in the appearance or function of the limb?  •   Is there a history of recent or old trauma?  
        A.  M.   Trescot ,  MD, ABIPP, FIPP      (*)   Pain and Headache Center ,   Anchorage ,  AK ,  USA    e-mail: DrTrescot@gmail.com       D.   Krashin ,  MD      Pain and Anesthesia and Psychiatry Departments ,  Chronic Fatigue Clinic, University of Washington ,   Seattle ,  WA ,  USA    
  2
drtres

   Is there a history of other medical conditions that might make the nerve more prone to other injury, including recent weight gain, pregnancy, diabetes, thyroid disease, malignancy, immune suppression, or HIV?  • D  oes the patient perform repetitive movements at work or during hobbies? (See Table  2.1 )
          Physical Exam
T he physical exam for peripheral nerve entrapments is very specifi c, directed by the patient pointing to “where it hurts” (Fig.  2.1) , followed by identifi cation of known nerve entrapment sites. Normal nerves are almost insensitive to pressure. Beyer described that normal nerves “can be rolled under the thumbnail at will” [ 4 ]. The infl amed, entrapped nerve, however, will be extremely sensitive, with the slightest pressure causing the patient “to literally jump out of the chair with pain” [ 3] . Gentle, open palm probing, specifi c thumb or fi nger pressure (Fig.  2.2 ), tapping ( Tinel’s sign ), and “strumming” across the affected structure are the more appropriate palpation techniques for specifi c identifi cation of tender structures.  Valleix phenomenon  may be present, which is ten
derness along the distribution of a peripheral nerve both proximal and distal to the site of entrapment [ 5 ]. This focused physical exam becomes even more important when the pain has spread “all over”; having the patient point to where the pain “fi rst started,” combined with the pattern of pain (“pattern recognition”), can give important clues as to the etiology.    Sensory testing of the affected area may help clarify the diagnosis, when paired with a good working knowledge of cutaneous innervation patterns and their common variations. Nerve entrapment may cause referred pain in the innervated area; it is also commonly accompanied by decreased sensation. Sensation should be assessed to both light touch and temperature or pinprick; patients will often be aware of areas with decreased sensation to touch but may be surprised to fi nd areas without temperature or pinprick sensation. Mechanical sensitivity can be assessed by a series of graded sizes of plastic fi laments called von Frey fi bers (Fig.  2.3 ). Assessment of two-point discrimination is particularly helpful in areas that normally have very good discrimination, such as the hands [ 6 ]. If the patient is asked to close their eyes, this approach can also help identify fabricated or embellished symptoms. In those nerves with combined motor and sensory function, motor impairment may also be elicited as a sign.   Knowledge of the common entrapment sites, the pattern of pain, and the specifi c examination can allow the provider to focus on the likely site of the entrapment, which is key for accurate injection therapy, which then confi rms the diagnosis and delivers therapeutic medication to the likely site of the nerve entrapment.     
   Table 2.1    Information to be obtained in the history [ 3 ]    Site of pain  Quality (looking for neuropathic features)  Radiation pattern  Duration  Intensity (at rest and with movement)  Temporal variation  Previous therapies and response  Precipitating factors  Mood  Relieving factors  Activities of daily living  Sleep  Current therapies  Patient beliefs regarding cause of pain
  Fig. 2.1    “Where does it hurt?’ (Image courtesy of Andrea Trescot, MD)       
  Fig. 2.2    A directed back examination (Image courtesy of Andrea Trescot, MD)         
A.M. Trescot and D. Krashin
drtrescot@gmail.com

 References
      1.    deSouza RM, Choi D. Peripheral nerve lesions. Neurosurgery. 2012;3(30):149–54.     2 .  D  orman TA. Diagnosis and injection techniques in orthopedic medicine. Baltimore: Williams and Wilkins; 1991.      3 .  H  icks F, Simpson KH. Nerve blocks in palliative care. Oxford: Oxford University Press; 2004. p. 129.      4.    Beyer TE. Idiopathic supraorbital neuralgia. Laryngoscope. 1949;59(11):1273–5.     5 .  K  ashuk K. Proximal peripheral nerve entrapment syndromes in the lower extremity. J Am Podiatry Assoc. 1977;67(8):529–44.      6.    Dellon AL, Mackinnon SE. Radial sensory nerve entrapment in the forearm. J Hand Surg Am. 1986;11(2):199–205

 Consequences of Peripheral Nerve Entrapment                     
     Andrea     M.     Trescot       and     Daniel     Krashin     
P       eripheral nerve entrapments can cause a variety of painful conditions as diverse as headache, backache, “sciatica,” “endometriosis,” and foot pain. Peripheral nerve entrapments can occur at sites where the nerve goes through a tunnel or canal, or pierces through fascia, or makes a sharp change in the direction of its path. Infl ammation, edema, or extrinsic compression will trigger entrapment; the sympathetic response to this entrapment leads to more infl ammation and edema, leading to more entrapment, creating a vicious cycle.  In nerves with a sensory component, chronic injury often causes increased excitability of the nerve. This can result in both  hyperalgesia  and  allodynia  in the peripheral nerve fi eld supplied by that nerve or the whole sensory dermatome, as is the case with injury to a spinal nerve root.  Nerve entrapments may be present in varying degrees, leading to a variety of clinical presentations. 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 or even years after the surgery, because of the scar cicatrix that gradually 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 compression. Clinical diagnosis is dependent upon 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 [ 1] . 
  Chronic peripheral neuroexcitability  may result in major disability. Severe sensitivity of the extremities is particularly impairing, especially with the upper extremities and hands. When mixed motor and sensory nerves are injured, the motor defi cit may compound the increased hypersensitivity. For example, an injury to the distal radial nerve may cause hyperalgia and allodynia in the peripheral nerve fi eld of that nerve, including the dorsum of the affected hand, as well as decreased grip and function of that hand. The combination of impaired function and hypersensitivity often leads the patient to avoid using that limb ( kinesiophobia) , even swaddling it in protective gloves or bandages and maintaining that limb in a guarded position. This restricts the patient’s ability to engage in rehabilitation and normal social activities and maintain or resume gainful employment [ 2 ]. I n a study of ulnar nerve entrapment, about half of the patients who did not have surgery were largely asymptomatic, while the rest had varying degrees of paresthesias, pain, and diffi culty with fi ne motor control of the fi ngers [ 3 ]. This was a retrospective, nonrandomized study and included patients who were seen by the surgeons but managed conservatively, likely with milder symptoms.   Strokes  or  cerebral vascular accidents (CVAs)  are a common cause of mortality and one of the most common causes of morbidity in the world [ 4 ]. Although there can be weakness, paresis, and dysarthria as a major cause of morbidity after CVA, pain can also be a signifi cant cause of distress, and some of that pain comes from entrapment neuropathies. Hunkar and Balci [ 4 ] evaluated 32 patients with ischemic or hemorrhagic stroke 6 months after the event and compared them to 10 age-matched controls. Nerve conduction studies showed that 12 patients (37.5 %) had median nerve neuropathy at the wrist, and 12 patients (37.5 %) had ulnar nerve neuropathy at the elbow in the symptomatic extremities. They concluded that entrapment neuropathies could be an important cause for morbidity after CVA.  The most dreaded consequence of peripheral nerve injury is  complex regional pain syndrome  (CRPS), which can be divided into “refl ex sympathetic dystrophy” or RSD
        A.  M.   Trescot ,  MD, ABIPP, FIPP        Pain and Headache Center ,   Anchorage ,  AK ,  USA    e-mail: DrTrescot@gmail.com       D.   Krashin ,  MD      (*)   Pain and Anesthesia and Psychiatry Departments ,  Chronic Fatigue Clinic, University of Washington ,   Seattle ,  WA ,  USA    e-mail: krashind@uw.edu  
 

( CRPS type I,  where there is no underlying nerve injury) and “causalgia” ( CRPS type II,  where there is an identifi ed nerve injury). This condition most commonly develops after a fracture or soft tissue injury of an extremity or after a surgical procedure. For instance, Irwin and Schwartzman published a case report of a patient with chest wall dystonia and CRPS after brachial plexus injury [ 5 ]. Factor analysis demonstrates that signs and symptoms of the syndrome cluster into four subgroups: (1) abnormalities in pain processing that cause allodynia, hyperalgesia, and hyperpathia, (2) skin color and temperature change, (3) neurogenic edema and vasomotor and sudomotor abnormalities, and (4) a movement disorder and trophic changes [ 6 ]. The movement disorder manifests as a combination of diffi culty initiating and maintaining movement, weakness, postural and intention tremor,  myoclonus , spasm, increased tone, abnormalities of reaching and grasping, and dystonia [ 7 ].  Dystonia  in CRPS is most likely a peripherally induced, focal dystonia [ 8 ]. O aklander et al. [ 9]  and Albrecht et al. [ 10] , both in 2006, felt that some form of initial nerve trauma (and the subsequent ischemia) was “an important trigger for the cascade of events leading to CRPS” [ 11 ]. Coderre and Bennett [ 12 ] proposed that “the fundamental cause of the abnormal pain sensation is ischemia.” They also suggested that ischemia provides a “unifying idea that relates the pathogenesis of CRPS-I to that of CRPS-II,” suggesting that the distinction between the two diagnoses is a matter of degree and not pathology.  CRPS associated with  shingles  or  herpes zoster (HZ)  was fi rst reported by Sudeck in 1901 [ 13]  but had been surprisingly unrecognized until recently [ 13 – 15] . One hypothesis of this relationship involves the provocation of local tissue infl ammation secondary to cytopathic changes induced by the HZ infection. These changes cause local trauma and a potential entrapment of the peripheral nerves [ 16 ], contributing to  postherpetic neuralgia (PHN) , the devastating complication of HZ outbreaks. PHN is most often found in patients who had CRPS-like symptoms [ 14 ]. Berry et al. [ 17 ] prospectively reviewed 75 patients over 50 years old with pain score ≥20/100 at 2–6 weeks post-HZ onset and followed these patients for 6 months, evaluating for CRPS-like symptoms. Of these patients, 25 had involvement of the extremities; 89 % of those with distal extremity involvement had symptoms of CRPS at 3 months. Although they did not specifi cally address the cause of these symptoms, infl ammation and subsequent entrapment of the peripheral nerve are likely.  Hypermobility may also contribute to both nerve entrapment and nerve stretch injury. Stoler and Oaklander described four patients with joint injuries who developed CRPS; all four also met criteria for Ehlers-Danlos hypermobility syndrome [ 18 ]. They hypothesized that the CRPS occurred via stretch injury to nerves crossing hypermobile joints, increased fragility of the nerve connective
tissue, or nerve trauma from the more frequent surgeries needed to treat the hypermobile joints.  Patients in the early phases of CRPS are more likely to respond to sympathetic ganglion blocks, as their symptoms are still sympathetically mediated. In a trial of stellate ganglion and lumbar sympathetic ganglion blocks, the duration of pain relief was shown to be more than three times longer in responding CRPS patients using local anesthetic when compared to saline [ 19 ]. Aggressive physical therapy is also a mainstay of treatment; in treatment-resistant cases, many other modalities have been used, including indwelling nerve catheters, ketamine infusions, and spinal cord stimulation [ 20] . Though widely practiced, the evidence base is slim and inconsistent in this area. H owever, these therapies presume that the  underlying process  is sympathetically mediated rather than being the  response to the process . Coderre and Bennett hypothesize that the role of the sympathetic nervous system in CRPS-I “is a factor that is not fundamentally causative, but may have an important contributory role in early-stage disease” [ 12 ]. D ellon et al. [ 21]  in 2009 reevaluated this entire concept and proposed that there is no real distinction between RSD (CRPS type I) and causalgia (CRPS type II). Rather, they hypothesized that chronic pain input to the dorsal spinal columns is misdiagnosed as CRPS-I and that chronic nerve compression and infl ammation (i.e., CRPS-II) can be the source of these painful dorsal column inputs. They performed a retrospective review of 100 consecutive patients with the diagnosis of “RSD” based on the following criteria from the International Association for Study of Pain [ 22 ]:
    Absolute : Pain extending outside the area of trauma, impaired extremity function, and either cold or warm perceptions or temperature changes in the affected extremity     Relative:  Edema, increased or decreased hair or nail growth, hyperalgesia, allodynia, abnormal skin coloring    
 They identifi ed 70 of those 100 patients who had documentation of chronic peripheral nerve entrapment based on abnormal sensory testing, a positive Tinel’s sign at the site of known anatomic narrowing, and temporary response to a local anesthetic injection (without steroid). Of note was the relatively large volume used (5 cc), which could have contributed to more entrapment. They noted “good” to “excellent” relief in 80 % of the patients after surgical release. In another paper in 2010, Dellon and colleagues [ 23 ] reviewed the results of 13 patients treated for lower extremity CRPS with surgical release of peripheral nerve entrapments; 75 % noted good or excellent relief a minimum of 24 month later. In both papers, they concluded that more than 80 % patients with a diagnosis of “CRPS-I” of the upper or lower extremity could have one or more injured and/or compressed peripheral nerves as the source of their continuing dorsal

column painful neural input and should actually have a diagnosis of treatable “CRPS-II.” 
    Summary
 Peripheral nerve entrapment can cause a wide number of clinical presentations, many of which are misdiagnosed (and therefore less likely to respond to treatment). Recognition (and appropriate treatment) of the peripheral nerve entrapment can increase the potential for successful treatment.     
   References
   1 .  K  line DG, Hudson AR. Nerve injuries: operative results for major nerve injuries, entrapments, and tumors. Philadelphia: W.B. Saunders; 1995.     2 .  D  avies E, Pounder D, Mansour S, Jeffery IT. Cryosurgery for chronic injuries of the cutaneous nerve in the upper limb. Analysis of a new open technique. J Bone Joint Surg Br. 2000;82(3):413–5.     3 .  P  adua L, Aprile I, Caliandro P, Foschini M, Mazza S, Tonali P. Natural history of ulnar entrapment at elbow. Clin Neurophysiol. 2002;113(12):1980–4.      4 .  H  unkar R, Balci K. Entrapment neuropathies in chronic stroke patients. J Clin Neurophysiol. 2012;29(1):96–100.      5.    Irwin DJ, Schwartzman RJ. Complex regional pain syndrome with associated chest wall dystonia: a case report. J Brachial Plex Peripher Nerve Inj. 2011;6:6.     6 .  H  arden RN, Oaklander AL, Burton AW, Perez RS, Richardson K, Swan M, et al. Complex regional pain syndrome: practical diagnostic and treatment guidelines, 4th edition. Pain Med. 2013;14(2): 180–229.      7.    Schwartzman RJ, Patel M, Grothusen JR, Alexander GM. Effi cacy of 5-day continuous lidocaine infusion for the treatment of refractory complex regional pain syndrome. Pain Med. 2009;10(2):401–12.      8.    Schott GD. Peripherally-triggered CRPS and dystonia. Pain. 2007;130(3):203–7.      9.    Oaklander AL, Fields HL. Is refl ex sympathetic dystrophy/complex regional pain syndrome type I a small-fi ber neuropathy? Ann Neurol. 2009;65(6):629–38.  
    10.    Albrecht PJ, Hines S, Eisenberg E, Pud D, Finlay DR, Connolly MK, et al. Pathologic alterations of cutaneous innervation and vasculature in affected limbs from patients with complex regional pain syndrome. Pain. 2006;120(3):244–66.      11.    Bruehl S. An update on the pathophysiology of complex regional pain syndrome. Anesthesiology. 2010;113(3):713–25.      1 2.  C  oderre TJ, Bennett GJ. A hypothesis for the cause of complex regional pain syndrome-type I (refl ex sympathetic dystrophy): pain due to deeptissue microvascular pathology. Pain Med. 2010;11(8):1224–38.       13.    Öztop P, Saraçgīl Coşar SN, Ümīt Yemīşcī O, Varol Üre RS. Complex regional pain syndrome associated with herpes zoster: a case report. Turk J Rheumatol. 2011;26(3):254–7.  1    4.  G  imenez-Mila M, Busquets C, Ojeda A, Fauli A, Moreno LA, Videla S. Neuropathic pain with features of complex regional syndrome in the upper extremity after herpes zoster. Pain Pract. 2014;14(2):158–61.  1    5.  L  ouizos L, Kremastinou F, Panaretou V, Skalistira M, Kouroukli I, Georgiou L. Complex regional pain syndrome after herpes zoster: case report. Eur J Pain. 2006;10(Suppl S1):S204.      16.    Ecker A. Pathogenesis of refl ex sympathetic dystrophy. Arch Neurol. 1989;46(5):482.  1    7.  B  erry JD, Rowbotham MC, Petersen KL. Complex regional pain syndrome-like symptoms during herpes zoster. Pain. 2004; 110(1–2):e1–12.      18.    Stoler JM, Oaklander AL. Patients with Ehlers Danlos syndrome and CRPS: a possible association? Pain. 2006;123(1–2):204–9.      19.    Price DD, Long S, Wilsey B, Rafi i A. Analysis of peak magnitude and duration of analgesia produced by local anesthetics injected into sympathetic ganglia of complex regional pain syndrome patients. Clin J Pain. 1998;14(3):216–26.      20.   O’Connell NE, Wand BM, McAuley J, Marston L, Moseley GL. Interventions for treating pain and disability in adults with complex regional pain syndrome. Cochrane Database Syst Rev. 2013;(4):Cd009416.      21.    Dellon AL, Andonian E, Rosson GD. CRPS of the upper or lower extremity: surgical treatment outcomes. J Brachial Plex Peripher Nerve Inj. 2009;4:1.      22.    Merskey H, Bogduk N. Classifi cation of chronic pain: descriptions of chronic pain syndromes and defi nitions of pain terms. 4th ed. Seattle: International Association for the Study of Pain (IASP) Press; 1994.      23.    Dellon L, Andonian E, Rosson GD. Lower extremity complex regional pain syndrome: long-term outcome after surgical treatment of peripheral pain generators. J Foot Ankle Surg. 2010; 49(1):33–6.    
3 Consequences of Peripheral Nerve Entrapment
drtrescot@gmail.com


Introduction
Many non-pharmacologic treatments for pain, such as
manipulation [
1
], massage therapy [
2
], and acupuncture,
date back thousands of years. With the rise of “Western” bio-
medicine and increasingly powerful drug companies in the
last century, these methods were often sidelined as quackery
[
3
]. The diffi
culty of evaluating many of these therapies with
the gold-standard randomized clinical trials, which are well
suited to medication trials, contributed to their marginaliza-
tion [
4
]. Because of their effi
cacy in many situations, how-
ever, patients continue to use a variety of non- pharmacologic
therapies. Currently, increasingly sophisticated visualization
[
5

10
], anatomic [
11

16
], biochemical [
17

21
], and system-
atic data evaluation [
22

30
] techniques are able to show
objective tissue characteristics and response to therapies.
Myofascial
pain syndrome
(MFPS) symptoms may mimic
other conditions commonly thought to require invasive inter-
ventions, such as carpal tunnel syndrome, herniated discs
with sciatica, and thoracic outlet syndrome, among others. If
the myofascial component is recognized and treated, symp-
toms often abate, leading to less need for analgesic and anti-
infl
ammatory medication, invasive procedures, and surgery.
Unfortunately, many primary care practitioners and pain
practitioners have not been taught about this cause of mor-
bidity [
31
].
Patients with severe acute injuries may initially need pas-
sive modalities (see below) and traditional pharmacologic
intervention to allow suffi
cient reduction of excess infl
am-
mation before beginning more intensive manual therapies
(Table
5.1
). Those with less severe acute injuries should be
encouraged to start manipulative intervention early, while
those with chronic pain will benefi
t from the addition of the
non-pharmacologic therapies with effects synergistic to
those achieved with traditional pharmacology.
Myofascial Pain Syndromes
MFPS are characterized by diffusely aching pain and tender-
ness in one or more taut and shortened muscles, as well as
hypersensitive areas known as
myofascial trigger points
(MTrPs) [
32
]. The pain is often referred, rarely in the distri-
bution of a peripheral nerve or spinal segment [
33
], but rather
in the predictable pattern mapped by Travell and Simons
[
32
]. Unless palpation of the painful site evokes signs of
acute tenderness, the source is likely a MTrP somewhere
H. W. Karl , MD
Department of Anesthesiology and Pain Medicine ,
University of Washington, Seattle Children’s Hospital ,
Seattle , WA , USA
e-mail:
helen.karl@seattlechildrens.org
H. Tick , MA, MD (
*
)
Family Medicine and Anesthesiology & Pain Medicine ,
University of Washington , Seattle , WA , USA
e-mail:
htick@uw.edu
K. A. Sasaki , DC, CCSP
Director , Vida Integrated Health , Seattle , WA , USA
e-mail:
drsasaki@vidaintegratedhealth.com
5
Table 5.1
Therapeutic approaches to MFPS, in order of intensity
Manual therapies Needle therapies
Patient education on postural
habits and activity modifi
cation
Acupuncture (acupressure,
traditional and
electroacupuncture)
Therapeutic exercise Direct or remote intramuscular
stimulation (dry needling)
Myofascial mobilization Local anesthetic injection
Massage (including Swedish,
shiatsu, self-massage, structural
integration (Rolfi
ng),
craniosacral)
Instrument assisted (Astym®,
Graston®)
Neural mobilization (neural
fl
ossing)
Joint manipulation or
mobilization
drtrescot@gmail.com
28
else. Pressure on the most tender area often reproduces the
pain pattern, and massage or injection of local anesthetic into
that site relieves the pain for a period of time, usually much
greater than the duration of the drug [
32
]. The onset of MFPS
is usually a muscle injury that activates an MTrP; this can be
due to acute trauma, cumulative repetitive overload, or a
peripheral nerve injury. The intensity of the symptoms
refl
ects the degree of irritability of the MTrP rather than the
size of the muscle.
In addition to taut and shortened painful muscles, patients
with MFPS may have localized weakness and autonomic
changes, such as abnormal pilomotor, sudomotor, and vaso-
motor phenomena. Tendons can become thickened or enthe-
sopathic, with traction on tendon attachments and the
potential for compression of other structures, particularly
peripheral nerves. Symptoms presenting in a specifi
c indi-
vidual depend on the surrounding anatomical structures; for
example, if myofascial dysfunction causes nerve entrapment,
it is likely to result in localized neuropathic pain with radia-
tion and dysesthesias.
Clinical characteristics of the MTrPs in these muscles
have been well described [
32
]. These extremely tender nod-
ules, associated with taut muscle bands, cause local and
referred pain, and they produce a spinal cord refl
ex known as
a
local twitch response (LTR)
when stimulated by snapping
palpation or needle penetration. Travell and Simons pro-
posed a theory of the etiology of myofascial abnormalities
known as the integrated trigger point hypothesis [
32
]. MTrPs
are thought to result from excess acetylcholine at the neuro-
muscular junction, leading to persistent muscle contraction
and an “energy crisis” in this localized area with increased
demand and decreased supply. Gunn’s postulate that muscle
dysfunction is caused by subtle compression of the nerve
roots, which creates nerve dysfunction equivalent to partial
denervation, remains controversial [
34
], although nerve root
compression likely contributes to the “double crush” phe-
nomenon [
35
] (see Chap.
1
).
The advent of technologies to assess the functional
derangements of these anatomic muscle disorders allows
more to be learned about their properties. In a selective
review of animal studies, Mense described the ways that
algesic (pain-causing) agents, most commonly ATP and
low tissue pH, excite muscle nociceptors. Muscle spasm
and other causes of chronic ischemia, abnormal posture,
infl
ammation, and MTrPs are all associated with low tissue
pH. Chronic activation of muscle nociceptors can lead to
central sensitization [
9
,
36
]. Sikdar et al. have demon-
strated hypoechoic areas on ultrasound that correspond to
MTrPs and have used elastography to show that MTrPs are
stiffer than normal muscle [
7
]. Shah et al. have microdial-
ysed the interstitial fl
uid at MTrPs and found an infl
amma-
tory milieu in the trigger points, but not in an unaffected
muscle [
17
].
Investigations at the tissue and cellular level have also
been useful to identify mechanisms underlying
fascial dys-
function
. Fascia is a three-dimensional continuous network of
cells (mostly fi
broblasts) and intercellular fi
bers which envel-
ops and divides all the other components of the body [
37

40
].
It supplies structural support, transmits forces between mus-
cles [
41
,
42
], is highly innervated with
mechanoreceptors
and
autonomic fi
bers
[
43
], and has
piezoelectric
properties [
44
,
45
]. Fascia may become shortened by acute injuries such as
trauma or infl
ammation and by chronically abnormal posture
or repetitive use [
44
], but it has a remarkable ability to reform
[
43
,
46
]. Any kind of mechanical loading affects the extracel-
lular matrix and increases the number and function of embed-
ded fi
broblasts. Application of acute or chronic mechanical
loads at higher “doses,” as seen in acute trauma or repetitive
motion strain, leads to the release of the infl
ammatory media-
tors described above. In contrast, lower loads, as seen in
cyclic mechanical stretch or massage, release anti-infl
amma-
tory compounds and stimulate collagen metabolism [
47
,
48
].
Clinically, muscle and fascia are usually injured and treated
in concert; fi
broblasts appear to provide important connec-
tions between them at a subcellular level [
48
,
49
].
Taken together, these and many more objective examina-
tions of muscle and fascial dysfunction provide insight into the
complex etiology of MFPS and an evidence base for the success
of a variety of clinical approaches to its relief. Manual medical
therapies and needle therapies are the two broad approaches
found to be effective for the relief of myofascial pain.
Manual Medical Treatments
( Table
5.2
)
Numerous manipulative techniques have developed over the
last two centuries and have been practiced by often compet-
ing professionals [
1
,
20
]. Modern scientifi
c publication on
manipulative methods began with Travell [
50
] and quickly
progressed to include the benefi
ts of combined therapies,
such as manipulation and local anesthetic infi
ltration [
51
].
The results of subsequent work have been published by
Table 5.2
Manual therapies
Treatment Practitioners
Physical modalities Physical therapist, chiropractor
Patient education Physical therapist, movement
therapist, chiropractor
Massage, self-massage Massage therapist, structural
integration practitioner (Rolfer)
Active release techniques,
myofascial release
Physical therapist, chiropractor
Neural mobilization (neural
fl
ossing)
Physical therapist, chiropractor,
osteopathic physician
Joint manipulation or
mobilization
Chiropractor, osteopathic
physician, physical therapist
H.W. Karl et al.
drtrescot@gmail.com
29
investigators in multiple disciplines, often using different
terms for essentially the same maneuvers [
52
]. This is one
reason it has been diffi
cult to demonstrate the short- and
long-term benefi
ts of these techniques [
53
]. As the evidence
base increases, it is hoped that practitioners will use the
strengths of their particular backgrounds to cooperate at all
levels, from diagnosis and treatment of individual patients to
research and teaching [
22
,
39
,
52
,
53
].
Physical Modalities
Application of ice, heat,
contrast baths
(for complex regional
pain syndrome (CRPS) symptoms), splinting, compression
stockings, and/or electrical stimulation can help decrease
pain and infl
ammation. Application of
low-level laser ligh
t
has also been shown to be helpful [
54
,
55
]. The routine use
of
ice
to reduce infl
ammation in acute injuries has recently
come into question; its use does temporarily decrease dis-
comfort, but normal infl
ammation is a constructive part of
healing [
56

58
]. These passive interventions should be used
to facilitate active stretching and strengthening exercises to
correct biomechanics [
59
].
Patient Education on Postural Habits,
Ergonomics, and Activity Modifi
cation
Identifi
cation of work-related or lifestyle habits that cause or
contribute to MFPS is key to treatment. For long-term relief to
be successful, the patient must understand the
ergonomics
of
their diagnosis and actively participate in rehabilitation [
59
].
Body awareness therapies to address postural habits such as
Feldenkrais
and the
Alexander technique
naturally complement
education, self-massage, and active therapeutic exercises [
60
].
Structural Integration (Rolfi
ng)
Dr. Ida Rolf developed in the 1920s a combination of move-
ment training and massage designed to maximize the body’s
vertical alignment [
61

63
]. In theory, when the body is not
aligned with gravity, additional energy must be used for any
task, and affected fascia will shorten and thicken. For example,
if the head is shifted forward, its effective weight can more than
double, causing pain and fatigue. One study showed improve-
ment of neck pain and range of motion after ten sessions [
62
].
Massage
Massage therapy
has been defi
ned as “soft tissue manipulation
by trained therapists for therapeutic purposes” [
2
]. It encom-
passes hundreds of different techniques and may be performed
with hands alone or with instruments [
64
]. Skilled practitioners
can identify taut muscle bands and MTrPs, improve local blood
fl
ow, and reduce pain and disability. A recent meta-analysis of
its effectiveness for diverse chronic pain conditions has shown
massage alone to be effective for low back pain and progres-
sively less effective for shoulder and headache pain (moderate
support), with only modest support to treat fi
bromyalgia, mixed
chronic pain, neck pain, and carpal tunnel syndrome [
2
]. One
area of debate is the optimal location at which to apply pressure
or friction. Stecco et al. addressed this question by developing
a biomechanical model of the myofascial system (Fascial
Manipulation©), dividing this continuous structure into seg-
ments, each served by myofascial units defi
ned by specifi
c
movements [
12
,
13
,
65

68
]. Analysis of abnormal motion
allows identifi
cation of areas requiring treatment [
69
].
Therapeutic Mechanical Load
Employing instruments to amplify and concentrate the
hands’ ability to affect the muscle and fascia have been used
for centuries [
44
,
70
]. The Astym® [
71
] and Graston
Technique® are two contemporary, instrument-assisted soft-
tissue mobilization methods [
64
].
Neural Mobilization (NM, Colloquially Termed
“Neural Flossing”)
NM consists of active or passive exercises to improve the
movement of peripheral nerves with respect to the other tis-
sues that surround them. In clinical studies, there is level 3
evidence of effectiveness for the upper quadrant (cervical
spine, shoulder, arm) with less conclusive evidence in the
lower quadrant (lumbar spine, pelvis, leg) [
72
]. Authors have
reported particular success treating median nerve entrapment
at the carpal tunnel (Chap.
37
) [
73

75
], neck and arm pain
[
76
,
77
], and the pain of lateral epicondylitis and neurogenic
cervicobrachial disorders [
78
]. Dr. Gabor Racz has also
encouraged this type of nerve mobilization after cervical and
lumbar epidural adhesiolysis [
79
,
80
]. Recent studies in ani-
mals have provided evidence for the mechanisms underlying
this practice [
18
,
19
].
Joint Manipulation or Mobilization
Removing restrictions on almost any joint limited in its range of
motion can improve joint function and reduce the stress on
nearby myofascial structures. Broadly speaking, this can be
achieved with manipulation using low-amplitude, high- velocity
movements or with mobilization using higher- amplitude, low-
5 Non-pharmacologic Treatment of Peripheral Nerve Entrapment
drtrescot@gmail.com