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This is to certify that the

dissertation entitled

USE OF MAGNETIC RESONANCE IMAGING EXAMINATION TO
ASSESS COMPARTMENT CHANGES IN THE FOREARM AND
WRIST WITH EXPOSURE TO REPETITIVE TYPING
presented by

Gail A. Shafer-Crane

has been accepted towards fulfillment
of the requirements for

Ph.D.

degree in Ana (1 omy

 

 
   

/ I Wjor professor

Date 3°/5'0'Z——

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6’01 cJCIRCJDatoDuopSS—p. 1 5

 

USE OF MAGNETIC RESONANCE IMAGING EXAMINATION T0 ASSESS
COMPARTMENT CHANGES IN THE FOREARM AND WRIST WITH
EXPOSURE TO REPETITIVE TYPING
By

Gail A. Shafer—Crane

A DISSERTATION

Submitted to
Michigan State University
In partial fulfillment of the requirements
for the degree of

DOCTOR OF PHILOSOPHY

Division of Anatomy and Structural Biology
Department of Radiology

2002

ABSTRACT
USE OF MAGNETIC RESONANCE IMAGING EXAMINATION T0 ASSESS
COMPARTMENT CHANGES IN THE FOREARM AND WRIST WITH
EXPOSURE TO REPETITIVE TYPING
By

Gail A. Shafer-Crane

Dimensional, positional and fluid content changes of soft tissues of the forearm
and wrist as a response to typing were analyzed in this study using magnetic resonance
imaging. Axial images were taken at the mid-forearm, proximal to the transverse carpal
ligament, at the longitudinal level of the pisiform, hamate and base of the metacarpals
levels. The intent was to contrast muscles more and less active through magnetic
resonance imaging (MRI) examinations, and note changes in morphology of the median
nerve at the wrist related to exposure to typing. Thirteen female professional typists, six
asymptomatic and seven symptomatic, underwent three MRI examinations of the
dominant forearm and wrist at baseline, after three hours of typing, and after eight hours
of rest. Three investigators blinded to the subjects’ exercise status analyzed forearm
muscle and wrist compartment images with respect to T2 signal intensity and nerve
morphology. Compartmental constituent fluid and shape changes were correlated with
typing. Forearm flexors were more active in typing than extensors and thumb muscles
(P=.0016). Progressive variations in T2 as well as size and shape of the median nerve
highly correlated to typing. MRI analysis following exercise (typing) in this study
revealed significant changes in both muscles and nerves, suggesting a relationship

between exposure to typing and these findings.

In loving memory of Esther Mary Loersch and Shirley Evelyn Barry, my grandmother
and mother and to the women who came before us, and will come after.

Carpi Diem.

iii

ACKNOWLEDGMENTS

My road to completion has taken many twists and turns through the maze of
classes, research projects, testing, teaching and finally writing. Through this long haul,
my family has shown heroic patience and support. We have given up much time together,
and delayed or rearranged every sort of family activity. Dan has patiently waited for his
college student wife to come home for meals, activities and just to be at home. Many
times Mike and his wife Elizabeth or Stephanie were drafted to help with the research
project, volunteer for imaging, or help in some way. Thanks to all of you.

This work would have never been started without the direction, patience and
vision of Robert Hubbard, PhD. He listened to an enthusiastic, naive graduate student
hopeful wandering about, looking for the entrance to the road to PhD, and heard the germ
of a worthy idea. Joseph Vorro admitted me into the Anatomy program, and assigned by
original committee: James Rechtien as my mentor, and Lawrence Ross, Kenneth
Stephens, and Robert Werner. Though the committee changed because of the loss of the
original project, these individuals have continued to offer their support and direction.
Particularly Dr. Rechtien, whose patience and perseverance is unmatched.

So many others were instrumental in my successful completion of this project.
Marcy Schlinger, the primary investigator of the study, helped format and edit many
forms of posters and preliminary articles. Drs. Lee Bennett, Kevin Robinson and Joseph
Pernicone radiologists spent countless hours pouring over images. Tom Cooper and Dr.
Ronald Meyer ran the MRI through our very lengthy imaging sessions on Sundays and

evenings.

iv

And, finally, thanks to my committee: James Rechtien, advisor, J .1. Johnson,
William Falls, Ron Meyer, Lee Bennett and Arlene Sierra. Each offered their time and
expertise in this endeavor. I have learned so much thanks to these people, and to so many

others. One may only hope to pass along the knowledge and opportunity to others.

TABLE OF CONTENTS

Page Number

List of Figures vii-viii
Table of Abbreviations ix
Glossary of Magnetic Resonance Imaging Terms x-xii
Chapter I. Introduction 1-25

1. Medical and Physical Costs of Repetitive Stress Injury 2-3

2. History of RSI 4-9

3. Definition of RSI 9-10

4. Neurocompressive Disorders 10-1 1

5. Similarities and differences between Neurocompressive

and Inflammatory Disorders 1 1-13
6. Normal Anatomy of Forearm Components _ 13-14
7. Altered Anatomy, Histology and Physiology in Peripheral
Nerves of the Forearm 14-15

8. Anatomical Considerations in Inflammatory Disorders 15-18

9. Examples of Neurocompressive Disorders 18-19

10. Examples of Inflammatory Disorders 20-21

1 1. Method of Study 21-23

12. Summary of Findings 23-24

13. Hypothesis Development 24-25
Chapter II. Anatomical review of the Upper Extremity 26-43

1. Neural and Vascular Pathways 26-27

2. Neck and shoulder 28

3. The Brachial Plexus 28-30

4. The Skeletal Armature 30

5. The course of neural and vascular structures 31-32

6. The Elbow 32-34

7. Compartments of the forearm 34-35

8. The Wrist 36-40

9. The Hand 41-43
Chapter III. Materials and Methods 44-54

1. Study Population 44

2. Study Objectives 45

3. Experimental design 45-50

4. Data collection 50-51

5. Hypothesis Development 51-54

vi

Chapter IV. Magnetic Resonance Imaging (MRI) Assessment of
Compartment Changes In Forearm and Wrist Following Exposure
to Typing In Asymptomatic Volunteers 55-74

Chapter V. Assessment of Changes in the Compartments of the

Forearm and Wrist When Exposed to Vocational Speed Typing

and Prolonged Rest in Symptomatic vs Asymptomatic Volunteers 75-92
References 93-99

Figures 99- 145

vii

Chapter 11
Figure 2.1:
Figure 2.2:
Figure 2.3:
Figure 2.4:
Figure 2.5:
Figure 2.6:

Chapter 111
Figure 3.1
Figure 3.2
Figure 3.3
Figure 3.4
Figure 3.5
Figure 3.6
Figure 3.7

Chapter IV
Figure 4.1
Figure 4.2
Figure 4.3
Figure 4.4
Figure 4.5
Figure 4.6
Figure 4.7
Figure 4.8

Figure 4.9

Figure 4.10
Figure 4.11
Figure 4.12
Figure 4.13

Figure 4.14
Figure 4.15

Figure 4.16

Chapter V
Figure 5.1
Figure 5.2
Figure 5.3

LIST OF FIGURES

Examples of sagittal and axial MRI Images ......................... 99
Fascia] compartments of the forearm in an axial image ....... 100
Proximal to the transverse carpal ligament .......................... 101
Imaging level of the pisiform bone ...................................... 102
Imaging level of the hook of the hamate bone ..................... 103
Imaging level of the base of the metacarpal bones ................ 104
Table of Subjects, ages, and diagnoses ................................ 105
Medical History and Release of Information forms ............. 106
U.C.R.I.H.S. Consent Form ................................................. 107
Levine CTS Symptom Severity Scale .................................. 108-10
Levine Functional Status Scale ............................................ l 11
Physical Examination Form ................................................. 112-13
Dual T2 weighted images with two TEs ............................... l 14
Wrist splint and coil in imaging position ............................. 1 15
Image used to establish Calculated T2 ................................. 1 l6
Carpal Tunnel of Subject 1 at hook of hamate ..................... 117
Carpal Tunnel of Subject 2 at hook of hamate ..................... 1 18
Scatter plot of Calculated T2 of forearm muscles ................. 1 19
Table of Calculated T2 changes in forearm muscle T2 ........ 120

Scatter plot of Calculated T2 forearm muscles of control ..... 121
Scatter plot of comparison of Typing vs. non typing control
extensor and thenar muscle Calculated T2 ............................ 122
Graph of Calculated T2 of extensor digitorum (typing) ...... 123
Graph of Calculated T2 of flexor digitorum profundus ....... 124
Median nerve T2 at TCL Typing subjects vs. control .......... 125
Surface to Area Ratio Typing subjects ................................. 126
Rank sum graph of changes in shape of the median nerve
identified by the radiologists at the hook of the hamate ....... 127

Median Nerve T2 at the TCL Typing vs. Control ................ 128
Pearson's Correlation Table of typing with changes in T2

of the Median nerve at the level of the TCL ......................... 129
Scatterplot comparing changes in median and ulnar nerve

T2 Relaxation times .............................................................. 130
Photo of the position used for Phalen's test .......................... 131
Chart of analyses performed by investigators 132

Axial MRI of the carpal tunnel comparing the median
nerve and ulnar nerves at three imaging levels .................... 133

viii

Figure 5.4
Figure 5.5
Figure 5.6
Figure 5.7

Figure 5.8
Figure 5.9
Figure 5.10

Figure 5.11

Figure 5.12

Figure 5.13
Figure 5.14
Figure 5.15
Figure 5.16

Figure 5.17

Axial MRI of the carpal tunnel as above, different

asymptomatic subject ........................................................... 134
Axial MRI of median nerves of symptomatic subjects

showing flattening and edema .............................................. 135
Tethered median nerve in an axial MRI of a symptomatic
subject at the three imaging levels taken at Baseline .......... 136
Axial MRI of the carpal tunnel of a symptomatic subject
showing flattening of the median nerve ................................ 137

Scatterplot of T2 relaxation times of the median

nerves of asymptomatic vs. symptomatic subjects with

typing and prolonged rest ...................................................... 138
Scatterplot of the change in ulnar nerve T2s, symptomatic

vs. asymptomatic subjects at Baseline, After Typing and

Post rest ................................................................................ 139
Graph of reported pain levels on a zero to ten scale ............. 140
Scatter plot of the Calculated T2 differences in the median
nerve at the TCL at Baseline, After typing and Post Rest... 141
Scatterplot of the differences in median nerve T2

relaxation times between symptomatic and asymptomatic

subjects .................................................................................. 142
Table of the average Calculated T23 of the asymptomatic
subjects' median nerves at four imaging levels .................... 143
Table of the average Calculated T25 of the asymptomatic
subjects' ulnar nerves at four imaging levels ....................... 143
Table of the average Calculated T25 of the symptomatic
subjects' median nerves at four imaging levels .................... 143
Table of the average Calculated T25 of the symptomatic
subjects' ulnar nerves at four imaging levels ....................... 144

The range of average T2 relaxation times of the median
and ulnar nerves, symptomatic vs. asymptomatic subjects
at Baseline, After typing and Post rest .................................. 145

ix

ANOVA
APL
AWS
C5,6,7,8
CNS
CTS
DIP
DOMS
DRUJ
ECR
ECRB
ECU
ED
EDM
EPB
EPL
ETL
FCRL
FCU
FDP
FDS
FOV
FPL
FSE
GRE
IP

MRI
NIOSH
PIP

RF

RSI

T 1

T 1

T2
TCL
TE

TR
UCRIHS
UNIX

Table of Abbreviations

Analysis of variance

Abductor pollicis longus

Advantage Windows Workstation

Cervical nerve number 5, 6, 7, and 8

Central Nervous System

Carpal Tunnel Syndrome

Distal interphalangeal joint

Delayed Onset Muscle Soreness

Distal radioulnar joint

Extensor carpi radialis

Extensor Carpi Radialis Brevis

Extensor carpi ulnaris

Extensor Di gitorum

Extensor digiti minimi

Extensor pollicis brevis

Extensor pollicis longus

Echo train length

Flexor carpi radialis longus

Flexor carpi ulnaris

Flexor digitorum profundus

Flexor digitorum superficialis

Field of view

Flexor pollicis longus

Fast spin echo

Gradient echo image, in this study T2 weighted
Interphalangeal joint

Magnetic Resonance Imaging

National Institute of Occupational Safety and Health
Proximal interphalangeal joint

Radio frequency pulse

Repetitive Stress Injury

MRI value T] where fat is brighter than water
Thoracic nerve number 1

MRI value T2 where water is brighter than fat
Transverse Carpal Ligament

Echo time

Relaxation time

University Committee on Research Involving Human Subjects
A proprietary computer operating system that allows simultaneous
multiple level interactions between software with multiple users

Fast Spin Echo

Fat saturation

Gradient Echo

Gyromagnetic ratio

Larmor equation

Glossary of Magetic Resonance Imaging Terms

In conventional spin echo, the radio frequency pulse is
applied to provide a 90° excitation pulse which is followed
by rephasing pulses at 180°. These pulse sequences are
adjusted for T1 (short TE and short TR), proton density
(short TE and long TR), and T2 weighting (long TE and
long TR). In fast spin echo multiple 180° rephasing pulses
are used during data acquisition. These are referred to as
echo train, and the total pulses used are defined as the echo
train length (ETL). The fast spin echo pulse sequence
allows more information to be recorded for each image in a
shorter period of time.

Fat saturation in image collection voids the signal from fat,
nullifying the signal. The hydrogen atom is linked to
carbon in fat, giving it a specific rate of precession. A 90°
radio frequency pulse can be applied to "pre-saturate" the
tissue in the FOV, followed by the excitation RF pulse is
then applied, and the signal from fat is voided.

Gradient echo images (GRE) require the application of
additional gradient echo pulses to refocus the echoes. This
takes less time than FSE, which requires application of the
radio frequency pulse. The result is a faster imaging time.
The GREs used in this study were T1 weighted, and
provided contrast between the median and ulnar nerves and
the surrounding connective tissue.

As the axis of an atom rotates, the vector of the axis caused
by its interaction with an applied magnetic field is called
the gyromagnetic ratio.

The Larmor equation (too=B0 x 7) provides the method for
calculating the value of the precession frequency under
different applied magnetic fields. The processional
frequency ((00) is equal to the applied magnetic field (Bo)
times the gyromagnetic ratio (7). Each type of molecule has
a different precessional frequency, allowing identification
of the substance through its unique electrical signature.

xi

Longitudinal magnetization

Precession

Resonance

RF pulse

T1 recovery time

T2 relaxation time

TE

TR

When a body is placed in a strong magnetic field, the axis
of the magnetic active atoms align with the magnetic field.

The axis of an atom rotates in a cone shaped path at a rate
that is consistent with the element's characteristics. This
rate varies with exposure to different magnetic fields, and
calculated using the Larmour calculation. Each element has
its own rate of precession.

Resonance causes the NMV to move out of alignment with
the applied magnetic field, forming a “flip angle.” The term
used to describe Bo is the longitudinal axis. The plane at
90° to the longitudinal axis is termed transverse plane.
During resonance, the magnetic moments also begin to
move in phase with one another. This is when the NMV’s
all precess at the same rate (the Larmor frequency for
hydrogen) and are located in the same position throughout
their paths of precession.

A radio frequency pulse is an applied radio frequency wave
that is at the same frequency as the precessional frequency
of an element, usually hydrogen. It is this pulse that
perturbs the atoms, causing some of them to spin into a
higher energy configuration, and to spin in phase with each
other (resonance).

T1 is determined by the length of time in milliseconds it
takes for the nuclei to recover longitudinal magnetization.

T2 relaxation time, or decay, is the length of time in
milliseconds that it takes for 63% of the transverse
magnetization to be lost following a radio frequency
perturbation. The energy loss resulting in T2 is through the
interaction of the magnetic fields of nearby nuclei, also
termed spin spin relaxation or spin lattice relaxation. The
energy lost takes the form of heat, which is dispersed
through the surrounding tissue or lattice.

Time between the application of the radio frequency pulse
and the peak of the signal induced in the coil measured in

milliseconds.

The time between radio frequency pulses

xii

Transverse magnetization

When an RF pulse is applied, the axis of atoms whose
natural oscillation matches the frequency of the pulse
absorb energy. This causes them to move out of alignment
with the longitudinal, applied magnetic field, or spin. If
sufficient energy is applied, the axes of these atoms will
move to 90 degrees out of alignment, this is transverse
magnetization. It is the degree of transverse magnetization
that produces the electrical field that is received by the
receiver coils and transformed into the MRI signal.

xiii

Chapter I

INTRODUCTION

Repetitive stress injuries (RSIs) are a plague on modern society. They affect the
quality of life for millions of people worldwide. Delayed onset pain or paresthesias are a
cardinal symptom of these disorders, and are poorly understood. This study was
undertaken to advance the understanding of the normal anatomical functions of nerves
and muscles exposed to repetitive activity, and how those functions might differ in
symptomatic individuals. A study model, which may be used in future studies, was
developed to examine the effects of a variety of vocational activities upon the muscles
and nerves of the forearm.

Societal and personal costs of R813 are significant. Knowledge of these costs
mandates that we explore the etiologies of these devastating syndromes. These disorders
have been observed throughout recorded history. Despite the attempts of the earliest
healers through modern physician scientists to define the etiologies of RSI, the causal
factors are not, as yet, completely understood.

A brief summary of these subjects will be presented in this chapter. A brief
history of RSIs and specifically the most prevalent RSI, carpal tunnel syndrome will be
presented. RSI will be defined, and several disorders of the forearm will be discussed.
Methods of study will be summarized, and the hypotheses of this study will be presented

at the conclusion of this introductory chapter.

Medical and Physical Costs of Repetitive Stress Injuries

The National Institute of Occupational Safety and Health (NIOSH) report of 2001
documents over 582,000 cases of repetitive stress injuries (RSIs) for the year 1995 [65].
Over the period included in that report, this number accounted for one out of three of all
injuries and illnesses with days away from work. Manufacturing and service industries
each account for around 26 percent of R815, followed by retail trade with nearly 16
percent. This NIOSH report focuses on injuries and illnesses resulting in the longest
periods of time away from work. This emphasis helps clarify risk levels of particular
vocations. The report uses median days away from work as the key survey measure of
severity. The median number of lost workdays for all cases of R81 was 6 days in 1999,
with one fourth of the cases resulting in 21 days or more away from work. The injury-
illness with the highest median of work days lost was carpal tunnel syndrome (CTS) at 27
lost days. Fractures were second with 20 days, and amputations required 18. Repetitive
motion resulted in the longest absences from work as a leading event and exposure
category at a median of 17 days [65].

Carpal tunnel syndrome, an entrapment neuropathy, is the most common of all
RSIs accounting for 90% of the compensable injuries reported through workers
compensation [65]. The Department of Labor statistics of 1999 reports CTS as the
diagnosis responsible for the most days missed from work for that year, and barely
second to back injuries as the most costly to rehabilitate. Cases involving surgery may
average $250,000 in medical costs alone [13]. Despite the epidemiological evidence, and
the increased incidence among workers in specific trades, a controversy remains over

categorization of CTS as an RSI in both research and clinical studies [34].

The prevalence of RSIs in the general population is significant. Actual
percentages vary widely depending on the study. NIOSH reports a 4.2 % prevalence in
women, and 1.3% in men in a 1996 survey. A similar Dutch study reports 6.8% in
women, and 1.2% in men [13, 18, 65]. Prevalence in working populations varies by task.
Chemiack reports the highest risk in fish and meat workers at 60%, followed by grocery
store clerks also at about 60%, with office workers at 10-26%. These figures were
determined by the Bureau of Labor Statistics Survey of Occupational Injuries and
Illnesses (1995), with high percentages either confirmed or identified by physical
examination [65].

The survey, which defined an expected number of cases, differs from the number
actually reported to either workers compensation by the Physician’s First Report, or to
the health department. The number of cases reported by workers compensation reports is
somewhat lower. This inconsistency may be because cases are not reported to either the
employer or workers compensation system, or because of the existence of a report latency
between case identification and the reports to various agencies responsible for ongoing
surveillance of RSIs.

Electrodiagnostic methods used in surveillance have defined cases not reported
clinically. These latent cases are reported as positives by some investigators and not
reported by others. They would not be included in reports of work related injuries to the
health department, for example, but would be included in longitudinal studies of specific
industries independent of governmental reporting mechanisms. Peak age ranges also vary
by study. Chemiack reports a peak age range of 45-54 years; other studies report a peak

age range of 35-44 years [13, 29, 56, 70].

History of Repetitive Stress Injuries

The earliest recording of RSI is from Egyptian hieroglyphics taken from the
Hanoverian obelisk now on display in the Louvre Museum in Paris, France. This refers to
“white finger disease” in stonecutters for the Pharaohs’ pyramids. References to this
problem have been made in the medical literature of the 19th and 20th centuries as well
[33, 52]. These more recent references are of fish and meat processors working with
knives in a cold environment, and stone masons and heavy construction workers using
jack hammers and other heavy tools with either a component of impact and/or vibration.
The exposure of the worker to low frequency vibration, prolonged power grasping, and
percussion also increases the risk of repetitive neural trauma that may lead to RSI [l3].

Carpal tunnel syndrome, thoracic outlet syndrome and cubital tunnel syndrome
were described in the medical literature of the 1800’s. Medical scientists of that period
often defined these entities as circulatory disorders of the nerves. It may be helpful to
review the history of CTS as an example of the evolution of modern understanding of the

etiologies of R815.

History of Carpal Tunnel Syndrome
(The following is paraphrased from The History of Carpal Tunnel Syndrome [66] with

additional information from other sources as cited).

Late Nineteenth Century

Sensory changes associated with CTS were first clearly defined by James Putnam
in 1880. He was the first to document nocturnal paresthesias. He eventually suggested
that this new disease entity was caused by circulatory disturbances affecting the median
nerve at the wrist. He ruled out more proximal lesions in the brachial plexus because
there is often bilateral involvement and the symptoms are inconsistent. Franz Schultz, a
contemporary of Dr. Putnam, described sensory symptoms in the median nerve
distribution in his patients. The Schultz study also reported a population similar to that of
Dr. Putnam. These patients were women of middle age who described nocturnal pain or

paresthesias [66].

Early Twentieth Century

Thenar atrophy was described as a separate, unrelated entity. James Ramsey Hunt
described thenar atrophy in 1909, 191 l, 1914 and 1950, relating atrophy to mechanical
compression of the motor branch of the median nerve by the transverse carpal ligament
(TCL). He determined that this disorder was caused by occupational overuse. However,
Dr. Hunt did not believe that the sensory nerve syndrome described by Dr. Putnam was

related to the motor impairment and thenar atrophy.

Pierre Marie and Charles Foix documented compression of the median nerve at
the TCL as the cause of thenar muscle atrophy in a report to the French Neurological
Society in 1913. They described the post mortem dissection of the median nerve of an 80-

year—old woman whose symptoms were known to the physicians before her death. They

were able to describe swelling of the median nerve, thinning distal to the TCL, formation
of a nodule or neuroma just proximal to the TCL, and demyelinization of the median

nerve beneath the TCL.

Early carpal tunnel/median nerve decompression surgeries were performed in the
1920’s [2],[52]. Further definition of “median neuritis” and eventually the term “carpal
tunnel syndrome” was attributed to Drs. Brain and Phalen in the 1940’s and 1950’s [2].
Advances in both diagnosis and treatment of carpal tunnel syndrome have been made as
the prevalence in the population has grown. According to Arle, only 12 cases were
known in the 1950’s, while as many as 15.8% of the working population is known to

have CTS in the current population [3].

Mid Twentieth Century

Post World War 11, women entered the work force in unprecedented numbers,
many taking jobs that required hours of typing, filing, and other tasks deemed “light
work”[34]. It was not expected that this type of work could elicit similar symptoms as the
heavy work previously associated with RSI. As reliance upon the computer expanded in
the 1980’s, studies began to suggest an epidemic of CTS. Dire predictions of 80-90% of
the workforce likely to experience some form of RSI during their work life began to gain
attention. In the 1990’s, CTS rivaled back injury for the most expensive of covered
injuries under workers’ compensation in most developed countries [3]. In recent years,
there has been a deluge of epidemiological, medical and ergonomic research in the area

of RSI and related workstations, physical and medical risk factors, and remedies. Yet no

precise cause and effect relationship between specific vocational tasks and characteristics

of CTS in particular, and RSIs in general, has been defined.

The History of Inflammation
Inflammation is often an early sign of RSI. Several disorders, which are
considered RSIs, are referred to as inflammatory disorders. They will be discussed in
greater detail later in this chapter. Knowledge of the historical development of the
understanding of inflammation may be helpful in understanding the anatomy, histology
and physiology of R81. (The following history of inflammation was paraphrased from

Inflammation, an Upjohn Company publication by Grueme B. Ryan and Guido Majno.)

I650 B.C.

The earliest references to inflammation have been translated from the Smith
Papyrus, a scroll writing in Egypt around 1650 BC, which was derived from an earlier
work that was as much as 1000 years older. This earliest reference to inflammation was
intermingled with the then current knowledge of wounds and infection. The Greeks
continued to relate inflammation and infection closely for a millennium. Roman medicine
did not alter this understanding of the close relationship between infection and
inflammation. However, the Roman writer Cornelius Celsus enumerated the four cardinal

clinical signs of inflammation: redness and swelling with heat and pain.

Late Eighteenth/Early Nineteenth Century

It was not until 1793 that Scottish surgeon John Hunter separated inflammation
from infection, as a “salutary reaction.” Julius Cohnheim, in 1867, wrote the first
description of inflammatory processes in frog mesentery that he was studying under the
microscope in the living state. He observed arteriole dilation with associated increased
blood flow, which eventually decreased. As blood flow slowed, he observed white blood
cells beginning to line the blood vessel walls. He then described diapedesis for the first
time. His hypothesis stated that the permeability of the blood vessels increased during the
inflammatory process. He related his observations to the four cardinal signs of
inflammation, and most of the basis for the modern understanding of the inflammatory
process was established.

Virchow, in his Cellular Pathology, published in 1858, added a fifth sign of
inflammation to the body of knowledge. This sign indicates that an inflamed organ does

not behave normally.

Nineteenth and Twentieth Century

The increase in permeability of the endothelium of the capillary system has been
gradually confirmed and defined over the last 100 years. Most recently, electron
microscopy has captured the various processes of inflammatory changes in the
endothelium. Diapedesis and the increased permeability of the venules to allow the
escape of antibodies and antitoxins and fluid have been documented by electron

microscopy.

The flow of fluid into the tissues, and subsequent accumulation of this fluid,
causes the acute edema in the early stages of inflammation. Fibroblast infiltration with
the exudate allows new connective tissue to be added to, or replace, the fluid that has
accumulated in the tissue. Inflammatory swelling is usually accompanied by pain, which

is either evident episodically or with motion or palpation [75].

Definition of Repetitive Stress Injuries

Repetitive stress injuries (RSI) refer to a category of conditions of the
neuromuscloskeletal system thought to be caused by the performance of repetitive tasks
[4, 33, 34], often including repetitive forceful grasping, pinching, pushing, lifting, pulling
or triggering. Examples of high risk activities include use of a computer mouse, air tools,
typing and hand tools. RSI is usually either vocational or avocational, resulting in a
cumulative trauma to soft tissue. This category of disorders is not a diagnosis. Many
terms are used in conjunction with these disorders. Cumulative trauma disorder, over-use
syndrome, repetitive motion disorder, repetitive strain injury, and musculo skeletal
disorders are among the most popular terms in the literature [33]. For the purposes of this
study, we will use the term repetitive stress injury (RSI) to represent these conditions.
Advances in technology continue to uncover the secrets of the various etiologies of
repetitive stress injuries. Clarification of the definitions of RSI as used in this study will
provide the basis for subsequent discussion of the Methods of Study and Hypotheses.

Clinicians divide repetitive stress injuries into two categories, neurocompressive
disorders and inflammatory disorders. Common neurocompressive disorders, carpal

tunnel syndrome, cubital tunnel syndrome, and Guyon’s canal syndrome, affect the

median and the ulnar nerves. They represent compression of these peripheral nerves in
specific compartments of the wrist and elbow. Inflammatory disorders of the forearm

include lateral and medial epicondylitis and tenosynovitis. These three disorders affect
specific muscles at their point of insertion or at their myotendinous junction, or in their

synovial tendon sheaths.

Neurocompressive disorders
Neurocompressive disorders are caused by mechanical compression, either because of
posture, invasive tissue, edema, or injury to a compartment that increases the pressure on
a nerve sufficiently to reduce or occlude perineural circulation. A brief review of normal

anatomy, histology and physiology as they relate to RSI follows.

Normal anatomy, histology and physiology

Peripheral nerves are usually mixed nerves, and have their beginnings as spinal
nerves [81]. The nerve cell is made up of three parts, the cell body, axon, and bouton or
terminus. Motor nerve cell bodies (efferent) are located within the gray matter of the
spinal cord [53]. The axon is often several feet long and branches to terminate on as few
as one, or as many as 30,000 muscle fibers to form a motor unit. As these axons exit the
spinal cord, they protrude between vertebrae through intervertebral foramina and proceed
through connective tissue compartments to their terminations in the extremities [60].
Sensory nerve cells (afferent) are housed within the dorsal root ganglion. Specialized
nerve endings, which are located in all tissues, may be chemoreceptors,

mechanoreceptors, or nociceptors. Action potentials initiated in these sensory organs, are

10

propagated along their long axons which are eventually housed within the spinal nerve.
They will finally synapse on the intemeurons of the central nervous system.

Nutrients, neural transmitters and other less known substances are manufactured
in the nerve cell body and transported to the terminus of the nerve in a process called
axonal transport [81]. Depending on the substance, either fast or slow axonal transport
moves it along toward the terminus of the nerve. Sustenance of both the nerve and the
muscle cells making up the motor unit is dependent on robust axonal transport [81].

Normal anatomy of the peripheral nerves permits sufficient mobility of the nerve
to allow it to slide as the position of the upper limb is moved through its normal range of
motion. This excursion of the nerve may be as much as 23 mm at the elbow or wrist [37,
87]. Along the length of the nerve, also gliding with it, is a capillary plexus. This plexus
is in two parts, the longitudinal and transverse capillaries. The capillaries are located

within and supply the perineurium, and penetrate deep between the fascicles [45].

Similarities between neurocompressive disorders and inflammatory disorders

Persistent nocturnal or delayed onset pain has been used for decades by clinicians
as the definitive symptom to diagnose repetitive stress injuries, including lateral
epicondylitis, tenosynovitis and CTS [64]. These symptoms often follow exposure to
prolonged exercise. Patient complaints are often transient, non-specific reports of pain,
weakness, and paresthesias in the upper limbs [33, 34]. These symptoms may crescendo
over time. With continued exposure to the injuring force, the symptoms of inflammation
increase until the patient is unable to tolerate the precipitating activity. Once the

individual has been subjected to a repetitive stress injury, the tissue involved continues to

11

be more susceptible to further injury. Recovery is lengthy, and may require a variety of
interventions including absolute rest, change in activity method or resistance, medication,
physical rehabilitation and/or surgery [2, 13, 34, 65]. If one is aware of causal factors,

these injuries are more easily prevented than treated.

Differences between neurocompressive disorders and inflammatory disorders

The most apparent difference between neurocompressive disorders and
inflammatory disorders is the anatomical structure involved in the injury. The mechanism
of injury is also different.

Neurocompressive disorders occur when there is an increase in
intracompartmental pressure inhibiting normal perineural circulation. This pressure
increase may occur because of an individual sustaining an awkward posture, repetitive
increases in finger tip pressure as in typing, or because of forceful grasp [71, 72, 86]. A
neurocompressive disorder often has an insidious onset. Seldom can a specific date or
incident be identified as the causal factor. It is more likely to be a lengthy exposure to an
aggravating activity. The more severe disorders may cause compression sufficient to
displace axons, or interrupt myelination. Diagnostic testing of neurocompressive
disorders is done through electrodiagnostic testing. Nerve conduction studies are the
“gold standard” for defining neurocompressive disorders [41, 52, 55, 56].

Inflammatory disorders often occur after a change in job status, a sudden
exposure to a new task or a change in equipment [33]. Inflammation of muscle is
characterized by an increase in interstitial fluid, complaints of soreness, stiffness or pain

at a specific point in the muscle. Tenosynovitis may be characterized by difficulty in

12

smoothly moving a digit (trigger finger), palpation of fibrous or fluid filled nodules along
the synovial tendon sheath, and pain with active range of motion of the joint moved by
the inflamed tendon. Clinical assessment including manual muscle testing, observation of
edema at the insertion of muscle, and/or pain with palpation over the muscle belly or

insertion of the muscle are classic signs.

Normal Anatomy of Forearm Compartments
The Carpal Tunnel
The carpal tunnel is a rigid, bony ‘C’ shaped canal formed from the eight carpal
bones that make up the wrist. Across the roof of the carpal tunnel is the transverse carpal
ligament, a thickened band of forearm fascia that closes the tunnel. The tendons of the
flexor digitorum profundus, flexor digitorum superficialis, and flexor pollicis longus

muscles, as well as the median nerve, traverse the wrist through the carpal tunnel.

The Cubital Tunnel and Guyon’s Canal

The ulnar nerve traverses the elbow in the cubital tunnel. The floor of the cubital
tunnel is the lateral collateral ligament, which covers a bony groove in the medial
proximal ulna; the roof is a connective tissue retinaculum. The tendon of the flexor carpi
ulnaris inserts into the retinaculum. The nerve then passes between the muscle bellies of
the flexor carpi ulnaris and flexor digitorum superficialis muscles in the forearm. The
ulnar nerve traverses the wrist with the ulnar artery and vein through Guyon’s canal, a

triangular connective tissue compartment. The floor of Guyon’s canal is the transverse

l3

carpal ligament, the roof is the palmar carpal ligament, and the medial wall is the medial

side of the pisiform bone.

Normal Accommodations of the Peripheral Nerves

The cross sectional shape of many peripheral nerves is typically elliptical. The
elliptical shape allows the nerve to alter shape as the flexible compartments are
compressed through muscle contraction or postural changes. The area of the nerve does
not change with the change in shape [48]. This has been shown to be a protective
response to changes in pressure within the compartment [71, 72, 86]. A more detailed
review of the normal anatomy and histology of the median and ulnar nerves may be

found in Chapter II on pages 24-41.

Altered anatomy, histology and physiology of the peripheral nerves of the forearm

Many authors have reported shape, circulatory and histological changes of the
peripheral nerves of the forearm resulting from increased intracompartmental pressure.
These changes may impact neural function in a transient, reversible way or they may
cause permanent, irreversible changes including axonal loss [17, 46, 47, 52, 63].

Carpal tunnel syndrome has been often studied, no doubt because it is vastly more
prevalent than other neurocompressive disorders [13, 18, 65]. Studies of median nerve
compression at the wrist document transient circulatory effects and the subsequent
symptoms, e. g. transient numbness and tingling or pain. Diagnostic testing may

document measurable effects, e. g. diminished circulation measured by Doppler

l4

flowometry and slowed nerve conduction [1, 17, 37, 46, 78]. More information on the
compartments of the wrist, including the carpal tunnel is in Chapter H on pages 32-37.
Compression within a compartment sufficient to occlude perineural circulation,
even if only briefly, will cause an interruption in the oxygen supply to the nerve axon and
a local, reversible physiological block [46]. If the compression is short lived, damage to
the axon may be completely reversed by relieving the compression. If the compression is
sustained for long periods, or is repeated with sufficient frequency, the injury may cause
demyelinzation and or retrograde degeneration of the nerve cell (Wallerian degeneration)
[46]. Ischemia is often mentioned as one of the most prevalent forces contributing to the

blockage of axonal transport, and to increased impact of compression on the nerve.

Anatomical Considerations in Inflammatory Disorders
Inflammation is generally thought of as a symptom. In the context of this study,
we will define inflammatory disorders as those whose primary characteristic is
inflammation. The culprit in these injuries is most often the connective tissue of the
bursa, tendon insertion, tendon sheath, or muscle belly. In order to understand the

implications of inflammation, it is necessary to review the normal anatomy, histology and

physiology.

Normal Anatomy, Histology and Physiology
Fascia covers all cellular components of the body. This is called myofascia when
it covers muscle. This continuous loose irregular connective tissue envelope is non-

contractile, or “inactive.” This is important because proprioceptors, pressure receptors

15

and other sensory organs that provide kinesthetic, proprioceptive, stretch, and
deformation feedback to the central nervous system are housed within this non-
contractile connective tissue [38, 39]. Muscle, tendon, and ligament sensors coordinate
with the fascial sensors to provide comprehensive postural and movement information to
the central nervous system (CNS). The CNS provides feedback to the muscles for

coordination of motion and protection from sprains and strains [38].

Dense Connective Tissue

Tendons, made up of dense regular connective tissue, attach muscles to bone.
Dense regular connective tissue is comprised of parallel collagen fibers with a noticeable
wave, or “crimp” [39]. This allows shock absorption and tolerance to prolonged or
repetitive strain without damage to either the tendon or muscle under normal loads. The
muscle fibers are also covered with loose irregular connective tissue (myofascia). This
tissue envelops the muscle, and as it nears the point of origin or insertion (myotendinous

junction), the connective tissue thickens and joins with the tissue of the tendon.

Muscle

Muscle is highly vascularized by prolific capillary beds that penetrate the muscle
along connective tissue layers, branch to supply adequate nutrition to the muscle fibers,
and transport waste materials out of the muscle [53]. During exercise, water is shifted
between intercellular muscle fiber compartments due to osmotic changes from the

accumulation of lactic acid, a by-product of exercise [80]. This is a simplification of one

16

theory that explains the changes in muscle tissue that allows the identification of active
muscle by magnetic resonance imaging. This will be discussed later in this chapter.
Muscle contraction may take one of three forms. Concentric contraction is when
the muscle shortens in length during activation. Isometric contraction is when there is no
change in muscle length during activation. And eccentric contraction is when the muscle
lengthens during activation [53, 79-81]. More information on muscle anatomy and

histology is available in the Anatomy chapter on pages 32-41.

Altered anatomy, histology and physiology

Increased strain in prolonged resistance, or repeated strain will cause connective
tissue fibers to straighten [38]. During cumulative repetitive activities a tendon may
lengthen and eventually remain in its lengthened state making it more susceptible to
damage at either the osteotendinous or the myotendinous junction [39]. Inflammatory
changes may occur when exposure to repetitive trauma accumulates, causing
microhemorrhages and dissociation between muscle fibers and their points of insertion
into the tendon [34, 69, 77]. Edema is one of the first signs of inflammation, which is

characterized by the accumulation of fluid in the intercellular space.

Delayed Onset Muscle Soreness
Delayed onset muscle soreness (DOMS) is the onset of muscle pain hours or days
after the exposure to the activity that caused the injury [53, 79]. Histological changes are

implicated in DOMS as evidenced by the accumulation of intercellular fluid [53, 79].

17

DOMS has been defined as one of the cardinal symptoms of repetitive stress injury [33,
34, 52].
Examples of Neurocompressive Disorders
Median neuropath y

Carpal Tunnel Syndrome

Carpal tunnel syndrome is the neurocompressive disorder of the median nerve at
the wrist. The median nerve is compressed beneath the transverse carpal ligament within
the carpal tunnel. Some causal factors include prolonged wrist flexion and repetitive
power grasp or pinch. These actions separately, or more powerfully in combination,
cause the long flexor tendons to compress the median nerve against the transverse carpal
ligament, collapsing the perineural circulation. Other common causal factors may include
wrist fracture, edema, and encroachment of muscle fibers from anomalous lumbricals that
invade the carpal tunnel. CTS is characterized by pain or paresthesias in the thumb and
radial two fingers, and the radial half of the third. Tinel’s sign is hypersensitivity of the
nerve to mechanical stimulation. Tinel’s sign is often elicited along the course of the
median nerve in CTS. If untreated, atrophy of the thenar muscles and subsequent loss of

grip and pinch strength may develop [33].

Pronator Syndrome

Compression of the median nerve may also occur as it passes through the pronator
teres muscle in the proximal forearm. The patient presents initially with complaints of
volar forearm pain that may follow repetitive forceful elbow motion [59]. Asking the

patient to pronate the forearm against resistance exacerbates the paresthesias or pain.

18

Ulnar neuropathies

Guyon’s Canal Syndrome

Ulnar nerve compression at the wrist occurs in Guyon’s canal, a small connective
tissue compartment located superficial to the transverse carpal ligament (TCL), beneath
the palmar carpal ligament and just lateral to the pisiform bone. Awkward postures of the
wrist, especially ulnar deviation and wrist flexion during power grasping are causal
factors [34]. Because Guyon's canal is a soft tissue compartment, this syndrome is vastly
less prevalent than CTS. Numbness, paresthesias, or pain in the small and ulnar half of

the ring fingers are symptoms of this disorder.

Cubital Tunnel Syndrome

Cubital tunnel syndrome is a common neurocompressive disorder of the ulnar
nerve caused by repeated valgus stress on the elbow. Because the cubital tunnel is
somewhat superficial, the ulnar nerve is exposed to potential mechanical trauma within
its confines. It may also be exposed to repetitive trauma from forceful flexion of the
elbow against resistance, or with percussive force as in hammering. The ulnar nerve may
also be tethered by anomalous connective tissue or scar tissue within the cubital tunnel.
Pain, paresthesia, and hypoesthesia that radiate about the elbow as well as proximally and
distally along the course of the ulnar nerve, are symptoms and signs of cubital tunnel

syndrome [34, 64].

19

Examples of Inflammatory Disorders

Lateral Epicondylitis

Lateral Epicondylitis is an inflammation of the common extensor tendon of the
forearm. The tendons of four wrist and finger extensor muscles combine to form this
broad tendon: the extensor carpi radialis brevis (ECRB), extensor carpi ulnaris, extensor
digitorum (ED), and extensor digiti minimi. The proximal attachment of the tendon arises
from the lateral epicondyle [60]. The tendon of the ECRB is most commonly inflamed in
this disorder [64]. The combined action of repetitive flexion of the index finger during
powerful grasping, as in activating the trigger of an air nailer, is a common causal factor
of lateral epicondylitis. This motion appears to require eccentric contraction of the ECRB
to stabilize the wrist. When the tolerance of this muscle is exceeded, it becomes inflamed
resulting in lateral epicondylitis. The backhand tennis strike is also such a common causal
factor, that this disorder is nicknamed “tennis elbow” [64]. Delayed onset muscle
soreness (DOMS) is a common symptom. The onset of pain may be delayed for hours or
days from the causal activity, which allows continuation of the activity and increased
severity of the disorder [72]. Once pain has begun, it recurs during the provocative

activity [34].

Medial Epicondylitis

Medial Epicondylitis is inflammation of the tendons of the pronator teres and/or
flexor carpi ulnaris as they insert into the medial epicondyle. Repetitive forceful flexion
of the wrist while grasping a fairly large object is a common causal factor. This disorder

is sometimes called golfer's elbow and housemaid's elbow. DOMS is a common

20

symptom. Once there is onset of pain, repetition of the provocative activity and/or

pressure on the insertion site will cause moderate to severe pain [34].

Tenosynovitis

Tenosynovitis and peritendinitis in the forearm, wrist and hand refers to
inflammation of the tendon sheaths of the long finger and wrist muscles [33, 34].
Forceful, repetitive use of the digits is a major causal factor. Often characterized by
palpable nodules along the length of the tendon sheaths or tendons, localized edema, and
palpable trigger points at the myotendinous junctions, these diagnoses are made through
clinical signs [34]. The patient may be able to indicate a specific date of overuse resulting
in the injury, or may relate a range of dates, wherein changes in the activity level were
noted. Onset of pain, while somewhat delayed, is often more acutely related to a specific
activity, where a specific incident of injury in a compressive disorder is less well defined.

[34].

Method of study
The characteristics of inflammation and repetitive stress suggest that exposure to
repetitive activity would present observable changes in muscles and nerves and their
respective compartments after a short exposure to the activity. These changes would
include vessel dilatation, changes in T2 relaxation times (T2 relaxation time is a
parameter of fluid content in tissue, see Glossary) of muscles and nerves, and increased

fluid levels in the compartments of the wrist and elbow. It would further be expected that

21

some or all of these changes would resolve with prolonged rest. The research design was

developed with these concepts in mind.

Typing as the exercise exposure of choice

Typing was chosen as the exercise exposure because clerical workers represent a
high percentage of the workforce who lose time from work because of RSI. Typing has
been shown to increase intracarpal tunnel pressure [72]. Furthermore, a design using
typing made possible the control of exercise posture, along with maintenance of

proximity to magnetic resonance imaging (MRI) equipment.

Study population

Women experience CTS and some other RSIs more frequently than men. The
ratio of women to men is as high as 5:1 in some populations [13]. For that reason, it was
decided that women would be recruited as subjects for this study. Clerical workers,
specifically professional typists, are more likely to experience some form of RSI, though
clerical workers are more likely to experience symptoms that are transient and poorly
localized. Our asymptomatic subjects were screened for history of previous injury,
diagnosis or recent symptoms. The symptomatic cohort was recruited because they were
experiencing symptoms of upper extremity pain or paresthesias at the time of the study.
Each individual also reported a diagnosis. Two reported diagnoses of CTS, four reported
diagnoses of lateral epicondylitis, and one reported a diagnosis of tenosynovitis. All had
similar symptoms of forearm pain and/or paresthesias. Some reported delayed onset

(DOMS) or nocturnal pain and/or paresthesias.

22

Imaging Method

Magnetic Resonance Imaging (MRI) was chosen as the evaluation technique. This
non-invasive technique provides high-resolution axial images that lend themselves well
to quantification of size, fluid content and changes in shape or position of the tissue under
study. More information on the MRI techniques used in this study is available on pages
45-46.

Summary of Findings

Muscle T2 Changes and active muscle identification

Investigators in this study were able to differentiate between muscles more and
less active during typing through the use of MRI T2 relaxation times. T2 weighted
images show unbound water as brighter than bound water. During exercise a number of
metabolic factors that are well documented in the literature combine to briefly increase
the T2 relaxation time in muscles performing concentric contraction [19-21, 68]. While
the most intense interval of T2 relaxation time increase is short lived, approximately 30

minutes, this phenomenon allowed the investigators to identify particular muscles active

in typing.

Changes in morphology of the nerves at the wrist
The investigators were further able to observe the median and ulnar nerves at the
wrist, and to compare and contrast their morphology at baseline, prior to activities of the

day, immediately after typing, and after 8 hours of rest. T2 changes were measured and

23

the visible morphologic changes in the nerves and their compartments were documented
in the dominant forearm of each subject by MRI.
More complete information on the methods used in this study is available in

Chapter III on pages 42-52.

Hypothesis development

Contrasting muscles more and less active in typing

At the outset of this study, several hypotheses were developed from the literature.
It is known, for example, that exercising muscle has a measurable increase in T2
relaxation time when compared to rest. One expectation of this study was to contrast
muscles active and inactive in typing. Inflamed tissue has the tendency to have increased
T2 relaxation time [55, 56] with MRI examination. For that reason it was expected that
the T2 relaxation time increases in muscles of symptomatic subjects after typing would

be more dramatic than those of asymptomatic individuals. This was not what was found.

Changes in Neural Morphology

Nerve morphology changes when challenged by increases in pressure from
muscle contraction or posture. Investigators in this study expected the shape and size of
the nerves of symptomatic subjects to change more than those of the asymptomatic
subjects. This proved to be incorrect. As the study progressed, an explanation became
apparent, and will be discussed in Chapters IV and V.

Study investigators also expected T2 relaxation times of nerves of both
symptomatic and asymptomatic subjects to vary with exposure to typing when compared

to rest. The variation and trend of the changes became one of the most interesting aspects

24

of this study. More information on results can be found in Chapters IV and V, pages 63-

72, 83-87.

25

CHAPER II

ANATOMICAL REVIEW OF THE UPPER EXTREMITY AS IT RELATES TO
REPETITIVE STRESS INJURY

Human function is unique, in part, because we are able to use our hands to carry
out complex tasks. The upper limb is designed to execute these tasks as quickly as the
brain invents them. High levels of communication between the central nervous system
and the upper extremity make this possible. The muscles that provide motor function to
the hand have one of the highest ratios of motor neurons, connecting the hand muscles
with the central nervous system, to muscle fibers [81]. The skin of the hand is similarly
invested with sensory receptors [81]. The combination of sensibility and motor control
creates one of the most sensitive and coordinated systems of the body. The distance these
neurons travel makes them vulnerable to compression as they twist and turn through a
system of compartments traveling from their origins in the central nervous system to their
points of termination. It is necessary to understand the course of the nerve and blood

supply from their beginnings to identify distal neural impairments.

Neural and Vascular Pathways
Neural and vascular structures have different origins. Nerves, veins and arteries
join to form neuro-vascular bundles that allow them to travel together from their
proximal origins to their distal terminations. The bony skeleton and connective tissue
compartments that provide conduits for the neuro-vascular bundles support the neuro-
vascular bundles. An understanding of the close physical and functional associations
between neural and vascular structures will be valuable in this study of repetitive stress

injuries (RSIs). Many RSI syndromes have both neural and vascular components,

26

etiologies, and symptoms. RSIs are usually associated with particular anatomical regions.
The following anatomical review of the upper extremity will define anatomical regions
and several of the associated repetitive stress injuries.

First, it is necessary to review a few terms that allow anatomical descriptions to
be consistent and concise. Examination of the body can be accomplished using many
imaging techniques (such as Magnetic Resonance Imaging, x-ray, or ultrasonography) or
through more hands on examination (such as physical, palpatory or goniometric
techniques). Anatomical nomenclature is used to identify consistent reference points and
perspectives. The present study will use a number of Magnetic Resonance Imaging
(MRI) methods. The images that are a result of MRI techniques are often referred to as
"slices." Sagittal sections (at the mid-line) and parasagittal sections (on either side of the
mid-line) divide the left side of the body from the right. Coronal slices run from side to
side, dividing anterior from posterior. Axial slices are perpendicular to the longitudinal
plane [60]. Axial examinations are the most useful for the assessment of the
compartments of the upper limb and are the images primarily used in this study (Figure
2.1).

A brief summary of the anatomical structures that are involved in repetitive stress
injuries follows. Included in the summaries of the anatomy are examples of the
mechanisms of common RSIs. Anatomical structures will be reviewed regionally,

proximal to distal.

27

The Neck and Shoulder

The head is borne by the vertebral column. The cervical vertebrae provide both
mobility and support for the head, while acting as a conduit for sensory and motor neural
components and sites of origin for neck and shoulder muscles. The vertebral foramina are
areas of potential impingement. Hemiation of the intervertebral discs, arthritic changes
reducing the size of the foramina, or an injury causing impingement of the nerve roots
(radicals) may cause a radiculopathy. A radiculopathy affects motor and sensory function
the full length of the peripheral nerve. Symptoms are usually exacerbated with range of

motion of the neck, which increases the pressure on the impinged spinal nerve [52].

The Brachial Plexus

The brachial plexus is the nerve center for the upper extremity. It is formed from
the anterior primary rami of cervical nerve roots C5 — Tl. As the anterior rami emerge
from the foramina, they form the trunks of the brachial plexus and pass between the
anterior and middle scalene muscles. If these muscles are hypertrophied from overuse or
are in spasm, they may compress the roots or trunks directly. The scalene muscles
originate from the transverse processes of the cervical vertebrae and insert on the first and
second ribs.

Hypertonicity or spasm of the anterior and middle scalenes may cause the first rib
to compress the brachial plexus and/or the subclavian artery, which travels with the
brachial plexus as it passes through the scalene muscles. This is one causal factor of
Thoracic Outlet Syndrome (TOS), which may be either a circulatory disorder of the upper

limb, or a neurogenic disorder. Neurogenic TOS is caused by direct compression of the

28

brachial plexus, and often causes poorly localized paresthesias, hypoesthesia and pain.
An anomalous cervical rib may compress either the brachial plexus or the subclavian
artery and cause TOS. Symptoms/signs of TOS are paresthesias, sometimes well
localized and sometimes spread throughout the upper extremity, and circulatory changes
including cyanosis of the affected arm. The patient will have decreased tolerance for

overhead activities such as washing, styling or drying their hair [52].

Trunks, Divisions, Cards and Branches

Distal to the nerve roots, the anterior rami combine to form the superior (C5 and
C6), middle (C7) and inferior (C8, Tl) trunks. The trunks then divide into the anterior
and posterior divisions. The lateral cord is formed by the anterior divisions of the
superior and middle trunks. The medial cord is formed by the continuation of the anterior
division of the inferior trunk. The posterior cord is comprised of the unification of all the
posterior divisions of the three trunks. The lateral, posterior and medial cords tuck under
the clavicle with the subclavian artery. The cords then divide into branches, which
become the named nerves supplying the shoulder, arm and forearm. The lateral pectoral
(thoracic), musculocutaneous, and lateral component of the median nerve derive from the
lateral cord. The ulnar nerve and medial contribution of the median nerve derive from the
medial cord, as do the medial pectoral, medial brachial cutaneous, and medial
antebrachial cutaneous nerves. The upper subscapular, thoracodorsal and lower
subscapular nerves derive from the posterior cord just proximal to the formation of its

terminal branches, the axillary and radial nerves [45, 60].

29

Nerves of the Upper Extremity

These nerves enter the arm just inferior to the glenohumeral joint. The
musculocutaneous nerve exits the axilla and is located between the biceps brachii and
brachialis after piercing the coracobrachialis muscle. The lateral antebrachial cutaneous
nerve is the continuation of the musculocutaneous nerve [60]. The median nerve exits the
axilla with the brachial artery. They traverse the arm on the surface of the brachialis
muscle. The ulnar nerve lies parallel to the median nerve, brachial artery and veins until
approximately mid-humerus. It then separates and penetrates the medial intermuscular
septum to enter the posterior compartment. It completes the path through the arm on the
medial aspect of the triceps muscle [74]. The radial nerve leaves the axilla between the
long and medial heads of the triceps muscle. It enters the radial groove with the radial

artery where it wraps around the humerus from medial to lateral.

The Skeletal Armature

The thoracic vertebrae not only support the cervical vertebrae, but the rib cage as
well. Each rib articulates first with the thoracic vertebra, then encircles the neck or chest
and articulates with the sternum, either directly through their own costal cartilage (true
rib) or indirectly through the costal cartilage of the rib immediately above (false ribs)
with the exception of the last two ribs which do not articulate with the sternum (floating
ribs) [60]. The clavicle, or collarbone, is an 'S' shaped long bone that articulates with the
sternum proximally and the scapula distally. The synovial stemoclavicular joint is the

only articulation between the axial skeleton and the upper extremity [60]. The very dense

30

interclavicular ligament provides limited mobility and tremendous strength to this

articulation. A fibrocartilage disc provides shock absorption within the joint.

Osteology of the Shoulder

The bony structure of the upper limb, the appendicular skeleton, is designed to
allow maximal mobility as a priority, with the sacrifice of some stability and weight
bearing ability compared to the more ligamentous and bony joints of the lower limb. The
proximal articulations of the arm include the shoulder joints. This complex joint includes
the articulation of three bones, the clavicle, scapula and humerus. The clavicle provides
the only direct articulation with the axial skeleton at the stemo-clavicular joint. Mobility
of the shoulder is enhanced by the muscular attachment of the scapula to the dorsal rib
cage and vertebral column. The concave anterior scapula, encased in muscle, glides over
the convex rib cage.

The shoulder joint is formed by a "ball and socket" joint at the apex of the
posterior scapula. The humeral head articulates with the scapula at the glenoid process
(glenohumeral joint). This relatively small articular fossa is enlarged by the glenoid
labrum, a ring of fibrocartilage, which increases the articular surface and depth of the
glenoid fossa. Shoulder stability is maintained through the acromioclavicular joint

superior to the glenohumeral joint [59, 60, 74].

The Course of Neural and Vascular Structures Supplying the Upper Limb

Circulatory structures that supply the upper extremity are of interest to the

investigators in this study of repetitive stress injuries. Arteries provide oxygenated blood

31

to the extremities. Deep veins accompany, and are usually named for, the associated
arteries. Deep veins, arteries and nerves often travel together in neuro-vascular bundles.
A description of the arterial pathways helps to summarize the course of the major
vessels through the upper limb. Arterial vessels branch from the arch of the aorta. The
brachiocephalic trunk branches into the right subclavian and carotid arteries; on the left
the subclavian and carotid arteries branch directly from the aorta. The subclavian artery
ascends and crosses the length of the clavicle, then crosses the first rib distally where it
becomes the axillary artery. The axillary artery changes names again, to the brachial
artery, after it crosses the teres major muscle and enters the arm. At approximately one
third of the length of the humerus, the deep brachial artery branches off to accompany the
radial nerve in the radial groove of the humerus, while the brachial artery continues
through the arm, accompanied by the median nerve, between the brachialis and biceps

brachii muscles [60].

The Elbow

The course of the Radial Nerve

The radial nerve emerges between the brachialis and the brachioradialis muscles
to cross the elbow laterally, entering the cubital fossa lateral to the biceps brachii tendon
as the biceps inserts into the radius. The radial nerve divides into the deep (muscular) and
superficial (sensory) branches. The deep branch pierces the supinator muscles in a fibrous
band, known as the “arcade of Frohse,” to become the posterior interosseous nerve, and is
vulnerable to impingement from spasm of the supinator [2]. This is sometimes diagnosed

as a vocational repetitive stress injury.

32

The Course of the Median Nerve

The median nerve also crosses the elbow in the cubital fossa medial to the biceps
brachii tendon, deep to the bicipital aponeurosis. It follows the continuation of the
brachial artery into the cubital fossa, and then accompanies the ulnar artery distally,
finally passing through the flexor/pronator compartment of the forearm between the
flexor digitorum superficialis (FDS) and flexor digitorum profundus (FDP) without an
accompanying artery, or less commonly, with the persistent branch of the median artery.
Here it innervates the majority of the extrinsic muscles and provides articular innervation
to the elbow [60]. The median nerve continues through the forearm between the FDS and

FDP until it enters the wrist.

The Course of the Ulnar Nerve

The ulnar nerve enters the arm anterior to the subscapularis muscle and teres
major and minor, and then follows the triceps muscle to the elbow. It traverses the elbow
within the cubital tunnel at the ulnar notch of the medial epicondyle. This tunnel is
formed by the aponeurosis between the two heads of the flexor carpi ulnaris muscle
distally, and a thin fibrous structure extending from the olecranon to the medial
epicondyle known as the cubital tunnel retinaculum. The ulnar nerve then joins the ulnar
artery in a neurovascular bundle between the ECU and FDS. The ulnar nerve continues
through the forearm between these muscles until it enters the wrist superficial to the

transverse carpal ligament in Guyon’s canal [25, 26, 60].

33

The cubital tunnel is an area of compression of the ulnar nerve, as is Guyon’s
canal. Ulnar neuropathies are the second most common peripheral neuropathy of the
upper extremity. One possible cause of compression is thickening of the cubital
retinaculum. According to Fritz, 22% of the population is subject to this anatomical
variation, which causes dynamic compression. In 11% of the population an anomalous
muscle, the anconeus epitrochlearis, which causes static compression of the ulnar nerve,
may replace the retinaculum [25]. Trauma to the ulnar nerve is more likely at the cubital
tunnel than at Guyon’s canal because Of the distance the ulnar nerve travels superficially,

exposing it to a higher potential for trauma [2].

Compartments of the Forearm
Muscles that move the wrist, hand and fingers attach at the elbow and along the
length of the forearm. The muscles are divided into flexor and extensor compartments
within the bony and fascial compartments of the forearm (Figure 2.2). These
compartments are defined by location, function and innervation. Neurovascular bundles

travel between muscles in fascial compartments [60].

The Extensor Compartment

The extensor-supinator compartment components are the extrinsic (outside the
hand) extensor muscles of the wrist, fingers and thumb. The radial nerve and its branches
innervate the muscles in this compartment. These muscles extend the wrist and fingers as
well as adduct, abduct, and supinate the forearm. The extensor carpi radialis longus

(ECRL) originates on the lateral supracondylar ridge of the lateral epicondyle. The

34

tendons of the extensor carpi ulnaris (ECU), extensor digitorum (ED), extensor carpi
radialis brevis (ECRB) and extensor digiti minimi (EDM) form the common extensor
tendon as it inserts on the lateral epicondyle. The supinator muscle partially originates on
the lateral epicondyle, as well as the radial collateral and annular ligaments of the elbow,
supinator fossa and crest of the ulna before it wraps around the circular radial head where
it inserts. The thumb muscle group (extensor pollicis brevis (EPB), extensor pollicis
longus (EPL) and abductor pollicis longus (APL)) is also within this forearm

compartment [59, 60, 74].

The F lexor-Pronator Compartment

The flexor-pronator compartment is on the anterior surface of the forearm,
separated from the extensor-supinator compartment by the interosseus membrane of the
radius and ulna. The flexor-pronator compartment is further divided into deep and
superficial muscles. The five superficial muscles primarily attach to the medial
epicondyle through the common flexor tendon. The pronator teres, flexor carpi radialis
(FCR), palmaris longus, flexor carpi ulnaris (FCU) and flexor digitorum superficialis
(FDS) are forearm pronators, wrist flexors and extrinsic finger flexors. Deep muscles in
this group include the flexor digitorum profundus (FDP), flexor pollicis longus (FPL) and
pronator quadratus. FDP and FDS are extrinsic (outside the hand) flexors of the digits
(fingers). The FDP flexes the distal interphalangeal joint of the fingers; the FDS flexes
the proximal interphalangeal joints (PIP). The FPL flexes the IP joint of the thumb [59,

60, 74].

35

The Wrist

The wrist is the highly dynamic link between the forearm and the hand. It is the
main conduit of nerves and circulatory vessels that serve the hand. The complex bony
joints of the wrist provide both strength and mobility for hand position and function. The
wrist provides the bony fulcrum for long flexor and extensor tendons, and allows infinite
repositioning of the hand during activity. Significant research has been done to
characterize “accessory motions”, the intercarpal motions of the carpal bones and their
ligaments, as they respond to the demands of voluntary activity.

In the current literature the accessory motions of the carpus, as well as primary
motions of the articulations of the long bones of the forearm and hand with the carpus,
have been described as causing minute deformations of the bony carpal tunnel and its soft
tissue constituents [43, 44, 71, 72]. These deformations create the potential for
compromise of neural, vascular, connective, and lymphatic tissues that pass through the
finite space of the carpal tunnel. Risk of repetitive trauma increases with the rates of
force, speed, and repetition of the task, which in turn, increases the effect upon the
contents of the carpal tunnel.

Magnetic Resonance Imaging studies of carpal tunnel syndrome (CTS) have
shown particular characteristics of the median nerve and other soft tissue constituents of
the carpal tunnel. These include increased T2 signal intensity of the median nerve,
increased fluid content of the tendon sheaths and other compartments, and bowing of the
flexor retinaculum over the median nerve [55, 56, 58, 61]. The axial imaging levels at
which these phenomena occur are identified by prominent bony landmarks of the wrist

clearly visible on magnetic resonance images. A description of these levels follows.

36

Proximal to the Transverse Carpal Ligament

For the purposes of this study, the area just distal to the distal radioulnar joint and
the radial and ulnar styloids, but before the appearance of the proximal lunate as it
articulates with the distal radius, is defined as “Proximal to the Transverse Carpal
Ligament” (Figure 2.3). The transverse carpal ligament (TCL) is used interchangeably in
the literature with the flexor retinaculum.

The distal radioulnar joint (DRUJ) is bound on the palmar aspect by ligaments,
which give rise to the floor of the carpal tunnel. The radius fits into the radial sulcus of
the distal ulna and is able to rotate about the ulna, permitting pronation and supination of
the forearm. The pronator quadratus is one of the prime movers of pronation in its
position covering the palmar surfaces of the distal radius and ulna. A thin layer of fat fills
the Parona space covering the pronator quadratus. This underlies the bed of the flexor
tendons, median and ulnar nerves, and the vessels of circulation that supply the wrist and
hand. The forearm fascia, which encases the forearm just deep to the skin, thickens and is
referred to as the palmar carpal ligament at this level [60].

Current studies of median nerve compression (carpal tunnel syndrome) describe
changes in the shape of the median nerve visible on MRI examination [6, 8, 12, 47, 55].
The median nerve is usually round or oval in undiagnosed or asymptomatic subjects at
this point, and is often flattened in symptomatic subjects [54]. The median nerve may be
swollen and demonstrate an increased T2 signal intensity in patients with CTS. The

sheath of connective tissue and fat surrounding the nerve is expected to be relatively thin

37

at this point. A definite separation between the nerve and connective tissue is often
visible as a dark line on T2 weighted images.

The ulnar nerve is usually oval at this level. It may be triangular or flattened in
patients with ulnar neuropathy at the wrist. While this has not been quantified to date,
characteristics similar to those of CTS may be noted. These include increased T2 signal
intensity, flattening or shape changes of the ulnar nerve, soft tissue inflammation and
fluid within Guyon's canal.

The long flexor tendons of the flexor digitorum profundus (FDP) and superficialis
(FDS), flexor pollicis longus (FPL) as well as the median nerve organize into layers as
they prepare to enter the carpal tunnel. They are enveloped in tendon sheaths from
proximal to the flexor retinaculum to the distal metacarpals (fifth finger to distal
phalanx). The flexor carpi radialis (FCR) tendon is not considered to be a constituent of
the carpal tunnel, even though it passes through the bony compartment. It enters the wrist
in its own fascial compartment along the radial aspect of the carpal tunnel before
inserting on the second metacarpal. The palmaris longus tendon is central and superficial
to the TCL, and terminates in a long thin tendon that blends into the palmar fascia. The
flexor carpi ulnaris tendon is the most medial structure in the volar wrist. It inserts first
on the pisiform bone, then the fifth metacarpal [60, 74].

The extensor, or dorsal, compartment proximal to the transverse carpal ligament
houses the extensor and abductor tendons of the digits. These tendons are housed within
tendon sheaths, which produce synovial fluid to provide lubrication. One surface
landmark used in examination of the wrist is the anatomical snuffbox. This hollow

depression in the lateral wrist is formed by the tendons of the abductor pollicis longus

38

(APL) and extensor pollicis brevis (EPB) ventrally, and the extensor pollicis longus
dorsally. The cephalic vein overlies the anatomic snuffbox and is one of the visible
landmarks helpful in orienting one’s self when one is studying images of the wrist.
Dorsally the radial artery passes deep to the APL and EPB to enter the anatomic
snuffbox. The extensor pollicis longus courses radially, superficial to the extensor carpi

radialis longus and brevis tendons.

Level of the Pisiform

The bony landmark used to define the proximal segment of the carpal tunnel is the
pisiform bone. The bones of the proximal carpal row, from lateral to medial are the
scaphoid, lunate, and triquetrum. The sesamoid bone, Pisiform, rests on the anterior
surface of triquetrum. The transverse carpal ligament (TCL) is formed when the volar
component of the antebrachial fascial thickens distal to the distal radioulnar joint. The
term "transverse carpal ligament" is used interchangably with the term "flexor
retinaculum of the wrist [31, 35]."

The TCL only attaches to carpals. The lateral attachments are proximally the
scaphoid and distally the trapezium. Medial attachments are the pisiform proximally and
the hook of the hamate distally. The TCL forms the roof of the carpal tunnel. The flexor
tendons, flexor digitorum superficialis (FDS), flexor digitorum profundus (FDP) and
flexor pollicis longus (FPL) organize into layers to pass through the finite space of the
carpal tunnel. The tendons of the FDP are deep, whereas the FDS tendons are more
superficial and medial to the FPL. The median nerve has some variability in its location.

However, it is usually superficial to the FDS, lying between the FDS and the tendon of

39

the FPL [51]. The retinaculum is least rigid in this region as it attaches on the mobile
Pisiform medially, with a rigid base at its lateral attachment to the scaphoid [60].
Guyon’s canal is medial and superficial to the carpal tunnel. The floor is the
transverse carpal ligament as it covers the pisiform and hamate bones (distally), the roof
is the palmar carpal ligament, and the medial wall is the pisiform bone. Guyon’s canal
houses the ulnar nerve (medial), artery and vein (lateral) (Figure 2.4). A small fat pad
provides cushion for the ulnar artery and nerve within the canal. The ulnar nerve, artery
and vein enter Guyon’s canal just palmar and external to the roof of the flexor
retinaculum on the ulnar side of the wrist. As the ulnar nerve and artery pass distally in
Guyon’s canal, they divide into their superficial and deep branches. The veins follow a

similar course to the arteries.

Level of the Hook of the Hamate

Bones of the distal carpal row from medial to lateral are the hamate, capitate,
trapezoid and trapezium. The hook of the hamate forms the ulnar wall of the carpal
tunnel, as well as the attachment site of the TCL and deep wall of Guyon’s canal [59, 60].

The TCL is generally seen as straight or slightly convex at this level as it extends
between the hamulus of the hamate to the tubercle of the trapezium on MRI. The palmar
capitate-scaphoid and palmar capitate-trapezium ligaments contribute to the deep walls of
this segment of the carpal tunnel (Figure 2.5) [59, 60, 74]. The median nerve maintains
its relationship to the other carpal tunnel structures as described at the level of the
proximal carpal tunnel, but may assume atypical positions and shapes depending on the

position of the wrist.

4o

The Hand
No anatomical review of the upper limb is complete without at least a brief
summary of the hand. Because the hand is the termination of the muscles, nerves and
blood vessels discussed throughout this study, a basic understanding of its systems

provides insight into the effects of RSI.

Osteology of the Hand

Distal to the carpal bones are the five metacarpals. These form the palm and the
base of the thumb. The transverse carpal ligament ends just proximal to the heads of these
long bones. The metacarpals maintain a concave transverse arch from their articulations
on the carpals (Figure 2.6). Articulating with each of the metacarpals are the phalanges,
or finger bones. These long bones provide the bony support and levers for grasp and
pinch. Each articulation is designed to provide either single plane motion, as in the hinge
joints of the interphalangeal joints, or mobility as in the saddle joint of the

carpometacarpal joint of the thumb.

Hand muscles: Intrinsic

Intrinsic muscles originate and insert within the hand. The intrinsic thenar, or
thumb, muscles originate from the TCL, trapezium and the scaphoid bones. The
hypothenar, or small finger, muscles arise from the pisiform bone, the hamate bone, the
tendon of the flexor carpi ulnaris, and the flexor retinaculum. The interosseous muscles

are divided into the palmar and dorsal interosseii. These muscles lie between the

41

metacarpals, where they attach in order to abduct and adduct the fingers. There are four
lumbrical muscles, numbered from lateral to medial, which flex the metacarpophalangeal
joints and assist in full extension of the proximal interphalangeal joints. They arise from
origins on the sides of the extensor expansions of the digits, and insert on the tendons of

the flexor digitorum profundus [60].

Hand muscles: Extrinsic

The tendons of the long finger and thumb flexors fan out from the carpal tunnel as
they approach their insertions on the digits. The flexor digitorum superficialis terminates
on the proximal middle phalanx of digits 2-5, where it is a primary flexor of the proximal
interphalangeal (PIP) joints. The flexor digitorum profundus inserts on the distal
phalanges of digits 2-5, where it is the only flexor of the distal interphalangeal (DIP)
joints. The flexor pollicis longus inserts on the base of the distal phalanx of the thumb,

where it is the only flexor of the interphalangeal joint of the thumb.

Integument and fascia

The skin of the palm is very thick and is characterized by deep flexion creases.
The palmar fascia is a continuation of the antebrachial fascia. It is well defined and thick
in the central palm, but it is thinner where it covers the thenar and hypothenar eminences.
This fascia provides excellent padding for the soft tissue structures of the hand [60].

The dorsal skin is wrinkled, with especially deep wrinkling present over the joints
of the digits. This permits the skin to stretch over the joints and enhances flexibility Of the

hand.

42

Nerves, Arteries and Veins of the Hand

The radial and ulnar arteries and veins form the superficial and deep arterial
arches of the palm. The superficial arch gives origin to the common and digital arteries
and veins of the digits. The median and ulnar nerves fan out as they emerge from the
carpal tunnel and Guyon’s canal to supply both motor and sensory innervation to the
hand. The median nerve supplies the lateral hand, as well as the thumb, index, long, and
lateral half of the ring fingers with sensation. The recurrent median, a branch that
typically arises just distal to the TCL, innervates the muscles of the thenar eminence.

The deep branch of the ulnar nerve innervates the adductor pollicis, the
hypothenar muscles, palmar and dorsal interosseii, and the medial two lumbricals. Its
sensory distribution includes the medial hand, medial half of the ring finger, and the little
finger. The superficial radial nerve terminates as it provides sensory innervation to the

lateral, dorsal hand and thumb [59, 60].

43

CHAPTER III

Materials and Methods

Clerical workers have been shown to be at higher risk than the general population
for repetitive stress injuries. Long hours of rapid data entry with minimal postural
changes, poorly designed workstations, and poor upper extremity conditioning for the
work are some of the risk factors [52, 65]. The population with the highest incidence of
repetitive stress injuries of the upper extremity includes women between the ages of 21

and 55 [3, 12, 13, 82].

Study Population

Thirteen female volunteers between the ages of 21 and 52 were recruited from the
patient base of physicians participating in the study as investigators and a local
rehabilitation center, Michigan State University clerical employees, and contract
transcriptionists associated with the physician practices, the rehabilitation center, or a
local hospital. All subjects were active as typists with a job requirement of three hours of
production typing per day. This is equal to the length and rate of typing exposure for this
study.

The asymptomatic cohort included 6 female typists; ages 21 - 52 mean age 38.
The symptomatic cohort included 8 female typist subjects 21 — 52, mean age 44 (Figure
3.1). A standard 'T' test was used to show that the difference in mean ages between
cohorts was not statistically significant. One subject from each cohort acted as a non-

typing control as well as a typing subject.

Study Objectives

The intent of this study was to establish an imaging and exercise protocol and test
hypotheses related to symptoms of delayed onset sensory disturbances including pain and
paresthesia. We elected to include symptomatic subjects previously diagnosed with any
repetitive stress injury of the forearm for this small cohort, as long as the subject reported
symptoms of forearm pain and/or paresthesias. All symptomatic subjects were
previously diagnosed with either carpal tunnel syndrome, tenosynovitis, or lateral

epicondylitis of the dominant limb.

Experimental Design

Subject Selection

Subjects were interviewed for medical and work history, and then placed in either
the asymptomatic or symptomatic cohort. Each subject identified her right hand as
dominant. Volunteers with a history of previous injury or surgery to the dominant wrist,
metabolic conditions such as diabetes or rheumatoid arthritis, or current pregnancy were
excluded from this study. Each subject completed a medical history questionnaire (Figure
3.2), an informed consent form (Figure 3.3) approved by the University Committee on
Research Involving Human Subjects (UCRIHS), and the Levine Carpal Tunnel
Syndrome Symptom Severity Scale (Figure 3.4), and Functional Status Scale (Figure
3.5). The investigators used the results from these surveys to quantify symptoms and
complaints [50, 76]. Subjects in the asymptomatic group scored 1.0-1.125 on the Levine

Symptom Severity Scale and 1.0 on the Functional Status Scale. Symptomatic subjects

45

scores ranged from 1.36 to 2.37 on the Levine Symptom Severity Scale, and from 1.0 to

3.0 on the Functional Status Scale.

Physical Examination

Following placement in the appropriate cohort, each subject was scheduled for a
physical examination of the dominant extremity. The physical examination was used to
document performance differences, if any, between subjects and between the
symptomatic and asymptomatic groups. The physiatrist or physiatry resident recorded the
results of the physical examinations on a standard form (Figure 3.6).

The physical examination included provocative testing used by many clinicians to
diagnose repetitive stress injuries. Among the provocative tests, the examiner attempted
to elicit Tinel' 5 sign. The examiner used percussion of his/her finger tips along the course
of the median and ulnar nerves at points as they approach the skin in an attempt to elicit
shooting pain or paresthesia. The examiner also performed Phalen's test, which elicits
radiating pain and/or paresthesia if positive. Each subject was directed to place the backs
of her hands together in what may be described as a reverse prayer position (Figure 5.1).
Proprioception screening of wrist and fingers, and reflex testing of the biceps, triceps and
brachioradialis tendons were performed.

Strength was quantified by manual muscle testing of shoulder flexion and
abduction, elbow flexion and extension, wrist flexion and extension, radial and ulnar
deviation, finger extension, finger abduction and thumb abduction. Each subject

performed three trials of power grasping using the Jamar dynamometer grip test at the

46

second setting. Each subject also performed three trials each of pinch testing of lateral,
three jaw chuck and tip pinches.

Sensory nerve conduction studies were done using the ulnar nerve on the
ipsilateral side as the control. A physiatrist or physiatry resident performed the physical
examination and sensory nerve conduction studies. A standardized data sheet was used to

record the physical examination results.

Magnetic Resonance Imaging Examination

Following the physical examinations, the examiner prepared each subject for the
first magnetic resonance imaging (MRI) examination of the dominant forearm. Precise
positioning and repositioning of the subject's right arm in the MRI magnet is vital for
accurate comparative measurements of diameter, area and signal intensity of the tissue
under study. Prior to the first imaging session, the investigator used an indelible marker
to place a crosshatch on the surface landmarks denoting the lateral epicondyle and the
approximate center of the forearm muscle bulk to assure accurate positioning for each
imaging session. The dorsum of the carpal tunnel was outlined using an 'H' that was
drawn on the skin with the parallel legs of the 'H' across the distal radius and ulna and
bases of the metacarpals with the cross bar in the longitudinal center of the wrist. The
markings were visible when the subject's arm was placed in either the extremity or wrist
coil. The cross hatch was used to indicate the "zero point" for imaging within the magnet

in a procedure called "land marking."

47

Imaging Position

A General Electric Signa 1.5 Tesla magnet and small extremity coil for the
forearm muscle bulk and elbow were used to image each subject’s right forearm. The
examiner positioned each subject in the magnetic resonance imaging magnet in a
modified swimmer’s position with the arm outstretched in shoulder flexion, elbow
extension, with the hand prone within the small extremity coil. The crosshatch mark on
the approximate center of the muscle bulk was used to center the forearm in the extremity
coil and “land mark” the forearm in the magnet core. Dual echo T2 weighted spin echo
images with different TE's (TR 1500/TE 60; TR 1500/T E 30) were obtained from the
proximal radial head through the musculotendinous junctions of the forearm flexors. TE,
or echo time, is the time in milliseconds between the radio frequency perturbation pulse
and the greatest induced signal. Each subject was then repositioned for imaging of the
elbow.

The mark on the lateral epicondyle was used to "landmark" each elbow within the
extremity coil. The elbow images were fast spin echo (FSE) (TR 1500 TE 80 and 15,
echo train length 8), FSE with fat saturation (TR 1500 TE 80 and 15 ETL 8), and gradient
echo (TR 700/TE 21, flip angle 40, Nex 2).

Each subject was then repositioned in side lying for the wrist images. The wrist
was placed in a small wrist coil with the wrist and hand supported in a neutral position,
wrist at 30°, fingers extended, by a thermal plastic resting pan splint (Figure 4.1). Fast
spin echo (TR 2000/ TE 16.0; TR 2000/T E 80.0 ETL 8, 512 x 256 Nex 2), fast spin echo
with fat saturation (TR2000/T E15, 512 x 256 Nex 2) and gradient echo (TR700/T E 21.0

flip angle 40, 512 x 256) images were obtained. Total image collection took one hour.

48

Typing as the Exercise Exposure

After the baseline MRI examinations were completed, the subjects then typed for
3 hours at a rate of approximately 50 words per minute. They were allowed one 15-
minute break mid way in the typing session. Each subject was provided with a
workstation that was adjusted for comfort and correct ergonomic position. Subjects were
encouraged to type as rapidly as they were able, and to continue until they were informed
of their break or the time to stop for the day. Typing material was not controlled, so each
typist either provided their own material, or they were provided with a book or magazine

IO USC.

Imaging After Typing

A second set of images was collected with the above protocol after the subjects
completed three hours of typing. Muscle bulk images were begun less than 10 minutes
after typing was discontinued, and collection of these images took approximately 6
minutes. As metabolites of muscle contraction are reabsorbed, particularly calcium and
sodium, free water and unbound hydrogen that increased in the muscle tissues during
eccentric contraction diminish in the tissue and return to a resting level. This causes T2
changes to begin to resolve between 20 and 30 minutes after discontinuation of the
exercise exposure [19, 57, 68]. Subjects needed to be moved quickly from typing into the
imaging position in the magnet for muscle studies.

Every attempt was made to duplicate the earlier imaging positions using surface
markings. Images from these studies were used to assess shape and size changes, making

it essential to precisely repeat the angle of imaging, slice content, and location of

49

important landmarks. When analyzing the images, examiners made use of bony

landmarks.

Rest Period and Related Imaging

Subjects were dismissed as each completed the post exercise imaging session, and
instructed to avoid repetitive tasks for 5 hours, then return for 3 hours of observed
inactivity to complete an 8-hour rest period. Television was provided during the observed
rest period in an attempt to lower the metabolic rate to simulate sleep. The third and final

set of images of each subject was then obtained after the rest period reported at 12 hours.

Data Collection
Three radiologists and the author, each of whom were blinded to the exercise
status and subjects' identity, analyzed images of the elbow, forearm and wrist
compartment constituents. Measurements of the area and shape of the median and ulnar
nerves, signal intensity, and fluid within the compartments of the wrist were made using
axial images at each of the following imaging positions:
Elbow: l. Proximal to the medial epicondyle
2. Distal to the medial epicondyle
Muscle bulk from elbow joint to teno-muscular junction
Wrist: l. Proximal to the flexor retinaculum
2. At the level of the Pisiform
3. At the level of the Hook of the Hamate

4. At the level of the base of the metacarpals.

50

Many investigators have used MRI examinations to identify actively exercising
muscle [19, 21, 22, 24, 57, 68] and characteristics of repetitive stress injuries at these
levels [6-8, 15, 36, 47, 52, 55, 61, 64, 69](for further review and definitions of these

imaging positions, please refer to the anatomical summaries in Chapter II, pages 27 - 41).

Hypothesis Development
Three hypotheses were tested in this study using different quantification
techniques. A review of each hypothesis precedes the explanation of method of data

analysis to clarify which methods are used for each hypothesis.

Hypothesis I : Calculated T2 of the Forearm Muscles can be used to identify muscles
more active in typing.

Two investigators graphically delineated each muscle of interest on an axial
image by tracing an area of the muscle belly. Software on a UNIX system (X-vessel
developed by Ronald A. Meyer at Michigan State University) applied the formula “T2:
Alli/1n (81. /S1 2),” to calculate T2 values where ATE is equal to the difference in TE
between two images, 81. is equal to the TE in the first image, S 12 is equal to the TB in
the second image (Figure 3.7). Muscles contracting concentrically (not isometrically)
have been demonstrated to show an increase in T2 relaxation time following the exercise
exposure. On T2 weighted images, tissue with high unbound hydrogen or water content is
brighter than tissue with high fat content. A mean T2 was established for each identified
muscle by averaging the Calculated T2s taken along its full length. The values were

analyzed for values at Baseline, After typing, and Post Rest. An increase in Calculated T2

51

following typing was expected. This was consistent with other studies where an increase
in Calculated T2 has been observed in exercising muscle. Statistical significance was
determined using a Repeated Measures ANOVA (Figure 4.6)(See Chapter IV, pages 63-
66).

Hypothesis 2: The median and ulnar nerves change shape within the wrist
compartments with exposure to typing.

Interpretation of images of the wrist structures demanded high resolution. Fast
spin echo and fast spin echo with fat saturation images were used (TR 2000/T E 16.0 and
TR 2000/T E 80 ETL 8, field of view 10x10, matrix 512 x 256/ Nex 2) to provide
adequate visualization of the small anatomical structures in the wrist. Voxel volume was
decreased to improve resolution. The field of view (FOV) was 10 x 10, matrix size 512 x
256/NEX 2, and this resulted in a pixel size of .008 mm squared (10mm/512 pixels by
10mm/256 pixels), 1 mm slice thickness. Gradient echo (TR 700 TE 21.0 flip angle 40;
FOV 10 x 10, matrix 512 x 256, 2 NEX) allowed very clear differentiation between
nerves and vessels (See Chapter IV and Chapter V, Pages 65-66, 83-86).

The chosen imaging techniques provided adequate resolution for identification of
most structures. Magnification was used for identification of the median nerve and the
ulnar neural vascular bundle at the wrist. Tethering of the nerve, nerve entrapment or
invasion of a nerve by fibroblasts and connective tissue proximal to the transverse carpal
ligament has been described in surgical and MRI literature [71, 73, 85]. Where evidence
of entrapment was noted in this study, identification of the nerve fascicles separate from
connective tissue structures was difficult, as was visualization of clear neural borders. In

many of the images of the median and/or ulnar nerves of the symptomatic subjects,

52

evidence of some impingement on the median and/or ulnar nerves was apparent, making
surface to area and T2 signal intensity calculations difficult.

The radiologists categorized the median and ulnar nerves as oval, flat or triangular
in images taken at Baseline (the first image of the day), After typing (following the 3
hour typing session), and Post rest (at the end of the day, following the 8 hour rest
period). These data were analyzed using Rank Sum, which is an analysis of the number
of images placed in each category. Images taken at each state of exposure, Baseline,
After typing and Post rest, were then compared using a Repeated Measure ANOVA to
determine statistical significance of the shape changes. Surface to area (S/A) ratios were
measured by delineating the outline of the median and ulnar nerves in images proximal to
the transverse carpal ligament, at the pisiform, hook of the hamate, and at the base of the
metacarpals. The investigator graphically delineated the outline of the nerves; then
surface to area ratios were calculated internally by X-vessel software designed by Ronald
A. Meyer, Ph.D. from Michigan State University on a computer using the UNIX
operating system. This served as an objective verification of the subjective shape changes
determined by the investigators. The ratios were analyzed using a repeated measures
ANOVA.

The investigators delineated the areas of the nerves at each level by tracing the
nerves with the computer mouse using the GE Advantage Windows workstation (AWS)
or the X-vessel program. The area was then calculated by the AWS or X-vessel and
recorded into an Excel file. Results were graphed and analyzed using Repeated Measures
ANOVA to determine statistical significance. T2 signal intensity of the median nerve

was determined by the method described for muscle calculated T2 (above) on the UNIX

53

system. Results were graphed with Excel and analyzed with correlation studies and
repeated measures ANOVA. The graphs are labled "Baseline, After typing and Post rest,"
which corresponds to Hours of O, 3 and 12. The "0" hour is equal to Baseline, "3" is
following 3 hours of typing, and "12" is following one hour of imaging, and eight hours
of rest.

Hypothesis 3: Changes in area, shape and T2 signal intensity of nerve and muscle will
be different in asymptomatic vs. symptomatic subjects.

Both asymptomatic and symptomatic subjects were exposed to the same
examinations, exercise and rest protocols. After data collection was complete,
investigators (blinded to exercise status and diagnosis) quantified shape, area, T2 signal
intensity, fluid content of the compartments and joints of interest. All of these
measurements were recorded on identical work sheets and analyzed using repeated
measures ANOVA's. Comparisons between and within groups were completed using
Pearson Correlation with significance determined in 2-tailed tests. Trends were identified

and graphed using Excel.

Human subjects

Physical and magnetic resonance imaging examination techniques used in this study are
all standard clinical examinations. They expose the subject to minimal risk if all
precautions are followed. The University Committee on Research Involving Human
Subjects (UCRIHS) at Michigan State University approved all methods of examination
and recruitment of subjects prior to data collection. All subjects signed informed consent

forms approved by UCRIHS prior to participation in the program.

54

CHAPTER IV
MAGNETIC RESONANCE IMAGING ASSESSMENT OF COMPARTMENT
CHANGES IN F OREARM AND WRIST FOLLOWING EXPOSURE TO TYPING

Gail Shafer-Crane OTR, CHT, Ronald Meyer, PhD, Marcy Schlinger, DO, D. Lee
Bennett, MD, Kevin Robinson, DO, James Rechtien, PhD, DO

ABSTRACT

Dimensional, positional and fluid content changes of soft tissues of the forearm
and wrist as a response to typing were analyzed in this study using magnetic resonance
imaging. Axial images were taken at the mid-forearm, proximal to the transverse carpal
ligament, at the longitudinal level of the pisiform, hamate, and base of the metacarpals
levels. The intent was to contrast muscles more and less active through magnetic
resonance imaging (MRI) examinations, and note changes in morphology of the median
nerve at the wrist related to exposure to typing. Asymptomatic female professional typists
(n=6) underwent three MRI examinations of the dominant forearm and wrist at baseline,
after three hours of typing, and after eight hours of rest. Three investigators blinded to the
subjects’ exercise status analyzed forearm muscle and wrist compartment images with
respect to T2 signal intensity and nerve morphology. Compartmental constituent fluid
and shape changes were correlated with typing. Forearm flexors were more active in
typing than extensors and thumb muscles (P=.0016). Progressive variations in T2 as well
as size and shape of the median nerve highly correlated to typing. MRI analysis following
exercise (typing) in this study revealed significant changes in both muscles and nerves,

suggesting a relationship between exposure to typing and these findings.

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INTRODUCTION

Computer data entry, hence typing, has been linked with repetitive stress injuries
(RSI) of the upper extremity [9, 13]. The mechanism of this relationship is poorly
understood. RSI is an all-encompassing term that includes disorders of nerves, muscles,
tendons, and their surrounding connective tissue. It is not a diagnosis, but a variety of
syndromes that have a proposed commonality of etiology. In the current study,
investigators studied muscles and nerves as they changed with exposure to typing. Soft
tissue compartmental constituents, synovium, tendons and their sheathes, joint spaces,
and the muscles activated in typing were assessed for fluid content, shape changes, and
other visible and quantifiable changes.

One cardinal symptom of some repetitive stress injuries is the patient’s report of
delayed or nocturnal onset of pain and paresthesias [50, 55]. These complaints are
common in both median and ulnar neuropathy. Delayed onset muscle soreness (DOMS)
has been documented as a common symptom in tendinopathy, tendinitis, and
epicondylitis [79]. The patient may continue to participate in the injurious activity
because of delayed onset of symptoms [62, 64].

The current investigation of the phenomenon of delayed onset of symptoms used
MRI to examine soft tissue changes in the forearm muscles and wrist compartments of
asymptomatic subjects with an exposure to typing followed by prolonged rest. Fluid
content as well as shape and positional changes of the median and ulnar nerves with
exposure to prolonged vocational speed typing followed by prolonged rest were also

analyzed.

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Identification of muscles that become active in typing

Typing is an activity that is becoming more and more common in everyday life. It
is also closely linked with repetitive stress injuries [65]. The muscles that are considered
more active in typing are assumed to be the finger and thumb flexors, flexor digitorum
superficialis (FDS), flexor digitorum profundus (FDP), and flexor pollicis longus (FPL).
Muscles considered to be supportive, or participating with an isometric contraction, and
therefore less likely to have a short term increase in T2 relaxation time during typing,
were the finger extensors, extensor digitorum (ED), and wrist stabilizers, flexor carpi
radialis (FCR), flexor carpi ulnaris (FCU), extensor carpi radialis longus and brevis
(ECRL, ECRB) and extensor carpi ulnaris (ECU). (T2 is the time in milliseconds
between the radio frequency pulse and the decay of longitudinal magnetization. This
allows calculation of unbound water content in the tissue.) These assumptions were
challenged when these muscles were analyzed using MRI.

Studies have been published that use magnetic resonance imaging to identify the
individual muscles of the forearm involved in pure exercise [20, 23]. Protocols to
distinguish active from inactive muscles are well established [19-21, 23, 42, 68].
However, these prior studies use pure exercise, e.g.: squeezing a dynamometer
repeatedly, whereas the current study uses a functional activity, typing, as its exercise

exposure.

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Changes in median and ulnar nerve shape in response to typing

In this study MRI examination was used to determine sequential changes in shape
of the median nerve in volunteers who typed at a vocational rate of approximately 50
words per minute. Many investigators have shown shape and positional changes during
postural changes at the wrist [71, 86]. The current study documented subtle shape
changes with the imaging position held constant. It is now fairly well accepted that
changes in shape are the nerve’s normal protective response to changes in
intracompartmental forces [30].

Studies related to typing have concentrated upon the effect of intracarpal tunnel
pressures on the median nerve [43, 44, 72, 86]. Cadaveric and in vivo studies have
demonstrated statistically significant intracarpal tunnel pressure increases related to
typing and application of fingertip pressure [43, 44, 71, 72, 86]. It is postulated in the
current study that these pressure changes will cause changes in the shape of the median
nerve that will be observed with MRI examination.

Observation of the ulnar nerve will be included in this study to assess its value as
a control. The ulnar nerve is considered by clinicians to be minimally affected by changes
in pressure within the carpal tunnel, and is used as a control for sensory nerve conduction
studies of the median nerve at the wrist.

The literature also describes changes in shape of the median nerve as it traverses
the wrist beneath the transverse carpal ligament (TCL) [5, 8, 16, 28, 36, 47, 49, 55, 56].
The most significant findings seemed to describe the effect of neural tethering [49] and

TCL pressure increases which impact the median nerve proximal to the TCL. Unless

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otherwise stated, the results discussed here will refer to changes in images proximal to

the TCL.

OBJECTIVES

Identification of Muscles Dominant in Typing

Identification of muscles more active in typing through documentation of short
term increased T2 relaxation time as an exercise response was undertaken in this study.
Compression neuropathies of the forearm are currently highly prevalent, and appear to
have a direct relationship to the impact of muscle activity. The median and ulnar nerves
are encased in the long wrist and finger flexor muscles of the forearm, and the radial
nerve courses through the extensor muscle compartment. The tendons of the finger
flexors surround the median nerve within the carpal tunnel. It is this very close physical
proximity that suggests a relationship between muscle activity and an effect on the
median nerve. It may be valuable to identify muscles active in typing that may be in close

proximity to the median nerve.

Quantification of volume and T2 relaxation time changes of wrist and forearm
compartmental constituents with exposure to typing

One cardinal sign of carpal tunnel syndrome or ulnar neuropathy is delayed onset
of pain and/or paresthesias in the fingers supplied with sensation by the median or ulnar
nerve. Many investigators have described these symptoms as the result of a cycle of
ischemia and reperfusion of the nerves dependent upon compartmental pressure increases

from position or exercise [44, 63, 71 , 72, 86]. The design of this study allowed

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investigators to observe the constituents of compartments of the elbow, forearm and wrist
at three stages of activity; Baseline (prior to activity), After typing (following 3 hours of

typing at 50 words per minute) and Post rest (following 8 hours of rest).

Materials and Methods

Population

Asymptomatic female professional typist volunteers (n=6), ages 21 — 52, mean
age 38 were recruited. One subject volunteered to act as both a typing subject and a non-
typing control. Volunteers were interviewed by telephone prior to participation to
determine medical and work history. Individuals were excluded if they had a positive
medical history for any injury to the dominant upper extremity, any metabolic disorder
including diabetes, or were currently pregnant or nursing. All volunteers were required to
be conditioned typists. This was defined to be individuals who routinely typed
continuously for a minimum of four hours. Each volunteer signed the informed consent
documents approved by the University Committee on Research Involving Human
Subjects of Michigan State University. The right arm was identified as the dominant

upper extremity in all subjects.

Study Protocol

On the day of the examinations, each subject reported for testing early in the
morning, after being instructed to limit activity prior to the examination. Physical
characteristics of the right arm of each subject were noted through the process of physical

examination and 3 MRI examinations, which were performed: prior to typing (Baseline),

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after three hours of vocational speed typing (After Typing), and following eight hours of
rest (Post Rest). Initially, a physical examination was performed on the right arm of each
subject, which included sensory nerve conduction studies, proprioception testing, strength
and range of motion screening tests, and provocative tests (Phalen’s and Tinel’s tests).
The physical examination was not used to eliminate any subjects from this study, but was
used to provide comparative information regarding their performance on the physical
examination and the MRI examinations. The physical examinations and sensory nerve
conduction studies were all within normal limits for all subjects in this study. All subjects
indicated they were without pain or paresthesias at each of the three examinations

conducted during this study.

Typing protocol

Uniform, ergonomic workstations were provided for the typing/exercise exposure.
Subjects were allowed to bring their own typing or use non-standardized typing material
provided by the investigators. Each subject was provided with an adjustable chair with
elbow rests, “natural” style keyboard, wrist rest and copy stand. Each workstation was
adjusted for position and comfort for each subject. The subjects were then directed to
type at a vocational rate (50 words per minute) for three hours, with one 15-minute break
half way through the typing time. Subjects used the same word processing software to
type un-standardized material. Keystrokes were counted through the word count feature.

MRI examinations were repeated immediately following the three-hour typing
time period, “After Typing”. Because exercise induced muscle T2 changes resolve within

30 - 60 minutes, the After Typing images were initiated within ten minutes of the

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cessation of typing. The final MRI examination was completed after the subjects had
completed 8 hours of rest, “Post Rest.” The last three hours of rest were observed. All
subjects watched television during the observed rest period in an attempt to decrease the
subjects’ metabolic rate and elicit delayed onset symptoms, which may have been

brought on during sleep.

Magnetic Resonance Imaging Protocol

Precise duplication of the MRI imaging positions was required for comparison of
changes in shape and size of the structures under study. Prior to the first images of the
day being taken, surface landmarks of the carpal tunnel, forearm extensor muscle bulk
and lateral epicondyle were marked on the skin with an indelible marker to facilitate
consistent repositioning of the subject within the MRI equipment. The right forearm of
each subject was positioned in a small extremity coil; then the subject was placed in the
General Electric Signa 1.5 Tesla magnet with the arm extended overhead in the
“swimmer’s position” for the forearm muscle images taken every centimeter (dual echo
axial T2 weighted spin echo images with different TE’s: T2 TR 1500, TE 30 and 60,
NEX 1); imaging duration 21 minutes.

The subject was then repositioned for imaging of the wrist. The right wrist of each
subject was positioned in a resting hand splint made to fit in the wrist coil (Figure 4.1) in
an unstressed position (wrist at 25 degrees of extension and fingers in full extension).
Images of the wrist and forearm compartments were collected after moving the subject to
side lying with the volar forearm opposite the subject’s face. T2 weighted fast spin echo

(TR 2000/TE 15&80, NEX 2, echo train length 8), fast spin echo with fat saturation (TR

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2000/T E 21, NEX 2, echo train length 8) and gradient echo (TR700/T E 21, NEX 2)
imaging methods were used to image the wrist compartments. Slices were one millimeter

thick. The full imaging session required approximately 45-60 minutes.

Method of Analysis
Analysis of Muscle

Two investigators, blinded to the subjects’ identity and exercise status,
graphically delineated a portion of the muscle bellies of the flexor pollicis longus (FPL),
abductor pollicis longus (APL), extensor pollicis longus (EPL), extensor digitorum (ED),
flexor digitorum profundus (FDP), flexor digitorum superficialis (FDS), flexor carpi
radialis (FCR), flexor carpi ulnaris (FCU), extensor carpi ulnaris (ECU), and extensor
carpi radialis longus (ECRL) in imaging slices throughout the length of the forearm
(Figure 4.2). T2 relaxation time for each muscle, which depends in part on intracellular
fluid content of the muscles, was quantified. An average "Calculated T2" in milliseconds
was determined for each muscle in each subject. The calculated T2s, reported in Results,
represent the average of the calculated T23 from each image throughout the length of
each muscle.

The average calculated T2 values for all muscles listed in this study were
calculated from the images taken at three different times of the day. These times were:
Early morning (Baseline), mid-day, (After Typing) and evening, (Post Rest). Subjects
were instructed to avoid typing activities prior to the Baseline images, and between the
After typing and Post rest images. A control subject participated in all examinations, but

was instructed to remain inactive during the typing exposure. The results of the control

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subject will be reported as “After Typing” to coincide with the typing subjects
examinations.

Two investigators blinded to the subjects’ identities and exercise status used a
UNIX computer system to delineate images of each muscle under study (Figure 4.2).
Two simultaneous fast spin echo T2 weighted images with 2 TE’s (echo time which
represents the interval between the radio frequency pulse and the maximum induced
signal) were used to calculate T2 in the muscles (TR 1500, TE 30 and 80 NEX 1).
Software on a UNIX system (x-vessel developed by Ronald A. Meyer at Michigan State
University) used the formula “T2: LIE/1n (S 11 IS 12),” to calculate T2 values where
ATE is equal to the difference in TE between two images, S 11 is equal to the TE in the
first image, S 1 2 is equal to the TE in the second image. Statistical significance of the data

was analyzed using repeated measures ANOVA.

Analysis of T2 Relaxation time of the Median and Ulnar Nerves

Changes in T2 relaxation times of the median and ulnar nerves at the wrist were
determined using the same formula as for muscle T2. However, images of the nerves
were delineated at four imaging levels at the wrist: l. Proximal to the transverse carpal
ligament, 2. Pisiform, 3.Hook of the hamate, 4.Base of the Metacarpals. As the effect of
intracarpal tunnel pressure may vary at each of these anatomical segments, it was
considered appropriate to measure the T2 of the median and ulnar nerves at each imaging
level as they progressed through the compartments instead of using an average T2 over

the length of each nerve at the wrist.

64

C ompartmental Analysis

Three radiologists blinded to the subjects’ identity and exercise status, analyzed
images selected at each of the four imaging levels listed above. They evaluated forearm
and wrist compartment constituents for changes in fluid content, shape, and size.
Investigators used the criteria defined by Mesgarzdeh, et. al. for categorization of the
shape of the median and ulnar nerves as well as definition of bowing of the transverse
carpal ligament [54-56]. Each nerve was categorized as flat (ratio of the major over the
minor axis >321), oval (ratio approximately 1:1) or triangular (a visible point was noted).
Bowing of the transverse carpal ligament was measured using the GE Advantage
Windows workstation to first measure the length of a straight line between the points of
medial and lateral attachments of the transverse carpal ligament (TCL), then measure the
distance of a second line drawn perpendicular to the first at the widest point between the
line and the inside, or deep edge, of the TCL. Bowing of the TCL was considered present
if less than I/2 of the TCL was straight [55].

Shape and size of the median and ulnar nerves were further quantified through the
use of surface to area ratios, where the investigator graphically delineated the nerve and
used the x-vessel software to compute the surface to area ratio. T2 of the median and
ulnar nerves was also quantified on the axial images of the wrist (Figures 4.3, 4.4). These
images were selected for analysis to correspond to bony landmarks along the length of
the wrist. Images corresponded with an axial image proximal to the transverse carpal

ligament, at the pisiform, at the hook of the hamate and at the base of the metacarpals.

65

RESULTS

Two methods of analysis were used in this study, one to contrast active from
inactive muscle using T2 Relaxation times, and the other was used to compare and
contrast the fluid content of the median and ulnar nerves (T2) at Baseline, After Typing,
and Post Rest. One control subject, who did not type but otherwise participated in all
examinations, was used to illustrate the effects of typing on the muscles and nerves of
typing subjects. The results of the muscle analysis will be presented first, followed by the

results of the nerve analysis.

Muscles Identified as Being Active in Typing

Muscles active in typing were found in the flexor/pronator group, including wrist
flexors (p=0.0016). In typing subjects the flexor digitorum superficialis (FDS), flexor
digitorum profundus (FDP), flexor carpi ulnaris (FCU), and flexor carpi radialis (FCR)
T2 relaxation times increased between Baseline and After Typing, and decreased between
After Typing and Post Rest. The T2 relaxation times of the extensor digitorum (ED),
extensor pollicis longus (EPL), and abductor pollicis longus (APL) remained the same
throughout the exposure to typing, then either increased with rest, or decreased to
Baseline levels or below (Figure 4.5).

The T2 values of the finger and wrist flexor muscles increased significantly with
typing and decreased more significantly after rest. The greatest difference between active
and inactive muscles was the T2 value decrease between After Typing and Post Rest

(Figure 4.6). Statistical significance was determined with a repeated measures ANOVA.

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Response of muscle in the control subject

In the control subject’s flexor muscle (FDP, FDS, FCU, and FCR) After Typing
values, which in the case of the control would represent a three-hour interval without
typing, decreased from Baseline, then remained level (Figure 4.7). In the muscles that
were not active in typing (ED, EPL, and APL), the control value followed a similar
pattern to the muscles of the subjects active in typing. The T2 of the muscles varied
slightly, and seemed to randomly increase or decrease with the passage of time (Figure
4.8). Typing subject’s ECU, ECR, ED, APL, and EPL seemed to randomly increase or
decrease between Baseline and After Typing, between After Typing and Post Rest, and

between Baseline and After Rest.

Differences Between Active and Inactive Muscles

If we graphically contrast the extensor digitorum and flexor digitorum profundus,
a muscle very active in typing, the pattern of T2 increase is apparent (Figure 4.9, 4.10).
The changes in T2 relaxation time of the FDP muscles are consistent, as opposed to the
T2 relaxation times of ED muscles which remain essentially constant.

The identification of active muscles was based on the statistically significant T2
relaxation time changes between Baseline and After Typing, between After Typing and
Post Rest, and a comparison between the non-typing control and typing subjects. It was
also noted that T2 relaxation times were often lower Post Rest compared to Baseline in

the majority of muscles found to be active in typing.

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Shape and T2 Relaxation time Responses in the Control Subject ’s Median and Ulnar
Nerves

Changes in shape of the median and ulnar nerves were subtle; however, they were
more evident in the visible categorizations (Flat, Oval or Triangular) made by the
radiologists (p=0.053) than in the surface to area ratios. Surface to area ratios (s/a) are
calculated by delineating the circumference (surface) then dividing this into the area. If a
shape changes, the s/a is expected to change as well. If the shape of the nerve were round,
a change in shape would correspond to a change in area, therefore there would be a
change in the surface to area ratio (s/a). Because the shape of the median and ulnar
nerves is elliptical, that shape may vary subtly without a corresponding s/a ratio change
[48].

The changes between Baseline, After typing and Post Rest in the control subject’s
T2 relaxation time values of the median and ulnar nerves were minimal. There was a
small increase in the median nerve, and a small decrease in the ulnar nerve on the “After
Typing” examination, compared to Baseline, on the axial images proximal to the TCL

(Figure 4.1 1).

Comparison Between Typing subjects and control

Changes in shape of the median nerve, between Baseline and After typing and
Post Rest, of typing subjects were compared with those of the non-typing control using
the surface to area ratios (Figure 4.12). The changes were subtle, and lacked statistical

significance. Statistical significance was noted, however, in the radiologists’ assessment

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of shapes at Baseline, After Typing and Post Rest (Figure 4.13) at the imaging level. This
apparent discrepancy is addressed in the Discussion.

T2 changes in both the median and ulnar nerves between Baseline, After Typing
and Post Rest where more apparent when compared to control (Figure 4.14). These
changes, while not statistically significant, were highly correlated with typing using
Pearson’s correlation table (Figure 4.15). The range of T2 changes were wider in images
of the median nerves than in images of the ulnar nerve. When contrasted with the T25 of
the control subject, the T25 of the ulnar nerves of the typing subjects were, for the most

part, equivalent to the control T25 of both the median and ulnar nerves (Figure 4.16).

DISCUSSION

This study was used to identify active muscles, and quantify some changes in the
median and ulnar nerves at the wrist, using a vocational activity considered to be high
risk for causing repetitive stress injuries. Use of the vocational activity of typing as the
exercise exposure introduces the potential for application of this protocol to study the
effects of other high-risk vocational activities. Methods well established in science to
study the effects of exercise on both muscles and nerves have been used in this clinical
application.

Delayed onset muscle soreness and delayed or nocturnal onset of paresthesias is a
cardinal symptom of repetitive stress injury. While this study analyzes the effects of
typing on an asymptomatic cohort, the information gathered following prolonged rest
provides information on the normal response to activity following a significant recovery

period.

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Muscles Identified as Being Active in Typing

Techniques that have been well established to identify muscles more active than
others in exercise were shown to be effective in this study. Muscles identified as being
active in typing in this study were limited to the flexor/pronator compartment of the
forearm. Included were the two wrist flexors, flexor carpi ulnaris and flexor carpi radialis.
It was expected that these muscles, because they are thought to be acting to stabilize the
wrist, would not show significant T2 changes during typing. The antagonists, the
extensor carpi radialis longus and brevis as well as the extensor carpi ulnaris, were not
shortening during typing, which would have caused an increase in T2. N0 long wrist or
finger extensors, long thumb flexors or long thumb extensors were identified as being as
active in typing as the muscles in the flexor group. It was expected that flexor pollicis
longus would have shown a significant T2 increase with typing, because this is the
muscle thought to be active in pressing the space bar. The results suggests that the FCR, a
wrist flexor, may be more involved in depressing keys requiring the thumb, than

previously thought.

Impact of Forearm Flexor Muscle Contraction on the Median and Ulnar Nerves
The median and ulnar nerves innervate the flexor/pronator group of muscles. The
flexor muscles encase neurovascular bundles that provide the conduits for the median and
ulnar nerves as they travel through the forearm. The forearm flexor muscle Random
Calculated T2 values increased significantly following exposure to vocational speed

typing (50wpm) for three hours. The tendons and bellies of these muscles are closely

70

associated with the median nerve within the carpal tunnel, and may be associated with the
increases in mechanical pressures within the carpal tunnel during typing noted in earlier

studies [43, 86].

Changes in Nerve Morphology Related to Typing

A relationship between delayed onset symptoms of paresthesias and pain related
to repetitive stress injuries and ischemia/reperfusion of the median nerve has been
supported in recent studies [63, 78, 86]. It may be surmised that intracarpal tunnel
pressure variation that is sufficient to cause alterations in the shape of the median nerve,
which are related to muscle activity, may also be sufficient to impair perfusion of the
perineural circulation, which in the region of the wrist is dependent on longitudinal
branches from various arteries in the vicinity. Investigators in previous studies using MRI
have demonstrated changes in shape of the median nerve related to changes in position of
the wrist during imaging, and surmise that this change in shape is a result of changes in

intracarpal tunnel pressure [44, 71, 86].

Shape Comparisons Between Baseline, After Typing and Post Rest in Typing Subjects
and the Control

In the current study, the shape of the median nerve in subjects exposed to typing
was seen to respond to activity levels when the imaging position was held constant.
Subtle changes in the shape of the median nerve are visible in each stage of activity and
rest. The ulnar nerve was not noted to change shape significantly in the same images. The

shapes of the median and ulnar nerves of the non-typing control subject were found to

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remain fairly constant. The axial magnetic resonance images were made prior to activity
(Baseline), following three hours of vocational speed typing (After typing), then after

sufficient rest to approximate sleep (Post Rest).

Changes in Median Nerve T2 Apparently Related to Intracarpal Tunnel Pressure

The most common RSI is carpal tunnel syndrome, or median nerve compression
at the wrist. For that reason, this study emphasized analysis of the median nerve, and the
carpal tunnel. Organization of the axons of the median nerve is similar to other peripheral
nerves, in that the sensory fibers (C6-C7 origin) are generally located more externally,
and the motor axons (C8-Tl origin) are more central [51]. Carpal tunnel syndrome is
often diagnosed through a medical history positive for nocturnal or delayed onset of
paresthesias. Delayed onset paresthesias seem to be caused by transient impairment of the
intraneural circulation that resolves within hours after normalization of intra-
compartmental pressure [17, 46].

In this study, typing appears to impact the fluid content of the median nerve of
asymptomatic subjects. When compared to the asymptomatic control subject more
significant changes in T2 relaxation times of the median nerve were noted in the
asymptomatic typing subjects. The ulnar nerve was also affected less than the median in

all but one subject (Figure 4.16).

The Use of a Specific, High Risk Vocational Task, Typing, for This Study

There are longitudinal studies where MRI has been used to document changes in

forearm and wrist compartments of subjects who have been diagnosed with compressive

72

disorders of the forearm peripheral nerves, or were exposed to repetitive vocational tasks
[67]. In those studies, increased pressure sufficient to impair perineural circulation was
noted in studies using pure exercise, e. g. repetitive grasping, lifting against resistance
[46]. Others have shown the effects of typing on increasing intracarpal tunnel pressure,
but did not use MRI, or record the recovery of the nerve following rest the same day as
was done in this study [71, 72, 86].

Exposure to typing is thought to have a cumulative effect. An increased
knowledge of the dimensional and extracellular fluid content changes of soft tissues as a
response to repetitive activity followed by rest as assessed in this study, may provide
insight regarding the onset and progression of forearm peripheral nerve compression

injuries.

CONCLUSION

In summary, this study has shown the feasibility of using T2 relaxation time
analysis to document muscles active in vocational activities. The identification of
muscles that are more active than their antagonists may be helpful in design, and
determination of efficacy, of ergonomic equipment and treatment techniques. Of
particular interest is the discovery that wrist flexors are more active in typing than thumb
muscles.

Furthermore, this study has shown a correlation between typing and changes in
the T2 of muscle and the median and ulnar nerves. The ulnar nerve, minimally affected
by these changes, is supported as an effective control for the median nerve in

electrodiagnostic studies.

73

Future studies will assess muscle and nerve T2 relaxation time changes, and shape
changes of the median and ulnar nerves with typing in symptomatic subjects. It will also
be of interest to image subjects exposed to other vocational activities that are defined as

high risk for carpal tunnel syndrome or other repetitive stress injuries.

74

CHAPTER V
Quantification of Shape and T2 Relaxation Time in the Median and Ulnar Nerves of

Asymptomatic vs. Symptomatic Female Volunteers Exposed to Vocational Speed
typing and Prolonged Rest

Gail Shafer-Crane, Ronald Meyer, Marcy Schlinger, Kevin Robinson, Joseph Pernicone

ABSTRACT
Introduction: A cardinal symptom of repetitive stress injuries (RSI) is nocturnal or
delayed onset muscle soreness and/or paresthesias. This may occur when perineural
capillaries of the median and ulnar nerves at the wrist are collapsed by increased pressure
in the compartments of the wrist, followed by reperfusion of the nerves when the pressure
resolves. Using magnetic resonance imaging, the length of T2 relaxation time has been
related to perineural circulation. Changes in shape of the median nerve have been linked
with an RSI. These shape changes may be related to changes in intracompartmental
pressure.
Objectives: The objectives of the study were to use MRI to: (l) observe the median and
ulnar nerves, at rest, after typing and after prolonged rest as they traverse the wrist; (2)
demonstrate changes related to typing and prolonged rest in median and ulnar nerve
morphology at the wrist; (3) compare and contrast observations of the median and ulnar
nerves at the wrist between symptomatic and asymptomatic subjects.
Methods: Thirteen professional, female typists between the ages of 21 and 52, mean age
44, were placed in symptomatic or asymptomatic categories by medical history. Each
subject was examined with MRI at Baseline, following three hours of vocational speed

typing (average 50 words per minute) and following prolonged rest. Images were

75

examined for changes in shape and T2 relaxation time by four investigators blinded to the
exercise status and identity of the subjects.

Results/Discussion: The investigators delineated the circumference of the median and
ulnar nerves, and then calculated the surface to area ratios. A visual categorization of the
shape of the median on images defined it as flat, oval, or triangular. The images taken
following typing were found to have significant changes related to typing in the normal
cohort (p=0.053) but not the symptomatic group (p=0.69). Changes in size followed the
same pattern. The changes in the asymptomatic cohort were significant (p=0.03), but not
in the symptomatic cohort (0.87). T2 changes for the median nerve of symptomatic
subjects tended to decrease below baseline then recover, while T2 relaxation times of
asymptomatic subjects tended to increase then return to baseline values.

Conclusions: The median and ulnar nerves respond to typing and prolonged rest with
dynamic changes as a normal response to activity. The nerves of symptomatic subjects
were less likely to respond to activity by changes in shape or size. T2 relaxation times of

both asymptomatic and symptomatic subjects were correlated to typing.

76

INTRODUCTION

Repetitive stress injury (RSI) is a broad term for a category of disorders that are
related to prolonged, repetitive activity. It is theorized that repetitious activities may
cause microtrauma that accumulates in soft tissue causing stereotypical symptoms. There
are at least 3 types of RSI: l. Neuropathy; 2. Inflammation of muscle or tendon; 3.
Synovitis or inflammation of the synovial membranes of the tendon sheath, joint capsule
or bursa. In this study, the RSI of primary interest is peripheral neuropathy of the median
nerve at the wrist. The neuropathies are generally thought to have one of two origins;
either mechanical compression of the nerve within a compartment or circulatory changes
to the nerves [44, 47, 78, 84].

Investigators in this study explored short-term effects of typing in asymptomatic
and symptomatic subjects in a single day. It focused on ischemia and reperfusion of the
median and ulnar nerves as evidenced by T2 relaxation time in the median and ulnar
nerves at the wrist. Changes in the shape of the nerves were documented as related to

typing in both the asymptomatic and symptomatic cohort.

Median and Ulnar Nerve Pathologies
Pathologies of the median and ulnar nerves at the wrist are described below. Two
such pathologies are carpal tunnel syndrome and Guyon’s canal syndrome. The
pathology of highest significance is carpal tunnel syndrome, or median nerve
compression at the wrist, beneath the transverse carpal ligament. The inclusion of the
term “syndrome” in their descriptions indicates that these are not true diagnostic terms,

but a description of a collection of symptoms.

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Median neuropathy/carpal tunnel syndrome

Median neuropathy at the wrist is synonymous with carpal tunnel syndrome
(CTS). Compression of the median nerve at the wrist may be caused by mechanical
compression or impingement of the perineural circulation.

The carpal tunnel is a bony trough bridged by the non-extensible transverse carpal
ligament (TCL). Flexor tendons of the fingers and thumb as well as the median nerve
pass through this tunnel. The TCL also acts as the pulley mechanism for the flexor
tendons [10, 43, 71 , 72]. The median nerve is typically located just deep to the TCL,
between the tendons of the flexor pollicis longus and flexor digitorum superficialis. In
this location, it is vulnerable to point contact pressure during wrist flexion from the
pulley action of the flexor tendons [44]. The median nerve is further vulnerable to
compression from fractures or dislocations of the carpal bones, edema or excess fluid in
the tendon sheaths, and invasion of the carpal tunnel by anomalous muscle development
[55, 56].

CTS is often identified through complaints of pain or paresthesia in the area of
sensory supply by the median nerve, which includes the palmar aspect of the thumb,
index and middle fingers, as well as the lateral half of the ring finger. The pathway for
this symptomatology is not well understood. It is theorized that compartmental
compression sufficient to collapse perineural capillaries may cause transient neural
ischemia [63, 86]. The collapse of these capillaries interrupts oxygenation of the nerve

fibers (transient neural ischemia), causing a reversible physiological block of neural

78

transmission [46, 66]. When the compression is resolved, gradual return of sensory nerve
function is marked by paresthesias.

Sensory nerve conduction studies are used to further diagnose CTS. The ulnar
nerve of the same hand is used as a control when assessing for a sensory nerve
conduction velocity slowing in the median nerve [14]. A number of studies show slowing
of nerve conduction can occur when the circulation of the nerve is impaired by
compression, then recovers quickly following resolution of the compression [17].

The median nerve is a mixed nerve, providing both sensory and motor nerve
supply to the hand. Sensory fascicles tend to be located directly beneath the contact point
of the TCL during wrist flexion, and are therefore thought to be more susceptible to
damage from increased intracarpal tunnel pressure [51]. It follows that sensory changes
of pain and paresthesia are the first noted symptoms identified in CTS. Atrophy of the
thumb flexor muscles is a finding in advanced or chronic CTS. As the motor fascicle is
more often located toward the radial side from the center of the nerve, where it is less

vulnerable to contact pressure from the TCL [51].

Ulnar Neuropath y/Gu yon ’s Canal Syndrome

Ulnar neuropathy at the wrist is much less prevalent than carpal tunnel syndrome.
The ulnar nerve at the wrist passes superficial to the TCL with the ulnar artery, just deep
to the pisohamate (volar-carpal) ligament [60]. Increases in pressure in this compartment
are linked to ulnar neuropathy at Guyon’s canal. In some cases, surgical release of the
TCL has had a secondary benefit of reduction of intracompartmental pressure of Guyon’s

canal as well as reduction of pressure within the carpal tunnel [l]. The ulnar nerve is

79

commonly entrapped at the entrance of Guyon’s canal in this syndrome [87]. Clinical
signs include numbness or hypesthesia, pain or paresthesias on the ulnar side of the hand
and in the ring and small fingers. Weakness of abduction of the fingers caused by

weakness of the interosseous muscles is another symptom [60].

Perineural circulation

Peripheral nerves are organized in fascicles surrounded by connective tissue. This
tissue encompasses a longitudinal capillary system that supplies the nerve axons. Many
of the nerve fascicles are imbedded in myelin sheaths. In part, these sheaths are made up
of Schwann cells. Spaces between the cells produce the Nodes of Ranvier. These nodes
are responsible for speeding the conduction of action potentials, and their efficacy is
dependent on spatial relationships between nodes. It has been theorized that there is
sufficient pressure within the compartments of the wrist to impact the conduction of the
action potential by displacing the Nodes of Ranvier. This seems unlikely in CT S. In
animal models, damage to the myelin sufficient to displace the Nodes of Ranvier required
1000 mm Hg [17, 46]. Typing was shown to increase carpal tunnel pressure to
approximately 45 mm Hg, sufficient to impact perineural circulation but not displace
myelin [72].

In addition to the myelin sheath, layers of connective tissue separate the neural
bundles. The epineurium (the outer layer of the nerve), perineurium (the layer that
surrounds each fascicle), and the endoneurium (the layer that surrounds each axon), are
interlaced with a network of longitudinal and interconnecting capillaries throughout the

length of the nerve [27, 84]. These in turn are supplied by arteries that maintain close

80

proximity to the nerve as it traverses the compartments of the arm, forearm and wrist. In
the case of the ulnar nerve, the nourishing artery is the ulnar artery in the forearm and
wrist. In the case of the median nerve, which has no accompanying artery in the forearm
or wrist, it depends on small branches from several arteries including the ulnar, radial and
anterior interosseous arteries which may not be in very close proximity to the nerve. It is
this capillary plexus of the median or ulnar nerves that is susceptible to either congestion
or ischemia caused by increased intracompartmental pressure [84, 86]. It is further noted
that surgical release of the median nerve has been shown to reverse ischemia measured
by Doppler flowmetry [78].

It has been demonstrated in several studies that changes in position of the wrist
and such activities as typing cause sufficient increases in intracarpal tunnel pressure to
collapse the perineural capillaries of the median nerve within the carpal tunnel [43, 44,
63, 86]. Intermittent collapse of these capillaries may be sufficient to reduce or block

axonal transport, but if of short duration will not cause axonal atrophy [l l, 14, 46, 63].

DIAGNOSTIC TESTS
Physical examination of a patient suspected of having a repetitive stress injury
may include imaging, strength testing, electrodiagnostic studies, and neurological testing
to assess pathology in the physical structures and function of the nerves. Emphasis has
been placed on provocative testing (see below) because of the ease of use in physical
examination, the volume of clinical information involving provocative testing, and the

reliance upon this method by clinicians for decades [52, 55].

81

Provocative testing

Provocative testing is targeted reproduction of paresthesias or pain in the
distribution of the nerve tested by mechanical means. One method used to test the median
nerve is Phalen’s test, or sign. The backs of the hands are placed together in a “reverse
prayer position” acutely flexing the wrists and holding that position for a minute or
longer (Figure 5.1). The subject will complain of paresthesias within one minute of
assuming this posture in a positive test. It is theorized that this is the result of increased
intracarpal tunnel pressure, which collapses the perineural circulation of the median nerve
[55, 83, 84]. Phalen’s sign is often positive in individuals who do not have a median
neuropathy, and therefore cannot be used independently to diagnose CTS.

Another test is Tinel’s sign, which is the reproduction of parethesias when the
examiner taps on the subject’s skin along the course of the nerve being tested. A Tinel's
sign is positive when the subject reports pain or paresthesias radiating out from the site of
percussion on the surface along the course of a nerve. It is often related to regeneration of
the nerve following degenerative changes, or irritation of the nerve [14, 46].

Provocative testing produces inconsistent results. Both Phalen’s sign (Figure 5.1),

and Tinel’s Sign are associated with both false positives and false negatives [l4].

Diagnosis Using Imaging

Magnetic Resonance Imaging (MRI) and ultrasonography studies have been used
to enumerate characteristics consistent in patients with CTS. Bowing of the transverse
carpal ligament, increased signal intensity of the median nerve, swelling of the median

nerve proximal to the transverse carpal ligament, inflammation of the synovial sheaths

82

within the carpal tunnel, and flattening of the median nerve at the pisiform and hook of
the hamate are often used to diagnose CTS [30, 47, 55].

T2 weighted spin echo and fast spin echo images have been used in other studies
to quantify fluid changes in peripheral nerves. Gradient echo images provide excellent
contrast between tissue types. T2 weighted images provide information on fluid content
within the tissue. Tissue that has a higher fluid content will appear brighter than tissue
with less fluid. T2 relaxation time is measured in milliseconds. Compression of a
peripheral nerve has been shown to cause an increase in the T2 relaxation time of the
nerve [32].

Tethering of a peripheral nerve is also one of the characteristics that can be
disclosed by imaging. Connective tissue invades the perineurium, causing the nerve to be
tethered to the surrounding compartmental structures. In CTS, the median nerve may be

tethered proximal to the transverse carpal ligament [40, 47, 52].

OBJECTIVES

This study was undertaken to use a high risk, vocational activity (typing) to
demonstrate changes in median and ulnar nerve morphology at the wrist in subjects. The
characteristics selected for quantification were shape and fluid content of the nerves.
Axial T2 weighted images of the right forearms were assessed for T2 relaxation time
changes of the median and ulnar nerves with the expectation that the T2 relaxation time
would increase with typing, and decrease with rest. In addition, it was expected that nerve
shape would visibly change and the area would increase with the exposure to typing. T2

weighted and gradient echo images were used to analyze changes in shape and size. It

83

was further expected that there would be a quantifiable difference between symptomatic

and asymptomatic subjects in both shape, size, and T2 relaxation time changes related to

typing.

METHODS

Subjects

Subjects were female, professional typists aged 21 to 52, mean age 44 years,
whose job required a minimum of four hours of continuous typing at a rate of 50 words
per minute or higher. Each subject was placed in either the asymptomatic or symptomatic
cohort following a telephone interview to determine medical history. No one was
accepted as a subject who had a history of metabolic disorder, current pregnancy or
injury to the dominant arm.

Six asymptomatic subjects and seven symptomatic subjects were recruited.
Medical histories of two individuals in the symptomatic cohort were positive for a
diagnosis of carpal tunnel syndrome. Four subjects in the symptomatic cohort had a
positive medical history for a diagnosis of lateral epicondylitis and one was positive for
tenosynovitis. One subject in the asymptomatic cohort, age 44, and one subject in the
symptomatic cohort, age 51, volunteered to serve as both non-typing controls and typing
subjects. These control subjects were tested on two days, once as a typing subject, once
as a control. On each day they underwent the full physical examination and all MRI
examinations. Each volunteer completed a medical history and “The Levine Scale of

Carpal Tunnel Syndrome Severity” [50]. All were right handed.

84

All subjects signed consent forms approved by the Michigan State University

Committee on Research Involving Human Subjects (UCRIHS).

Examination procedure

Each subject was given a physical examination that tested muscle strength,
proprieoception, and reflexes of the right arm as well as sensory nerve conduction of the
median and ulnar nerves at the wrist. Either a physiatrist or physiatry resident performed
all physical examinations. Subjects were then examined with MRI at Baseline (before
typing), following three hours of vocational speed typing, and following eight hours of
rest, the last three hours observed. Subjects watched television for the three hours of
observed rest to lower their metabolic rates in an effort to elicit delayed onset symptoms

associated with sleep.

Magnetic Resonance Imaging Examinations

All MRI examinations were performed using a 1.5 Tesla General Electric Signa
Magnetic Resonance Imager. Spin echo (TR1500,TE 36 and 60 NEX 1), fast spin echo
(TR 2000, TE 15 and 80 NEX 2, echo train length 8), and fast spin echo with fat
saturation (TR2000/ TE 21 NEX 2 echo train length 8), and gradient echo (TR 700, TE
21 NEX 2) images were obtained. Axial images of the forearm were used in all data

collection. (Please refer to the MRI glossary of terms for an explanation of TR, TE, etc.)

85

Data Collection

Three radiologists and a third investigator blinded to the subjects and their
exercise status analyzed the images (Figure 5.2). Visible categorization of the shape of
the median nerve just proximal to the transverse carpal ligament, at the level of the
pisiform and the hook of the hamate identified the nerves as either oval, flat or triangular.

The examiner delineated the area of interest in either a nerve or muscle, then
using X-vessel software for the UNIX computer, developed by Ronald A. Meyer at
Michigan State University, was able to calculate T2 relaxation time by averaging the T2
relaxation times between simultaneously collected T2 weighted images with different
TE's. The X-vessel formula is: T2=ATE/ln (Sh/S12), where T2 refers to the calculated
value of T2 relaxation time; ATE refers to the difference between the echo times in
milliseconds; In is the natural log; $11 is the T2 relaxation time in milliseconds in the first
image; and SI; is the T2 relaxation time in milliseconds in the second image.

Surface to area ratios were performed to provide additional information regarding
nerve shape change. An investigator graphically delineated the circumference of the
nerves under study. The X-vessel software was used in conjunction with a UNIX

operating system to calculate the surface to area ratios.

Methods of Analysis
Results were compared using Repeated Measures ANOVA. The results of each of

the investigators were analyzed separately and results were then compared. If there were

86

disparate results each examiner was asked to review their data for accuracy and

repeatability, which resolved most disparities.

RESULTS

Morphology of the median and ulnar nerves with exposure to typing at Baseline

The shape of the median nerve is different at each imaging level (Figure 5.3, 5.4).
The median nerve is expected to be oval proximal to the transverse carpal ligament in the
asymptomatic subject [54]. Our study demonstrates variability of the shape of the median
nerve, but for the most part, the median nerve was oval at the TCL in asymptomatic
subjects. Symptomatic subjects’ median nerves were sometimes very flat, making them
difficult to differentiate from the TCL, or rounded suggesting edema (Figure 5.5).

Statistically significant changes in the shape of the median nerve were noted when
a comparison was made between Baseline and After Typing, and between After Typing
and Post Rest images of the median nerves of asymptomatic subjects (p=0.053). Surface
to area ratios of asymptomatic subjects did not show significant changes (p=0.64).

Images of the ulnar nerves of both symptomatic and asymptomatic subjects were
nearly all oval. Surface to area ratios and the radiologists’ categorizations were in
agreement. No statistically significant shape changes were noted in the ulnar nerve with
exposure to typing or following rest, or between symptomatic and asymptomatic subjects.

The ulnar nerve remained, for the most part, elliptical in shape.

87

Median nerves of symptomatic subjects had anomalous morphology

Tethering of the median nerve proximal to the transverse carpal ligament
was observed in two ways. The median nerve was seen to be edematous, surrounded by
connective tissue, which appeared to be tethering the nerve proximal to the TCL (Figure
5.6). In the second type, the nerve is flattened against the TCL (Figure 5.7). The borders
of the nerve can barely be discerned. While this nerve is visible with a border that can be
delineated, obliteration of the median nerve by connective tissue proximal to the TCL
associated with long-standing carpal tunnel syndrome has been described in other studies

[47].

Shape of the Median Nerve as it Traverses the Wrist

The shape of the median nerve is subject to the pressures it encounters proximal
to the TCL, and as it traverses the wrist. The imaging levels of this study provide views
of the nerve at each of three levels (Figure 5.3, 5.4). Compression beneath the TCL from
the bony carpal walls, anomalous muscle within the carpal tunnel, and forces from the

flexor tendons become obvious at each level.

Comparison of Changes in T2 relaxation times of the median and ulnar nerves of the
Controls

The T2 relaxation time Of both the asymptomatic and symptomatic control
subjects' median nerves did not vary significantly between Baseline and after three hours.
The T2 relaxation time value then decreased to below Baseline. The ulnar nerve of the

control subjects demonstrated a slight drop in the T2 relaxation time between Baseline

88

and 3 hours later (After Typing). Between this observation and the After Rest, the T2
relaxation time remained essentially unchanged. T2 relaxation time values decreased in
the median (Figure 5.8) and ulnar (Figure 5.9) nerves in both the symptomatic and
asymptomatic controls when comparing Baseline to Post Rest. Please note, that although
control subjects did not type, in the graphs control results are labeled “After typing”. This

allows a comparison at that time interval with the subjects who were typing.

Symptomatic Subjects Report Pain With Typing

All of the symptomatic subjects reported at least a pain level of one on a scale
from zero to ten (Figure 5.10). The two subjects who had been diagnosed with carpal
tunnel syndrome prior to this study reported delayed onset pain with prolonged rest, as
did the subject who acted as both a non-typing control (Subject l3) and a typing subject

(Subject 16).

Comparison of Changes in T2 relaxation times of the median and ulnar nerves,
Symptomatic vs. Asymptomatic Subjects

T2 relaxation times of the asymptomatic subjects had a tendency to increase with
the exposure to typing, then decreased to Baseline levels. T2 relaxation time values of the
symptomatic subjects either increased very slightly, or decreased between Baseline and
After Typing (Figure 5.1 1). Between After Typing and Post Rest, T2 relaxation time
values of the median and ulnar nerves of the asymptomatic subjects returned

approximately to Baseline, while the T2 relaxation times of Symptomatic subjects'

89

median nerve in all cases but one, increased to above Baseline values (Figure 5.12).
Tables in Figures 5.13, 5.14, 5.15, and 5.16 include the values depicted in the graphs.

As shown in Figure 5.17, the average T2 relaxation times of the median and ulnar
nerve of all symptomatic subjects maintained a higher range of values than all but one of

the asymptomatic subjects. The exact interpretation of these findings is unclear.

DISCUSSION
There is a correlation in changes and shape of the median nerve with typing

The median nerve was seen to change shape significantly in the asymptomatic
subjects with exposure to typing. This appears to be a response to activity. The shape
changes noted in the median nerves of symptomatic subjects, while still undergoing some
subtle shape changes when exposed to typing, were less significant than the shape
changes seen in the asymptomatic subjects.

The shapes of the median nerves of symptomatic subjects were often swollen,
very flat, nearly obliterated by connective tissue, or were subjected to tethering in images
taken proximal to the TCL in images taken at Baseline. These findings agree with many
others, that the median nerve is often misshapen in symptomatic subjects at rest [47, 49,
55, 56]. This study shows a tendency for these median nerves to respond less robustly to

typing by changing shape.

T2 Relaxation Time Values Respond differently in Controls vs. Typing Subjects
As was expected, the T2 relaxation times in non-typing control subjects varied
less than in subjects engaged in typing. This may be related to dilatation of perineural

capillaries as an exercise response. It is interesting to note that the average T2 relaxation

90

times of both the median and ulnar nerves of asymptomatic subjects were seen to be
higher than those of the symptomatic subjects.

A pattern of ischemia of the nerves brought on by impaired perineural circulation
followed by reperfusion is discussed in the literature. It would follow that delayed onset
symptoms, either delayed onset muscle soreness (DOMS) or delayed/noctumal onset
paresthesias may be closely linked to this phenomenon. A change in neural T2 relaxation
time was affected by typing in this study. Those T2 relaxation time changes may be
evidence of the cycle of ischemia and reperfusion. If symptomatic individuals have less
robust perineural circulation than asymptomatic individuals, they may be more sensitive
to pressure changes suggested in this study.

As shown in Figure 5.17, the average T2 relaxation times of the median and ulnar
nerves of symptomatic subjects maintained a higher range than those of the asymptomatic
subjects. Higher T2 relaxation time is used as a diagnostic sign of neural inflammation,
and is diagnostic in carpal tunnel syndrome. It was of interest that while this cohort was
not homogenous in diagnosis, only two subjects were diagnosed with CTS, all
symptomatic subjects' average T2 relaxation times in both the median and ulnar nerves

were higher than those of asymptomatic subjects.

CONCLUSIONS
MRI studies of functional activity, typing, has been shown to be efficacious. It is
valuable to study subjects performing a functional activity in order to quantify the effects
of the activity. Facsimiles of the activity have value in establishing the protocols for

scientific analysis. However, the use of the actual, functional activity has the benefit of

91

direct observation over conjecture. Further investigation into the effects of other high-risk
vocational tasks on shape, size and T2 relaxation time changes would provide additional
information on this subject.

In this study, both the median and ulnar nerves showed T2 relaxation time
changes related to typing, while changes in shape were less apparent. Results should be
substantiated by a larger study, with higher numbers of both asymptomatic and
symptomatic subjects, and with symptomatic subjects with greater homogeneity of

diagnosis.

92

10.

ll.

12.

l3.

l4.

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98

 

Coronal Axial

Figure 2.1: Anatomical terms, sagittal, coronal, axial are ways to describe “slices” of
images. The sagittal image on the left is taken longitudinally and used to locate the area
that will be imaged in the study. This "Localizer" image is 90 degrees from the axis of the
images that will be used. The axial image on the right provides excellent detail and
sufficient resolution for quantification of size, shape and fluid content of tissues in the
Image.

99

 

Figure 2. 2: Fascia] compartments can be seen in this axial image of forearm muscles.
The interosseous membrane appears as a dark line, which divides the image top to bottom
(heavy white arrow). The extensor compartment is in the upper third of the image, the
flexor/pronator compartment is in the lower two-thirds of the image. Boundaries between
muscles (light white arrows) are also visible.

Radius

Ulnar styloid

 

Figure 2.3: The most proximal of the imaging levels used in this study, this image is
"Proximal to the Transverse Carpal Ligament." The radius and ulnar styloid are visible at
this level, but not the lunate. The median nerve (heavy white arrow) and ulnar nerve
(light white arrow) are easily identified.

101

Guyon's canal

Pisiform bone

 

Figure 2.4: Level of the pisiform bone. The transverse carpal ligament (light white
arrows) can be seen as a dark line enclosing the contents of the carpal tunnel. The median
nerve (heavy white arrow) can be identified just beneath the TCL. Guyon's canal is a
triangular space just outside the carpal tunnel.

102

Hamulus or hook of hamate bone

 

Figure 2.5: Level of the hook of the hamate is well within the carpal tunnel. The
transverse carpal ligament (light arrows) appears as a dark border to the carpal tunnel.
The median nerve (heavy white arrow) is just deep to the TCL, surrounded by flexor
tendons.

103

First metacarpal

Second metacarpal

 

Figure 2.6: Level of the base of the metacarpals. The metacarpals form an arch beginning
with the first metacarpal (of the thumb). The transverse carpal ligament (light white
arrows) can still be seen as a dark border of the carpal tunnel.

Study Subjects by Age and Diagnosis

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Subject Number Age Diagnosis

1 38 None

2 51 None

3 46 None

4 21 None

5 46 None

6 21 None

9 31 Carpal Tunnel Syndrome
10 52 Lateral Epicondylitis

l 1 38 Lateral Epicondylitis

12 44 Lateral Epicondylitis

13 40 Tenosynovitis

14 51 Lateral Epicondylitis

18 52 Carpal Tunnel Syndrome

 

Figure 3.1: This table lists all of the subjects with age and diagnosis. Asymptomatic
subjects have diagnoses listed as "None."

105

Subject Name:
Subject number: 00__xxxx

 

Date

 

PROLONGED TYPING/MRI RESEARCH STUDY
QUESTIONNAIRE

Please indicate if you have ever had the symptoms of, or have ever been told you have the following by
circling the correct response, if yes, describe.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Heart disease YES NO
High blood pressure YES NO
Stroke YES NO
Diabetes YES NO
Rheumatoid arthritis YES NO
Osteo arthritis YES NO
Lupus YES NO
Fibromyalgia YES NO
Carpal Tunnel Syndrome YES NO
Lateral Epicondylitis YES NO
Fracture of arm, forearm or wrist YES NO
Surgery YES NO
Implants of any kind YES NO
Could you be pregnant now? YES NO
Do you use caffeine? YES NO How much
Do you use nicotine? YES NO How much

 

List medicines you use daily or as needed:

 

 

Indicate how many hours you routinely type at one time/in one day 1-3 4-6 8-10
DATE OF BIRTH
MEDICAL RELEASE

 

I GIVE MY CONSENT FOR Michigan State University MRI RESEARCH TEAM MEMBERS TO
RELEASE INFORMATION REGARDING ANY DIAGNOSITIC INFORMATION TO THE
PHYSICIAN LISTED BELOW IN THE UNLIKELY EVENT THE RADIOLOGIST DISCOVERS AN
ABNORMALITY IN MY RESEARCH MRI EXAMINATION.

PHYSICIAN NAME

 

ADDRESS PHONE NUMBER

 

I AM VOLUNTEERING TO PARTICIPATE IN THIS RESEARCH STUDY. I HAVE READ AND
ACCEPTED THE TERMS OF THE INFORMED CONSENT. I GIVE MY CONSENT FOR THE MRI
RESEARCH TEAM TO USE THE INFORMATION OBTAINED THROUGH THE REPETITIVE
STRESS INJURY MRI PROJECT THAT PERTAINS TO ME FOR RESEARCH, PUBLICATION AND
FURTHER STUDY. I UNDERSTAND MY NAME WILL NOT BE USED, HOWEVER
DEMOGRAPHIC INFORMATION AND THE RESULTS OF ANY RELATED TESTS MAY BE USED
FOR THIS RESEARCH PROJECT, AND FOR FUTURE PROJECTS OF THIS NATURE. MY NAME
AND OTHER IDENTIFYING INFORMATION WILL BE HELD AS CONFIDENTIAL
INFORMATION, AND NOT RELEASED WITHOUT MY SPECIFIC INFORMED CONSENT.

PARTICIPANT'S SIGNATURE
Figure 3.2

 

106

RSI/TYPING RESEARCH STUDY INFORMED CONSENT

You have been asked to volunteer in a research study involving the use of a Magnetic Resonance
Imaging (MRI) examination. The purpose of this examination is to study what occurs in the
tissues of the forearm and wrist when exposed to prolonged typing and during rest. Because many
symptoms, especially numbness, tingling and pain, occur at night, a portion of this study will
involve nighttime tests. You have been selected because you are either diagnosed with or
experience symptoms of a repetitive stress injury in your forearms or wrists, and continue to work
with a primary work requirement of typing.

Magnetic Resonance Imaging requires the use of a very large permanent magnet made in the
shape of a large tube with a movable table on tracks that carries the person into the center of the
imaging magnet. It is imperative that the subject of these examinations avoids wearing or
carrying any metal objects that may be magnetic during the test. As a participant in this
study, you will be asked to lie face down, then on your side on the imaging table with your
dominant arm over your head inside a smaller “extremity coil” for about thirty minutes for each
test. Use of a positioning splint helps position your forearm and wrist comfortably inside the
extremity coil. There will be three examinations, one before you begin typing, one immediately
following typing and one at night. If you request one, we will schedule a visit to the MRI area, in
order for you to see the magnet and experience the experimental position inside the magnet.
When you agree to participate, you will be given several questionnaires including a general health
questionnaire, the Magnetic Resonance Imaging questionnaire, and a questionnaire to determine
your level of symptoms of repetitive stress injury.

If selected for the study, you will be asked to participate in a physical examination of your arms.
This will include strength testing, sensory testing, range of motion, nerve conduction studies, and
MRI examination the morning of the experiment. You will then report for your normal work
duties. Immediately following vocational typing of at least three hours, you will be given a
second MRI examination. You will be asked to return between 6 and 8 pm that evening for a
period of absolute rest followed by a final MRI examination. You will be compensated $60.00 for
participation as a subject in this study.

We hope that if you agree to participate in the experiments, you will complete all requirements of
the study. However, should you decide not to complete any portion of the experiments, there will
be no attempt to force you to continue, and there will be no penalty for stopping your
participation at any time, for any reason.

It is not expected that there is any potential for harm in this study. However, it is necessary that
you understand that Michigan State University and the faculty and students participating in this
project do not compensate for injuries incurred as a result of your participation in this research.
The questionnaire is provided to screen volunteers with health risks that are inappropriate for this
study.

 

 

 

I agree to take part in this project as described above.
Signature Date

Witness Date

Figure 3.3

107

LEVINE CARPAL TUNNEL SYNDROME SYMPTOM SEVERITY

SUBJECT NUMBER DATE

SCALE
TABLE I

 

The Following questions refer to your symptoms for a typical twenty-four-hour period during the

past two weeks (Circle one answer to each question).

How severe is the hand or wrist pain that you have at night?

1.)
2.)
3.)
4.)
5.)

I do not have hand or wrist pain at night.
Mild pain

Moderate pain

Severe pain

Very severe pain

How often did hand or wrist pain wake you up during a typical night in the past two weeks?

I.)
2.)
3.)
4.)
5.)

Never

Once

Two or three times
Four or five times

More than five times

Do you typically have pain in your hand or wrist during the daytime?

r.)
2.)
3.)
4.)
5.)

I never have pain during the day

I have mild pain during the day

I have moderate pain during the day
I have severe pain during the day

I have very severe pain during the day

How often do you have hand or wrist pain during the daytime?

l.)
2.)
3.)
4.)
5.)

Never

Once or twice a day

Three to five times a day
More than five times a day

The pain is constant

How long, on average, does an episode of pain last during the daytime?

l.)

I never get pain during the day

108

2.)
3.)
4.)
5.)

Less than 10 minutes
10 to 60 minutes
Greater than 60 minutes

The pain is constant throughout the day

Do you have numbness (loss of sensation) in you hand?

I.)
2.)
3.)
4.)
5.)

No

I have mild numbness

I have moderate numbness
I have severe numbness

I have very severe numbness

Do you have weakness in your hand or wrist?

l.)
2.)
3.)
4.)
5.)

No weakness

Mild weakness
Moderate weakness

I have severe numbness

I have very severe numbness

Do you have tingling sensations in your hand?

1.)
2.)
3.)
4.)
5.)

No tingling

Mild tingling
Moderate tingling
Severe tingling

Very severe tingling

How severe is numbness (loss of sensation) or tingling at night?

1.)
2.)
3.)
4.)
5.)

I have no numbness or tingling at night
Mild

Moderate

Severe

Very severe

How often did hand numbness or tingling wake you up during the past two weeks?

1.)
2.)
3.)
4.)
5.)

Never

Once

Two or three times
Four to five times

More than five times

109

Do you have difficulty with the grasping and use of small objects such as keys or pens?
1.) No difficulty
2.) Mild difficulty
3.) Moderate difficulty
4.) Severe difficulty
5.) Very severe difficulty
SUBJECT NUMBER: DATE:

 

Figure 3.4

110

LEVINE FUNCTIONAL STATUS SCALE

TABLE II

On a typical day the past two weeks have hand and wrist symptoms caused you to
have any difficulty doing the activities listed below? Please circle one number that
best describes you ability to do the activity.

 

 

 

 

 

 

 

 

 

 

Activity N o Mild Moderate Severe Cannot Do at
difficulty Difficulty Difficulty Difficulty All Due to
Hand and Wrist
Symtoms

Writing 1 2 3 4 5

Buttoning of clothes 1 2 3 4 5

Holding a book 1 2 3 4 5

while reading

Gripping of a 1 2 3 4 5

telephone handle

Opening of jars l 2 3 4 5

Household chores l 2 3 4 5

Carrying of grocery 1 2 3 4 5

bags

Bathing and dressing 1 2 3 4 5

 

 

 

 

 

 

Figure 3.5

111

 

PHYSICAL EXAMINATION TYPING/RSI RESEARCH STUDY

 

 

 

 

Subject Number: Date of examination:
Date of Birth Time of examination:
Examiner

Hand Tested: Right Left

Dominant hand: Right Left

Completion of questionnaire: note all questions answered yes, and explain:

 

Subject indicates she routinely types four hours at a time: YES NO
Right Left
Phalen’s test: Indicate positive or negative

Proprioception: Index finger
Normal/abn N ormal/abn

Reflexes:
Location Scale 0-4/4 Right Scale 0-4/4 Left Normal/Abnormal
Biceps
Triceps
Brachioradialis

 

 

 

 

 

 

 

 

 

 

Manual muscle tests:

 

 

 

 

 

 

 

 

 

Muscle Strength Right Strength Left 1-5/5 Normal/Impaired
1-5/5

Deltoid /5 /5
Biceps /5 /5
Triceps l5 /5
Wrist extension /5 /5
Wrist flexion l5 /5
Interosseous /5 l5
Extensor indicus /5 /5
Abductor Pollicus /5 /5
Brevis

 

 

 

 

 

 

Nerve ' Normal/Abnormal
Radial — Thumb
Median- Index f.

Ulnar — Small f.
Nerve root 6
Nerve root 7
Nerve root 8

 

112

PHYSICAL EXAMINATION TYPING/RSI RESEARCH STUDY

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Page 2 of 2
Grasp andminch strength in pounds: Right Left
[three trials)
Right Right Right Left Left Left
Trial 1 Trial 2 Trial 3 Trial 1 Trial 2 Trial 3
Mass gray
Lateral pinch
Three jaw chuck
Tip pinch
Nerve conduction study
Right Nerve Stimulation] D.L MSEC AMP Dist. Normal]
Record Microvolt cm Abnormal
Median / / 14/6
Ulnar 14/6

 

 

 

 

 

 

 

 

Figure 3.6: This physical examination for provided a standardized method of recording results.

113

 

 

 

Figure 3.7: Dual T2 weighted images used to establish Calculated average T2 for individual
muscles.

114

 

Ktr'i 1"}. UNI," "'1'

 

 

Figure 4.1: Position of wrist and hand using thermoplastic splint within the wrist coil

115

Radial nerve

Flexor digitorum profundus

Median nerve
Flexor digitorum superficialis

Ulnar nerve

Flexor carpi ulnaris

 

Figure 4.2: Forearm muscles and neurovascular compartments in an axial image used to
calculate Random Calculated Muscle T2 in Milliseconds.

116

         

Before Exercise After Typing Post Rest
Figure 4.3: Carpal tunnel of Subject 1 at the hook of the hamate. The arrow indicates the
median nerve.

117

      

' . ' » ' 1
Before Exercise After Typing Post Rest
Figure 4.4: Carpal tunnel at the hook of the hamate of Subject 2, arrow indicates the
median nerve. Note the change from triangular/flat to triangular to oval.

118

Calculated T2 Forearm Muscle
Typing Subjects

 

32

 

;+—ml
—i—am
—i—em'
—a—edl
+fdp :

 

T2 in Milliseconds

—+—MS

—+—mr

—+—mu

 

 

O 3 6 9 12
Hours
Baseline After typing Post Rest

Figure 4.5: Averaged Calculated T2 of forearm muscles of all typing subjects
demonstrates the increase in T2 relaxation time immediately following typing in the more
active muscles contrasted with the flat or less acute increase in T2 of the less active
muscles.

119

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Random Calculated T2 Forearm Baseline After Post P
Muscle typing Rest value
Flexor pollicis longus (FPL) 28.82 29.45 29.43 0.51
Abductor Pollicis Longus (APL) 31.02 31.58 30.43 0.34
Extensor Pollicis Longus (EPL) 30.13 30.10 29.58 0.51
Extensor Digitorum (ED) 28.89 29.27 28.74 0.76
Flexor Digitorum Profundus (FDP) 28.38 29.44 28.48 0.02
Flexor Digitorum Superficialis 28.76 29.90 0.01
(FDS) 28.28

Flexor Carpi Radialis (FCR) 28.87 29.30 27.73 0.02
Flexor Carpi Ulnaris (FCU) 28.82 30.38 28.51 0.01
Extensor Carpi Radialis Longus 0.10
(ECRL) 30.07 28.79 29.07
Extensor Carpi Ulnaris (ECU) 30.62 26.00 30.11 0.10

 

Figure 4.6: Forearm muscle Random Calculated T2 in milliseconds with corresponding

significance level.

120

 

Muscle T2 Relaxation Times of Control Subject

 

 

 

 

 

31
+ ECU
30 ‘ \\_ + FPL ‘
g 4 -. + ECR
§ 29 \ /____A ~1~ APL
to v—
2 28 7 a , ' 7'" +ED
g l i + FDP
27 \.\_‘ ‘ —— FDS ,
1 —~ PCB
26 . ‘ + FCU
0 3 6 9 12
Hours
Baseline After typing Post Rest

Figure 4.7: The T2 relaxation time in milliseconds of the non-typing control is depicted
in this graph. Note that the T2 decreases or remains flat in all muscles analyzed here. The
control subject did not type, and therefore her muscles would not be expected to
demonstrate an increase in T2 After Typing. The Post Rest T2s are as expected- as well.

121

Typing vs. Control
Extensor and Thenar Muscle Calculated T2

    
 
 

 

‘ "‘7 — — l—+-ECU

;—-l—-ECFI
32 l ED
I -aI —APL

 

. —+— ECU control

\j + ECR control

 

 

 

 

Calculated T2 in Milliseconds
to
CD

 

\7— MW 1 .. \f —I—ED control

_ l —-— APL control

261*— 7777 u“““~~-~~-- ]-----FPL
- ‘ ““~-u —o——FPLcontroI

24 l I “ ‘ - A - —I— — EPL
22 . : + EPL control

0 3 6 9 12
Hours
Baseline After typing Post Rest

Figure 4.8: Comparison of the extensor and thenar muscle groups calculated mirscle T2
of the control subject with typing subjects showing no significant change in T2 with
passage of time (control solid line) or typing (broken line).

122

Extensor Digitorum Calculated T2 Relaxation Times
With Control Subject

 

 

 

 

 

 

 

 

 

 

i+Subject 5 l
l—o—Subect6 ‘1
.fControl] .

 

W

.5 _- - h I-
g +Subject 2
§ ~ar~ Subject 3 .
g —--a—- Subject 4 '
2 .
.E

N

'—

 

 

Hours
Baseline After typing Post Rest

Figure 4.9: Scatterplot of Calculated T23 of Extensor Digitorum all study subjects
including the non-typing control.

123

Flexor Digitorum Profundus T2
With exposure to Typing

 

+ SUbjeci 1

+ Subject 2 A

+ Subject 3 1 .
. ——+— Subject 4 I
.. l + Subject 5 l I

T2 in Milliseconds

j + Subject 6 ' ?

 

 

‘ --Control 7 : ,

 

O 3 6 9 1 2
Hours

Baseline After typing Post Rest

4.10: Scatterplot of Calculated T2 of Flexor Digitorum. Compared to the previous graph,
the consistent increase in the T2 Relaxation times of the active muscles compared to the
Control is significant. This demonstrates the pattern of T2 increases with exercise,
decrease with rest in an active muscle.

124

Median Nerve T2
TCL
Typing vs control
90

 

—°-r Subject 1
+ Subject 2 j
. --— Subject 3 ~

 

—-— Subject 4 ‘

 

 

. —I— Subject 5 ‘

T2 in Milliseconds

+ Subject 6 .
‘-°-Control ~

 

 

Hours
Baseline After typing Post Rest

Figure 4.1 1: Graphic representation of the pattern of T2 changes in the median nerve with
exposure to typing.

125

Median Nerve Surface to Area Ratio Typing Subjects

 

 

 

0.5

0.45 , , - , - , - -
2
g 0.4. - - -
D.
5 0.35 - , - ~ ~ ~ , -
8
i 0.3 ,
2
o 0.25 - - - -
8
‘g 0.2 -
m
3,015
8
2 0.1 A ,
<

0.05 ,

0

TCL Pisiform Hamate Metacarp

Baseline - Typing - Post Rest

Figure 4.12: This chart graphically depicts the surface to area ratios at each of the four
imaging levels. The bar to the left represents "Baseline," the center bar represents "After
typing," and the right bar represents "Post Rest." Variation at the hook of the hamate and
metacarpal level, while more noticeable, still do not approach statistical significance.

126

Shape of the Median Nerve at the Hook of Hamate
Mean and Standard Devlation

Rank Sum

 

Baseline After typing Post rest

Figure 4.13: Graph of Rank Sum comparing the changes in shape of the median nerve at
the imaging level hook of the hamate. Variation is seen between at Baseline, After
Typing and Post Rest. This imaging level was chosen because it is beneath the TCL and
is suggestive of compression from both the TCL and flexor tendons within the carpal
tunnel.

127

Median Nerve T2 at the TCL
Typing vs control

100

 

I Subject 2
E1 Subject 3
E1 Subject 4
I Subject 5 ‘
I Subject 6
VIControl ‘

T2 in Milliseconds

 

 

 

0 3 12
Hours

Baseline After typing Post Rest
Figure 4.14: This histogram compares T25 of the median nerve of each subject with error

bars. While the trends are apparent, the lack of statistical significance is graphically
demonstrated.

128

Asymptomatic Cohort Median Nerve Level of TCL

 

 

 

 

 

Correlations
BASELINE TYPING REST
BASELINE Pearson Correlation 1.000 .879‘ .832
Sig. (2-tailed) . .050 .080
N 5 5 5
TYPING Pearson Correlation .879‘ 1.000 .478
Sig. (2-tailed) .050 . .416
N 5 5 5
BEST Pearson Correlation .832 .478 1.000
Sig. (2-tailed) .080 .416 .
N 5 5 5

 

 

 

 

 

 

'- Correlation is significant at the 0.05 level (2-tailed).

Figure 4.15: This Pearson Correlation Table illustrates the significant correlation between
changes in the calculated T2 of the median nerve of typing subjects.

129

Changes in Median vs Ulnar Nerve T2
Typing Subjects Compared to Control

 

 

 

 

 

 

 

7° ’—.’—subj3MN‘
6° ’ +Subj4MN
5° ’ ’ ” ” ’ ' " —I—Subj5MN‘
f: 40 ’ ' " ' ' ” ”L—o—SubjeMN‘
.5 30 .
3: —o—Sub13UN‘
E 20 __ Subj4UN.
o 10’ ' Subj5UN
0 \ —o—Subj6UN
'10 ' ._ — — — — I—O—Control
_20..__ . , MN,
0 3 6 9 12
Baseline After typing Hours Post Rest

Figure 4.16: This graph demonstrates the range of T2 Relaxation time variation in the
median nerves of typing subjects compared to the narrower range of the T2 values of
both the ulnar nerves of typing subjects and the median and ulnar nerves of the non-
typing control subjects.

130

 

Figure 5.1: Phalen’s test requires the subject to place the backs of the hands together with
the wrists acutely flexed. This increases carpal tunnel pressure, and often elicits
complaints of paresthesias or pain in the thumb, index, long and ring fingers in less than
one minute.

131

 

 

 

 

 

 

Investigator Surface Calculated Asymptomatic Symptomatic Visible Visible
to Area T2 Cohort Cohort shape T2

of the signal
nerve intensity

Radiologist X X X

LB

Radiologist X X X X X

KR

Radiologist X X X

JP

Author X X X X X X

 

 

 

 

 

 

 

Figure 5.2: Images analyzed were axial T2 and gradient echo images of the forearm of
each of the subjects.

132

 

     

  

Level proximal to the TCL Level of the pisiform Level of the hook of hamate
Figure 5.3: This asymptomatic subject’s median nerve is somewhat flattened at each
level. It changes shape subtlety at each of the imaging levels. The ulnar nerve (black
arrow) remains oval or rounded at each of the imaging levels. These images are of the
same subject taken at baseline.

133

          

, . _.'-r .‘ 2"" ~ -'. r,
. ,, .41. 4| . .
t. . -. .. . 1
Level proximal to TCL Level of pisiform bone Level of the hook of hamate

 

Figure 5.4: This asymptomatic subject’s median nerve (heavy white arrow) is oval. It

widens and flattens at the TCL, but remains essentially oval. A distinct point becomes
apparent at the hook of the hamate. The ulnar nerve remains oval (light white arrow).

Note the change in shape of the carpal tunnel at the different imaging levels.

134

              

Level proximal to TCL Level proximal to TCL Level of pisiform bone
Figure 5.5: These images of the median nerves of symptomatic subjects just proximal to
the transverse carpal ligament and at the level of the pisiform illustrate the two
deformities of the median nerve most reported in the literature, flattening (heavy white
arrow) and edema (right image, white arrow).

135

         

Level proximal to TCL Level of pisiform bone

 

Level of hook of amate

Figure 5.6: Fast Spin Echo T2 images at the imaging levels: Proximal to transverse carpal
ligament, Level of Pisiform, and Hook of Hamate, magnified x 3. The white arrow
indicates the Median nerve. This is a symptomatic subject, diagnosis carpal tunnel
syndrome. Note size of median nerve and presence of thickened connective tissue
surrounding the median and ulnar nerves proximal to the TCL. This connective tissue
“tether” disappears at the pisiform level, and the size of the median nerve diminishes as it
passes through the carpal tunnel denoting swelling of the median nerve prior to entry into
the carpal tunnel. The signal intensity of the median nerve visibly increases from TCL to
pisiform, and from pisiform to hamate.

136

 

 

1’

Level of the pisiform Level of the hook of the hamate

Figure 5.7: Note the dramatic flattening of the median nerve (large arrow) in an image of

a symptomatic subject at the level of the pisiform, left, and hook of the hamate, right. The
ulnar nerve (small arrow) is ovoid, suggesting minimal compression of the ulnar nerve.

137

Change in Median Nerve T2

Asymptomatic vs. Symptomatic Subjects

 

I

Change in T2

 

 

-15

 

9
Hours

Baseline After typing

 

‘—-I—-Subj3MN
‘——A—vSubj4MN
.—-—-Subj5MN
--o—-Subj6MN
+Subj9MN

—o—Subj10 MN
—I—Subj11MN
+Subj 15 MN .
—-—Subj16 MN

I
—-—Subj17 MN
A—O—Subj 18 MN

-—l—Cont Subj 7 ‘

12 —Cont 8qu 147‘

Post Rest

Figure 5.8: T2 relaxation time changes in the median nerve when the subject was exposed
to typing. This scatterplot depicts symptomatic subjects (solid) tend to have minimally
increased or decreased T2 after typing, while asymptomatic subjects (broken) tend to
have increased T2 SI. Following the prolonged rest period, T25 of several of the
symptomatic subjects increased slightly above Baseline levels. Heavy, solid lines indicate
controls. Changes in T2 are defined as the calculated T2 at each time period minus the T2

relaxation time at Baseline.

138

Ulnar Nerve T2 Differences
Symptomatic Vs Asymptomatic

 

 

 

 

.E 40 7 7 7 7
a --—3
E —-I- 4
a -.-5
2 _.-._ 6
8 «n ‘
u —I-7control
.E =
o 8 +9
%3 +10
.53; ‘—-—11
E ——15
e ~—+—-16
'3', +17
g ,—A—18
5 —-—14control

 

 

Hours

Baseline After typing Post Rest

Figure 5.9: Less variation in T2 is noted in this graph of ulnar nerves of all subjects. T2
of control subjects (Black lines) remains below Baseline, while the majority of typing
subjects’ T25 (Dashed line) increase to above Baseline in the Post Rest interval.
Symptomatic subjects’ ulnar nerve T25 both increase and decrease below Baseline levels
After Typing. Changes in T2 are defined as the calculated T2 at each time period minus
the T2 relaxation time at Baseline.

139

Symptomatic Subjects Reported Pain

 

+ Subject 9
+ Subject 10
- - era—Subject 11 ‘
»+ Subject 12
+ Subject 13

7 7 l + Subject 14
—1— Subject 15
- - -0- Subject 16

—--— Subject 17
+ Subject 18'

 

 

Pain Zero to Ten Scale

 

 

O 3 6 9 12
Hours

Baseline After typing Post Rest

Figure 5.10: Subjects 9 and 18 were diagnosed with carpal tunnel syndrome prior to this
study. The heavy black line represents the subject who acted both as a typing subject and
control. Her reported pain was zero while acting as a non-typing control, and
demonstrated delayed onset of pain after rest.

140

Change in Median Nerve T2 Asymptomatic vs.
Symptomatic Subjects

 

 

 

 

Change in calculated T2 Relaxation
Time In Milliseconds

 

Hours

Baseline After typing Post Rest

Figure 5.1 l: Asymptomatic subjects (dashed lines) increased T2 relaxation times, while
symptomatic subjects (solid lines) were more likely to decrease T2’s or remain
unchanged. Changes in T2 are defined as the calculated T2 at each time period minus the
T2 relaxation time at Baseline.

141

Change in Median Nerve T2 Asymptomatic vs.
Symptomatic Proximal to TCL With controls

 

+ 6
+7control
+ 9

 

——10
—-—11
+15
+16

Change in calculated T2 in
milliseconds

 

+ 14wcontrol‘

 

 

 

 

Hours

Baseline After typing Post Rest

Figure 5.12: Median nerve T2 relaxation time trends are noted in this scatter plot. The
median nerves of symptomatic subjects (red lines) tend to vary less than those of
asymptomatic subjects (green lines). Several T2 relaxation times remain fairly constant
After Typing, then increase above Baseline, while others decrease After Typing, then
recover to a value above Baseline. Only one asymptomatic subject’s T2 relaxation time
decreases After Typing. Changes lack statistical significance. Changes in T2 are defined
as the calculated T2 at each time period minus the T2 relaxation time at Baseline.

142

 

 

 

 

 

 

Median Nerve Average T25: Baseline After typing Post Rest
Asymptomatic Subjects

Proximal to TCL 39.73 49.15 45.59
Pisiform 39.57 42.38 43.23
Hook of Hamate 41.92 46.63 42.13
Metacarpal heads 38.79 37.57 43.09

 

 

 

 

 

Figure 5.13: Average T25 of the asymptomatic subjects’ median nerve at the four
imaging levels. Changes are not statistically significant using a repeated measures

ANOVA (p=0. 14).

 

 

 

 

 

Ulnar Nerve: Asymptomatic Subjects Baseline After typing Post Rest
Proximal to TCL 48.56 45.61 52.31
Pisiform 47.45 39.71 47.96
Hook of Hamate 47.65 38.86 48.68

 

 

 

 

Figure 5.14: T2 values of the Ulnar nerve were not available at the metacarpal heads. The

ulnar nerve branches before it reaches this imaging level.

 

 

 

 

 

 

Median Nerve: Symptomatic Subjects Baseline After typing Post Rest
Proximal to TCL 50.17 53.02 55.15
Pisiform 50.25 48.26 48.22
Hook of Hamate 49.42 49.15 51.67
Metacarpal heads 53.24 51.84 52.98

 

 

 

 

 

Figure 5.15: The T2 value changes were not statistically significant at After Rest

(p=0.56).

I43

 

 

Ulnar Nerve: Symptomatic Subjects Baseline After typing Post Rest

 

 

 

 

Proximal to TCL 55.2 58.15 50.25
Pisiform 54.05 54.88 55
Hook of Hamate 51.2 49.97 58.87

 

 

 

 

 

Figure 5.16: No statistical significance was noted After Rest in symptomatic subjects’
average T25 of the ulnar nerve (p=0. 17).

144

 

Median and Ulnar Nerves
Symptomatic vs Asymptomatic
T2 Relaxation Times

 

+ MN TCL

+ UN TCL

+ MN Pisiform

—-— UN Pisiform

+ MN Hamate

-o- UN hamate

+ MN TCL Sympto
+ UN TCL sympto
--— MN Pisiform Sympto
+ UN Pisiform Sympto
+ MN Hamate Sympto
+ UN Hamate Sympto

T2 relaxation times

 

 

 

 

0 3 6 9 12
Hours
Baseline After typing Post Rest

 

 

 

Figure 5.17: For the most part, asymptomatic subjects' average T28 maintained a lower
average T2 than those of symptomatic subjects. The one exception is the average of the
ulnar nerve at the transverse carpal ligament of one of the asymptomatic subjects.

145