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About the Author
Sally Caldwell earned her Ph.D. in Sociology from the University of North
Texas. The author of Romantic Deception (Adams Media, 2000), Caldwell
focuses her primary research interest on the topic of deception in social rela-
tionships. Caldwell resides in a small village in the hill country of south central
Texas and serves on the faculty of the Department of Sociology at Texas
State University|San Marcos.
Copyright 2012 Cengage Learning. All Rights Reserved. May not be copied, scanned, or duplicated, in whole or in part. Due to electronic rights, some third party content may be suppressed from the
eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional
content at any time if subsequent rights restrictions require it.
Brief Contents
Introduction: Methods, Material, and Moments to Remember 1

1 The What and How of Statistics 4
2 Describing Data and Distributions 21
3 The Shape of Distributions 54
4 The Normal Curve 74
5 Four Fundamental Concepts 96
6 Confidence Intervals 114
7 Hypothesis Testing With a Single Sample Mean 155
8 Hypothesis Testing With Two Samples
(Mean Difference and Difference Between Means) 185
9 Beyond the Null Hypothesis 210
10 Analysis of Variance 229
11 The Chi-Square Test 263
12 Correlation and Regression 283
Appendix A Table of Areas Under the Normal Curve (Distribution of Z ) 318
Appendix B Family of t Distributions (Two-Tailed Test) 320
Appendix C Family of t Distributions (One-Tailed Test) 321
Appendix D Distribution of F (.05 Level of Significance) 322
Appendix E Distribution of F (.01 Level of Significance) 323
Appendix F Distribution of Q (.05 Level of Significance) 324
Appendix G Distribution of Q (.01 Level of Significance) 325
Appendix H Critical Values for Chi-Square (χ2) 326
Appendix I Critical Values of r (Correlation Coefficient) 327
Appendix J Data Sets and Computer-Based Data Analysis 328
Appendix K Some of the More Common Formulas Used in the Text 334
Answers to Chapter Problems 337
Glossary 343
References 349
Index 351
vii
Contents
Introduction: Methods, Material,

and Moments to Remember 1
1 The What and How of Statistics 4

Before We Begin 5
A World of Information 5
Levels of Measurement 8
Samples and Populations 12
The Purposes of Statistical Analysis 14
Descriptive Statistics 15
Inferential Statistics 15
Chapter Summary 17
Some Other Things You Should Know 18
Key Terms 19
Chapter Problems 19
2 Describing Data and Distributions 21

Before We Begin 22
Measures of Central Tendency 22
The Mean 22
The Median 26
The Mode 28
Measures of Variability or Dispersion 30
The Range 30
Deviations From the Mean 31
ix
x Contents
The Mean Deviation 34

The Variance 36
The Standard Deviation 39
n Versus n – 1 46
Chapter Summary 50
Key Terms 51
Chapter Problems 51
3 The Shape of Distributions 54

Before We Begin 55
The Basic Elements 55
Beyond the Basics: Comparisons and Conclusions 58
A Special Curve 63
Chapter Summary 70
Key Terms 72
Chapter Problems 72
4 The Normal Curve 74

Before We Begin 75
Real-World Normal Curves 76
Into the Theoretical World 79
The Table of Areas Under the Normal Curve 82
Finally, an Application 89
Chapter Summary 93
Key Terms 94
Chapter Problems 95
5 Four Fundamental Concepts 96

Before We Begin 97
Fundamental Concept #1: Random
Sampling 97
Fundamental Concept #2: Sampling Error 100
Fundamental Concept #3: The Sampling Distribution
of Sample Means 103
Fundamental Concept #4: The Central Limit Theorem 105
Contents xi
Chapter Summary 110

Key Terms 112
Chapter Problems 112
6 Confidence Intervals 114

Before We Begin 115
Confidence Interval for the Mean 115
Confidence Interval for the Mean With s Known 116
An Application 117
Reviewing Z Values 118
Z Values and the Width of the Interval 120
Bringing in the Standard Error of the Mean 120
The Relevance of the Central Limit Theorem
and the Standard Error 123
Confidence and Interval Width 126
A Brief Recap 128
Confidence Interval for the Mean With σ Unknown 129
Estimating the Standard Error of the Mean 129
The Family of t Distributions 132
The Table for the Family of t Distributions 134
An Application 138
A Final Comment About the Interpretation
of a Confidence Interval for the Mean 140
A Final Comment About Z Versus t 141
Confidence Intervals for Proportions 142
An Application 143
Margin of Error 145
Chapter Summary 147
Key Terms 150
7 Hypothesis Testing With

a Single Sample Mean 155
Before We Begin 156
Setting the Stage 156
A Hypothesis as a Statement of Your Expectations:
The Case of the Null Hypothesis 157
Single Sample Test With s Known 159
Refining the Null and Phrasing It the Right Way 160
The Logic of the Test 161
xii Contents
Applying the Test 163

Levels of Significance, Critical Values,
and the Critical Region 166
But What If . . . 170
But What If We’re Wrong? 171
Single Sample Test With s Unknown 176
Some Variations on a Theme 178
Chapter Summary 179
Key Terms 181
8 Hypothesis Testing With Two Samples (Mean

Difference and Difference Between Means) 185
Before We Begin 186
Related Samples 186
The Null Hypothesis 191
Combining the Logic and the Null 191
The Estimate of the Standard Error of the Mean
Difference 192
Interpreting the Results 193
Some Additional Examples 194
Independent Samples 195
Combining the Logic and the Null 199
The Estimate of the Standard Error
of the Difference of Means 199
Interpreting the Results 202
Some Additional Examples 203
Chapter Summary 204
Key Terms 206
9 Beyond the Null Hypothesis 210

Before We Begin 211
Research or Alternative Hypotheses 211
Contents xiii
One-Tailed and Two-Tailed Test Scenarios 213

Testing a Non-directional Research Hypothesis 214
Testing a Directional Research Hypothesis 217
Power and Effect 221
Chapter Summary 225
Key Terms 226
10 Analysis of Variance 229

Before We Begin 231
The Logic of ANOVA 231
From Curves to Data Distributions 233
The Different Means 234
From Different Means to Different Types of Variation 236
The Application 239
Calculating the Within-Groups Sum of Squares (SSW) 240
Calculating the Between-Groups Sum of Squares (SSB ) 243
From Sums of Squares to Estimates of Variance 245
Calculating the F Ratio 249
The Interpretation 250
Interpretation of the F Ratio 250
Post Hoc Testing 252
Chapter Summary 256
Key Terms 258
11 The Chi-Square Test 263

Before We Begin 264
The Chi-Square Test of Independence 264
A Focus on the Departure From Chance 269
The Application 271
The Formula 275
The Calculation 275
Conclusion and Interpretation 276
Chapter Summary 278
Key Terms 279
xiv Contents
12 Correlation and Regression 283

Before We Begin 284
Scatter Plots 284
Linear Associations: Direction and Strength 286
Other Types of Association 288
Correlation Analysis 289
Two Variables: X and Y 290
The Logic of Correlation 292
The Formula for Pearson’s r 293
Application 296
Interpretation 298
An Additional Step: Testing the Null 300
Conclusion and Interpretation 301
Regression Analysis 302
An Application 302
The Logic of Prediction and the Line of Best Fit 304
The Regression Equation 306
The Standard Error of the Estimate 309
Chapter Summary 311
Key Terms 312
Appendix A Table of Areas Under the Normal Curve
(Distribution of Z) 318
Appendix B Family of t Distributions (Two-Tailed Test) 320
Appendix C Family of t Distributions (One-Tailed Test) 321
Appendix D Distribution of F (.05 Level of Significance) 322
Appendix E Distribution of F (.01 Level of Significance) 323
Appendix F Distribution of Q (.05 Level of Significance) 324
Appendix G Distribution of Q (.01 Level of Significance) 325
Appendix H Critical Values for Chi-Square (χ2) 326
Appendix I Critical Values of r (Correlation Coefficient) 327
Appendix J Data Sets and Computer-Based Data Analysis 328
It Usually Starts with Rows and Columns 328
Good News; Words of Caution; It’s Up to You 332
Appendix K Some of the More Common Formulas Used in
the Text 334
Answers to Chapter Problems 337
Glossary 343
References 349
Index 351
Preface
The idea behind this book came from my students, after I watched countless
semesters unfold in a predictable fashion. The scene repeats itself each year in
a classroom largely populated with panic-stricken students facing their first for-
mal encounter with the field of statistical analysis. I like to think that my passion
for the subject matter allows me to connect with most of the students, but there
are always some students who remain locked in the throes of fear. For those
students, mere passion on my part won’t get the job done. What’s called for,
I’ve discovered, is constant attention to the students’ perspective—a willingness
to respect the roadblocks (real or imaginary) that exist in their minds.
For some students, the roadblock is what I call the fear of the formula
factor—the tendency to recoil at the mere mention of a mathematical formula.
For other students, it’s the so what? scenario—the tendency for many students
to question the relevance of the subject matter and why they have to take the
course in the first place. I believe there’s a way to overcome these roadblocks,
and that’s the method I’ve attempted to present in Statistics Unplugged.
For those who are familiar with the second edition, I trust that you’ll find
the fundamental approach has remained the same in this third edition. I’ve
maintained the emphasis on the logic behind statistical analysis and the focus
on an intuitive understanding that I believe lies within virtually every student.
I’ve also tried to keep the language simple and friendly—something that seems
to work for the students.
Changes to the Fourth Edition

As with previous editions, the changes to the fourth edition were driven by re-
viewers and students. I was fortunate to have suggestions from a valuable cadre
of professors who teach introductory statistics, as well as a host of students who
took the time to let me know how I might improve the text. When it comes
time to update a text, it doesn’t get any better than to check with the folks who
are in the trenches.
xv
xvi Preface
As to the specific changes, there are content and technological changes

that have been implemented. On the content side of the ledger, the number
of learning checks in the book has increased markedly, and the discussion
of some fundamental topics has been expanded to a noticeable degree. For
example, the discussion of the standard deviation, variance, and Z scores has
been expanded, as has the treatment of two other central concepts—namely,
the notion of a sampling distribution and the concept of the standard error.
I am increasingly convinced that these two concepts are linchpins to devel-
oping a solid understanding of inferential statistics. As for the technological
changes, Statistics Unplugged now has an interactive counterpart in the form
of CourseMate, a major addition that should promote more student engage-
ment in the process of statistical reasoning. The CourseMate element also will
provide students with increased opportunities for self-evaluation through online
tests and work problems.
Acknowledgments
In many ways, a book, and particularly a statistics text, is but a string of ideas
woven together in what the author hopes will be a coherent or otherwise useful
fashion. Eventually, it falls to a team of dedicated individuals to bring the proj-
ect to life. In the case of Statistics Unplugged, it is the team of talented people
at Cengage and their associates who have made the fourth edition a reality.
Accordingly, the following individuals have my sincere appreciation:
Tim Matray, Acquisitions Editor
Nicole Richards, Editorial Assistant
Janay Pryor, Marketing Project Manager
Carolyn Deacy, Art Director
Lynn Lustberg, Project Manager
Kathleen Cunningham, Cover Designer
Equally important were the reviewers who offered a critical reading of and
suggestions for material from the first edition of this book through the current
edition. With their firsthand knowledge of what it means to teach inferential
statistics, the value of contributions from the reviewers cannot be overstated.
And with the list of reviewers growing ever longer, I now think of Statistics
Unplugged as a collaborative effort.
Reviewers for the first edition were:
James Knapp, Southeastern Oklahoma State University
Paul Ansfield, University of Wisconsin, Oshkosh
Lora Schlewitt-Haynes, University of Northern Colorado
Ida Mirzaie, Ohio State University
Charles Harrington, University of Southern Indiana
Steve Weinert, Cuyamaca Community College, Rancho
San Diego, California
J. Oliver Williams, North Carolina State University
Preface xvii
Holly Straub, University of South Dakota

Faye Plascak-Craig, Marian College
Michael Hurley, George Mason University, Fairfax County, Virginia
Susan Nolan, Seton Hall University, South Orange, New Jersey
Reviewers for the second edition were:
Robert Abbey, Troy University, Troy, Alabama
David Hardy, Loyola Marymount University, Los Angeles
Steven Scher, Eastern Illinois University
Alvin Shoemaker, Calvin College, Grand Rapids, Michigan
Beverley Whalen-Schmeller, Tennessee State University
Reviewers for the third edition were:
David J. Hardy, Loyola Marymount University
Heather Gelhorn, University of Colorado, Boulder
Colleen Swain, University of Florida
Andrew Garner, University of Mississippi
Allan R. Barnes, University of Alaska, Anchorage
Reviewers for the fourth edition were:
Stephen Weinert, Cuyamaca College, Rancho San Diego, California
Steve Bounds, Arkansas State University
Kathleen C. McCulloch, Idaho State University
Stewart Shankman, University of Illinois at Chicago
Deborah Carroll, Southern Connecticut State University
Alisha Janowsky, University of Central Florida
Barbara E. Rowan, Wesleyan College, Middletown, Connecticut
At my institution, I am lucky to be surrounded by wonderful colleagues, and
two in particular remain central to my efforts with Statistics Unplugged. First,
there is my department chair, Susan Day, who has created the most affirming
work environment I could ever imagine. I think it’s safe to say that all of my
colleagues join me in praise of Susan’s leadership abilities. There’s no doubt
about it: Susan manages to keep the ship afloat in a way that lets us get our
work done. Then there is another colleague of mine, Kay Newing, who shares
my passion for the field of statistics and who is always willing to hear me out if
I have a question or comment. Kay brings some very valuable ingredients to the
table of camaraderie; namely, a passion for teaching, a truly fine intellect, and
a wonderful sense of humor.
Equally important, the students who serve as tutors and lab instructors in
our department have been a constant barometer on course content. This corps
of very bright students has always been a valuable resource and is deserving of
my deepest appreciation:
Melanie Moody
Patricia Morton
Blanca Davilla
xviii Preface
Daniel Japko
Kellie Cochran
Brittany (Bee) Barnett
Patrick Dew
Victoria Munoz
April Hudson
Margot Hake
Colin Pierson
Nick Lalone
Apart from those wonderfully talented students in the Tutoring
Office and Statistics Lab, there are two other students who deserve special
mention—Thomas Garcia and J.L. Bailey. Thomas Garcia served as my intern
during the time that I was putting some of the finishing touches on the revision
material. Thomas went way beyond the call of duty to keep me organized and
bring good humor to my life on a daily basis. I don’t know that I will ever think
about the fall semester of 2011 without thinking about Thomas Garcia. As for
J.L. Bailey, he served as my graduate assistant for two years and was a statistics
tutor for two years before that. Over the years, J.L. came to be a central figure
in my life. He covered classes when I was ill; he graded tests; he fielded student
questions; he served as my all around sounding board. He reviewed and edited
my work, and he also laughed at my jokes. I will never think about my teach-
ing career without thinking about J.L. Bailey. He’s the type of student who
reminds me of the true rewards that are to be found in the world of academia.
Finally, when it comes to acknowledgments, there is the very special col-
lection of people who have brought an untold amount of joy into my life. Each
has, in some way, contributed to the completion of this effort. Whether in the
form of encouragement or an understanding of my schedule, the folks in this
circle of special people have made major contributions.
For example, nobody brings any more laughter into my world than John
Friedli. A simple phone call from John will stay in my mind for days, just
because of his unlimited wit. And in the same way, even a brief conversation
with my friend Steve Klepfer will linger in my mind as I think through his astute
observations about politics or life in general.
And then there is Eric Groves. Even though he’s been a part of my life
for decades, words still fail me when the topic is Eric. But Eric understands all
of that, and that’s what matters. Finally, there are Marilee Wood and Tevis
Grinstead—two people who live life on a grand scale and allow me to vicari-
ously partake of their adventures. Marilee and Tevis are generous beyond mea-
sure. Dinner at their home here in the Hill Country or a trip to their home in
Santa Fe is like a retreat into a very different world—a world in which time
immediately slows down, good wine is poured, and the conversation flows—a
world that reminds me of the true importance of friendship.
Introduction
Methods, Material, and Moments
to Remember
S tatistics, Quantitative Methods, Statistical Analysis—words, phrases, and

course titles that can shake the confidence of nearly any student. Let me put
your mind at ease right away. Your experience with statistics doesn’t have to
be a horror story. In fact, your experience with statistics can be an enjoyable
one—a venture into a new way of thinking and looking at the world. It’s all a
matter of how you approach the material.
Having taught statistics to legions of undergraduate students, I’ve spent
a lot of time trying to understand how students react to the material and why
they react the way they do. In the process, I’ve developed my own approach
to the subject matter, and that’s what I’ve tried to lay out in this book. As we
get started, let me tell you a little more about what to expect as you work your
way through this book.
First, let me explain my method. I’m committed to the idea that the subject
matter of statistics can be made understandable, but I’m also convinced that
it takes a method based on repetition. Important ideas and concepts can be
introduced, but they have to be reintroduced and reemphasized if a student is to
get the connection between one concept and the next. Repetition—that’s the
method I’ve used in this book, so you should be prepared for that.
At times you may wonder why you’re rereading material that was empha-
sized at an earlier point. Indeed, you’ll likely start muttering “not that again!” If
that happens, enjoy the moment. It signals that you’re beginning to develop a
sense of familiarity with the central concepts.
I’ve also tried to incorporate simplicity into the method—particularly in
the examples I’ve used. Some examples will probably strike you as extremely
simplistic—particularly the examples that are based on just a few cases and the
ones that involve numbers with small values. I trust that simplistic examples
won’t offend you. The goal here is to cement a learning process, not to master
complicated mathematical operations.
My experience tells me that a reliance on friendly examples, as opposed
to examples that can easily overwhelm, is often the best approach. When
numbers and formulas take center stage, the logic behind the material can get
1
2 Introduction Methods, Material, and Moments to Remember
lost. That point, as it turns out, brings us to the essence of the material you’re
about to encounter.
In the final analysis, it’s often the logic behind statistics that proves to be
the key to success or failure. You can be presented with formulas—simple or
complex—and you can, with enough time and commitment, memorize a string
of them. All of that is well and good, but your ability to grasp the logic behind
the formulas is a different matter altogether. I’m convinced that it’s impossible
to truly understand what statistics is all about unless you understand the logic
behind the procedures. Consequently, it’s the logic that I’ve tried to emphasize
in this book.
Indeed, it’s safe to say that numbers and formulas have taken a back seat
in this book. Of course you’ll encounter some formulas and numbers, but that’s
not where the emphasis is. Make no mistake about it—the emphasis in this
book is on the conceptual basis behind the calculations.
There’s one other thing about the material that deserves comment. Like it
or not, the traditional approach to learning new material may come up short
when you want to learn about statistical analysis. The reason is a simple one:
The field of statistics is very different from other subjects you’ve studied in
the past.
If, for example, you were taking a course to learn a foreign language, you’d
probably figure out the goal of the course fairly early. You’d quickly sense that
you’d be learning the basics of grammar and vocabulary, trying to increase your
command of both over time. I suspect you’d have a similar experience if you
signed up for a history course. You’d quickly sense that you were being intro-
duced to names, dates, places, and overall context with the goal of increasing
your understanding of the how and why behind events.
Unfortunately, the field of statistical analysis doesn’t fit that learning model
very well. You may be able to immediately sense where you’re going in a lot
of courses, but that’s not necessarily the case in the field of statistics. In fact,
my guess is that a command of statistical analysis is probably best achieved
when you’re willing to go along for the ride without really knowing at first where
you’re going. A statement like that is close to heresy in the academic world, so
let me explain.
There is an end game to statistical analysis. People use statistical analysis
to describe information and to carry out research in an objective, quantifiable
way. Indeed, the realm of statistical analysis is fundamental to scientific inquiry.
But the eventual application of statistical analysis requires that you first have a
firm grasp of some highly abstract concepts. You can’t even begin to appreci-
ate the very special way in which scientists pose research questions if you don’t
have the conceptual background.
For a lot of students (indeed, most students, I suspect), it’s a bit much
to tackle concepts and applications at the same time. The process has to be
broken down into two parts—first the conceptual understanding, and then the
applications. And that’s the essence of my notion that you’re better off if you
don’t focus at the outset on where you’re going. Concentrate on the con-
ceptual basis first. Allow yourself to become totally immersed in an abstract,
Introduction Methods, Material, and Moments to Remember 3
c onceptual world, without any thought about direct applications. In my judg-

ment, that’s the best way to conquer the field of statistical analysis.
If you’re the sort of student who demands an immediate application of
concepts—if you don’t have much tolerance for abstract ideas—let me strongly
suggest that you lighten up a bit. If you’re going to master statistics—even at
the introductory level—you’ll have to open your mind to the world of abstract
thinking.
Toward that end, let me tell you in advance that I’ll occasionally ask you to
take a moment to seriously think about one notion or another. Knowing stu-
dents the way I do, I suspect there’s a chance (if only a small chance) that you’ll
ignore my suggestion and just move ahead. Let me warn you. The approach of
trying to get from Point A to Point B as quickly as possible usually doesn’t work
in the field of statistics. When the time comes to really think about a concept,
take whatever time is necessary.
Indeed, many of my students eventually come to appreciate what I mean
when I tell them that a particular concept or idea requires a “dark room mo-
ment.” In short, some statistical concepts or ideas are best understood if con-
templated in a room that is totally dark and void of any distractions. Those
should become your moments to remember. I’m totally serious about that, so
let me explain why.
Many statistical concepts are so abstract that a lot of very serious thought
is required if you really want to understand them. Moreover, many of those
abstract concepts turn out to be central to the statistical way of reasoning.
Simply reading about the concepts and telling yourself that you’ll remember
what they’re all about won’t do it. And that’s the purpose behind a dark room
moment.
If I could give you a single key to the understanding of statistics, it would
be this: Take the dark room moments seriously. Don’t be impatient, and don’t
think a few dark room experiences are beneath your intellectual dignity. If I tell
you that this concept or that idea may require a dark room moment, heed the
warning. Head for a solitary environment—a private room, or even a closet.
Turn out the lights, if need be, and undertake your contemplation in a world
void of distractions. You may be amazed how it will help your understanding
of the topic at hand.
Finally, I strongly urge you to deal with every table, illustration, and work
problem that you encounter in this text. The illustrations and tables often con-
tain information that can get you beyond a learning roadblock. And as to the
work problems, there’s no such thing as too much practice when it comes to
statistical applications.
Now, having said all of that as background, it’s time to get started. Welcome
to the world of statistics—in this case, Statistics Unplugged!
1
The What and How of Statistics
Before We Begin
A World of Information
Levels of Measurement
Samples and Populations
The Purposes of Statistical Analysis
Descriptive Statistics
Inferential Statistics
Chapter Summary
Some Other Things You Should Know
Key Terms
Chapter Problems
We start our journey with a look at the question of what statisticians do and
how they go about their work. In the process, we’ll explore some of the funda-
mental elements involved in statistical analysis. We’ll cover a lot of terms, and
most of them will have very specific meanings. That’s just the way it is in the
field of statistics—specific terms with specific meanings. Most of the terms will
come into play repeatedly as you work your way through this book, so a solid
grasp of these first few concepts is essential.
4
A World of Information 5
Before We Begin
One question that seems to be on the mind of a lot of students has to do
with relevance—the students want to know why they have to take a course
in statistics in the first place. As we begin our journey, I’ll try to answer that
question with a few examples. Just to get started on our relevance mission,
consider the following:
Let’s say that you’re applying for a job. Everything about the job is to your
liking. You think that you’re onto something. Then you encounter the last line
of the job description: Applicants must have a basic knowledge of statistics
and data analysis.
Perhaps you’re thinking about applying to graduate school in your chosen
field of study. You begin your research on various graduate programs across
the nation and quickly discover that there’s a common thread in program re-
quirements: Some background in undergraduate statistics or quantitative
methods is required.
Maybe you’re starting an internship with a major news organization and
your first assignment is to prepare a story about political races around the
state. Your supervisor hands you a stack of recent political polls, and you hit
the panic button. You realize that you really don’t know what is meant by the
phrase margin of error, even though you’ve heard that phrase hundreds of
times. You have some idea of what it means, but you don’t have a clue as to
its technical meaning.
Finally, maybe it is something as simple as your employer telling you that
you’re to attend a company year-end review presentation and report back.
All’s well until you have to comprehend all of the data and measures that are
discussed in the year-end review. You quickly realize that your lack of knowl-
edge about statistics or quantitative analysis has put you in a rather embarrass-
ing situation.
Those are just a few examples that I ask you to consider as we get started.
I can’t promise that your doubts about the relevance of statistics will immedi-
ately disappear, but I think it’s a good way to start.
A World of Information
People who rely on statistical analysis in their work spend a lot of time dealing
with different types of information. One person, for example, might collect
information on levels of income or education in a certain community, while
another collects information on how voters plan to vote in an upcoming elec-
tion. A prison psychologist might collect information on levels of aggression in
inmates, while a teacher might focus on his/her latest set of student test scores.
There’s really no limit to the type of information subjected to statistical analysis.
Though all these examples are different, all of them share something
in common. In each case, someone is collecting information on a particular
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2 “The Myography of Nerve-degeneration in Animals and Man,” Archives of Medicine,
viii., No. 1, 1882.
In the period of recovery or regeneration of the nerve the musculo-

galvanic reactions slowly reacquire their normal characters; the
normal suddenness and completeness of the contractions gradually
appear, and faradic excitation causes slight responses. Lastly, the
nerve also begins to exhibit excitability under galvanism and
faradism. These various abnormal electrical reactions, also
frequently observed in diseases of the spinal cord, constitute the so-
called reaction of degeneration, or De R. The subject is one of much
practical importance, and for details the reader is referred to the
treatises on electro-therapeutics of Erb and De Watteville.
Just as we depend upon the De R. to prove interruption of motor

nerve-fibres (or, in other cases, destruction of ganglion cells in the
anterior horns of the cord), so do we rely upon the demonstration of
complete anæsthesia to prove interruption of sensory fibres. In
seeking for the area of anæsthesia several points must be borne in
mind: (1) The normal distribution of the principal nerve-trunks as
taught by ordinary anatomical works; (2) the remarkable anomalies
of distribution which sometimes occur; (3) that many nerves near
their endings exchange filaments in very variable numbers; loops for
collateral innervation, which will supply some sensibility to parts
which, judging by ordinary anatomical rules, should be made
anæsthetic by section of a given nerve-trunk; (4) another
consideration is the degree of anæsthesia. Before pronouncing upon
the complete and fatal division of a nerve-trunk (by injury or by
disease), absolute anæsthesia should be demonstrated in its area of
principal and isolated distribution. Ordinary tests are not, as a rule,
sufficient for this purpose. The best means in our experience
consists in the use of a very strong induction (faradic) current, as
follows: The skin of the suspected region to be thoroughly dried and
rubbed with chalk or powdered starch; one pole, consisting of an
ordinary wet electrode, to be applied just above the part to be tested,
and the other pole, consisting of a single wire, with which different
parts of the anæsthetic area are to be touched. By this means
partially insensible regions, not responding to pricking and burning,
may be made to yield reaction, and the area of absolute anæsthesia
be thereby much reduced. Malingering may also be readily exposed
by this test, which presents another advantage—viz. of not causing
local injury or scars as burning will.
It follows from the preceding statements that in cases of limited

atrophic paralysis with De R. the diagnosis between a central lesion
(destruction of ganglion cells of the anterior horns of the cord) and a
strictly peripheral (or neural) lesion is to be chiefly based upon two
considerations: (1) The distribution of the paralysis, which in the first
case affects muscles which are physiologically grouped or
associated, while in the second case the simple law of anatomical
associations or grouping is observed; (2) by the state of sensibility,
which is normal in disease of the anterior horns of the cord, and is
frequently impaired or abolished in nerve lesions.
Lesions affecting the cauda equina cause all the above-mentioned

symptoms of peripheral lesions in a limited (partial) paraplegic
distribution. If the lesion or injury be in the sacro-coccygeal region,
the symptoms will, as a rule, be found confined to parts below the
knee, occasionally also involving the muscles on the posterior aspect
of the thigh (flexors of the leg). Below the knees we find an atrophic
paralysis with De R., anæsthesia of the foot and part of the leg, loss
of plantar and achillis reflexes, and the sphincter ani will be
paralyzed. The patellar reflex is preserved or exaggerated. In case
the lesion be in the lumbar region, below the first lumbar vertebræ,
the symptoms will be found to extend as high as the groin, involving
also the buttocks and sphincter ani; state of the bladder variable. All
reflexes will be lost in the paralyzed extremities, except in some
cases the cremasteric reflex.
Strange as it may appear, physicians do not always remember that

there is practically no lumbar spinal cord (vide Fig. 2.), and that
injuries, etc. of the lumbar vertebræ and dura tend to affect nerves,
and not a nervous centre.
II. Localization of Lesions in the Spinal Cord.
Diseases of the spinal cord are distinguished by the following

general characters, positive and negative:
Positive Characters.—Tendency to primary bilateral or paraplegic

distribution of all the symptoms. In the majority of cases preservation
of electro-muscular excitability, and in one well-defined group of
cases De R. more or less typically developed in the paralyzed parts.
Frequent vesical and rectal paralysis, either of the retaining or of the
ejecting apparatus. Pains and other paræsthesiæ in the extremities,
the pains often possessing the electric or fulgurating character.
Anæsthesia of paraplegic distribution. Sensations of constriction or
cincture about a limb or about the body at various levels. Occurrence
of ataxia without paralysis. Progressive muscular atrophy without
actual paralysis. Easy production of eschars (bed-sores).
Negative Characters.—Absence of typical hemiplegic or monoplegic

distribution of symptoms. Rarity of head symptoms, as headache,
vertigo, mental disturbance; of lesions of the optic nerve. Absence of
epileptiform convulsions. Absence of such grouping of motor and
sensory symptoms as would exactly correspond to the area of
distribution of one or more large nerve-trunks.
The above symptomatic indications are, of course, of the most

general meaning only, and are liable to exceptions and subject to
varying conditions.
The DIAGNOSIS of the exact localization of lesions in the spinal cord,

considered from the clinical standpoint, is perhaps best arrived at by
following an anatomical and physiological order of subdivision of the
problem into three questions, as follows:
FIRST QUESTION.—BEING GIVEN SYMPTOMS INDICATING DISEASE LIMITED TO

ONE OR MORE SYSTEMS OF THE SPINAL CORD, TO DECIDE WHICH ARE
AFFECTED.
Physiology and the results of embryological and pathological
researches justify us in making a general division of the spinal cord,
for purposes of diagnosis, into two great systems, whose limits are
fairly well known—viz. the æsthesodic or sensory system, and the
kinesodic or motor system. The following outline diagram (Fig. 5) of
section through the spinal cord exhibits the ascertained limits of the
two systems.
FIG. 5.
Diagram of a Transverse Section of the Spinal Cord through the Cervical

Enlargement: The æsthesodic system is shaded, the kinesodic system
unshaded. Parts of the æsthesodic system: (1) Posterior nerve-roots; (2)
posterior gray horns; (3) fasciculi cuneati (columns of Burdach, inclusive
of posterior root-zones); (4) fasciculi graciles (columns of Goll or posterior
median columns); (5) ascending cerebellar fasciculi; (6) columns of
Clarke. Parts of the kinesodic system: (7) Anterior roots; (8) anterior
columns (inclusive of anterior root-zones); (9) anterior gray horns; (10)
crossed pyramidal fasciculi; (11) direct pyramidal fasciculi (columns of
Türck); [10 and 11 are the intraspinal prolongation of the cerebral motor
tract]; (12) lateral columns, of ill-defined limits and unknown functions; P.
R., posterior roots; P. S., posterior septum; A. R., anterior roots; A. F.,
anterior fissure.
A. Lesions of the Æsthesodic System.—Limits of the Æsthesodic
System.—By this term we mean that combinations of ganglion-cells
and nerve-fibres whose functions are locally sensory, and of those
fibres which transmit impressions centripetally (frontad) to the
encephalon. The following are the recognized parts of this system,
as outlined on the diagram: (1) the posterior (dorsal) nerve-roots and
attached ganglia; (2) the posterior gray horn and central gray
substance to an unknown distance ventrad; (3) the fasciculi cuneati
(columns of Burdach), whose lateral parts are more particularly
designated as posterior root-zones; (4) the fasciculi graciles
(columns of Goll) or posterior median columns; (5) the fasciculi ad
cerebellum; (6) the vesicular columns of Clarke (most developed in
the dorsal part of the cord). All of these parts have sensory functions,
or at least transmit impressions centripetally, and they undergo
secondary (Wallerian) degeneration toward the encephalon—i.e.
frontad of a transverse lesion of the cord.3
3 There are some results of physiological experiments and a few isolated pathological
facts which would seem to point to the existence of other sensory (centripetal)
fasciculi in the lateral columns, but it would be wholly premature to make use of these
facts in a practical consideration of the subject.
At the present time there is only one lesion of the æsthesodic system
which can be diagnosticated during the patient's life from positive
symptoms.
(a) Lesions of the fasciculi cuneati (posterior root-zones, 3). The

symptoms of lesion (usually sclerosis) in this region are wholly
sensory and ataxic. At an early stage acute pains, fulgurating pains,
occur in the extremities; later paræsthesiæ, anæsthesia, and ataxia.
The fulgurating pains caused by the slowly-progressive lesion of the
posterior root-zones are very peculiar, and almost pathognomonic
(vide preceding article for their description). In some cases
paræsthesiæ precede the pains, which inversion of the usual order
must be due to a difference in the starting-point of the sclerosis
within the large fasciculi cuneati. Tendinous reflexes (especially the
patellar) are lost at an early period in the disease, and by noting the
disappearances of the different reflexes we can trace with some
accuracy the longitudinal extension of the sclerosis (vide Fig. 2). In
many cases the pupillary reflex is also abolished, constituting the
Argyll-Robertson pupil.
As negative characters of lesions of the posterior root-zones (and of

the rest of the æsthesodic system) we note absence of paralysis,
contracture, atrophy, and De R.
In the present state of our knowledge of spinal physiology and

pathology we think that a lesion in this location should be recognized
by the physician early and positively—in some cases years before
ataxia and other grosser symptoms make the diagnosis of locomotor
ataxia obvious even to a layman's eye.
(b) Lesions of the fasciculi graciles (column of Goll, 4) cannot, we

believe, be recognized directly by positive symptoms. There are a
few cases on record of primary (?) sclerosis of these columns, in
which during life vague sensory symptoms had been noted, but we
cannot build upon such data. Indirectly, however, we can in many
cases diagnosticate degeneration of these fasciculi, reasoning from
the data of pathological anatomy. Thus, for example, in advanced
cases of sclerosis of the fasciculi cuneati (posterior spinal sclerosis)
we know that in the dorsal and cervical regions of the cord the
columns of Goll are in a state of secondary degeneration. After
complete transverse division of the cord by injury, extreme pressure,
or focus of myelitis, etc. the same (centripetal) degeneration exists
above the lesion.
The same remarks apply fairly to our clinical knowledge of the

remaining parts of the æsthesodic system, columns of Clarke (6),
and fasciculi ad cerebellum (5). We know absolutely nothing of
lesions of the posterior horns (2) in their clinical and diagnostic
relations.
B. Lesions of the Kinesodic System.—Limits of the Kinesodic

System.—In general this includes the antero-lateral parts of the cord.
In a trans-section of the cord (vide Figs. 5 and 6) the following
columns and fasciculi are recognized, their location and limits being
made known to us by embryology, descriptive and pathological
anatomy: (7) The anterior (ventral) nerve-roots emerging from (8) the
true anterior columns or anterior root-zones; (9) the ventral (anterior)
gray horns with their groups of ganglion cells; (10) the crossed
pyramidal fasciculus, which is the caudal continuation of the cerebral
motor tract of the opposite hemisphere; (11) the direct pyramidal
column (column of Türck), which is the caudal continuation of the
cerebral motor part of the hemisphere on the same side; (12) the
antero-lateral column. Fasciculi 10 and 11 bear an inverse relation to
each other—i.e. 11 is larger in proportion as 10 is smaller.
FIG. 6.
Diagram of a Transverse Section of the Spinal Cord through the Lumbar

Enlargement: The æsthesodic system is shaded; the kinesodic system
unshaded. Parts of the æsthesodic system: (1) Posterior nerve-roots; (2)
posterior gray horns; (3) fasciculi cuneati (columns of Burdach, inclusive
of posterior root-zones); (4) fasciculi graciles (columns of Goll, or
posterior median columns); (5) ascending cerebellar fasciculi; (6)
columns of Clarke. Parts of the kinesodic system: (7) Anterior roots; (8)
anterior columns (inclusive of anterior root-zones); (9) anterior gray
horns; (10) crossed pyramidal fasciculi; (11) direct pyramidal fasciculi
(columns of Türck) [10 and 11 are the intraspinal prolongation of the
cerebral motor tract]; (12) lateral columns of ill-defined limits and
unknown functions; P. R., posterior roots; P. S., posterior septum; A. R.,
anterior roots; A. F., anterior fissure.
In a general way it may be stated that lesions of the kinesodic

system are characterized positively by the isolated existence or
predominance of motor symptoms, by impairment of muscular
nutrition, and by De R.; also by contractures. The reflexes are almost
never normal, being either exaggerated or lost. Negative symptoms
are—absence of sensory symptoms, of ataxia, and of vesical or
rectal symptoms.
(a) Lesions of the anterior gray horns (9) are revealed by most
definite and characteristic symptoms. There occurs a flaccid
paralysis involving more or less extensive groups of muscles in the
extremities, rarely truncal muscles, and never those of organic life. In
a few weeks the paralyzed muscles undergo atrophy, sometimes to
an extreme degree, and various degrees of De R. are present.
Cutaneous and tendinous reflexes are abolished. The bladder and
rectum are normal. Sensory symptoms absent, and if present consist
only of mild paræsthesiæ, which are probably due to postural
pressure upon nerve-trunks or to disturbance of the peripheral
circulation. There is no tendency to the formation of bed-sores, but
circulation and calorification are reduced in the paralyzed members.
It should be remembered that paralysis due to systematic lesion of
the anterior gray horns is never typically paraplegic, with horizontal
limit-line of sensory symptoms, a cincture feeling, and vesical
paralysis.
The above symptom-grouping is characteristic of lesion of the

anterior horns en masse; in other words, of poliomyelitis. In that form
of systematic disease of the anterior horns which consists primarily
and chiefly of a degeneration or molecular death of the ganglion cells
there is no true paralysis; the atrophy of muscles is infinitely slower,
and it proceeds in various muscles fasciculus by fasciculus, the
wasting being usually preceded by fibrillary contractions, and being
almost always symmetrically located on the two sides of the body
(affecting analogous or homologous parts). The electrical reactions
are abnormal, in that musculo-faradic reaction is lost in exact
proportion to the wasting; so that in a large muscle one part may
contract normally, while the adjacent fasciculi do not. It is as yet
uncertain whether De R. occur in this disease (progressive muscular
atrophy). Calorification and circulation are much less impaired than
in poliomyelitis; the negative symptoms are much the same.
It is sometimes difficult to distinguish poliomyelitis from generalized

neuritis. The diagnosis is to be made by the presence in the latter
disease of marked sensory symptoms—neuro-muscular pains,
numbness, slight anæsthesia—and by a grouping of symptoms
coinciding with the distribution of nerve-trunks and branches. No
assistance can be derived from electrical tests, as both diseases
yield more or less typical De R.
(b) Lesions of the spinal pyramidal tract (of fasciculi 10 and 11) are
followed by motor symptoms only—viz. paralysis and contracture—
or, in other words, by a spastic paralysis. Sensibility is unaffected;
the bladder, rectum, and truncal muscles are not distinctly paralyzed;
the reflexes are much increased, and ankle-clonus is often present.
The electrical reactions of the paralyzed muscles are normal,
qualitatively at least. The diagnosis of localization may be pushed
still farther by the following considerations:
(1) When the condition of spastic paralysis is unilateral, of

hemiplegic distribution, and follows an attack of cerebral disease of
some sort, we may feel sure that both the crossed and the direct
fasciculi of the pyramidal (10 and 11) belonging to one cerebral
motor tract are degenerated throughout the length of the spinal cord,
the crossed fasciculus on the paralyzed side and the direct on the
healthy side (same side as injured hemisphere). It would thus appear
that lesion of the direct pyramidal fasciculus (11) produces no
symptoms,4 except, of course, in those rare cases in which it is
larger than its associated crossed fasciculus.
4 Unless it be the increase of reflexes which is so often observed on the non-
paralyzed side in hemiplegics.
(2) The above symptoms may be bilateral, as observed in children

as a congenital or early-acquired condition. In such cases the four
fasciculi of the motor tract are degenerated or undeveloped, in
correspondence with a symmetrical bilateral lesion of the motor area
of the cerebrum—imperfect development or early destruction.
(3) When the legs alone are the seat of spastic paralysis, with
increased reflexes, spastic or tetanoid gait, without sensory
symptoms, the diagnosis of a primary sclerosis of both lateral
columns (inclusive of 10) of the spinal cord is justified.
(c) Lesions of antero-lateral columns of the cord (8 and 12), primary

and independent of lesions of the anterior horns or of the crossed
pyramidal fasciculus, cannot now be diagnosticated during life.
These large masses of fibres include fasciculi whose functions are
probably motor; others (especially in 12) whose functions, according
to recent experiments, may be sensory; and still others which are
associating or commissural.
(d) Various combinations of the above lesions occur, and may be

recognized positively during life: (1) Combined sclerosis of the
posterior columns and of the crossed pyramidal fasciculi (3 and 10),
indicated by ataxia with paralysis, absence of patellar reflex,
tendency to contracture, pains, and anæsthesia less marked than in
typical posterior spinal sclerosis. This symptom-group is usually
found in children; it is pre-eminently a family disease, and is known
as Friedreich's disease. Similar cases also occur in adults as a
strictly personal disease. (2) Secondary degeneration of the
pyramidal tract (10 and 11), with more or less localized atrophy of
cells in the anterior horns (9) coexists in two forms: First, in a few
cases of cerebral hemiplegia with contracture, and pathological
atrophy of various muscles on the paralyzed side; second, as a
distinctly spinal bilateral affection, characterized by a spastic or
tetanoid state of the lower extremities, and a mixture of atrophic
paralysis (vide (a)), with contracture in the arms and hands. This
latter form is the amyotrophic lateral sclerosis of Charcot.
SECOND QUESTION.—BEING GIVEN SYMPTOMS INDICATING A TOTAL

TRANSVERSE LESION OF THE SPINAL CORD, ONE INVOLVING ITS VARIOUS
SYSTEMS AT A CERTAIN LEVEL, TO DETERMINE THE ELEVATION OR FRONTO-
CAUDAL SITUATION OF THE LESION.
This question is usually easy of solution by the following method:

Since a transverse lesion of the spinal cord gives rise to both motor
and sensory symptoms of horizontal, paraplegic distribution caudad
of the lesion, the first thing to do is to determine accurately the upper
level of the symptom, either the line of anæsthesia or the limit of
paralysis. The former is always much more definite than the latter,
and usually serves as the guide to diagnosis, indicating accurately
the uppermost part of the lesion. In the thorax the levels of sensory
and motor symptoms nearly coincide, but in the extremities the
operation of Van der Kolk's law of distribution of motor and sensory
fibres of nerve-trunks must be borne in mind, although it does not
apply as strictly in this case as in nerve lesions strictly speaking.
Gowers's diagram will prove very serviceable in making a diagnosis
of transverse lesions, and will also prove of use in the study of
vertebral injury and disease, as it indicates with sufficient accuracy
the relation between vertebræ (spinous processes) and segments of
the spinal cord. (Vide Fig. 2.)
The following are the principal transverse localizations of disease

which are usually recognized during life by the above procedure:
(a) Lesions of the cauda equina (by tumors, caries, or fracture of the
bones, etc.) produce paralysis, anæsthesia, atrophy of muscles, with
De R., in the range of distribution of the sciatic nerves mainly. The
sphincter ani is paralyzed and relaxed, while the bladder remains
normal as a rule. In all essential respects this paraplegiform, but not
paraplegic, affection resembles that following injury to mixed nerve-
trunks. It is in reality an intra-spinal peripheral paralysis. The more
exact location of the lesion, in the absence of external physical signs
(fracture, etc.), may be approximately determined by a study of the
distribution of the symptoms and their relation to nerve-supply.
(b) Lesions of the lower end of the lumbar enlargement, or conus

medullaris, behind the first lumbar vertebra, will give rise to the same
symptoms as (a). The expression, lumbar part of the spinal cord,
should be more carefully used than it is at present in the discussion
of spinal injuries and spinal-cord diseases, disease of the lumbar
enlargement being common enough, but disease of the lumbar part
of the cord very rare. In the discussion of railway cases, more
especially, it is often forgotten that the spinal cord practically ends
behind the first lumbar vertebra.
(c) Lesions of the middle and upper parts (segments) of the lumbar
enlargement are evidenced by true paraplegia, without paralysis of
the abdominal muscles. In some cases the quadriceps group,
supplied by the crural nerve, is not paralyzed. The constriction and
the limit of anæsthesia are about the knees, at mid-thigh, or near the
groin in different cases. The paralyzed muscles, as a rule, retain
their irritability and show normal electrical reactions; the cutaneous
and tendinous reflexes are preserved or increased. The sphincter is
usually paralyzed, while the bladder is relatively unaffected.
(d) Transverse lesion of the dorsal spinal cord produces the classical
type of paraplegia—i.e. paralysis and anæsthesia of all parts caudad
of the lesion. The limit of anæsthesia and the constriction band are
nearly horizontal, and their exact level varies with the height of the
lesion, from the hypogastric region to above the nipples. Below the
level of anæsthesia, which indicates by the number of the dorsal
nerve the upper limit of the cord lesion, there are complete paralysis,
retention of urine, constipation with relaxed sphincter ani, greatly
exaggerated reflexes in the lower extremities, even to spinal
epilepsy; the muscles preserve their volume fairly well, and their
electrical reactions are normal—sensibility in all its modes is
abolished; bed-sores are easily provoked. Retention of urine is an
early symptom in lesion of the middle dorsal region of the cord—
sometimes, in our experience, preceding symptoms in the legs.
(e) A transverse lesion of the cord at the level of the last cervical and
first dorsal nerves—i.e. in the lower part of the cervical enlargement
—gives rise to typical paraplegia with a sensory limit-line at or just
below the clavicle, but also with some very peculiar symptoms
superadded. These characteristic symptoms are in the upper
extremities, and consist of paralysis and anæsthesia in the range of
distribution of the ulnar nerves. In the arms the anæsthesia will be
found along the lower ulnar aspect of the forearm, the ulnar part of
the hands, the whole of the little fingers, and one half of the annuli.
There will be paralysis (and in some cases atrophy with De R.)
affecting the flexor carpi ulnaris, the hypothenar eminence, the
interossei, and the ulnar half of the thenar group of muscles,
producing in most cases a special deformity of the hand known as
claw-hand or main-en-griffe. Another important symptom of a
transverse lesion in this location is complete paralysis of all the
intercostal and abdominal muscles, rendering respiration
diaphragmatic and making coughing and expectoration impossible.
The breathing is abdominal in type, and asphyxia is constantly
impending.
(f) A transverse lesion of the upper part of the cervical enlargement,

below the origin of the fourth cervical nerve, gives rise to symptoms
designated as cervical or total paraplegia. The lower extremities and
trunk are as in (d) and (e), but besides both arms are completely
paralyzed and anæsthetic. The limit of anæsthesia usually extends
along the clavicles to the acromion processes, or a little below, near
the deltoid insertions. All reflexes caudad of this line are vastly
increased, either with tonic or clonic contractions. In some cases of
pressure upon the cervical cord by tumors, caries of vertebræ, etc.
the tetanoid or spastic state of the extremities (the lower more
especially) may precede paralysis for a long time; as the
compression increases paralysis becomes more and more marked,
while the reflexes remain high. This constitutes the clinical group we
described in 1873 as tetanoid pseudo-paraplegia.
(g) Transverse lesions of the spinal cord from the decussation of the
pyramids to the fourth cervical nerve are very rare, and usually of
traumatic origin. They produce complete paralysis of the entire body,
and also of the diaphragm (third and fourth cervical nerves), thus
causing death by apnœa in a very short time.
(h) In ascending paralysis (Landry) the above symptom-groups,

excepting (a), (b), are met with at successive stages of the disease,
often by almost daily accession, until finally respiration ceases.
(i) The height of a transverse localized lesion (e.g. a stab-wound) of

one lateral half of the spinal cord is to be determined by the various
groupings of symptoms stated in the preceding paragraphs, the chief
guide being the limit-line between the sensitive and anæsthetic
portions of the body, measured vertically. The symptoms are,
however, distributed in a very remarkable manner on either side of
the median line. The paralysis will be found on the same side as the
lesion, often accompanied by hyperæsthesia, vaso-motor paralysis,
and loss of muscular sense, while the anæsthesia is on the other
side of the body. When such a lesion occurs below the first dorsal
nerve, the symptom-group is designated as hemiparaplegia; when
the lesion is higher up, so as to paralyze the arms, the affection is
termed spinal hemiplegia (Brown-Séquard).
Above the decussation of the pyramids total transverse lesions are

practically unknown, so that the second question need not be
followed farther.
By means of the data above given we are also enabled to determine

the length—i.e. fronto-caudal extension—of the systematic lesions of
the cord.
The symptoms of transverse lesions of the spinal cord are not

exclusively caudad of the lesion, and some very striking ones are
observable in the head. In lesions of the upper part of the dorsal cord
and of the cervical enlargement (e, f, g) we observe vaso-motor and
pupillary symptoms, due to injury of the spinal origin of the cervical
sympathetic nerve; the pupils are contracted; the cheeks and ears
congested and unnaturally warm; the cutaneous secretions are
increased. In other words, the symptoms about the head, frontad of
the lesion, are the same as those we produce experimentally in
animals by section of the cervical sympathetic or of the lower
cervical cord. In hemi-lesion of the cord, in man as in animals, these
symptoms are unilateral, on the same side as the injury.
Another point to be remembered in the study of transverse lesions of

the spinal cord is that the lesion may involve enough of the anterior
gray horns to give rise to atrophic paralysis with De R. in some few
muscles deriving their motor innervation from the focus of disease.
This is not rarely seen in cervical paraplegia.
THIRD QUESTION.—BEING GIVEN VERY LIMITED MOTOR OR SENSORY

SYMPTOMS OF SPINAL ORIGIN, TO DETERMINE THE EXACT LOCATION OF THE
FOCAL LESIONS CAUSING THEM.
(a) In the range of sensory disturbances this question rarely presents

itself for solution. Localized anæsthesia and pain of spinal origin
(except the fulgurating pains of tabes) are rare, and we do not know
the relation of cutaneous areas with the spinal segments as well as
we know the motor innervations. It should be stated here, however,
that the location of a fixed pain and of a zone of anæsthesia is often
of great value in determining what spinal nerve is affected, just
outside of the cord itself, by such directly-acting lesions as vertebral
caries, spinal pachymeningitis, tumors upon the spinal cord, etc.
Among the various symptoms of Pott's disease of the spine, fixed
pains in one side of the trunk, in one thigh, or in the upper occipital
region, etc. is a sign against which the physician should always be
on his guard, as it is a very early and valuable indication of the
existence of an affection which requires special treatment as soon as
a diagnosis can be made.
(b) Localized motor symptoms of spinal origin calling for a diagnosis

of the focal lesions causing them are frequent, and are mostly met
with in two affections—viz. progressive muscular atrophy and
poliomyelitis. The problem is now capable in many cases of an
approximately exact solution by the deductive application of our
knowledge of the intimate connection between certain muscles and
muscular groups and limited portions or segments of the spinal cord
(anterior gray horns more especially). This knowledge has been
accumulated and organized from ordinary anatomy, physiological
experiments, and more especially from carefully-made autopsies
with microscopic examination of the cord. We cannot present this
subject better than by reproducing a tabular statement of these
results prepared by M. Allen Starr.5 Future autopsies may correct this
table, and in making use of it the occurrence of anomalous nerve-
distribution should be remembered:
LOCALIZATION OF FUNCTIONS IN THE VARIOUS SEGMENTS OF

THE SPINAL CORD.
5 “The Localization of Functions of the Spinal Cord,” American Journal Neurology and
Psychiatry, iii., 1884.
The above table should be studied in connection with Gowers's

diagram of the vertebral column and spinal cord (Fig. 2, p. 53), for
the thorough study of cases of neural and spinal localization.
Additional details of much value with respect to the peripheral nerve
distribution are accessible in the works of Ranney6 and Ross7.
6 The Applied Anatomy of the Nervous System, N. Y., 1881, p. 355 et seq.
7 Handbook of Diseases of the Nervous System, Am. ed., Philada., 1885, p. 356 et
seq.
III. The Localization of Lesions in the Medulla Oblongata.
In general terms, lesions of the oblongata are characterized by the

early appearance and prominence of motor symptoms in the mouth,
throat, and larynx, and by bilaterality of the symptoms. Remote
symptoms consist of disturbances in the cardiac action and in the
functions of some intra-abdominal organs. There may also be more
or less paralysis of all the extremities. These lesions may
conveniently be classified, like those of the cord, into systematic and
focal.
A. SYSTEMATIC LESIONS OF THE OBLONGATA.—1. Systematic lesions of
the æsthesodic system of the oblongata are, for purposes of
practical diagnosis, unknown at the present time.
2. Systematic lesions of the kinesodic system of the oblongata, on

the other hand, are often positively recognizable during the patient's
life.
(a) The most strictly systematic and most frequent of these lesions is
that of secondary (Wallerian) degeneration of the pyramids, the
prolongation of the cerebral motor tract. This morbid change gives
rise to no distinct bulbar symptoms, and it can only be diagnosticated
inferentially or inclusively by determining the existence of secondary
degeneration of the entire pyramidal tract, from the occurrence of
hemiplegia followed by contracture and increased reflexes. If the
phenomena present be those of double spastic hemiplegia, there is
surely degeneration of both pyramids.
(b) A systematic lesion affects the nuclei (origins) of the facial,

hypoglossal, pneumogastric, spinal accessory, and the motor root of
the trigeminus nerves, giving rise to a classical symptom-group. The
symptoms thus produced are exclusively (?) motor and trophic,
consisting of progressively increasing paresis, with atrophy of the
muscles about the lips and cheeks, the intrinsic lingual muscles, the
laryngeal and pharyngeal muscles. Later, the masseters, temporals,
and pterygoids are sometimes involved; and, finally, extremely rapid
action of the heart with pneumonic symptoms indicates the gravest
extension of the morbid process. An early symptom in such cases is
abnormal salivation. These affections, generally designated as
varieties of bulbar paralysis, subacute or chronic, are usually readily
recognized intra vitam, and recent discoveries in morbid anatomy
have enabled us to correctly diagnosticate the seat of the lesion in its
various extensions. The laryngeal paralysis represents disintegration
(atrophy) of ganglion-cells in the bulbar origin of the spinal accessory
nerve; lingual atrophic paralysis indicates the same lesion in the
nuclei of the hypoglossal nerves; the labio-buccal symptoms are
produced by lesion of the facial nerve nucleus (inferior facial nucleus
of older writers); the paralysis of the muscles of mastication is due to
extension of cell-degeneration to the motor nucleus of the trigeminus
in the pons; and the final cardio-pulmonary symptoms indicate an
extension of the lesion into the sensory (?) origin of the
pneumogastric nerves.
It is evident that this systematic lesion of the oblongata is the

equivalent or analogue of the various acute and chronic lesions of
the anterior horns of the spinal cord, described supra, and in practice
we sometimes find these bulbar and spinal lesions associated:
progressive muscular atrophy of the extremities and amyotrophic
lateral sclerosis being complicated with bulbar paralysis.
B. FOCAL LESIONS OF THE MEDULLA OBLONGATA, as at present known,

occur mostly in the kinesodic system, but may also involve several
fasciculi and nuclei at one time. The symptoms of such lesions are
grouped in two principal types:
(a) Single symptoms, such as atrophy or atrophic paralysis of some

one muscle or muscular group innervated by the hypoglossal, facial,
or spinal accessory nerves. For example, unilateral atrophy of the
tongue, when not due to neural injury, is quite surely the
representative of destruction of one hypoglossal nucleus. It is
possible that some cases of peripheral facial paralysis, so-called, or
Bell's palsy, and cases of paralysis of the sterno-mastoid and
trapezius, are not due to neural lesion, but to primary disease of the
nuclei of the facial and spinal accessory nerves, either as
poliomyelitis or as progressive cell-degeneration and atrophy.
A similar reserve must be used in speaking of the localization of

small lesions in the oblongata, causing diabetes mellitus, polyuria,
albuminuria, and salivation. From experiments upon animals and a
few post-mortem examinations in human cases we know that such
lesions may occur and cause the symptoms, but their recognition
during the patient's life is at the present time next to impossible.
(b) The symptoms may be complex and belong to the general class
of crossed paralysis, the mouth, face, tongue, and larynx being

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Introduction: Methods, Material, and Moments to Remember 1

Introduction: Methods, Material,

1 The What and How of Statistics 4

2 Describing Data and Distributions 21

The Mean Deviation 34

3 The Shape of Distributions 54

4 The Normal Curve 74

5 Four Fundamental Concepts 96

Chapter Summary 110

6 Confidence Intervals 114

7 Hypothesis Testing With

Applying the Test 163

8 Hypothesis Testing With Two Samples (Mean

9 Beyond the Null Hypothesis 210

One-Tailed and Two-Tailed Test Scenarios 213

10 Analysis of Variance 229

11 The Chi-Square Test 263

12 Correlation and Regression 283

Changes to the Fourth Edition

As to the specific changes, there are content and technological changes

Holly Straub, University of South Dakota

S tatistics, Quantitative Methods, Statistical Analysis—words, phrases, and

c­ onceptual world, without any thought about direct applications. In my judg-

In the period of recovery or regeneration of the nerve the musculo-

Just as we depend upon the De R. to prove interruption of motor

It follows from the preceding statements that in cases of limited

Lesions affecting the cauda equina cause all the above-mentioned

Strange as it may appear, physicians do not always remember that

Diseases of the spinal cord are distinguished by the following

Positive Characters.—Tendency to primary bilateral or paraplegic

Negative Characters.—Absence of typical hemiplegic or monoplegic

The above symptomatic indications are, of course, of the most

The DIAGNOSIS of the exact localization of lesions in the spinal cord,

FIRST QUESTION.—BEING GIVEN SYMPTOMS INDICATING DISEASE LIMITED TO

Diagram of a Transverse Section of the Spinal Cord through the Cervical

(a) Lesions of the fasciculi cuneati (posterior root-zones, 3). The

As negative characters of lesions of the posterior root-zones (and of

In the present state of our knowledge of spinal physiology and

(b) Lesions of the fasciculi graciles (column of Goll, 4) cannot, we

The same remarks apply fairly to our clinical knowledge of the

B. Lesions of the Kinesodic System.—Limits of the Kinesodic

Diagram of a Transverse Section of the Spinal Cord through the Lumbar

In a general way it may be stated that lesions of the kinesodic

The above symptom-grouping is characteristic of lesion of the

It is sometimes difficult to distinguish poliomyelitis from generalized

(1) When the condition of spastic paralysis is unilateral, of

(2) The above symptoms may be bilateral, as observed in children

(c) Lesions of antero-lateral columns of the cord (8 and 12), primary

(d) Various combinations of the above lesions occur, and may be

SECOND QUESTION.—BEING GIVEN SYMPTOMS INDICATING A TOTAL

This question is usually easy of solution by the following method:

The following are the principal transverse localizations of disease

(b) Lesions of the lower end of the lumbar enlargement, or conus

Introduction: Methods, Material, and Moments to Remember 1

c onceptual world, without any thought about direct applications. In my judg-