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Undergraduate Lecture Notes in Physics

Jakob Schwichtenberg

Physics from
Symmetry
Second Edition
Undergraduate Lecture Notes in Physics
Undergraduate Lecture Notes in Physics (ULNP) publishes authoritative texts covering topics
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Department of Physics, University of Oslo, Oslo, Norway

Michael Inglis
SUNY Suffolk County Community College, Long Island, NY, USA

More information about this series at http://www.springer.com/series/8917

Jakob Schwichtenberg

Physics from Symmetry

Second Edition

123
Jakob Schwichtenberg
Karlsruhe
Germany

ISSN 2192-4791 ISSN 2192-4805 (electronic)

Undergraduate Lecture Notes in Physics
ISBN 978-3-319-66630-3 ISBN 978-3-319-66631-0 (eBook)
https://doi.org/10.1007/978-3-319-66631-0
Library of Congress Control Number: 2017959156

1st edition: © Springer International Publishing Switzerland 2015

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N AT U R E A L W AY S C R E AT E S T H E B E S T O F A L L O P T I O N S

ARISTOTLE

A S F A R A S I S E E , A L L A P R I O R I S TAT E M E N T S I N P H Y S I C S H A V E T H E I R

O R I G I N I N S Y M M E T R Y.

HERMANN WEYL

T H E I M P O R TA N T T H I N G I N S C I E N C E I S N O T S O M U C H T O O B TA I N N E W F A C T S

A S T O D I S C O V E R N E W W AY S O F T H I N K I N G A B O U T T H E M .

W I L L I A M L AW R E N C E B R AG G
Dedicated to my parents
Preface to the Second Edition

In the two years since the first edition of this book was published I’ve
received numerous messages from readers all around the world. I
was surprised by this large number of responses and how positive
most of them were. Of course, I was cautiously confident that read-
ers would like the book. Otherwise I wouldn’t have spent so many
months writing it. However, there is certainly no shortage of books
on group theory or on the role of symmetries in physics. To quote
Predrag Cvitanovic1 1
Predrag Cvitanović. Group Theory:
Birdtracks, Lie’s, and Exceptional Groups.
Almost anybody whose research requires sustained use of group Princeton University Press, 7 2008.
theory (and it is hard to think of a physical or mathematical problem ISBN 9780691118369
that is wholly devoid of symmetry) writes a book about it.

Moreover, I’m not a world renowned expert. Therefore, I knew no

one would buy the book because my name is written on the cover. So
the chances were high that "Physics from Symmetry" would simply
drown in the flood of new textbooks that are published every year.

Therefore, it’s reasonable to wonder: Why and how did "Physics

from Symmetry" avoid this fate?

I think the main reason for the success of the first edition is what I
framed as something negative above: it wasn’t written by a world
renowned expert. I wrote the book while I was still a student and,
as I remarked in the preface to the first edition, "I wrote the book I
wished had existed when I started my journey in physics". So my
motivation for writing the book wasn’t to create an authoritative ref-
erence or a concise text that experts would love. Instead, my only fo-
cus was to write a book that helps students understand. As a student
myself I always had still fresh in memory what I found confusing
and what finally helped me understand.

This point of view is nicely summarized in the following quote by

C.S. Lewis2 2
C. S. Lewis. Reflections on the Psalms.
HarperOne, reprint edition, 2 2017.
It often happens that two schoolboys can solve difficulties in their work ISBN 9780062565488
for one another better than the master can. When you took the problem
X

to a master, as we all remember, he was very likely to explain what

you understood already, to add a great deal of information which you
didn’t want, and say nothing at all about the thing that was puzzling
you. [...] The fellow-pupil can help more than the master because
he knows less. The difficulty we want him to explain is one he has
recently met. The expert met it so long ago he has forgotten. He sees
the whole subject, by now, in a different light that he cannot conceive
what is really troubling the pupil; he sees a dozen other difficulties
which ought to be troubling him but aren’t.

While most readers liked the student-friendly spirit of the first edi-
tion, it was, of course, not perfect. Several readers pointed out typos
and paragraphs with confusing notation or explanations. This feed-
back guided me during the preparation of this second edition. I
focused on correcting typos, improving the notation and I rewrote
entire sections that were causing confusion.

I hope these changes make "Physics from Symmetry" even more

3
No book is ever perfect and I’m al- student-friendly and useful3 .
ways happy to receive feedback. So if
you find an error, have an idea for im-
provement or simply want to comment Karlsruhe, September 2017 Jakob Schwichtenberg
on something, always feel free to write
me at mail@jakobschwichtenberg.com
Preface to the First Edition

The most incomprehensible thing about the world is that it is at all

comprehensible.

- Albert Einstein4 4
As quoted in Jon Fripp, Deborah
Fripp, and Michael Fripp. Speaking of
Science. Newnes, 1st edition, 4 2000.
In the course of studying physics I became, like any student of ISBN 9781878707512
physics, familiar with many fundamental equations and their solu-
tions, but I wasn’t really able to see their connection.

I was thrilled when I understood that most of them have a com-

mon origin: symmetry. To me, the most beautiful thing in physics is
when something incomprehensible, suddenly becomes comprehen-
sible, because of a deep explanation. That’s why I fell in love with
symmetries.

For example, for quite some time I couldn’t really understand

spin, which is some kind of curious internal angular momentum that
almost all fundamental particles carry. Then I learned that spin is
a direct consequence of a symmetry, called Lorentz symmetry, and
everything started to make sense.

Experiences like this were the motivation for this book and in
some sense, I wrote the book I wished had existed when I started my
journey in physics. Symmetries are beautiful explanations for many
otherwise incomprehensible physical phenomena and this book is
based on the idea that we can derive the fundamental theories of
physics from symmetry.

One could say that this book’s approach to physics starts at the
end: Before we even talk about classical mechanics or non-relativistic
quantum mechanics, we will use the (as far as we know) exact sym-
metries of nature to derive the fundamental equations of quantum
field theory. Despite its unconventional approach, this book is about
standard physics. We will not talk about speculative, experimentally
unverified theories. We are going to use standard assumptions and
develop standard theories.
XII
5
Starting with Chapter A. In addition,
the corresponding appendix chapters
are mentioned when a new mathemati-
cal concept is used in the text.
6
On many pages I included in the
margin some further information or
pictures.
Depending on the reader’s experience in physics, the book can be
used in two different ways:
• It can be used as a quick primer for those who are relatively new
to physics. The starting points for classical mechanics, electro-
dynamics, quantum mechanics, special relativity and quantum
field theory are explained and after reading, the reader can decide
which topics are worth studying in more detail. There are many
good books that cover every topic mentioned here in greater depth
and at the end of each chapter some further reading recommen-
dations are listed. If you feel you fit into this category, you are
encouraged to start with the mathematical appendices at the end
of the book5 before going any further.
• Alternatively, this book can be used to connect loose ends for more
experienced students. Many things that may seem arbitrary or a
little wild when learnt for the first time using the usual historical
approach, can be seen as being inevitable and straightforward
when studied from the symmetry point of view.
In any case, you are encouraged to read this book from cover to
cover, because the chapters build on one another.
We start with a short chapter about special relativity, which is the
foundation for everything that follows. We will see that one of the
most powerful constraints is that our theories must respect special
relativity. The second part develops the mathematics required to
utilize symmetry ideas in a physical context. Most of these mathe-
matical tools come from a branch of mathematics called group theory.
Afterwards, the Lagrangian formalism is introduced, which makes
working with symmetries in a physical context straightforward. In
the fifth and sixth chapters the basic equations of modern physics
are derived using the two tools introduced earlier: The Lagrangian
formalism and group theory. In the final part of this book these equa-
tions are put into action. Considering a particle theory we end up
with quantum mechanics, considering a field theory we end up with
quantum field theory. Then we look at the non-relativistic and classi-
cal limits of these theories, which leads us to classical mechanics and
electrodynamics.
Every chapter begins with a brief summary of the chapter. If you
catch yourself thinking: "Why exactly are we doing this?", return
to the summary at the beginning of the chapter and take a look at
how this specific step fits into the bigger picture of the chapter. Every
page has a big margin, so you can scribble down your own notes and
ideas while reading6 .
 XIII

I hope you enjoy reading this book as much as I have enjoyed writing
it.

Karlsruhe, January 2015 Jakob Schwichtenberg

Acknowledgments

I want to thank everyone who helped me create this book. I am espe-

cially grateful to Fritz Waitz, whose comments, ideas and corrections
have made this book so much better. I am also very indebted to Arne
Becker and Daniel Hilpert for their invaluable suggestions, comments
and careful proofreading. I thank Robert Sadlier for his proofreading,
Jakob Karalus for his comments and Marcel Köpke and Paul Tremper
for many insightful discussions.
I also want to thank Silvia Schwichtenberg, Christian Nawroth,
Ulrich Nierste and my editor at Springer, Angela Lahee, for their
support.
Many thanks are due to all readers of the first edition who sug-
gested improvements and pointed out mistakes, especially Meir
Krukowsky, Jonathan Jones, Li Zeyang, Rob Casey, Ethan C. Jahns,
Bart Pastoor, Zheru Qiu, Rudy Blyweert, Bruno Jacobs, Joey Ooi,
Henry Carnes, Jandro Kirkish, Vicente Iranzo, Rohit Chaki, Jonathan
Wermelinger, Achim Schmetz, RubingBai, Markus Pernow, Gleb
Klimovitch, Enric Arcadia, Cassiano Cattan, Martin Wong, Marco
Smolla, Alexander Zeng, Mohammad Mahdi AlTakach, Jonathan
Hobson, Peter Freed, Daniel Ciobotu, Telmo Cunha, Jia-Ji Zhu, An-
drew J. Sutter, Rutwig Campoamor-Stursberg and Andreas Wipf.
Finally, my greatest debt is to my parents who always supported
me and taught me to value education above all else.

If you find an error in the text I would appreciate a short email

to errors@jakobschwichtenberg.com. All known errors are listed at
http://physicsfromsymmetry.com/errata .
Contents

Part I Foundations

1 Introduction 3
1.1 What we Cannot Derive . . . . . . . . . . . . . . . . . . . 3
1.2 Book Overview . . . . . . . . . . . . . . . . . . . . . . . . 5
1.3 Elementary Particles and Fundamental Forces . . . . . . 7

2 Special Relativity 11
2.1 The Invariant of Special Relativity . . . . . . . . . . . . . 12
2.2 Proper Time . . . . . . . . . . . . . . . . . . . . . . . . . . 14
2.3 Upper Speed Limit . . . . . . . . . . . . . . . . . . . . . . 16
2.4 The Minkowski Notation . . . . . . . . . . . . . . . . . . 17
2.5 Lorentz Transformations . . . . . . . . . . . . . . . . . . . 19
2.6 Invariance, Symmetry and Covariance . . . . . . . . . . . 21

Part II Symmetry Tools

3 Lie Group Theory 25

3.1 Groups . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26
3.2 Rotations in two Dimensions . . . . . . . . . . . . . . . . 29
3.2.1 Rotations with Unit Complex Numbers . . . . . . 31
3.3 Rotations in three Dimensions . . . . . . . . . . . . . . . 33
3.3.1 Quaternions . . . . . . . . . . . . . . . . . . . . . . 34
3.4 Lie Algebras . . . . . . . . . . . . . . . . . . . . . . . . . . 38
3.4.1 The Generators and Lie Algebra of SO(3) . . . . 42
3.4.2 The Abstract Definition of a Lie Algebra . . . . . 45
3.4.3 The Generators and Lie Algebra of SU (2) . . . . 46
3.4.4 The Abstract Definition of a Lie Group . . . . . . 47
3.5 Representation Theory . . . . . . . . . . . . . . . . . . . . 50
3.6 SU (2) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 54
3.6.1 The Finite-dimensional Irreducible Representations
of SU (2) . . . . . . . . . . . . . . . . . . . . . . . . 54
XVIII

3.6.2 The Representation of SU (2) in one Dimension . 61

3.6.3 The Representation of SU (2) in two Dimensions 61
3.6.4 The Representation of SU (2) in three Dimensions 62
3.7 The Lorentz Group O(1, 3) . . . . . . . . . . . . . . . . . . 62
3.7.1 One Representation of the Lorentz Group . . . . 66
3.7.2 Generators of the Other Components of the
Lorentz Group . . . . . . . . . . . . . . . . . . . . 69
3.7.3 The Lie Algebra of the Proper Orthochronous
Lorentz Group . . . . . . . . . . . . . . . . . . . . 70
3.7.4 The (0, 0) Representation . . . . . . . . . . . . . . 72
3.7.5 The ( 12 , 0) Representation . . . . . . . . . . . . . . 72
3.7.6 The (0, 2)
1
Representation . . . . . . . . . . . . . . 74
3.7.7 Van der Waerden Notation . . . . . . . . . . . . . 75
3.7.8 The ( 12 , 12 ) Representation . . . . . . . . . . . . . . 80
3.7.9 Spinors and Parity . . . . . . . . . . . . . . . . . . 84
3.7.10 Spinors and Charge Conjugation . . . . . . . . . . 86
3.7.11 Infinite-Dimensional Representations . . . . . . . 87
3.8 The Poincaré Group . . . . . . . . . . . . . . . . . . . . . 89
3.9 Elementary Particles . . . . . . . . . . . . . . . . . . . . . 91
3.10 Appendix: Rotations in a Complex Vector Space . . . . . 92
3.11 Appendix: Manifolds . . . . . . . . . . . . . . . . . . . . . 93

4 The Framework 95
4.1 Lagrangian Formalism . . . . . . . . . . . . . . . . . . . . 95
4.1.1 Fermat’s Principle . . . . . . . . . . . . . . . . . . 96
4.1.2 Variational Calculus - the Basic Idea . . . . . . . . 96
4.2 Restrictions . . . . . . . . . . . . . . . . . . . . . . . . . . . 97
4.3 Particle Theories vs. Field Theories . . . . . . . . . . . . . 98
4.4 Euler-Lagrange Equation . . . . . . . . . . . . . . . . . . . 99
4.5 Noether’s Theorem . . . . . . . . . . . . . . . . . . . . . . 101
4.5.1 Noether’s Theorem for Particle Theories . . . . . 101
4.5.2 Noether’s Theorem for Field Theories - Spacetime
Symmetries . . . . . . . . . . . . . . . . . . . . . . 105
4.5.3 Rotations and Boosts . . . . . . . . . . . . . . . . . 108
4.5.4 Spin . . . . . . . . . . . . . . . . . . . . . . . . . . . 110
4.5.5 Noether’s Theorem for Field Theories - Internal
Symmetries . . . . . . . . . . . . . . . . . . . . . . 110
4.6 Appendix: Conserved Quantity from Boost Invariance
for Particle Theories . . . . . . . . . . . . . . . . . . . . . 113
4.7 Appendix: Conserved Quantity from Boost Invariance
for Field Theories . . . . . . . . . . . . . . . . . . . . . . . 114
 XIX

Part III The Equations of Nature

5 Measuring Nature 117

5.1 The Operators of Quantum Mechanics . . . . . . . . . . . 117
5.1.1 Spin and Angular Momentum . . . . . . . . . . . 118
5.2 The Operators of Quantum Field Theory . . . . . . . . . 119

6 Free Theory 121

6.1 Lorentz Covariance and Invariance . . . . . . . . . . . . . 121
6.2 Klein-Gordon Equation . . . . . . . . . . . . . . . . . . . . 122
6.2.1 Complex Klein-Gordon Field . . . . . . . . . . . . 124
6.3 Dirac Equation . . . . . . . . . . . . . . . . . . . . . . . . 124
6.4 Proca Equation . . . . . . . . . . . . . . . . . . . . . . . . 127

7 Interaction Theory 131

7.1 U (1) Interactions . . . . . . . . . . . . . . . . . . . . . . . 133
7.1.1 Internal Symmetry of Free Spin 12 Fields . . . . . 134
7.1.2 Internal Symmetry of Free Spin 1 Fields . . . . . 135
7.1.3 Putting the Puzzle Pieces Together . . . . . . . . . 136
7.1.4 Inhomogeneous Maxwell Equations and Minimal
Coupling . . . . . . . . . . . . . . . . . . . . . . . . 139
7.1.5 Charge Conjugation, Again . . . . . . . . . . . . . 140
7.1.6 Noether’s Theorem for Internal U (1) Symmetry . 141
7.1.7 Interaction of Massive Spin 0 Fields . . . . . . . . 142
7.1.8 Interaction of Massive Spin 1 Fields . . . . . . . . 143
7.2 SU (2) Interactions . . . . . . . . . . . . . . . . . . . . . . 143
7.3 Mass Terms and "Unification" of SU (2) and U (1) . . . . 150
7.4 Parity Violation . . . . . . . . . . . . . . . . . . . . . . . . 158
7.5 Lepton Mass Terms . . . . . . . . . . . . . . . . . . . . . . 162
7.6 Quark Mass Terms . . . . . . . . . . . . . . . . . . . . . . 165
7.7 Isospin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 166
7.7.1 Labelling States . . . . . . . . . . . . . . . . . . . . 168
7.8 SU (3) Interactions . . . . . . . . . . . . . . . . . . . . . . 170
7.8.1 Color . . . . . . . . . . . . . . . . . . . . . . . . . . 172
7.8.2 Quark Description . . . . . . . . . . . . . . . . . . 173
7.9 The Interplay Between Fermions and Bosons . . . . . . . 174

Part IV Applications

8 Quantum Mechanics 177

8.1 Particle Theory Identifications . . . . . . . . . . . . . . . . 178
8.2 Relativistic Energy-Momentum Relation . . . . . . . . . . 178
8.3 The Quantum Formalism . . . . . . . . . . . . . . . . . . 179
8.3.1 Expectation Value . . . . . . . . . . . . . . . . . . 181
XX

8.4 The Schrödinger Equation . . . . . . . . . . . . . . . . . . 182

8.4.1 Schrödinger Equation with an External Field . . . 185
8.5 From Wave Equations to Particle Motion . . . . . . . . . 185
8.5.1 Example: Free Particle . . . . . . . . . . . . . . . . 185
8.5.2 Example: Particle in a Box . . . . . . . . . . . . . . 186
8.5.3 Dirac Notation . . . . . . . . . . . . . . . . . . . . 189
8.5.4 Example: Particle in a Box, Again . . . . . . . . . 191
8.5.5 Spin . . . . . . . . . . . . . . . . . . . . . . . . . . . 192
8.6 Heisenberg’s Uncertainty Principle . . . . . . . . . . . . . 196
8.7 Comments on Interpretations . . . . . . . . . . . . . . . . 197
8.8 Appendix: Interpretation of the Dirac Spinor
Components . . . . . . . . . . . . . . . . . . . . . . . . . . 198
8.9 Appendix: Solving the Dirac Equation . . . . . . . . . . . 203
8.10 Appendix: Dirac Spinors in Different Bases . . . . . . . . 205
8.10.1 Solutions of the Dirac Equation in the Mass Basis 207

9 Quantum Field Theory 209

9.1 Field Theory Identifications . . . . . . . . . . . . . . . . . 210
9.2 Free Spin 0 Field Theory . . . . . . . . . . . . . . . . . . . 211
9.3 Free Spin 12 Field Theory . . . . . . . . . . . . . . . . . . . 216
9.4 Free Spin 1 Field Theory . . . . . . . . . . . . . . . . . . . 219
9.5 Interacting Field Theory . . . . . . . . . . . . . . . . . . . 219
9.5.1 Scatter Amplitudes . . . . . . . . . . . . . . . . . . 220
9.5.2 Time Evolution of States . . . . . . . . . . . . . . . 220
9.5.3 Dyson Series . . . . . . . . . . . . . . . . . . . . . 224
9.5.4 Evaluating the Series . . . . . . . . . . . . . . . . . 225
9.6 Appendix: Most General Solution of the Klein-Gordon
Equation . . . . . . . . . . . . . . . . . . . . . . . . . . . . 229

10 Classical Mechanics 233

10.1 Relativistic Mechanics . . . . . . . . . . . . . . . . . . . . 235
10.2 The Lagrangian of Non-Relativistic Mechanics . . . . . . 236

11 Electrodynamics 239
11.1 The Homogeneous Maxwell Equations . . . . . . . . . . 240
11.2 The Lorentz Force . . . . . . . . . . . . . . . . . . . . . . . 241
11.3 Coulomb Potential . . . . . . . . . . . . . . . . . . . . . . 243

12 Gravity 245

13 Closing Words 251

Part V Appendices

A Vector calculus 255

 XXI

A.1 Basis Vectors . . . . . . . . . . . . . . . . . . . . . . . . . . 256

A.2 Change of Coordinate Systems . . . . . . . . . . . . . . . 257
A.3 Matrix Multiplication . . . . . . . . . . . . . . . . . . . . . 259
A.4 Scalars . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 260
A.5 Right-handed and Left-handed Coordinate Systems . . . 260

B Calculus 263
B.1 Product Rule . . . . . . . . . . . . . . . . . . . . . . . . . . 263
B.2 Integration by Parts . . . . . . . . . . . . . . . . . . . . . . 263
B.3 The Taylor Series . . . . . . . . . . . . . . . . . . . . . . . 264
B.4 Series . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 266
B.4.1 Important Series . . . . . . . . . . . . . . . . . . . 266
B.4.2 Splitting Sums . . . . . . . . . . . . . . . . . . . . 268
B.4.3 Einstein’s Sum Convention . . . . . . . . . . . . . 269
B.5 Index Notation . . . . . . . . . . . . . . . . . . . . . . . . 269
B.5.1 Dummy Indices . . . . . . . . . . . . . . . . . . . . 269
B.5.2 Objects with more than One Index . . . . . . . . . 270
B.5.3 Symmetric and Antisymmetric Indices . . . . . . 270
B.5.4 Antisymmetric × Symmetric Sums . . . . . . . . 271
B.5.5 Two Important Symbols . . . . . . . . . . . . . . . 272

C Linear Algebra 273

C.1 Basic Transformations . . . . . . . . . . . . . . . . . . . . 273
C.2 Matrix Exponential Function . . . . . . . . . . . . . . . . 274
C.3 Determinants . . . . . . . . . . . . . . . . . . . . . . . . . 274
C.4 Eigenvalues and Eigenvectors . . . . . . . . . . . . . . . . 275
C.5 Diagonalization . . . . . . . . . . . . . . . . . . . . . . . . 275

D Additional Mathematical Notions 277

D.1 Fourier Transform . . . . . . . . . . . . . . . . . . . . . . . 277
D.2 Delta Distribution . . . . . . . . . . . . . . . . . . . . . . . 278

Bibliography 281

Index 285
 Part I
Foundations

"The truth always turns out to be simpler than you thought."

Richard P. Feynman
as quoted by
K. C. Cole. Sympathetic Vibrations.
Bantam, reprint edition, 10 1985.
ISBN 9780553342345
1
Introduction

1.1 What we Cannot Derive

Before we talk about what we can derive from symmetry, let’s clarify
what we need to put into the theories by hand. First of all, there is
presently no theory that is able to derive the constants of nature.
These constants need to be extracted from experiments. Examples are
the coupling constants of the various interactions and the masses of
the elementary particles.

Besides that, there is something else we cannot explain: The num-

ber three. This should not be some kind of number mysticism, but
we cannot explain all sorts of restrictions that are directly connected
with the number three. For instance,

• there are three gauge theories1 , corresponding to the three fun- 1

Don’t worry if you don’t understand
some terms, like gauge theory or
damental forces described by the standard model: The electro-
double cover, in this introduction. All
magnetic, the weak and the strong force. These forces are de- these terms will be explained in great
scribed by gauge theories that correspond to the symmetry groups detail later in this book and they are
included here only for completeness.
U (1), SU (2) and SU (3). Why is there no fundamental force follow-
ing from SU (4)? Nobody knows!
• There are three lepton generations and three quark generations.
Why isn’t there a fourth? We only know from experiments with
high accuracy that there is no fourth generation2 . 2
For example, the element abundance
in the present universe depends on the
• We only include the three lowest orders in Φ in the Lagrangian number of generations. In addition,
(Φ0 , Φ1 , Φ2 ), where Φ denotes here something generic that de- there are strong evidence from collider
experiments. (See e.g. Phys. Rev. Lett.
scribes our physical system and the Lagrangian is the object we 109, 241802) .
use to derive our theory from, in order to get a sensible theory
describing free (=non-interacting) fields/particles.
• We only use the three lowest-dimensional representations of the
double cover of the Poincaré group, which correspond to spin 0, 12

© Springer International Publishing AG 2018

J. Schwichtenberg, Physics from Symmetry, Undergraduate
Lecture Notes in Physics, https://doi.org/10.1007/978-3-319-66631-0_1
4 physics from symmetry

and 1, respectively, to describe fundamental particles. There is no

fundamental particle with spin 32 .

In the present theory, these things are assumptions we have to

put in by hand. We know that they are correct from experiments,
but there is presently no deeper principle why we have to stop after
three.
In addition, there is one thing that can’t be derived from symme-
try, but which must be taken into account in order to get a sensible
theory:

We are only allowed to include the lowest-possible, non-trivial order

in the differential operator ∂μ in the Lagrangian. For some theories
these are first order derivatives ∂μ , for other theories Lorentz in-
variance forbids first order derivatives and therefore second order
derivatives ∂μ ∂μ are the lowest-possible, non-trivial order. Otherwise,
we don’t get a sensible theory. Theories with higher order derivatives
are unbounded from below, which means that the energy in such the-
ories can be arbitrarily negative. Therefore states in such theories can
always transition into lower energy states and are never stable.

Finally, there is another thing we cannot derive in the way we de-

rive the other theories in this book: gravity. Of course there is a beau-
tiful and correct theory of gravity, called general relativity. But this
theory works quite differently than the other theories and a complete
derivation lies beyond the scope of this book. Quantum gravity, as an
attempt to fit gravity into the same scheme as the other theories, is
still a theory under construction that no one has successfully derived.
Nevertheless, some comments regarding gravity will be made in the
last chapter.
 introduction 5

1.2 Book Overview

Double Cover of the Poincaré Group

Irreducible Representations


s  +
(0, 0) : Spin 0 Rep ( 12 , 0) ⊕ (0, 12 ) : Spin 1
2 Rep ( 12 , 12 ) : Spin 1 Rep
acts on acts on acts on
  
Scalars Spinors Vectors
Constraint that Lagrangian is invariant Constraint that Lagrangian is invariant Constraint that Lagrangian is invariant
  
1
Free Spin 0 Lagrangian Free Spin 2 Lagrangian Free Spin 1 Lagrangian
Euler-Lagrange equations Euler-Lagrange equations Euler-Lagrange equations
  
Klein-Gordon equation Dirac equation Proka equation

This book uses natural units, which means we set the Planck
constant to h̄ = 1 and the speed of light to c = 1. This is helpful
for theoretical considerations, because it avoids a lot of unnecessary
writing. For applications the constants need to be added again to
return to standard SI units.

Our starting point will be the basic assumptions of special relativ-

ity. These are: The velocity of light has the same value c in all inertial
frames of reference, which are frames moving with constant velocity
relative to each other and physics is the same in all inertial frames of
reference.

The set of all transformations permitted by these symmetry con-

straints is called the Poincaré group. To be able to utilize them, we
discuss the mathematical theory that enables us to work with sym-
metries. This branch of mathematics is called group theory. We will
derive the irreducible representations of the Poincaré group3 , which 3
To be technically correct: We will
derive the representations of the
you can think of as basic building blocks of all other representations.
double-cover of the Poincaré group
These representations are what we use later in this text to describe instead of the Poincaré group itself. The
particles and fields of different spin. On the one hand, spin is an ab- term "double-cover" comes from the
observation that the map between the
stract label for different kinds of particles/fields and on the other double-cover of a group and the group
hand can be seen as something like internal angular momentum. We itself maps two elements of the double
cover to one element of the group. This
will discuss in detail how this comes about.
is explained in Section 3.3.1 in detail.

Afterwards, the Lagrangian formalism is introduced, which

makes working with symmetries in a physical context very conve-
6 physics from symmetry
4
Without the Higgs mechanism, terms
describing mass in the Lagrangian
spoil the symmetry and are therefore
forbidden.
5
Non-relativistic means that everything
moves slowly compared to the speed of
light and therefore especially curious
features of special relativity are too
small to be measurable.
nient. The central object is the Lagrangian. Different Lagrangians
describe different physical systems and we will derive several La-
grangians using symmetry considerations. In addition, the Euler-
Lagrange equations are derived. These enable us to derive the equa-
tions of motion from a given Lagrangian. Using the irreducible rep-
resentations of the Poincaré group, the fundamental equations of
motion for fields and particles with different spin can be derived.
The central idea here is that the Lagrangian must be invariant
(=does not change) under any transformation of the Poincaré group.
This makes sure the equations of motion take the same form in all
frames of reference, which we stated above as "physics is the same in
all inertial frames".
Then, we will discover another symmetry of the Lagrangian for
free spin 12 fields: Invariance under U (1) transformations. Similarly
an internal symmetry for spin 1 fields can be found. Demanding
local U (1) symmetry will lead us to coupling terms between spin 12
and spin 1 fields. The Lagrangian with this coupling term is the cor-
rect Lagrangian for quantum electrodynamics. A similar procedure
for local SU (2) and SU (3) transformations will lead us to the correct
Lagrangian for weak and strong interactions.
In addition, we discuss symmetry breaking and a special way to
break symmetries called the Higgs mechanism. The Higgs mecha-
nism enables us to describe particles with mass4 .
Afterwards, Noether’s theorem is derived, which reveals a deep
connection between symmetries and conserved quantities. We will
utilize this connection by identifying each physical quantity with
the corresponding symmetry generator. This leads us to the most
important equation of quantum mechanics
[ x̂i , p̂ j ] = iδij (1.1)
and quantum field theory
[Φ̂( x ), π̂ (y)] = iδ( x − y). (1.2)
We continue by taking the non-relativistic5 limit of the equation
of motion for spin 0 particles, called Klein-Gordon equation, which
result in the famous Schrödinger equation. This, together with the
identifications we made between physical quantities and the genera-
tors of the corresponding symmetries, is the foundation of quantum
mechanics.
Then we take a look at free quantum field theory, by starting
 introduction 7

with the solutions of the different equations of motion6 and Eq. 1.2. 6
The Klein-Gordon, Dirac, Proka and
Afterwards, we take interactions into account, by taking a closer look Maxwell equations.

at the Lagrangians with coupling terms between fields of different

spin. This enables us to discuss how the probability amplitude for
scattering processes can be derived.

By deriving the Ehrenfest theorem the connection between quan-

tum and classical mechanics is revealed. Furthermore, the fun-
damental equations of classical electrodynamics, including the
Maxwell equations and the Lorentz force law, are derived.

Finally, the basic structure of the modern theory of gravity, called

general relativity, is briefly introduced and some remarks regarding
the difficulties in the derivation of a quantum theory of gravity are
made.

The major part of this book is about the tools we need to work
with symmetries mathematically and about the derivation of what is
commonly known as the standard model. The standard model uses
quantum field theory to describe the behavior of all known elemen-
tary particles. Until the present day, all experimental predictions of
the standard model have been correct. Every other theory introduced
here can then be seen to follow from the standard model as a special
case. For example in the limit of macroscopic objects we get classical
mechanics or in the limit of elementary particles with low energy,
we get quantum mechanics. For those readers who have never heard
about the presently-known elementary particles and their interac-
tions, a really quick overview is included in the next section.

1.3 Elementary Particles and Fundamental Forces

There are two major categories for elementary particles: bosons and
fermions. There can be never two fermions in exactly the same state,
which is known as Pauli’s exclusion principle, but infinitely many
bosons. This curious fact of nature leads to the completely different
behavior of these particles:
• fermions are responsible for matter

• bosons for the forces of nature.

This means, for example, that atoms consist of fermions7 , but the 7
Atoms consist of electrons, protons
and neutrons, which are all fermions.
electromagnetic-force is mediated by bosons. The bosons that are
But take note that protons and neutrons
responsible for electromagnetic interactions are called photons. One are not fundamental and consist of
of the most dramatic consequences of thie exclusion principle is that quarks, which are fermions, too.

there is stable matter at all. If there could be infinitely many fermions

in the same state, there would be no stable matter8 . 8
We will discuss this in Chapter 6
8 physics from symmetry

There are four presently known fundamental forces

• The electromagnetic force, which is mediated by massless photons.

• The weak force, which is mediated by massive W+ , W− and Z-

bosons.

• The strong force, which is mediated by massless gluons.

• Gravity, which is (maybe) mediated by gravitons.

Some of the these bosons are massless and some are not and this
tells us something deep about nature. We will fully understand this
after setting up the appropriate framework. For the moment, just
take note that each force is closely related to a symmetry. The fact
that the bosons mediating the weak force are massive means the
related symmetry is broken. This process of spontaneous symmetry
breaking is responsible for the masses of all elementary particles.
We will see later that this is possible through the coupling to another
fundamental boson, the Higgs boson.

Fundamental particles interact via some force if they carry the

9
All charges have a beautiful common corresponding charge9 .
origin that will be discussed in Chapter
7. • For the electromagnetic force this is the electric charge and conse-
quently only electrically charged particles take part in electromag-
netic interactions.
10
Often the charge of the weak force • For the weak force, the charge is called isospin10 . All known
carries the extra prefix "weak", i.e. is
fermions carry isospin and therefore interact via the weak force.
called weak isospin, because there
is another concept called isospin for • The charge of the strong force is called color, because of some
composite objects that interact via the
strong force. Nevertheless, this is not a
curious features it shares with the humanly visible colors. Don’t
fundamental charge and in this book let this name confuse you, because this charge has nothing to do
the prefix "weak" is omitted. with the colors you see in everyday life.

The fundamental fermions are divided into two subcategories:

quarks, which are the building blocks of protons and neutrons, and
leptons. Famous leptons are, for example, electrons and neutrinos.
The difference is that quarks carry color charge and therefore take
part in strong interactions, whereas leptons do not. There are three
quark and lepton generations, which consist each of two particles:

Generation 1 Generation 2 Generation 3 Electric charge Isospin Color

Up Charm Top +2 e 1

3 2
Quarks: Down Strange Bottom −1 e −1 
3 2

Electron-Neutrino Muon-Neutrino Tauon-Neutrino 0 +1 -

2
Leptons: Electron Muon Tauon −e −1 -
2
 introduction 9

Different particles can be identified through labels. In addition

to the charges and the mass there is another incredibly important
label called spin, which can be seen as some kind of internal angular
momentum. Bosons carry integer spin, whereas fermions carry half-
integer spin. The fundamental fermions we listed above have spin
1
2 and almost all fundamental bosons have spin 1. There is only one
known fundamental particle with spin 0: the Higgs boson.

There is an anti-particle for each particle, which carries exactly the

same labels with opposite sign11 . For the electron the anti-particle 11
Maybe except for the mass label.
This is currently under experimental
is called positron, but in general there is no extra name and only a
investigation, for example at the AEGIS,
prefix "anti". For example, the antiparticle corresponding to an up- the ATRAP and the ALPHA exper-
quark is called anti-up-quark. Some particles, like the photon12 are iment, located at CERN in Geneva,
Switzerland.
their own anti-particle.
12
And maybe the neutrinos, which is
All these notions will be explained in more detail later in this text. currently under experimental investi-
Now it’s time to start with the derivation of the theory that describes gation in many experiments that search
for a neutrinoless double-beta decay.
correctly the interplay of the different characters in this particle zoo.
The first cornerstone towards this goal is Einstein’s famous theory of
special relativity, which is the topic of the next chapter.
2
Special Relativity

The famous Michelson-Morley experiment discovered that the speed

of light has the same value in all reference frames1 . Albert Einstein 1
The speed of objects we observe in
recognized the far reaching consequences of this observation and everyday life depend on the frame
of reference. For example, when an
around this curious fact of nature he built the theory of special rela- observer standing at a train station
tivity. Starting from the constant speed of light, Einstein was able to measures that a train moves with
50 kmh , another observer running with
predict many interesting and strange consequences that all proved
15 kmh next to the same train, measures
to be true. We will see how powerful this idea is, but first let’s clarify that the train moves with 35 kmh . In
what special relativity is all about. The two basic postulates are contrast, light always moves with
1, 08 · 109 km
h , no matter how you move
• The principle of relativity: Physics is the same in all inertial relative to it.
frames of reference, i.e. frames moving with constant velocity
relative to each other.

• The invariance of the speed of light: The velocity of light has the
same value c in all inertial frames of reference.
In addition, we will assume that the stage our physical laws act on
is homogeneous and isotropic. This means it does not matter where
(=homogeneity) we perform an experiment and how it is oriented
(=isotropy), the laws of physics stay the same. For example, if two
physicists, one in New-York and the other one in Tokyo, perform ex-
actly the same experiment, they would find the same2 physical laws. 2
Besides from changing constants,
Equally a physicist on planet Mars would find the same physical as, for example, the gravitational
acceleration
laws.

The laws of physics, formulated correctly, shouldn’t change if

you look at the experiment from a different perspective or repeat
it tomorrow. In addition, the first postulate tells us that a physical
experiment should come up with the same result regardless of if
you perform it on a wagon moving with constant speed or at rest in
a laboratory. These things coincide with everyday experience. For
example, if you close your eyes in a car moving with constant speed,
there is no way to tell if you are really moving or if you’re at rest.

© Springer International Publishing AG 2018

J. Schwichtenberg, Physics from Symmetry, Undergraduate
Lecture Notes in Physics, https://doi.org/10.1007/978-3-319-66631-0_2
12 physics from symmetry

Without homogeneity and isotropy physics would be in deep

trouble: If the laws of nature we deduce from experiment would hold
only at one point in space, for a specific orientation of the experiment
such laws would be rather useless.

The only unintuitive thing is the second postulate, which is con-

trary to all everyday experience. Nevertheless, all experiments until
the present day show that it is correct.

2.1 The Invariant of Special Relativity

Before we dive into the details, here’s a short summary of what we
want to do in the following sections. We use the postulates of special
relativity to derive the Minkowski metric, which tells us how to com-
pute the "distance" between two physical events. Another name for
physical events in this context is points in Minkowski space, which
is how the stage the laws of special relativity act on is called. It then
follows that all transformations connecting different inertial frames of
reference must leave the Minkowski metric unchanged. This is how
we are able to find all transformations that connect allowed frames
of reference, i.e. frames with a constant speed of light. In the rest of
the book we will use the knowledge of these transformations, to find
equations that are unchanged by these transformations. Let’s start
with a thought experiment that enables us to derive one of the most
fundamental consequences of the postulates of special relativity.

Imagine, we have a spectator, standing at the origin of his co-

ordinate system and sending a light pulse straight up, where it is
Fig. 2.1: Illustration of the thought reflected by a mirror and finally reaches again the point from where
experiment
it was sent. An illustration of this can be seen in Fig. 2.1

We have three important events:

• A : the light leaves the starting point

• B : the light is reflected at a mirror

• C : the light returns to the starting point.

3
For constant speed v we have v = Δs
Δt , The time-interval between A and C is3
with the distance covered Δs and the
time needed Δt, and therefore Δt = Δs
2L
v Δt = tC − t A = , (2.1)
c
where L denotes the distance between the starting point and the
mirror.

Next imagine a second spectator, standing at t A at the origin of his

coordinate system and moving with constant velocity u to the left,
 special relativity 13

relative to the first spectator4 . For simplicity let’s assume that the 4
Transformations that allow us to trans-
origin of this second spectators’ coordinate system coincides at t A form the description of one observer
into the description of a second ob-
with the coordinate origin of the first spectator. The second spectator server, moving with constant speed
sees things a little differently. In his frame of reference the point relative to first observer, are called
boosts. We derive later a formal de-
where the light ends up will not have the same coordinates as the scription of such transformations.
starting point (see Fig. 2.2).

We can express this mathematically

x A = 0 = xC = uΔt → Δx  = uΔt , (2.2)

where the primed coordinates denote the moving spectator. For the
first spectator in the rest-frame we have of course

x A = xC → Δx = 0. (2.3)

We assume movement along the x-axis, therefore

yA = yC

and zA = zC

→ Δy = 0 and Δz = 0
(2.4)
and equally of course

y A = yC and z A = zC → Δy = 0 Δz = 0.
and
(2.5)
The next question is: What about the time interval the second
spectator measures? Because we postulate a constant velocity of Fig. 2.2: Illustration of the thought
light, the second spectator measures a different time interval between experiment for a moving spectator. The
second spectator moves to the left and
A and C! The time interval Δt = tC  − t is equal to the distance l the
A therefore the first spectator (and the
light travels, as the second spectator observes it, divided by the speed experiment) moves relative to him to
the right.
of light c.
l
Δt = (2.6)
c
We can compute the distance traveled l using the good old Pythagorean
theorem (see Fig. 2.2)

 2
1
l=2 uΔt + L2 . (2.7)
2

Using Eq. 2.6, we therefore conclude


 2
1
cΔt = 2 uΔt + L2 . (2.8)
2

If we now use Δx  = uΔt from Eq. 2.2, we can write


 2
1 
cΔt = 2 Δx + L2
2
Another random document with
no related content on Scribd:
 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