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Models for Design
Electrical Calculations for
Industrial Plants
Models for Design
Electrical Calculations for
Industrial Plants

Robert E. Henry, PE
CRC Press
Taylor & Francis Group
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Boca Raton, FL 33487-2742

© 2018 by Taylor & Francis Group, LLC

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 The help in editing this book by Mark E. Henry is gratefully

acknowledged. The support and review by Sharon A. Henry, Atty,

is deeply appreciated. Kyra Lindholm and Deepa Kalaichelvan

helped in so many ways. This book is dedicated to all of them.

Contents

List of Figures..........................................................................................................xi
List of Tables......................................................................................................... xiii
Acknowledgments.................................................................................................xv
Author................................................................................................................... xvii

1. Introduction......................................................................................................1
Fun Test..............................................................................................................4
Questions.......................................................................................................4
Answers.........................................................................................................5

Section I Plant Equipment

2. Using an Uninterruptible Power Supply to Feed

a Variable-Speed Drive...................................................................................9
Introduction.......................................................................................................9
Variable-Frequency Drives............................................................................ 11
Uninterruptible Power Supplies...................................................................12
Harmonic Distortion......................................................................................13
Torque..........................................................................................................14
Rotating Inertia...........................................................................................14
Starting a Fan..............................................................................................17
Starting Ramp Time...................................................................................18
Mechanical Resonance..............................................................................20
Response Time of a UPS with a Drive’s Load........................................21
Fan Start Time and Torque........................................................................21
Motor Efficiency Requirements............................................................... 23
An Example.....................................................................................................24
Normal Operation......................................................................................25
Time Where Load Exceeds Steady Torque.............................................27
Setting the Drive’s Torque Limit in the Drive’s Firmware...................27
Sizing the UPS for Its Load.......................................................................27
Sizing the UPS Battery...............................................................................29
Light Loads on Large Motors...................................................................30

3. Storage Batteries.............................................................................................33
The DC System................................................................................................33
Valve-Regulated Lead–Acid Battery............................................................36
Battery Selection..............................................................................................37

vii
viii Contents

Battery Heat Flow...........................................................................................39

The Battery..................................................................................................39
The Stack.....................................................................................................39
Heat Flow Analysis of the Stack..............................................................40
Exponential Temperature Response of the Stack..................................42
Battery Specific Heat..................................................................................42
Heat Flow Analysis of the Stack in the Cabinet.....................................43
A Different Use of This Battery.....................................................................45
Charging the Battery and Thermal Runaway.............................................46

Section II One-Line Designs

4. The Largest Demand for 13.8 kV Switchgear...........................................49

Large-Motor Fault Current Contribution....................................................50
Large Motors...............................................................................................51
Small Motor Contribution.............................................................................51
Medium-Voltage Motor Control Centers....................................................52
Maximum Plant Motor Load....................................................................53
Fault Analysis of the Maximum Plant....................................................54
Conclusions......................................................................................................56
Exceptions........................................................................................................57

5. The Minor Influence of the Grid Thevenin

Impedance on Plant Faults...........................................................................59

6. Use of a Three-Winding Step-Up Transformer........................................61

Introduction.....................................................................................................61
The Small Off-Power Generating Unit........................................................62
The Small-Unit Auxiliary Load.....................................................................62
The Transformer..............................................................................................64
Specifying the Transformer...........................................................................66
Fault Current in the Auxiliary Distribution................................................66
Transformer Impedance Values....................................................................68
Calculating Wye Values.................................................................................69
Values on the Transformer’s Nameplate.....................................................70
Fault-Current Analysis for the Protective Relay System...........................71
Larger Units.....................................................................................................72

Section III Fast Transient Calculations

7. Analysis of Power Cables Conducting Fast Transient Loads................75

Cables in Air....................................................................................................76
Cables Installed in Conduit...........................................................................78
Underground Feeders....................................................................................81
Contents ix

Calculation of Time Constants......................................................................81

Cooldown.........................................................................................................84
Simple Fast Transient Response....................................................................86
Power Cables Rated 600 V.............................................................................89
Sizing Power Feeders Using the Tables.......................................................89
Cable Assemblies............................................................................................90

8. Sizing Power Cables for Fast Transient Loads.........................................91

Developing the Summary Tables 7.2 and 7.5..............................................92
Low Voltage.....................................................................................................92
Fast Transient Loading of the Motor............................................................93
Fast Transient Loading of the Motor’s Feeder............................................93
Fast Transient Loading of Variable-Speed Drives......................................94
Summary..........................................................................................................94

9. Introduction to Motor Fast Transient Loading.........................................95

A Mining Company Project...........................................................................95
General Response............................................................................................96

10. Fast Transient Motor Analysis.....................................................................99

Background......................................................................................................99
The Circuit Used for Analysis.....................................................................101
Varying Reactance.........................................................................................102
Torque.............................................................................................................103
Summary........................................................................................................104

11. Calculation of the Motor’s Temperatures................................................105

Thermal Model..............................................................................................105
Motor Thermal Capacitances......................................................................105
Temperature Rise Rating..............................................................................106
Evaluating Thermal Circuit Elements........................................................107
Operating Time at 1300 lb-ft of Torque......................................................107
Cooldown to 200 Hp Operation: Extended Cycle....................................109
The More Severe Operating Cycle.............................................................. 110
Afterthought on the Thermal Resistances................................................. 111
Summary........................................................................................................ 112

12. Motor Conclusions...................................................................................... 113

Frame Size...................................................................................................... 113
Purchasing Requirements............................................................................ 114

13. Line Design................................................................................................... 117

The Load......................................................................................................... 117
Cable Ampacity and Size............................................................................. 118
Cable Temperature........................................................................................ 119
x Contents

Voltage Drop.................................................................................................. 119

Line Length....................................................................................................120
Auxiliary Power Feeder Size and Signal Cable........................................120
Alternative Conductor Sizes.......................................................................122
Transmission at 2400 V.................................................................................122

14. Comparisons of Line Alternative Costs..................................................127

Cable Prices for 600 V Lines........................................................................127
Motor Feeder.................................................................................................127
Aux Power Feeder........................................................................................128
Signals Cable.................................................................................................128
Galvanized Steel Messenger Cable and Spiral Wrapping Tape.............128
Alternative 2400 V Line................................................................................129
Summary........................................................................................................130

15. Preliminary Cost Estimate..........................................................................133

The Process Plant Cost.................................................................................133
The Line Cost.................................................................................................133
Skid Costs.......................................................................................................134
Summary........................................................................................................135
Costs per Foot................................................................................................135

Appendix A: Derivation of Equations for Transient Heat

Flow from Cables in Conduit...........................................................................137
Appendix B: Finding the Electrical Characteristics
of the 400 Hp Motor......................................................................................... 143
Glossary................................................................................................................155
Codes and Standards..........................................................................................157
Bibliography........................................................................................................159
Index......................................................................................................................161
List of Figures

Figure 2.1 Turbocompressor performance....................................................10

Figure 2.2 Torque–speed curve for a fan or air compressor........................18
Figure 2.3 Starting torques of a motor driving a fan...................................19
Figure 2.4 Large motor efficiencies at loads below one-fourth..................31
Figure 4.1 One-line sketch of a 96 MVA plant..............................................50
Figure 4.2 Impedance network sketch of a 96 MVA plant..........................55
Figure 6.1 One-line diagram of a small off-power generating unit...........63
Figure 6.2 The impedance diagram of the unit with 4160 V base............. 65
Figure 10.1 The equivalent circuit of an induction motor...........................100
Figure 10.2 The equivalent circuit used for analysis...................................102
Figure 11.1 Motor thermal model...................................................................106
Figure 11.2 Stator temperature response to the operating profile............. 111
Figure A.1 Schematic representation of cable heat flow.............................138
Figure B.1 The equivalent circuit used for analysis.....................................144

xi
List of Tables

Table 2.1 Typical Motor Performance Data...................................................16

Table 2.2 Rough Motor Characteristics at 20 Hz..........................................23
Table 2.3  Battery Characteristics Valve-Regulated Lead–Acid Cell
1.75 V/Cell kW/Cell at 25°C..........................................................30
Table 3.1  Battery Performance (VRLA Type at 25°C
1.8 V/Cell Discharge)......................................................................38
Table 3.2 Battery in Table 3.1 Discharge Losses and Efficiencies...............38
Table 3.3 Battery Module Component Weights and Specific Heats..........42
Table 4.1 Universal Common Load Makeup................................................53
Table 7.1 K Factors in Table 43 for Equations in 8.5.2.4...............................78
Table 7.2 Summary Cable Heating Tabulation.............................................82
Table 7.3 Cable Heating Tabulation...............................................................83
Table 7.4 Cable Heating Tabulation...............................................................85
Table 7.5 480 V Cable Heating Tabulation....................................................89
Table 10.1 Manufacturer’s Data for the 400 Hp Motor...............................101
Table 11.1 Thermal Capacitances................................................................... 106
Table 11.2 O
 peration at 460 and 414 V with 400 Hp Output
(Xtot = 0.2382 Ohms).......................................................................108
Table 13.1 Voltage Drop and Line Length.....................................................121
Table 14.1 Alternative 480 V Costs for Messengers and Poles...................129
Table 14.2 Alternative Cable Costs.................................................................129
Table 14.3 Total Alternative 480 V Line Costs..............................................130
Table 14.4 Total Alternative Line Cost for a 2400 V Line............................130
Table 15.1 Costs of a 450 Hp Motor with a 2300 V or 460 V Winding......134
Table 15.2 Estimated Total Cost and Breakdown.........................................135
Table 15.3 Alternative Costs per Foot............................................................135
Table B.1 Results of Characteristics and Values..........................................153

xiii
Acknowledgments

Grateful acknowledgment is made for authorization and permission to use

and reprint material from the following sources:

© 2003 IEEE, Proceedings, Cable Sizing for Fast Transient Loads, R. E.

Henry, 2003 Industrial and & Chemical Power Society Conference,
St. Louis, MO
© 2004 IEEE, Proceedings, Response of Power Cables to Fast Transient
Loads, R. E. Henry, IEEE Industry Appl. Conf. 39th Annual Meeting,
Seattle, WA
© 2015 IEEE, Proceedings, Fast Transient Loads of Low Voltage Power
Cables, R. E. Henry, Ind. and Commercial Power Systems 51st
Technical Conf. Ind. Applications Soc., Calgary, Alberta, Canada
© 2002 IEEE, IEEE Std. 242, Recommended Practice for Protection and
Coordination of Industrial and Commercial Power Systems—Buff
Book, ANSI/IEEE Std. 242-86

xv
Author

Robert E. Henry, PE, has more than 50 years

of engineering experience and earned a BSEE
and an MS in industrial management. He
spent his early years in the aerospace industry
and worked on the design of the navigation
and power systems for the Apollo spacecraft.
Most of his career has been in industrial plant
design. Power generation, substations, and
design of nuclear plants constitute most of his
experience. He also has experience in food,
petrochemical, mining, and paper industries.
He authored a paper for the Institute of Navigation on orbital rendezvous.
He has also authored papers on heat flow in electronic equipment and on
power cables conducting kiloampere loads lasting several minutes. He is
president of R. E. Henry P.E., LLC.

xvii
1
Introduction

The chapters herein are intended as go-bys. Each is an example of an anal-

ysis and included calculations. The relations and formulas are all given in
the references. However, cable tables are developed in Chapters 7 and 8.
Nothing illustrates a relation like a calculation. Working problems at the end
of a chapter is how one learns the material. With this in mind, I thought that
presenting the topics herein in a traditional-text format would be a useful
undertaking. I haven’t included problems at the end of the chapter, but I do
include examples. The level of knowledge would be for the engineer reader
with an undergraduate degree not competent with a specialist’s background.
There are a few relationships that I do expect the reader to know. An exam-
ple is that for finding the rated current of a transformer, given the number
of phases, the rated voltage, and the kVA rating. Also see Question 5 in the
Fun Test at the end of this chapter. And the reader should be familiar with
current transformers (CTs) and voltage transformers (VTs, and rarely PTs.)
These are readily learned from the examples herein if the reader doesn’t
know these relationships. Also, the reader should know the inside of an oil-
filled transformer, what its core looks like, and have a rough idea of what
a winding looks like. The same for a motor. He must know the difference
between power and energy.
A long time ago, my math professor said that when he was giving oral
examinations to his master’s degree candidates, he would ask them to name
the fundamental theorem of differential calculus. He said that none of his
candidates could ever name it. Years later, I thought I would compose a
little test for newly graduated electrical engineers whom I was interview-
ing, who were applying for employment with my company. The test was to
be comprised of a few questions like my math professor’s, designed so that
few could answer any of the questions even though they should know the
answers. How many thousandths of an inch is the setting of a spark plug’s
gap was one question, as well as what is the fundamental theorem of dif-
ferential calculus. The test was to make the candidate squirm and think he
would not receive an offer. It was a great ice breaker. (If you are curious, the
test is included at the end of this chapter, and with answers.)
It taught me that no one knows everything, and don’t assume that
knowledge of a topic is widely known. I know many competent design
engineers who know a great deal about variable-speed drives and unin-
terruptable power supplies, how to model a motor, and how do motors
perform at other than 50 or 60 Hz. I also know many, many more engineers

1
2 Models for Design: Electrical Calculations for Industrial Plants

who don’t know much about these topics. Also, few electrical engineers
know how a power cable’s ampacity is arrived at, and very, very few know
how a power cable responds to kiloampere current spikes lasting several
minutes.
Engineering schools have not taught variable frequency effects in motors
until recently. Nor did they teach the big energy savings that can be realized
by not including traditional valves that control flow in industrial applica-
tions. Decades ago, I was taught analog audio circuits and their response
to variable voice frequencies. This did not give me much preparation for
variable frequency effects in motors. These effects are within the scopes of
both electrical and mechanical engineering. Few universities teach electrical
power and its applications anyway. And the development of power tran-
sistors, which made variable-speed motors practical, is only about three
decades old.
I also thought I might include other topics in industrial power, such as
uninterruptable power supplies. Other related topics are storage batteries
and switchgear at 13.8 kV in a main-tie-main arrangement, the maximum
demand that medium-voltage switchgear can supply. Three-winding trans-
formers used as step-ups in generating plants is another favorite topic. Also,
not all of the calculations are electrical. Some analyze the heat flow in a
battery, cable, or motor. Here, the physics of heat flow is drawn upon. My
models are usually crude. Thereby, the calculation results are approximate.
However, they offer insight and are suitable for verifying computer calcula-
tions based on detailed models.
Motors are fundamental to industrial plants. They are among the few old-
est electrical products. Their complication isn’t widely familiar. Where their
operation is required for short periods at loads beyond their rated horse-
power, is covered in two chapters and Appendix B.
This book is in units of feet, pounds of force, seconds, degrees Celsius,
watts, hertz, amperes, and volts. These are electrical engineering units found
in most texts that were published during the last half of the last century. Also,
for heat, watts and watt-hours, not Btu per hour and Btu’s. Watts and watt-
hours are easier and more direct with electrical heat dissipation, and to heat
flow in power cables and motors. Motor units are horsepower and lb-ft of
torque. The focus is also on 60 Hz and American circular mils. Most product
data on the Internet is in these units. Not that the methods cannot be applied
to 50 Hz and square millimeters. I leave that to the reader. Also, my circuit
calculations use impedance values, not per-unit values. I believe the number
crunching is the same either way. In seeing the results, I believe impedance
values are closer to Ohm’s law and better show the sense of the calculation.
Use what is easier for you.
I have designed European industrial plants and generating stations. Once
one starts working on a European project, thinking in European units is easy.
Introduction 3

The engineering standards used in the western hemisphere are equivalent

to European and Asian standards. With many products, their electrical
standards are the same or used intermingled. The performance standards
and test procedures for uninterruptible power supplies are common in both
hemispheres, for example. The most compelling equivalence is that univer-
sal electrical units are common throughout the world and have been since
the beginning of electricity as a commodity. Electricity as a tariffed com-
modity began in Chicago with Commonwealth Edison’s AC system about
1900. And Edison, with the others, used volts and amperes as electricity
evolved in the 1870s. Volts and amperes came from the scientific flowering
in late-eighteenth-century Europe. An effort to drop feet, mass, and pounds
of force in favor of European units continues.
In calculations, I use four significant figures. To think this improves accu-
racy is ridiculous. It is simply convenient for me. Three significant figures
are plenty. Usually, the elements of what the calculation addresses aren’t
known well enough to justify more than two significant figures. Knowledge
of the calculation’s elements determines accuracy, not the number of signifi-
cant figures. It used to be that the number of significant figures signified how
accurately the calculation’s elements were known, but this seems to have
fallen away.
The topics presented in this book are listed in the Table of Contents. Start at
any chapter, there is no beginning or end. Although some of the chapters are
linked, each stands on its own, more or less. Computer programs for electri-
cal analysis are not part of the topics. They have their place with batches of
data and repetition of calculations. But garbage in is garbage out. There is
no substitute for mastery of the engineering behind the computer programs.
Independently verifying results by plain old analysis with a pencil, paper,
and calculator isn’t going out of style.
Fast transient loads are kiloampere loads that last for several m ­ inutes.
I did a lot of original engineering work with fast transient heating of
power cables and sizing them for such loads. That work is included
herein. Shown herein is that sizing motor feeders by methods per the
National Electrical Code using tables for motor current is overly conserva-
tive and needlessly costly. The methods using tables for motor currents
are inappropriate for motors with varying load. (The code allows other
methods applied under engineering supervision.) Nine of this book’s
15 chapters address fast transient loads. Four of the nine chapters are
about fast transient heating of motors.
Engineering is the art of applying science to human needs. It is a learned
profession. In my case, the science was mostly physics, of the Newtonian
kind. I have the honor of having helped to design the Apollo Lunar Module,
which was done mostly at Bethpage, New York, by Grumman Aerospace
Corp. now absorbed by Northrop Grumman. (Through performing tests
4 Models for Design: Electrical Calculations for Industrial Plants

in a vacuum chamber, I also established that the accuracy of the naviga-

tion sextant in the command module was 2.3 s of arc, and not the intended
1.2 s of arc. The fix was to energize the trunnion’s resolver’s stator, not
its rotor.)
There is a void between the capability of a product and its application. The
product development engineer of a variable-frequency drive is intimate with
its control software but may be weak in the range of required performance
and relative costs of installations. From knowing the design of the plant, the
particular needs that the drive must meet is a separate specialty. This per-
spective, of requirements for transformers, cables, motors, and the like, is the
perspective of this book.
I hate errors in texts. Errors stop the reader just when she is working hard
to follow the topic in the sentence. It makes the reader angry. I have worked
hard to correct all errors I have found, but some must remain. All errors
herein are mine, and I’m sorry for them.

Robert E. Henry, PE

Fun Test
Questions

1. What is the fundamental theorem of differential calculus?

2. During factory testing, at what output kVA is a transformer’s capacity
measured (standard procedure)?
3. How is a transformer’s impedance measured?
4. In balanced three-phase circuit analysis, how many phases are modeled
at a time?
5. If analyzing a transformer in its connected circuits, if the transformer’s
load impedance on the secondary side is 1, what is this transformer’s
load impedance on the primary side if the turns ratio is 3:1?
6. What causes transformer inrush when a transformer is energized?
7. What is the setting of a spark plug’s gap?
8. In music theory, what is the classical sonata form? (asked if testee said
yes when asked if testee took a music appreciation course)
9. If charging a storage device with an available source of energy, can all
of the available energy be coupled into the storage device?
10. What fundamental law governs this process?

Answers on the Next Page

Introduction 5

Answers

1. Given a function, y = f(x), for the value of delta y = f(delta x), as the
value of delta x approaches zero, delta y approaches dy.
2. Zero output. The secondary terminals are shorted together with shunts
(or using CTs) in the shorting bars to measure phase currents.
3. With the transformer so connected, the primary voltages are raised from
zero to the value where secondary currents are at their rated value. The
percent of measured primary voltage, at rated shorted secondary cur-
rent, is the percent impedance. (It results from, of all the flux generated
by the windings, not all is being induced into the core, and losses.)
4. One. It represents each of the balanced phases. Its applied voltage is the
single-phase value, the rated primary voltage divided by the square
root of three.
5. Nine.
6. The residual flux in the core. If the transformer is somehow turned off
at the exact instant when the core is at zero flux, and if turned back on at
the same voltage when turned off, there will be no inrush. This is pos-
sible with three phases, each shifted 120° from the other, if each phase
has the same current–voltage relationship.
7. From 15 to 75 thousands of an inch, depending on the engine require-
ments and the spark plug.
8. Two themes (songs) are in a movement. Each is introduced, then devel-
oped in the middle of the movement and mixed, then restated at the
end.
9. It is impossible to store all of the available transformed energy because
losses are inherent. Also, losses are inherent if discharging the storage
device.
10. The First Law of Thermodynamics: Energy cannot be created or
destroyed but can only be transformed.

We beat on, with our models, against the stronger wind of skeptics,
back into the past. Were they skeptics? Or were they just green shackled,
unable to grasp change? Unable to spend the grueling labor of the mind
to gain the visions that the models radiated?
 Section I

Plant Equipment
2
Using an Uninterruptible Power Supply
to Feed a Variable-Speed Drive

Introduction
This chapter presents the application of a variable-frequency drive ­connected
to a motor driving a fan. The fan is ventilating a building with airflow that is
essential to a process within the building. With loss of normal building power,
the process is interrupted, but airflow must be maintained for 20 min longer dur-
ing the power outage. This flow purges the process of gases that could otherwise
accumulate and become explosive. However, 40% flow, reduced from full nor-
mal, is required. Because there is no backup ­generator, the variable-frequency
drive is switched to an uninterruptible power supply having a 20 min battery.
It may be uncommon to find an uninterruptible power supply feeding a
drive that supplies a fan.
However, this application is necessary

• Where power interruption cannot be tolerated

• Where a backup generator isn’t available
• Where power quality is poor

Sometimes, critical loads must operate after loss of normal power and during
the interval when the backup source is being started, especially when start-
ing attempts are prolonged.
The combination of an uninterruptible power supply (UPS) supplying a
variable-frequency drive first begs the question: why isn’t a front end of a
UPS, with its rectifier, battery, and DC bus, married to a variable-­frequency
drive’s back end? The drive’s part would have a controller, with its inverter
and motor control. The answers are that the demand for such a combina-
tion is uncommon, and UPS design requirements and variable-frequency
drive requirements are different. The analysis presented herein is useful in
other separate applications of drives and UPSs. The examples are usable for
matching UPSs to other loads besides drives. An example of a drive sup-
plying a motor with a fast transient load is given in Chapter 10.

9
10 Models for Design: Electrical Calculations for Industrial Plants

This discussion focuses on sizing an uninterruptible power supply (UPS)

to power a variable-frequency drive (VFD), which drives a motor and its fan
load. Although pumps follow the same principles as fans, addressed herein
are only fans. This discussion is limited to

a. A fan forcing airflow and driven by a motor

b. A variable-frequency drive driving the motor
c. A standard 460 V three-phase 60 Hz induction motor, totally enclosed
and fan cooled, with horsepower rating from 60 to 600 Hp
d. A variable-frequency drive supplied from a 480 V source
e. Both VFDs and UPSs of the low-harmonic type with active filtering

The airflow is regarded as incompressible, and the Fan Laws apply

(see Bibliography). However, in some applications, a large flow head requires
a turbocompressor, and then compressible flow applies. Air compressor flow
is an isentropic process, with the process inefficient in the turbocompres-
sor. Hence, the turbocompressor manufacturer provides the performance
characteristics tailored to the needed flow. The manufacturer of a fan or a
turbocompressor provides performance data and curves to define the most
accurate information for the VFD’s operation. Figure 2.1 is an example of a
turbocompressor’s performance curves and data.

140 80
Rated 1500 CFM @ 78 in WTR COL
107 F inlet temp 11.6 psia inlet press
0.932 SP GR1.382 K value 2145
1995 rpm –78 in WC inlet
0 in WC outlet Horsepower
120 60
1995
Differential pressure in WC

Shaft horsepower input

100 40
em

2145
st
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Surge limit
80 20
Press
ure
1995

60 0
1000 1500 2000 2500 3000 3500
Inlet CFM

FIGURE 2.1
Turbocompressor performance.
Another random document with
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 fatty degen.
vessels. Sclerosis
ant. columns.
Atrophy ant. roots.
Foci of softening
in ant. cornua.
Roger and Fatty degen.
29 1871 2 2½ Variola. Both legs. Ibid.
Damaschino. blood-vessels,
circumscribed
myelitis.
Roger and Foci of softening,
30 1871 2 3 Fever. Ibid. Ibid.
Damaschino. as above.
Focus myelitis on
both sides.
Disappearance Virch. Arch.,
31 1873 Roth. 1 2 Ibid. Ibid. ganglion-cells, 1873, Bd.
abundant lviii.
exudation
corpuscles.
Extensive myelitis
ant. and central Med.-Chir.
After
32 1868 L. Clarke. 1 32 Both arms. part gray matter. Trans., li. p.
inoculation.
Disappearance 219.
ganglion-cells.
Atrophy lumbar
cord ant. lat.
columns. Atrophy
Virch.
Acute ganglion-cells.
33 1876 Schultze. 3 22 Both legs. Archiv, Bd.
disease. Abundant exud.
lxviii., 1876.
corpuscles.
Proliferation
neuroglia.
34 1876 Leyden. 2 60 Fall from L. leg. Circumscribed Archiv f.
table. cicatrix with Psych.,
complete 1876, Bd. vi.
destruction gray
substance.
Amyloid
 degeneration.
Atrophy ant. roots.
Atrophy ganglion-
cells. Cellular
35 1876 Leyden. ¾ 1¾ Suddenly. L. leg. diffused infilt. Ibid.
(myelitis) gray
subst'ce.
Amyloid infiltration
ant. horns,
atrophy ganglion-
Sudden
36 1876 Leyden. 4 58 L. leg. cells left lumbar Ibid.
over night.
horn. Diffuse
atrophy gray
substance.
Sclerotic focus in
right lumbar and
in left cerv. region.
R. leg, L. Diffuse meningo-
37 1876 Leyden. 3 20 Ibid. Ibid.
arm. myelitis. Atrophy
ant. lat. columns.
Encapsulated
myelitis.
Purulent focus in
Quoted by
ant. cornua
Seeligmüller,
38 1876 Demme. ? 3½ ? — lumbar region.
loc. cit., p.
Atrophy ganglion-
18.
cells.
Diffuse
inflammation
39 1876 Eisenlohr. ? ¾ ? B. legs. Ibid.
anterior horns and
ant. lat. columns.
Myelitic
disorganization Trans. Path.
40 1879 Turner. 2½ 2¾ ? gray substance Soc. Lond.,
ant. cornua 1879.
lumbar cord.
41 1883 Archambault 30 m's 31 m's, Malaise Left leg Focus red Le Union
et or 26 and and right softening ant. médicale,
Damaschino. arm. horns left lumbar; 1883.
 d'ys fr. prostration right cervical
début. one day. region. Enormous
enlargement
vascular network,
and distension
blood-vessels;
granular
corpuscles in
lymphatic
sheaths; marked
atrophy cells and
of myeline
sheaths of fibres
in ant. roots;
myeline balls in
sheath; axis-
cylinders
disappeared.
Lesions more or
less marked
throughout cord.
Nerves not
examined.
Red area both
anterior cornua
lumbar region.
Fever and Here distension Trans. Path.
42 1884 Money. 2 yrs. 28 m's. vomiting Paraplegia. and thrombosis Soc. Lond.,
for a week. vessels; infiltration 1884.
leucocytes;
absence
multipolar cells.
1884 Money. Unknown 7 yrs. Unknown. Right leg. Wasting anterior
horn almost
throughout lumbar
region. Atrophy
cells chiefly in
ant., ant.-lat.,
post.-lateral, and
central groups,
 replaced by dense
nucleated tissue.

It will be useful to add another table, which will group together the cases
in which the autopsies were made within two years after the occurrence
of the paralysis. Of these, all but the two made by Laborde, in which the
cornua are declared to be healthy and the lesion limited to the white
columns, show traces of destructive morbid processes in the gray
substance of the cord, greatly predominating in the anterior cornua, but
not absolutely limited to them, nor even to the part of the cord which
corresponds to the paralyzed limb:

TABLE VI.
Date of Autopsy Year of
Case No. Name of Author. after Paralysis. Publication.
41 Damaschino. 6 weeks. 1883
40 Turner. 26 days. 1879
28 Roger and Damaschino. 2 mos. 1871
42 Money. 4 mos. 1884
27 Echeverria. 6 mos.
39 Eisenlohr. 6 mos.
29 Roger. 6 mos. 1871
31 Roth. 9 mos. 1873
35 Leyden. 11 mos. 1876
14 Bouvier and Laborde. 12 mos. 1864
30 Roger. 13 mos. 1871
15 Cornil and Laborde. 16 mos. 1864
12 Recklinghausen. 24 mos. 1863
38 Demme. 24 mos. 1876
23 Taylor. 18 mos. 1879
25 Humphrey. 24 mos. 1879

AUTOPSIES OF RELATIVELY RECENT CASES.—In cases relatively recent all

macroscopic changes in the cord may be entirely wanting. There may be
some degree of asymmetry in the surface of section, patches of white
coloration in the anterior gray substance, or of gray or yellow color in the
white columns; the anterior roots may be congested or even already
atrophied.94 On the other hand, there have several times been found foci
of visible red softening, much more frequently at a point corresponding to
the origin of the paralyzed nerves, but not absolutely confined to them,
and sometimes existing at points where they have given rise to no
symptoms whatever.95
94 Roger's first case, No. 28 of Table V.

95 Case 1st of Roger, Tab. V.

Microscopic Lesions.—In striking contrast with this paucity of macroscopic

lesions are the interesting structural changes revealed under the
microscope. These lesions are usually comprised within circumscribed
foci whose size may vary from a long diameter of 2 mm.96 to one of from
10 to 30 mm.97 Sometimes bilateral foci are found with monoplegic
paralysis; thus one side or the other preponderates in the morbid process.
96 Case Roth, Tab. V.

97 Case Schulze, Tab. V.

In recent cases (Damaschino's, at twenty-six days; Roger's, at two

months; Turner's, at six weeks) patches of red softening existed at the
portions of the cord containing the nuclei of origin of the paralyzed
nerves. In Turner's case the focus contained hemorrhagic extravasation,
and the traces of this were clearly perceptible in Roger's first case. The
blood-vessels are dilated; their lymphatic sheaths infiltrated with
leucocytes and with granular corpuscles; their walls are thickened,
pigmented, or fatty.

Leucocytes are often disseminated through the diseased area, and in one
case (Demme) were accumulated into a focus of pus. Besides the
leucocytes, the foci are often infiltrated with large round granular cells that
seem to be transformed neuroglia-cells (Leyden). In one case neuroglia
nuclei were accumulated in a ring around the focus, seeming to indicate
the beginning of encapsulation.

The most striking lesion, however, and the one which is common to the
most recent as well as to old cases, is the deformation, atrophy, and final
disappearance of the large ganglionic cells of the anterior cornua. The
first change consists in granular pigmentation;98 then the prolongations
disappear, leaving the body of the cell shrunken and deformed; at last the
whole cell disappears. Sometimes all the cells of an anterior horn have
disappeared throughout the entire depth of the focus; quite as often, in
certain sections at least, the atrophy is limited to certain groups, as the
external,99 or the external in one focus, the antero-lateral in another,
situated on the opposite side of the cord.100
98 Case of Echeverria, Tab. V.

99 Case by Schultze (this is a case of ancient lesion), Tab. V. (Virch. Arch., Bd. lviii.).

100 Case by Taylor, Tab. IV. (Path. Trans., London, 1879.)

In a case rendered celebrated by Charcot it is stated that in many

sections of the cord atrophy of ganglionic cells constituted the unique
alteration, the tissue immediately surrounding the place whence they had
disappeared being perfectly healthy. It is on this appearance that has
been built up the theory of a primary idiopathic atrophy of the ganglionic
cells as the characteristic lesion of infantile paralysis. But in other portions
of the same cord Charcot himself describes destruction of the gray
reticulum imbedding the cells; and this destruction is insisted upon in
many other observations. In other words, there is a general disintegration
of the gray nervous tissue of the anterior cornua which contain the focal
lesion. The normal tissue is then replaced by a reticulum of conjunctive
fibres, more or less dense according to the age of the case.

These focal lesions of the cord explain admirably, as will be seen, the
permanent symptoms of the disease. But of great importance for
understanding its initial period is the fact that structural changes—similar
to, but less severe than, those just described—have beer found diffused
throughout the cord. In several cases hyperæmia, partial atrophy of
ganglionic cells and nerve-fibres, infiltration with exudation corpuscles, in
the anterior cornua and even central gray canal from the lumbar to the
cervical region.101 In Damaschino's case, besides the focal lesions which
corresponded to the paralyses of the right arm and left leg, were others
corresponding to the left arm and right leg where no paralysis existed.
101 See cases by Leyden, Roth, Schultze, Clarke, Damaschino.

This case (1883) is also interesting in bringing out another lesion not
usually noticed. This is the breaking up into balls of the myeline in the
medullated tubes, both of the anterior intraspinal nerve-roots and of such
fibres as traversed the anterior nerves. In balsam preparations these
myeline drops are dissolved; but in osmic acid and glycerin preparations
they appear as black balls all over the field. The lesion is identical with
that already described by Dejerine (1875) in both nerves, roots, and white
columns. The columns of Clarke have always been found intact.

In the recent cases no lesions of the white columns have been observed
—a fact upon which reposes the doctrine that such lesions, when
existing, are secondary to those of the cornua.

SECOND GROUP OF CASES.—The next group of cases contains 16, where

the autopsy was made more than two years after the début of the
paralysis.

TABLE VII.—AUTOPSIES SHOWING LESIONS OLDER THAN TWO YEARS.

Year of
Case No. Name of Author. Date of Lesion. Publication.
11 Longet. 7 yrs. 1842
27 Echeverria. 7 yrs. 1866
43 Money. 7 yrs. 1884
16 Lancereaux. 16 yrs. 1873
38 Leyden. 17 yrs. 1876
33 Schultze. 19 yrs. 1876
17 Charcot and Joffroy. 25 yrs. 1870
20 Müller. 30 yrs. 1871
22 Clarke. 31 yrs. 1868
10 Hutin. 42 yrs. 1825
13 Cornil. 47 yrs. 1863
36 Leyden. 54 yrs.
34 Leyden. 58 yrs. 1876
19 Vulpian. 64 yrs. 1870
22 Raymond. 70 yrs. 1875
16 Prévost. 76 yrs. 1866

The date of these lesions varies from seven to seventy-six years. In two
or three cases, where the autopsy was made on very old people, the
early history of the disease was unknown, but the probable date of the
paralysis was calculated.
In this group of cases patches of atrophy, semi-transparent and grayish in
color, focal or diffused, are clearly perceptible to the naked eye. As a rule,
the atrophy is unilateral, and sensibly affects the entire half of the cord. In
some cases of paraplegia, however, there is a bilateral, symmetrical
shrinkage of the entire lumbar cord, which has been reduced to the size
of a quill.

The atrophy involves, first and most markedly, one or both anterior
cornua; second, the anterior nerve-roots arising from them; third, the
antero-lateral columns.

In both the latter localities the microscope will often find individual nerve-
tubes wasted and deprived of their myeline. The atrophied patches are
generally sclerosed as the seat of a proliferated neuroglia, coloring deeply
with carmine. In Laborde's cases, published at the very beginning of what
may be called the anatomical period, the atrophy and sclerosis were said
to be limited to the antero-lateral columns and the nerve-roots, while the
cornua remained intact. In all more recent observations, however, the
lesion of the white columns and roots has been found strictly proportioned
to that of the gray horns. The sclerosis extended into the latter,
constituted by a reticulum of connective-tissue fibres, sometimes fine,
sometimes so matted together as to form a dense felt-like substance,
sometimes offering the ordinary aspect of sclerosis.

Amyloid corpuscles have been found infiltrated in great numbers through

both the gray and white substance in these old cases (case by Cornil),102
seeming to replace the infiltration with exudation corpuscles observed in
the more recent ones.103 When the lesion is distinctly circumscribed the
focus is often surrounded by a zone of embryonic cells, seeming to
indicate a reactive proliferation on the periphery.104
102 Loc. cit., Soc. Biol.,1863.

103 Seguin (loc. cit.) observes that the opinion is gaining ground which ascribes these to a
transformation of the neuroglia corpuscles.

104 Case by Schultze, loc. cit.

As in the relatively fresh cases, the circumstance which has attracted the
most attention is the atrophy of the ganglionic cells from the sclerosed
patches of the anterior cornua. The completeness with which these have
disappeared in any focus seems to be proportioned to the completeness
of the paralysis in the corresponding limb. Partial atrophy or
disappearance of spinal groups of cells from the cornua may sometimes
be correlated with paralysis of special muscles.105
105 Thus in Schultze's case, already quoted, the external group of cells had disappeared
from the focus in one gray horn, and the extensors of the foot were alone paralyzed. This
seems to confirm the opinion advanced by Spitzka, that this external group of motor-cells
corresponds to the extensor, the internal groups to the flexor muscles.

Study of the pathology of infantile paralysis is not completed when the

above series of spinal lesions has been enumerated. Most various
interpretations have been made of these lesions as they have been
successively discovered. Thus, after the theory of congestion came the
theory of primary sclerosis, built upon Laborde's two autopsies;106 then
the theory of primary atrophy of ganglionic cells;107 then the theory of
myelitis;108 finally, a theory of complex and variable lesion.109
106 Laborde, loc. cit.; Cornil, loc. cit.

107 Charcot, Leçons sur les Maladies du Syst. nerveux; Prévost, Soc. Biol., 1864; Joffroy,
Arch. de Physiol., 1870; Petitfils, “De l'Atrophie aigue des Cellules matrices,” Thèse de
Paris, 1873.

108 Schultze, Virch. Arch., Bd. lxviii.; Roth, Ibid., Bd. lviii.; Henoch, loc. cit., p. 208; Ross, loc.
cit., p. 125; Seguin, loc. cit., 1877; Erb, Ziemssen's Handbuch; Seeligmüller, Gerhardt's
Handbuch; Roger and Damaschino, Gaz. méd., 1871; Turner, Path. Trans. Lond., 1879;
Hammond, loc. cit.

109 Leyden, Archiv für Psych., Bd. vi., 1876.

It was Prévost who first ascribed a predominant importance to the atrophy

of the ganglionic cells of the anterior cornua; but it was in the hands of
Vulpian, Joffroy, and more especially Charcot and his pupils, that the
theory was fully developed. Infantile paralysis was ranked in a newly-
formed group of diseases, all characterized by atrophy of these same
cells, and differing from each other principally in the acuteness of the
process and in its complications.110 Seguin, in his original lecture in 1874,
supported the same views, but in 1877 fully adopted that of myelitis. The
objections to this theory are: 1st, that by it two diseases so different in
their course, localization, electrical reactions, and form of paralysis as
atrophic paralysis and progressive muscular atrophy are essentially
identified on account of the identity of one lesion, the atrophy of the
anterior ganglionic cells;111 2d, the presence of other lesions or of traces
of them peremptorily proves the pre-existence of a complex morbid
process which involves the ganglionic cells, but is neither limited to them,
nor, necessarily, originates in them.
110 Thus, acute anterior poliomyelitis, subacute anterior poliomyelitis, progressive muscular
atrophy, amyotrophic lateral sclerosis, bulbar paralysis.

111 When this objection is accepted, Barlow's remark falls to the ground, that “the similarity
of lesion found in two such different diseases as infantile paralysis and progressive muscular
atrophy proves the failure of anatomical characters, taken alone, to serve as a basis of
nosology” (Brain, April, 1879, p. 74).

This inference was drawn by Roger from the hemorrhagic softening,

dilatation, and degeneration of blood-vessels, infiltrations with exudation-
corpuscles, and hyperplasia of conjunctive nuclei present in his case.
Similarily, Schultze, in a case examined nineteen years after the
occurrence of the paralysis, found traces of an extensive myelitis in the
diffusion of the lesions,112 in the exquisite cellular infiltration, the
proliferation of the neuroglia, and the atrophy of axis-cylinders of nerve-
fibres together with the cells; and inferred an anterior myelitis, diffused in
the long axis of the cord, but limited to the antero-posterior region.
Schultze defines Charcot's theory to be an hypothesis of such an acute
atrophy of ganglionic cells as leads to a rapid melting down of these
bodies, whereby reactionary inflammation is excited in the surrounding
tissue. This implies that the dying cells are able to act like a virulent
substance on the imbedding tissue, and of this, declares Schultze,
“Charcot has offered no proof.”113
112 In this case of paraplegia without lesion of the upper extremity, to which we have several
times alluded, there was bilateral atrophy of the lumbar cord, atrophy of the right anterior
nerve in the dorsal and lower cervical region, also in the cervical enlargement.

113 It might be said that the fall of the fever as soon as the paralysis is declared and the
motor cells presumably melted down should contradict the idea that their dying substance
acts as an irritant upon surrounding tissues.
A third objection has been brought forward by Leyden, and is really an
enlargement on the second. It is, that various lesions or morbid processes
may underlie the same clinical history. In four autopsies of cases
presenting all the clinical history of acute anterior poliomyelitis this author
has found three different lesions. In one an extensive lepto-meningitis,
together with irregular focal sclerosis of the white columns, evidently
depended upon the latter, and in turn caused sclerosis of the anterior
cornua with consequent destruction of their cells.114 In two other cases an
anterior poliomyelitis was accompanied by diffused lesions of the central
canal. Finally, in a fourth case the lesions were limited to the anterior
cornua, as is most usual.
114 This case of Leyden's throws light on the two autopsies by Laborde with sclerosis of the
white columns and intact cornua. It seems probable that a process originating in the cornua
had then been arrested or had receded, while continuing its evolution in the white columns.

The theory of acute atrophy of ganglionic cells is not sensibly different

from that of a parenchymatous myelitis.115 But all the objections which can
be urged against the former theory apply to the latter also, with the
exception that the hypothesis of inflammation suggests a cause for the
otherwise inexplicable atrophy. Observation of the pathological
appearances alone could not decide whether the irritation started in the
parenchymatous or interstitial tissues. Reference to the etiology of the
disease shows that of the two most frequent apparent causes, blood-
poisoning and traumatisms, the first would indicate that the inflammation
started in the connective tissue supporting the blood-vessels; the second
suggests that the irritation began in the spinal elements constituting the
origin of the nerves.
115 Hammond assumes such a form of myelitis in his classification of inflammations limited
to the anterior part of the gray matter of the spinal cord:

1. Inflammation of motor and trophic nerve-cells: (a) Infantile spinal paralysis; (b) Spinal
paralysis of adults; (c) Pseudo-hypertrophic spinal paralysis.

2. Inflammation of motor cells: (a) Glosso-labia-laryngeal paralysis.

3. Inflammation of trophic cells: (a) Progressive muscular atrophy; (b) Progressive facial
atrophy (Dis. Nerv. Syst., 6th ed., p. 464).

We think this classification open to several fundamental criticisms.

Whatever be the starting-point, however, it is very evident that the morbid
process soon involves all the tissues contained in the gray matter of the
anterior horns, and constitutes, therefore, a real anterior poliomyelitis.

A question of much interest is the relation to this of the lesions of the

anterior roots and of the white columns. Is the atrophy of nerve-tubes a
passive consequence of their separation from the ganglionic cells, the
sclerosis a secondary consequence of this? or is the sclerosis the cause
of the atrophy, itself the result of an irritation propagated downward from
the myelitic focus, according to the usual law for secondary
degenerations in motor tracts? or, finally, is it a residuum of a
leucomyelitis (or of the white substance), complicating by simple
extension the inflammation of the gray substance?

Review of the autopsies recorded would indicate that the lesions in

question are brought about sometimes in one, sometimes in another, of
these ways—sometimes even, as in Leyden's case, by extension from a
meningitis. That sclerosis of the white columns is most frequently a
secondary degeneration is indicated by the frequency with which it
appears below the lesion of the cornua, by the rarity with which it is found
above, and also by the general proportion between its intensity and that
of the disease of the gray matter.

We have devoted so much space to consideration of spinal-cord lesions,

because they are by far the most constant and the most important; after
these rank the structural alterations of the muscles, which received for a
while such a preponderance of attention.

Hammond has studied the progress of these changes on the living

subject by fragments of fibre successively removed with Duchenne's
harpoon. In an incipient stage of degeneration the fibrillæ are found to be
irregular and torn,116 the transverse striæ dim; oil-globules are seen
arranged according to the long axis of the fibre. In a more advanced
stage the transverse striæ nearly disappear, the oil-globules are in large
numbers, and fat-corpuscles are also abundant. Finally, the whole
specimen is seen as a mass of air-globules. Six weeks later, however,
these had in turn disappeared, and there remained a mass of connective
tissue.
 116 Though, from the method of removal, this appearance cannot be considered as certainly
pathological.

This series of changes, however, does not always take place, as

Hammond himself recognizes. Laborde117 first described a granular form
of muscle atrophy, where the muscular substance gradually wastes away
without ever becoming fatty, and leaving a transparent and hyaline
sheath. The two forms of fatty and of simple atrophy can be distinguished
by the naked eye. In the latter the muscle begins by being thinner or
lighter and softer than usual, ultimately turning light brown. The fatty
muscle becomes a homogeneous yellowish-white, diversified by
occasional remnants of reddish fibres.
117 Loc. cit., p. 131.

Proliferation of the interstitial connective tissue may be combined with

either simple or fatty atrophy. A combination of abundant sclerosis and
abundant fatty infiltration may lead to a pseudo-hypertrophy of the
muscles.

“There cannot be the slightest doubt,” observes Erb, “that the lesions
described constitute a degenerative atrophy similar to what may be
caused by section or sense traumatism of a peripheric nerve.”

The peripheric nerves have been much less thoroughly studied than the
spinal cord. Leyden first directed special attention to the nerves. He found
the sciatic altered in two cases,118 in the first by an interstitial neuritis; in
the second by partial atrophy. In 1880 the same writer, in an extensive
article on poliomyelitis and neuritis,119 greatly extends his views as earlier
expressed. Not only does he claim the coexistence of neuritis with spinal-
cord disease in atrophic paralysis, but thinks that many cases of this, and
also of other forms of paralysis, “lately supposed to originate in the spinal
cord, may really begin in any part of the motor apparatus,” thence
sometimes generalize throughout the whole apparatus, sometimes
remain limited to the original portion affected. Thus, progressive muscular
atrophy may sometimes begin in the nerves, sometimes in the muscles,
and sometimes in the ganglionic cells of the cord; and this variety of origin
explains the discrepancies of opinion which have been held upon the
nature of this disease. Similarly, all forms of acute or chronic atrophic
paralysis in either children or adults may begin in either the nerves or
cord, thence become generalized to both, or remain limited to one part of
the spinal motor system. Cases of atrophic paralysis which recover are
probably not cases of poliomyelitis at all, but of multiple neuritis,
rheumatic, traumatic, or infectious in nature. The regeneration of
peripheric nerves is a well-demonstrated possibility, but not that of the
cells of the cord. Lead-paralysis is usually confined to the nerves, but
sometimes extends to the cord. In diphtheritic paralysis Buhl has found
injection, thickening, and granular infiltration of nerves at the union of their
anterior and posterior roots;120 and as long ago as 1876, Dejerine, in a
case of atrophic paralysis in a syphilitic woman, found varicose swelling
of the medullary sheath in the nerves of the paralyzed lower extremities,
together with heaping up of the myeline into large drops, colored black in
glycerin and osmic-acid preparations. Coincidently, in the cord, at the
origin of the same nerves, the number of motor-cells was diminished, and
of those that remained the prolongations, and even the body, of the cell
were atrophied.121
118 Cases 34 and 35 of Table V., quoted from Arch. de Psychiatrie, Bd. vi., 1876.

119 Zeitschrift für Klin. Med., 1880.

120 Zeitschrift für Biol., 1867.

121 Arch. de Phys., 1876.

These views of Leyden's are extremely interesting, and should stimulate

future research into the condition of nerves in all cases of atrophic
paralysis. It is quite incorrect to say, as Archambault and Damaschino
have recently done,122 that Leyden denies the existence of anterior
poliomyelitis in such cases, especially in such as prove permanent. He
only insists on the frequent coincidence of neuritis, on a varying point of
departure for the morbid process, and on the probability that in cases of
recovery this process has always remained peripheric.
122 Le Union méd., 1883, 7, 35, case quoted in Table V. It is much to be regretted that
Damaschino, who strongly controverts Leyden's views, did not examine the nerves in his
own most interesting case.

The strongest objection to Leyden's theory is the absence in most

recorded cases, either infantile or adult, of the usual signs of nerve
inflammation, local pain, or tenderness. Autopsies of old cases are not
able to differentiate an inflammation from an atrophic process in the
nerves, followed by a secondary thickening of the endoneurium. This
thickening was found in three cases examined by Edmonds in 1882,
whose subjects had suffered from infantile paralysis in early life, and had
had the paralyzed limb amputated at the age of fifteen or sixteen.
Transverse sections were made from the internal popliteal nerves. The
specimens showed some healthy nerve-fibres, presumed to be sensory;
others much smaller, with the axis-cylinders wasted or degenerated; while
strands of connective tissue traversed the nerve-bundles, resulting from
hypertrophy of the endoneurium. The vessels showed inflammation of
their coats, with proliferation of the endothelium.123
123 Trans. Path. Soc. London, 1883.

The brain is usually normal, unless indeed the paralysis has affected
children previously rendered idiotic by congenital atrophia cerebri.
Sandie, however, examined one brain with an interesting positive
result.124 The brain was taken from a boy of fifteen paralyzed since the
age of three in almost all his muscles, with even paresis of the muscles of
the trunk and neck. The paralysis was more marked upon the right than
on the left side. At the autopsy, in addition to atrophy of the muscles and
of the motor nerves, with exquisite atrophy of the anterior columns and
anterior cornua, was found a decided atrophy of the left central
convolution, and, less marked, of the paracentral lobule. This was shown
by comparative measurements with the opposite side of the same brain,
and also with the corresponding convolution and lobule in two other
brains. The child's intelligence had not been affected.
124 Centralblatt f. d. Med. Wissensch., No. 15, 1875.

The arrest of development of the bones has been already mentioned, as

well as that of their epiphyses and apophyses. The compact osseous
tissue is atrophied: the medullary, on the contrary, abundantly developed
and rich in fat.

PATHOGENY OF INFANTILE PARALYSIS.—In the pathological anatomy of

infantile paralysis there are two principal facts to be correlated with its
clinical phenomena—namely, the limitation of the myelitis to the anterior
gray horns of the spinal cord; the destruction of the ganglionic nerve-cells
in these gray horns. That the other lesions observed are subordinate to
these is shown by their variableness as compared with the constancy of
the anterior poliomyelitis. These lesions are, in the cord, the atrophy and
sclerosis of the anterior nerve-roots and white columns; in the muscle, the
fatty degeneration or simple atrophy of the fibre; in the nerve, breaking
down, and finally atrophy of the myeline sheath, sometimes of the axis-
cylinder; proliferation of the endoneurium.

Consequence of Limitation of Myelitis.—Limitation of the morbid process

to a portion of the motor tract, the anterior cornua, and exclusion of the
posterior horns and roots, readily explain the predominant positive
symptom of motor paralysis, together with the absence of sensory
disturbance. The absence of muscular rigidity, spasm, active contraction,
and of exaggerated reflexes is similarly explained by the immunity from
the morbid process of the posterior white columns and the portion of the
lateral columns immediately adjacent to them. The motor paralysis
resulting from destruction of the anterior ganglionic cells of the cord is
much more complete than that which depends on simple interruption of
the motor tracts passing from the brain. The manner in which the motor
tracts are connected by a succession of arching fibres with these cells
already indicates that the latter are dépôts for the reinforcement of the
motor impulses. We must believe, indeed, that the centrifugal impulses
reaching the anterior cornua are not yet motor in character, but to become
so must sustain a new elaboration in the ganglionic cells of this region.
Evidently, the network of gray fibres connecting the arcuate strands of the
antero-lateral columns with the cells become, in virtue of that fact alone,
essential to the process. But it is also probable that the multiplied
transmission of impressions, which lies perhaps at the basis of the
process of their higher elaboration in ganglionic centres, is carried on in
the larger network of gray fibres as well as in the smaller network
contained in the ganglionic cells. Destruction of a portion of this network
would therefore interfere with the elaboration of the motor impulse, in the
same manner, though to a relatively less extent, as destruction of the
ganglionic cells themselves.

Trophic Lesions.—The rapid wasting of the paralyzed muscles, with their

degenerative electrical reactions, seems, however, to be an effect
altogether peculiar to lesions of the ganglionic bodies.125 According to
Charcot, who has so especially formulated the laws of amyotrophic
paralysis, all the ganglionic cells essential to the elaboration of motor
impulses exercise a trophic influence upon muscles. The spinal cell,
nerve-fibre, and muscle-fibre combine into a complex indissoluble unity or
element. One part of this lesion of complex elements is necessarily
followed by proportionate lesion of all its other parts.
125 The amyotrophic lateral sclerosis of Charcot exhibits in an exquisite manner the
difference between paralysis without atrophy, caused by sclerosis of the antero-lateral
columns, and paralysis with atrophy when the morbid process has extended to the anterior
cornua.

According to Erb, however, who extends Samuel's doctrine of special

trophic nerves, it is not the motor cells which influence the nutrition of the
muscle-fibres with which they are connected, but special trophic cells
lying among the others in the anterior cornua. This theory is principally
based on the existence of muscular atrophies of central origin
(progressive muscular atrophy, bulbar paralysis), unaccompanied for a
long time by paralysis.126 Hammond cites as a converse example the
anterior poliomyelitis “where the peripheric disturbance is, in the first
place, solely one of motility; this is paralysis without atrophy. After a time,
which may be as much as six months or even more, the trophic changes
begin.”127
126 Ziemssen's Handbuch.

127 Loc. cit., p. 429.

But surely this is an exaggerated emphasis on the exception, rather than

the true inference from the rule of rapid wasting in anterior poliomyelitis—
a rule so general as to have originated the title atrophic paralysis. Erb
gives an ingenious scheme (Fig. 55) of the mental relations of motor and
trophic cells with cerebral and spinal nerve-fibres. It will be seen that
isolated lesions of one or the other trophic apparatus might occur without
paralysis of motor tracts, while simultaneous lesion of the trophic
apparatus and of the ganglion-cells, or of the latter, involving the tracts
coming from the trophic cells, would cause, as in anterior poliomyelitis,
motor paralysis, muscular atrophy, loss of the reflexes, degenerative
reaction in nerves and muscles.

FIG. 55.
c, trophic cell for nerve; a, cerebral fibre; b, trophic cell for muscle; d,
ganglionic cell; s, sensory fibre; f, trophic path to muscle; m, muscle. (From
Ziemssen's Handbuch der Speciellen Pathol., Bd. xi. Zweite H., Zweite Abtheil,
p. 313.)
Duchenne and Joffroy128 also argue the existence of special trophic
nerve-cells. The absence129 of the nutritive lesions of the skin and cellular
tissue which are so conspicuous when the gray matter around the central
canal or posterior to it is involved,130 the dependence of the nutrition of the
motor apparatus, nerves, muscles, bones on the integrity of the anterior
horns, are facts which, taken together, seem to indicate that the
maintenance of nutrition depends on the unbroken continuity of the motor
or sensory apparatus from the periphery to the ultimate central element,
rather than on any special central cells endowed with trophic functions.131
Erb's hypothesis, as his own scheme moreover denotes, demands not
only trophic cells distinct from motor cells, but separate trophic cells for
the muscles, for the motor, and for the sensory nerves.
128 “De l'Atrophie aigue et chronique des Cellules nerveuses,” Arch. de Phys., No. 4, 1870.

129 Money, and also Gowers, have signalized a condition of the skin resembling myxœdema
(Tr. Path. Soc. London, 1884, and Brit. Med. Journ., 1879).

130 Mayer (Herman's Handbuch Physiol.) sums up the great mass of evidence now
accumulated, which demonstrates the trophic influence of the central gray mass of the cord
upon the tissue.

131 Nepveu (La France médicale, 1879) mentions some cases of infantile paralysis
complicated with trophic lesions of the skin. The facts, if accepted, could only indicate an
extension of the myelitis to the central and posterior regions of the gray columns. The
relations between non-atrophic paralysis caused by interruptions of the motor tracts and
muscular atrophy dependent on lesion of the anterior cornua are exquisitely shown in a case
reported by Sander. An adult suffered from chronic motor paralysis, gradually increasing, in
the right arm, with paresis of the lower extremities. In the hand, arm, and shoulder the
paralysis was followed by gradual atrophy and diminution of the faradic contractility; in the
lower extremities no atrophy occurred. At the autopsy was found a gliomatous tumor seated
in the anterior cornua predominating on the right side, extending from the level of the sixth
dorsal to that of the eighth cervical vertebra. The ganglion-cells were pigmented and
compressed, not altogether destroyed. The lumbar cord was intact, and the non-atrophic
paresis of the lower extremities evidently resulted from the interruption of the motor tract
above.

The peculiar grouping of nerve-centres within the cord that seems to be

indicated by some of the groupings of infantile paralysis shows, as has
been said, a probable divergence within the cord of nerve-fibres which
run together in the same nerve-stem. The associations to be expected
from the data of functional association and of clinical history are by no
means fully decided. It is even a matter of dispute whether the tibialis
anticus is functionally more associated with the flexors or with the
extensors of the thigh, and whether its experimental irritation or clinical
paralysis really coincides with that of the first or of the second group. This
entire field of observation is new and promises fertile results.132
132 It is from this field that has come a new argument for the spinal nature of lead-paralysis,
from its peculiar grouping, and from analogy with that of anterior poliomyelitis of the upper
extremities (Remak, “Ueber die Local. Atropa. Spinal Lahm.,” Archiv für Psych., Bd. ix.; also,
Ferrier, loc. cit.).

Relation between Limitation of Myelitis and Age.—From the relative

frequency of anterior poliomyelitis in childhood, as compared with its
much greater rarity in adult life, we must infer the existence of some
special conditions in childhood which tend to limit the morbid process to
such a portion of the cord. The theory of a primitive spontaneous atrophy
of the motor cells would serve, indeed, to explain this limitation. The
reasons already alleged for regarding the morbid process as a systematic
myelitis decisively hinder the acceptance of such an explanation as it
stands. On the assumption, however, that the myelitis is usually of
functional origin, and starts, therefore, in the elements of the anterior
cornua essentially involved in the motor functions, the morbid
susceptibility of these elements may be ranked with the liability to disease
of the entire locomotor system which is known to be so predominant in
children. From pathological evidence, even without anatomical proof, we
may reasonably infer an incompleteness of development in the anterior
cornua of the cord correlative with that well demonstrated in the bones
and functionally inexperienced muscles. If the antero-posterior fibres
which connect the anterior cornua with the central and posterior gray
masses be also incomplete, the radiation of irritations, and consequent
vascular irritation, would also be arrested within the boundaries of the
original lesion. Thus a peculiarly circumscribed, instead of the common
diffused, myelitis of adults.

Money133 points out that for the gray matter of the cord, as of the brain,
the centre or maximum force of the circulation is on the periphery, and the
nutritive supply of the centre is thus easily cut off. Moreover, while the
blood-vessels of the cervical and dorsal regions of the cord pass to it