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page v
Contents
Preface ix
Acknowledgments x
Walkthrough xii
About the Author xiv
Safety xv
Chapter 1 Digital Electronics 1

1-1 What Is a Digital Signal? 2
1-2 Why Use Digital Circuits? 4
1-3 Where Are Digital Circuits Used? 8
1-4 How Do You Generate a Digital Signal? 9
1-5 How Do You Test for a Digital Signal? 15
1-6 Simple Instruments 19
Summary 22
Correlated Experiments 22
Chapter Review Questions 22
Critical Thinking Questions 24
Answers to Self-Tests 25
Chapter 2 Numbers We Use in Digital Electronics 26

2-1 Counting in Decimal and Binary 26
2-2 Place Value 27
2-3 Binary to Decimal Conversion 29
2-4 Decimal to Binary Conversion 30
2-5 Electronic Translators 31
2-6 Hexadecimal Numbers 34
2-7 Octal Numbers 36
2-8 Bits, Bytes, Nibbles, and Word Size 37
Summary 39
Chapter 3 Logic Gates 43

3-1 The AND Gate 43
3-2 The OR Gate 46
3-3 The Inverter and Buffer 48
3-4 The NAND Gate 50
3-5 The NOR Gate 51
3-6 The Exclusive OR Gate 53
3-7 The Exclusive NOR Gate 54
3-8 The NAND Gate as a Universal Gate 56
3-9 The NOR Gate as a Universal Gate 59
3-10 Gates with More Than Two Inputs 63
3-11 Using Inverters to Convert Gates 65
3-12 Practical TTL Logic Gates 68
3-13 Practical CMOS Logic Gates 71
3-14 Troubleshooting Simple Gate Circuits 75
3-15 IEEE Logic Symbols 77
3-16 Simple Logic Gate Applications 79
3-17 Logic Functions Using Software (BASIC Stamp Module) 83
Summary 88
Chapter 4 Combining Logic Gates 96

4-1 Constructing Circuits from Boolean Expressions 97
4-2 Drawing a Circuit from a Maxterm Boolean Expression 98
4-3 Truth Tables and Boolean Expressions 99
4-4 Sample Problem 103
4-5 Simplifying Boolean Expressions 105
4-6 Boolean Algebra 106
4-7 Karnaugh Maps 114
4-8 Karnaugh Maps with Three Variables 115
4-9 Karnaugh Maps with Four Variables 117
4-10 More Karnaugh Maps 118
4-11 A Five-Variable Karnaugh Map 119
4-12 Using NAND Logic 120
4-13 Computer Simulations: Logic Converter 122
4-14 Solving Logic Problems: Data Selectors 126
4-15 Programmable Logic Devices (PLDs) 130
4-16 Using De Morgan’s Theorems 138
4-17 Solving a Logic Problem (BASIC Stamp Module) 140 page vi
Summary 145
Chapter 5 IC Specifications and Simple Interfacing 155

5-1 Logic Levels and Noise Margin 155
5-2 Other Digital IC Specifications 160
5-3 MOS and CMOS ICs 165
5-4 Interfacing TTL and CMOS with Switches 167
5-5 Interfacing TTL and CMOS with LEDs 171
5-6 Interfacing TTL and CMOS ICs 175
5-7 Interfacing with Buzzers, Relays, Motors, and Solenoids 179
5-8 Optoisolators 182
5-9 Interfacing with Servo and Stepper Motors 185
5-10 Using Hall-Effect Sensors 193
5-11 Troubleshooting Simple Logic Circuits 200
5-12 Interfacing the Servo (BASIC Stamp Module) 201
Summary 204
Chapter 6 Encoding, Decoding, and Seven-Segment Displays 212

6-1 The 8421 BCD Code 212
6-2 The Excess-3 Code 214
6-3 The Gray Code 215
6-4 The ASCII Code 218
6-5 Encoders 219
6-6 Seven-Segment LED Displays 221
6-7 Decoders 224
6-8 BCD-to-Seven-Segment Decoder/Drivers 225
6-9 Liquid-Crystal Displays 229
6-10 Using CMOS to Drive an LCD Display 234
6-11 Vacuum Fluorescent Displays 237
6-12 Driving a VF Display 240
6-13 Troubleshooting a Decoding Circuit 243
Summary 245
Chapter 7 Flip-Flops 252

7-1 The R-S Flip-Flop 252
7-2 The Clocked R-S Flip-Flop 255
7-3 The D Flip-Flop 257
7-4 The J-K Flip-Flop 259
7-5 IC Latches 263
7-6 Triggering Flip-Flops 265
7-7 Schmitt Trigger 267
7-8 IEEE Logic Symbols 268
7-9 Application: Latched Encoder-Decoder System 270
Summary 273
Chapter 8 Counters 278

8-1 Ripple Counters 278
8-2 Mod-10 Ripple Counters 281
8-3 Synchronous Counters 282
8-4 Down Counters 283
8-5 Self-Stopping Counters 285
8-6 Counters as Frequency Dividers 286
8-7 TTL IC Counters 288
8-8 CMOS IC Counters 292
8-9 A Three-Digit BCD Counter 296
8-10 Counting Real-World Events 300
8-11 Using a CMOS Counter in an Electronic Game 304
8-12 Using Counters—An Experimental Tachometer 307
8-13 Troubleshooting a Counter 311
Summary 314
page vii
Chapter 9 Shift Registers 321

9-1 Serial-Load Shift Registers 323
9-2 Parallel-Load Shift Registers 324
9-3 A Universal Shift Register 327
9-4 Using the 74LS194 IC Shift Register 329
9-5 An 8-Bit CMOS Shift Register 331
9-6 Using Shift Registers: Digital Roulette 333
9-7 Troubleshooting a Simple Shift Register 338
Summary 340
Critical Thinking Questions 342 page viii
Chapter 10 Arithmetic Circuits 345

10-1 Binary Addition 345
10-2 Half Adders 347
10-3 Full Adders 348
10-4 3-Bit Adders 350
10-5 Binary Subtraction 351
10-6 Parallel Subtractors 353
10-7 IC Adders 355
10-8 Binary Multiplication 358
10-9 Binary Multipliers 360
10-10 2s Complement Notation, Addition, and Subtraction 363
10-11 2s Complement Adders/Subtractors 368
10-12 Troubleshooting a Full Adder 370
Summary 372
Chapter 11 Memories 377

11-1 Overview of Memory 378
11-2 Random-Access Memory (RAM) 381
11-3 Static RAM ICs 383
11-4 Using a SRAM 386
11-5 Read-Only Memory (ROM) 388
11-6 Using a ROM 391
11-7 Programmable Read-Only Memory [PROM] 393
11-8 Nonvolatile Read/Write Memory 397
11-9 Memory Packaging 400
11-10 Computer Bulk Storage Devices 403
11-11 Digital Potentiometer: Using NV Memory 410
Summary 414
Chapter 12 Simple Digital Systems 419

12-1 Elements of a System 419
12-2 A Digital System on an IC 422
12-3 Digital Games 423
12-4 The Digital Clock 425
12-5 The LSI Digital Clock 429
12-6 The Frequency Counter 434
12-7 An Experimental Frequency Counter 439
12-8 LCD Timer with Alarm 441
12-9 Simple Distance Sensing 447
12-10 JTAG/Boundary Scan 453
Summary 456
Chapter 13 Computer Systems 461

13-1 The Computer 461
13-2 The Microcomputer 463
13-3 Microcomputer Operation 466
13-4 Microcomputer Address Decoding 470
13-5 Data Transmission 473
13-6 Detecting Errors in Data Transmissions 477
13-7 Data Transmission in a Computer System 480
13-8 Programmable Logic Controllers 485
13-9 Microcontrollers 489
13-10 The BASIC Stamp Microcontroller Modules 491
13-11 Digital Signal Processing 498
13-12 DSP in a Digital Camera 502
13-13 Microcontroller: Photo Input and Servo Motor Output 504
Summary 509
Chapter 14 Connecting with Analog Devices 515

14-1 D/A Conversion 516
14-2 Operational Amplifiers 517
14-3 A Basic D/A Converter 518
14-4 Ladder-Type D/A Converters 520
14-5 An A/D Converter 522
14-6 Voltage Comparators 524
14-7 An Elementary Digital Voltmeter 526
14-8 Other A/D Converters 528
14-9 A/D Converter Specifications 532
14-10 An A/D Converter IC 533
14-11 Digital Light Meter 536
14-12 Digitizing Temperature 539
Summary 541
Appendix A Solder and the Soldering Process 546

Appendix B 2s Complement Conversions 551
Glossary of Terms and Symbols 552

Index 566
page v
Preface
Digital Electronics: Principles and Applications, ninth edition, is an easy-to-read

introductory text for students new to the field of digital electronics. Providing entry-level
knowledge and skills for a wide range of occupations is the goal of this textbook and its
ancillary materials. Prerequisites are general math and introductory electricity/electronics.
Binary math, Boolean concepts, simple programming, and various codes are introduced and
explained as needed. Concepts are connected to practical applications, and a systems
approach is followed that reflects current practice in industry. Earlier editions of the text have
been used successfully in a wide range of programs: electronic technology, electrical trades
and apprenticeship training, computer repair, communications electronics, and computer
science, to name a few. This concise and practical text can be used in any program needing a
quick and readable overview of digital principles.
New to This Edition

Over 100 Multisim simulation files have been developed to bring the examples within these
chapters to life. These simulation files can be run within Multisim, to provide students with a
firsthand experience with the examples presented in the textbook. Multisim simulation files
have also been developed for the laboratory experiments to provide an improved learning
experience for the student.
The experiments in the Experiments Manual are designed to provide a hands-on learning
experience, to reinforce the topics covered in this textbook. The titles of the individual
experiments associated with each chapter are listed in a new section, Correlational
Experiments, following the summary at the end of each chapter in this textbook. This listing
will help the reader identify the experiments in the Experiments Manual associated with the
topics covered in each chapter.
Chapter 1
• Expanded the formulas and examples.
• Revised the section on the oscilloscope.
Chapter 2
• Revised and expanded the section on binary to decimal conversion.
• Expanded the Bit, Bytes, Nibbles, and Words section.
Chapter 3
• Revised and expanded the section on the universal NAND gate.
• Added a new section on the use of a NOR gate as a universal gate.
• Revised the coverage of DeMorgan’s theorem.
• Revised the Summary section.
Chapter 4
• Added a new section on Boolean algebra.
• Expanded the coverage of Karnaugh maps.
• Revised the Summary section.
Chapter 5
• Expanded the section on digital IC specifications.
• Added new examples for the calculation of fan-out and power dissipation.
Chapter 6
• Revised the coverage of the ASCII codes.
Chapter 8
• Revised and expanded the section on ripple counters.
Chapter 11
• Revised the coverage of optical storage devices.
Chapter 12
• Introduced a real-time clock IC in the LSI digital clock section.
• Expanded the coverage of distance measurement using ultrasound.
Chapter 13
• Expanded the section on the microcomputer.
Chapter 14
• Revised the coverage of operational amplifiers in D/A conversion.
page 321
Additional Resources
An Experiments Manual for Digital Electronics contains a comprehensive test, a variety of
hands-on lab exercises and experiments, and additional problems for each chapter in the
textbook.
McGraw-Hill Connect includes comprehensive Multisim files, keyed to circuits found in
the ninth edition, and a Multisim primer, which provides a tutorial on the software for new
users.
Instructors can access instructor resources on McGraw-Hill Connect to find a wide
selection of information including:
• An Instructor’s Manual that includes a list of the parts and equipment needed to
perform lab experiments, learning outcomes for each chapter, answers to chapter
review questions and problems, and more.
• PowerPoint presentations that provide comprehensive coverage of the topics in each
chapter. A set of questions at the end of each chapter’s slide deck provides a review of
the topics covered.
• An image library that contains all of the figures presented in this textbook.
• A test bank with questions for each chapter.
Remote Proctoring & Browser-Locking Capabilities
New remote proctoring and browser-locking capabilities, hosted by Proctorio within

Connect, provide control of the assessment environment by enabling security options and
verifying the identity of the student.
Seamlessly integrated within Connect, these services allow instructors to control students’
assessment experience by restricting browser activity, recording students’ activity, and
verifying students are doing their own work.
Instant and detailed reporting gives instructors an at-a-glance view of potential academic
integrity concerns, thereby avoiding personal bias and supporting evidence-based claims.
page x
Acknowledgments
Roger Tokheim thanks family members Marshall, Rachael, Dan, Jack, Ben, and Carrie for
their help on this project.
Patrick Hoppe would like to thank his wife Rose and the team at McGraw-Hill for their
invaluable help on this project: Theresa Collins, Product Development Coordinator; Beth
Baugh, Product Developer; Carey Lange, Copy Editor; Sandy Wille and Jane Mohr, Content
Project Managers; David Hash, Designer; and Lorraine Buczek, Content Licensing
Specialist.
page xi
page xii
Walkthrough
Digital Electronics: Principles and Applications, ninth edition, is designed for a first course
in digital electronics. It provides a concise, modern, and practical approach that’s suitable for
a range of electricity and electronics programs. With its easy-to-read style, numerous full-
color illustrations, and accessible math level, the text is ideal for readers who need to learn
the essentials of digital electronics and apply them to on-the-job situations.
page xiii
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the structural, condition of the optic nerve. That such an influence
may be exerted is shown by cases of transverse myelitis low down in
the cord, which, according to Erb and Seguin, were complicated by
double optic-nerve atrophy. The second theory is that the involved
part of the cord and the optic nerve present a similar vulnerability to
the same morbid influences. This is illustrated in some cases of
chronic alcoholic and nicotine poisoning, in ergotism, and in the
spinal affections due to hereditary influences and developmental
defects.
To discuss the nature of the disturbing influence which is responsible

for the most characteristic evidence of the disease, the ataxia, would
be equivalent to reviewing almost every mooted question in spinal
physiology. It is to be borne in mind that ataxia is a collective term
designating any inco-ordination of movement which is independent
of motor paralysis. It may be due to abolition or impairment of tactile
perception; it may be due to loss of the muscular sense; it may be
due to hampered motor co-ordination; and, finally, it may be due to a
disturbance of the space-sense. In my opinion it is only in
exceptional cases that any one of these factors can be positively
excluded. Occasionally, one has been noted when the ataxia was
grave but the tactile sense was unimpaired, or where the muscular
sense was perfect but ataxia was well developed. The difficulty with
most such records is that no discrimination is made as to the kind of
ataxia present. That loss of skill which the patient shows when he
shuts his eyes and attempts to perform certain movements without
their aid is undoubtedly due to diminished sensation, either tactile or
muscular, and usually both. The inability to stand with the eyes
closed is probably a cerebellar phenomenon, and in this respect we
are on the way to return to Duchenne's opinion. It is true that the
cerebellar organ is healthy in most tabic subjects, but its centripetal
informer, the direct cerebellar tract, is either itself involved or affected
in its origin in the columns of Clarke. But, besides the static ataxia
and that motor ataxia which can be neutralized by the use of the eye,
there is another disturbance, which, as Erb and his followers hold,
cannot be accounted for on the strength of any sensory disturbance.
It consists in an interference with the proper succession and rhythm
of movement. It seems as if that automatic mechanism by which the
individual or grouped muscular contractions engaged in locomotion
follow each other with the smoothness of the action of perfectly-
fitting cog-wheels were disturbed; the correct after-movement is
hesitated over or skipped, or even takes place at the wrong moment,
neutralizing some other step in the co-ordination required. The
tendency of physiologists and pathologists is to attribute this form of
ataxia to the disease of the intrinsic co-ordinating apparatus of the
cord itself. The experiments of Tarchanoff on a headless duck, and
the determination of the existence of cursorial co-ordinating tracts
uniting the brachial and lumbar nuclei in mammals, as well as the
observations made on automatic co-ordinate movement in
decapitated criminals, demonstrate the existence in the cord of such
an apparatus. The combination of the ganglionic centres which
underlies this co-ordination is affected by the so-called short tracts of
the cord,48 and it is precisely a portion of these which are involved in
the lesion of the column of Burdach. A number of arguments have
been advanced against regarding the lesion of this column, or
indeed any of the lesions of the posterior column, as explaining the
ataxia-producing effect of tabes. Westphal has interposed some
potent objections. He holds that lesion of these columns will be
found more frequently when examinations shall no longer be limited
to those cases where disease is suspected because ataxia was
observed during life. He found extensive disease of the posterior
columns in sufferers from paretic dementia who did not exhibit the
characteristic ataxic gait of tabes. I believe this objection can be met
by the very cases cited by Westphal in its support. Where the spinal
disorder preceded the cerebral—that is, where paretic dementia
occurred as a complication of tabes dorsalis—true locomotor and
static ataxia had been present before the insanity exploded. On the
other hand, where the spinal disease followed the cerebral, typical
ataxia did not ensue. This would seem to indicate that the
destruction of cortical control is inimical to the development of typical
tabes. Leyden has made a suggestion in the same direction when he
attributes the lesser manifestness of locomotor ataxia in tabic
females to their inferior cerebral organization.49 A more convincing
proof of the correctness of this conclusion is furnished by the fact
that if the pathological process, after destroying the posterior
columns and producing ataxia, invades the voluntary motor tract, the
ataxic symptom becomes less palpable.50 This antagonism between
lateral-column and posterior-column lesion is frequently exemplified
in the combined forms of sclerosis. It would seem, then, that where
the brain is healthy and the controlling voluntary tracts are
unimpaired, the ataxia is aggravated, supporting the beautiful theory
of Adamkiewicz, which assumes that the locomotor ataxia is due to a
disturbance of the balance normally existing between the psycho-
motor centres and those controlling the muscular tone as well as
those mediating reflex excitability.51
48 Intersegmental tracts.
49 In one out of three female eases I found the active disturbance of gait as severe as
in males, but Leyden's observation is supported by all who have seen a sufficiently
large number of female cases.
50 Not because of paresis altogether, for it diminishes materially out of proportion to

the paresis.
51 Archiv für Psychiatrie, x. p. 545. There is another observation which bears in this
direction: James of Boston observed that absolute deaf-mutes in a large percentage
of cases are insusceptible to vertigo or to the allied phenomenon of sea-sickness.
Certainly, the auditory nerve is a space-sense nerve; its physiological elimination is,
however, accompanied by an immunity against a symptom which may be an evidence
of disturbed space-sense transmission. In like manner, the destruction of the central
perceptive and voluntary centres in the paretic dement inhibits the legitimate results of
posterior spinal sclerosis.
The degeneration of the crossed-pyramid tracts in typical tabes seem to be strictly an

atrophy from disuse, perhaps facilitated by the general malnutrition of the cord. It is
limited to that part supplying the most or solely affected extremities. Thus, where the
lower extremities are alone grossly involved it is totally degenerated in the lumbar
area, and only in its outer parts in higher levels. As if to fortify this comparison by
analogous observations from every great segment of the nervous axis, a similar
inhibiting influence of pyramid lesion on co-ordinating disturbance (muscular sense) is
noted in secondary degeneration of the interolivary layer; when uncomplicated with
pyramid lesion (Meyer and my own case,) ataxia is present; when so complicated
(Schrader, Homén) it is not observed, even if determinable.
Lissauer52 has recently determined the existence of a degeneration

of certain fine nerve-fibres, apparently derived from the outermost of
the radicles into which the posterior nerve-roots divide on entry. They
are situated on that border of the apex of the posterior horn which is
in contact with the lateral column, and were found degenerated in all
cases except such as were in the initial period. No symptomatic
relation has been claimed for this lesion.
52 Neurologisches Centralblatt, 1885, No. 11.
One of the most important questions which have grown out of the
pathological studies of tabes is the relationship between the lesions
and the not infrequently observed restoration of functions which had
been more or less seriously impaired in an earlier period of the
disease. Even those symptoms which ordinarily comprise the
continuous and essential clinical background of tabes may exhibit
remarkable changes in this direction. I have two well-established
observations—one of tabes of eight years' standing, the other of
more recent date—in which that symptom which, once established,
is the most constant, the reflex iridoplegia, disappeared, to reappear
in two months in one case where it had been associated with
myosis, and to reappear in eight months in the other, repeating this
oscillation the following year. I have now under observation a tabic
patient in the sixth year of his illness who two years ago had a return
of both knee-phenomena to a nearly normal extent, to lose them in
two months, and to regain the reflex on the left side four months ago,
retaining it up to the present. These three cases were of syphilitic
subjects. In a fourth advanced non-syphilitic tabic patient, whose
ataxia had reached a maximal degree, I found a return of both knee-
phenomena for three days after its absence had been established by
medical examiners for over a year, and had probably been a feature
for a much longer period. Hammond the younger and Eulenburg
have reported similar cases. Nothing is more surprising to those
unfamiliar with the progress of this disease than to find gross ataxia
or the electrical pains and anæsthesia to disappear or nearly so; and
the alleged success of more than one remedial measure is based on
the fallacious attributing to the remedy what was really due to the
natural remittence of the disease-process or of its manifestations.
The financial success of quacks and the temporary but rapidly
evanescent popularity of static electricity, Wilsonia belts, and like
contrivances are owing to the hopefulness inspired in the credulous
patient by the mere coincidence of spontaneous improvement and
the administration of a new remedy, supplemented, it may be, by the
influence of mind on body in his sanguine condition. It is to be
assumed that the influences which are at work in provoking the
trophic and visceral episodes of tabes are of an impalpable
character, and that all theorizing regarding the reason of their
preponderance in one and their absence in another case are as
premature as would be any speculation regarding their rapid
development and subsidence in the history of one and the same
case. But we have better grounds for explaining the remissions of
the ataxia and anæsthesia.
It is only in the most advanced stages of tabes that the destruction of

the axis-cylinder becomes absolute or nearly so. Contrary to the
opinion of Leyden,53 who held that the tabic sclerosis differs from
disseminated sclerosis in the fact that the axis-cylinder does not
survive the myelin disappearance, it is now generally admitted that a
certain number of exposed or practically denuded axis-cylinders may
be preserved in the sclerotic fields.54 It is on the theory that these
delicate channels may be oppressed at one time, perhaps by
inflammatory or congestive pressure, and relieved at another by its
subsidence, that we may assume them to be the channels through
which the now limited, now liberated, functions are mediated. It is
also reasonable to suppose that vicarious action may supplement
the impaired function, and to some extent overcome the disturbing
factors. This is illustrated by the controlling influence of the visual
function—yea, even of the unconscious and ineffectual co-operation
of completely amaurotic eyes—in neutralizing both locomotor and
static ataxia. One patient who was well advanced in the initial period
of tabes, and who had been encouraged to consider the medical
opinion to that effect as the result of an exaggerated refinement of
diagnosis, made repeated tests of the Romberg symptom in his own
case, and deluded himself into the belief that the physician was
mistaken because he succeeded in practically overcoming it with an
effort that too plainly told its own story; but still he overcame it.
Certain peripheral influences have the power of stimulating the
dormant activity of potentially vicarious tracts, and perhaps also the
blunted activity of those whose function is impaired. The outside
temperature, certain barometric conditions, all may exert an
influence in this direction for good or evil.
53 Op. cit., p. 328, vol. ii.
54 Babinski (Neurologisches Centralblatt, 1885, p. 324) notes this feature, and,

consistently with the findings of most modern observers, discovers much more
resemblance to disseminated sclerosis than to the systemic sclerosis with which
Strümpell and Westphal (in part) incline to classify tabes. Similar objections to the
system-disease theory are advanced by Zacher (Archiv für Psychiatrie, xv. p. 340). I
may not pass over in silence the fact that Babinski considers his observations to
militate also against regarding any phase of the tabic sclerosis as a secondary
process. But while it may fairly be asked that a sclerosis to be regarded as systemic
must be shown to be total, this is not necessary for a secondary process, unless the
primary involvement be total also; and that is not the case in tabes.
ETIOLOGY.—Authorities are now agreed that no single cause can be

regarded as the sole responsible factor in all cases of tabes, and that
a number of etiological influences are combined in the provocation of
this disease in most instances. When the distinctiveness of the
affection was first recognized it was customary to attribute it to
sexual excesses, and the unfortunate sufferer had frequently to bear
the implied reproach of having brought his misery on himself, in
addition to the hopeless prospect which those who followed
Romberg and other authorities of the day held out to him.55
55 This opinion survives in a large portion of the German laity and in French novels.
About the time that the poet Heine was dying from an organic spinal affection two
other prominent literary characters of Paris were affected with tabes. It so happened
that all three were popularly regarded as libidinous, and one of their leading
contemporaries, whose name escapes me, took occasion to issue a manifesto
addressed to the jeunesse dorée which closed with the apostrophe, “Gardons à nos
moelles.”
Heredity plays a very slight part in the etiology of tabes. Writers of

ten and fifteen years ago attributed a greater importance to it than is
now done. But this was due to the incorporation with tabes of the so-
called family form of locomotor ataxia—a disease which is now
regarded as a distinct affection.56
56 There is but one record of direct heredity (the father and son being affected nearly
at the same time), to my knowledge. It was observed at the Berlin Hospital by Remak
(Berliner klinische Wochenschrift, 1885, No. 7). Both father and son were syphilitic.
More importance may be attached to individual predisposition, but

thus far no distinct formulation of this factor has been attempted
except by Schmeichler,57 who offers the suggestion that there are
persons with a predisposition to the development of connective-
tissue proliferation in various organs of the body, and that in them
tabes and other sclerotic affections are consequently more frequent
than in others. This suggestion appears plausible, but it is
unconfirmed by positive observations.
57 Op. cit.
Sex appears on a superficial view to be one of the most important

elements. It is generally admitted that at most one female becomes
tabic for every ten males who do so. Of 81 cases in private practice,
I observed but 3 females. Rockwell, Seguin, Birdsall, and Putnam
give similar figures. This comparative immunity is probably due to
the fact that the female is less exposed to over-exertion, to surface
chilling of the feet, to the injurious consequences of sexual excess,
and to syphilis58 than the male. As a rule, the affection in females is
more insidiously developed, progresses more slowly, is less marked
by crises and trophic disturbances, and not accompanied by as
severe pains and profound disturbance of co-ordination as is the
corresponding affection in males.
58 Whether the shorter vitality of the syphilitic female as compared with that of the
male is a factor in diminishing the accumulation of chronic tertiary sequelæ in that
sex, or whether it be the lesser vulnerability of the inferior nervous system, I am
unable to decide from the facts at my disposal. In private and clinical experience I
have been struck by the fact that women affected with syphilis in the same way and
under similar circumstances with tabic syphilitic males develop symptoms of
functional disorder of the brain and cord, such as spinal and cerebro-spinal irritation.
My cases referred to had in no instance any indication of a syphilitic condition or
history, and a distinct and different cause was found in all three.
The most important element in creating an acquired predisposition to

tabes is undoubtedly the existence of constitutional syphilis. Some
difference of opinion still exists regarding the proportion of syphilitic
tabic patients, chiefly due to the neglect of Erb—when he first
announced the prevailing view, and which is generally attributed to
him—to differentiate between cases of demonstrated constitutional
syphilis and the so-called spurious or soft chancre. But although
there occurred a reaction against his view which went to as great an
extreme in the opposite direction, the careful and critically registered
statistics accumulated in the mean time strengthen the view that
there are more syphilitic subjects among the tabic than among any
class of sufferers from other nervous affections.59 Reumont, a
physician at Aix-la-Chapelle, to which place syphilitic patients in
general resort in large numbers, found that of 3400 cases of syphilis,
290 had nervous affections, 40 being afflicted with tabes. Bernhardt60
took occasion to examine a group of hospital patients who were free
from tabes, and found that not fully 16 per cent. were syphilitic, while
of 125 tabic patients, over 46 per cent. were determined to have had
positive syphilitic manifestations. Several of those observers who
have paid attention to the question of the syphilitic origin of tabes
have admitted that the more searching their inquiry the larger the
proportion of detected syphilitic antecedent histories. Thus, Rumpf's
earlier table shows 66, and his later 80, per cent. of such
antecedents. This latter figure exactly corresponds to the percentage
of syphilis in my private cases. At a discussion held by members of
the American Neurological Association in 1884, Webber gave 54,
Putnam 49, Rockwell 40, Birdsall 43,61 and Seguin 22 per cent.62 as
the proportion in their experiences.
59 Excepting always those having the distinctive and undisputed syphilitic character.
60 Archiv für Psychiatrie, xv. p. 862.
61 Derived from over five hundred cases which had presented themselves at the clinic
of the College of Physicians and Surgeons.
62 In the Archives of Medicine he tabulates 54 (private) cases as follows:
Chancre alone 23
Chancre followed by secondary symptoms 16
Total of those with history of chancre 39
No history of chancre in 15
Total 54
Of European writers, aside from those already mentioned, Berger

claims 43 per cent., and Bernhardt, in commenting on the increasing
percentage obtained by accurate investigation, reports an additional
series of 7 new cases in private practice, all of which were syphilitic.
Fournier, Voigt, Œhnhausen, and George Fisher estimate the
syphilitic tabic patients at respectively 93, 81, and 72 per cent. of the
whole number. The almost monotonous recurrence of a clear
syphilitic history in my more recent records is such that in private
practice I have come to regard a non-syphilitic tabic patient as the
exception. Among the poorer classes the percentage of discoverable
syphilitic antecedents is undoubtedly much less. The direct exciting
causes of tabes, exposure and over-exertion, are more common with
them and more severe in their operation.
The proof of a relationship between syphilis and tabes dorsalis does

not rest on statistical evidence alone. A number of observations
show that the syphilitic virus is competent to produce individual
symptoms which demonstrate its profound influence on the very
centres and tracts which are affected in tabes. Thus, Finger63
showed that obliteration of the knee-jerk is a frequent symptom of
the secondary fever of syphilis, and that the relation is so intimate
between cause and effect that after the return of the reflex, if there
be a relapse of the fever, the obliteration of the knee-jerk is repeated.
Both the permanent loss of the knee-jerk (Remak) and the peculiar
pupillary symptoms of tabes are sometimes found in syphilitic
subjects who have no other sign of nervous disorder; and Rieger and
Foster64 regard the syphilitic ocular disturbances, even when they
exist independently, as due, like those of tabes, to the spinal, and not
to a primarily cerebral, disturbance. Another argument in favor of the
syphilitic origin of tabes is derived from the occasional remedial
influence of antisyphilitic treatment. The force of this argument is
somewhat impaired by the fact that the same measures occasionally
appear to be beneficial in tabes where syphilis can be excluded. Still,
the results of the mixed treatment in a few cases of undoubted
syphilitic origin are sometimes unmistakable and brilliant.65 As some
cases, even of long standing, yield to such measures, while others,
apparently of lesser gravity and briefer duration, fail to respond to
them, the question as to whether syphilis is a direct cause or merely
a predisposing factor may be answered in this way: That in the
former class it must have been more or less directly instrumental in
provoking the disease, while in the latter class it is to be regarded as
a remote and predisposing factor, to which other causes, not
reached by antisyphilitic treatment, became added. The claim of Erb,
that “tabes dorsalis is probably a syphilitic disease whose outbreak is
determined by certain accessory provocations,” is not subscribed to
unreservedly by a single writer of eminence.
63 “Ueber eine constante nervöse Störung bei florider Syphilis der Secundärperiode,”
Vierteljahrschrift für Dermatologie und Syphilis, viii., 1882.
64 “Auge und Rückenmark,” Graefe's Archiv für Ophthalmologie, Bd. xxvii. iii.
65 In one case already referred to a return of both knee-phenomena and complete

disappearance of locomotor and static ataxia were effected after a duration of four
years. The treatment was neglected and the knee-jerks disappeared, and one has
now returned under the resumed treatment, but accompanied by lightning-like pains.
At a meeting of the Société médicale des Hôpitaux, held November 10, 1882,
Desplats reported a case in which even better results were obtained. Reumont
(Syphilis und Tabes nach eigenen Erfahrungen, Aachen, 1881) reports 2 out of 36
carefully observed syphilitic cases cured, and 13 as improved under antisyphilitic
treatment.
The question has been raised whether the influence of syphilis is

sufficiently great to justify a clinical demarcation between syphilitic
and non-syphilitic cases. A number of observers, including Reumont,
Leonard Weber, and Fournier, incline to the belief that there are
more atypical forms of tabes in the syphilitic group. Others, including
Rumpf, Krause, and Berger, are unable to confirm this, but the
former admits, what seems to be a general impression among
neurologists, that an early preponderance of ptosis, diplopia, and
pupillary symptoms is more common with syphilitic than with non-
syphilitic tabes. Fournier66 believes that syphilitic patients show more
mental involvement in the pre-ataxic period; but it is evident that he
has based this belief on a study of impure forms. The advent of
tabes in syphilitic cases does not in this respect differ from the rule.
The most protracted and severe diplopia I have yet encountered in a
tabic patient is one, now under observation, in the initial period of the
disease, syphilis being positively excluded as an etiological factor.
66 L'Éncephale, 1884, No. 6.
It seems to be a prevalent opinion that the cases of syphilis in which

tabes is developed include a large proportion of instances in which
the secondary manifestations were slight and unlike that florid
syphilis with well-marked cutaneous and visceral lesions which is
more apt to be followed by transitory or severe vascular affections of
the cord and brain.
Excesses in alcohol, tobacco, and abuse of the sexual function are

among the factors which frequently aggravate the tendency to tabes,
and one or more of them will usually be found associated with the
constitutional factor in syphilitic tabes. Both alcohol and nicotine
have a deleterious effect on nervous nutrition and on the spinal
functions, as is illustrated in the effect of the former in producing
general neuritis, and of both in provoking optic-nerve atrophy and
general paralysis of the insane, not to speak of the pupillary states
which often follow their abuse, and the undeniable existence of a
true alcoholic ataxia. Sexual excesses were, as stated, at one time
regarded as the chief cause: the reaction that set in against this
belief went to the extreme of questioning its influence altogether. It is
to-day regarded as an important aggravating cause in a large
number of cases, and this irrespective of whether it be the result of a
satyriacal irritation of the initial period or a precedent factor. In a
large number of my patients (18 out of 23 in whom this subject was
inquired into) the habit of withdrawing had been indulged in,67 and,
as the patients admitted, with distinct deleterious effects, such as
fulness and throbbing in the lumbo-sacral region, tremor and rigidity,
with tingling or numbness, in the limbs, blurred vision, and
sometimes severe occipital headache; in one case lightning-like
pains in the region of the anus ensued.68
67 Coitus reservatus, the real crime of the Onan of Scripture.
68 Leyden states that coitus in the upright position has been accused of producing
tabes, without mentioning his authority. I have no observation on this subject touching
tabes, but am prepared to credit its bad effect from the account of a masturbator, who
during the orgasm produced while standing felt a distinct shock, like that from a
battery, shooting from the lumbar region into his lower limbs, and causing him to fall
as if knocked down. He consulted me in great alarm—was scarcely able to walk from
motor weakness, and had no knee-phenomenon; in a few weeks it returned, and no
further morbid sign appeared. Masturbators of the worst type occasionally manifest
ataxia, and in three cases I have been able to establish the return of the knee-jerk,
together with other improvements in the spinal exhaustion of these subjects. The loss
and diminution of the patellar jerk, and the frequently associated urinary incontinence,
as well as certain of the peripheral pains found in masturbators, certainly prove that
undue repetition of the sexual act (be it natural or artificial) is competent to affect the
cord in a way that cannot but be injurious in case of a predisposition to tabes, if not
without the latter.
Of single causes, none exerts so direct and indisputable an influence

on the production of tabes as the action of cold and wet upon the
lower segment of the body. It is usually the case that such exposure
is frequently repeated and combined with over-exertion before the
disease is produced, but it is occasionally possible to trace the very
first symptom of the disease directly to a single exposure. A soldier
who stands up to his knees in a rifle-pit half full of water finds his
limbs numb or tingling; develops slight motor weakness, then
lightning-like pains, and ultimately a typical tabes. In the case of a
peddler who presented an advanced form of the disease, the first
symptoms had developed after a single wetting of his feet: while
walking along one of our watering-places with his wares the swell of
a steamer inundated the beach. He had been subject to perspiring
feet before that, and the perspiration remained checked from that
time on.69 The influence of surface chilling was remarkably manifest
in all three of my female cases. In one of them it was due to frequent
wetting of the feet; in the second, a midwife, the first symptoms
began immediately after standing on a cold hearthstone while
preparing some article needed in a lying-in case. In the third case, a
lady who contracted and safely passed through a scarlatina in her
twenty-eighth year was taken out driving while desquamation was
going on. She became thoroughly chilled, experienced numbness in
the fingers and toes, and from that day on developed a slowly
progressing tabes involving all extremities alike.70
69 Checking of habitual perspiration by violent measures is mentioned by the German
textbook writers as a frequent cause, but occurs quite rarely in the modern tables.
70 In view of the absence of spinal—or, in fact, any nervous—symptoms prior to the

exposure referred to, it does not seem necessary to insist that this was not an
instance of a true post-scarlatinal tabes; and possibly the case thus designated by
Tuczek (Archiv für Psychiatrie, xiii. p. 147) may have been really due to chilling of the
delicate body-surface after desquamation or during that process. The typical form of
myelitis and sclerosis after exanthematous fevers is rather of the disseminated type.
Spinal concussion has been mentioned by a number of authorities

as a possible cause for tabes, as for other forms of sclerotic spinal
disease. In 1 of 81 cases in my own observation the development of
the disorder could be distinctly traced to a railway injury; in 2 a
sudden aggravation was as distinctly referable to a similar cause.71
To what extent railroad travelling, with its attendant continual jarring
of the body, may predispose to the development of tabes or of other
spinal diseases is as yet a matter of mere conjecture. That railroad
travelling exerts a bad influence in some cases of the established
disease is evident; but in others the patients rather like the motion,
and claim to feel benefited by it.
71 A fall from a chair, striking on the back of the latter, while endeavoring to keep a
row of books from coming down in one case, and the shock of the Ashtabula disaster
in the other. The latter patient, the same one who is referred to as describing the
electric-storm sensation in an earlier part of this article, had his foot amputated in
consequence of that disaster; but, like one of the characters in Jacob Faithful, who felt
his toes when the weather changed, though he left both legs at Aboukir, he felt the
terrific pains of the disease in the absent foot as distinctly as in the other. Dumenil and
Petit (Archives de Névrologie, ix. Nos. 25 and 26) relate cases in which a spinal
concussion was the only ascertainable cause.
A number of toxic agents have been charged with producing tabes:

thus, Bourdon maintains this of absinthe; Oppenheim attributes one
case to poisoning by illuminating gas, the exposure to its influence
being immediately followed by a gastric crisis, and this by a
regulation tabes.72 It is supposed that most of the poisons acting on
the cord in this or a similar way, such as arsenic, cyanogen,73
barium, and chloral,74 do not produce a spinal lesion directly, but
through the medium of a secondary cachexia. Of no agent is the
effect in producing tabes so well studied as ergot of rye. It had long
been known that ergot-poisoning provoked certain co-ordinating,
motor, and sensory disturbances, but it was left for Tuczek75 to show
that this vegetable parasite produces a lesion of the spinal cord
which in its character and distribution apes typical posterior sclerosis
so closely as to justify the designation of a tabes ergotica. Possibly,
pellagra, which is sometimes manifested in a similar way,76 may yet
be shown to have a like influence.
73 Bunge, Archiv für experimentelle Pathologie, xii.

74 Transactions of the Clinical Society of London, xiii. p. 117, 1880.
75 Archiv für Psychiatrie, xiii. p. 148.
76 Bouchard, “Étude d'Anatomie pathologique sur un Cas de Péllagrie,” Gaz. méd. de

Paris, 1864, No. 39.
Among the occasional and exceptional causes of tabes, Leyden and

Jolly mention the puerperal state; Bouchut, diphtheria; and several
instances are recorded in which psychical shock was responsible for
the outbreak of the disease. In a small number of cases I found that
mental worry and anxiety coincided with the period of presumable
origin of the disease.
Age seems to have no special determining influence. It is true that

most sufferers from this disease are men in the prime of life or in the
period following it. But it is precisely at these periods that the
exposure to the recognized causes of tabes is greatest. It seems as
if there were very little liability to the development of tabes after the
fiftieth and before the twenty-fifth year; still, some cases of infantile
tabes have been recorded.77
77 Excluding the so-called family form of locomotor ataxia: 6 rather imperfectly
described cases are cited by Remak (loc. cit.), and 3 additional ones related by
himself. Of the latter, 2 had hereditary syphilis, and of 1 the father was both syphilitic
and tabic.
In the majority of cases tabes is due to a combination of a number of

the above-mentioned factors. The majority of tabic patients in the
middle and wealthy classes have had syphilis, and of these, in turn,
the majority have been guilty of sexual excesses or perverted sexual
acts, while excesses in tobacco and of alcohol are often superadded.
Among the poorer patients we find syphilis less frequently a factor,
but still present, according to various estimates, in from 20 to 60 per
cent. of the cases. Excesses in tobacco play a lesser, and excesses
in alcohol a larger, part in the supplemental etiology than in the other
class, while exposure to wet and cold and over-exertion are noted in
the majority; indeed, in a fair proportion they are the only assignable
causes.
DIAGNOSIS.—The recognition of advanced tabes dorsalis is one of the

easiest problems of neurological differentiation. The single symptom
which has given one of its names to the disease—locomotor ataxia
—is so manifest in the gait that even the sufferers from the affection
learn to recognize the disease in their fellow-sufferers by the peculiar
walk.78
78 At present I have six tabic patients under treatment, who are acquainted with each
other, and who have made each other's acquaintance in the singular way of
addressing one another on the strength of mutual suffering at Saratoga, at the Hot
Springs of Arkansas, and in New York City.
Although there are other chronic affections of the cord which

manifest ataxia, such as myelitis predominating in the posterior
columns, disseminated sclerosis in a similar distribution, and some
partially recovered cases of acute myelitis, the gait is not exactly like
that of tabes. The uncertainty may be as great, but the peculiarly
stamping and throwing motions are rarely present in these
affections. The clinical picture presented by the ataxic patient, aside
from his gait, is equally characteristic in advanced cases. Absence of
the knee-jerk and other deep reflexes, the bladder paralysis, sensory
disturbance, delayed pain-conduction, trophic disturbances, and
reflex iridoplegia are found in the same combination in no other
chronic disorder of the cord. It is supposable that an imperfect
transverse myelitis in the lumbar part of the cord might produce the
reflex, ataxic, sensory, sexual, and vesical symptoms of ataxia, but
the brachial symptoms found in typical tabes as well as gastric crises
would be absent. The pupillary symptoms would also fail to be
developed, in all probability. It is to be remembered that only
fascicular cord affections can produce a clinical picture exactly like
that of tabes in more than one important respect. In analyzing the
individual symptoms of the early stage the more important differential
features can be most practically surveyed.
The discovery of no single symptom of tabes dorsalis marks so
important an epoch in its study as Westphal's observation that the
knee-phenomenon is usually destroyed in it. Had this symptom not
been detected, so Tuczek admits, ergotin tabes would have eluded
recognition.79 It was claimed by a majority of neurologists at first that
this jerk is always abolished in tabes, but it is now recognized that
there are exceptions, as is shown by cases of Hirt,80 Westphal, and
others, not to mention some well-established cases of its return
during the progress of the disease.
79 It is not to be wondered that, like most new discoveries, that of the pathological
changes of the patellar reflex should have been made the basis of premature
generalizations. The attempt of Shaw (Archives of Medicine) to establish a relation
between disturbances of the speech-faculty and an increased knee-jerk has not met
with any encouragement or confirmation, and has been rebutted by Bettencourt,
Rodrigues (L'Éncephale, 1885, 2), and others.
80 Berliner klinische Wochenschrift, 1886, 10.
The knee-phenomenon is supposed to be a constant attribute of

physiological man. It is difficult to elicit it in children, and frequently
impossible to obtain it in young infants. It also disappears in old age,
without having any special signification, except that this occurrence
seems to be in direct relation to senile involution. In 2403 boys
between the ages of six and thirteen years, Pelizæus81 found it
absent in one only. It is customarily elicited by having the patient
while sitting in a chair throw one leg over the other; hereupon the
ligamentum patellæ is struck a short, quick blow. Under physiological
circumstances the leg is jerked outward involuntarily after an interval
of about one-fifth of a second—one that is scarcely appreciated by
the eye. But if it be found absent by this mode of examination, the
case is not to be regarded as one of absence of the jerk without
further ado. The patient is made to sit on a table, his legs dangling
down and his body leaning back, while he clenches his fists. By this
means the jerk will often be produced where it appears to be
impossible to evolve it by the ordinary means. It is also well to try
different parts of the ligament, and when comparing both sides to
strike on the corresponding spot and in the same direction. Many
subjects who appear to be irresponsive will respond very well when
a point on the outer edge near the tibial insertion is percussed. The
elbow reflex, which has the same signification for the upper extremity
that the knee-jerk has for the lower, is elicited in the same manner.
The absence of the knee-jerk is usually regarded as a suspicious

circumstance in persons of middle life; and where it can be
demonstrated that it has been present years previously and
subsequently disappeared, it is looked upon as of grave import. I,
however, published three years ago an authentic case of
disappearance of the knee-jerk in a physician now in active practice
in New York City who to this day enjoys excellent health and has
developed no other sign of spinal disease. The knee-jerk is also
abolished in a number of conditions not belonging to the domain of
strictly spinal diseases, such as diphtheria, diabetes, secondary
syphilis, and severe cases of intermittent fever. Of these, diabetes
alone can be possibly confounded with tabes dorsalis. The difficulty
of differentiating early tabes and diabetes is enhanced by the fact
that on the one hand there are often ataxic symptoms with diabetes,
while on the other both glycosuria and diabetes insipidus may
complicate tabes. Senator, Frerichs, Rosenstein, Leval-Piquechef,
Charcot, Raymond, Demange, Féré, Bernard, and T. A. McBride all
recognize the occasional presence of the ataxic gait, paræsthesia,
belt sensation, and even fulgurating pains, besides the abolition of
the jerk, in diabetes mellitus.82 In pure cases of diabetes, however, I
am not aware that spinal myosis or the reflex paralytic pupil has
been found.
82 I have now under observation a case of myelitis with predominating sclerosis of the
posterior columns of five years' standing in a merchant who has been under
antidiabetic treatment for eleven years.
Abolition of the knee-jerk is found in all organic diseases of the

spinal cord which destroy any part of the neural arch at the upper
lumbar level, where the translation of the reflex occurs, whether it be
in the posterior root-zones or in the gray matter of the origin of the
crural nerves. Thus, acute or chronic myelitis, disseminated sclerotic
foci of this level, may cause obliteration of the reflex at any time of
the disease; so may acute or chronic anterior poliomyelitis,
neoplasms, and amyotrophic lateral sclerosis of the anterior cornua
type if the destruction of the anterior cornua be complete enough. It
is also found abolished with all diseases of the peripheral nerves—
traumatic and neuritic—which produce absolute motor paralysis of
such nerves.
Among the sources of error possibly incurred in examining for this

important symptom the presence of rheumatism is one. There is
sometimes a tetanic rigidity of the joints which prevents the reflex
from becoming manifest. It is also sometimes found to be absent
immediately after severe epileptic attacks, according to Moeli.83
83 In three examinations after severe attacks of epilepsy I found it normal.
The condition of the pupil is perhaps a more constant sign of early

tabes than the loss of the knee-jerk; at least it has been found well
marked in cases where the jerk had not yet disappeared. It may be
regarded as a rule in neuro-pathology that wherever reflex
iridoplegia is at any time accompanied by other oculo-motor
disturbance, it is either of spinal origin or in exceptional cases due to
disease of the pons varolii. The peculiar character of the pupillary
disturbance of tabes furnishes us with a criterion for distinguishing it
from one affection which in common with it exhibits loss of the knee-
jerk—diphtheria. In diphtheria there is also a reflex disturbance of the
pupil, but it is the reverse of that of early tabes. In the latter reaction
to light is lost, but the accommodative contraction power is retained;
in diphtheria accommodative contraction power is lost, but reaction
to light is retained.
The bladder disturbance has already been described. It is found as a

marked symptom so prominently in no other systemic affection of the
cord, and in few of the non-systemic forms, of sclerosis. In none of
these is it associated with absence of the patellar jerk, reflex
iridoplegia, and fulminating pains, as in tabes, except there be also
some motor paresis. It is the combination of any two of the important
initial symptoms of tabes without paralysis or atrophy that is
regarded as indicative of the disease by most authorities. Thus the
swaying in closing the eyes, if associated with the Argyll-Robertson
pupil, is considered as sufficient to justify the diagnosis of incipient
tabes, even if the knee-jerk be present and fulminating pains and
bladder trouble absent. Undoubtedly, the tabic symptoms must begin
somewhere. But at what point it is justifiable to give a man the
alarming information that he is tabic is a question. I have a number
of neurasthenic subjects now under treatment who have had reflex
iridoplegia for years; in one the knee-jerk is slowly becoming
extinguished; in two it has been becoming more marked after
becoming less; in all the three mentioned there is slight swaying in
closing the eyes and some difficulty in expelling the last drops of
urine while micturating. I do not believe that such a condition justifies
a positive opinion, although the surmise that they are on the road to
developing tabes may turn out correct for all these and for some of
those who have merely reflex iridoplegia.
Incipient tabes cannot be readily confounded with any other chronic

disease of the spinal cord. Some of the cases produced by sudden
refrigeration resemble a beginning myelitis. But the absence of true
paralysis seems to distinguish it from the latter. In all the cases of so-
called acute locomotor ataxia of myelitic origin that I can find a
record of, paralytic symptoms were marked, if not throughout the
disease, at least in the initial period.
Other forms of sclerosis occasionally limited to the posterior columns

imitate the symptoms of tabes. It is unusual, however, for such
sclerosis to be distributed through so great an extent of the posterior
columns as to produce symptoms consistent with tabes in both the
upper and lower extremities. And even where this condition is
complied with, the typical progress so characteristic of tabes is not
adhered to. As previously stated, the progress is weakened by
variations in certain symptoms. Such variations are found in other
forms of sclerosis, but they are not as great, trophic disturbances not
so common, and visceral crises not so violent, as a rule.

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Chapter 1 Digital Electronics 1

Chapter 2 Numbers We Use in Digital Electronics 26

Chapter 3 Logic Gates 43

Chapter 4 Combining Logic Gates 96

Chapter 5 IC Specifications and Simple Interfacing 155

Chapter 6 Encoding, Decoding, and Seven-Segment Displays 212

Chapter 7 Flip-Flops 252

Chapter 8 Counters 278

Chapter 9 Shift Registers 321

Answers to Self-Tests 343

Chapter 10 Arithmetic Circuits 345

Chapter 11 Memories 377

Chapter 12 Simple Digital Systems 419

Chapter 13 Computer Systems 461

Chapter 14 Connecting with Analog Devices 515

Appendix A Solder and the Soldering Process 546

Glossary of Terms and Symbols 552

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To discuss the nature of the disturbing influence which is responsible

50 Not because of paresis altogether, for it diminishes materially out of proportion to

The degeneration of the crossed-pyramid tracts in typical tabes seem to be strictly an

Lissauer52 has recently determined the existence of a degeneration

It is only in the most advanced stages of tabes that the destruction of

54 Babinski (Neurologisches Centralblatt, 1885, p. 324) notes this feature, and,

ETIOLOGY.—Authorities are now agreed that no single cause can be

Heredity plays a very slight part in the etiology of tabes. Writers of

More importance may be attached to individual predisposition, but

Sex appears on a superficial view to be one of the most important

The most important element in creating an acquired predisposition to

60 Archiv für Psychiatrie, xv. p. 862.

62 In the Archives of Medicine he tabulates 54 (private) cases as follows:

Of European writers, aside from those already mentioned, Berger

The proof of a relationship between syphilis and tabes dorsalis does

65 In one case already referred to a return of both knee-phenomena and complete

The question has been raised whether the influence of syphilis is

It seems to be a prevalent opinion that the cases of syphilis in which

Excesses in alcohol, tobacco, and abuse of the sexual function are

Of single causes, none exerts so direct and indisputable an influence

70 In view of the absence of spinal—or, in fact, any nervous—symptoms prior to the

Spinal concussion has been mentioned by a number of authorities

A number of toxic agents have been charged with producing tabes:

73 Bunge, Archiv für experimentelle Pathologie, xii.

75 Archiv für Psychiatrie, xiii. p. 148.

76 Bouchard, “Étude d'Anatomie pathologique sur un Cas de Péllagrie,” Gaz. méd. de

Among the occasional and exceptional causes of tabes, Leyden and

Age seems to have no special determining influence. It is true that

In the majority of cases tabes is due to a combination of a number of

DIAGNOSIS.—The recognition of advanced tabes dorsalis is one of the

Although there are other chronic affections of the cord which

80 Berliner klinische Wochenschrift, 1886, 10.