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2015v1.0
The
ECGMade Practical
This page intentionally left blank
The
ECGMade Practical
SEVENTH EDITION

JOHN HAMPTON DM MA DPhil FRCP FFPM FESC

Emeritus Professor of Cardiology, University of Nottingham, UK
DAVID ADLAM BA BM BCh DPhil FRCP FESC
Associate Professor of Acute and Interventional Cardiology and Honorary
Consultant Cardiologist, University of Leicester, Leicester, UK

EDINBURGH LONDON NEW YORK OXFORD PHILADELPHIA ST LOUIS SYDNEY 2019

© 2019 Elsevier Ltd. All rights reserved.

First edition 1986

Second edition 1992
Third edition 1997
Fourth edition 2003
Fifth edition 2008
Sixth edition 2013
Seventh edition 2019

The right of John Hampton and David Adlam to be identified as author(s) of this work has been asserted by them in
accordance with the Copyright, Designs and Patents Act 1988.

No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical,
including photocopying, recording, or any information storage and retrieval system, without permission in writing from
the Publisher. Details on how to seek permission, further information about the Publisher’s permissions policies and our
arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at
our website: www.elsevier.com/permissions.

This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may
be noted herein).

Notices
Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any
information, methods, compounds or experiments described herein. Because of rapid advances in the medical sciences,
in particular, independent verification of diagnoses and drug dosages should be made. To the fullest extent of the law, no
responsibility is assumed by Elsevier, authors, editors or contributors for any injury and/or damage to persons or property as
a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or
ideas contained in the material herein.

ISBN 978-0-7020-7460-8
978-0-7020-7461-5

Printed in China

Last digit is the print number: 9 8 7 6 5 4 3 2 1

The
Content Strategist: Laurence Hunter publisher’s
policy is to use
Content Development Specialist: Fiona Conn
paper manufactured
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Design: Brian Salisbury
Illustration Manager: Karen Giacomucci
Illustrator: Helius and Gecko Ltd
Contents
Preface vii
12-lead ECGs ix

1. The ECG in healthy people 1

2. The ECG in patients with palpitations and syncope:
initial assessment 57
3. The ECG in patients with palpitations and syncope:
ambulatory ECG monitoring 85
4. The ECG when the patient has a tachycardia 93
5. The ECG when the patient has a bradycardia 147
6. The ECG in patients with chest pain 195
7. The ECG in patients with breathlessness 255
8. The effects of other conditions on the ECG 283
9. Conclusions: four steps to making the most of the
ECG 313

Index 317

v
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Preface
What to expect of this book understand them so there is a series of changes in the
text compared with previous editions: for example,
This book is the seventh edition of The ECG in Practice,
there is more focus on ambulatory monitoring and
but we have changed the title to The ECG Made Practical
newer monitoring devices and developments in pacing
to emphasize its relationship to The ECG Made Easy
systems and defibrillators are described. We have made
We assume that the reader of this book will have the
a clearer link between the ECGs of myocardial infarc-
level of knowledge of the ECG that is contained in The
tion, coronary anatomy and the site of myocardial
ECG Made Easy. The ECG is indeed easy in principle, but
injury. To make room for these changes, and to give
the variations in pattern seen both in normal people and
more space to ECG interpretation, there is now less
in patients with cardiac and other problems can make the
focus on patient management.
ECG seem more complex than it really is. This book con-
The new edition of the third title in the series is being
centrates on these variations, and contains several exam-
published simultaneously and again we have changed the
ples of each abnormality. It is intended for anyone who
title, from 150 ECG Problems to 150 ECG Cases to empha-
understands the basics, but now wants to use the ECG to
size the central place of the patient rather than the ECG.
its maximum potential as a clinical tool.
This new edition is divided into two sections, one con-
The ECG is not an end in itself, but is an extension of
taining numerous examples of ‘everyday’ ECGs which are
the history and physical examination. Patients do not visit
suitable for those who have mastered The ECG Made Easy,
the doctor wanting an ECG, but come either for a health
and the other including more esoteric and difficult ECGs
check or because they have symptoms. Therefore this
which provides more examples than can be included the
book is organized according to clinical situations, and the
this new edition of The ECG Made Practical. Those who
chapters cover the ECG in healthy subjects and in patients
want to practice their skills after reading The ECG Made
with palpitations, syncope, chest pain, breathlessness or
Practical will find their challenge in the fifth edition of 150
non-cardiac conditions. To emphasize that the ECG is
ECG Cases.
part of the general assessment of a patient, each chapter
begins with a brief section on history and examination.
This seventh edition continues the philosophy of What to expect of the ECG
its predecessors in that the patient is considered more The ECG has its limitations. Remember that it provides a
important than the ECG. However, the ECG is a vital picture of the electrical activity of the heart, but gives only
part of diagnosis and, increasingly, influences treat- an indirect indication of the heart’s structure and func-
ment. Electrical devices of various sorts are standard tion. It is, however, invaluable for assessing patients whose
treatment in cardiology, and patients with such devices symptoms may be due to electrical malfunction in the
commonly present with non-cardiological problems. heart, especially patients with conduction problems and
Those who are not specialists in cardiology need to those with arrhythmias.

vii
Preface
In healthy people, finding an apparently normal
ECG may be reassuring. Unfortunately, the ECG can be
totally normal in patients with severe coronary disease.
Conversely, the range of normality is such that a healthy
subject may quite wrongly be labelled as having heart
disease on the basis of the ECG. Some ECG patterns
that are undoubtedly abnormal (e.g. right bundle branch
block) are seen in perfectly healthy people. It is a good
working principle that it is the individual’s clinical state
that matters, not the ECG.
When a patient complains of palpitations or syncope,
the diagnosis of a cardiac cause is only certain if an ECG
is recorded at the time of symptoms – but even when
the patient is symptom-free, the ECG may provide a
clue for the prepared mind. In patients with chest pain
the ECG may indicate the diagnosis, and treatment can
be based upon it, but it is essential to remember that
the ECG may remain normal for a few hours after the
onset of a myocardial infarction. In breathless patients a
totally normal ECG probably rules out heart failure, but
viii
it is not a good way of diagnosing lung disease or pul-
monary embolism. Finally it must be remembered that
the ECG can be quite abnormal in a patient with a variety
of non-cardiac conditions, and one must not jump to
the conclusion that an abnormal ECG indicates cardiac
pathology.
Acknowledgements
In this seventh edition of The ECG Made Practical we have
been helped by many people. In particular, we are grate-
ful to our development editor, Fiona Conn, for her enor-
mous attention to detail that led to many improvements
in the text. We are also grateful to Laurence Hunter and
his team at Elsevier for their encouragement and patience.
As before, we are grateful to many friends and colleagues
who have helped us to find the wide range of examples
of normal and abnormal ECGs that form the backbone of
the book.
JH, DA
12-lead ECGs
AAI pacing Fig. 5.31
Accelerated idionodal rhythm Fig. 1.47
Accelerated idioventricular rhythm Fig. 1.28
Anorexia nervosa Fig. 8.24
Aortic stenosis, severe, left ventricular hypertrophy
with Fig. 7.8
Aortic stenosis and left bundle branch block
Fig. 7.6
Atrial fibrillation Fig. 4.21, Fig. 4.22, Fig. 5.10
Atrial fibrillation, uncontrolled Fig. 7.1
Atrial fibrillation and anterior ischaemia Fig. 6.26
Atrial fibrillation and coupled ventricular
extrasystoles Fig. 7.2
Atrial fibrillation and inferior infarction Fig. 4.37
Atrial fibrillation and left bundle branch block
Fig. 4.26, Fig. 4.27
Atrial fibrillation and right bundle branch block
Fig. 4.32
Atrial fibrillation and Wolff–Parkinson–White
syndrome Fig. 4.45
Atrial flutter and 1 : 1 conduction Fig. 4.20
Atrial flutter and 2 : 1 block Fig. 4.17
Atrial flutter and 4 : 1 block Fig. 4.19
Atrial flutter and intermittent VVI pacing Fig. 5.27
Atrial flutter and variable block Fig. 5.9
Atrial flutter in hypothermia Fig. 8.2
Atrial septal defect and right bundle branch
block Fig. 8.9
Atrial tachycardia Fig. 4.16
Atrioventricular nodal re-entry tachycardia (AVNRT)
and anterior ischaemia Fig. 4.14, Fig. 6.27
Bifascicular block Fig. 2.22
Biventricular pacing Fig. 7.22
Broad complex tachycardia of uncertain origin
Fig. 4.34, Fig. 4.35
Brugada syndrome Fig. 2.14, Fig. 2.15
Chronic lung disease Fig. 7.19
Complete heart block Fig. 5.13
Complete heart block and Stokes–Adams attack
Fig. 5.15
Congenital long QT syndrome Fig. 2.12
DDD pacing, atrial tracking Fig. 5.34
DDD pacing, atrial and ventricular pacing Fig. 5.33
DDD pacing, intermittent Fig. 5.35
Dextrocardia Fig. 1.11
Dextrocardia, leads reversed Fig. 1.12
Digoxin effect Fig. 8.17
Digoxin effect and ischaemia Fig. 6.41
Digoxin toxicity Fig. 8.18
Ebstein’s anomaly, right atrial hypertrophy and right
bundle branch block Fig. 8.8
Ectopic atrial rhythm Fig. 1.8
ix
12-lead ECGs
Electrical alternans Fig. 8.12
Exercise-induced ischaemia Fig. 6.44
Exercise-induced ST segment depression Fig. 6.46
Exercise testing, normal ECG Fig. 6.43, Fig. 6.45
Fallot’s tetralogy, right ventricular hypertrophy
in Fig. 8.7
Fascicular tachycardia Fig. 4.33
First degree block and left bundle branch block
Fig. 2.20
First degree block and right bundle branch
block Fig. 2.21, Fig. 5.7, Fig. 5.14
Friedreich’s ataxia Fig. 8.26
His pacing Fig. 5.31
Hyperkalaemia Fig. 8.13
Hyperkalaemia, corrected Fig. 8.14
Hypertrophic cardiomyopathy Fig. 2.6, Fig. 7.11
Hypokalaemia Fig. 8.16
Hypothermia Fig. 8.3
Hypothermia, atrial flutter Fig. 8.2
Hypothermia, re-warming after Fig. 8.4
Intermittent VVl pacing Fig. 5.26
Ischaemia, anterior Fig. 6.24
Ischaemia, anterior and atrial fibrillation Fig. 6.26
Ischaemia, anterior and AV nodal re-entry
tachycardia Fig. 6.27
Ischaemia, anterior and inferior infarction and right
bundle branch block Fig. 6.21
Ischaemia, anterior and possible old inferior
infarction Fig. 6.23
Ischaemia, anterior and right bundle branch
block Fig. 6.20
Ischaemia, anterolateral Fig. 6.25
x
Ischaemia, digoxin effect and Fig. 6.41
Ischaemia, exercise-induced Fig. 6.44
Ischaemia, ?left ventricular hypertrophy
Fig. 7.10
Ischaemia, probable Fig. 7.9
Junctional tachycardia with right bundle branch
block Fig. 4.33
Left anterior hemiblock Fig. 7.12
Left atrial hypertrophy Fig. 2.7
Left atrial hypertrophy and left ventricular
hypertrophy Fig. 7.3
Left bundle branch block Fig. 2.3, Fig. 6.17
Left bundle branch block and aortic stenosis
Fig. 7.6
Left ventricular hypertrophy Fig. 2.2, Fig. 6.34,
Fig. 6.39, Fig. 7.5, Fig. 7.7, Fig. 8.6
Left ventricular hypertrophy and ?ischaemia
Fig. 7.10
Left ventricular hypertrophy and left atrial
hypertrophy Fig. 7.3
Left ventricular hypertrophy and severe aortic
stenosis Fig. 7.8
Limb lead switch Fig. 1.3
Lithium treatment Fig. 8.22
Long QT syndrome, congenital Fig. 2.12
Long QT syndrome, drug toxicity Fig. 4.43
Malignant pericardial effusion Fig. 8.11
Mediastinal shift Fig. 1.22
Mitral stenosis and pulmonary hypertension
Fig. 7.4
Myocardial infarction, acute anterior and old
inferior Fig. 6.16

Myocardial infarction, acute anterolateral, with left
axis deviation Fig. 6.8
Myocardial infarction, acute inferior Fig. 6.2
Myocardial infarction, acute inferior and anterior
ischaemia Fig. 6.13
Myocardial infarction, acute inferior infarction
(STEMI) and anterior NSTEMI Fig. 6.15
Myocardial infarction, acute inferior and old
anterior Fig. 6.14
Myocardial infarction, acute inferior and right bundle
branch block Fig. 6.18
Myocardial infarction, acute lateral Fig. 6.6
Myocardial infarction, anterior Fig. 6.5
Myocardial infarction, anterior NSTEMI Fig. 6.22
Myocardial infarction, anterolateral, ?age Fig. 6.9
Myocardial infarction, evolving inferior Fig. 6.3,
Fig. 6.4
Myocardial infarction, inferior and atrial
fibrillation Fig. 4.37
Myocardial infarction, inferior and right bundle
branch block Fig. 6.18
Myocardial infarction, inferior and right bundle
branch block and ?anterior ischaemia Fig. 6.21
Myocardial infarction, inferior and right ventricular
infarction Fig. 6.12
Myocardial infarction, inferior and ventricular
tachycardia Fig. 4.38
Myocardial infarction, lateral (after 3 days) Fig. 6.7
Myocardial infarction, old anterior Fig. 6.10
Myocardial infarction, old anterolateral NSTE-
ACS Fig. 6.40
Myocardial infarction, old inferior (possible) and
anterior ischaemia Fig. 6.23
Myocardial infarction, old posterior Fig. 6.35
Myocardial infarction, posterior Fig. 6.11
12-lead ECGs
Normal ECG Fig. 1.10, Fig. 1.13, Fig. 6.43, Fig. 6.45
Normal ECG, accelerated idionodal rhythm Fig. 1.47
Normal ECG, people of African origin Fig. 1.41,
Fig. 1.42
Normal ECG, child Fig. 1.50
Normal ECG, ectopic atrial rhythm Fig. 1.8
Normal ECG, exercise testing Fig. 6.44, Fig. 6.46
Normal ECG, high take-off ST segment Fig. 1.32
Normal ECG, junctional escape beat Fig. 1.6
Normal ECG, left axis deviation Fig. 1.49
Normal ECG, ‘leftward’ limit of normality Fig. 1.17
Normal ECG, notched S wave (V2) Fig. 1.27
Normal ECG, P wave inversion Fig. 1.8, Fig. 1.35
Normal ECG, P wave inversion (lead VR, VL) Fig. 1.35
Normal ECG, partial right bundle branch block
pattern Fig. 1.34
Normal ECG, pre-exercise Fig. 6.47
Normal ECG, R wave dominance (lead II) Fig. 1.14
Normal ECG, R wave dominance (V1) Fig. 1.23,
Fig. 7.17
Normal ECG, R wave dominance (V3) Fig. 1.21
Normal ECG, R wave dominance (V4) Fig. 1.19
Normal ECG, R wave dominance (V5) Fig. 1.20,
Fig. 1.25
Normal ECG, R wave size Fig. 1.14, Fig. 1.15
Normal ECG, right axis deviation Fig. 1.16
Normal ECG, ‘rightward’ limit of normality
Fig. 1.15
Normal ECG, R–R interval variation Fig. 1.4
Normal ECG, RSR1 pattern Fig. 1.26
Normal ECG, RSR1S1 pattern Fig. 1.27
Normal ECG, S wave dominance (V3) Fig. 1.19
Normal ECG, S wave dominance (V4) Fig. 1.20
Normal ECG, septal Q wave Fig. 1.29, Fig. 1.49
Normal ECG, small Q wave Fig. 1.30, Fig. 1.37
xi
12-lead ECGs
Normal ECG, ST segment, isoelectric and sloping
upward Fig. 1.31
Normal ECG, ST segment depression Fig. 1.34
Normal ECG, ST segment depression
(nonspecific) Fig. 1.35
Normal ECG, ST segment elevation Fig. 1.33
Normal ECG, T wave, peaked Fig. 8.15
Normal ECG, T wave, tall peaked Fig. 1.44
Normal ECG, T wave flattening Fig. 1.43
Normal ECG, T wave inversion (lead III) Fig. 1.37
Normal ECG, T wave inversion (lead V1) Fig. 1.37
Normal ECG, T wave inversion (lead V2) Fig. 1.40
Normal ECG, T wave inversion (lead V3) Fig. 1.41
Normal ECG, T wave inversion (lead VR) Fig. 1.36
Normal ECG, T wave inversion (lead VR, V1–V2)
Fig. 1.39
Normal ECG, T wave inversion in people of African
origin Fig. 1.41, Fig. 1.42
Normal ECG, U wave, prominent/large Fig. 1.45,
Fig. 1.46, Fig. 1.48
Pericardial effusion, malignant Fig. 8.11
Pericarditis Fig. 6.33
Pre-exercise normal ECG Fig. 6.47
Prolonged QT interval due to amiodarone Fig.
2.13, Fig. 8.20
Pulmonary embolus Fig. 6.29, Fig. 6.30, Fig. 6.31,
Fig. 6.32, Fig. 7.20
Pulmonary hypertension and mitral stenosis Fig. 7.4
Pulmonary stenosis Fig. 8.5
Re-warming after hypothermia Fig. 8.4
Right atrial hypertrophy Fig. 7.14
Right atrial hypertrophy and right bundle branch
block, in Ebstein’s anomaly Fig. 8.8
xii
Right atrial hypertrophy and right ventricular
hypertrophy Fig. 7.15
Right bundle branch block and acute inferior
infarction Fig. 6.18
Right bundle branch block and anterior
infarction Fig. 6.19
Right bundle branch block and anterior
ischaemia Fig. 6.20
Right bundle branch block and atrial septal
defect Fig. 8.9
Right bundle branch block and inferior infarction,
?anterior ischaemia Fig. 6.21
Right bundle branch block and right atrial
hypertrophy, in Ebstein’s anomaly Fig. 8.8
Right ventricular hypertrophy Fig. 2.4, Fig. 7.18
Right ventricular hypertrophy, marked Fig. 7.16
Right ventricular hypertrophy in Fallot’s
tetralogy Fig. 8.7
Right ventricular hypertrophy and right atrial
hypertrophy Fig. 7.15
Right ventricular outflow tract ventricular tachycardia
(RVOT-VT) Fig. 4.3, Fig. 4.41
RSR1 pattern Fig. 1.26, Fig. 2.14
RSR1S1 pattern Fig. 1.27
Second degree block (2 : 1) Fig. 5.12
Sick sinus syndrome Fig. 5.2
Sinus arrhythmia Fig. 1.4
Sinus bradycardia Fig. 1.6, Fig. 5.1, Fig. 5.2
Sinus rhythm, after cardioversion Fig. 4.18,
Fig. 4.36
Sinus rhythm, in Wolff–Parkinson–White syndrome
type A Fig. 4.12
Sinus rhythm and left bundle branch block Fig.
4.25

Sinus rhythm and normal conduction, post-
cardioversion Fig. 4.36
Sinus tachycardia Fig. 1.5
ST segment, nonspecific changes Fig. 6.1
ST segment depression, exercise-induced Fig.
6.46
Subarachnoid haemorrhage Fig. 8.25
Supraventricular extrasystole Fig. 1.7, Fig. 4.7
Supraventricular tachycardia Fig. 4.11
T wave, nonspecific changes Fig. 6.1
T wave, nonspecific flattening Fig. 6.42
T wave, unexplained abnormality Fig. 6.38
Thyrotoxicosis Fig. 8.10
Torsade de pointes Fig. 2.11
Trauma Fig. 8.23
Trifascicular block Fig. 2.23
Ventricular extrasystole Fig. 1.9, Fig. 4.8
Ventricular extrasystoles, coupled and atrial
fibrillation Fig. 7.2
12-lead ECGs
Ventricular fibrillation Fig. 4.50
Ventricular tachycardia Fig. 4.29, Fig. 4.30, Fig.
4.31
Ventricular tachycardia, fusion and capture
beats Fig. 4.39
Ventricular tachycardia and inferior infarction
Fig. 4.38
Ventricular tachycardia torsade de pointes Fig. 2.11
VVl pacing, bipolar Fig. 5.24
VVl pacing, intermittent Fig. 5.26
VVl pacing, unipolar Fig. 5.25
VVl pacing in complete block Fig. 5.28
Wolff–Parkinson–White syndrome and atrial
fibrillation Fig. 4.45
Wolff–Parkinson–White syndrome type A Fig. 2.8,
Fig. 2.9, Fig. 4.12, Fig. 4.44, Fig. 6.36, Fig. 7.13
Wolff–Parkinson–White syndrome type B Fig. 2.10,
Fig. 6.37
xiii
This page intentionally left blank
The ECG in healthy people

Types of ECG 1
1
The ECG is frequently used as a screening tool whether
from a truly asymptomatic, apparently ‘healthy’, subject
The ‘normal’ ECG 2
(e.g. for an employment medical) or as part of the battery
The normal cardiac rhythm 2 of initial investigations in patients presenting with new
symptoms of uncertain significance or cause. ECG find-
The heart rate 2
ings should always be interpreted in the clinical context
Extrasystoles 5 in which it was taken. Over-interpretation of normal
variations in the ECG may lead to misdiagnosis and risk
The P wave 9
initiation of unnecessary investigations and inappropri-
The PR interval 13 ate management. Understanding variations in the ECG
that we can expect to find in completely healthy people is
The QRS complex 15
therefore a key prerequisite to the accurate interpretation
The ST segment 35 of ECGs that appear ‘abnormal’.
The T wave 39
The QT interval 47
TYPES OF ECG
The ECG in athletes 49
ECG traces come in many guises including continuous
The ECG in pregnancy 52
single channel heart monitoring, 3-lead rhythm assess-
The ECG in children 52 ment, and even internal electrograms obtained from
implanted devices or during cardiac procedures. The most
What is a ‘normal ECG’? 53
‘complete’ external ECG is the traditional 12-lead trace
What to do 55 (Fig. 1.1). Accurate lead position (Fig. 1.2) is key as mis-
placed leads change the appearances of the trace and may
Further investigations 55
lead to misinterpretation. For example, limb lead switches
Treatment of asymptomatic ECG abnormalities 55 can resemble abnormalities of the cardiac axis (Fig. 1.3),

1
1 The ECG in healthy people
whilst alterations of chest lead position, for example due
to displacement in obese patients or by breast tissue, may
resemble cardiac rotation with delayed anterior R-wave
progression (see Fig. 1.20).
THE ‘NORMAL’ ECG
The normal cardiac rhythm
Sinus rhythm is the only normal sustained rhythm (see
Fig. 1.1). In young people the R–R interval is reduced (i.e.
the heart rate is increased) during inspiration, and this is
called sinus arrhythmia (Fig. 1.4). When sinus arrhythmia
is marked, it may mimic an atrial arrhythmia. However, in
sinus arrhythmia each P–QRS–T complex is normal, and
it is only the interval between them that changes.
Sinus arrhythmia becomes less marked with increas-
ing age of the subject, and is lost in conditions such as
Fig. 1.1
Normal ECG
I VR
II VL
III VF
2
diabetic autonomic neuropathy due to impairment of
vagus nerve function.
The heart rate
There is no such thing as a normal heart rate, and the
terms ‘tachycardia’ and ‘bradycardia’ should be used
with care. There is no point at which a high heart rate
in sinus rhythm has to be called ‘sinus tachycardia’ and
there is no lower limit for ‘sinus bradycardia’. Nev-
ertheless, unexpectedly fast or slow rates do need an
explanation.
Sinus tachycardia
The ECG in Fig. 1.5 was recorded from a young woman
who complained of a fast heart rate. She had no other
symptoms, but was anxious. There were no other abnor-
malities on examination, and her blood count and thyroid
function tests were normal.
V1 V4
V2 V5
V3 V6
 Fig. 1.2

R Y

VR VL

I
V1 V2 V3 V4 V5 V6

6 chest leads looking at heart from the front

B
G

III II

VF
6 limb leads looking at heart
from the sides and from below
ECG lead positions for the chest and upper limb leads. Correct positioning of the lower limb leads is also required for
a 12-lead ECG (not shown here).
1 The ECG in healthy people

Fig. 1.3
I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

II

Fig. 1.4
I VR V1 V4

II VL V2 V5

III VF V3 V6

II

4
 The ‘normal’ ECG 1

BOX 1.1 Possible Causes of Sinus Rhythm With a Fast

Limb lead switch Heart Rate
NOTE • Pain, fright, exercise
• Prominent R wave in a VR • Hypovolaemia
• Inverted limb lead complexes • Myocardial infarction
• Normal chest leads • Heart failure
• Pulmonary embolism
• Obesity
• Lack of physical fitness
• Pregnancy
• Thyrotoxicosis
• Anaemia
• CO2 retention
• Autonomic neuropathy
• Drugs:
• sympathomimetics
• salbutamol (including by inhalation)
• caffeine
• atropine

Box 1.1 shows possible causes of sinus rhythm with a

Sinus arrhythmia
fast heart rate.
NOTE
• Marked variation in R–R interval Sinus bradycardia
• Constant PR interval
The ECG in Fig. 1.6 was recorded from a young profes-
• Constant shape of P wave and QRS complex
sional footballer. His heart rate was 44 bpm, and at one
point the sinus rate became so slow that a junctional
escape beat appeared.
The possible causes of sinus rhythm with a slow heart
rate are summarized in Box 1.2.

Extrasystoles
Supraventricular extrasystoles, either atrial or junctional
(atrioventricular [AV] nodal), occur commonly in normal
people and are of no significance. Atrial extrasystoles (Fig.
1.7) have an abnormal P wave; in junctional extrasystoles
either there is no P wave or the P wave may follow the
QRS complex.

5
1 The ECG in healthy people

Fig. 1.5
I VR V1 V4

II VL V2 V5

III VF V3 V6

Fig. 1.6
I VR V1 V4

II VL V2 V5

III VF V3 V6

II

6

Sinus tachycardia
NOTE
• Normal P–QRS–T waves
• R–R interval 500 ms
• Heart rate 120 bpm
Sinus bradycardia
NOTE
• Sinus rhythm
• Rate 44 bpm
• One junctional escape beat
Junctional escape beat
The ‘normal’ ECG 1
BOX 1.2 Possible Causes of Sinus Rhythm With a
Slow Heart Rate
• Physical fitness
• Vasovagal attacks
• Sick sinus syndrome
• Acute myocardial infarction, especially inferior
• Hypothyroidism
• Hypothermia
• Obstructive jaundice
• Raised intracranial pressure
• Drugs:
• beta-blockers (including eye drops for glaucoma)
• calcium channel blockers (e.g. verapamil)
• digoxin
• ibabradine
In healthy people, normal sinus rhythm may be
replaced by what are, in effect, repeated atrial extrasysto-
les. This is sometimes called an ‘ectopic atrial rhythm’ and
it is of no particular significance (Fig. 1.8).
Ventricular extrasystoles are also commonly seen in
normal ECGs (Fig. 1.9). Ventricular extrasystoles are
almost universal, but when very frequent they indicate
populations at increased risk and may merit further inves-
tigation (see Ch. 4, p. 101).
7
1 The ECG in healthy people

Fig. 1.7
I VR V1 V4

II VL V2 V5

III VF V3 V6

II

Fig. 1.8
I VR V1 V4

II VL V2 V5

III VF V3 V6

II

8
 The ‘normal’ ECG 1

Supraventricular extrasystole
NOTE
• In supraventricular extrasystoles the QRS complex and the
T wave are the same as in the sinus beat
• The fourth beat has an abnormal P wave and therefore an
atrial origin
The P wave
In sinus rhythm, the P wave is normally upright in all leads
except VR. When the QRS complex is predominantly down-
ward in lead VL, the P wave may also be inverted (Fig. 1.10).
In patients with dextrocardia the P wave is inverted
in lead I (Fig. 1.11). In practice this is more often seen if
the limb leads have been wrongly attached (Fig. 1.3), but
dextrocardia can be recognized if leads V5 and V6, which
normally ‘look at’ the left ventricle, show a predominantly
downward QRS complex.

Early abnormal P wave

Normal variant: ectopic atrial rhythm

NOTE
• Sinus rhythm
• Inverted P wave in leads II–III, VF, V4–V6
• Constant PR interval

Inverted P waves in lead II

9
1 The ECG in healthy people

Fig. 1.9
I VR V1 V4

II VL V2 V5

III VF V3 V6

II

Fig. 1.10
I VR V1 V4

II VL V2 V5

III VF V3 V6

10
 The ‘normal’ ECG 1
If the ECG of a patient with dextrocardia is repeated
with the limb leads reversed, and the chest leads are
Ventricular extrasystole placed on the right side of the chest instead of the left, in
NOTE corresponding positions, the ECG becomes like that of a
• Sinus rhythm, with one ventricular extrasystole normal patient (Fig. 1.12).
• Extrasystole has a wide and abnormal QRS complex and A notched or bifid P wave (P mitrale) is the hallmark of
an abnormal T wave left atrial hypertrophy, and peaked P waves (P pulmonale)
indicate right atrial hypertrophy – but bifid or peaked P
waves can also be seen with normal hearts (Fig. 1.13) and
are not particularly clinically useful features.

Ventricular extrasystole

Normal ECG
NOTE
• In both leads VR and VL the P wave is inverted, and the
QRS complex is predominantly downward

Inverted P wave in lead VL

11
1 The ECG in healthy people

Fig. 1.11
I VR V1 V4

II VL V2 V5

III VF V3 V6

Fig. 1.12
I VR V1 V4

II VL V2 V5

III VF V3 V6

12
 The ‘normal’ ECG 1

The PR interval
Dextrocardia In sinus rhythm, the PR interval is constant and its
NOTE normal range is 120–200 ms (3–5 small squares of ECG
• Inverted P wave in lead I paper) (see Fig. 1.1). In atrial extrasystoles, or ectopic
• No left ventricular complexes seen in leads V5–V6
atrial rhythms, the PR interval may be short, and a PR
interval of less than 120 ms suggests pre-excitation (see
Figs 2.8, 2.9, 2.10).
A PR interval of longer than 220 ms may be due to
first degree block, but the ECGs of healthy individuals,
especially athletes, may have PR intervals of slightly longer
than 220 ms – which can be ignored in the absence of any
other indication of heart disease.

Inverted P wave and Persistent S

dominant S wave in lead I wave in lead V6

Dextrocardia, leads reversed

NOTE
• Same patient as in Fig. 1.11
• P wave in lead I upright
• QRS complex upright in lead I
• Typical left ventricular complex in lead V6

Upright P wave Normal QRS

and QRS complex complex in lead
in lead I V6

13
1 The ECG in healthy people

Fig. 1.13
I VR V1 V4

II VL V2 V5

III VF V3 V6

II

Fig. 1.14
I VR V1 V4

II VL V2 V5

III VF V3 V6

14
 The ‘normal’ ECG 1

The QRS complex

The cardiac axis
Normal ECG
NOTE There is a fairly wide range of normality in the direction of
• Sinus rhythm the cardiac axis. In most people the QRS complex is tallest
• Bifid P waves, best seen in leads V2–V4 in lead II, but in leads I and III the QRS complex is also
• Peaked T waves and U waves, best seen in leads V2–V3 – predominantly upright (i.e. the R wave is greater than the
normal variants S wave) (Fig. 1.14).

Bifid P wave in lead V3

Normal ECG
NOTE
• QRS complex upright in leads I–III
• R wave tallest in lead II

15
1 The ECG in healthy people

Fig. 1.15

I VR V1 V4

II VL V2 V5

III VF V3 V6

Fig. 1.16
I VR V1 V4

II VL V2 V5

III VF V3 V6

16
 The ‘normal’ ECG 1
The cardiac axis is still perfectly normal when the R
wave and S wave are equal in lead I: this is common in tall
Normal ECG people (Fig. 1.15).
NOTE When the S wave is greater than the R wave in lead
• This record shows the ‘rightward’ limit of normality of the I, right axis deviation is present. However, this is very
cardiac axis common in perfectly normal people. The ECG in Fig. 1.16
• R and S waves equal in lead I is from a professional footballer.
It is common for the S wave to be greater than the R
wave in lead III, and the cardiac axis can still be consid-
ered normal when the S wave equals the R wave in lead
II (Fig. 1.17). These patterns are common in obese people
and during pregnancy.
When the depth of the S wave exceeds the height of the
R wave in lead II, left axis deviation is present (see Figs
2.22 and 2.23).
Limb lead switches can sometimes be misinterpreted
as abnormalities of cardiac axis (see Fig. 1.3).

Normal ECG
NOTE
• Right axis deviation: S wave greater than R wave in lead I
• Upright QRS complexes in leads II–III

Dominant S wave
in lead I

17
1 The ECG in healthy people

Fig. 1.17
I VR V1 V4

II VL V2 V5

III VF V3 V6

Fig. 1.18
I VR V1 V4

II VL V2 V5

III VF V3 V6

18
 The ‘normal’ ECG 1

Normal ECG
NOTE
• This shows the ‘leftward limit’ of normality of the cardiac
axis
• S wave equals R wave in lead II
• S wave greater than R wave in lead III

S wave = R S wave > R

wave in lead II wave in lead III

Normal ECG The size of R and S waves in the chest leads

NOTE In lead V1 there should be a small R wave and a deep S
• Lead V1 shows a predominantly downward complex, with wave, and the balance between the two should change
the S wave greater than the R wave progressively from V1 to V6. In lead V6 there should be a
• Lead V6 shows an upright complex, with a dominant R tall R wave and no S wave (Fig. 1.18).
wave and a tiny S wave Typically the ‘transition point’, when the R and S waves
are equal, is seen in lead V3 or V4 but there is quite a lot of
variation. Fig. 1.19 shows an ECG in which the transition
point is somewhere between leads V3 and V4.
Fig. 1.20 shows an ECG with a transition point between
leads V4 and V5, and Fig. 1.21 shows an ECG with a transi-
tion point between leads V2 and V3.
The transition point is typically seen in lead V5 or even
S wave > R wave in lead V1 Dominant R wave in lead V6 V6 in patients with chronic lung disease (see Ch. 7), and
this is called ‘clockwise rotation’. In extreme cases, the
chest leads need to be placed in the posterior axillary line,
or even further round to the back (leads V7–V9) before the
transition point is demonstrated. A similar ECG pattern

19
1 The ECG in healthy people

Fig. 1.19
I VR V1 V4

II VL V2 V5

III VF V3 V6

Fig. 1.20
I VR V1 V4

II VL V2 V5

III VF V3 V6

20

Normal ECG
NOTE
• In lead V3 there is a dominant S wave
• In lead V4 there is a dominant R wave
• The transition point is between leads V3 and V4
Normal ECG
NOTE
• Dominant S wave in lead V4
• R wave just bigger than S wave in lead V5
The ‘normal’ ECG 1
may be seen in patients with an abnormal chest shape,
particularly when depression of the sternum shifts the
mediastinum to the left. The patient from whom the ECG
in Fig. 1.22 was recorded had mediastinal shift. An appar-
ent ‘clockwise rotation’ ECG pattern can sometimes arise
from lateral displacement of the ECG chest leads, particu-
larly in larger patients or by breast tissue.
Occasionally the ECG of a totally normal subject will
show a ‘dominant’ R wave (i.e. the height of the R wave
exceeds the depth of the S wave) in lead V1. There will
thus, effectively, be no transition point, and this is called
‘counterclockwise rotation’. The ECG in Fig. 1.23 was
recorded from a healthy footballer with a normal heart.
However, a dominant R wave in lead V1 is usually due to
either right ventricular hypertrophy (see Ch. 7) or a true
posterior infarction (see Ch. 6).
Excessive R wave voltages may be an indication of left
ventricular hypertrophy (see page 263). Provided that the
ECG is properly calibrated (1 mV causes 1 cm of vertical
deflection on the ECG), the limits for the sizes of the R
and S waves in normal subjects are usually said to be:
• 25 mm for the R wave in lead V5 or V6
• 25 mm for the S wave in lead V1 or V2
• Sum of R wave in lead V5 or V6 plus S wave in lead V1
or V2 should be less than 35 mm.
However, R waves taller than 25 mm are commonly seen
in leads V5–V6 in fit and thin young people, and are per-
fectly normal. Thus, once again, interpretation of these
‘limits’ depends on the clinical context. The ECGs in Figs
1.24 and 1.25 were both recorded from fit young men with
normal hearts.
21
1 The ECG in healthy people

Fig. 1.21
I VR V1 V4

II VL V2 V5

III VF V3 V6

Fig. 1.22
I VR V1 V4

II VL V2 V5

III VF V3 V6

22
 The ‘normal’ ECG 1

Normal ECG
NOTE
• Dominant S wave in lead V2
• Dominant R wave in lead V3
• The transition point is between leads V2 and V3

V7 Mediastinal shift
NOTE
• ‘Abnormal’ ECG, but a normal heart
• Shift of the mediastinum means that the transition point is
under lead V6
• Ventricular complexes are shown in leads round the left
V8 side of the chest, in positions V7–V9

V9

23
1 The ECG in healthy people

Fig. 1.23
I VR V1 V4

II VL V2 V5

III VF V3 V6

Fig. 1.24
I VR V1 V4

II VL V2 V5

III VF V3 V6

24
 The ‘normal’ ECG 1

Normal ECG
NOTE
• Dominant R waves in lead V1

Dominant R wave
in lead V1

Normal ECG
NOTE
• S wave in lead V2 is 36 mm

S wave > 25 mm in lead V2

25
1 The ECG in healthy people

Fig. 1.25
I VR V1 V4

II VL V2
V5

III VF
V3
V6

Fig. 1.26
I VR V1 V4

II VL V2 V5

III VF V3 V6

26
 The ‘normal’ ECG 1

The width of the QRS complex

Normal ECG The QRS complex should be less than 120 ms in duration
NOTE (i.e. less than 3 small squares) in all leads. If it is longer
• R wave in lead V5 is 42 mm
than this, then either the ventricles have been depolarized
from a ventricular rather than a supraventricular focus (i.e.
a ventricular rhythm is present), or there is an abnormal-
ity of conduction within the ventricles. The latter is most
commonly due to bundle branch block. An RSR1 pattern,
resembling that of right bundle branch block (RBBB) but
with a narrow QRS complex, is sometimes called ‘partial
right bundle branch block’ and is a normal variant (Fig.
1.26). An RSRV pattern is also a normal variant (Fig. 1.27)
and is sometimes called a ‘splintered’ complex.
In perfectly normal hearts the normal rhythm may be
replaced by an accelerated idioventricular rhythm, which
looks like a run of regular ventricular extrasystoles, with
wide QRS complexes (Fig. 1.28).

R wave > 25 mm in lead V5

Normal ECG
NOTE
• RSR1 pattern in lead V2
• QRS complex duration 100 ms
• Partial right bundle branch block pattern

RSR1 pattern and QRS complex 100 ms in lead V1

27
1 The ECG in healthy people

Fig. 1.27
I VR V1 V4

II VL V2 V5

III VF V3 V6

Fig. 1.28
I VR V1 V4

II VL V2 V5

III VF V3 V6

II

28
 The ‘normal’ ECG 1

Normal ECG
NOTE
• RSR1S1 pattern in lead V1
• Notched S wave in lead V2
• QRS complex duration 100 ms
• Partial right bundle branch block pattern

RSR1S1 pattern in Notched S

lead V1 wave in lead V2

Accelerated idioventricular rhythm

NOTE
• Sinus rhythm
• First and last beats are ventricular extrasystoles
• The fifth beat starts a run of ventricular rhythm at about
80 bpm

Idioventricular rhythm in lead II

29
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operator then takes hold of the patient's hand and the other
electrode is passed over the muscles of the neck, back, trunk, and
extremities.

When the patient is in bed, as in the regular rest treatment, this

method has to be modified, and then the best treatment is by direct
muscular faradization. Two sponge electrodes are employed. The
sponges are moistened, so that the current may pass through the
skin and reach the muscles. Both electrodes are taken in one hand,
the handle of one, pointing backward, being between the first and
second fingers, while the handle of the other is between the third and
fourth fingers. In this way the distance between the points of
application can be readily altered. The current is then applied to the
muscles everywhere, beginning with those of the feet. Muscles
should be relaxed before passing the current through them. The
whole body can be gone over in this way in the course of half an
hour.

The hydropathic treatment of hysteria is one that has much in it to be

commended. Jolly approves the systematic external application of
cold water; Chambers advocates the daily morning use of shower-
baths, holding that the bracing up of the mind to the shock of a cold
shower-bath is a capital exercise for the weak will-power of the
hysterical individual, and some admirable results have been reported
by Charcot in inveterate neurasthenics and hysterics.
Hydrotherapeutic treatment, continued perseveringly for a long time,
says Rosenthal, “diminishes the extreme impressionability of
hysterical patients, strengthens them, and increases their power of
resistance to irritating influences, stimulates the organic functions,
combats the anæmia, calms the abnormal irritability of the peripheral
nervous system, and by diminishing the morbid increase of reflex
power relieves the violence of the spasmodic symptoms. Even
chronic forms which are combined with severe paroxysms of
convulsions are susceptible of recovery under this plan of treatment.”

The hydrotherapeutic treatment may be contrasted with the

treatment by seclusion, rest, massage, and electricity. Undoubtedly,
one class of hysterical patients is greatly benefited by the latter
method systematically carried out; these have already been
described. In other cases, however, this method of treatment is
useless; in some of them it has a tendency to prolong or aggravate
the hysterical disorder, while in the same cases a well-managed
hydrotherapeutic treatment will answer admirably. This is applicable
in hysterical patients who eat and drink well, who, as a rule, preserve
a good appearance, but whose mind and muscles are equally flabby
and out of tone, and need to be stirred up both physically and
mentally.

Dujardin-Beaumetz recommends prolonged warm baths of from one

to two hours' duration, and believes that the therapeutic virtues of
these baths are augmented by infusions of valerian.

In order to obtain satisfactory results from hydrotherapy, as well as

from massage, electricity, etc., it is best to remove patients from their
family surroundings. Good sanitariums near our large American
cities where hydrotherapy and other special methods of treatment
can be carried out are sadly needed. Hydrotherapeutic treatment is
much more efficacious when conducted at a well-regulated
institution, for several reasons. Measures troublesome in themselves
are here carried out as a matter of daily routine. Numerous patients
permit of the employment of competent attendants. The change is
often of great benefit. The close personal supervision which
hysterical patients are likely to have in a hydrotherapeutic
establishment is also to be taken into consideration. Better modes of
living, proper forms of exercise, regulated diet, etc. also enter; but
still, a fair share of the good which results can be attributed to the
water treatment.

While, however, it is better to remove hysterical patients, for

hydrotherapeutic as well as for other treatment, from their family
surroundings, and to place them in some well-regulated
establishment, it is not by any means impossible to carry out such
treatment in private practice, particularly in a house supplied with a
bath-room. Many of our hydrotherapeutic institutions are in the
hands of charlatans or of individuals who are not practically well
fitted for their work. Not infrequently, however, good results are
obtained even under these circumstances. Much more can be done
in this direction with modest buildings and appliances than is
generally supposed. It is not necessary to have numerous
apartments: three or four rooms in a well-appointed house, if the
arrangements for carrying out the hydrotherapeutic treatment are of
a proper kind, will suffice for a large amount of good work. In almost
any house provided with bath-rooms with hot and cold water some
useful hydrotherapy may be attempted. The spinal douche or pour
can be used by placing the patient in a sitz- or ordinary hip-bath and
pouring the water from a spout or hose held at a certain height, the
distance being regulated according to the patient's condition. Again,
the patient sitting in a tub, water can be poured upon her, beginning
at first with a high temperature and gradually lowering it. The
shower-bath may also be used. An extemporaneous shower-bath
can be provided by an ordinary watering-pot. Whole, three-quarters,
or half baths at different temperatures can be given. One method of
carrying out the wet pack is very simple. A comforter is spread upon
the bed; next to this is placed a woollen blanket, and over the
blanket a wet linen sheet, upon which the patient rests, with the head
on a low pillow. The wet sheet, blanket, and comforter are then
wrapped closely about the patient, bottles of hot water being placed
at the feet. The cold drip-sheet method is another easily used. It
consists in placing about the patient, while sitting up or standing, a
sheet wet with cold water, and then vigorously rubbing her through
the sheet.

Baths to the head may be used in some cases; cool head-baths are
most frequently applied. One method of using these baths is to have
the patient lie in such a position that the head projects a little beyond
the edge of the bed and over a basin or receptacle of some kind.
Water of a suitable temperature is then poured gently or squeezed
out of a sponge over the head. For some forms of insomnia or some
of the disorders of sleep in hysteria this treatment is a valuable
auxiliary to other measures.
For the hysterical spine cold compresses may be used along the
spine. On the other hand, hot fomentations may be found of benefit
in some cases. Where hydrotherapeutic measures are employed
attention should be paid to the condition of the circulation,
particularly in the extremities. If the feet or hands are cold, hot
applications or frictions should be used.

For certain of the vaso-motor disorders of hysteria, such as cold or

hot feet, flushings, etc., local hydrotherapeusis will be of service. In
hysterical contractures local stimulation by the douche method or by
the steam bath may be tried. For the excitable rectum cold enemata
in small quantities, so as not to be expelled, will be found to be very
efficacious. For spasmodic attacks, whether purposive or involuntary,
the use of the wet pack or the plunge-bath will sometimes be found
of good service. In neuralgias and other painful local disorders of
hysteria, frictions, fomentations, Turkish or Russian baths, and the
wet pack are often very beneficial.

When hysteria is complicated, as it very often is, with disorders of

the liver and stomach, hydrotherapeutic measures will be of added
efficacy. When it is associated with genito-urinary disorders, even
though the latter are not regarded as the cause of the former, special
beneficial effects, both local and general, can be obtained from
hydrotherapeutic measures. Locally, sitz-baths, hip-baths, douche-
baths, hot and cold injections, and foot-baths may act as revulsives,
astringents, or local tonics, while at the same time they are
measures which tend to strengthen the system as a whole.

Sea-bathing is often of the greatest value, although it is sometimes

difficult to induce hysterical patients, who are willing enough to go to
the seashore, to resort to surf-bathing. Few measures are better
calculated to bring up the tone of the nervous system of an hysterical
or neurasthenic patient than well-directed sea-bathing. Where sea-
bathing cannot be employed sea-water may be used indoors. Sea-
water establishments, where baths at various temperatures may be
had, are now to be found at all the best seaside resorts. In a few
cases the internal use of large quantities of either hot or cold water,
or of the ferruginous mineral waters, may be associated with the
external treatment.

The climatic treatment of hysteria has received little or no attention;

undoubtedly, much could be said in this connection. In a great
country like ours a climate suited to the requirements of almost every
form of disease can be had. The climate of those regions, either of
the seaboard or inland, particularly well suited to cases of lung
trouble, will often be useless, and sometimes harmful, to neurotic
patients. For a certain class of hysterical patients a sojourn at the
seashore, if not too protracted, will prove of great value. On the
whole, for most hysterical patients of the neurasthenic type the best
plan is to go first to the seashore for a few weeks, and then resort to
an inland hilly or mountainous country, but not at too great an
elevation. I have known the climate of some of the high altitudes of
Colorado to be of positive injury by depressing the nervous system.
Resorts like Capon Springs in West Virginia, out of the reach of
steam and worry, with prevailing south-west winds, are desirable
places.

The treatment of hysteria by the method of metallotherapy is worthy

of some consideration. It is a method by no means new. It was
known and practised by the ancients with rings and amulets.
Popularized at the beginning of the present century by certain
travelling charlatans, it was later, for a time, wholly ignored. In recent
years it has been received with considerable attention. One Burq for
many years practised metallotherapy in Paris disregarded or scouted
by the profession, but claiming many remarkable cures. Finally,
Charcot was induced to give him an opportunity of demonstrating the
truth or falsity of his claims at Salpêtrière.124 Cases of grave hysteria
were submitted to the treatment, and in certain instances with
striking results.
124 Lancet, Jan. 19, 1878.

After having determined by a series of experiments the particular

metal to which the patient is sensitive, bits of metal may be applied
to the surface of the body in various places; this constitutes external
metallotherapy. Or the metal, in the form of powder (as reduced iron)
or an oxide or some other salt, may be administered; this is internal
metallotherapy. That certain definite effects may be produced by the
application of metals to the surface of the body is unquestionable.
Some of the results which have followed their employment are the
removal of anæsthesia and analgesia, relief of hysterical paralysis,
improvement in the circulation, removal of achromatopsia, relief of
contracture.

Many investigations in Germany, England, France, and this country

have demonstrated that the same or similar effects can be produced
by the application of other non-metallic substances, such as discs of
wood, minerals, mustard plasters, etc. Hammond, among others,
has shown this. How the results are obtained is still a matter of
dispute. On the one hand, it is claimed, principally by the French
observers, that the cures are due to the metals themselves, either by
virtue of some intrinsic power or through some electrical currents
generated by their application. On the other hand, it is asserted,
particularly by the English observers, that the phenomena are best
explained on the doctrine of the influence of the mind on the body; in
other words, by the principle of expectant attention. Some at least of
the effects are to be explained on the latter hypothesis, but it is likely
that the monotonous impressions made upon the peripheral sense-
organs by different substances applied locally may act reflexly on the
brain.

Seguin125 reports a case of convulsion and hemianæsthesia in an

adult male cured by metallotherapy; the metal used was gold. Two
ordinary twenty-dollar gold pieces were placed in the patient's
hands, and afterward on his forearm, cheek, and tongue. Nothing
else was suggested or done to him; sensibility returned, and the
staggering and other symptoms disappeared. The patient left the
hospital claiming to be perfectly well. The same author reports
several other successful cases of metallotherapy, all of them
reactions to gold. One was a girl sixteen years old with analgesia.
125 Arch. of Medicine, New York, 1882.
Not a few cases are now on record of the cure of hysterical
contracture and other forms of local hysterical disorders by the
application of a magnet. Charcot and Vigouroux cured one case of
hysterical contracture of the left arm by repeated applications of the
magnet to the right or healthy arm. Debove by prolonged application
of magnets relieved hemianæsthesia and hemiplegias—not only the
hysterical varieties, but also, it is said, when dependent upon such
conditions as alcoholism, plumbism, and even cerebral lesions.
Maggiorani of Rome studied the physiological action of the magnet
and laid down the first rules for its therapeutic use. In the case of
powerful magnets we have more room for believing that an actual,
tangible force is at work in producing the results than in the case of
simple metals.

The question has been sometimes asked whether hypnotism can be

used with success in the treatment of hysteria. Richer reports a few
cures of hysteria through this agency. Braid has put on record
between sixty and seventy cases which he claims to have cured by
the same means. This list undoubtedly includes some hysterical
cases—of paralysis, anæsthesia, aphonia, blindness and deafness,
spinal irritation, etc. Both on theoretical grounds and from
experience, however, I believe that the practice of hypnotization may
be productive of harm in some cases of hysteria, and should be
resorted to only in rare cases of mental or motor excitement.

By some, special measures during the hysterical fit are regarded as

unnecessary. Jolly, for instance, says that we must merely take care
that the patients do not sustain injury in consequence of their
convulsive movements, and that respiration is not impeded by their
clothing. Rothrock126 reports several cases of hysterical paroxysms
relieved by the application of either snow or ice to the neck. The
applications were made by stroking up and down either side of the
neck along the line of the sterno-cleido-mastoid muscles. He
believed that the most probable explanation of the results obtained
was the shock received from the cold substance, but that
supplemental to this there may have been supplied through the
pneumogastric nerve a besoin de respirer. This measure and the use
of the cold spinal douche are both to be recommended.
126 Philada. Med. Times, 1872-73, iii. 67.

Emetics are sometimes valuable. Miles127 reports several cases of

severe hysterical seizure in which tobacco was promptly efficient in
controlling the affection. He used the vinum tabaci in doses of one
drachm every half hour or hour until the system was relaxed and
nausea induced, the effects usually being produced after taking
three or four doses. Fifteen grains of sulphate of zinc may be used in
adult cases. James Allen for a case of hysterical coma successfully
used a hypodermic injection of one-tenth of a grain of apomorphia.
Recently, at the Philadelphia Hospital this remedy has been
successfully employed in two cases, one of hysterical coma and the
other of hysterical mania. Inhalations of nitrite of amyl are often of
surprising efficiency. This and other measures referred to under
HYSTERO-EPILEPSY are also applicable in the treatment of any form of
hysterical spasm.
127 Clinical Med. Reporter, 1871, iv. 25-27.

For hysterical convulsions occurring during pregnancy an enema of

asafœtida, camphor, the yolk of an egg, and water, such as has
been recommended by Braun of Vienna, will often be found promptly
efficacious.

Fagge128 mentions a procedure which he had often seen adopted by

Stocker—namely, pressure upon the arteries and other structures on
each side of the neck.
128 British Medical Journal, March 27, 1880.

For hysterical paralysis faradism and galvanism hold the chief place.
Metallic-brush electricity should be used in the treatment of
anæsthesia.
Whenever, in local hysteria, particularly of the paralytic, ataxic, or
spasmodic form, it is possible to coax or compel an organ or part to
perform its usual function long unperformed or improperly performed,
treatment should be largely directed to this end. Thus, as Mitchell
has shown, in some cases of aphonia, especially in those in which
loss of voice is due to the disassociation of the various organs
needed in phonation, by teaching the patient to speak with a very full
chest an involuntary success in driving air through the larynx may
sometimes be secured. Once compel a patient by firm but gentle
means to swallow, and œsophageal paralysis begins to vanish.

Mitchell makes some interesting remarks upon the treatment of the

peculiar disorders of sleep, which he describes and to which I have
referred. When the symptoms are directly traceable to tobacco, he
believes that strychnia and alcohol are the most available remedies,
but gives a warning against the too liberal use of the latter. A
treatment which was suggested to him by a clever woman who
suffered from these peculiar attacks consists in keeping in mind the
need of breaking the attack by motion and by an effort of the will. As
soon as the attack threatens the patient should resolutely turn over,
sit up, or jump out of bed, and move about, or in some such way
overcome the impending disorder. Drugs are of little direct use.
Small doses of chloral or morphia used until the habit is broken may
answer, but general improvement in health, proper exercise, good
food, and natural sleep are much more efficient.

Fagge says that he has seen more benefit in hysterical contracture

from straightening the affected joints under chloroform, and placing
the limb upon a splint, than from any other plan of treatment.
Hammond129 (at a meeting of the New York Neurological Society,
Nov. 6, 1876) reports a case of supposed hysterical contracture in
the form of wry neck, in which he divided one sterno-cleido-mastoid
muscle; immediately the corresponding muscle of the other side
became affected; he cut this; then contraction of other muscles took
place, which he kept on cutting. The case was given up, and got well
spontaneously about two years later. Huchard130 entirely relieved an
hysterical contracture of the forearm by the application of an elastic
bandage.
129 Philadelphia Medical Times, vol. vii., Nov. 25, 1876.

130 Revue de Thérapeutique, quoted in Med. Times, vol. xiii., June 16, 1883.

A lady with violent hysterical cough was chloroformed by Risel of

Messeberg131 for fourteen days at every access of the cough, and
another for eight days. In both the symptoms were conquered. Nitrite
of amyl is useful in similar cases.
131 Allg. Med. Centralzeitung, Oct. 9, 1878.

Graily Hewitt132 reports a case of hysterical vomiting of ten months'

duration, caused by displacement of the uterus, and cured by
reposition of that organ. The same authority, in a paper read to the
London Congress, advanced the opinion that the exciting cause of
attacks of hysteria and hystero-epilepsy was a distortion of the
uterus produced by a flexion of the organ upon itself, either forward
or backward. He believed the attacks were the result of reflex
irritation. He recited eighteen cases, all of which were relieved.
Flechsig133 favors the gynæcological treatment of hysteria, including
castration or oöphorectomy. He reports three cases with good
results. His article favors the idea that any morbid condition of the
genital organs present ought to be remedied before treating the
hysterical symptoms. Zeuner,134 on the other hand, refers to a
number of cases in which gynæcological treatment gave either
entirely negative results or was productive of positive injury to
hysterical patients. He quotes Perreti,135 physician to an asylum for
the insane, who gives the details of a number of cases in which
gynæcological examinations or treatment were directly productive of
injury. He mentions a case of a female patient who had delusions
and hallucinations of a sexual type in which the physician was the
central figure. He reports cases in which proper constitutional
treatment, without gynæcological interferences, led to a full recovery.
Playfair, also quoted by Zeuner, states that he has often known the
condition of hysterical patients to be aggravated by injudicious
gynæcological interference. Oöphorectomy will be more fully
discussed under HYSTERO-EPILEPSY.
132 Med. Press and Circ., June 2, 1880.

133 Neurol., 7 Abt., 1885, Nos. 19, 20.

134 Journ. American Med. Ass., Chicago, 1883, i. 523-525.

135 Berliner klinische Wochenschrift, No. 10.

HYSTERO-EPILEPSY.

BY CHARLES K. MILLS, M.D.

DEFINITION.—Hystero-epilepsy is a form of grave hysteria

characterized by involuntary seizures in which the phenomena of
hysteria and epilepsy are commingled, and by the presence in
unusual number and severity, between the paroxysms, of symptoms
of profound and extensive nervous disturbance, such as paralysis,
contracture, hemianæsthesia, hyperæsthesia, and peculiar psychical
disorders.
SYNONYMS.—Hystero-epilepsy has long been known under various
names, as Epileptiform hysteria, by Loyer-Villermay and Tissot; as
Hysteria with mixed attacks, by Briquet; as Hysteria major or Grave
hysteria, by Charcot. The term hystero-epilepsy has been used with
various significations, and often without due consideration, and for
these reasons some authorities advise that it should not be used at
all. Gowers,1 for instance, refers to epileptic hysteria, hysterical
epilepsy, and hystero-epilepsy as hybrid terms which tend rather to
hinder than to advance the study of the nature of these convulsive
attacks and their relations to other forms of hysteria. He holds that it
is a clear advantage to discard them as far as possible, and
suggests the use of the term hysteroid, as proposed by W. W.
Roberts, or that of co-ordinate convulsions, as describing accurately
the character of the attack. These suggested terms do not strike me
as improvements upon those which he wishes the profession to
avoid. The word hysteroid, while good enough in its way, is certainly
objectionable on the ground of indefiniteness. Co-ordinate is
proposed, because the convulsive movements are of a quasi-
purposive appearance; that is, they are so grouped as to resemble
phenomena which may be controlled by the will. This meaning of co-
ordinate, however, as applied to the disorder in question, would not
be easily grasped by the average physician. When it is impossible to
name a disease from the standpoint of its pathological anatomy, the
next best plan is to use a clinical term which in a plain common-
sense manner gives a fair idea of the main phenomena of the
affection. Hystero-epilepsy, if it means anything, means simply a
disorder in which the phenomena of both hysteria and epilepsy are
to some degree exhibited. Certainly, this is what is seen in the cases
known as hystero-epileptic. In forming the compound the hysterical
element is, very properly, expressed first, the disease being a
hysteria with epileptic or epileptoid manifestations, rather than an
epilepsy with hysterical or hysteroid manifestations. A study of the
definition of hystero-epilepsy which has been given will show that it
is intended to restrict the application of the term in the present article
to cases with involuntary or non-purposive attacks, the voluntary or
purposive having been considered in the last article.
 1 Epilepsy and other Chronic Convulsive Diseases: their Causes, Symptoms, and
Treatment, by W. R. Gowers, M.D., F. R. C. P., etc., London, 1881.

HISTORY.—The greatest impulse to the study of hystero-epilepsy in

recent years has been given by the brilliant labors of Charcot and his
pupils and assistants in his famous service at La Salpêtrière. In his
lectures on diseases of the nervous system2 (edited by Bourneville),
and in various publications in Le Progrès médical and other journals,
Charcot has reinvestigated hysteria major with great thoroughness,
and has thrown new light upon many points before in obscurity. He
deserves immense credit also for the work which he has stimulated
others to do. Bourneville, well known as the editor of some of
Charcot's most valuable works, has published, alone or with others,
several valuable monographs upon hysteria and epilepsy.3 The most
valuable work on hystero-epilepsy, however, because the most
elaborate and comprehensive, is the treatise of Richer.4 Richer was
for a time interne in the Salpêtrière Hospital, and with Regnard
pursued his investigations under the superintendence and direction
of Charcot. His book is a volume of more than seven hundred pages,
containing a vast amount of information and profusely illustrated, in
large part by original sketches by the author. Charcot himself has
written for it a commendatory preface.
2 Leçons sur les Maladies du Système nerveux. A portion of these lectures have been
translated by G. Sigerson, M.D., and published by the New Sydenham Society of
London, and reprinted in 1878 and 1879 in Medical News.

3 Bourneville, Recherches clinique et therapeutique sur l'Épilepsie et l'Hystérie, 1876;

Bourneville et Voulet, De la Contracture hystérique-permanente, 1872; Bourneville et
Regnard, Iconographie photographique de la Salpêtrière. I have made special use of
the second volume of the last of these works.

4 Études cliniques sur l'Hystero-épilepsie, ou Grande Hystérie, par le Dr. Paul Richer,
Paris, 1881.

No article on hystero-epilepsy can be written without frequent use of

this work of Richer, and also of the numerous contributions of
Charcot. To them we are indebted for new ways of looking at this
disease, as well as for an almost inexhaustible array of facts and
illustrations of the diverse phases of this disorder.

While the curious, grotesque, or outrageous manifestations now

known as hystero-epileptic have been discussed with more or less
minuteness by authors from the time of Sydenham to the present,
usually, and more especially in all countries but France, these
manifestations have been studied as isolated phenomena. Charcot
and Richer, however, present a comprehensive view of hysteria as a
disease of a certain typical form, but often manifesting itself in an
imperfect or irregular manner. This regular type is characterized
particularly by a frequently- or infrequently-recurring grave attack,
which is divided into distinct periods, and these periods into phases.

This regular type of grave hysteria once understood, a place of

advantage is gained from which to study the disease in its imperfect,
irregular, and abortive forms. Whatever its pathology may be, such
striking symptoms as loss of consciousness with spasm,
hallucinations, and illusions show at least temporary disturbance of
the integrity of the cerebrum.

Hystero-epilepsy of imperfectly developed or irregular type is a not

uncommon affection in this country, but the disease in its regular
type is comparatively rare.

VARIETIES.—Hysteria and epilepsy, so far as seizures are concerned,

may show themselves in two ways in the same patient; but I believe
that it is best that the term hystero-epilepsy should be restricted in its
application, as Charcot, Bourneville, and Richer have advised, to the
disorder in which hysterical and epileptic symptoms are commingled
in the same attack—what is spoken of by the French as hystero-
epilepsy with combined crises. The other method of combination is in
the affection known as hystero-epilepsy with separate crises, in
which the same patient is the victim of two distinct diseases, hysteria
and epilepsy, the symptoms of which appear independently of each
other.
The fact that hysteria is at times associated with true epilepsy is
often overlooked. A patient who is known to have had pure hysterical
seizures of the grave type has also a genuine paroxysm of epilepsy,
and thus the medical attendant is deceived. I will dismiss the
consideration of hystero-epilepsy with separate crises with a few
paragraphs at this place, devoting the rest of the article to the
disorder with combined crises.

The coexistence of hysteria and epilepsy, with distinct manifestations

of the two neuroses, has been most thoroughly considered by
D'Olier.5 Beau in 1836, and Esquirol in 1838, first showed this
coexistence. Landouzy in 1846 first made use of the name hystero-
epilepsy with separate crises.
5 Memoir which obtained the Esquirol prize in 1881, by M. D'Olier, interne of the
hospitals of Paris, on “Hystero-Epilepsy with Distinct Crises, considered in the Two
Sexes, and particularly in Man,” translated and abstracted by E. M. Nelson, M.D., in
the Alienist and Neurologist, April, 1882.

In France the distinct existence of hysteria and epilepsy in the same

individual is not, according to D'Olier, a very exceptional fact. Beau
has reported it 20 times in 276 cases. The different modes of
coexistence have been summed up by Charcot as follows: “1,
Hysteria supervening in a subject already epileptic; 2, epilepsy
supervening in a subject previously hysterical; 3, convulsive hysteria
coexisting with epileptic vertigo; 4, epilepsy developing upon non-
convulsive hysteria (contracture, anæsthesia).”

The following case, now in the Philadelphia Hospital, illustrates the

first of these modes of combination: S——, aged thirty-nine, female,
a Swede, came to this country in 1869. She said that her mother had
fits of some kind. The patient had her first fit when she was four
years old. Her menses did not come on until she was nineteen. With
the appearance of her periods she had fainting-spells off and on for
two years, and in these spells she would fall to the ground. After two
years she improved somewhat, but still would have an occasional
seizure like petit mal. Four years ago she had a severe fit, in which
she bit her tongue. This was a paroxysm of true epilepsy. It was
witnessed by the chief nurse in the hospital, a competent observer.
Since then she has had attacks of some kind every month or oftener.
She rarely had a true epileptic seizure. Often, however, she had
hysterical and hystero-epileptic attacks. These paroxysms have
been witnessed by myself and by the resident physician and nurse.
Rarely they were epileptic, frequently they were hysterical. Mental
excitement will often induce an hysterical spasm.

PATHOLOGY.—Holding that hystero-epilepsy is a form of grave

hysteria, the remarks which have been made in the last article on the
probable nature of severe convulsive attacks will be applicable here.
In hystero-epilepsy with the typical grave attack we have the highest
expression of that disturbance of cerebro-spinal equilibrium which
constitutes the pathology of hysteria.

ETIOLOGY.—It will also be unnecessary to go at length into the

discussion of the predisposing and exciting causes of hystero-
epilepsy. In general, its predisposing causes are those of hysteria of
any form. Certain causes or conditions, however, predispose to
certain types or forms of hysteria. The Latin races are more inclined
to the hystero-epileptic form of hysteria than are the natives of more
temperate or colder climates. Bearing upon this point, I have already
quoted the letter of Guiteras with reference to hysteria and hystero-
epilepsy in Cuba and semi-tropical America. Forms of religion which
cultivate to an extreme degree the emotional or the sentimental side
of human nature tend to produce hystero-epilepsy.

With reference to sex it may be said that hystero-epilepsy prevails to

a greater extent among females than males, even proportionately to
a larger degree than some of the other marked phases of hysteria. It
does, however, occur in men and boys, although rarely. Richer
records, from the practice of Charcot, a case in a lad of twelve years.
Several cases have fallen under my own care.

Ten years since I saw a case of hystero-epilepsy, which in some

respects closely simulated tetanus, in a youth nineteen years old. He
was well until seventeen years of age, when he slightly wrenched his
back. Shortly afterward he felt some pain between the shoulders.
From that time, at irregular intervals, generally of a few days only, he
was subject to attacks of dull pain, which seemed to run up the spine
to the head. About two months after this injury he first had a
spasmodic attack. A spasm would come on while he was quietly
sitting or working. The body assumed the backward-arched position.
As his father described the case, there was always space enough
under his back for a baby to crawl through. Generally, he would have
more than one seizure on a given occasion. He would sometimes
have as many as six or seven in one hour. On coming to, he would
stare and mutter and work his mouth and lips, at the same time
pointing around with his hands and fingers in a wild way. Sometimes
he would sleep for several hours afterward if not disturbed, but his
sleep was not of a stertorous character. He said that he could feel
the attacks coming on; his body felt as if it was stretching, his head
going back. He thought he was not conscious during the whole of the
attacks, but between the spasms he could take medicine when
directed. When first examined he had decided tenderness on
pressure over the second, third, and fourth dorsal vertebræ.
Pressure in this region would sometimes bring on a convulsive
paroxysm. When first seen he had been for three months having
seizures every two or three weeks. He was under observation for
several months, during which time he was treated with faradization
to the spine, the hot spinal douche, tonics, and bromides, and made
a complete recovery.

W. Page McIntosh6 has reported several cases of hystero-epilepsy in

the male, one of which is doubly interesting because it was in a
negro. This patient was twenty-one years old, stout, and previously
in good health. He complained of intense pain in the stomach, and
soon passed into a violent convulsion. To show the importance of
diagnosis in these cases, it is interesting to note that the doctor first
thought of strychnia-poisoning, then of acute indigestion, next of
tetanus. Soon, however, he decided that he had a case of hysteria.
The patient had other convulsions on the day following the first
attack. The seizures were evidently hystero-epileptic or hysterical.
He was not unconscious, and believed that on a recent previous
evening he had been conjured by an old negress. The spell was to
work in three days, which it did. The doctor counter-spelled him with
a hypodermatic syringe, after which he promptly recovered.
McIntosh reports another case in a man forty years old and the
father of six children, who was laboring under strong mental
excitement because of the sufferings of a dangerously ill child. His
whole form was convulsed, and his body underwent a variety of
peculiar contortions. He had had similar attacks before, and had
subsequent recurrences.
6 Med. News, vol. xlviii., No. 1, Jan. 2, 1886, pp. 5-8.

The following case was observed in the Philadelphia Hospital: W. F.

——, aged twenty-eight years, married, has one child. His seizures
began seven years ago, when he had an attack while playing a
game of pool. At this time he had, according to his account, a
sudden feeling of giddiness or vertigo in which he fell over and had a
spasm, during which he thinks he was unconscious. After the seizure
he suffered from headache, but had no disposition to sleep.

From that time until the present he has been subject to these spells,
though the paroxysms are very irregular in frequency. Sometimes he
will have several attacks in a day; again, he will be free from them for
days, and perhaps for two or three weeks, but never for more than a
month at a time. They have come on him while walking in the street,
and on several occasions he has been taken to different hospitals.
He was admitted to the Philadelphia Hospital four times. On his first
admission he only remained over night; on his second and third he
remained for two or three weeks. On the last admission he remained
four weeks, and had spasms every day and night after admission.
He had, by actual count, from five to six hundred after he went in;
and in one evening, from seven P.M. to midnight, he had no less than
thirty-eight. These seizures, which were witnessed by myself and
two resident physicians, differed but little from each other, although
at times some were more violent than others. They began with a
forced inspiration; then the patient straightened himself out and
breathed in a stertorous or pseudo-stertorous manner. The pulse in
that stage became slow, and at times was as low as 48 per minute.
The temperature was normal or subnormal. The arched position was
sometimes taken, but the opisthotonos was not marked. The
paroxysm ceased by an apparent forced expiration, and the
breathing then became normal; the patient remained in a somewhat
dazed condition, which was only momentary. During the attack the
patient said that he was unconscious of his surroundings. In the
interval between the attacks he suffered from headache and from
pain over the region of the stomach. He also had tenderness on
pressure over the lumbar vertebræ. He never bit his tongue.

Age has some influence in the development of hystero-epilepsy. It is

of most common occurrence at the period of pubescence; it is rare in
old age, but occurs with comparative frequency in middle life; or,
rather, it should be said that middle-aged hystero-epileptics are not
uncommonly met with, individuals who have for many years been
subject to the attacks. In young children, girls or boys, it is certainly
rare.

With reference to the exciting causes of hystero-epilepsy, it will only

be necessary to say that of those which have already been
enumerated in the general discussion of the etiology of hysteria, a
few, such as domestic troubles, abnormal sexual excitement, and
painful menstruation, are likely to induce the paroxysm, but fright,
excitement, anxiety, sudden joy, and other psychical disturbances
are the most frequent of the exciting causes of the seizures. A threat
or a blow has been known to precipitate an attack. The use or abuse
of alcohol is sometimes an exciting cause. Reflex irritation, such as
that from intestinal worms, and digestive disorders sometimes
produces hystero-epileptic attacks in children.

SYMPTOMATOLOGY.—In considering the symptoms of hystero-epilepsy

the subject must be approached from several points of view. In the
first place, the disorder can be divided (1) into the regular or typical
grave attack; and (2) into the irregular attacks. These irregular
seizures can be greatly subdivided, but their discussion will be
confined to those types which have been most observed in this
country, although I do not think that any variety of hystero-epilepsy is
distinctively American; and this is what might be supposed from the
largeness of our country and the different nationalities of which it is
composed.

I have seen but few cases of hystero-epilepsy of the regular type.

One of these was first described at some length in the American
Journal of Medical Sciences for October, 1881. I will here give the
case, with illustrations, somewhat condensed from the accounts as
first published.7
7 For the opportunity of studying and treating this case I was under obligations to
Charles S. Turnbull and J. Solis Cohen, the patient having been for several months
under their care at the German Hospital of Philadelphia. Carefully prepared notes of
the case were furnished to me by H. S. Bissey and H. W. Norton, resident physicians
at the hospital. I was also under great obligations to my friend J. M. Taylor for a series
of sketches of the positions assumed by the patient at different stages of the attack.

R——, æt. 21, single, was first admitted to the German Hospital Nov.
13, 1879. Between her ninth and twelfth years she had had several
attacks of chorea. During childhood she was often troubled with
nightmare and unpleasant dreams; she often felt while asleep as if
she were held down by hands. She was frequently beaten about the
head and body. Her menses did not appear until she was nearly
eighteen. Before and at her first menstrual epoch she suffered
severe pain and cramp. During the first year of her menstruation,
while at Atlantic City, the flow appeared in the morning, and she went
in bathing the same afternoon. She stayed in the water two hours,
was thoroughly chilled, and the discharge stopped. Ever since that
time she had only menstruated one day at each period, and the flow
had been scanty and attended with pain. When about eighteen she
kept company with a man for five months, and after having put much
confidence in him learned that he had a wife and two children. This
episode caused her much worriment. She positively denied
seduction. She became much depressed. September 2, 1879, she
was seized in a street-car with a fainting fit. On coming to, she found
her left arm was affected with an unremitting tremor. Seven weeks
later she was admitted to the German Hospital. She had severe