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Bipolar II Disorder
Bipolar II Disorder
Modelling, Measuring and Managing
Third Edition
Edited by
Gordon Parker
University of New South Wales
University Printing House, Cambridge CB2 8BS, United Kingdom
One Liberty Plaza, 20th Floor, New York, NY 10006, USA
477 Williamstown Road, Port Melbourne, VIC 3207, Australia
314–321, 3rd Floor, Plot 3, Splendor Forum, Jasola District Centre, New Delhi – 110025, India
79 Anson Road, #06-04/06, Singapore 079906
Cambridge University Press is part of the University of Cambridge.

It furthers the University’s mission by disseminating knowledge in the pursuit of education,
learning, and research at the highest international levels of excellence.
www.cambridge.org
Information on this title: www.cambridge.org/9781108414111
DOI: 10.1017/9781108333252
© Cambridge University Press 2019
This publication is in copyright. Subject to statutory exception and to the provisions of relevant
collective licensing agreements, no reproduction of any part may take place without the written
permission of Cambridge University Press.
First published by Cambridge University Press 2008
Second Edition 2012
Third Edition 2019
Printed and bound in Great Britain by Clays Ltd, Elcograf S.p.A.
A catalogue record for this publication is available from the British Library.
ISBN 978-1-108-41411-1 Paperback
Cambridge University Press has no responsibility for the persistence or accuracy of URLs for
external or third-party internet websites referred to in this publication and does not guarantee
that any content on such websites is, or will remain, accurate or appropriate.
Every effort has been made in preparing this book to provide accurate and up-to-date information
that is in accord with accepted standards and practice at the time of publication. Although case
histories are drawn from actual cases, every effort has been made to disguise the identities of the
individuals involved. Nevertheless, the authors, editors, and publishers can make no warranties
that the information contained herein is totally free from error, not least because clinical
standards are constantly changing through research and regulation. The authors, editors, and
publishers therefore disclaim all liability for direct or consequential damages resulting from the
use of material contained in this book. Readers are strongly advised to pay careful attention to
information provided by the manufacturer of any drugs or equipment that they plan to use.
Bipolar II Disorder
Bipolar II Disorder
Modelling, Measuring and Managing
Third Edition
Edited by
Gordon Parker
University of New South Wales
University Printing House, Cambridge CB2 8BS, United Kingdom
One Liberty Plaza, 20th Floor, New York, NY 10006, USA
477 Williamstown Road, Port Melbourne, VIC 3207, Australia
314–321, 3rd Floor, Plot 3, Splendor Forum, Jasola District Centre, New Delhi – 110025, India
79 Anson Road, #06-04/06, Singapore 079906
Cambridge University Press is part of the University of Cambridge.

It furthers the University’s mission by disseminating knowledge in the pursuit of education,
learning, and research at the highest international levels of excellence.
www.cambridge.org
Information on this title: www.cambridge.org/9781108414111
DOI: 10.1017/9781108333252
© Cambridge University Press 2019
This publication is in copyright. Subject to statutory exception and to the provisions of relevant
collective licensing agreements, no reproduction of any part may take place without the written
permission of Cambridge University Press.
First published by Cambridge University Press 2008
Second Edition 2012
Third Edition 2019
Printed and bound in Great Britain by Clays Ltd, Elcograf S.p.A.
A catalogue record for this publication is available from the British Library.
ISBN 978-1-108-41411-1 Paperback
Cambridge University Press has no responsibility for the persistence or accuracy of URLs for
external or third-party internet websites referred to in this publication and does not guarantee
that any content on such websites is, or will remain, accurate or appropriate.
Every effort has been made in preparing this book to provide accurate and up-to-date information
that is in accord with accepted standards and practice at the time of publication. Although case
histories are drawn from actual cases, every effort has been made to disguise the identities of the
individuals involved. Nevertheless, the authors, editors, and publishers can make no warranties
that the information contained herein is totally free from error, not least because clinical
standards are constantly changing through research and regulation. The authors, editors, and
publishers therefore disclaim all liability for direct or consequential damages resulting from the
use of material contained in this book. Readers are strongly advised to pay careful attention to
information provided by the manufacturer of any drugs or equipment that they plan to use.
To my wife Heather. Ever supportive and ever
generous of spirit.
Contents
List of Contributors ix
Preface to the Third Edition xi
Acknowledgements xiii
Section 1 – Domain Chapters 9 The Neurobiology of Bipolar II

Disorder 91
1 Mapping the Terrain of Bipolar II Emre Bora and Christos Pantelis
Disorder 1
10 Methodological Nuances in
Gordon Parker
Undertaking and Interpreting
2 Bipolar Disorder in Historical Efficacy Studies of Medications for
Perspective 6 Bipolar II Disorder 108
Edward Shorter Gabriela Tavella and Gordon Parker
3 The Bipolar Spectrum 16 11 The Role of Antidepressants in

Chris B. Aiken Managing Bipolar II Disorder 113
Joseph F. Goldberg
4 Defining and Measuring Bipolar
II Disorder as a Categorical 12 Mood Stabilisers in the Treatment
Condition 33 of Bipolar II Disorder 129
Gordon Parker David J. Bond, George Hadjipavlou
and Lakshmi N. Yatham
5 Bipolar II Disorder in Context:
13 The Use of Antipsychotic Drugs in
A Review of Its Epidemiology,
Bipolar II Disorder 143
Disability and Economic
Burden 49 Eduard Vieta
Trisha Chakrabarty, George 14 Perinatal Nuances in Managing
Hadjipavlou, David J. Bond and Bipolar II Disorder 151
Lakshmi N. Yatham Gabriela Tavella and Philip Boyce
6 Comorbid Conditions Associated 15 Psychological Interventions for
with Bipolar II Disorder 60 Bipolar II Disorder 163
Gordon Parker and Stacey McCraw Vijaya Manicavasagar and
David Gilfillan
7 Personality and Temperament
Styles Associated with Bipolar II 16 The Role of Well-Being Plans in
Disorder 69 Managing Bipolar II Disorder 177
Tahlia Ricciardi Margo Orum
8 Differentiating Bipolar II 17 The Trajectory of Illness
Disorder from Personality-based Experienced by Those with a
Dysregulation Disorders 77 Bipolar II Disorder 192
Joel Paris and Adam Bayes Tessa Cleradin
vii
viii Contents
Section 2 – Management 29 Management Commentary 255

Robert M. Post
Commentaries
30 Management Commentary 263
18 Introduction to Management Joshua D. Rosenblat and Roger S.
Commentaries 211 McIntyre
Gordon Parker
19 Management Commentary 213 Ayal Schaffer
Jay D. Amsterdam and Lorenzo
Lorenzo-Luaces 32 Management Commentary 272
Michael E. Thase
Darryl Bassett 33 Management Commentary 276
Mauricio Tohen
David Castle 34 Management Commentary 278
Eduard Vieta
Konstantinos N. Fountoulakis 35 Management Commentary 281
Lakshmi N. Yatham
Sophia Frangou 36 Management Commentary 285
Allan Young
Heinz Grunze
Section 3 – Conclusion
Tadafumi Kato 37 Rounding Up 289
Gordon Parker
Gin S. Malhi
Philip B. Mitchell Index 299
Lawrence T. Park and Carlos A.
Zarate, Jr.
Contributors
Chris B. Aiken Sophia Frangou

Mood Treatment Center, North Carolina, Department of Psychiatry, Icahn School of
USA Medicine at Mount Sinai, New York, USA
Jay D. Amsterdam David Gilfillan
Depression Research Unit, Department Clinical Psychologist, Leura and Sydney,
of Psychiatry, University of Pennsylvania, Australia
Philadelphia, USA
Joseph F. Goldberg
Darryl Bassett Icahn School of Medicine at Mount Sinai,
School of Medicine, Division of New York, USA
Psychiatry, University of Western
Australia, Perth, Western Australia Heinz Grunze
Klinikum am Weissenhof, Weinsberg;
Adam Bayes Paracelsus Medical University,
School of Psychiatry, University of New Nuremberg, Germany
South Wales; Black Dog Institute. Sydney,
Australia George Hadjipavlou
Department of Psychiatry, University of
David J. Bond British Columbia, Vancouver, Canada
University of Minnesota Medical School,
Minnesota, USA Tadafumi Kato
Laboratory for Molecular Dynamics of
Emre Bora Mental Disorders, RIKEN Brain Science
Department of Psychiatry, Dokuz Eylul Institute, Saitama, Japan
University, Izmir, Turkey
Lorenzo Lorenzo-Luaces
David Castle Department of Psychological and Brain
St Vincent’s Hospital; University of Sciences, Indiana University, Indiana, USA
Melbourne, Melbourne, Australia
Gin S. Malhi
Trisha Chakrabarty Sydney Medical School, University of
Department of Psychiatry, The Sydney, Sydney, Australia
University of British Columbia,
Vancouver, Canada Vijaya Manicavasagar
School of Psychiatry, University of New
Tessa Cleradin South Wales; Black Dog Institute, Sydney,
Consumer advocate, Higher Education Australia
and Training Institute, Sydney
Stacey McCraw
Konstantinos N. Fountoulakis School of Psychiatry, University of New
Third Department of Psychiatry, Aristotle South Wales; Black Dog Institute. Sydney,
University of Thessaloniki, Greece Australia
ix
x List of Contributors
Roger S. McIntyre Ayal Schaffer

Mood Disorder Psychopharmacology Sunnybrook Health Sciences Centre,
Unit, University Health Network, Toronto, Toronto, Canada
Canada
Edward Shorter
Philip B. Mitchell Jason A. Hannah Chair Professor of the
School of Psychiatry, University of New History of Medicine, Faculty of Medicine,
South Wales; Black Dog Institute. Sydney, University of Toronto, Toronto, Canada
Australia
Gabriela Tavella
Margo Orum School of Psychiatry, University of New
Open Sky Psychology, Sydney, Australia South Wales; Black Dog Institute. Sydney,
Australia
Christos Pantelis
Melbourne Neuropsychiatry Centre, Michael E. Thase
Department of Psychiatry, University of Department of Psychiatry
Melbourne, Melbourne, Australia Perelman School of Medicine of the
University of Pennsylvania and the
Joel Paris Corporal Michael J Crescenz Veterans
Institute of Community and Family Affairs Medical Center Philadelphia,
Psychiatry. SMBD-Jewish General Pennsylvania, USA
Hospital, McGill University, Montreal,
Quebec, Canada. Mauricio Tohen
Department of Psychiatry and
Lawrence T. Park Behavioural Sciences, University of New
Experimental Therapeutics and Mexico Health Sciences Centre, New
Pathophysiology Branch, National Institute Mexico, USA
of Mental Health, Maryland, USA
Eduard Vieta
Gordon Parker Department of Psychiatry and Psychology,
School of Psychiatry, University of New Hospital Clinic, Institute of Neuroscience,
South Wales; Black Dog Institute. Sydney, University of Barcelona, IDIBAPS,
Australia CIBERSAM, Barcelona, Catalonia, Spain
Robert M. Post Lakshmi N. Yatham
Bipolar Collaborative Network, George Mood Disorders Centre, University of
Washington University School of British Columbia, Vancouver, Canada
Medicine, Maryland, USA
Allan Young
Tahlia Ricciardi Centre for Mental Health Imperial
School of Psychiatry, University of New College, London, UK
South Wales; Black Dog Institute. Sydney,
Australia Carlos A. Zarate, Jr.
Experimental Therapeutics and
Joshua D. Rosenblat Pathophysiology Branch, National
Department of Psychiatry, University of Institute of Mental Health, Maryland,
Toronto, Ontario, Canada USA
Preface to the Third Edition
This book is designed
To detail what is known
What needs to be clarified and
What issues should be debated
About bipolar II disorder
Especially the extent to which its management
Should be extrapolated
From the strategies used in managing bipolar I disorder, or
Should differ to reflect bipolar II’s categorical status.
The first edition of this book was published in 2008 and it was – as far as we can
establish – the first monograph to focus on bipolar II disorder for the academic com-
munity. This reflected the condition being defined and detailed only since the seven-
ties, having its very diagnostic status challenged by many, being viewed as a minor
condition (e.g. ‘bipolar lite’) and, as a consequence, its lack of coverage in treatment
guidelines.
A second edition was published in 2012 and now we publish the third edition,
principally reflecting increasing recognition of BP II and need by clinicians and con-
sumers for information about the condition and its management. To capture changes
in emphases in the published literature, some chapters have been deleted, new ones
added and previous chapters updated. The appeal of the first two editions appeared
to very much reflect the commentary section in the second half of the book – where
instead of seeking or presenting a ‘consensus’ of views (a common strategy but cri-
tiqued in this edition), we allowed bipolar experts to be in two minds about many
management aspects. The appeal comes less from observing experts argue and more
from observing the strength of their arguments based on their clinical observations,
allowing the reader to then make their own judgments – either resolving or tolerating
the many ambiguities. Reviewer John Gottlieb (2010) not only observed that the 2008
edition was ‘the first publication out of the gate on this important area,’ but went on
to observe that
Eschewing the standard . . . format of blandly compiling the accumulated data . . . and
striving for a deadening impartiality . . . [and] draining the lifeblood out of the subject . . .
[the book] makes room for the full cacophony of opinion, debate, agreement and conflict
that constitutes the field of research at this time . . . The result is less a compilation than a
real-time, street fight amongst respected colleagues.
In this edition, instead of asking experts to critique a management template (as
reviously), we invited them to respond to a set of questions central to the management
p
of bipolar II disorder. A cacophony of opinion is still observable.
While the book was initially designed
For academic and clinical mental health professionals
It has progressively been used as a reference
xi
https://doi.org/10.1017/9781108333252.001
xii Preface to the Third Edition
By those with a bipolar disorder

And by their family members
We hope that this edition
Will go even further
To meet the needs of the last constituency
For up to date information.
https://doi.org/10.1017/9781108333252.001
Acknowledgements
My sincere thanks to Gabriela Tavella and Tahlia Ricciardi who have assisted me with
addressing so many production tasks with great acumen and skill, to Kerrie Eyers
who again provided editorial wisdom, and to Jessica Papworth and Nigel Graves
from Cambridge University Press who thoughtfully and carefully steered this book to
production.
xiii
Section 1 Domain Chapters
Mapping the Terrain of Bipolar

Chapter
1 II Disorder
Gordon Parker
Any consideration of bipolar II (BP II) disorder requires addressing a number of funda-
mental issues. Firstly, does such a bipolar condition exist – whether differing from bipolar
I (BP I) disorder dimensionally or categorically? As detailed earlier (Parker and Paterson,
2017) the concept of hypomania (a key BP II construct) was first defined by Mendel in
1881 – who essentially described a milder version of mania – while, in 1882, Kahlbaum
used the term ‘cyclothymia’ to describe alterations between elation without psychosis and
melancholic episodes. During the early twentieth century both cyclothymia and hypo-
mania were lumped together as milder forms of manic depressive psychosis. From the
1930s to the 1970s, the concept of hypomania’ or a ‘milder form’ of bipolar disorder all
but disappeared until Dunner identified a putative BP II category in his research studies.
Dunner (personal communication) identified a subset of bipolar patients who appeared
to be ‘in between’ those with unipolar depression and those who experienced mania, and
who reported less severe ‘hypomanic’ episodes.
BP II disorder has now been formally categorized for several decades with Shorter
(Chapter 2) detailing how it was accorded separate status in the final version of the RDC
(Research Diagnostic Criteria) in 1978. In 1980, DSM-III listed an ‘Atypical Bipolar
Disorder’ and positioned it as a ‘residual category’ (p. 223) for ‘individuals with manic
features that cannot be classified as Bipolar Disorder or as Cyclothymic Disorder’ – exem-
plified by individuals who have had a previous major depressive episode and who are
then presenting with ‘some manic features (hypomanic episode) but not of sufficient
severity and duration to meet the criteria for a manic episode. Such cases are referred to
as “Bipolar II’”. In 1987, DSM-III-R allowed those who had had one or more hypomanic
episodes (but ‘without Cyclothymia or a history of either a Manic or a Major Depressive
Episode’) to be listed in a category of ‘Bipolar Disorder Not Otherwise Specified’. It
achieved formal DSM status (as Bipolar II Disorder) in the 1994 DSM-IV manual, where
its essential features were captured by a clinical course of one or more major depressive
episodes accompanied by at least one hypomanic episode, albeit with its seven symp-
tom criteria (p. 338) being identical to those defining a manic episode (p. 332). In the
2013 DSM-5 manual Bipolar II Disorder is clearly separated from Bipolar I disorder in
the introduction to the relevant chapter. In addition, BP II was formally classified in the
1994 ICD-10 system. Thus, it exists as a formalized psychiatric condition and has for an
extended period.
It is likely, however, that BP II long existed prior to its formal classification. Davidson
(2011) reviewed the mental health ‘afflictions’ of the first 51 British Prime Ministers, pro-
viding evidence suggestive of a BP II disorder in 16% (Canning, Churchill, Disraeli, Grey,
https://doi.org/10.1017/9781108333252.002
2 Section 1: Domain Chapters
Lloyd George and Macmillan). None received such a diagnosis (as the condition was not
then formally classified), and as Davidson details, none lost office as a consequence of
their mood swings and with most being judged as superior prime ministers than the oth-
ers who, if not experiencing depression, were commonly anxious and self-doubting. Most
of those with a putative BP II disorder were recognized as having depressive states but
their oscillating elevated mood states were either not observed or given differing inter-
pretations, consistent with the longstanding tendency to view those with the condition as
simply having mercurial states or a cyclothymic personality style.
Despite its formal categorization for several decades, a diagnostic category may
or may not have validity and psychiatry can provide many examples, both historical
(e.g. masturbatory madness) and current (e.g. DSM-5’s Disruptive Mood Dysregulation
Disorder – a formalised depressive disorder which is defined by irritability and temper
outbursts while lacking any depressive symptom criteria). Again, despite BP-II’s listing,
there are many who doubt its existence, most commonly positioning it simply as a milder
expression of a bipolar disorder spectrum or as a personality style marked by emotional
dysregulation or normative mood swings (qua cyclothymia).
A key objective of this book is to argue directly and indirectly for its existence. Simply
offering a ‘believing is seeing’ argument is scientifically unacceptable. Instead, any argu-
ment for its entity status requires BP II disorder to be defined by a number of clinical
symptoms (both in relation to hypomanic and depressive states) that, as a set, are dis-
tinctive and not able to be positioned as simply reflecting a personality style. Failure to
identify its status as a categorical mood disorder has contributed to its remaining under
the radar. For example, in a recent paper (Parker et al., 2017) we considered its coverage
in a large set of evidence-based guidelines for managing bipolar disorders. Most made
no reference to the condition. Of those making reference, few offered any specific recom-
mendations for managing bipolar II, and most offered an ‘extrapolation’ management
model (i.e. recommending the same medications as for those with a BP I condition). The
structuring of those guidelines again provides evidence suggesting that there is limited
recognition of the existence of BP II disorder and, secondly, if conceded, that the domi-
nant model is a dimensional one.
Separate chapters in this book allow authors to debate its status either as a dimen-
sional condition (reflecting a milder state lying on a spectrum that, at the more severe
end, captures BP I disorder) or as a categorical condition separate from bipolar I disorder.
Its ‘existence’ would be advanced if a substantive case can be made for its status as a cat-
egorical condition. Two chapters focus on offering arguments for each model. I favour a
categorical binary model as detailed in Chapter 4, albeit recognizing the limitations to
any simple binary model. For example, one wit stated that: ‘There are two classes of people
in the world: those who divide the people in the world into two classes and those who do not’.
Another wit (qua twit) observed ‘There are only ten types of people in the world. Those who
understand binary and those who don’t’.
There are major consequences to establishing whether BP II disorder differs dimen-
sionally or categorically from BP I disorder. If the two conditions lie along a dimension,
then it might be anticipated that the same management models would be relevant to each
condition (i.e. the extrapolation model). If BP II disorder differs categorically, then it may
respond quite differently to medications established as beneficial for those with a BP I
disorder subject to the studies employing rigorous methodologies.
https://doi.org/10.1017/9781108333252.002
Chapter 1: Mapping the Terrain of Bipolar II Disorder 3
In relation to the last point, we have prepared a new chapter (Chapter 10) reviewing a
number of major limitations to the design of studies evaluating the efficacy of treatments
for the bipolar disorders, capturing key issues detailed in a recently published paper
(Parker and Tavella, 2018), and limitations that are particularly salient in relation to BP II
disorder. The short duration of many trials, the tendency to test mood stabilizers during
acute episodes as against testing their efficacy as maintenance treatments, the many limi-
tations to the measures most commonly applied and the frequency of their administra-
tion, all confound and limit our capacity to truly evaluate whether a treatment modifies
both the highs and lows of a bipolar condition. Such limitations are particularly salient
in evaluating interventions for BP II states when mood oscillations are more frequent in
terms of episode frequency, duration and severity, and in assessing the comparative effi-
cacy of differing management strategies.
There also remains a clear need to improve detection and diagnosis. BP II disorder
seemingly attracts two positions – ‘over-diagnosis’ (often by expanding the spectrum or
dimensional model into domains of personality and temperament) and ‘under-diagnosis’.
The latter concern is worthy of extension. As noted throughout the book, very high
percentages of individuals with a BP II disorder never receive that diagnosis over their
lifetime – and instead are most often diagnosed and managed as if they have a unipolar
depressive disorder or given a personality disorder diagnosis (most commonly ‘border-
line’). For those who experience a distinct delay to obtaining a BP II diagnosis, the risks
are of considerable ‘collateral damage’ from the condition (in terms of disruption to work
and relationships in particular), of ‘social suicide’ (from engaging in activities that per-
manently damage the individual’s reputation) and of actual suicide. Over the last decade
I continue to be surprised by the high rates of colleagues who have failed to diagnose a
seemingly characteristic BP II condition, either by neglecting to screen for the possibility
during routine consultations or, sadly, when a patient seeks confirmation of such a diag-
nosis from a professional who does not accept or concede the existence of a BP II disorder.
I suspect that one of the principal explanations for ‘failure to detect’ is training – or, in
this instance, the lack of it. Most psychiatrists train in facilities where they observe psy-
chotic BP I states. Few mental health professionals over the age of forty have ever received
a lecture on BP II disorder during their training course. Most professionals who have
developed an interest in this diagnostic condition over the last few decades have generally
‘learned on the job’, observing a condition that varies in so many ways from BP I disorder.
But perhaps the most common reason for failure to so diagnose is – as noted earlier – simply
not asking screening questions for all patients who present for assistance with ‘depres-
sion’. There is therefore a need for much greater professional and community awareness,
and this has proceeded to a reasonable degree in Australia over the last decade following
orthodox educational strategies and especially from prominent people in the community
detailing features of their BP II condition in the media, a process encouraged by Stephen
Fry’s 2006 BBC series ‘The Secret Life of the Manic-Depressive’. Such concerns argue for
readily available assessment tools and that health professionals screen all patients pre-
senting with signs and symptoms of ‘depression’ for the presence of a bipolar disorder.
Finally, there is the key issue of management. Evaluating management options is gen-
erally advanced by assessing ‘the evidence’. In psychiatry, as in medicine, there is a gen-
erally accepted hierarchy or clinical evidence pyramid. Low-level ‘evidence’ is provided
by ideas, opinions and case reports. At the next level lie case series, as well as both case
https://doi.org/10.1017/9781108333252.002
control and cohort studies. At the next level lie randomised controlled studies. At the
highest level lie systematic reviews of the aggregated evidence and which are often sup-
ported by quantifying meta-analyses.
Low-level evidence is easy to criticize as, for example, it may simply reflect idiosyn-
cratic opinion (and which may be erroneously persuasive simply if ‘eminence-based’).
But high-level evidence also has its limitations. Such evidence can be skewed by a number
of factors. For example, medications (such as lithium) that have been prescribed for an
extended period have a theoretical advantage over newer medications, when the latter
may have been evaluated in few studies. Medications that have been evaluated in multiple
studies are likely to be recommended above those that have been minimally evaluated.
Efficacy studies tend to weigh evaluating benefit with less attention to ‘costs’ (i.e. side-
effects). Findings from efficacy studies (most commonly generated from randomized
controlled studies) may not cross-walk to real world clinical practice, most commonly
reflecting the composition of those who take part in clinical trials. Trial participants tend
to have milder disorders (with suicidal ideation being a representative exclusion crite-
rion), may sometimes only enter the trial to obtain medication for free, are judged to
have no history of drug or alcohol problems, no co-morbid symptom states or personal-
ity disorder, and are therefore quite pristine in comparison to those who attend clinical
psychiatrists. Thus, randomized controlled trials and meta-analyses provide some evi-
dence about the degree to which a medication works and may (subject to all potential
side-effects being inquired about) provide important information about rates of risks and
side-effects. But the actual ‘effectiveness’ of a medication in a clinical setting is generally
not able to be assessed from such studies.
A common approach by clinicians is therefore to prescribe a medication to a set num-
ber of their own patients. If the medication is likely to be effective, the clinician may only
require a dozen or so patients to obtain an effectiveness ‘signal’. If a signal is not obtained
until 20–50 patients have received the medication, then its real-world utility is likely to be
low. A second common approach by clinicians is to ask a small set of ‘experts’ (i.e. clini-
cian researchers who have prescribed the medication to a large number of patients) for
their evaluation of the particular medication. Subject to such experts not having a conflict
of interest, such information can be highly informative. Thus, rather than management
guidelines being derived only from randomized controlled trials, there is an advantage to
an iterative process whereby the trial efficacy data is melded with the opinions of unbi-
ased experts. This approach is addressed in several individual chapters, including a new
chapter addressing perinatal nuances in relation to the prescription of medication in
pregnant or breastfeeding women with a bipolar II disorder.
In the absence of clear prescriptive evidence-based guidelines for the management of
BP II the abhorred vacuum can best be filled by the views of practitioners who are clini-
cally skilled and observant until the evidence base is more definitive. This book there-
fore offers an iterative process for the reader. Separate chapters overview and evaluate
the efficacy data from clinical trials of differing medications, before offering a series of
commentaries and where the commentators offer their clinically weighted observations.
We encourage the reader to make their judgments on the basis of those two ‘worlds’ of
evidence.
https://doi.org/10.1017/9781108333252.002
Chapter 1: Mapping the Terrain of Bipolar II Disorder 5
References
Davidson, J. (2011). Downing Street Blues. A Parker, G., Graham, R. and Tavella, G. (2017).
History of Depression and Other Mental Is there consensus across international
Afflictions in British Prime Ministers. evidence-based guidelines for the
Jefferson, NC: McFarland & Company, Inc.. management of bipolar disorder? Acta
Parker, G. and Paterson, A. (2017). Should Psychiatrica Scandinavica, 135, 515–26,
the bipolar disorders be modelled Parker, G. and Tavella, G. (2018). Design
dimensionally or categorically? In A. F. limitations to bipolar II treatment efficacy
Carvalho and E. Vieta (Eds.), The Treatment studies: a challenge and a revisionist
of Bipolar Disorder: Integrative Clinical strategy. Journal of Affective Disorders, 229,
Strategies and Future Directions. Oxford, 334–41.
UK: Oxford University Press.
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Bipolar Disorder in Historical
Chapter
2 Perspective
Edward Shorter
Bipolar disorder is, in a sense, as old as the hills. Yet its diagnosis as a distinct disor-
der is quite recent. Physicians have always recognized alternating states of melancholia
and mania. It would be as idle to ask who was the first to describe this alternation as it
would be to ask who first described mumps. Aretaeus of Cappadocia, around 150 years
after the birth of Christ, wrote of the succession of the two illnesses. It is clear from the
context (Jackson, 1986, pp. 39–41) that he was using the two terms to describe what we
today would consider mania and melancholia. Yet Aretaeus did not consider the alterna-
tion of mania and melancholia to be a separate disease. Etienne Esquirol, director of the
Charenton asylum outside of Paris and one of the founders of modern psychiatry, noted
in 1819 (Esquirol, 1819, p. 169), ‘sometimes melancholia passes into mania; indeed it is
the ease with which this . . . transformation occurs that has led all the authors to confuse
melancholia with mania’. There is no hint in Esquirol’s writing that he considered the
alternation of melancholia and mania to constitute a separate disorder.
For these remote centuries I use ‘bipolar disorder’ to mean the succession of melan-
cholia and mania. A word of clarification: in the twentieth century, after the writing of
Kleist and Leonhard, ‘bipolar disorder’ implies that there is a separate unipolar depressive
disease. By contrast, the term ‘manic-depression’ suggests that there is only one depres-
sion, whether linked to mania or not. But the term ‘manic-depressive insanity’ itself did
not surface until 1899. To describe mania, melancholia, and their alternation in previous
centuries, I shall simply call it bipolar disorder and crave the reader’s indulgence.
So the big question is not who first described bipolar disorder, but rather if it is one
disease or two? The centuries of clinical experience that lie behind us constitute a moun-
tain of evidence of some weight. And in this tremendous accumulation of practical learn-
ing, has bipolar disorder been considered one disease? Or two: the alternation of two
separate diseases, mania and melancholia? A third possibility: is bipolar disorder an
alternation of several different kinds of mood disorders that includes episodes of catato-
nia, melancholia, psychotic depression, mania, and hypomania, each an independent ill-
ness entity in its own right? Conrad Swartz has suggested that, in this kind of alternation,
the term ‘multipolar disorder’ might be more appropriate than ‘bipolar disorder’ (Swartz,
personal communication, 24 October 2006). When we find these syndromes occurring
over the years in the same patient, is it one illness or several?
For psychiatrists of the past, it was quite common to see melancholia cede to mania.
Vincenzo Chiarugi, a psychiatrist at the Bonifazio mental hospital in Florence, Italy, at
the end of the eighteenth century, described a female patient, aged 35, who switched
from deep melancholia to mania. Chiarugi thought this a case of ‘true melancholy’ and
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Chapter 2: Bipolar Disorder in Historical Perspective 7
by no means out of the ordinary. The clinicians of the day often used such terms as mania
and melancholia in a sense quite different from ours, yet, on the basis of the case report
(Chiarugi, 1794, pp. 95–6), Chiarugi was dealing with manic-depression.
In the world of patients as well, alternating mania and melancholia have been known
since time out of mind. As Thomas Penrose, the curate of Newbury in Berkshire, England,
penned (Penrose, 1775, p. 19) in the 1780s of a young woman disappointed in love:
Dim haggard looks, and clouded o’er with care,
Point out to Pity’s tears, the poor distracted fair.
Dead to the world – her fondest wishes crossed
She mourns herself thus early lost.
Now, sadly gay, of sorrows past she sings,
Now, pensive, ruminates unutterable things.
She starts – she flies – who dares so rude
On her sequester’d steps intrude?
In the Voitsberg district of Austria early in the nineteenth century, such alternations
of melancholia and mania were regarded by the valley dwellers as quite typical, and one
of the features that distinguished them from the hill dwellers. Said a Dr. Irschitzky in
1838, ‘We know from experience, that among the valley folk now and then melancholia
occurs, mostly for religious reasons, and frequently acute insanity (mania). These mental
illnesses follow in a quite natural manner from the constitution and the character of these
people . . . whereby frequently mania serves as an interlude’ (Irschitzky, 1838, p. 243).
These authors regarded mania and melancholia as two illnesses succeeding each
other. Among the first observers to see this alternation of mania and melancholia as parts
of the same disease was Spanish court physician Andrés Piquer Arrufat, who described
in 1759 the mentally ill king Fernando VI has having ‘el afecto mélancolico-maniaco’, and
penned a quite careful clinical description. Piquer regarded the illness as a unitary condi-
tion (‘son una misma enfermedad’) different from either melancholia or mania, in the
broad sense in which those diagnoses were then understood (Piquer, 1759/1846, pp. 6, 27).
Piquer’s manuscript account was, however, not published until 1846, which makes his
priority a bibliographic curiosity rather than a fundamental building stone in the his-
tory of psychiatric illness classification. Jésus Pérez and co-workers, who have studied
the Piquer account carefully, point out that Piquer apparently launched the diagnosis in
a 1764 textbook, yet without the careful characterization of it that we find in the memoir
published in 1846 (Pérez et al., 2011, p. 72), nor do they mention the 1846 publication.
In 1818, German psychiatrist Johann Christian August Heinroth in Leipzig pro-
posed four versions of ‘mixed mood disorders’ (gemischte Gemüthsstörungen), in each
of which some kind of insanity alternated with melancholia. One form, for example,
Heinroth described as the alternation of ‘madness’ (Wahnsinn) and melancholia. Calling
the disorder ‘quiet madness (ecstasis melancholica)’, Heinroth said that in the illness,
madness ‘loses its monstrousness’, and melancholia loses its ‘lifelessness, and the whole
illness proceeds in alternating exaltation and depression’. Heinroth also threw in a dollop
of German romanticism, and had the patient spending the melancholic phase ‘dragging
about the fields and woods or isolated mountain tops giving full expression to his still
sobs and sighs, or weaving in quiet contemplation wreaths of white flowers . . .’ (Heinroth,
1818, pp. 355–6).
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By the 1840s such accounts were numerous. In 1844, Carl Friedrich Flemming, direc-
tor of the Sachsenberg mental hospital in Germany, described ‘Dysthymia mutabilis’, the
kind of mood disorder that arises when Dysthymia atra (black depression) and Dysthymia
candida (low-level mania) alternate. ‘Between both of them (atra and candida) there is a
not infrequent connection, Dysthymia mutabilis, which sometimes shows the character of
one, sometimes the character of the other’. Flemming saw other kinds of depression too,
such as melancholia attonita, or stuporous melancholia (Flemming, 1844, pp. 114, 129).
Flemming’s proposed coinage, appearing in a then obscure German language journal,
was soon forgotten in an era when Paris was the centre of the enlightened world. And it
was in Paris that bipolar disorder as a separate entity was famously announced a few years
later. In 1850 Jean-Pierre Falret, a staff psychiatrist of the Salpêtrière Hospice in Paris
gave a lecture to the Psychiatric Society in which he briefly mentioned ‘circular insanity’
(la folie circulaire), thus giving the alternation of mania and melancholia a separate name.
He incorporated the idea into the clinical lectures he offered at the hospital in the early
1850s and published those lectures in 1854. Whatever Falret might have said in the early
lectures, by the 1854 book, the alternation of mania and melancholia in la folie circulaire
had become a disease of its own, not just the succession of two separate illnesses. Falret:
‘[La folie circulaire] is generally neither mania nor melancholia as such, with their cus-
tomary characteristics; it is, in some manner, the core of these two kinds of mental disease
without their depth [sans leur relief]’ (Falret, 1854a, pp. 249–50). He went on to explain
how bipolar mania and melancholia differed from the regular versions. There was in 1854
a vigorous exchange between Jules Baillarger, who claimed to have described the same
disease under another label (la folie à double forme), claiming priority, and Falret, who
insisted on his own priority of la folie circulaire (Baillarger, 1854a, 1854b; Falret, 1854b).
In 1864, Falret attempted to strangle the entire debate by insisting that neither mania
nor melancholia existed as separate diseases and the only natural entity was la folie
circulaire, in which these phases alternated, sometimes at prolonged intervals (Falret,
1864). The issue of which of these squabbling clinicians has priority is secondary. But
it would be fair to say that in Paris in the early 1850s bipolar disorder was born for
an international audience, yet without the careful apparatus of psychopathology and
nosology that came later.
The baton now passed to the Germans, and for the next hundred years the principal
contributions to bipolar disorder would be made by German professors. In 1878 Ludwig
Kirn, a psychiatry resident who had trained at the Illenau asylum, published a postdoc-
toral thesis on ‘the periodic psychoses’ in which he gave a detailed psychopathological
account of bipolar disorder, something the French clinicians had omitted in favour of
grand generalizations (Kirn, 1878). German nationalists, with their dislike of the French,
considered this the first description of the disorder tout court, but it in fact was not
(Kirchhoff, 1924, p. 167).
In these years many German psychiatrists such as Wilhelm Griesinger and Heinrich
Neumann described bipolar disorder in one form or another. For most, the usual course
was switching from melancholia into mania, and then into terminal dementia, more or
less as Falret had first described. But in 1882, Karl Kahlbaum, one of the great names
in the history of German psychiatry – because of his insistence on using the ‘clinical
method’ to study psychopathology – proposed the term ‘cyclothymia’ for recoverable
alternations of melancholia and mania. Yet these cases did not tip into dementia (as in
Heinrich Neumann’s ‘typical insanity’). Instead, the patients got better.
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Another such cyclical episode might then occur, and so forth. Also, the ‘mania’ that
Kahlbaum described was not a full-blast onslaught affecting all mental functions but
a kind of exaggerated elation without psychosis (Kahlbaum, 1882). It corresponded
roughly to what Berlin psychiatrist Emanuel Ernst Mendel had a year previously called
‘hypomania’ (Mendel, 1881), and is – in essence – the ancestor of ‘bipolar II disorder’.
Then came the great earthquake in German nosology: Emil Kraepelin and his historic
classification of psychiatric illnesses, the basic outlines of which have endured more or
less intact until the present. The classification, based on course and outcome, became the
first real conceptualization of manic-depressive illness, a disease having an undulating
course rather than an irreversible downhill slide as in chronic psychosis (which Kraepelin
called ‘dementia praecox’). Building on the work of Kahlbaum in 1863 – who was the first
psychiatrist to have classified mental illnesses on the basis of clinical course (Kahlbaum,
1863) – Kraepelin spelled out the importance of illness course in detail for mania and
melancholia. Thomas Ban once observed, ‘Many people described what was to become
manic-depressive illness but it was Emil Kraepelin who conceptualised it as a class of
illness because of his adoption of temporality as an organizing principle of psychiatric
nosology’ (Ban, personal communication, 9 November 2006).
In 1899, in the sixth edition of his textbook, Kraepelin lumped together all depression
(except that beginning in middle age) and all mania under the category manic-depression
(Kraepelin, 1899). For him, it was the sole mood disorder. There was no ‘unipolar’ depres-
sion. Kraepelin thought it a matter of indifference whether the illnesses recurred peri-
odically, or whether mania and melancholia were linked together or not. Thus, with
Kraepelin’s work what we most emphatically call ‘bipolar disorder’ ceased to be a separate
disease. The concept of alternating mania and melancholia as a disease of its own became
lost from sight because Kraepelin considered all mood disorders to be part of ‘manic-
depressive insanity’ (das manisch-depressive Irresein). Although we commonly say that
bipolar disorder is the successor of Kraepelin’s manic-depressive insanity, this is errone-
ous: Kraepelin incorporated all cases of depression and mania, alternating or not, into
manic-depression. By contrast, our use of the term ‘bipolar disorder’ implies that there is
a separate class of unipolar depression.
Two further comments about Kraepelin’s manic-depressive illness should be made.
Firstly, in later editions, he popularized Wilhelm Weygandt’s concept of the existence
of ‘mixed psychoses’; that is, manic and depressive symptoms appearing simultaneously.
Weygandt had ventured the notion in a post-doctoral thesis, which was not an automatic
guarantee of international acceptance (Weygandt, 1899, 1904).
Secondly, Kraepelin doubted that Kahlbaum’s cyclothymia represented a separate ill-
ness but was rather just a form of manic-depressive insanity in which there might be
long lucid intervals between episodes. Today’s Diagnostic and Statistical Manual (DSM-5)
positions cyclothymic disorder as separate from the main bipolar disorders (I and II)
because the hypomania and depression of cyclothymia both fall below the threshold of a
full episode of mania or of major depression (American Psychiatric Association, 2013).
The main problem with Kraepelin’s manic-depressive illness was not its nosologi-
cal adequacy – there is really no reason why the concept would not serve us quite well
today – but its prognostic desperateness: Kraepelin had a dim view of the prognosis of
most illnesses. He believed that dementia praecox went relentlessly downhill, but that
lifetime prospects for ‘MDI’ were those of unceasing recidivism. Oswald Bumke, soon to
succeed Kraepelin as Professor of Psychiatry in Munich, wrote in 1908, ‘Many physicians
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today view the chances of recovery of a patient who once falls ill with mania or melan-
cholia as far too unfavourably – because a relapse is possible but certainly not necessary’
(Bumke, 1908, p. 39). Of treatment in those days there was, with the exception of opium
for melancholia, very little talk.
The next development was elaborating the ‘two depressions’, the depression of uni-
polar disorder and the depression of bipolar disorder. Kraepelin taught in Heidelberg
and Munich. But the charge back towards bipolar disorder as a disease of its own, à la
Française, began in a different academic fortress entirely: Karl Kleist’s university clinic in
Frankfurt. Kleist was not an adept of Kraepelin and his circle identified with the intensely
biological approach to psychiatry of Carl Wernicke. It was actually Wernicke (1900) who
adumbrated in part three of his textbook, published in 1900, the first of these new bipolar
entities: hyperkinetic and akinetic motility psychosis.
For Wernicke, bipolarity was not a major issue. But for Kleist it was. Kleist’s ambition
was to continue the series of independent disease entities between manic-depressive ill-
ness and dementia praecox, which were the two great diseases that Kraepelin had estab-
lished. Between these bookends, Kleist (1911) started to insert a number of diagnoses,
some unipolar and some bipolar. It is therefore Kleist who restored bipolar thinking to
psychiatry in 1911, without challenging the existence of Kraepelin’s manic-depressive ill-
ness (which was, of course, not a bipolar illness because Kraepelin did not conceptualize
a separate unipolar depression).
In the following years Kleist identified several other cyclical psychoses, including ‘con-
fusional psychoses’ that alternate between ‘agitated confusion’ and ‘stupor’ (Kleist, 1926,
1928). The point was, for Kleist and other investigators in these years, to open up space
in between Kraepelin’s two great diseases, which were manic-depression and dementia
praecox, to find room in the middle for diagnoses with prognoses that were perhaps more
benign than Kraepelin’s terrible dementia praecox. Yet, against the great Kraepelinian
‘two-disease’ tide, Kleist’s ideas made little headway at this point.
Kleist had two very productive students, Edda Neele and Karl Leonhard, who after the
Second World War carried forward Kleist’s teachings about bipolarity. In a 1948 textbook,
Leonhard said, ‘Manic-depressive or circular insanity demonstrates two poles, which are
characterized through the manic phase or mania and the depressive phase or melancho-
lia’. Leonhard used the term ‘bipolarity’ (Bipolarität) (Leonhard, 1948, p. 88). Then in a
1949 study of all ‘cyclical psychoses’ admitted to the Frankfurt university clinic between
1938 and 1942, Neele (1949, p. 6) reinforced the terms ‘unipolar disorder’ and ‘bipolar
disorder’ (einpolige und zweipolige Erkrankungen). Kleist must have used these previously
in a teaching setting but Neele’s post-doctoral thesis (Habilitation) is their first major
public airing.
Throughout the 1940s and 1950s Leonhard burrowed away at the periodic and the
cyclical psychoses – at Frankfurt until 1955, then at Erfurt and Berlin – trying to insert
them in the larger scheme of psychiatric illness. In 1957, Leonhard’s magisterial study –
The Classification of the Endogenous Psychoses – appeared and definitively separated what
we call bipolar affective disorder from ‘pure depression’. This separation of depressive
illness by polarity remains in force in most circles today. ‘Undoubtedly there is a manic-
depressive illness’, wrote Leonhard (1957, pp. 4–5) ‘having in its very nature the tendency
to mania and melancholia alike. But next to this there are also periodically appearing
euphoric and depressive states that show no disposition at all to change to the opposite
form. Thus, there exists this basic and very important distinction between bipolar and
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monopolar psychoses’. This is the true birth, or rebirth if one will, of bipolar disorder in
contemporary psychiatry. This is the part of Leonhard’s work that went into the DSM
of the American Psychiatric Association in 1980 (see below) and, on such matters see
Shorter (2015, pp. 79–80).
Yet for the most part, Leonhard did not use the terms unipolar or bipolar in describ-
ing manic-depressive illness or the ‘pure’ depressions and manias, even though they cor-
respond nicely to our concepts of bipolar and unipolar today. Instead, in his detailed
discussions he reserved bipolar and unipolar for the ‘cyclic psychoses’, such as ‘anxiety-
euphoria psychosis’ and Wernicke’s ‘hyperkinetic-akinetic motility psychosis’. He stated
that the ‘cyclic psychoses are related to the phasic psychoses – indeed directly linked to
them. [These are] are the psychoses that Kleist brought together as cyclic. They are bipo-
lar and multiform and never result in lasting disability’ (Leonhard, 1957, p. 120).
Leonhard’s cyclic psychoses did not make it into the DSM system. He differentiated
them from the ‘periodic psychoses’ (phasic psychoses) such as manic-depressive illness
and pure depression and pure euphoria. Yet manic-depression is also cyclical, while pure
depression and pure euphoria are not. These refinements would be almost too trivial to
mention were it not for the fact that Leonhard’s schema as a whole deserves a well-informed
second look. The main point here is that Leonhard is the first author to separate depres-
sions by polarity (though generally he reserved the polarity terms for other illnesses).
Leonhard’s separation of manic-depressive illness from depression was taken up by a
handful of scholars outside of Germany, and 1966 became ‘a very good year’ for the study
of bipolar illness (for this phrase see Winokur, 1991, p. 28). In that year, three studies
appeared that distinguished among depressions by polarity, meaning the depression of
bipolar disorder (manic-depressive illness) versus the unipolar depression termed ‘mel-
ancholia’ at that time. All three studies found greater family histories of mood disorder in
bipolar patients than unipolar. However, as observed by Michael Alan Taylor: ‘they and
all others found that among the families of bipolar patients there was always more unipo-
lar than bipolar illness’ (Taylor, personal communication, 12 November 2006).
In one of these studies, Jules Angst in Zurich compared patients with bipolar disor-
der to those with endogenous depression, involutional melancholia and mixed affective-
schizophrenia. He ended up questioning ‘the nosological unity of the (Kraepelinian)
manic-depressive illness. The purely depressive monophasic and periodic psychoses are
statistically differentiated from those that have a cyclic course’ (Angst, 1966, p. 106).
Meanwhile, Carlo Perris in Sweden, adopting a specifically Leonhardian approach,
compared bipolar and unipolar depressive patients at the Sidsjon Mental Hospital in
Umea, arguing that ‘they are two different nosographic entities’ (Perris, 1966, p. 187).
It is worth noting that some feel that Angst and Perris created a monster by permitting
the use of terms such as bipolar depression and monopolar depression in suggesting the
existence of fundamentally different entities, albeit of great commercial use in registering
pharmaceutical agents for ‘bipolar depression’ and the like.
Finally, in 1966, Leonhard’s distinction between monopolar and bipolar depression
made its first American beachhead. In June 1966, at a meeting of the Society of Biological
Psychiatry in Washington DC, George Winokur and Paula Clayton of Washington
University in St. Louis, the then premier American institution for biological approaches
to psychiatry, showed that ‘the family background for manic-depressive patients differed
from that of patients who showed only depression’ (Winokur, 1991, p. 29; Winokur and
Clayton, 1967). Interestingly, despite Winokur’s presence on the team, manic-depressive
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illness did not make it into the so-called ‘Feighner criteria’, the attempt to recast psychiatric
diagnosis launched at Washington University in the early 1970s, by Feighner et al. (1972).
In the 1970s, the evolution of bipolar disorder became a primarily American, rather
than a German, story. In a reaction to the diagnostic indifference of psychoanalysis, these
years saw a new fervour in nosological thinking in the United States. Led by Robert Spitzer,
a group of researchers at the New York State Psychiatric Institute – that also included Eli
Robins of Washington University – set about defining ‘Research Diagnostic Criteria’ (the
RDC) as a way of recasting American psychiatric diagnosis. A preliminary paper pro-
duced by the group in the mid-70s (Spitzer et al., 1975) included ‘major depressive illness’
(and ‘minor depressive illness’) but made no reference to bipolar disorder. Yet by the time
a final version of the RDC was published in 1978, ‘bipolar depression with mania (bipo-
lar I)’ and ‘bipolar depression with hypomania (bipolar II)’ had been added to the RDC,
alongside ‘major depressive disorder’. There were now two big depressions firmly fixed in
American psychiatric nosology, one linked to mania as bipolar disorder and the other a
unipolar depression called ‘major depression’, although the RDC system also included a
host of other depressive subtypes and atypical forms of depression (Spitzer et al., 1978).
The RDC became the template in 1978 for the dramatic reshaping of psychiatric diag-
nosis that took place two years later, also under the leadership of Robert Spitzer, in the
American Psychiatric Association’s third edition of the APA’s Diagnostic and Statistical
Manual (American Psychiatric Association, 1980). DSM-III provided for a Leonhardian
division between unipolar depression (called Major Depression), and bipolar manic-
depression (called Bipolar Disorder). Although by this time everyone had forgotten who
Leonhard was, DSM-III represented the international triumph of one of the core con-
cepts of Leonhard’s system. The distinction between major depression and bipolar dis-
order was preserved in subsequent editions of the DSM series. Both depressions were
called ‘major depression’, but the latter was more severe in terms of chronicity and shorter
length of time between episodes.
In the following years, a large body of clinical and pharmacological opinion upheld
the distinction between bipolar and unipolar mood disorders; in other words, the dis-
tinction between two kinds of serious depression (Ban, 1990). Bernard Carroll called
bipolar disorder ‘the most extreme case of mood instability’ and said that any theory of
brain function would have to come to terms with, quoting Donald Klein, ‘this striking
phenomenon’. Carroll argued that there were fundamental biological differences between
bipolar and unipolar disorders, and although those with bipolar disorder had more life-
time episodes, the excess was: ‘entirely accounted for by the manias . . . in other words,
manic depressive patients are not just more unstable than unipolar patients in mood
regulation in both directions’ (Carroll, 1994, p. 304). Yet there must be a pendular move-
ment between the view that depression and mania are separate illnesses and the view
that linked depression-mania constitutes an illness of its own. In the 1990s, the pendu-
lum began to swing back from DSM-III and Leonhard to a more Kraepelinian view. This
movement was initiated as early as 1980 by Michael Taylor and Richard Abrams, then at
the Chicago Medical School, who wrote, after reviewing genetic and biological studies,
‘These data suggest that the separation of affective disorders by polarity may have been
premature’ (Taylor and Abrams, 1980, p. 195). Unlike previous investigators, Taylor and
Abrams based their work on well-defined rating scales and treatment response.
In 2006 Taylor, now at the University of Michigan, and Max Fink at SUNY’s Stony
Brook campus, in a major review of the diagnosis of melancholia, said of the bipolar
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versus unipolar dichotomy, ‘The scientific evidence fails to distinguish unipolar and bipo-
lar depressive disorders . . . bipolarity as a separate psychiatric disorder is not supported
by psychopathology, family studies, laboratory tests, or treatment response’ (Taylor and
Fink, 2006, p. 24). What other people see as unipolar illness, Taylor and Fink consid-
ered to be non-melancholic depression and what is bipolar depression, they considered
melancholia.
Outside of the DSM sphere, other investigators, using pharmacological ‘torches’,
proposed forms of bipolar II not envisioned in the Manual. In 2016, Jay D. Amsterdam
and Janusz K. Rybakowski, in the Oxford Handbook of Mood Disorders, recognized ‘clas-
sical’, ‘atypical’, and ‘rapid cycling’ forms of bipolar II on the basis of differential phar-
macological response to lithium, valproate, lamotrigine, and so forth (Amsterdam and
Rybakowski, 2016).
David Dunner and associates, then at the Laboratory of Clinical Science of the
National Institute of Mental Health, had differentiated bipolar II from bipolar I early in
the 1970s, writing of the ‘bipolar II group’ (Dunner et al., 1972). It was, however, only
in 1976 that Dunner and associates, now at the New York State Psychiatric Institute,
reported a large-scale clinical study of differences among bipolar I, bipolar II and uni-
polar depressed patients. The group concluded, ‘The data from the Hamilton rating scale
suggest that the symptoms of depression in patients classified as bipolar II are more simi-
lar to unipolar than to bipolar I patients’ (Dunner et al., 1976).
As the DSM series evolved after 1980, bipolar II disorder became ever more elabo-
rated. DSM-III itself dilated simply upon ‘bipolar disorder’, yet added an ‘atypical bipolar
disorder’ among the ‘atypical affective disorders’. Of this atypical form, DSM-III com-
mented, ‘Such cases have been referred to as “Bipolar II.”’ Thus, bipolar II was born.
DSM-III-R in 1987 referred to these formerly ‘atypical’ forms as ‘bipolar disorder not
otherwise specified’. One ‘example’ of this ‘NOS’ diagnosis was ‘Bipolar II’: ‘at least one
Hypomanic Episode and at least one Major Depressive Episode . . . Such cases have been
referred to as “Bipolar II”’.
DSM-IV in 1994 opened the floodgates. ‘Bipolar II Disorder’ acquired its own mono-
graph and code (296.89). It acquired its own ‘specifiers’, or variants (without codes) and
its own discussion of ‘familial pattern’, ‘differential diagnosis’, and the other standard fea-
tures of a full-fledged DSM monograph. The frequency of the diagnosis now increased
immeasurably, especially in children.
Indeed, by the time of DSM-5 in 2013, the over-diagnosis of ‘bipolar II’ in children
had become an embarrassment to the manual’s sponsors and to child psychiatry. To take
the pressure off ‘bipolar II’, DSM-5 created a new paediatric diagnosis, ‘Disruptive Mood
Dysregulation Disorder’. The manual explained, ‘DSM-IV did not include a diagnosis
designed to capture youths whose hallmark symptoms consisted of very severe, non-
episodic irritability, whereas DSM-5 . . . provides a distinct category for such presentations’
(p. 157). This, of course, was a major change. The section ‘Highlights of Changes from
DSM-IV to DSM-5’ passed over it, in the paragraph on ‘Bipolar and Related Disorders’, in
silence (p. 810). The main discussion of bipolar II in DSM-5 was close to that of DSM-IV.
As a historian, it is not my place to comment on the scientific merits of the polarity
debates, both the initial one detailed earlier and the current debate as to whether bipolar
II is an entity differing dimensionally or categorically from bipolar I disorder. Subsequent
research may well establish that bipolar II disorder is an illness in its own right, requir-
ing a distinctive therapeutic approach involving mood stabilization. In the meantime,
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however, the frequency of diagnosing the bipolar disorders seems to be growing by leaps
and bounds (Healy, 2006), and arguing for its proponents to provide rigorous diagnostic
criteria and validation data to redress such diagnostic boundary concerns.
Acknowledgements
For comments on an earlier draft I should like to thank Thomas Ban, Tom Bolwig,
Bernard Carroll, Max Fink and Michael Alan Taylor.
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The Bipolar Spectrum
Chapter
3 Chris B. Aiken
Introduction
Attempts to understand the margins of psychiatric disorders are almost as old as the
disorders themselves. Spectrum concepts have developed around schizophrenia, autism,
compulsivity, and bipolar disorder. Some of these concepts have become official classifi-
cations in their own right. The schizophrenia spectrum evolved into the Cluster A per-
sonality disorders, and the subject of this book, bipolar II (BP II) disorder, took its first
steps as part of a bipolar spectrum model.
The spectrum model differs from official nosology in taking a dimensional, rather
than a categorical, approach to diagnosis. In the categorical model, distinct disorders are
identified and clear diagnostic boundaries are presumed or proposed. In the spectrum
view, those boundaries are arbitrary markers along a continuum.
These two lenses are not incompatible, and their interplay has enriched our understand-
ing of psychiatric diagnoses. Angst (2006), who over his long career has furnished research
supporting both the categorical and dimensional models, wrote that ‘categorical classifica-
tion is fully compatible with the dimensional view.. .. The continuous distribution of both
depressive and hypomanic symptoms in the population makes the distinction between
normal and pathological difficult, just as with blood pressure and pulse rate’.
The spectrum approach has been used in several diagnostic models of mood disor-
ders. This chapter will focus on two versions of the bipolar spectrum construct:
The unipolar–bipolar spectrum, which proposes that signs, symptoms, and biologi-
cal markers of bipolar disorder range along a continuum between unipolar and bipolar
disorders.
The affective temperaments, which describes a spectrum of dimensional traits that
bridge manic-depressive illness with styles of temperament. These include dysthymic,
cyclothymic, hyperthymic, and irritable types.
Finally, this chapter will look at how concepts from the bipolar spectrum are being
applied in predictive tests of bipolar disorder, drawing from the field of evidence-based
diagnostics that has gained acceptance in general medicine. These tools, which include
the Bipolarity Index and Bipolar Risk Calculator, aim to improve the recognition of clas-
sic bipolar cases and identify those at risk for conversion to bipolar disorder.
The Unipolar–Bipolar Spectrum

As detailed in Chapter 2, Kraepelin (1921 [English Translation]) viewed the two poles
of manic-depressive illness as part of a ‘single morbid process’. That view predominated
16
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Chapter 3: The Bipolar Spectrum 17
throughout most of the twentieth century when the term manic-depressive illness was used
inclusively to describe ‘a single disorder of mood, either extreme depression or elation,
that dominates the mental life of the patient’ (DSM-II, 1968). Kraepelin had considered
separating the poles into two disorders, but concluded that ‘this classification, apparently
so simple, really encounters manifold difficulties’.
Such a division was later formulated by Leonhard (1957) and further validated in the
1960s when Angst, Perris and Winokur presented evidence that the distal ends of manic-
depressive illness were unique enough in their familial patterns and clinical course to
warrant separation into distinct disorders (Angst and Marneros, 2001). That led to the
separation of bipolar and unipolar disorders in DSM-III (1980). Almost as soon as DSM-III
was published, journal articles emerged arguing for a return to Kraepelin’s unitary
model. Taylor and Abrams (1980a, 1980b) contended that the separation was premature,
citing phenomenological, genetic, neuropsychological, electroencephalogram (EEG), and
treatment studies that suggested significant overlap within the unipolar–bipolar dichotomy.
Others began subtyping this unipolar–bipolar overlap, drawing from Kraepelin’s
observations to propose entities that had been left out of DSM-III. One of the first of
these entities was BP II, proposed by Dunner et al. (1976) while DSM-III was still being
drafted. Subsequently, Angst (1978) and Klerman (1981) presented various categories of
subthreshold bipolarity. Those models eventually culminated in a more detailed division
by Akiskal’s group (see Table 4.1) (Akiskal and Pinto, 1999; Ng et al., 2008).
Although these models divide the spectrum into categories, they view those categories as
points along a continuum that runs from depression to mania and, in some models, to psy-
chotic disorders. The propensity to mania determines where each category rests on the spec-
trum. For example, patients whose mania is unmasked only by a dementing illness are the
furthest removed from true bipolar disorder in Akiskal’s 2008 model – detailed in Box 3.1.
Akiskal’s model was followed by a proposal from Ghaemi et al. (2001) that used DSM-
style criteria to bring together the most widely accepted subtypes of the bipolar spectrum
into a single condition (see Box 3.2). Their criteria predicted conversion from unipolar
to bipolar status over a five-year period with high sensitivity (0.87) and specificity (0.92)
in a retrospective study (Woo et al., 2015), but it failed to predict non-response to anti-
depressant treatment in a secondary analysis of the Sequenced Treatment Alternatives to
Relieve Depression (STAR-D) trial (Perlis et al., 2011).
In a novel approach to defining the bipolar spectrum, Akiskal (2005) devised the ‘rule
of threes’ – effectively a list of biographical signs that were associated with bipolar disor-
der in series of 1,000 affective patients (Box 3.3). These signs appear soft, but their asso-
ciation with bipolar disorder was validated by a large internet survey of 71,247 Brazilians,
about a quarter of whom reported a history of mood disorders (Lara et al., 2015). The
Brazilian data identified further markers that differentiated those with a bipolar disorder
from those with a unipolar depressive condition, including: ≥3 provoked car accidents,
≥3 religion changes, ≥60 sexual partners, pathological love ≥2 times, reversed circadian
rhythm, high debts, frequent book reading, talent for poetry in men, and heavy cursing
and an extravagant style of dress in women. These behavioural signs can be informative
when queries of hypomanic symptoms yield ambiguous responses, but their predictive
value is limited to patients who have a history of recurrent depression.
In Akiskal’s list, the triad of trait ‘mood lability’, ‘energy activity’, and ‘daydream-
ing’ was derived from an 11-year prospective study of an National Institute of Mental
Health (NIMH) collaborative depression cohort. The presence of all three traits predicted
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Box 3.1 Akiskal’s subtypes of the bipolar spectrum

Bipolar 0 Schizophrenia
Bipolar ½ Schizobipolar disorder (manic states associated with mood incongruent
psychotic features)
Bipolar I Manic depressive illness, where mania causes severe problems
Bipolar I ½ Depression with protracted hypomania that causes moderate problems
Bipolar II Depression with spontaneous discrete hypomanic episodes that cause no
more than minor problems
Bipolar II ½ Depression superimposed on cyclothymic temperament
Bipolar III Depression with hypomania occurring solely in association with
antidepressant or other somatic treatment
Bipolar III ½ Marked mood swings in the context of substance and/or alcohol (ab)use
Bipolar IV Depression superimposed on a hyperthymic temperament
Bipolar V Recurrent depressions with mixed hypomanic symptoms during the
depression but without discrete hypomanias
Bipolar VI Manic symptoms with onset during dementia
Box 3.2 Bipolar spectrum disorder as defined by Ghaemi et al. (2001)
A. At least one major depressive episode

B. No spontaneous hypomanic or manic episodes
C. Either of the following, plus at least two items from criterion D, or both of the following plus one
item from criterion D:
1. A family history of bipolar disorder in a first-degree relative
2. Antidepressant-induced mania or hypomania
D. If no items from criterion C are present, six of the following nine criteria are needed:
1. Hyperthymic personality (at baseline, non-depressed state)
2. Recurrent major depressive episodes (>3)
3. Brief major depressive episodes (on average, <3 months)
4. Atypical depressive symptoms (DSM-IV criteria)
5. Psychotic major depressive episodes
6. Early age of onset of major depressive episode (<age 25)
7. Postpartum depression
8. Antidepressant ‘wear-off’ (acute but not prophylactic response)
9. Lack of response to ≥3 antidepressant treatment trials
conversion from unipolar to bipolar disorder with a sensitivity of 91% and specificity of
45% (Akiskal et al., 1995).
Spectrum Models of Mixed States and of Mania

In the categorical system, mania is the defining feature that separates bipolar from uni-
polar disorders. In the spectrum view, manic symptoms rise continuously from unipolar
to bipolar disorder and from normality to bipolar disorder. This view has been validated
by studies of mixed symptoms in unipolar depression and subthreshold hypomania in
community samples.
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Box 3.3 Biographical markers of hypomania (Akiskal’s ‘Rule of Three’)
>3 Major depressive episodes

3 Failed marriages
3 Failed antidepressants
3 First-degree relatives with affective illness
3 Generation family history for affective illness
Eminence in 3 fields in the family
3 Simultaneous jobs
Proficiency in 3 languages (for US-born citizens)
3 Distinct professions (exercised simultaneously)
3 Comorbid anxiety diagnoses
Triad of past histrionic, psychopathic or borderline diagnoses
Triad of trait ‘mood lability’, ‘energy activity’ and ‘daydreaming’
Flamboyance expressed in a triad of bright colours
3 Substances of abuse
3 Impulse control behaviours
Simultaneous dating of 3 individuals
DSM-III took a categorical approach to mixed states, requiring that they meet full cri-
teria for both a manic and depressive episode and allowing their diagnosis only in bipo-
lar I (BP I) disorder. When viewed through a dimensional lens, mixed symptoms occur
in unipolar as well as bipolar disorders. These are now recognized in DSM-5 as mixed
features, and a recent meta-analysis of 17 studies concluded that they are common in
both bipolar (35%) and unipolar depression (24%) when defined as three or more manic
symptoms during a depressive episode (Vázquez et al., 2018). These rates are two to three
times higher than the rates identified with DSM-5 criteria, due to the more restrictive
approach of excluding ‘overlapping’ symptoms of irritability, distractibility and psycho-
motor agitation from the mixed features specifier in DSM-5 (Perugi et al., 2015).
As suggested by the spectrum model, mixed symptoms rise dimensionally between
unipolar and bipolar disorders, without a clear cut-off separating the two (Benazzi, 2003;
Cassano et al., 2004; Kumar et al., 2017). The frequency of bipolar markers, includ-
ing family history, age of onset, course of illness, comorbid conditions, and treatment
response, also rises continuously along this spectrum, with unipolar-mixed depression
forming an intermediate zone between the extremes of pure unipolar and full bipolar
conditions (Akiskal and Benazzi, 2003; Cassano et al., 2004; Diler et al., 2017; Ferentinos
et al., 2017; Perugi et al., 2015). However, unipolar mixed states appear to be a stable
entity and convert to full bipolar disorder at a relatively low rate, which Stahl et al. (2017)
quantified at 13–16%.
Much as yellow and blue make green, the overlap of hypomanic and depressive symp-
toms creates a unique presentation that is more complex and severe than the purer mood
states (see Box 3.4 and ‘Dark Hypomania’ in Table 4.7). Treatment of mixed states is dif-
ficult, with higher rates of side-effects and lower rates of response. Compared to the purer
moods, these patients have more comorbid conditions, including anxiety, substance abuse,
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Box 3.4 Clinical presentation of depressive mixed states (from Koukopoulos et al., 1992)
Objective findings Mood lability from melancholic to dysphoric, despair, dramatic expressions
of suffering, bouts of weeping, vivacious facial expression, talkativeness,
psychic and/or motor agitation, emotional lability, impulsive suicidal
attempts, high diastolic blood pressure
Patient complaints Anxiety, inner tension, irritability, anger, despair, suicidal impulses, crowded
and/or racing thoughts, rumination, initial or middle insomnia
Family report Incessant complaints, irritability, occasional verbal outbursts, occasional
physical aggression, occasional hypersexuality
Box 3.5 The bipolar specifier
Episode of elevated mood, irritable mood, or increased activity with at least 3 of the DSM-IV criteria
B mania symptoms
At least one of the following consequences: (a) unequivocal and observed change in functioning
uncharacteristic of the person’s usual behaviour, (b) marked impairment in social or occupational
functioning observable by others, (c) requiring hospitalization or outpatient treatment
No minimum duration of symptoms, no exclusion criteria
personality disorders, trauma, head injury, and medical disorders (Vázquez et al., 2018).
Suicide rates are elevated in this population and have been associated with antidepressant
treatment (Stahl et al., 2017).
Pure hypomania also occurs on a spectrum between unipolar and bipolar disorders,
with short duration hypomanias bridging the two disorders. As with the unipolar mixed
states, patients with short duration hypomania also represent an intermediate phenotype
between unipolar and bipolar disorder, according to studies of associated illness markers
(e.g., family history, age of onset, recurrence of depression, comorbid conditions, and
treatment response) (Miller et al., 2016; Nusslock and Frank, 2011).
Manic symptoms also rise dimensionally between the normal and bipolar popula-
tions. This was explored in the Zurich study, which prospectively evaluated hypomanic
symptoms over 20 years in a community sample of 4,547 young adults. The Zurich study
offered a rare glimpse of hypomanic symptoms in the normal population. Though these
subjects lacked a history of clinical depression, they were not simply ‘the happier nor-
mals’ and had elevated rates of impulsivity, irritability, sleep disturbance, binge eating,
and substance abuse (Gamma et al., 2008). Validators of bipolarity, such as family history
and associated features, rose continuously as the number and duration of hypomanic
symptoms increased (Angst and Dobler-Mikola, 1984; Angst et al., 2003).
The Zurich study was designed to explore the optimal cut-off criteria for hypomania.
From that work Angst developed the Bipolar Specifier (2011), a simplified definition of
hypomania that removed the duration and exclusion criteria from DSM-IV and, at the
same time, tightened the definition by requiring an unequivocal change in functioning
(Box 3.5). The Bipolar Specifier was compared to the DSM-IV criteria in a multinational
study of 5,635 patients with depression. Although only one-third of the patients who met
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Table 3.1 The affective temperaments
Temperament Limitations Strengths

Dysthymic Self-critical, non-assertive, avoidant, Hard-working, dependable, fair-minded
rejection sensitive and ruminative and realistic
Hyperthymic Glutinous, meddlesome, impatient, Extroverted, charismatic, energetic,
hot-tempered, distracted, impulsive, upbeat, confident, many interests,
and unfaithful leadership ability. They have a low need
for sleep (<6 hours) but also complain of
sleep disturbance
Cyclothymic Inconsistent cycling from energized Intuitive, empathic, open, creative,
to sluggish, extroverted to withdrawn, spontaneous, and sensitive to the
passionate to disinterested, impulsive environment. These traits can lead to
to inhibited. This leads to instability in success in the arts, hospitality industry
relationships, work, and avocations and customer service
Irritable Dissatisfied, on edge, reactive, quick Skeptical, iconoclastic, independent, and
tempered, and jealous assertive
the Bipolar Specifier criteria also qualified for a DSM-IV bipolar diagnosis by their symp-
toms, markers of bipolarity were similar among both the DSM-IV and Bipolar Specifier
defined-group, such as age of onset, family history, course of illness, comorbid condi-
tions, and response to antidepressants (Angst et al., 2011).
The Affective Temperaments

Temperament is a component of personality that refers to stable, enduring traits with
a strong biological foundation, such as energy, sleep, chronotype, emotional reactivity,
novelty seeking, harm avoidance, and reward dependence. The affective temperaments
are positioned as unique traits that exist in those who lie on a continuum between mood
disorders and normal personality.
Although rooted in works of the ancient Greeks, the modern affective temperaments
were first described by Kraepelin (1921 [English Translation]). He described depressive,
manic, irritable, and cyclothymic types that occurred with ‘special frequency. . . in the
families of manic-depressive patients’. Kraepelin’s rich descriptions were later formalized
by Akiskal in the Temperament Evaluation of Memphis, Pisa and San Diego (TEMPS)
scale, which has since been extensively validated in 27 studies spanning 15 countries and
involving over twenty thousand subjects (Elias et al., 2017).
Table 3.1 outlines the cardinal features of these temperaments with an emphasis on
their healthier aspects that can be leveraged in psychotherapy. The hyperthymic and
dysthymic types are considered pure forms, corresponding to the two poles of manic-
depressive illness, while the other two are thought to arise from the continuous overlap
(irritable) or rapid alteration (cyclothymia) of the purer types (Gonda and Vázquez, 2014).
Prominent affective temperaments are found in 13–20% of the general population
(Vázquez et al., 2012) and approximately half of the bipolar population (Vöhringer et al.,
2012). The hyperthymic and cyclothymic temperaments predominate in bipolar popula-
tions, the dysthymic in unipolar, and the irritable seemingly evenly distributed in both
(de Aguiar Ferreira et al., 2013; Gassab et al., 2008; Serra et al., 2015).
The hyperthymic trait has a variable relationship to bipolar disorder. While some
studies have linked it to bipolarity (DeGeorge et al., 2014; Gandotra et al., 2011), others
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have observed it more frequently in those in the normal population (Evans et al., 2005;
Mendlowicz et al., 2005; Vázquez et al., 2008). As a predictor of conversion from unipolar
to bipolar disorder, its capacity is poor (Woo et al., 2015). Pharmacologic studies also
point toward significant heterogeneity. In bipolar populations, the hyperthymic trait is a
risk factor for antidepressant-induced hypo/mania (de Aguiar Ferreira et al., 2014; Henry
et al., 2001; Tondo et al., 2013), while in unipolar populations it predicts complete remis-
sion on antidepressants (de Aguiar Ferreira et al., 2014).
Temperament is a stable trait while mood disorders are episodic, but the two can
overlap in ways that influence the presentation of episodes. When superimposed on
dysthymic traits, hypomania may manifest through overwork rather than more pleasur-
able pursuits. Those with dysthymic, cyclothymic, and irritable temperaments are more
prone to mixed than pure presentations of mania (Röttig et al., 2007). Temperament also
influences predominant polarity, shifting the expression of bipolar disorder towards the
depressive pole among dysthymic types and the manic pole among hyperthymic types
(Henry et al., 1999).
Among the affective temperaments, cyclothymia has stronger associations with BP II,
while the others distribute more evenly between BP I and BP II (Gonda and Vázquez,
2014). The overlap of BP II and cyclothymia creates a constellation of symptoms of some
relevance to borderline personality disorder.
Cyclothymia, Bipolar II ½ and Borderline Personality Disorder

When cyclothymic traits overlap with BP II they shift the expression of hypomania toward
mixed (or ‘dark’) states. The nature of those ‘dark’ symptoms, as shown in Table 3.2, her-
ald a stormier course, with earlier onset and more comorbid conditions, suicidality, and
borderline personality features evident than in their pure BP II counterparts. Akiskal
called this overlap condition bipolar II ½ and hypothesized that it represented the affec-
tive component of a borderline personality disorder (Akiskal et al., 2003).
Akiskal et al. (2003) identified bipolar II ½ in a substantial minority (i.e., 38%) of BP II
patients. That 38% figure is identical to the rate of borderline personality disorder in
those with a BP II condition, according to a recent meta-analysis (Fornaro et al., 2016),
raising the possibility that investigators are identifying the same patients with different
diagnoses.
Table 3.2 Sunny vs. dark hypomania (Akiskal et al., 2003)
Sunny hypomania Dark hypomania

Less sleep More traveling, imprudent driving
More drive and energy Excess shopping and spending
More self-confident Foolish ventures in business
Increased work motivation More irritable, impatient
Increased social activity Attention easily distractible
Increased physical activity Increased sex drive and interest in sex
More plans and ideas Increased consumption of coffee, cigarettes
Less shy, less inhibited Increased consumption of alcohol
More talkative than usual
Extremely happy mood, over-euphoric
More laughing
Faster thinking, more puns and jokes
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Other lines of research have identified shared personality traits in cyclothymic and
borderline personality disorders. Both are high in neuroticism and low in agreeableness
and conscientiousness (Kendler et al., 2011; Rózsa et al., 2008; Walsh et al., 2012). The two
disorders also share elevations in the seemingly opposing traits of harm avoidance and
novelty seeking (Fassino et al., 2009; Maremmani et al., 2005), a paradoxical constellation
that may explain the elevated rates of substance abuse, self-harm, and suicide attempts
described in both these groups (Apfelbaum et al., 2013; Guerreiro et al., 2013).
It is the overlap of these two disorders that has stirred much of the controversy around
the bipolar spectrum. There is a concern that viewing borderline personality disorder as
a mood disorder will steer clinicians towards pharmacotherapy in place of psychotherapy
(Paris, 2012). That is a valid concern, but it derives more from the DSM’s classification of
cyclothymia as a mood disorder than from the spectrum model, which recognizes it as a
temperament-based condition.
In reality, psychotherapy has the best evidence for the treatment of cyclothymic dis-
order, but there are no randomized, placebo-controlled pharmacotherapy trials for this
condition (Fava et al., 2011). Akiskal warns against ‘aggressive mood stabilization’ for
those with the affective temperaments, writing that ‘for the patient to trust a psychiatrist,
he or she must respect the patient’s temperament and individuality, that indeed his or her
aim is to bring out the optimum in what is positive and desirable in [the] patient’s tem-
perament’ (Akiskal and Akiskal, 2011).
An integrated view of cyclothymia and borderline personality disorder need not
favour pharmacotherapy of necessity and could lead instead to a helpful cross-fertilization
of psychotherapies. For example, both groups have irregular circadian rhythms (Fleischer
et al., 2012). Techniques to modulate those rhythms are well-established in bipolar disorder
and are beginning to be explored in borderline personality disorder (Bromundt et al., 2013).
The skill-building therapies commonly used for borderline personality disorder could
also be helpful for cyclothymia. The Systems Training for Emotional Predictability and
Problem Solving (STEPPS), which builds skills for impulsivity and anger, is currently
undergoing a controlled trial for patients with comorbid bipolar and borderline person-
ality disorder (Riemann et al., 2014), and a skill-building psychoeducational group has
recently been developed for cyclothymic disorder (Perugi et al., 2017).
Medication is sometimes used in those with a borderline personality disorder, and
an understanding of its relationship to bipolar disorder may also prove useful there. For
example, a recent Cochrane review of borderline personality disorder drew conclusions
similar to the guidelines for bipolar disorder. Second-generation antipsychotics, mood
stabilizers, and omega-3 fatty acids had the best support, and there was ‘inadequate evi-
dence’ for antidepressants (Stoffers et al., 2010). Such conclusions present a challenge to
current standards of practice, as antidepressants are often used in this population, but
the conclusion has been confirmed in two recent reviews (Hancock-Johnson et al., 2017;
Ripoll, 2012). Other studies have identified borderline personality disorder as a risk fac-
tor for antidepressant-induced mood destabilization (Barbuti et al., 2017), particularly
with the tricyclic class (Links et al., 1990; Soloff et al., 1986, 1987).
Recognition of the Bipolar Spectrum in DSM

Since DSM-III, each successive edition of the manual has absorbed concepts previ-
ously relegated to the bipolar spectrum in refining the classification of mood disorders,
https://doi.org/10.1017/9781108333252.004
Table 3.3 Evolution of bipolar spectrum concepts in recent DSM manuals
DSM disorder Entry into DSM Spectrum concept

Bipolar I disorder DSM-III (1980) Not applicable
Cyclothymic disorder DSM-III (1980) Cyclothymic temperament
Hypomanic syndrome DSM-III-R (1987) Bipolar II (Dunner et al., 1976)
Bipolar II disorder DSM-IV (1994) Bipolar II (Dunner et al., 1976)
Antidepressant-induced hypo/ DSM-5 (2013) Bipolar III (Akiskal and Pinto, 1999)
mania1
Substance/medication-induced DSM-5 (2013) Bipolar III ½ (Akiskal and Pinto, 1999)
bipolar and related disorder2
Major depressive disorder and DSM-5 (2013) Various models describing partial mixed
bipolar disorder with mixed states in bipolar and unipolar disorder (e.g.,
features Akiskal, Angst, Benazzi and Koukopoulos)
Short duration hypomania Conditions for further Bipolar specifier (Angst et al., 2011)
study in DSM-5 (2013)
1
DSM-5 allows antidepressant-induced hypo/mania to count toward a diagnosis of bipolar disorder as long
as the symptoms persist at a full syndromal level beyond the physiological effects of the medication.
2
Before DSM-5, mania due to substance use was not recognized as a variant of bipolar disorder and instead
was classified as substance-induced mood disorder.
including the addition of BP II in DSM-IV (1994). Although the current edition (DSM-5,
2013) maintains the separation of unipolar and bipolar disorders, its overall organization
bears a closer resemblance to Kraepelin’s unitary hypothesis than DSM-III had in 1980.
For practical reasons, DSM-5 remains a categorical system. Categories are useful for
controlled trials, and standardized boundaries, however arbitrary, allow the results of
those trials to be more readily translated into clinical practice. A closer look at the man-
ual, however, reveals the influence of a dimensional approach. Kupfer, the DSM-5 com-
mittee chair, wrote that depression and bipolar are part of ‘a continuum, with variable
expressions of vulnerability to hypomania or mania’ (Phillips and Kupfer, 2013).
Table 3.3 traces the evolution of spectrum concepts through the different editions of
DSM, with most of the shift occurring in DSM-5. More research is needed on the preva-
lence of these DSM-5 disorders, but initial studies suggest that their rates approach those
suggested by the bipolar spectrum concept. The Bipolar Disorders: Improving Diagnostic
Guidance and Education (BRIDGE) studies applied some of the DSM-5 criteria to two
large multi-national samples (total n = 8,446), and offer an approximation of their fre-
quencies in a sample of depressed patients (Angst et al., 2011; Perugi et al., 2015): 10%
having BP I by DSM-IV criteria, 6% having BP II by DSM-IV criteria, 18% being cases
of antidepressant-induced hypo/mania that were excluded by DSM-IV criteria but would
count towards a bipolar diagnosis in DSM-5, 7% having unipolar depression with mixed
features by DSM-5 criteria, and 59% having unipolar depression without mixed features.
Taken together, those figures suggest that 41% of depressed patients would be rec-
ognized in DSM-5 with a disorder previously considered part of the bipolar spectrum,
including BP I and II. This study needs replication as it may have been prone to selection
bias, but it does approach the rate of bipolar spectrum disorders reported before DSM-
5, which ranged from 40 to 50% of depressed patients (Angst et al., 2011; Nusslock and
Frank, 2011).
https://doi.org/10.1017/9781108333252.004
The Bipolar Spectrum as a Predictive Tool

With much of the bipolar spectrum construct absorbed into DSM-5, many of its concepts
have been repurposed as predictive diagnostic tools. These are modelled after similar
tools in general medicine, where signs, symptoms, and laboratory tests are considered in
light of their diagnostic sensitivity and specificity. Evidence-based tests are much needed
for mood disorders, given the problem of both over-diagnosis and under-diagnosis of
bipolar disorder (Nusslock and Frank, 2011), the poor reliability of structured diagnostic
interviews for detecting mania (Regier et al., 2013), and the long delays in making an
accurate diagnosis (Hirschfeld et al., 2003).
Among the features associated with the bipolar spectrum, antidepressant-induced
hypo/mania is the strongest predictor of conversion from unipolar to bipolar disorder,
which explains why it is now recognized as a bipolar type in DSM-5. In two studies,
100% of patients who experienced that reaction went on to develop full bipolar disorder
after an average follow-up of three years (Akiskal et al., 1983; Strober and Carlson, 1982).
Other predictors of conversion include: family history of bipolar disorder, younger age
of onset, male gender, certain comorbidities (psychosis, substance abuse, eating disor-
ders, anxiety disorders), mixed features, antidepressant treatment-resistance, and a more
severe, chronic, or recurrent course of depression (Kessing et al., 2017; Serra et al., 2015;
Takeshima and Oka, 2013).
The Bipolarity Index

The Bipolarity Index is a clinician-rated scale that gives an estimate of diagnostic con-
fidence about the presence of a bipolar disorder (Aiken et al., 2015). The scale is based
on the work of Robins and Guze (1970), who proposed validating psychiatric disorders
along five dimensions: signs and symptoms, age of onset, course of illness, response to
treatment, and family history. The Bipolarity Index consists of 50 items across those five
dimensions, each weighed according to the strength of their association with the classical
form of bipolar disorder.
The Index encourages clinicians to think in probabilistic terms about a bipolar diag-
nosis. Higher scores are not indications of severity but of a greater likelihood of a true
bipolar diagnosis. In line with that emphasis, higher scores in the STEP-BD study were
associated with a more favourable response to mood stabilizers (Del Debbio et al., 2007).
Clinical trials have used the Index to improve the specificity of the diagnostic process
by minimizing false positive subjects. For example, it can identify patients who endorse
manic symptoms but lack other features of bipolarity, a scenario that often occurs with
post-traumatic stress disorder, attention deficit disorder, and borderline personality dis-
order (Aiken et al., 2015).
A cut-off point of 50 has been suggested from cross-national studies (total n = 3,305),
where it performed with very high sensitivity (0.8–0.9) and specificity (0.8–0.9) in distin-
guishing DSM-based bipolar disorder from unipolar depression (Aiken et al., 2015; Ma
et al., 2016; Zaravinos-Tsakos et al., 2017), and, in one study, from Cluster B personality
disorders (Apfelbaum et al., 2013).
The Index can be quickly completed during an intake interview and is available online
at www.moodtreatmentcenter.com/bipolarityindex.pdf, while a modified patient-rated
version called the MoodCheck is available through www.psycheducation.org. Although
its ability to predict the conversion from unipolar to bipolar disorder has not been tested,
https://doi.org/10.1017/9781108333252.004
most of the individual items on the scale have been validated for that use (Kessing et al.,
2017; Serra et al., 2015; Takeshima and Oka, 2013; Woo et al., 2015).
Bipolar Risk Calculator

The spectrum concept has also been applied to staging systems for bipolar disorder, simi-
lar to those used in cancer and renal disease. Here, the spectrum runs from those with
prodromal features who are at risk for bipolar disorder to those with the full disorder
and, at the later stages, experience frequent recurrences or a persistent unremitting illness
(Kapczinski et al., 2014). Spectrum concepts help identify prodromal cases of bipolar dis-
order, and the Bipolar Risk Calculator is a tool that can estimate that risk in the offspring
of a bipolar parent (Hafeman et al., 2017).
The calculator was built from broad symptom-based scales and is available online at
www.pediatricbipolar.pitt.edu. It performed well in a five-year study, with a balance of
sensitivity and specificity that compared favourably to risk calculators used in general
medicine. A younger age of onset in the parent was the strongest predictor of conversion.
Although the study measured symptoms of depression, mania, and anxiety, it was the
overall severity of symptoms rather than any particular cluster that predicted conversion
to bipolar disorder (Hafeman et al., 2017).
Conclusions and Implications for Treatment

The bipolar spectrum construct proposes that bipolar disorders are connected to other con-
ditions along continuous dimensions of signs and symptoms. Evidence has been presented
supporting continuums between both bipolar and unipolar disorders as well as between
bipolar disorder and the normal population (via personality traits). Manic symptoms rise
continuously between these groups, and signs of bipolarity rise in concert along with them,
such as rates of family history, course of illness, and treatment response variables.
This theory has led to a probabilistic approach that uses disease markers to enhance
diagnostic accuracy. This is an important advance for bipolar disorder, where symptom-
driven tools evidence low sensitivity and poor reliability (Aiken et al., 2015; Zimmerman
et al., 2011), particularly in BP II patients who often present with mixed states, com-
plex comorbid conditions, and mercurial symptoms that cross into many diagnostic
categories.
A limitation of the spectrum concept is the difficulty of applying continuous dimen-
sions to clinical trials. The categorization of spectrum concepts in DSM-5 has led to pro-
gress in that area, and treatment guidelines are now available for two categories on the
spectrum: depression with mixed features (Stahl et al., 2017) and the bipolar prodrome
(i.e., adolescents who have mood symptoms and a first-degree relative with bipolar dis-
order) (Schneck et al., 2017).
One point of consensus is that antidepressant monotherapy should be avoided in
patients with mixed features, whether unipolar or bipolar, due to the risk of mood desta-
bilization with these agents. This is especially true in children and adolescents, where
antidepressants carry the additional risk of suicidality. Thus, in the guidelines for mixed
depression, antidepressants are only used in combination with a mood stabilizer, and
even then are generally third-line options. For adolescents with the bipolar prodrome,
antidepressants are avoided altogether in the presence of mixed features (Schneck et al.,
2017; Stahl et al., 2017).
https://doi.org/10.1017/9781108333252.004
That caution extends to patients with short-duration hypomania. In the large, inter-
national BRIDGE study, the rate of mood destabilization with antidepressants rose in
concert with the length of hypomania: 0.7% for no hypomania, 8.7% for 1 day, 14% for
2–3 days, 27% for 4–6 days and 37.9% for ≥ 7 days (Angst et al., 2012).
Treatment is less clear for unipolar patients who lack mixed or manic symptoms but
have markers of bipolarity such as family history of bipolar disorder, early age of onset, or
a high recurrence of depression. Studies are mixed on whether those features predict anti-
depressant treatment-resistance (Correa et al., 2010; Perlis et al., 2011), although they do
appear predictive of antidepressant-induced hypo/mania (Barbuti et al., 2017). Outside
of antidepressants, treatments with efficacy in both unipolar and bipolar depression are
useful options for this group including lithium, pramipexole, and certain atypical antip-
sychotics; as well as light therapy, omega-3 fatty acids, and psychotherapy (Aiken, 2007;
Bromundt et al., 2013; Stahl et al., 2017).
Long-term medication treatment may be necessary for highly recurrent cases, but
it should not be the default option for all patients on the spectrum as it is for BP I.
Lamotrigine and lithium have good data for long-term prevention, and their benefits
against the depressive pole make them good options for spectrum disorders (Phelps,
2016). Research also supports lamotrigine’s benefits in two of the most common sub-
types on the spectrum: depression with short-duration hypomania and the constellation
of cyclothymia and/or borderline personality disorder (Hancock-Johnson et al., 2017;
Manning et al., 2005; McCraw and Parker, 2016), but lamotrigine has not proven benefi-
cial in pure unipolar depression (Reid et al., 2013).
Some patients on the spectrum can be treated with psychotherapy alone. Controlled
trials support this approach for cyclothymia and, in the form of family therapy, for ado-
lescents with prodromal bipolarity (Fava et al., 2011, Schneck et al., 2017).
Weaknesses of the bipolar spectrum model relate to its potential for misuse, whether
through diagnostic or pharmaceutical expansion, or through stigmatization of those
identified with it. The bipolar spectrum should not be confused with a bipolar diagnosis,
and its treatment may diverge from standard bipolar therapies. The spectrum is not a
diagnosis at all, but a marker of risk and a guidepost in a zone of uncertainty.
Further Reading
For professionals: Phelps, J. (2016). A Spectrum For patients: Aiken, C. and Phelps, J. (2017).
Approach to Mood Disorders: Not Fully Bipolar, Not So Much: Understanding Your
Bipolar but Not Unipolar – Practical Mood Swings and Depression. New York:
Management. New York: W. W. Norton. W. W. Norton.
Online: www.psycheducation.org
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Carolina; She Makes Her Appearance, Destroys One Union Vessel, and
Injures Several Others; Lieutenant Cushing; His Singular Character and
Daring Adventures; He Sinks the Albemarle with a Torpedo, while she is
Lying at a wharf; His Official Report; His Subsequent Career; His Death.
FORT FISHER. DECEMBER A. D. 1864,

JANUARY A. D. 1865.
mportance of the Place to the Confederates; The Largest Fleet That Ever
Sailed Under the American Flag Invests It, Under Admiral Porter; The
Army Co-operates With the Fleet; Failure of the First Attack; Gen. Terry
Arrives With Reinforcements, and a Fresh Investment of the Place Begins
January 13th, 1865; Details of This Famous Engagement; Fort Fisher
Surrenders; Appearance After the Battle; Other Incidents; Blockade-
runners. II-273
DEEDS OF VALOR ON THE SEAS.

Captain Silas Talbot; Ancestry; In the American Camp; Commands a Fire- II-289
Ship; Grapples the “Asia”; Promoted; Captures the “Pigot”; Again
Promoted; Fits Out the “Pigot” and the “Argo”; Captures three Prizes from
the West Indies; The “King George”; A Terror to the Coast; Talbot Captures
the “King George”; “Argo” Returned to her Owners; Talbot in Command of
a Private Armed Ship; Captured by an English Fleet; The Notorious Prison
Ship “Jersey”; Taken to England; Dartmoor Prison; Three Attempts at
Escape; Exchanged for an English Officer; At Paris; Sails for America;
Captured by a Privateer; Reaches New York; Retires to a Farm; Selected
to Command a New Frigate; In Command of “Old Ironsides”; Captures the
“Sandwich”; Questions of Rank; Withdraws from the Service; Buys Land in
Kentucky; Characteristics; Death; Burial in Trinity Church, New York; The
Whaleboat Men of the Revolution; George Raymond; The Connecticut
Fleet; A Terror to the British; Daring Leaders; Captain Mariner; Captain
Hyde; Mariner Visits a Tavern in Disguise; Major Sherbook Denounces
Mariner; Mariner Searches the Major’s House; Captures the Major;
Captain Hyler at Egg Harbor; Captures an English Corvette; Hyler Visits
New York in Disguise; Searches for a Notorious Tory; Captures an East
Indiaman; Hyler on Land; Captures a Hessian Major; Captures four
Trading Sloops; Usefulness of the Whaleboat Men ended with the War;
Captain James Drew; In the English Service; Persecuted by a Lieutenant;
Knocks his Persecutor Down; Escape by Swimming; Arrives at
Philadelphia; Goes to France; In Command of the “De Brock”; Loaded with
Gold and War Material; Lands in Maryland; Cargo Escorted to Wilmington;
Arms to Headquarters; Treasure to a Mansion; The Gold Stolen; Drew
Mans his Ship; Fights an English Ship; Drew’s Former Persecutor in
Command; The Duel on the Deck; Drew Kills the Commander and
Captures the Ship; Drew’s Marriage; Captures two Prizes of Immense
Value; Drew’s Fatal Banquet; Loss of the “De Brock”; Drew’s Body
Washed Ashore; The Churchyard at Lewes, Delaware; Stephen Decatur;
Story of the Barbary Pirates; The Frigate “Philadelphia”; Captured by
Pirates; The Bashaw of Tripoli; The “Philadelphia” added to the Bashaw’s
Fleet; The “Mastico”; Decatur Burns the “Philadelphia”; Chased by Pirates;
Commodore Preble; Submission of the Bashaw; McDougall and the
“Wyoming”; Searching for the “Alabama”; In Japanese Seas; The Prince of
Nagato; Independent Pirate; His Captures; Fires on the “Pembroke”;
McDougall at Simonoseki; Fights three Japanese Vessels and Shore
Batteries; Disables the Ships; Silences the Batteries; Demands Indemnity;
The Share of the United States; Captain McGiffen; Graduate of Annapolis;
In the Chinese Service; Battle of the Yalu; Battle between Modern Ships;
The Chen Yuen; Desperate Fighting; McGiffen Thrashes a Coward; Five
Hours Action; McGiffen Terribly Wounded; Returns to America a Physical
Wreck; His Death.
OUR NEW NAVY.

Use of Armor for Ships; Harveyized Nickel Steel; Modern Explosives;
Vessels of the New Navy; The Question of Fuel; Torpedo Boats; Torpedo
Catchers; Speed; The Navies of Europe; Of China and Japan; Need of a
Better Navy; Merchant Vessels; Ship Yards; Machinery; Duty of Officers;
Training of Officers; The Naval Academy; History of the Institution; Course
of Instruction; Marine Corps; Revenue Marine; Marine Hospital Service;
Light Houses; Training Ships; Life Saving Service; The Flag. II-337
THE EXPLOSION OF THE MAINE.

The Maine at Havana; The Explosion; Loss of Life; Captain Sigsbee’s
Telegram; Description of the Maine; Divers and Wrecking Apparatus; The
Flag Hauled Down; Naval Board of Inquiry; The Testimony; The Finding of
the Court; Feeling in the United States; Forbearance of the Nation;
Chaplain Chidwick; Rumors of Retaliation; The President and his Advisers. II-398
DEWEY’S ACTION AT MANILA.

First Serious Encounter between the United States and Spain; The II-415
Philippine Islands; Area and Population; Discovery of the Group; Religious
Orders; Island of Luzon; City of Manila; Commerce and Manufactures; Bay
of Manila; Arrival of the United States Squadron; Partial Destruction;
Breakfast; Bombardment Resumed; Complete Destruction of the Spanish
Ships and Forts; Dewey’s Despatch; Vessels Composing American Fleet;
The Action in Detail; Secretary of the Navy Congratulates Dewey;
Congress Votes a Sword for Dewey; Medals for Officers and Men; Dewey
Made a Rear Admiral.
List of Illustrations
Page
0. Deck of Battleship Indiana Frontispiece.
1. Engagement between Serapis and Bonhomme Richard II-16
2. Medal Awarded to John Paul Jones II-43
3. The Wasp Boarding the Frolic II-44
4. Capture of the Guerriere by the Constitution II-51
5. Perry’s Victory on Lake Erie II-66
6. McDonough’s Victory on Lake Champlain II-134
7. Capture of the Cyane and Levant by the Constitution II-151
8. Engagement between the Monitor and Merrimac II-170
9. New Orleans—Fleet Passing Forts Jackson and St.
Philip II-187
10. Sinking of the Alabama by the Kearsarge II-211
11. The New Battleship Kearsarge II-218
12. Farragut Entering Mobile Bay II-242
13. Le Solferino, 1865 II-255
14. Lieut. Cushing’s Torpedoboat Sinking the Albemarle II-259
15. Monitor Fleet in a Gale off Fort Fisher II-278
16. The Miantonomoh II-295
17. Gunboats on Western River II-295
18. The Clermont—Fulton’s First Steamboat—1807 II-319
19. Fight with Algerine Pirates II-319
20. Cruiser Following Torpedo into Action II-330
21. Battleship Indiana II-347
22. Cruiser Baltimore II-354
23. Battleship Texas II-363
24. Cruiser Chicago II-370
25. Battleship Oregon II-375
26. Cruiser Cincinnati II-386
27. Cruiser Newark II-391
28. Blowing Up of the Maine in Havana Harbor II-399
29. Ram Katahdin II-405
30. Admiral Dewey and his Flagship Olympia II-414
31. Map of Manila Bay II-419
32. The Battle of Manila—The American Fleet II-424
33. The Battle of Manila—The Spanish Fleet II-425
Naval Battles of America.
SERAPIS AND BONHOMME RICHARD. A. D. 1779.
his remarkable action is interesting not only on

account of its bloody and desperate character, and
on account of the sensation it produced at the time,
but because it illustrates one phase of our great
struggle for independence; a considerable space is
therefore devoted to it.
The hero of this action, John Paul, was born at
Kirkcudbright, in Scotland, July 6th, 1747; and was
sent to sea, as an apprentice, at the age of twelve.
He afterwards made voyages as mate of a slaver,
then an honored and recognized employment for a
portion of the English merchant marine.
At twenty-one he had command of a vessel in
the West India trade, so that his merits as a seaman were early
recognized. He afterwards became a trader in a vessel of his own.
At the age of twenty-six he left the sea; and adopted the name of
Jones. The reason for this does not clearly appear. He may have
had some old scores to clear; and, settling in a new world, may have
thought a new name necessary.
In December, 1775, he was appointed a First Lieutenant in the
United Colonial Navy, and ordered to the Alfred, our first flag-ship.
He hoisted the first flag of the Colonies afloat; a yellow flag, with the
pine tree and rattlesnake. In this ship he participated in several
actions; and was afterwards in command of the Providence, when he
only escaped capture by excellent seamanship. He made many
prizes in this ship.
On Oct. 10th, 1776, he was named the 18th naval captain, and, in
command of the Alfred and Providence, captured a valuable armed
ship, and other prizes, again eluding recapture by good seamanship.
He next went to European waters in command of the Ranger, 18,
and there received, from a French squadron, the first salute to the
Stars and Stripes, by this time adopted.
He cruised in English waters, burning ships at White Haven, and
spiking guns in batteries on shore; and then attempted to carry off
the Earl of Selkirk. In this he failed, but having carried off some of
that nobleman’s plate, was branded by the English as a pirate. This
epithet came with a bad grace from a nation then celebrated for
thorough “looting” of every place which came into their hands, in
India, and elsewhere. The real offence was that Jones was an
English subject, who had renounced his allegiance, and was serving
against the mother country; like all the rest of those engaged in the
Revolution. During this cruise in the Ranger he took the Drake, of 20
guns.
After this he received from the French government an old
Indiaman, called the Duc de Duras, which he renamed the
“Bonhomme Richard,” or Poor Richard, in allusion to the publication
by Benjamin Franklin.
He had some other armed vessels, mostly “letters of marque,”
under his command.
The Bonhomme Richard had 40 guns, and a mixed crew, of
various nationalities. Jones sailed under such hampering restrictions
that he was prevented from carrying out many promising projects;
but at last, on the 23d of September, he fell in with a Baltic fleet of
merchantmen, convoyed by the English frigate Serapis, 44, and the
Countess of Scarborough, 20. The result of the engagement which
ensued will be given hereafter.
To continue the sketch of Jones himself, we may say that, in 1780,
the year after this action, he sailed for the United States, in the Ariel,
20, but lost his masts in a severe gale of wind, and was obliged to
return to France; whence he sailed again and arrived safely, about
the beginning of 1781.
He was then launched in the America, 74, which was presented by
our Government to the French; and he made a cruise in her as a
volunteer.
In 1783 he was prize agent of the United States in Europe; and
finally, in 1787, while in Denmark, he resigned, and entered the
Russian Navy—hoisting his flag, as Rear Admiral, in the “Vladimir,”
on the 28th of June, 1788. He found so much jealousy and enmity
towards him that he resigned in about a year.
Afterwards he resided in Holland and France, and was appointed
Commissioner of the United Slates to Algiers—but his death
occurred at this time, at the age of forty-five.
And now, to return to his cruise in the Bonhomme Richard:—
Paul Jones had obtained so much celebrity for his cruise in the
Ranger, that, after that ship departed for America he remained in
France, in the hope of receiving a more important command.
During the years 1778-9 various projects were discussed, in which
he was to have a part. One idea was to make a descent upon
Liverpool, with a body of troops to be commanded by La Fayette.
These plans all came to nothing, and his offers of service were
repulsed; until at last a singular arrangement was proposed to him.
M. de Sartine, French Minister of Marine, in a letter of February,
14th, 1779, states that the King of France had decided to purchase,
and put at the disposition of Captain Jones, the Duras—an old
Indiaman of some size, then at l’Orient. To this vessel were added
three more, procured by means of M. le Ray de Chaumont, a banker
who had connections with the French Ministry.
Dr. Franklin, who, as Minister of the United States, was supposed,
in a legal sense, to direct the whole affair, added the Alliance, 32, by
virtue of authority from Congress.
The vessels thus procured formed a little squadron, composed of
the Bonhomme Richard, Alliance, Pallas, Cerf, and Vengeance. The
Pallas was a purchased merchantman; the Vengeance a small
purchased brig; the Cerf was a large cutter, and, with the exception
of the Alliance, the only vessel of the squadron built for war
purposes. All but the Alliance were French built, and they were
placed under the American flag by the following arrangement: the
officers received appointments, which were to remain valid for a
limited period only, from Dr. Franklin, who had been furnished blank
commissions, to fill at his own discretion, ever since he had arrived
in Europe. The vessels were to show the American ensign and no
other. In short, the French ships were to be considered as American
ships during this particular service: and when it was terminated they
were to revert to their former owners. The laws and provisions made
for the American navy were to govern, and command was to be
exercised, and to descend, according to its usages. Such officers as
already had rank in the American Navy took precedence, agreeably
to dates of commission, and new appointments were regulated by
priority of appointment.
ENGAGEMENT BETWEEN THE SERAPIS AND BONHOMME RICHARD.
By especial provision, Captain Jones was to be Commander-in-

chief, a post which his original commission entitled him to fill, as
Captain Landais, the only other regular captain in the squadron, was
his junior. The joint right of the American Minister and of the French
Government to direct the movements of the squadron was
recognized.
It is not exactly known from what source the money was obtained
to fit out this squadron; and it is likely that it never will be known,
especially as the French Revolution destroyed so many records,
public and private. Although the name of the King was used, it is
possible that private adventure was at the bottom of the enterprise,
although the French Government furnished vessels and the use of
its stores. Dr. Franklin expressly stated that he made no advances
for the ships employed.
As everything connected with this remarkable expedition has
interest for us, it is as well to go a little further into the composition of
the force fitted out by Jones.
After many delays, the Bonhomme Richard was equipped and
manned. It was intended to cast 18-pounders for her, but as that
would take too much time, old 12’s were substituted. With this
change in armament, the Richard, as she was called by the sailors,
got ready for sea.
She was, properly, a single-decked ship, that is, carrying her
armament on one gun-deck, with the usual additions on the quarter-
deck and forecastle.
But Commodore Jones, with a view to attacking the enemy’s large
convoys, caused twelve ports to be cut in the gun-room, below,
where six old 18-pounders were mounted, with the intention of
fighting all of them on the same side, in smooth water. It was
foreseen that these guns could only be of use in moderate weather,
or when engaged to leeward, but the ship’s height admitted of them,
and it was done.
On her gun-deck proper the ship had twenty-eight ports, the
regular construction of an English 38-gun ship at that time. Here the
12-pounders were placed. On her quarter-deck and forecastle were
mounted eight 9’s; making, in all, a mixed armament, rather light, to
be sure, of 42 guns. If the six 18’s were taken away, the ship would
have been what was called a 32-gun frigate.
She was a clumsy vessel, built many years before, with the high,
old-fashioned poop, which resembled a tower.
With a vessel of this singular armament and unwieldy construction,
Jones was compelled to receive on board a crew of very doubtful
composition. A few Americans filled officers’ positions; but the crew
embraced representatives of more than twelve nationalities. To keep
this motley crew in order, one hundred and thirty-five marines, or
soldiers, were put on board. These were nearly as much mixed, as
to nationalities, as the sailors.
Just as the squadron was about to sail M. le Ray de Chaumont
appeared at l’Orient, and presented a concordat or agreement, for
the signature of all the commanders. This looked very much like a
partnership in a privateering expedition, and was the cause of much
after disobedience among Jones’ captains.
On June 19th, 1779, the ships sailed, bound south, with a small
convoy of vessels. These they escorted safely into the Garonne, and
other ports; but not without repeated exhibition, thus early, of
disobedience of orders, and unseamanlike conduct, which marked
the whole career of this squadron, so ill assorted and manned.
While lying to, off the coast, the Alliance, by lubberly handling, got
foul of the Richard, and lost her mizzen-mast; carrying away, at the
same time, the head, cutwater and jib-boom of the Richard. This
necessitated a return to port, to refit.
When at sea again, and steering to the northward, the Cerf cutter
was sent in chase of a strange sail, and parted company.
The next morning she engaged a small English cruiser, of 14
guns, and caused her to strike, after a sharp fight of an hour; but she
was forced to abandon her prize by the approach of an enemy’s
vessel of superior force. The Cerf went into l’Orient again.
On the 23d three enemy’s vessels-of-war were seen by the
squadron; and, having the wind, they ran down in a line abreast,
when, most probably deceived by the height and general
appearance of the Richard, they hauled up and escaped under a
press of sail. On the 26th the Alliance and Pallas parted company
with the Richard, leaving that ship with the Vengeance brig only, for
consort. On reaching the Penmarks, a headland of Finisterre, the
designated rendezvous, the missing vessels did not appear. On the
29th, the Vengeance having gone, by permission, into Groix Roads,
the Richard fell in with two more of the English cruisers, which, after
some hesitation, also ran, evidently under the impression that the
Richard was a two-decker.
Jones had reason to be satisfied with the spirit of his crew on this
occasion, the people manifesting a strong disposition to engage.
At last, on the 30th, the Richard ran into Isle Groix, off l’Orient; and
about the same time the Pallas and Alliance came in.
Then another delay occurred. A court was convened to inquire into
the conduct of Captain Landais, of the Alliance, in running foul of the
Richard. Both ships also had to undergo repairs. Luckily, just then a
cartel arrived from England, bringing more than one hundred
exchanged American seamen, most of whom joined the squadron.
This was a most important accession to the crew of the Richard,
and that of the Alliance. Neither of these ships had had many
Americans among their crews. Among those who came from the
English prisons was Mr. Richard Dale, who had been captured as a
Master’s Mate, in the Lexington, 14.
This young officer did not reach France in the cartel, however, but
had previously escaped, came to l’Orient, and joined the Richard.
Jones soon learned his worth, and, in reorganizing his ship, had
made him First Lieutenant.
The Richard had now nearly one hundred American seamen on
board, and all the officers were native Americans, but the
commander and one midshipman. Many of the petty officers were
Americans also. In a letter of August 11th, Jones states that the crew
of the Richard consisted of 380 souls, including 137 soldiers, or
marines.
On the 14th of August the squadron sailed a second time, from
Groix Roads; having the French privateers Monsieur and Granville in
company, and under Jones’ orders. The first parted company almost
immediately, on account of differences concerning a valuable prize;
and another was taken the day she left.
On the 23d the ships were off Cape Clear, and while towing the
Richard’s head round, in a calm, the crew of the boat, which
happened to be manned by Englishmen, cut the tow-line, and
escaped. Mr. Lunt, the sailing-master, manned another boat, and
taking four marines, pursued the fugitives. A fog came on, and Mr.
Lunt not being able to find the ships again, fell into the hands of the
enemy. Through this desertion, and its immediate consequences, the
Richard lost twenty of her best men.
The day after this escape the Cerf cutter was sent close in, to
reconnoitre, and to look for the missing people; and, for some
unexplained reason this useful vessel never rejoined the squadron.
There appeared to have been no suspicion of any treachery on her
part, and we are left to conjecture the cause of her disappearance.
A gale of wind followed, during which the Alliance and Pallas
separated, and the Granville parted company, by order, with a prize.
The separation of the Pallas was caused by the breaking of her tiller;
but that of the Alliance was due to the unofficerlike and
unseamanlike conduct of her commander.
On the morning of the 27th the brig Vengeance was the only
vessel in company with the Commodore.
On August 31st the Bonhomme Richard, being off Cape Wrath,
the northwest extremity of Scotland, captured a large English letter-
of-marque, bound from London to Quebec; a circumstance which
proves the expedients to which their ship-masters were then driven
to avoid capture, this vessel having gone north about, to escape the
cruisers on the ordinary track. While in chase of the letter-of-marque,
the Alliance hove in sight, having another London ship, from
Jamaica, as a prize.
Captain Landais, of the Alliance, was an officer who had been
obliged to quit the French Navy on account of his unfortunate
temper. He now began to show a disorganizing and mutinous spirit;
pretending, as his ship was the only real American vessel in the
squadron, that that fact rendered him superior to Jones, and that he
should do as he pleased with his ship.
That afternoon a strange sail was made, and the Richard showed
the Alliance’s number, with an order to close. Instead of obeying the
signal, Captain Landais wore, and laid the head of his ship in the
opposite direction. Other signals were disobeyed; and the control of
Commodore Jones over the ship, which ought to have been the most
efficient of the squadron, may be said to have ceased.
Jones now shaped his course for the rendezvous he had
appointed, in hopes of meeting the missing ships, and the Pallas
rejoined him, having captured nothing.
From then until the 13th of September the squadron continued its
course round Scotland; the ships separating and rejoining constantly,
and Captain Landais assuming power over the prizes, as well as
over his own vessel, that was altogether opposed to discipline and to
marine usage.
On the 13th of September the Cheviot Hills were in sight from the
ships. Understanding that a 20-gun ship, with two or three man-of-
war cutters, were lying at anchor off Leith, in the Frith of Forth,
Commodore Jones planned a descent upon that town. At this time
the Alliance was absent, and the Pallas and Vengeance having
chased to the southward, the necessity of communicating with those
vessels caused a fatal delay, and ruined a promising project. The
attempt was at last made, but when the men were actually in the
boats the ships were driven out of the Frith by a heavy blow; and
when in the North Sea one of their prizes actually foundered.
The design was so audacious that it is probable the English would
have been taken by surprise; and no doubt much damage would
have been done to them, but for the gale. Dale, a modest and
prudent man, thought so.
After this bold project was abandoned, Jones appears to have
meditated another still more daring; but his colleagues, as he bitterly
styles his captains, refused to join in it. We do not know what it was;
but only that the officers of Jones’ own ship heartily approved it.
Jones had much respect for the judgment of Captain Cottineau, of
the Pallas, and as he disapproved of it, it was dropped.
The Pallas and Vengeance even left the Richard—probably with a
view to prevent the attempt to execute this nameless scheme; and
the Commodore was compelled to follow his captains to the
southward or lose them altogether.
Off Whitby they came together again, and on Sept. 21st the
Richard chased a collier ashore, near Flamborough Head.
The next day she was at the mouth of the Humber, the Vengeance
being in company, and several vessels were taken or destroyed.
Pilots were enticed on board, and a knowledge of the state of things
inshore obtained. It appeared that the whole coast was alarmed, and
that many persons were burying their plate. By this time about a
dozen vessels had been taken, and rumor increased the number. No
vessels had ever before excited such local alarm on British shores,
for centuries.
Under the circumstances Commodore Jones did not think it
prudent to remain so close in with the land, and he accordingly stood
out under Flamborough Head. Here he was joined, next day, by the
Pallas and Alliance. This was on the 23d of September.
The wind was light from the southward, the water smooth, and
many vessels in sight, steering in different directions. About noon the
squadron, with the exception of the Cerf and the two privateers,
being all in company, Jones manned one of the pilot-boats he had
detained, and sent her in chase of a brig, which was lying to, to
windward. On board the little vessel were Mr. Lunt, the Second
Lieutenant, and fifteen men, all of whom were absent from the ship
for the rest of the day.
In consequence of the loss of the two boats off Cape Clear, the
absence of the party in the pilot-boat, and the number of men that
had been put in prizes, the Richard was now left with only one
lieutenant, and with but little more than three hundred souls on
board, exclusive of prisoners. Of the latter there were about one
hundred and fifty in the Richard.
The pilot-boat had hardly left the Richard when the leading ships
of a fleet of more than forty sails were seen stretching out on a
bowline from behind Flamborough Head, turning down to the south.
From previous intelligence this fleet was immediately known to be
the Baltic ships, under the convoy of the Serapis, 44, Captain
Richard Pearson, and a hired ship that had been put into the King’s
service, called the Countess of Scarborough. The latter was
commanded by Captain Piercy, and mounted 22 guns.
As the interest of the succeeding details will principally centre in
the two ships, the Serapis and Bonhomme Richard, it may be well to
give a more minute account of the actual force of the former. At that
period 44’s were usually built on two decks; and such was the
construction of this ship, which was new, and was reputed to be a
fast vessel. On her lower gun-deck she mounted 20 18-pound guns;
and on her upper gun-deck 20 9-pound guns; and on her quarter-
deck and forecastle ten 6-pound guns; making an armament of fifty
guns.
She had a regularly trained man-of-war’s crew of 320 souls, of
whom fifteen are said to have been Lascars.
When Jones made out the convoy, the men-of-war were inshore,
astern, and to leeward, probably with a view to keeping the
merchantmen together. The officials at Scarborough, perceiving the
danger into which this fleet was running, had sent a boat off to the
Serapis, to apprise her of the presence of a hostile force, and
Captain Pearson fired two guns, signaling the leading vessels to
come under his lee. These orders were disregarded, however, the
headmost ships continuing to stand out from the land.
Jones, having ascertained the character of the fleet in sight,
showed signal for a general chase; and another to recall the
lieutenant in the pilot-boat.
The Richard then crossed royal-yards. These signs of hostility
alarmed the nearer English merchant ships, which hurriedly tacked,
fired alarm guns, let fly their top-gallant-sheets, and made other
signals of the danger they found themselves in; while they now
gladly availed themselves of the presence of the men-of-war to run
to leeward, or else seek shelter close in with the land.
The Serapis, on the contrary, signaled the Scarborough to follow,
and hauled boldly out to sea, until she got far enough to windward,
when she tacked, and stood inshore again, to cover her convoy.
The Alliance being much the fastest vessel of the American
squadron, took the lead in the chase, speaking the Pallas as she
passed. It has been proved that Captain Landais told the
commander of the latter vessel, on this occasion, that if the stranger
proved to be a fifty-gun ship, they had nothing to do but to escape.
His subsequent conduct fully confirms this; for no sooner had he run
down near enough to the two English vessels-of-war to ascertain
their force, than he hauled up, and stood off from the land again.
This was not only contrary to all regular order of naval battle, but
contrary to the positive command of Jones, who had kept the signal
to form line flying; which should have brought the Alliance astern of
the Bonhomme Richard, and the Pallas in the van. Just at this time
the Pallas spoke the Richard, and inquired what station she should
take, and she was directed to fall into line.
Captain Cottineau was a brave man, who subsequently did his
duty in the action, and he had only thought that, because the Richard
had suddenly hauled up from the land, her crew had mutinied, and
that she was being run away with. Such was the want of confidence
in the force so singularly composed, and such were the
disadvantages under which this celebrated combat was fought.
So far, however, from meditating retreat or mutiny, the crew of the
Richard had gone cheerfully to their quarters, although every man on
board was conscious of the force of the enemy with whom they were
about to contend; and the spirit of the commanding officer appears to
have communicated itself to his men.
It was now quite dark, and Jones was compelled to use a night-
glass, to follow the movements of the enemy. It is probable that the
darkness added to the indecision of the captain of the Pallas, for
even after the moon rose it was thick, and objects at a distance were
seen with difficulty. The Richard continued to stand steadily on; and
at about half-past seven she came up with the Serapis; the
Scarborough being a short distance to leeward. The American ship
was to windward, and, as she slowly approached, Captain Pearson
hailed. The answer returned was purposely equivocal, and both
ships delivered their broadsides at almost the same moment.
As the water was quite smooth, Jones had relied very much upon
the eighteen-pounders which were in the Richard’s gun-room; but at
this first discharge, two of the six that were fired bursted, blowing up
the deck above, and killing or wounding many of the people
stationed below. This disaster rendered it impossible to make the
men stand at the other heavy guns, as they could have no
confidence in them. It at once reduced the broadside of the Richard
to about one-third less than that of her opponent; and the force
which remained was distributed among the light guns, in a
disadvantageous manner. In short, the battle was now between a
twelve-pounder and an eighteen-pounder frigate; with the chances
almost preponderatingly in favor of the latter.
Jones himself said that after this accident his hopes rested solely
upon the twelve-pounders that were immediately under the
command of his First Lieutenant, Dale.
The Richard, having backed her top-sails, exchanged several
broadsides, when she filled again and shot ahead of the Serapis;
which ship luffed across her stern, and came up on the weather
quarter of her antagonist, taking the wind out of her sails, and, in her
turn, passing ahead.
All this time, which was about half an hour, the fire was close and
furious. The Scarborough now drew near; but it is uncertain whether
she fired or not. The officers of the Richard state that she raked them
at least once; but her commander reported that, owing to the smoke
and darkness, he was afraid to discharge his guns, not being able to
make out which ship was friend and which foe.
Unwilling to lie by and be uselessly exposed to shot, Captain
Piercy edged away from the combatants, exchanging one or two
broadsides, at a great distance, with the Alliance, and shortly
afterward was engaged at close quarters by the Pallas, which ship
compelled him to strike to her, after a creditable resistance of about
an hour.
Let us now return to the principal combatants:—
As the Serapis kept her luff, sailing and working better than the
Richard, it was the intention of Captain Pearson to pay broad off,
across the Richard’s fore-foot, as soon as he had got far enough
ahead. But making the attempt and finding he had not room, he put
his helm down, to keep clear of his adversary, and this double
movement brought the two ships nearly in a line, the Serapis
leading.
By these evolutions the English ship lost some of her way, while
the American, having kept her sails trimmed, not only closed, but
actually ran on board of her antagonist, bows on, a little on her
starboard quarter. The wind being light, much time was consumed in
these manœuvres, and nearly an hour had elapsed between the
firing of the first gun and the moment when the vessels got foul of
each other, in the manner just described. The English thought it was
the intention of the Americans to board; and for some minutes it was
uncertain whether they would do so or not, but the position was not
safe for either party to pass into the opposing ship.
There being at this time a complete cessation of the firing, Captain
Pearson hailed, and asked whether the Richard had struck. “I have
not yet begun to fight,” was the answer from Jones.
The Richard’s yards were then braced aback, and the sails of the
Serapis being full, the ships separated.
As soon as they were far enough apart, the Serapis put her helm
hard down, laid all aback forward, shivered her after sails, and wore
short round on her heel, with a view, most probably, of luffing up
across the Richard’s bow, in order to rake her. In this position the
Richard would have been fighting her starboard, and the Serapis her
port guns; but Jones, by this time, had become convinced of the
hopelessness of success against so much heavier metal; and so
backed astern some distance, filled on the other tack, and luffed up,
with the intention of meeting the enemy as he came to the wind, and
of laying him athwart hawse.
In the smoke and dim light, one or the other party miscalculated
the distance, for the vessels came foul again, the bowsprit of the
English vessel passing over the poop of the American. As neither
had much way the collision did but little injury, and Jones, with his
own hands, immediately lashed the enemy’s head-gear to his
mizzen-mast. The pressure on the after sails of the Serapis, which
vessel was nearly before the wind at the time, brought her hull
round, and the two ships gradually fell close alongside of each other,
head and stern; the jib-boom of the Serapis giving way with the
strain. A spare anchor of the English ship now hooked in the quarter
of the American, and additional lashings were got out on board the
latter, to secure her opponent in this position.
Captain Pearson, who was a brave and excellent officer, was fully
aware of his superiority in weight of metal; and he no sooner
perceived that the vessels were foul than he dropped an anchor, in
the hope that the Richard would drift clear of him. But, of course,
such an expectation was futile, as the yards were interlocked, the
hulls pressed close together, there were lashings fore and aft, and
every projection aided in holding the two ships together. When the
cable of the Serapis took the strain, the vessels slowly tended, with
the bows of the Serapis and the stern of the Richard, to the tide.

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Bipolar II Disorder Modelling Measuring

and Managing 3rd Edition Gordon

Bipolar Disorder For Dummies. 4th Edition Candida Fink

Bipolar Disorder A Guide for You and Your Loved Ones

Developing the Curriculum 9th Edition William Gordon Ii

Managing Substance Use Disorder - Practitioner Guide

Managing Children with Developmental Language Disorder

Measuring the User Experience Collecting Analyzing and

Calculus II 3rd Edition Mark Zegarelli

A Social Psychology of Leisure 3rd Edition Gordon J.

Cambridge University Press is part of the University of Cambridge.

Cambridge University Press is part of the University of Cambridge.

Section 1 – Domain Chapters 9 The Neurobiology of Bipolar II

3 The Bipolar Spectrum 16 11 The Role of Antidepressants in

Section 2 – Management 29 Management Commentary 255

Chris B. Aiken Sophia Frangou

Roger S. McIntyre Ayal Schaffer

By those with a bipolar disorder

Mapping the Terrain of Bipolar

Jackson, S. (1986). Melancholia and Depression depressive psychoses. Acta Psychiatrica

The Unipolar–Bipolar Spectrum

Box 3.1 Akiskal’s subtypes of the bipolar spectrum

Box 3.2 Bipolar spectrum disorder as defined by Ghaemi et al. (2001)

A. At least one major depressive episode

Spectrum Models of Mixed States and of Mania

Box 3.3 Biographical markers of hypomania (Akiskal’s ‘Rule of Three’)

>3 Major depressive episodes

Box 3.5 The bipolar specifier

Table 3.1 The affective temperaments

Temperament Limitations Strengths

The Affective Temperaments

Cyclothymia, Bipolar II ½ and Borderline Personality Disorder

Table 3.2 Sunny vs. dark hypomania (Akiskal et al., 2003)

Sunny hypomania Dark hypomania

Recognition of the Bipolar Spectrum in DSM

Table 3.3 Evolution of bipolar spectrum concepts in recent DSM manuals

DSM disorder Entry into DSM Spectrum concept

The Bipolar Spectrum as a Predictive Tool

The Bipolarity Index

Bipolar Risk Calculator

Conclusions and Implications for Treatment

Akiskal, H. S. and Akiskal, K. K. (2011). Angst, J. and Marneros, A. (2001). Bipolarity

KEARSARGE AND ALABAMA. JUNE

MOBILE BAY. AUGUST 5th, A. D. 1864.

CUSHING AND THE ALBEMARLE.

FORT FISHER. DECEMBER A. D. 1864,

DEEDS OF VALOR ON THE SEAS.

OUR NEW NAVY.

THE EXPLOSION OF THE MAINE.

DEWEY’S ACTION AT MANILA.

SERAPIS AND BONHOMME RICHARD. A. D. 1779.

his remarkable action is interesting not only on

ENGAGEMENT BETWEEN THE SERAPIS AND BONHOMME RICHARD.

By especial provision, Captain Jones was to be Commander-in-

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