Depression and the Erosion of the Self

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Barbara Dowds
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DEPRESSION AND THE EROSION OF
THE SELF IN LATE MODERNITY
Taylor & Francis
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 DEPRESSION AND THE
EROSION OF THE SELF IN
LATE MODERNITY
The Lesson of Icarus

Barbara Dowds
ROUTLEDGE

Routledge
Taylor & Francis Group

LONDON AND NEW YORK

First published 2018
by Routledge
2 Park Square, Milton Park, Abingdon, Oxon OX14 4RN

and by Routledge
711 Third Avenue, New York, NY 10017

Routledge is an imprint of the Taylor & Francis Group, an informa business

© 2018 Barbara Dowds

The right of Barbara Dowds to be identified as author of this work has been
asserted by her in accordance with sections 77 and 78 of the Copyright,
Designs and Patents Act 1988.

All rights reserved. No part of this book may be reprinted or reproduced or

utilised in any form or by any electronic, mechanical, or other means, now
known or hereafter invented, including photocopying and recording, or in any
information storage or retrieval system, without permission in writing from
the publishers.

Trademark notice: Product or corporate names may be trademarks or registered

trademarks, and are used only for identification and explanation without
intent to infringe.

British Library Cataloguing-in-Publication Data

A catalogue record for this book is available from the British Library

Library of Congress Cataloging-in-Publication Data

A catalog record has been requested for this book

ISBN: 978-1-78220-590-6 (pbk)

Typeset in Palatino
by V Publishing Solutions Pvt Ltd., Chennai, India
 To the memoir writers and all who struggle with depression

It would be a poor result of all our anguish and our wrestling, if we

won nothing but our old selves at the end of it—if we could return to
the same blind loves, the same self-confident blame, … the same feeble
sense of that Unknown towards which we have sent forth irrepressible
cries in our loneliness.

George Eliot, Adam Bede

Taylor & Francis
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CONTENTS

ACKNOWLEDGEMENTS ix

ABOUT THE AUTHOR xi

INTRODUCTION xiii

PART I: THE SELF: EXPERIENCE AND DEVELOPMENT

CHAPTER ONE
The experience of depressive breakdown: the role of
loss and rejection 3

CHAPTER TWO
The many ways of not being true to yourself 21

CHAPTER THREE
Depression as consequence and cause of somatic conditions 47

CHAPTER FOUR
Childhood development: what does it take to build a self? 59
vii
viii CONTENTS

PART II: THE SCIENCE OF DEPRESSION

CHAPTER FIVE
Low mood as an appropriate adaptive response: an evolutionary
perspective on depression 85

CHAPTER SIX
What science can tell us about depression: neuroscience; genetics
and epigenetics; gut microbiota 107

PART III: A DEPRESSIVE SOCIETY? THE IMPACT ON THE SELF,

RELATIONSHIPS, AND MEANING

CHAPTER SEVEN
A non-facilitating environment? The role of contemporary
society and culture 137

CHAPTER EIGHT
Empty (narcissistic), false, or fragmented: disorders of the
self in late modernity 167

CHAPTER NINE
Relatedness under threat: anxiety and ambivalence 195

CHAPTER TEN
Depression and meaninglessness: the loss of connecting and
experiencing 223

CHAPTER ELEVEN
Fundamental human needs: a conclusion 249

REFERENCES 261

INDEX 283
ACKNOWLEDGEMENTS

Special thanks to Ted Dinan, Trish Morgan, and Paschal Preston for
casting expert eyes over sections of the manuscript that are on the
fringes of my own territory. In particular, Paschal and Trish’s generos-
ity and enthusiasm affirmed my confidence and gave me the energy
to keep going with the long haul. I also want to thank former science
colleagues Ann Burnell, Martin Downes, Christine Griffin, and Thecla
Ryan for reading one of the chapters. I am grateful to my clients for all
they continue to teach me, and to my friends and therapy colleagues Ger
Byrne, Pauline Macey, Josephine Murphy, and Marjorie Travers for lov-
ing support. Also warm appreciation to Sean Rothery for his fellowship
and coffees as we shared the progress of our respective manuscripts.
Most of all, as usual, I owe an enormous debt to Peter Labanyi: for
particular help with the contents of Chapter Seven, for reading the
entire manuscript multiple times, for access to the library of his mind,
for his inspired discussions, suggestions, and corrections, and above all,
for his Winnicottian mothering and mood regulation.
Finally I want to thank Rod Tweedy at Karnac for believing in this
project, and for his continuing encouragement and support. And thanks
also to Constance Govindin, Kate Pearce and the rest of the team at
Karnac for all their help and assistance.
ix
Taylor & Francis
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ABOUT THE AUTHOR

Barbara Dowds, B.A. Ph.D. MIAHIP MIACP SIACP SIAHIP, was

educated at Trinity College Dublin (TCD) and had a previous career
in science as a researcher at the University of California and TCD, and
later as a senior lecturer in molecular genetics at Maynooth University.
She completed her therapy training in 2002, and then began to work as
a humanistic and integrative psychotherapist. Barbara taught on vari-
ous psychotherapy trainings between 2003 and 2014, and was on the
editorial board of Eisteach (the journal of the Irish Association for Coun-
selling and Psychotherapy) for seven years. She is the author of numer-
ous articles and of Beyond the Frustrated Self (Karnac, 2014). Barbara is
currently in private practice as therapist and supervisor and presents
postgraduate training workshops. For more information, see www.
barbaradowds.net

xi
Taylor & Francis
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INTRODUCTION

I was motivated to research and write this book because so much I read
or hear about depression seems wrong, trivial, unhelpful, or unethi-
cal. It is wrong that something that is escalating so fast is put down
to genetics or an imbalance of brain chemicals. It is trivial to focus
therapy on symptoms, such as negative thinking, rather than the fun-
damental causes. It is unhelpful to put so much research funding into
neuroscience, where the outcome is a detailed understanding of physi-
ological mechanisms without any understanding of what it means to
be a human being living in a particular society and time. It is unethical
to condemn so many to drug dependence and the belief that they are
defective, that the problem is theirs individually, rather than ours col-
lectively. My aim is to explore the origins of depression and why the
rate is increasing so rapidly (by twenty per cent per year according to
Healthline—www.healthline.com). I began my inquiry by examining
personal accounts of depressive breakdown for clues about possible
childhood influences and adult triggers. I then moved on to search for
socio-cultural changes that might make sense of what is an epidemic of
depression, given that as many as one quarter of people in the devel-
oped world have a lifetime risk of suffering from it.

xiii
xiv INTRODUCTION

The lack of any biological marker or indeed of any simple cause of

depression tells us that it is not a disease. Our genetic makeup changes
slowly over thousands of years, so the current increase in depression
cannot be ascribed to faulty genes. While the statistical rise may partly
be due to greater reporting of the condition now that there are more
effective treatments available, it must also be connected to changes in
the way we are living. I have written this book to get people to wake up:
living the way we increasingly are in the twenty-first century is endan-
gering our psychic health. We are living in the best of times and the
worst of times. Health, longevity, material well-being, and freedom of
mobility and action are all unprecedented in the developed world. But
our freedom is restricted to a limited range of things, many of which
don’t ultimately matter; and it is restricted to certain people, the poor or
socially disenfranchised being excluded. Even for the privileged, there
is a price to pay for our affluence and, like the obese on junk food diets
who have vitamin deficiencies, we seem to be starving in the midst of
plenty.
Depression may be experienced as intense sadness, or as numbness
or emptiness, and it is usually accompanied by anxiety. It is a somewhat
vague term that can refer to an ongoing minor experience of low mood
or to suicidal misery. Deep depression manifests as a mood disturbance
that equals or exceeds the diagnostic threshold for major depression.
This is characterised by having five or more of the nine symptoms listed
by DSM-5: depressed mood; loss of interest or pleasure; sleep distur-
bance; guilt; low energy; psychomotor changes; inability to concentrate;
change in weight or appetite; self-harm or thoughts of death. Neverthe-
less, depression is a term that is applied to low mood that lasts from
minutes to years, to the condition of a morose temperament or to a sui-
cidal breakdown.
Subjectively there are vast differences in the depth and length of
depressive episodes, but it appears that while the experience may vary
enormously, the roots of shallow and deep depression are the same.
There are common risk factors, and longitudinal studies show that low-
grade depression is a precursor of deep depression (Rottenberg, 2014).
Likewise, after recovery from the worst of deep depression, patients
typically continue to experience periods of shallow depression. Patients
with a clinical diagnosis of minor depression have the same kinds of
symptoms as patients with major depression, but fewer of them; and
the condition is persistent, with most people still experiencing some
 INTRODUCTION xv

symptoms a year later. Alarmingly, the chances of developing major

depression are five times greater if you already have minor depression
(ibid.). For these reasons, this book does not distinguish between differ-
ent degrees of depression.
The book opens with an analysis of twenty-one memoirs of depres-
sive breakdown. The authors represent a subgroup of educated, ambi-
tious, middle-class people who write as part of their professional lives
and thus have the wherewithal to produce and publish a memoir. But
while they are not therefore typical of the general population, it will
become evident that not just the experiences but the underlying causes
of their distress are representative of depression in our twenty-first cen-
tury society. Recently I witnessed a distressing scene at a livestock mar-
ket in a part of Romania where horses have not yet been replaced by
tractors. A horse had been harnessed to a very large block of concrete
to demonstrate its strength. The owner was whipping the horse, who
frantically jumped and struggled but could not move the heavy weight.
The man continued to beat the horse, refusing to accept that it was not
strong enough for the job. In the same way have the memoir writers
used the will to whip the embodied self. When we no longer have the
strength, energy, or libido for a life task, when its goal is not authenti-
cally ours but imposed by pressure to perform, compete, and win, we
give up and lie down: we become depressed.
What I am presenting here is a biopsychosocial model, which locates
the origins of depression in interactions between childhood relation-
ships, the social environment, and genetic vulnerability. Low mood has
evolved as an adaptive response to conditions of helplessness, hope-
lessness, chronic stress, separation from or loss of a major attachment
figure, indeed frustration of any of our fundamental needs. The varia-
tion in susceptibility to depression within a population can be partially
attributed to genetic makeup, but only to a limited extent (heritability
of thirty-seven per cent). Most of the roots lie in the childhood rela-
tionships that shape the formation of the self and determine our resil-
ience to life’s stressors, and in our adult socio-cultural conditions in
the degree to which they generate or protect against stress, loss, and
meaning. While it is impossible to prove causality in any simple way,
one can build up evidence from many different angles and sources that
weigh the probability. It is like showing that smoking increases your
chances of getting lung cancer—there is not just one single piece of evi-
dence. Some who smoke don’t get cancer, but your chances are greatly
xvi INTRODUCTION

increased if you do smoke. It will be clear on almost every page of the

book that the division into chapters is artificial. It conceals the real and
complex interactions between multiple internal and external influences
from the distant or recent past. The division is merely a regrettable con-
sequence of the need for linear presentation.
A major risk factor for depression is having a depressed mother, par-
ticularly in the early years, and we will see that in societies where the
extended family or friends support the mother there is a lower inci-
dence of postnatal depression. Anything that interferes with the main-
tenance of an attuned relationship between carer and child increases
the child’s risk for a range of emotional and developmental disorders.
Such adverse circumstances include stressed caregivers, emotionally
unavailable parents, or being reared in a crowded environment with-
out attuned one-to-one care during the first two years of life. We will
see that, alongside the rise in depression and anxiety, there are parallel
increases in narcissism (i.e., deficient self-structure) and insecure attach-
ment, especially the avoidant kind. My core argument is that we should
view depression less as a mood disorder—which merely describes the
symptoms—but more fundamentally as a disorder of the self. An empty,
false, fragmented, or otherwise fragile self leaves us with an underlying
depression that can be activated in later life by stress, loss, or even quite
trivial setbacks.
The book explores the kinds of changes in society that may be impact-
ing on our self-formation and relationships and that affect our sense of
life as being meaningful—changes that leave us vulnerable to depres-
sion. I criticise our current society not just because I don’t like many
aspects of it, but, as I argue with the help of theories of human needs,
because our most fundamental psychosocial needs are no longer being
adequately met. Human beings cannot flourish without close, support-
ive relationships; without authenticity, stability, meaning, and a wider
context for their lives; without contact with the earth; and without an
understanding of what is going on around them. We cannot thrive
when our sense of self is increasingly shrinking: from the connected
self to the individualised self to the postmodern sense of self that is little
more than a wilful ego masking an inner void.
Technology and a maximising ethos of productivity have disen-
chanted, de-souled the world and its inhabitants and reframed them
as resources to be exploited. We are living in an atomised society that
has been taken over by the toxic values of competitive individualism,
 INTRODUCTION xvii

where trusting, co-operative communities have been replaced by

anxious monads in an endlessly mutating and inhospitable world. We
instrumentalise both ourselves and others: instead of inhabiting the
authentic self, young people increasingly perform a persona for the
benefit of the ego and the audience, and simultaneously try to eliminate
the competition. A population of narcissists, for whom a belief in enti-
tlement far exceeds any sense of personal responsibility, exacerbates
individualism and aggression—even hatred—in the public sphere, and
adds to the erosion of the social matrix. Our culture is both impinging
and abandoning (try ringing a help-line), at the same time too much
(speed, stimulus, change, pressure) and too little (meaning, holding,
support, boundaries, control over our own lives). We no longer know
where power resides, but we suspect that actually nobody is in charge
and that the system is out of control, in a chaotic state. Late modernity
fosters vulnerability to depression because of the increasingly adverse
conditions for raising infants, and at the same time provides adult trig-
gers for depression in the shape of endemic stress and loss. Like Icarus,
our late-capitalist society is flying too close to the sun. Increasing num-
bers of people who are compelled to buy into its ideology are crashing
to the ground. Depression is the collapse of the individual with an over-
reaching ego that rejects all authority (from the deeper self) other than
its own will-driven impulses. Such an ego-focused identity may be free,
but it is a negative freedom: from both containment and nourishment,
from connection and therefore meaning.
It is beyond the scope of this book to compare different cultures and
their experience of depression, and the reader is referred to other sources
such as Eshun and Gurung (2009). Overall we can say that culture influ-
ences the awareness of symptoms, the meaning people attribute to their
suffering as well as the treatments they may find useful and acceptable.
Thus, depression is always embedded in a particular socio-cultural
context, which may be a contributory or a protective factor. Low mood
equips us to respond appropriately to our social and material environ-
ments and is therefore saturated with meaning. We ignore the messages
of depression at our peril.
An important and relevant work was published just too late to influ-
ence and focus my book. The Political Self: Understanding the Social Con-
text for Mental Illness argues that psyche and society are interpenetrated.
Highlighted in particular is the prevalence of left hemisphere-mediated
dissociation and dehumanisation of others under late capitalism.
xviii INTRODUCTION

Coming from quite different starting points from my own argument,

the editor nevertheless reaches similar conclusions, while ending with
an inspiring flourish (Tweedy, 2017). Symptoms (such as depression)
“—the displayed symbols of our broken world—are … both indicators
of sickness and also latent signs of life”. Tweedy argues for a two-fold
response: not just therapy taking note of social reality, but also “putting
the psyche back in the world” (p. lii) and thereby de-dissociating and
revitalising the public sphere.
 PART I
THE SELF: EXPERIENCE AND
DEVELOPMENT
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CHAPTER ONE

The experience of depressive breakdown:

the role of loss and rejection

E
mpirical research into depression provides data on demographics—
how different population groups and locations fare in the
depression stakes. It indicates possible causes of depression in
generalised terms—childhood abuse, significant life events, etc. How-
ever, none of these statistics convey either the experience of depression
or the sheer complexity of a life and how many possible causes interact
to generate clinical depression. While the statistics may show that a cer-
tain percentage of those who have a major depressive episode go on to
have second, third, and more relapses, they fail to reveal the systemic
and relational aetiology and the dynamic process of a life punctuated
by depressive illness. Thus, there is a real benefit in examining the first-
hand descriptions of individual lives: what we lose in scale and rigour,
we gain in concreteness, depth, and complexity, and we can generate
fruitful hypotheses that might guide future population research.
In this section, I analyse twenty one memoirs of depressive break-
down, among which two (Jamison, Merritt) or possibly three (Wurtzel
received varying diagnoses) of the authors suffer from bipolar disorder,
and the remainder from unipolar depression. The writers comprise four-
teen women and seven men, the same ratio in which depression occurs
in the population at large. They include two poets, three fiction writers,
3
4 D E P R E S S I O N A N D T H E E R O S I O N O F T H E S E L F I N L AT E M O D E R N I T Y

two non-fiction writers, eight journalists (in a perilous profession), one

biologist, three psychologists, one psychiatrist, and one actor. I have
included one fictionalised account—Sylvia Plath’s The Bell Jar—amongst
them because it is so closely based on the author’s own experience of
depression and early suicide attempt. Depression amongst the poor
and indigent does not benefit from this first-hand description, though
Andrew Solomon (2014) has provided space for their voices in his book
The Noonday Demon. Inevitably I am constrained by the narrative choices
and level of self-awareness of the memoir writers: in particular, some
tell us a great deal about childhood experiences, others very little.
I will attempt to categorise the memoirs according to my under-
standing of likely causes of the depression. I will leave the question
of genetics aside in this section (but return to it in Chapter Six) and
restrict myself to environmental causes, whether originating in child-
hood, familial, or societal culture, or current lifestyle causes. Any sim-
ple notion that depression is caused by an unhappy childhood where
the individual suffers rejection, abuse, or neglect is confounded by
some of these accounts. Some of these writers record happy, stable
childhoods (e.g., McEvoy, Rice-Oxley, and Jamison), while several oth-
ers had happy home lives but were unpopular at school. Some were
much loved, but perhaps overprotected (e.g., Kelly), while others were
rejected by a parent, had a depressed and/or anxious parent, an unsta-
ble childhood, or lived in a psychologically unhealthy culture (of guilt
or lies, for example).
While I have categorised the memoirists according to one major
factor contributing to their depression, most could have—and some
have—been located under several different headings, showing how
multifactorial the condition is. The various causative factors also inter-
act with each other in complex ways. In addition to possible genetic
vulnerability, depression usually has distal causes in childhood
upbringing that result in a fragile sense of self (next chapter and later)
and/or insecure relationships (this chapter and later). Proximal initiat-
ing events in adulthood, such as stress or loss, may then provoke an
apparently mystifying slide into depression. At the same time, child-
hood primary causes and adulthood secondary triggers are not inde-
pendent of each other. Loss in adulthood is far more likely to induce
depression if it restimulates insecurity from the past. A stressful life-
style in adulthood is often a defence against an empty sense of self or
poor self-esteem, and cannot therefore be separated from the childhood
 THE EXPERIENCE OF DEPRESSIVE BREAKDOWN 5

origins of depression. The challenge for each individual is to make sense

of what the depression is telling her and what needs to be attended to in
therapy or in her manner of living.
Amongst the memoir writers who had other family members who
suffered from depression, almost all of them attributed the family pat-
tern to genetic propensity. This shows how the genetic/medical model
has infiltrated the general population as well as the physicians and
therapists with whom they come into contact. In reality, as we will see
in Chapter Six, there is no way for the individual to know whether
familial similarity originates in inherited susceptibility or in upbringing
or other environmental patterns shared by the family members.

Depression as a result of loss or separation anxiety

Loss of major attachment figures
One theory of depression centres on our innate need for attachment to
parents in childhood and the effect of the loss or absence of that secure
base in generating grief and panic (see Chapter Five). It doesn’t take
a great leap to envisage depression and anxiety as more long-term
versions of grief and panic. Indeed, while focusing on grief, Wolpert
(1999) has suggested that depression is a “malignant” version of the
normal response of sadness, analogous to cancer being a malignant
form of normal cell division. The loss of an attachment figure such as
a spouse, partner, or parent may provoke depression. But so too can
other losses—of physical health, home, career, religious faith, or any-
thing that we cathect and love that is of defining importance for our
identity or security or that shapes the world as we know it. A world that
is changing too rapidly will bring ongoing loss, which can contribute to
depression, though more likely as a low-level, chronic condition.
We are more vulnerable to loss if we have not internalised a child-
hood experience of secure attachment. Such insecurely attached chil-
dren are likely to carry that attachment pattern into adulthood: by not
having a spouse or partner or by forming a physically or emotionally
distant, unreliable, entangled, or abusive relationship. Insecure attach-
ment can be generated by permanent or temporary loss (death, hospi-
talisation, etc.) of a parent in childhood, but it is more frequently driven
by the inability of the parents to “read” the child in an empathic and
attuned manner. A sensitively attuned parent consistently intuits and
6 D E P R E S S I O N A N D T H E E R O S I O N O F T H E S E L F I N L AT E M O D E R N I T Y

responds appropriately to the child’s needs, with the result that the
child feels safe and valued, learns to be aware of and respect his own
feelings and needs, and to develop emotional intelligence towards him-
self and others. In the absence of this attunement, a child is emotionally
abandoned, which generates both anxiety and depression. Emotionally
or physically abandoned children may suffer severe separation anxiety
which can continue into adult life. “No one told me that grief felt so
much like fear,” observed C. S. Lewis (2013, p. 1), reflecting the insecu-
rity that accompanies loss of an attachment figure.
Bereavement that is not grieved plays a role in the aetiology of
depression, as was the case for Sylvia Plath and her alter ego Esther
Greenwood (childhood loss of her father), William Styron (whose
mother died when he was thirteen), and Linda Gask whose father died
just as her career in medicine was beginning. Styron—significantly
given his failure to mourn—writes at arms-length in the third person
about “the young person [who] … carries within himself … an insuf-
ferable burden of which rage and guilt, and not only dammed-up sor-
row, are a part, and become the potential seeds of self-destruction”
(1992, pp. 79–80). Lewis Wolpert (1999) was convinced that his depres-
sion was triggered by his new heart drug. His wife believed that it was
linked with his planned trip to South Africa where his father had been
murdered some years before, but Wolpert doesn’t tell us enough about
his feelings for us to know whether this was another case of unproc-
essed grief or horror (though the exclusion of these details is surely sig-
nificant). Elizabeth Wurtzel’s father disappeared for a few years during
her adolescence, leaving his family of origin with instructions not to tell
her of his whereabouts. This was both more and less cruel than a death:
less in being reversible, more in the rejection explicit in his behaviour.
The only way to recover from a loss, however many years have passed,
is to grieve; only then can the individual move on.
Sally Brampton was a successful journalist, novelist, and magazine
editor, including launch editor of Elle Magazine, who in her early fif-
ties slid into three years of catastrophic depression. This included two
suicide attempts, developing alcohol dependency, and three stays in
psychiatric wards. The immediate triggers for her depression were a
succession of losses: the (amicable) breakup of her marriage with the
loss of home as well as husband; the loss of a job in which she did not
fit; as well as falling in love with a man who reciprocated but was not
available because of family responsibilities. She was physically unwell
 THE EXPERIENCE OF DEPRESSIVE BREAKDOWN 7

and lost a close friend (Paula Yates) to suicide as she sank deeper into
depression. She tried two psychoanalysts but didn’t like them or their
approach and didn’t continue with either. Three months passed before
she was admitted to hospital with severe clinical depression. Her adult
losses replicated her childhood experience of being repeatedly plucked
from home as she followed her father to his latest work posting. As she
says, “In all these losses, I had lost myself” (2008, p. 64).
Brampton’s parents did not speak the language of emotions, so she
learned to be stoic, without wants or needs—in other words, to abandon
herself. Superficially she engaged with others, but she hid how she was
really feeling. She noted: “my natural default setting is to shut down and
hide … Yet every time I manage to answer the phone, make a call or
seek out the company of friends, I am amazed at the way that my mood
can lift” (ibid., p. 123). While she loved and felt loved by her parents,
she didn’t feel seen or understood. Developmentally, love is not enough
for self-formation if mirroring, understanding, and attunement are lack-
ing, as we will see in later chapters. Her mother probably suffered from
dysthymia, a condition that has fewer or less serious symptoms than
major depression, but which lasts longer. Sally realised in adulthood
that her father almost certainly had undiagnosed Asperger’s syndrome:
he couldn’t understand or empathise with body language or the more
subtle emotions, interpret social cues, or grasp implied meanings. Thus
Brampton’s feelings were not recognised or addressed, and she learned to
ignore and override them herself. It is not surprising that all three children
(Brampton and her two brothers) of the family developed depression.
There is a strong pattern of depression in Brampton’s family: her mother,
two brothers, and—since her book was published—a major depressive
episode in her seventeen-year-old daughter. This could be due to either
common genetic and/or environmental/upbringing factors.
The trigger experience for Andrew Solomon’s first depressive break-
down was his much-loved mother’s death, after a two-year battle with
cancer when he was twenty-seven. Once there was no hope left for
recovery she killed herself, having previously ordered the drugs with
the help of her husband and sons. Solomon describes her suicide as
the “cataclysm” of his life (2014, p. 268) despite admiring her for it and
believing in what she did. After her death, he felt great sorrow and
anger, but was not yet “crazy”. He started psychoanalysis, and the fol-
lowing year he fell in love with a woman, but after a tumultuous two
years they broke up by mutual agreement. When, a few months later,
8 D E P R E S S I O N A N D T H E E R O S I O N O F T H E S E L F I N L AT E M O D E R N I T Y

his analyst announced her plan to retire, he felt “devastatingly lonely

and entirely betrayed” (ibid., p. 45), despite the fact that he had been
considering ending the therapy anyway. These losses along with his
coming out as a gay man (following the publication of his first novel
with its overtly gay content) appear to have been the triggers that initi-
ated his breakdown.
In reflecting on the sadness of his depression, Solomon speaks about
the loss of past joy and love. He finds this loss harder to process than
past pain. This he can leave in the past, but past joy is experienced as
current loss: “The worst of depression lies in a present moment that
cannot escape the past it idealizes” (ibid., p. 99). One could interpret
this as an inability to live intensely in the present. Holding on to the
past may block or compensate for the present, but one could alterna-
tively argue that letting go of what is most precious in the past impov-
erishes the present. As Proust proclaimed wistfully: “the true paradises
are the paradises that we have lost” (1992, p. 222).

Grief and bereavement

Freud (1917e) viewed melancholia as a consequence of inner conflicts
between love and hatred for the deceased, which block the healthy
process of grieving. Self-reproach on account of these unconscious
feelings of hostility—repression of anger—was thought to generate
depression. Karl Abraham and Melanie Klein both believed that inter-
nalisation of the loved one and conflict of emotions were intrinsic to
all forms of mourning because our relations to others begin in ambiva-
lence (Leader, 2009). Klein argued that once children move beyond the
splitting defence, they see that the individual who has bad attributes
also has good ones. This realisation is followed by a phase of sorrow
and concern during which we attempt to make amends for our earlier
aggression. This is the depressive position, and it must be re-entered
again and again with every loss we suffer. If such early struggles have
not been dealt with, depression is more likely to develop.
Loss may be followed by depression when the work of mourning
is blocked. In Anita Brookner’s novel Latecomers (1989), a Jewish boy
Fibich is sent to England at the age of seven to escape the Nazis. His
parents do not survive the death camps, and his last memory is of
being torn from them at the train station and his mother fainting into
his father’s arms. He lives with anxiety and depression all his life: to
 THE EXPERIENCE OF DEPRESSIVE BREAKDOWN 9

make Brookner’s favourite distinction, he is not viable, not compared

to his robust and valiant friend Hartmann who vigorously repudiates
the value of looking back on his very similar fate. Fibich is irresistibly
drawn back into his past, but at the same time can remember virtually
nothing of his childhood. It is only when, in his sixties, he feels the grief
of separating from his parents and his burning regret that he didn’t get
off the train, that he can begin to inhabit the present, and the future in
the shape of his son. In the very different responses of the friends to
similar circumstances, we can see the role of temperament and earlier
childhood experience in the kind of defensive stance adopted.
The grief from bereavement can feel just like depression. Within a
six-month period, Tracy Thompson’s father died and she also lost a
long-term and a short-term boyfriend. “The grief I felt … was exac-
erbated by the extent to which I had depended on these men for my
self-worth” (1995, p. 72). As she says perceptively: “That winter, grief
made its acquaintance with depression, its near neighbor” (ibid., p. 73).
Likewise, when Wolpert’s wife died he felt as if his depression was
starting again, but his daughter reassured him that he was confusing
normal mourning with depression (1999). However, Rottenberg (2014)
has argued persuasively that the two are indistinguishable except in
the way society responds to them. While depression often remains a
stigmatised secret, the healing of grief is supported by culturally based
rituals and practical and emotional support. Likewise Keedwell (2008)
notes that depression and grief overlap in terms of triggers as well as
subjective experience and duration, and we will see in Chapter Five
that low mood may offer a selective advantage to young animals under-
going the distress of separation from the mother.

Other losses
Loss of faith
In Bergman’s grief-saturated film Winter Light and in some of the
memoirs, loss of faith contributes to depression. Stephanie Merritt,
for example, grew up in a family that were committed members of a
conservative, charismatic, Christian church, which formed the cen-
tre of their social lives. At university she gave up attending church
and had to cope with the disappointment of her parents and others
in the church as well as with “a kind of severance that would not be
10 D E P R E S S I O N A N D T H E E R O S I O N O F T H E S E L F I N L AT E M O D E R N I T Y

easily mended” (Merritt, 2009, p. 73) because the loss simultaneously

encompassed family, community, and a whole worldview and sense of
meaning. She chose reason over faith, but at the time “had no sense of
the cost involved” (ibid., p. 110). The depression returned the summer
she graduated, when she felt expelled from the place where she had
belonged, and had broken up with her boyfriend; she had no job, no
future, no money, and nowhere to live. Her perception of the distance
from her family generated by her departure from the church also meant
she could not go home. While hanging round Cambridge in the months
following, she slid into “anomie” (ibid., p. 78), often unable to get out
of bed or see people, and cancelling job interviews. Though Merritt suf-
fered an earlier depression before losing her faith, the two experiences
have remained inseparable for her and she felt intensely pressurised to
fit everything into this short and finite life now that there was no eternal
hereafter.
After a brief four-year vocation Michael Harding, aged thirty-two,
left the Catholic priesthood for the woman who became his wife, but
he remained highly conflicted about the role of religion in his life. He
became aware that “the priesthood embodied my depression. It was the
glove. The wrap-around numb bodysuit that I put on to isolate myself
from ordinary life” (Harding, 2013, p. 47). He still wanted to have the
kudos of being a priest without losing the woman he loved, and felt
guilty for forgetting “the ecstasy to be found in solitude and prayer”
(ibid., p. 78). He calls his religious faith “magical thinking”, a belief that
a “benign deity” (ibid., p. 118) was intervening on his behalf to smooth
and bless his path in life.
In his late fifties Harding suffered from depression linked to physi-
cal illness and a mid-life crisis. “In the months that followed, my usual
melancholy transformed into a swamp of sorrow, an ocean of grief …”
(ibid., p. 168). While he lay in bed for the four months of the worst of
his depression, Harding’s wife tended him and gave him the “time to
mourn and to cry for all the lives that I had never lived. Before I let them
go” (p. 188). He contemplated the role that faith played in his life and
realised that it was fear that kept him clinging to religion, and at the heart
of that “the fear of death that lies at the root of all depression” (p. 280).
And he notes: “whether it’s in society or in an individual, whether it is
gradually over years or suddenly in trauma, the ebbing away of reli-
gious belief causes sorrow and loneliness, melancholy and depression”
(p. 161). The book ends when he realises that he has “returned once
Another random document with
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organs, as the lung, the testicle, the liver, the spleen, etc. The
dependence of miliary tuberculosis of the pia upon previously-
existing caseous or other inflammatory deposits in some part of the
body is acknowledged by most modern pathologists. Seitz3 states
that out of 130 cases, with autopsies, of adults, upon which his work
is based, such deposits were found in 93.5 per cent. General
constitutional weakness, either congenital or resulting from grave
disease or from overwork, from insufficient or unwholesome food,
and from bad hygienic surroundings, also favors the deposit of
tubercle in the meninges. Sometimes two or more predisposing
causes exist at once. Thus, a child born of tuberculous parents may
be fed with artificial diet instead of being nursed, or may live in a
house whose sanitary condition is bad. Hence the disease is
common among the poor, although by no means rare in the higher
classes of society. In some cases it is difficult or impossible to assign
any predisposing cause. A single child out of a numerous family may
be stricken with the disease, while the rest of the children, as well as
the parents and other ascendants, are healthy. For instance, while
writing this article I had under observation a little boy six years old
whose parents are living and healthy, with no pulmonary disease in
the family of either. The only other child, an older brother, is healthy.
While apparently in perfect health the child was attacked with
tubercular meningitis, and died in seventeen days with all the
characteristic symptoms of the disease. At the autopsy there was
found much injection of the cerebral pia everywhere, a large effusion
of lymph at the base of the brain and extending down the medulla,
abundance of miliary tubercles in the pia and accompanying the
vessels in the lateral regions of the hemispheres, lateral ventricles
distended with nearly clear fluid, ependyma smooth, choroid
plexuses covered with granulations, convolutions of brain much
flattened. Careful investigation, however, will usually enable us to
detect some lurking primary cause, either in the family predisposition
or in the history of the patient himself.
3 Die Meningitis Tuberculosa der Erwachsenen, von Dr. Johannes Seitz, Berlin, 1874,
p. 317.
Season appears to have but little influence on the production of the
disease. The largest number of cases is observed during winter and
spring, owing doubtless to the influence of the temperature and
weather, and to the exclusion from fresh air, in favoring the
development of tubercle and the scrofulous diathesis. Males, both
children and adults, are somewhat more frequently attacked than
females.

In regard to the exciting causes it may be said that where a

disposition to the deposit of tubercle exists, anything which tends to
lower the vitality of the individual is likely to hasten the event. In
infants with hereditary tendency to tubercle, an improper diet is
especially liable to develop meningeal tubercle. In older children,
besides unwholesome or insufficient food and unfavorable hygienic
surroundings, the acute diseases common to that period of life, such
as the eruptive fevers, intestinal disorders, whooping cough, etc.,
often act as immediate causes. Sometimes the development of the
disease may be traced to over-stimulation of the nervous system by
excessive study, often aided by imperfect ventilation or overheating
of the school-room. Caries of the temporal bone from disease of the
middle ear may act as an immediate cause of tubercular meningitis,
although simple meningitis is of course a more frequent result of that
condition. The disease has been known to follow injuries of the head
from blows or falls. In a larger number of cases the exciting cause is
not discoverable, especially when the meningeal affection is simply
an extension of the disease from some other part of the body, as the
lungs, the bronchial or mesenteric glands, etc. This is often the case,
both in adults and in children, when tubercular meningitis
complicates pulmonary consumption.

SYMPTOMS.—The disease is most frequently observed in children

between the ages of two and seven years. It is much less common in
adults, who are generally attacked between the ages of twenty and
thirty years. In the majority of cases the invasion of the malady is
preceded by a prodromic stage, usually occupying from a few days
to several weeks, though sometimes extending over a considerably
longer period. This stage probably represents the process of deposit
of miliary tubercles in the pia mater before their presence has given
rise to much structural change in the tissue. The characteristic
symptoms of the prodromic stage consist chiefly in an alteration of
the character and disposition of the patient, varying in extent in
different cases. In general, it may be said that he becomes sad,
taciturn, apathetic, irritable, indisposed to play, often sitting apart
from his companions, gazing in a strange way into vacancy. There is
diminution or loss of appetite and some emaciation. He is restless at
night, is disturbed by nightmare, or grinds his teeth. The digestion is
deranged. Usually there is constipation, but occasionally diarrhœa,
or these conditions may alternate with each other. Squinting and
twitching of the facial muscles are sometimes noticed. Headache
may occur early in this stage, but it is usually observed later, and it
then forms a prominent symptom. Vomiting is also frequent, usually
not preceded by nausea, sometimes provoked by sudden
movement, as in sitting up in bed, and is apt to occur when the
stomach contains little or no food. These symptoms vary much in
degree, and they are often so slight that they pass unnoticed by the
parents or friends. Occasionally the patient, if a child, will manifest a
strange perversity or an unusual disobedience, for which he is
perhaps punished under the belief that his misconduct is intentional.
In older children and in adults delirium, especially at night,
sometimes followed by delusions which may be more or less
permanent, is frequent at this stage. The above symptoms often
remit from time to time, and during the interval the patient may seem
to have recovered his health. The prodromic symptoms are rarely
altogether wanting in children, although they may have escaped
notice from lack of opportunity of observation on the part of the
physician. On the other hand, as Steffen4 justly observes, the most
characteristic symptoms may be present, and lead even an
experienced observer to a confident diagnosis of tubercular
meningitis during the early stage of a case of typhoid fever or of
cerebral congestion without tuberculosis.
4 “Meningitis Tuberculosa,” by A. Steffen, in Gerhardt's Handb. der Kinderkrankheiten,
5 B., 1ste Abth., 2te Hälfte, p. 465.
For convenience of description it is customary to divide the disease
proper, after the prodromal period, into three stages—viz. of
irritation, compression, and collapse. In some cases it is not difficult
to observe these divisions, but it must be borne in mind that in others
the symptoms do not follow any regular sequence, so that no
division is possible. In infants profound slumber may be the only
morbid manifestation throughout the entire disease. Steffen records
such a case, and I have seen two similar ones.

First Stage: The interval between the prodromic period and the first
stage is usually so gradual that no distinction between the two can
be detected. In other cases the disease is ushered in suddenly by
some striking symptom, such as an attack of general convulsions,
with dilated pupils and loss of consciousness. This is not often
repeated, though partial twitchings of the limbs or of the muscles of
the face may follow at intervals. In young children a comatose
condition, with unequal pupils, is apt to take the place of these
symptoms. The principal phenomena of the first stage are headache,
sensitiveness to light and sound, vomiting, and fever. The latter
varies much in intensity from time to time, but is not usually high, the
temperature seldom rising above 103° F., and usually, but not
always, higher at night than in the morning; but there is no
characteristic curve. The pulse varies in rate, but is usually slow and
irregular or intermittent. The respiration is irregular, with frequent
sighing. The tongue is dryish and covered with a thin white coat. The
bowels are costive. Delirium is frequent at night, and the sleep is
disturbed, the patient tossing about and muttering or crying out. The
eyes are half open during sleep. These symptoms become more
marked from day to day. The pain in the head is more frequent and
severe; the patient presses the hands to the forehead or rests the
head against some support if sitting up. During sleep he occasionally
utters a loud, sharp cry, without waking. There is increasing apathy,
and some intolerance of light, shown by an inclination to turn toward
the wall of the room or to lie with the face buried in the pillow. The
appetite is lost, the constipation becomes more obstinate, the
slowness and irregularity of the pulse persist. With the rapid
emaciation the belly sinks in, so that the spinal column can be easily
felt. Soon the child falls into a state of almost continual somnolence,
from which, however, he can be awakened in full consciousness,
and will answer correctly, generally relapsing again immediately into
slumber. His restlessness diminishes or ceases altogether, and he
lies continuously on the back with the head boring into the pillow. He
becomes more passive under the physician's examination, in strong
contrast to his previous irritability. At the end of a week or more from
the beginning of this stage symptoms of irritation of some of the
cerebral nerves begin to show themselves, in consequence of
pressure from the increasing exudation at the base of the brain and
into the ventricles. Strabismus (usually convergent), twitching of the
facial muscles and grimaces, grinding of the teeth, or chewing
movements of the mouth are noticed. The somnolence deepens into
sopor, from which it becomes more and more difficult to arouse the
patient, who gradually becomes completely insensible.

Notwithstanding the alarming and often hopeless condition which

this assemblage of symptoms indicates, intervals of temporary
amendment not unfrequently take place. The child may awake from
his lethargy, recognize those about him, converse rationally, take his
food with relish, and exhibit such symptoms of general improvement
that the parents and friends are led to indulge in fallacious hopes,
and sometimes the physician himself ventures to doubt the accuracy
of his diagnosis. Such hopes are of short duration; the unfavorable
symptoms always return after a brief interval. The duration of the first
stage may be reckoned at about one week.

Second Stage: This period is not separated from the preceding one
by any distinct change in symptoms. The patient lies in a state of
complete insensibility, from which he can no longer be aroused by
any appeal. The face is pale or of an earthen tint, the eyes are half
closed. If the anterior fontanel be still open, the integument covering
it is distended by the pressure beneath. Often one knee is flexed, the
opposite leg extended; one hand applied to the genitals, the other to
the head. Sometimes one leg or arm is alternately flexed and
extended. The head is apt to be retracted and bores into the pillow.
The pupils are dilated, though often unequal and insensible to light:
the sclerotica are injected; a gummy exudation from the Meibomian
glands forms on the edges of the lids. The patient sighs deeply from
time to time, and occasionally utters a loud, piercing cry. Paralysis,
and sometimes rigidity of one or more of the extremities, are often
observed, and occasionally there is an attack of general convulsions.
The pulse continues to be slow and irregular, the emaciation
progresses rapidly, and the abdomen is deeply excavated. The
discharges from the bladder and rectum are involuntary. The
average duration of the second stage is one week.

Third Stage: No special symptoms mark the passage of the second

stage into the third, which is characterized by coma, with complete
resolution of the limbs. The constipation frequently gives place to
moderate diarrhœa. The distended fontanel subsides, and often
sinks below the margin of the cranial bones. A striking feature of this
stage is a great increase in the rate of the pulse, the heart being
released from the inhibitory influence of the par vagum in
consequence of the complete paralysis of the latter from pressure.
The pulse varies in rapidity from 120 to 160 or more in the minute.
For the same reason the respiration also increases in frequency,
though not to the same degree. The eyelids are widely open; the
pupils are dilated and generally motionless, even when exposed to a
bright light. The eyes are rolled upward, so that only the lower half of
the iris is visible; the sclerotica is injected from exposure to the air
and dust. Convulsions may occur from time to time. Death
terminates the painful scene, usually in from twenty-four to forty-
eight hours, but sometimes the child lives on for days, unconscious,
of course, of suffering, though the afflicted parents and friends can
with difficulty be brought to believe it.

Certain points in the symptomatology of tubercular meningitis

demand especial consideration.

I have already observed that the division of the disease into definite
stages is purely arbitrary, and is employed here merely for
convenience of description; in fact, few cases pursue the typical
course. A period of active symptoms and another of depression can
often be observed, but these frequently alternate. Stupor and
paralysis may characterize the early stage, and symptoms of
irritation, with restlessness, screaming, and convulsions,
predominate toward the end. Certain characteristic symptoms may
be wholly or in part wanting, such as vomiting, constipation, or
stupor.

The temperature shows no changes which are characteristic of the

disease. Throughout its whole course it varies from time to time,
without uniformity, except that it usually rises somewhat toward
night. It seldom exceeds 102° or 103° F., unless shortly before
death, when it may rise to 104° F., or even higher, and may continue
to rise for a short time after death.

During the premonitory stage the pulse offers no unusual

characteristics. Its frequency is often increased, as is usual in any
indisposition during the period of childhood, but it preserves its
regularity. Toward the close of this period, and especially during the
first stage of the disease proper, a remarkable change takes place. It
becomes slow and irregular, the rate often diminishing below that in
health. The irregularity varies in character; sometimes the pulse
intermits, either at regular or irregular intervals. An inequality in the
strength of different pulsations is also observed. These peculiarities
of the circulation are due to the irritation of the medulla and the roots
of the par vagum, by which the inhibitory function of that nerve upon
the action of the heart is augmented. During the last period, on the
other hand, the increasing pressure on the vagus paralyzes its
function, and the heart, freed from its control, takes on an increased
action, the pulse rising to 120 beats, and often many more, in the
minute. Robert Whytt, in his interesting memoir,5 dates the beginning
of the second stage from the time that the pulse, being quick but
regular, becomes slow and irregular; the change again to the normal
frequency, or beyond it, marking the commencement of the third
stage.
5 “An Account of the Symptoms in the Dropsy of the Ventricles of the Brain,” in the
Works of Robert Whytt, M.D., published by his son, Edinb., 1768, p. 729.
In the early stage the respiration presents nothing abnormal, but
when the pulse becomes slow and irregular the breathing is similarly
affected. Sighing is very common in the prodromal period and first
stage. Toward the end of the second stage the increasing paralysis
of the respiratory centre gives rise to the phenomena known as the
Cheyne-Stokes respiration, consisting of a succession of respiratory
acts diminishing in force until there is a complete suspension of the
breathing, lasting from a quarter to three-quarters of a minute, when
the series begins again with a full inspiration. In general, the
variations in the rate of the respiration follow those of the pulse,
though the correspondence is not always exact.

In the early stage of the disease the pupils are usually contracted
and unequal. They are sluggish, but still respond to the stimulus of
light. At a later period they become gradually dilated, and react even
more slowly to light or not at all, the two eyes often differing in this
respect. Ophthalmoscopic examination frequently shows the
appearance of choked disc and commencing neuro-retinitis. In rare
cases tubercles are seen scattered over the fundus of the eye. They
are about the size of a small pin's head, of a yellowish color, and of
sharply-defined contour. Neuro-retinitis and choked disc are not, of
course, pathognomonic of tubercular meningitis, and choroidal
tubercles are so rarely seen as to be of little avail in diagnosis. In
fact, they are less frequent in this disease than in general
tuberculosis without meningitis. In twenty-six cases of tubercular
meningitis examined by Garlick at the London Hospital for Sick
Children they were found only once.6 The effect upon the conjunctiva
of the unclosed lids has been already described.
6 W. R. Gowers, M.D., Manual and Atlas of Medical Ophthalmoscopy, Philada., 1882,
p. 148. See, also, Seitz, op. cit., p. 347; Steffen, op. cit., pp. 452 and 472; and
“Tubercle of the Choroid,” Med. Times and Gazette, Oct. 21, 1882, p. 498.

The tongue is somewhat coated soon after the beginning of the

disease, and the breath is offensive. The appetite is lost, and there is
decided emaciation in many cases during the prodromic period. The
thirst is usually moderate. Vomiting is one of the most constant
symptoms during the first period, and its occurrence on an empty
stomach is characteristic of tubercular meningitis. It is not usually
preceded by nausea, and often takes place without effort, by mere
regurgitation, the rejected fluid consisting chiefly of bile mixed with
mucus. Although constipation is the most common condition in the
early stage, and is often rebellious to treatment, yet in some cases
diarrhœa is observed, which may mislead the physician in respect to
the diagnosis. From the beginning of the second stage, and
sometimes earlier, the discharges from the bowels and the bladder
are involuntary.

DURATION.—The duration of tubercular meningitis, apart from the

prodromic period, which often can hardly be determined, averages
from two weeks to two weeks and a half. In exceptional cases death
may take place in a few days or a week, and occasionally a patient
may linger for several weeks,7 the difference being apparently due to
the rapidity of the tubercular deposit and of the resulting
inflammation and exudation. The patient usually takes to his bed at
the beginning of the first stage, but he may be up during a part of the
day until the beginning of the second. In rare instances the child will
be about, and even out of doors, until a few days before death.
7 Such a case is reported by Michael Collins in the London Lancet, March 8, 1884.

PATHOLOGICAL ANATOMY.—The essential lesion of tubercular

meningitis consists in a deposit of miliary tubercles in the pia mater
of the brain, giving rise to inflammation of that membrane and
exudation of serum and pus. In the early stage both surfaces of the
pia are reddened and more or less thickened, and present an
opaline appearance, while between them—that is, in the meshes of
the pia—we find a colorless and transparent fluid which is effused in
greater or smaller amount, resembling jelly when viewed through the
arachnoid. These conditions are sometimes observable on the
convexity of the hemispheres, but are much more abundant on the
lateral surfaces, and especially at the base. More distinct evidence of
inflammation is shown by the presence of a yellowish or greenish-
yellow creamy deposit on the surface of the pia, consisting chiefly of
pus, which is also much more abundant at the base than elsewhere,
especially about the optic commissure, infundibulum, pons Varolii,
and the anterior surface of the medulla. The cranial nerves may be
deeply imbedded in the deposit, which often extends into the fissure
of Sylvius, gluing together the adjacent surfaces of the lobes, and
accompanies the vessels, forming narrow streaks along the sides of
the brain up to the convexity.

The miliary tubercles or granulations consist of semi-transparent

bodies, grayish or whitish in color, varying in size from that of the
head of the smallest pin, indeed almost invisible to the naked eye, to
that of a millet-seed (whence their name). Larger masses are
frequently seen, formed by the aggregation of smaller granulations.
The tubercles are usually found on the inner surface of the pia,
always in the immediate neighborhood of the blood-vessels, which
they accompany in their ramifications, and are also scattered, in
greater or less numbers, throughout the purulent exudation from the
surface of the pia. They are most abundant at the base of the brain,
ascending the sides along the course of the vessels. Sometimes,
though rarely, they are more abundant on the convexity. The total
number varies; it is usually very large, but sometimes only a limited
number exists, even in well-marked cases, and along with intense
inflammation of the pia. The granulations are found in different
degrees of development—sometimes all of them similar in color,
size, and consistency, at others in various stages of fatty
degeneration. The distribution may be symmetrical in the two
hemispheres or irregular. Under the microscope (after suitable
preparation of the part) the bacillus tuberculosus in considerable
numbers may be found in the pia, in places adjacent to the
arterioles.8
8 See a case reported by Y. Dawson in the London Lancet, April 12, 1884, in which
tubercles were visible only by the microscope with numerous bacilli.

The ventricles of the brain are usually distended with a clear or

opalescent, rarely bloody, fluid, the amount of which generally
corresponds to the intensity and extent of the meningeal
inflammation, although sometimes it is not above the normal
quantity. The two lateral ventricles are affected in an equal degree;
the third and fourth ventricles are more rarely implicated. According
to Huguenin,9 it is doubtful whether acute inflammation of the
ependyma takes place in tubercular meningitis. Steffen also10 says
that the ependyma is not inflamed, and that it is not the seat of the
deposit of tubercles. This latter statement is denied by other
authorities, and Huguenin is inclined to believe that they may exist in
that membrane. In the following case, under my care, abundant
granulations were found on the surface of the ependyma:
9 G. Huguenin, op. cit., p. 499.

10 Op. cit., p. 449.

Olaf M—— (male), æt. 8 years, born in Denmark, entered

Massachusetts General Hospital Sept. 13, 1881. Maternal
grandmother died of consumption; paternal grandfather lived to the
age of ninety-five years. One brother had some disease of hip.
Patient was the child of poor parents and lived in an unhealthy
suburb of Boston. During the two preceding winters he had a bad
cough. He was apparently well till four weeks before his entrance,
when he complained of bellyache, and became listless, but he was
out of doors ten days before he came to the hospital. It was noticed
that he was sensitive to sound. No vomiting, no diarrhœa, no
epistaxis, no cry; some cough. He had been somnolent, and was
observed to swing his arm over his head while asleep. June 14,
when first seen by me, he was lying on his back, unconscious, eyes
half closed, pupils dilated, jaw firmly closed, much emaciated, belly
retracted, left leg occasionally flexed and extended. No priapism.
The optic discs were reddened. June 15, there is some intelligence,
he answers questions; keeps one hand on the genitals. June 16,
pupils contracted, does not swallow. June 18, left eye divergent,
conjunctiva injected, whole surface livid, cries out occasionally. Died
at midnight.

FIG. 30.
Autopsy.—General lividity of surface, much emaciation. Much fine
arborescent injection on outer surface of dura mater. Numerous
Pacchionian bodies. Yellow matter beneath arachnoid along course
of vessels on each side of anterior lobes. Abundant fine granulations
along course of vessels on each anterior lobe, on upper margins of
median fissure, along fissure of Sylvius, and on choroid plexuses.
Very little lymph at base of brain. Six or eight ounces of serum from
lateral ventricles, and abundant fine transparent granules over
ependyma of both. Numerous opaque granulations in pia mater of
medulla oblongata. Surface of right pleura universally adherent.
Mucous membrane of bronchia much injected; a considerable
amount of pus flowed from each primary bronchus. No tubercles in
lungs nor in peritoneum. No ulcerations in intestines. No other
lesions.

The choroid plexuses are generally involved in the inflammatory

process, and are sometimes covered with yellow purulent
exudations. As in the above case, large numbers of tubercles may
be found in them, notwithstanding the opinion of Huguenin that their
number is always small.

The substance of the brain in the vicinity of the tubercular deposit is

generally found in a more or less œdematous condition, owing to the
obstruction of the circulation resulting from compression of the
vessels by the tubercles and effused lymph. Softening, sometimes
even to diffluence, not unfrequently occurs in the neighborhood of
the deposit, probably from ischæmia (necrobiosis). If there be any
considerable amount of exudation in the ventricles, the convolutions
are flattened by compression against the cranial bones.

The above-described lesions are not confined to the brain, but may
extend to the cerebellum, the pons, the medulla, and the spinal cord.
If examinations of the latter were more frequent in autopsies of this
disease, we should doubtless find, as has been done in some
instances, that the membranes often show the characteristic
alterations of tubercular meningitis, and even the presence of
granulations in the cord itself. The lesions may extend throughout
the cord, and are especially noticed in the dorsal region and in the
vicinity of the cauda equina. Their presence explains some of the
symptoms evidently due to spinal origin, such as retraction of the
head with rigidity of the neck and of the trunk, contractions of the
limbs, tetanic spasms, priapism, paralysis of the bladder and rectum,
etc., which are common in simple spinal meningitis.
The deposit of miliary tubercles in the pia mater, with little or no
accompanying meningitis, is met with in rare instances. The
tubercles are few in number, but vary in dimensions, being
sometimes united together in masses of considerable size, which are
frequently encysted. Beyond thickening and opacity of the
membrane, their presence seems to excite but little inflammatory
reaction, but they are generally accompanied by ventricular effusion
which by its pressure gives rise to characteristic symptoms.

The principal lesions found in other organs of the body consist of

tubercle in various stages of development, caseous matter, diseases
of the bones, etc. Miliary granulations are chiefly seen in the lungs,
peritoneum, intestinal mucous membrane, pleura, spleen, liver, and
kidneys. The bronchial and mesenteric glands often contain caseous
masses, some of which are broken down and suppurating. The
testicles sometimes present the same appearances. In adults, the
most frequent lesion which is found external to the brain is
pulmonary tuberculosis in a more or less advanced stage. Tubercles
are also sometimes present in the eye. Angel Money11 states that out
of 44 examinations made at the Hospital for Sick Children, London,
the meninges were the seat of gray granulations in 42. The choroid
(one or both) showed tubercles 14 times (right 3, left 5, both 6), and
11 times there were undoubted evidences of optic neuritis. Twice the
choroid was affected with tubercle when the meninges were free; in
one of these instances there was a mass of crude tubercle in the
cerebellum; in the other, although there were tubercles in the belly
and chest, there were none in the head. So that 12 times in 42 cases
of tubercles in the meninges there were tubercles in the choroid—i.e.
about 31 per cent.
11 “On the Frequent Association of Choroidal and Meningeal Tubercle,” Lancet, Nov.
10, 1883.

DIAGNOSIS.—In many cases tubercular meningitis offers but little

difficulty in the diagnosis. Although the symptoms, taken singly, are
not pathognomonic, yet their combination and succession, together
with their relation to the age, previous health, and antecedents of the
patient, are usually sufficient to lead us to a correct opinion. The
prodromic period of altered disposition (irritability of temper or
apathetic indifference), headache, constipation, vomiting, and
emaciation, followed by irregularity and slowness of the pulse,
sighing respiration, sluggishness and irregularity of the pupils; the
progress from somnolence to unconsciousness and coma; the
sudden lamentable cry; the convulsions and paralysis; the return of
rapid pulse and respiration in the last stage,—are characteristic of no
other disease. Our chief embarrassment arises during the insidious
approach of the malady, before its distinctive features are visible or
when some important symptom is absent. Its real nature is then apt
to be overlooked, and, in fact, in some cases it is impossible to
decide whether the symptoms are indicative of commencing cerebral
disease, or, on the other hand, are owing to typhoid fever, to a
simple gastro-intestinal irritation from error in diet, to worms in the
alimentary canal, to overwork in school, or to some other cause.
Under these circumstances the physician should decline giving a
positive opinion until more definite signs make their appearance. It
must be remembered that very important symptoms may be absent
in cases which are otherwise well marked. In all doubtful cases the
family history should, if possible, be obtained, especially whether
one or both parents or other near relatives have been consumptive
or have shown symptoms of scrofula or tuberculosis in any form, and
whether the patient himself has signs of pulmonary tuberculosis, of
enlarged or suppurating glands, or obstinate skin eruptions. The
presence or history of those conditions would add greatly to the
probability of tubercular meningitis.

The diseases for which tubercular meningitis is most liable to be

mistaken are acute simple meningitis, typhoid fever, acute gastro-
intestinal affections, eclampsia of infants and children, worms in the
intestines or stomach, the hydrencephaloid disease of Marshall Hall,
and cerebro-spinal meningitis.

Acute meningitis is distinguished from the tubercular disease by its

sudden invasion without prodromatous stage, by the acuteness and
intensity of the symptoms, the severity of the headache, the activity
of the delirium, the greater elevation of the temperature, and by its
brief duration, which rarely exceeds one week. In those exceptional
cases of tubercular meningitis in which the prodromal period is
absent or not observed and the course is unusually rapid, it would be
perhaps impossible to distinguish between the two diseases. A
family history of tubercle, or the discovery of the granulations in the
choroid by ophthalmoscopic examination, might save us from error
under such circumstances. The great rarity of idiopathic simple
meningitis should be remembered. Meningitis from disease of the
ear sometimes resembles the tubercular affection, but the history of
the attack, usually beginning with local pain and otorrhœa, will in
most cases prevent any confusion between the two forms of
disease.

The early period of typhoid often bears considerable resemblance to

that of tubercular meningitis. Headache, languor, restlessness, and
mild delirium are common to both. Typhoid can be distinguished by
the coated tongue, the diarrhœa, the enlargement of the spleen, the
tympanites, abdominal tenderness and gurgling, the eruption, and,
above all, by the characteristic temperature-curve, which, if
accurately observed, is conclusive. The course of typhoid fever is
comparatively uniform, while that of tubercular meningitis is often
extremely irregular. It should not be forgotten that the two diseases
may coexist.

The presence of worms in the alimentary canal may cause

symptoms somewhat like those of tubercular meningitis, and the
symptoms of the latter disease are occasionally erroneously
attributed to those parasites. The administration of an anthelmintic,
which should never be omitted in doubtful cases, will clear up all
uncertainty.

Cerebro-spinal meningitis is usually an epidemic, and therefore not

likely to be confounded with the tubercular disease. In sporadic
cases it can be recognized by its sudden onset and acute character,
by the eruption, and by the prominence of the spinal symptoms.
The so-called hydrencephaloid disease of Marshall Hall is a
condition of exhaustion and marasmus belonging to infancy, caused
by insufficient or unsuitable nourishment, by diarrhœa, and by the
injudicious depletive treatment so much in vogue in former times,
when the affection was much more common than at present. Some
of its symptoms, such as sighing respiration, stupor, pallor, and
dilated pupils, bear a certain resemblance to those of tubercular
meningitis, though it would be more easily confounded with chronic
hydrocephalus. The absence of constipation, headache,
convulsions, and vomiting, and the favorable results of suitable
nourishment and stimulants, serve to distinguish it from cerebral
disease.

Eclampsia, or sudden convulsion, is common in infants and young

children, and, since the occurrence of a fit may be the first or the
most striking symptom in tubercular meningitis, it is important to
ascertain its origin. In the majority of cases convulsions in children
arise from some peripheral irritation, such as difficult dentition,
worms in the alimentary canal, constipation, fright, etc., acting
through the reflex function of the spinal cord, which is unusually
sensitive in the early period of life. The absence of previous
symptoms, and the discovery of the source of the irritation, with the
favorable effect of its removal by appropriate treatment, will in most
cases suffice to eliminate structural disease of the brain. In others
we must withhold a positive opinion for a reasonable time in order to
ascertain whether more definite symptoms follow. Convulsions also
occasionally form the initial symptom of the eruptive fevers,
especially scarlatina. Here the absence of prodromal symptoms, and
the speedy appearance of those belonging to the exanthematous
affection, will remove all sources of doubt. Convulsions, with or
without coma, occurring in the early stage of acute renal
inflammations, may simulate the symptoms of tubercular meningitis.
An examination of the urine will show the true nature of the disease.

In addition to the above diseases there are some cerebral affections

of uncertain pathology which resemble tubercular meningitis, but
which are not generally fatal. As Gee justly remarks,12 “Every
practitioner from time to time will come across an acute febrile
disease accompanied by symptoms which seem to point
unmistakably to some affection of the brain, there being every
reason to exclude the notion of suppressed exanthemata or
analogous disorders. After one or several weeks of coma, delirium,
severe headache, or whatever may have been the prominent
symptom, the patient recovers, and we are left quite unable to say
what has been the matter with him. To go more into detail, I could not
do otherwise than narrate a series of cases which would differ from
each other in most important points, and have nothing in common
excepting pyrexia and brain symptoms. There is, generally,
something wanting which makes us suspect that we have not to do
with tubercular meningitis. Brain fever is as good a name as any
whereby to designate these different anomalies; cerebral congestion,
which is more commonly used, involves an explanation which is
probably often wrong, and certainly never proved to be right.” No
doubt such cases are occasionally cited as examples of recovery
from tubercular meningitis.
12 “Tubercular Meningitis,” by Samuel Jones Gee, M.D., in Reynolds's System of
Medicine, Philada., 1879, vol. i. p. 832.

PROGNOSIS.—Although there are on record undoubted instances of

recovery from tubercular meningitis, yet their number is so small that
practically the prognosis is fatal. It is safe to say that in almost all the
reported cases of recovery the diagnosis was erroneous.13 Even
should the patient survive the attack, he is usually left with paralyzed
limbs and impaired mental faculties, and dies not long afterward from
a recurrence of the disease or from tuberculosis of the lungs or other
organs.
13 Hahn, “Recherches sur la Méningite tuberculeuse et sur le Traitement de cette
Maladie” (Arch. gén. de méd., 4e Série, vols. xx. and xxi.), claims to have cured 7
cases, but of 5 of them there is no evidence that they were examples of tubercular
meningitis at all. The subject of the curability of tubercular meningitis is ably treated
by Cadet de Gassicourt (Traité clinique des Maladies de l'Enfance, vol. iii., Paris,
1884, p. 553 et seq.). His conclusion is that most of the alleged cures are cases of
 meningitis of limited extent, arising from the presence of tubercular tumors, syphilitic
gummata, cerebral scleroses, and neoplasms of various kinds.

TREATMENT.—In view of the fatality of the disease, and of its frequent

occurrence in childhood, the prophylactic treatment is of great
importance. Every effort should be made to protect children whose
parents or other near relatives are tuberculous or scrofulous, and
who are themselves delicate, puny, or affected with any
constitutional disorder, from tubercular meningitis, by placing them in
the best possible hygienic conditions. Pure air, suitable clothing,
wholesome and sufficient food, and plenty of out-of-door exercise
are indispensable. Sedentary amusements and occupations should
be sparingly allowed. Especial pains should be taken to prevent
fatigue by much study, and school-hours should be of short duration.
The hygiene of the school-room is of paramount importance, and if
its ventilation, temperature, and light are not satisfactory, the child
should not be permitted to enter it. The bed-chamber should be well
ventilated night and day. A sponge-bath, cold or tepid according to
the season or to the effect on the patient, should be given daily,
followed by friction with a towel. The bowels must be kept regular by
appropriate diet if possible, or by simple laxatives, such as magnesia
or rhubarb. For delicate, pale children some preparation of iron will
be useful. The choice must be left to the practitioner, but one of the
best in such cases is the tartrate of iron and potassium, of which
from two to six grains, according to the age, may be given three
times daily after meals. Cod-liver oil is invaluable for scrofulous
patients or where there is a lack of nutrition. A teaspoonful, given
after meals, is a sufficient dose, and it is usually taken without
difficulty by children, or if there be much repugnance to it some one
of the various emulsions may be tried in proportionate dose. Along
with this, iodide of iron will in many cases be found useful or as a
substitute for the oil when the latter cannot be borne. It is best given
in the form of the officinal syrup, in the dose of from five to twenty
drops. Change of air is useful in stimulating the nutritive functions,
and a visit to the seashore or mountains during warm weather will
often be followed by general improvement.
Since it is not possible to arrest the disease when once begun, the
efforts of the physician must be directed toward relieving the
sufferings of the patient as far as possible. In the early period the
restlessness at night and inability to sleep will call for sedatives, such
as the bromide of sodium or of potassium, in the dose of ten or
fifteen grains at bedtime or oftener. This should be well diluted with
water, sweetened if necessary. The addition of five to twenty drops of
the tincture of hyoscyamus increases the effect. Sometimes chloral
hydrate, either alone or combined with the bromide when the latter
fails, will procure quiet sleep. From five to ten grains may be given at
a dose, according to the age. Compresses wet with spirit and water
or an ice-cap may be applied to the head if there be much pain in
that region, or it may be necessary to give opium in some of its forms
by the mouth, such as the tincture or fluid extract, in doses of from
one to five drops. Constipation is best overcome by means of
calomel in three- to five-grain doses, to which may be added, when
necessary, an equal amount of jalap powder, or an enema of
soapsuds may be administered. Active purging should be avoided.
Liquid nourishment, such as milk, gruel of oatmeal, farina, or barley,
beef-tea, broths, etc., must be given in moderate quantities at
intervals of a few hours so long as the patient is able to swallow.
Occasional sponging of the whole surface with warm or cool water,
and scrupulous attention to cleanliness after defecation, especially
when control of the sphincters is lost, will add to his comfort. He
should occupy a large and well-ventilated chamber, from which all
persons whose presence is not necessary for his care and comfort
should be excluded. He should be protected from noise and from
bright light, and should lie on a bed of moderate width for
convenience of tending.

There is no specific treatment at present known which is likely to be

of any benefit in this disease, any more than in tuberculosis of other
organs than the brain. Common experience has shown that mercury,
which formerly had so high a reputation in the treatment of cerebral
diseases of early life, not only fails completely, but adds to the
sufferings of the patient when pushed to salivation. The iodide of
potassium is recommended by almost all writers, but, so far as I