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O A P L
OX F O R D A M E R I C A N P S YC H I AT RY L I B R A RY

Major Depressive
Disorder
O A P L
OXF OR D AM ER I C AN P S YC H I AT RY L I BR ARY

Major
Depressive
Disorder
Stephen M. Strakowski, MD
Erik B. Nelson, MD

1
1
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You must not circulate this work in any other form

and you must impose this same condition on any acquirer.

Library of Congress Cataloging-in-Publication Data

Strakowski, Stephen M., author.
Major depressive disorder / Stephen Strakowski, Erik Nelson.
p. ; cm.
Includes bibliographical references.
ISBN 978–0–9–02068–5 (alk. paper)
I. Nelson, Erik, 964– author. II. Title.
[DNLM: . Depressive Disorder—Handbooks. WM 34]
RC537
66.85'27—dc23
204047696

9 8 7 6 5 4 3 2 
Printed in the United States of America
on acid-free paper
 Contents

. Introduction 
2. Making a Diagnosis of Depression 5
3. Epidemiology of Depressive Disorders 5
4. Illness Comorbidity and Co-occurrence
with Depressive Disorders 23
5. Neurophysiology of Depressive Disorders 3
6. Genetics of Depression 43
7. Psychopharmacology and Other Biological
Therapies in the Management of Depression 49
8. Psychotherapy and Related Techniques 69
9. A Programmatic Approach to Treatment 75
0. Managing Special Populations 87

Appendix: Example Mood Chart 99

Index 0
Dr. Strakowski would like to dedicate this book to his family, for their
unwavering support, and to his patients who serve as a constant inspiration.

Dr. Nelson would like to dedicate this book to his mother, whose struggle
with depression has not prevented her from being a wonderful teacher, wife,
and parent.
Chapter 

Introduction
Depressive disorders, often referred to as “clinical depression,” include
major depression, dysthymia, and other related conditions that have
plagued humanity throughout history. Unfortunately, this epidemic has often
been nearly invisible; affected people have typically been stigmatized and
ostracized, so they suffered in silence rather than seeking help. For much
of human history, “help” was quite barbaric, ranging from blood-letting to
witch burning, both of which managed to decrease the rates of depression
by eliminating the sufferer! In the past few years, stigma surrounding depres-
sion has dramatically decreased as a number of well-known individuals pub-
licly acknowledged personal experiences with depression. Newscaster Mike
Wallace (Sixty Minutes) was one of the first to use his own experiences with
depression and suicidality, coupled with his celebrity, to raise awareness of
this often mysterious malady. In his book Darkness Visible, the noted author

1
(of Sophie’s Choice) William Styron provides a heart-wrenching and gripping
attempt to describe the indescribable—the depth, darkness, and despair of
his experience with major depression. Actress Brooke Shields wrote of her
struggles with postpartum depression in Down Came the Rain, only to be pub-
licly criticized by fellow actor Tom Cruise, who expressed the depth of igno-
rance and stigma still maintained by the uninformed when faced with mental
illness. Ms. Shields’s courageous response to this criticism opened doors for
other women to seek help for postpartum depression. Terry Bradshaw, one
of the best quarterbacks in NFL history, taught us that depression attacks
even the toughest among us. Tipper Gore, Amanda Beard, Halle Berry,
J. K. Rowling, Jim Carrey, Ashley Judd, David Letterman, and many others
joined the battle against depression by discussing their own experiences; in
doing so, they demonstrated that depression cuts across social boundaries
with impunity. These brave celebrities put a public face on depression and
encouraged acceptance of it as a medical illness. However, the apparent
sudden increasing frequency of these announcements gives the misleading
impression that depression is somehow new or fashionable. Nothing could
be further from the truth.
The history of depression dates back millennia to the beginning of recorded
human history. Descriptions of depression appear in Ancient Egyptian papyri
as well as the Indian Mahabharata. As early as 400 bc, Hippocrates declared
that, rather than being of magical or spiritual origin, mental disorders arose
from imbalance among the various humors that comprised human health,
namely blood, phlegm, yellow bile, and black bile. Specifically, depression,
called “melancholia,” was believed to result from an excess of black bile
(melancholia translates literally as “black bile”). The great physician Galen
Major Depressive Disorder supported this humoral view of depression so that it persisted, more or less
intact, for nearly 500 years.–3 In the nineteenth century, European psychia-
trists began to delineate among different mental disorders, culminating in the
early twentieth-century work of Emil Kraepelin, who distinguished dementia
praecox from manic-depressive illness, the latter of which included both uni-
polar and bipolar depressive disorders. Indeed, the unipolar/bipolar distinc-
tion did not prevail until 957, when Leonhard proposed that the occurrence
of mania (bipolar disorder) defined a separate illness from one involving only
recurrent (unipolar) depressive episodes. With this long track record, then, it
should be no surprise that a number of famous individuals throughout history
recorded their struggles with depression (Table .).
As the stigma surrounding depression steadily diminishes, it becomes
increasingly obvious how troublesome it is. Epidemiological studies sug-
gest that at least 5% of individuals suffer from depression at some point
in their lives, with 5% in any given year; consequently, depression is one
of the most common medical conditions affecting humankind.4–6 Rates of
depression in medical settings are even higher as depression is comorbid
in more than half of people suffering from major neurological, psychiat-
ric, and other medical conditions. Although women experience depres-
sion more commonly then men, depression strikes across gender, race,
age, and class boundaries. By the year 2020, depression is expected to be
the leading cause of disability worldwide and, with suicide occurring in up
2

to 7–8% of depressed individuals; it is also one of the leading causes of

premature mortality. Although depression represents a major (if not the
major) current public health problem, less than half of affected individuals
receive evidence-based treatment.
Despite the prevalence and importance of depression, its causes are
not well understood. Many people who experience depression appear to
inherit a genetic risk, although environmental effects, especially stress and

Table . Historical Figures Suffering From

Probable Depression
Individual Role When
Lived
Winston Churchill UK Prime 874–965
Minister
Charles Darwin Naturalist 809–882
Francisco Goya Painter 746–828
Ernest Hemingway Writer 899–96
William James Psychologist 842–90
Meriwhether Lewis Explorer 774–809
Abraham Lincoln US President 809–865
Isaac Newton Physicist 642–727
Friedrich Nietzsche Philosopher 844–900
Mark Twain Humorist/Author 836–90
Walt Whitman Poet 89–892
the occurrence of other illnesses, appear to significantly contribute to the

Introduction
onset of depression. Moreover, the specific genes that impart increased risk
for depression have not yet been identified. In fact, depression is so com-
mon in certain neurological, medical, and psychiatric conditions, we won-
dered whether it represents a nonspecific response to brain insult or injury.7
Contrary to this suggestion, however, there are individuals who develop

Chapter 
depression in the absence of any clear precipitants. Regardless, the end result
is a condition in which the healthy neural mechanisms that maintain emotional
homeostasis in the brain become disrupted. Nonetheless, as the neurobiol-
ogy of depression is clarified, treatment advances will hopefully move from
reliance on strictly empirical and often serendipitous treatment findings to
more targeted approaches.
It is truly unfortunate that most people suffering from depression do not
receive evidence-based treatment in a timely manner, since both medical
and psychological interventions significantly improve symptoms, function,
and outcome. In part, the sheer volume of depression stresses psychiatric,
medical, and therapeutic care delivery systems, so that many affected indi-
viduals simply land in the wrong clinic at the wrong time. Moreover, despite
advances, because society continues to stigmatize and minimize depres-
sive symptoms, people are often reluctant to seek help or to discuss their
concerns with caregivers. Indeed, the cognitive dissonance and negativity
that accompany depression leave many sufferers with the (false) a priori

3
assumption that “nothing will help me.” Also, as noted, depression often
occurs within the context of other medical and psychiatric conditions, so
sometimes it gets lost in the treatment of the other illness. Consequently,
effective treatment of depression can be challenging, particularly if it fails to
respond to the first intervention. Indeed, in these instances, successful treat-
ment is programmatic, incorporating sophisticated psychopharmacology,
evidence-based therapies, lifestyle modifications, and general good health
practices.
With these considerations in mind, in this Oxford American Psychiatry
Library (OAPL) volume, we review practical and succinct descriptions of
depression and its management in order to provide a quick reference for
the busy practitioner. This volume may also be useful for nonmedical people
suffering from depression and their families, as well as medical or psychol-
ogy students who are trying to better understand these common conditions.
A major focus of this volume will be to provide a programmatic approach to
the management of depression in order to develop systematically the best
treatment, as opposed to the common situation in which people receive
inadequate treatment that changes prematurely and too frequently, leading
to submaximal outcomes. Ultimately, the goal of this volume is to improve
the lives of people suffering from depression and to bring hope to them and
their loved ones.
[Authors’ Note: In this book we use the term “depression” (singular form)
to represent multiple conditions that perhaps more correctly would be called
“depressive disorders” (plural form). We made this choice because the sin-
gular form is more common in the vernacular; however, when distinctions
among depression subtypes are relevant, we use the plural form.]
Major Depressive Disorder References
. Davison K. Historical aspects of mood disorders. Psychiatry 2008; 8:47–5.
2. Paykel ES. Basic concepts of depression. Dialogues Clin Neurosci 2008;
0:270–289.
3. Goodwin FK, Jamison KR. Chapter : Conceptualizing manic-depressive
illness: the bipolar-unipolar distinction and the development of the
manic-depressive spectrum. In: Manic-Depressive Illness: Bipolar Disorders and
Recurrent Depression. New York: Oxford University Press, 2007.
4. Weissman MM, Bruce ML, Leaf PJ, Florio LP, Holzer C. Affective disorders.
In: Robins LN, Regier DA, eds., Psychiatric Disorders in America: The Epidemiologic
Catchment Area Study, pp. 53–80. New York: Free Press, 99.
5. Kessler RC, McGonagle KA, Zhao S, Nelson CB, Hughes M, Eshleman S,
Wittchen H-U, Kendler KS. Lifetime and 2-month prevalence of DSM-III-R
psychiatric disorders in the United States. Arch Gen Psychiatry 994; 5:8–9.
6. Kessler RC, Chiu WT, Demler O, Walters EE. Prevalence, severity and comor-
bidity of 2-month DSM-IV disorders in the National Comorbidity Survey
Replication. Arch Gen Psychiatry 2005; 62:67–627.
7. Strakowski SM, Adler CM, DelBello MP. Is depression simply a nonspecific
response to brain injury? Curr Psychiatry Rep 203; 5:386–294.
4
Chapter 2

Making a Diagnosis of
Depression

2.. Brief Historical Overview

As noted in Chapter , depression has accompanied humanity throughout its
history. Descriptions of depressive-like conditions are found in the ancient
Egyptian Ebers papyrus (ca. 500 bc), the Indian Ramayana and Mahabharata
(ca. 4th–5th century bc), and the Biblical Old Testament (perhaps as old as ca.
000 bc). The ancient Greeks considered depression (called “melancholia”)
a medical condition that arose from an imbalance of humeral constituents,
namely an excess of “black bile”; indeed, “melancholia” translates as “black
bile.” Hippocrates (ca. 400 bc) described melancholia as prolonged despon-

5
dency, loss of appetite, insomnia, and agitation. Aretaeus of Cappadocia
linked melancholia to suicide. These ancient descriptions are reminiscent of
the same symptoms used today to diagnose major depression.
The black bile hypothesis of melancholia persisted through the Middle
Ages, although it was unfortunately at times linked to the sin of “sloth,” and
so was attributed to demons or immorality to be remedied by forced manual
labor, beatings, or even witch burnings. With the Renaissance, some scholars
challenged the spiritual basis of melancholia, perhaps culminating in Richard
Burton’s The Anatomy of Melancholia (62 ad). Burton was a clergyman who
returned to the humoral (as opposed to moral) theory of melancholia, and
suggested it could be remedied by healthy diet, sleep, meaningful work, and
intellectual pursuits. Although he typically attributed the humoral imbalance
to specific causes, such as poor diet, he recognized that melancholia also
occurred de novo. As the focus of medicine shifted to hemodynamic theories
of disease in the eighteenth century, melancholia was increasingly considered
a physiological condition. With increasingly indiscriminate definitions of mel-
ancholia, the term “depression” began to be used by the late 800s, with
melancholia reserved for a subtype with psychosis.
In the late nineteenth and early twentieth century, Emil Kraepelin dra-
matically influenced psychiatry by separating manic-depressive insanity
from dementia praecox, based primarily on course of illness. Specifically,
manic-depressive insanity exhibited improvement between episodes,
whereas dementia praecox was unrelenting and deteriorating; the latter
became the basis for our current conceptualization of schizophrenia. This
distinction placed depression firmly into a single category with all other mood
disorders. Kraepelin’s conceptualization of affective illness was viewed as too
Major Depressive Disorder broad by many psychiatrists, however, leading Leonhard in 957 to coin the
term “bipolar disorder” in order to distinguish individuals who experienced
mania and depression (i.e., two poles) from those with only recurrent major
depression (i.e., one pole, or “unipolar” depression). Several landmark stud-
ies and the relative specificity of lithium for the treatment of bipolar disorder
reinforced this classification.2 Given that specific causes of depression remain
uncertain, the current diagnostic systems3,4 are based on empirical data
that have identified commonly co-occurring symptoms historically linked to
depression. Consequently, diagnoses of major depression and related condi-
tions rely on clinical assessment of these symptoms, more or less devoid of
hypotheses regarding underlying etiology. As discussed in Chapter , multiple
potential causes have been identified, suggesting that depression represents a
nonspecific response to a variety of brain insults.5 Nonetheless, for diagnostic
purposes, depression is defined as a collection of commonly co-occurring
symptoms, that is, a syndrome.

2.2. Symptoms and Diagnosis of

Major Depression
Major depression, then, is defined by the co-occurrence of several specific
symptoms that are listed in Box 2.; these symptoms serve as the basis for
6

the two most widely used criteria sets, namely the American Psychiatric
Association’s Diagnostic and Statistical Manual of Mental Disorders (5th edi-
tion; DSM-5) and the International Classification of Diseases (0th revision;
ICD-0 [with ICD- currently under development and likely remaining

Box 2. Symptoms of Major Depression

• Persistent sadness or low mood,2,3
• Anhedonia—loss of interest in pleasurable experiences,2
• Fatigue or low energy2
• Feelings of worthlessness or low self-confidence3
• Excessive guilt or self-blame
• Change in appetite and weight3
• Psychomotor agitation or retardation
• Anxiety and nervousness
• Disturbed sleep—insomnia or hypersomnia3
• Impaired concentration or indecisiveness3
• Somatic complaints (e.g., back pain, headache)
• Hopelessness3
• Suicidal thoughts or behavior

Considered a core symptom in DSM-5.
2
Considered a core symptom in ICD-0.
3
Included as DSM-5 criteria for dysthymia.
largely similar]). A diagnosis of depression requires at least four (ICD-0) or

Making a Diagnosis of Depression

five (DSM-5) of the symptoms from Box 2., including at least two of the core
symptoms. Moreover, these symptoms must represent a change in a person’s
typical behavior and must be relatively persistent nearly every day for at least
2 weeks (DSM-5) to  month (ICD-0). Symptoms must also cause functional
impairment in order to warrant a diagnosis of major depression.
Despite its name, perhaps the most defining and relatively specific symp-
tom of major depression is anhedonia, that is, the loss of the ability to
experience pleasure or a disinterest in pleasurable activities that a person
would normally enjoy. In many circumstances, depressed individuals do not
acknowledge feeling sad or down, but do express a loss of interest in hob-
bies, relationships, or other life pursuits. As part of the clinical assessment
of major depression, identifying these life pursuits and tracking them over
time helps to define the course of illness and recovery. One common and
relatively easily tracked expression of anhedonia in adults is a decrease in sex

Chapter 2
drive; clinicians often fail to inquire about sexual activity, potentially ignoring
an important clinical clue. As noted in Box 2., anhedonia is a core symptom
of major depression.
Another core symptom of depression is low or dysphoric mood, namely
persistent despondency and sadness. In adolescents, irritability often accom-
panies or substitutes for low mood during a depressive episode. Alternatively,
depressed individuals may report reactive dysphoria in which minor problems

7
lead to excessive negative emotional responses. Low mood is expressed in
many ways, depending on culture and sex, and men tend to be less likely to
describe these feelings than women.
The final core symptom is low energy or fatigue (Box 2.). Accompanying
low energy is often the cognitive experience of a loss of motivation, so that
even simple tasks, like showering, seem insurmountable to someone who
is depressed. These three core symptoms—anhedonia, low mood, and low
energy—commonly co-occur and in many ways define depression in and of
themselves. However, as noted, current criteria sets require one or more
additional symptoms from Box 2..
These additional symptoms reflect disturbances in neurovegetative
functions, behavior, and cognition. Sleep and appetite can be increased
or decreased. Weight loss accompanies appetite loss in some individuals.
Psychomotor changes range from retardation, in which movement and
thinking are slowed, to anxious agitation and restlessness. Anxiety and ner-
vousness occur in many depressed individuals such that the intersection
between anxiety and depressive disorders can be complex (see Chapter ),
and an anxious subtype of depression is recognized. Cognitive symptoms
include loss of self-esteem and thoughts of low self-worth and hopelessness.
During depression, individuals become self-accusatory, taking responsibil-
ity for negative circumstances in situations in which they had no impact or
control. Concentration difficulties occur and are sometimes misinterpreted
as memory loss as people fail to store information due to inattention. In
older patients, this symptom can be difficult to distinguish from early demen-
tia, although complicating this interpretation is that memory loss in depres-
sion may be a sign of incipient dementia in the elderly. Somatic complaints
Major Depressive Disorder are common during depression and typically include nonspecific pain syn-
dromes. Psychosis (hallucinations and delusions) and catatonia may occur
during a severe depressive episode. Delusions in depression often involve
themes of guilt, persecution or loss as part of the overall negative cognitive
presentation.
The most concerning behavioral expression of depression is suicidality.
Suicide represents a terrible permanent solution for a temporary and treat-
able problem. People with major depression have a high rate of suicide, with
a lifetime risk of perhaps 8%; depressed men are 5–7 times more likely to
commit suicide than women, although women make more attempts. People
who are untreated have up to a 5 times higher risk of suicide than those who
receive care. Hopelessness also increases the risk for suicide.

Key Point: Major depression is a syndrome characterized by persistent

anhedonia, low or dysphoric mood, low energy or fatigue, and a num-
ber of other neurovegetative and cognitive symptoms.

2.3. Subtypes of Major Depression

Different combinations of the various symptoms that occur during a major
depressive episode define a few subtypes. Identifying subtypes may help to
8

guide treatment decisions (discussed briefly here, but in detail in Chapters 7

and 0).
2.3.. Anxious Depression
As noted, anxiety is common during major depression, affecting up to 80%
of people during an episode.6 Many of these individuals will concurrently
meet criteria for major depression and an anxiety disorder (e.g., generalized
anxiety or panic disorder). High levels of anxiety are associated with poorer
treatment response and increased risk of suicide. Anxious depression may be
more common in women than men.
2.3.2. Melancholic Depression
The term “melancholic depression” dates to ancient Greece, but in cur-
rent nomenclature refers to a specific presentation that includes severe
anhedonia, mood nonreactivity to life events, late insomnia (early morn-
ing awakening), marked loss of appetite, and psychomotor symptoms.
Melancholic depression is associated with greater likelihood of excessive
hypothalamic-pituitary-adrenal (HPA) axis activity and may be more respon-
sive to antidepressants (perhaps particularly tricyclic antidepressants) and
electroconvulsive therapy (ECT) than non-melancholic depression.7
2.3.3. Atypical Depression
Atypical depression is somewhat the converse of melancholic depression.
Namely, it involves hypersomnia instead of insomnia, weight gain instead of
weight loss, psychomotor “leaden paralysis” rather than agitation, excessive
rejection sensitivity in interpersonal relationships, and mood reactivity such
that people can be “cheered up” with positive events. Some studies suggest

Making a Diagnosis of Depression

that atypical depression may be linked to bipolar disorder, although this rela-
tionship is not definitive.2 It may also be more common in women, begin ear-
lier in life, and have a more chronic course than other types of depression.
Atypical depression may be less treatment responsive than other subtypes of
depression.
2.3.4. Psychotic Depression
Psychosis (that is, hallucinations and delusions) occurs in up to 5% of depres-
sive episodes, or about 0.6% of the population.8 In some individuals, these
symptoms can be difficult to identify, as responses to questions may be too
guarded or sparse to elicit delusional concerns. Delusions can be mood con-
gruent (i.e., themes of loss, sadness, or persecution) or incongruent (i.e.,
themes of grandiosity or physical impossibility). Mood-incongruent psychosis
may be less treatment responsive or may herald the onset of a primary psy-

Chapter 2
chotic disorder (e.g., schizophrenia) in young people or dementia in older
people. The presence of psychosis requires a combination of antidepressants
and antipsychotics, as neither medication by itself is particularly helpful. ECT
often is a first-line choice as well. The role of psychotherapy is limited.
Although relatively unusual now in Western culture, catatonia appears to
be more common in psychotic depression or bipolar mania than schizophre-
nia. Catatonia can be life-threatening, so warrants aggressive intervention.

9
ECT is often the treatment of choice in these cases, and benzodiazepines may
also acutely relieve symptoms.
2.3.5. Postpartum Depression
The perinatal period is characterized by a number of significant hormonal,
social, and physical changes that underlie an increased risk of depression. Up
to 6% of women experience a major depressive episode within the first
3 months after childbirth, and many develop symptoms even before deliv-
ery. In this period, major depression may be overlooked due to so-called
“excuses” for symptoms that include sleep deprivation, a change in social
roles, and physical changes associated with nursing and delivery; clinically it
is important to maintain a high index of suspicion for new depression post-
partum, particularly in high risk groups that include women with bipolar dis-
order, prior postpartum depression, recurrent prior depressive episodes, or
personality disorders. Indeed, the stresses from the so-called “excuses” may
increase the risk of depression.
2.3.6. Seasonal Affective Disorder
Certain individuals experience regular onset of depression during specific
times of the year. The more common pattern is the onset of depression
in the fall or early winter, with resolution in the spring. However, summer
depression also occurs in some individuals. People with bipolar disorder or
a history of recurrent depression are at higher risk of developing seasonal
patterns. Seasonal affective disorder is more common in higher latitudes. It
may respond to light therapy, preferentially compared with other depressive
subtypes.
Major Depressive Disorder 2.3.7. Treatment-Resistant Depression
Treatment-resistant depression has been variably defined, but typically refers
to cases in which symptoms do not improve with at least two adequate anti-
depressant trials from different medication classes. Although not formally
defined in DSM-5, it is common in clinical practice. Treatment-resistant
depression is common, affecting perhaps one-third to one-half of depressed
individuals. It has been associated with bipolar disorder, although is not lim-
ited to that condition. Approaches to treatment-resistant depression are pro-
vided in Chapter 7.
2.3.8. Severity Measures
Major depression is classified as mild, moderate, or severe, based on the
number of symptoms and level of functional impairment. Mild cases exhibit
a number of symptoms that just meets threshold with minimal functional
impairment. Severe cases meet all or nearly all of the symptoms, experience
psychosis, or demonstrate marked functional limitations. Moderate depres-
sion lies between these two extremes. Scores from rating scales are some-
times used to quantify severity.

Key Point: A number of subtypes of major depression exist, based

largely on the severity and combination of various symptoms.
These subtypes exhibit some differences in prognosis and treatment
10

response.

2.4. Other Depressive Disorders

2.4.. Dysthymia
Dysthymia is now called “Persistent Depressive Disorder” in DSM-5, which is
descriptive since it is a condition in which depressive symptoms continue for
more than 2 years ( year in youth) and are largely unremitting, other than for
brief periods (2 months maximum). The definition in ICD-0 is similar. The
intent of these definitions is to identify cases of persistent depressed mood
accompanied by other symptoms from Box 2. that do not always meet cri-
teria for a full major depressive episode. Unlike major depression, anhedo-
nia is less characteristic of dysthymia. However, major depressive episodes
may occur during the course of dysthymia, a condition sometimes referred to
as “double depression.” Although currently classified as a mood disorder, at
times in the past dysthymia was considered a disorder of personality or tem-
perament, highlighting its persistent nature. Dysthymia tends to begin relatively
early in life and persist for years, if not a lifetime; it can be difficult to treat.
2.4.2. Disruptive Mood Dysregulation Disorder
“Disruptive Mood Dysregulation Disorder” (DSMDD) is a new diagnosis
in DSM-5 that may be included in ICD- as well.9 The key characteristics
are persistent irritable or low mood, accompanied by relatively frequent
and severe temper outbursts beginning in childhood. Criteria for DSMDD
were largely developed by a research group at the National Institute of

Making a Diagnosis of Depression

Mental Health (NIMH).9 This group was working with a group of irritable
children who were commonly referred with a diagnosis of bipolar disorder,
but lacked evidence of clear manic or hypomanic episodes. Family history
and outcome data suggested that these children suffered from a condition
associated with later developing depression rather than mania (i.e., bipolar
disorder). Although DSMDD appears to be relatively common, occurring in
up to 5% of children, controversy around the diagnosis continues, given its
recent addition to the psychiatric lexicon. Consequently, DSMDD should be
diagnosed only after other more commonly recognized conditions, such as
bipolar disorder, major depression, attention deficit hyperactivity disorder
(ADHD), oppositional defiant disorder, intermittent explosive disorder, or
autism, are ruled out.
2.4.3. Premenstrual Dysphoric Disorder

Chapter 2
“Premenstrual Dysphoric Disorder” is also a relatively new diagnosis,
although it arises from a long-standing history of behavioral and neuroveg-
etative symptoms that accompany menses that are popularly referred to as
premenstrual syndrome. Premenstrual Dysphoric Disorder includes affective
lability, commonly with periods of both depression and irritability, accompa-
nied by other typical depressive symptoms (Box 2.) and frequently physi-
cal agitation. The symptoms occur predictably during or a few days before

11
menses, every month or nearly so, and typically resolve within a few days.
Although discomfort with menses is nearly universal, Premenstrual Dysphoric
Disorder appears to affect perhaps up to 8% of premenopausal women and
exists across cultures.0
2.4.4. Secondary Depression
Major depression may be the singularly most common form of medical
comorbidity, as it occurs with brain insult or injury and many other stress-
ors and medical events. This co-occurrence is discussed in more detail in
Chapter 4.

2.5. The Affective Spectrum

Some clinicians and scientists have advocated for the notion of an affective
spectrum that extends from minor depressive symptoms (e.g., dysthymia)
through recurrent depressive episodes that progress with the addition of
increasing manic symptoms (e.g., cyclothymia) through full hypomania (bipo-
lar II disorder) and mania (bipolar I disorder).2 Additionally, a number of
other conditions are sometimes added to the spectrum, such as anxiety disor-
ders, eating disorders, and some types of personality disorders. The rationale
for including these somewhat disparate conditions is that they not only com-
monly overlap with major depression, but also respond to antidepressants.
Unfortunately, this overlap may more accurately reflect the nonspecificity of
both the causes of depression and the effects of antidepressant medications,
Major Depressive Disorder rather than a spectrum per se. Nonetheless, the affective spectrum may have
heuristic value for research.

Key Point: The concept of an affective spectrum defined by various

combinations and severity of affective and other behavioral symptoms
is insufficiently developed to guide clinical decision making at this time.

2.6. Course and Patterns of Illness of

Major Depression
Major depression can begin at any time across the life span, although it is
relatively uncommon prior to puberty. In the United States, the peak onset of
recurrent major depression is in the late teens or early twenties, but onsets
at other ages are not uncommon. Once initiated, without treatment a major
depressive episode typically lasts many weeks or months. Twenty percent
of individuals will continue to experience symptoms more than a year after
onset;3 some of these will develop persistent symptoms consistent with a
diagnosis of dysthymia that may continue for years and even to the end of
life. Treatment can dramatically decrease the duration and severity of symp-
toms in 3–8 weeks in perhaps one-half to two-thirds of individuals. Estimates
suggest that after a single episode of depression, 50% of individuals will, at
12

some point, experience at least one more episode; after a second episode,
the likelihood of recurrence increases to 80%. Although early episodes are
often associated with a precipitating stressor, this link decreases with each
recurrence. Consequently, over time the strongest predictor of future epi-
sodes is a history of past recurrences. Individuals with underlying psychiatric
(e.g., bipolar disorder) and medical (e.g., heart disease) conditions known
to increase risk for depression are also at higher risk of recurrence. Onset
of depression in childhood or adolescence predicts a likely course of recur-
rent depressive episodes later in life, as does significant childhood stress or
loss. The likelihood of recurrence steadily decreases as the time since the
last episode increases; hence, after two episodes, most treatment guidelines
recommend ongoing antidepressant treatment or therapy for prevention.
Depression, then, is a common, lifelong, recurrent illness.

2.7. Differential Diagnosis of

Major Depression
2.7.. Bipolar Disorder
Depressive symptoms that occur in the course of bipolar disorder are not
unique, but look like any other case of depression. As noted, there may be
higher rates of atypical depression in bipolar individuals, but this occurrence is
not frequent enough to be diagnostic. Indeed, a diagnosis of bipolar disorder
requires the occurrence of either mania or hypomania, which differentiates it
from unipolar depression.
2.7.2. Schizophrenia or Schizoaffective Disorder

Making a Diagnosis of Depression

Depressive symptoms and episodes commonly occur in schizophrenic disor-
ders. Conversely, a small percentage of people with major depression also
experience psychosis, the defining symptoms of schizophrenia. Schizophrenia
and schizoaffective disorders are distinguished from psychotic depression
by the persistence of psychosis for a significant period of time (at least 2–4
weeks) prior to and beyond the depressive episode(s).
2.7.3. Sadness/Grief
The experience of bereavement following a loss can include symptoms like
those in Box 2.. Sadness following negative life events similarly is part of the
human condition and can be accompanied by the other symptoms of Box 2..
Depressive symptoms that do not meet full criteria for major depression and
that follow a stressor are sometimes referred to as an Adjustment Disorder.
The primary differentiator between “normal” sadness or grief and depression

Chapter 2
is that, in the former, the symptoms () follow a clear precipitant that would
make others sad in a similar situation; (2) typically resolve spontaneously;
and (3) most importantly, do not significantly impair psychosocial function.
However, stress and loss can precipitate a depressive episode, so monitoring
psychosocial function following a negative life event may permit early detec-
tion of a new depressive episode.

13
2.7.4. Drug/Alcohol Use Disorders
Chronic drug or alcohol use is commonly associated with low mood, anhedo-
nia, and most of the other symptoms in Box 2.. Alcohol abuse, in particular,
is known to be associated with, and to cause, high rates of depression. A pri-
mary depressive disorder can be differentiated from depression secondary
to substance abuse by occurrence of affective symptoms during periods of
sobriety and onset of affective symptoms prior to onset of substance abuse
in the former, or rapid resolution of affective symptoms following detoxifica-
tion in the latter.
2.7.5. Other Neurological and Medical Illnesses
As noted, depression is a common, nonspecific response to nearly any con-
dition that impacts brain function. Medical causes can occur anytime in life,
although they become more likely as individuals move into their fifties and
sixties. A first onset of a depressive episode after age 50, and especially after
age 60, warrants a careful medical evaluation to rule out conditions like those
discussed in Chapter 4.

References
. Davison K. Historical aspects of mood disorders. Psychiatry 2008; 8:47–5.
2. Strakowski SM. Making a diagnosis of bipolar disorder. Chapter 2 in Bipolar
Disorder: OAPL Library. New York, NY: Oxford University Press, 204,
pp. 5–6.
3. American Psychiatry Association. Diagnostic and Statistical Manual of Mental
Disorders (5th edition). Washington, DC: American Psychiatric Press, 203.
Major Depressive Disorder 4. World Health Organization. ICD-0 Classifications of Mental and Behavioural
Disorder: Clinical Descriptions and Diagnostic Guidelines. Geneva: World Health
Organization, 992.
5. Strakowski SM, Adler CM, Delbello MP. Is depression simply a nonspecific
response to brain injury? Curr Psychiatry Rep 203; 5:386–396.
6. Schuch JJ, Roest AM, Nolen WA, Penninx BW, de Jonge P. Gender differences
in major depressive disorder: results from the Netherlands study of depres-
sion and anxiety. J Affect Disord 204; 56:56–63.
7. Moussaoui D, Agoub M, Khoubila A. How should melancholia be incorpo-
rated in ICD-. World Psychiatry 202; (suppl. ):69–72.
8. Chakrabarti S. Psychotic and catatonic presentations in bipolar and depressive
disorders. World Psychiatry 202; (suppl. ):59–64.
9. Leibenluft E, Uher R, Rutter M. Disruptive mood dysregulation with dysphoria
disorder: a proposal for ICD-. World Psychiatry. 202; (suppl. ):77–8.
0. Figueira ML, Videira Dias V. Postpartum depression and premenstrual dys-
phoric disorder: options for ICD-. World Psychiatry 202; (suppl.
):73–76.
14
Chapter 3

Epidemiology of
Depressive Disorders

3.. Population Prevalence and Incidence

Major depressive disorders are exceptionally common, perhaps the most
common medical conditions affecting humanity that are not associated with
aging or a self-limited virus. Although the specific prevalence of depressive
disorders varies somewhat across studies, nonetheless, based upon sev-
eral large US epidemiological investigations, the lifetime prevalence rate of
depression converges around 0–5%, with an annual rate of 3–5% (Table
3.).–4 European and other cross-national studies show similar rates of
depression in their populations (Table 3.).5 Several factors likely contrib-

15
15
ute to the variability observed among studies and populations. First, most
of these studies used different diagnostic criteria and ascertainment meth-
ods, thereby leading to different thresholds across individuals about the pres-
ence or absence of depression. Related to this factor, different cultures and
demographic groups likely express the symptoms of depression in different
ways, leading to variable validity and sensitivity of any specific criteria set or
ascertainment method. Third, depression is highly comorbid with a variety of
other medical and psychiatric conditions; consequently, depending upon how
these co-occurring and secondary cases were managed within various study
methods, and depending on differences in rates of these other conditions
across samples, the apparent rate of depression would change. With these
considerations in mind, coupled with the association of depression through-
out the course of humankind, perhaps the most parsimonious conclusion
is that depression is similarly common across humanity, although perhaps
somewhat variable in how it is expressed.

Key Point: Major depression is among the most common conditions

affecting humankind with rates up to 5% of the population; it is simi-
larly common across nations and cultures.

3.2. Subgroups and Other Factors

3.2.. Sex
Depressive disorders are more common in women than men. Relatively
consistently across studies, women appear to be .5 to 2 times more
Major Depressive Disorder Table 3. Prevalence (%) of Major Depression and Dysthymia
in Epidemiological Studies
Study Major Depression Dysthymia
Lifetime 2-month Lifetime 2-month
ECA, 980 4.9 2.7 3.2 —
NCS, 994 7. 0.3 6.4 2.5
NCS-R, 2005 — 6.7 — .5
CNCG, 996 9.6* 3.0+ — —
ECA = Epidemiologic Catchment Area study; NCS = National Comorbidity Survey;2
NCS-R = National Comorbidity Survey-Revised;3 CNCG = Cross-National Collaborative
Group.4
*Mean calculated across 9 countries. +Mean calculated across 7 countries.

likely to develop a depressive disorder. Although the specific reasons for

this sex-linked increased risk are not known, almost certainly some of the
variance is due to risks associated with the peripartum period, menarche,
menopause, and menstruation (i.e., premenstrual dysphoric disorder) that
are unique to women. In addition, since most cultures are more tolerant of
women expressing emotions than of men doing so, it is likely that depression
is under-recognized in the latter. Regardless, depression is common in both
sexes, so it should not be considered a uniquely female condition.
16

Key Point: Women are more likely than men to develop depression;
nonetheless, it is very common in both.

3.2.2. Age
Risk for depressive disorders extends across the life span, although is rela-
tively rare prior to puberty. When depression occurs in childhood or early
adolescence, it is often associated with later progression to (commonly)
bipolar disorder, (less commonly) schizophrenia, or (perhaps) other psychi-
atric conditions. The mean age at onset of depression is in the mid- to late
20s, with the largest peak of new cases occurring in the mid-20s to mid-30s.
Smaller peaks of increased rates of new onset depression are also seen in the
mid-teens and mid-50s.
The Epidemiologic Catchment Area (ECA) study observed that older age
groups demonstrated a relatively lower lifetime prevalence rate of depres-
sion than the younger cohorts, which is inconsistent with the notion that pop-
ulation rates of depression should accumulate with age. These findings raised
the question of whether depression is becoming more prevalent over time,
that is, increasing rates with each generation, which is called the “birth cohort
effect.” Later findings from the National Comorbidity Survey supported this
suggestion.2 However, there are other alternatives. Since depression can only
be diagnosed with clinical interviews, these findings might reflect generational
differences in awareness of or willingness to acknowledge behavioral symp-
toms. There is little doubt that stigma against mental illness has declined with
each generation over the past century, so these changes might impact how
people report behavioral conditions. Moreover, depression is associated with

Epidemiology of Depressive Disorders

increased risk of premature mortality (see Section 3.3), so that people with
depression may become under-represented in elderly samples. Finally, since
depression has been recognized and common since the dawn of civilization,
it would seem that if there was a history of birth cohort effects, then rates
of depression would be even higher than they are now, having accumulated
over the millennia of human history. Although some posit that the stresses
or experiences of modern life predispose people to depression, this sug-
gestion is inconsistent with the steady increase in human rights, health, and
opportunities, and the associated decreased level of stress simply to survive,
relative to centuries past. Indeed, claims that urban living increases the risk of
depression have not been substantiated by research. Currently, then, these
age-cohort effects are poorly understood. Regardless, depression can begin
at any time in life with no age group immune.

Key Point: Depressive disorders can begin at any time in life.

Chapter 3
3.2.3. Race/Ethnicity
As noted previously, depressive disorders are common across a wide range
of countries and cultures. Consequently, there are few racial and ethnic dif-
ferences. Within the United States, studies have been mixed as to whether

17
African Americans have somewhat lower rates of affective disorders in gen-
eral, and depressive disorders specifically, than other ethnic groups. Typically,
however, once other demographic differences are controlled, rates of
depression appear to be similar among US racial and ethnic groups.
In contrast to epidemiologic studies, for decades investigators have
reported that individuals of African descent in the United States and western
Europe are clinically diagnosed with schizophrenia at higher rates than whites,
with corresponding lower rates of affective disorders. African Americans
with mood disorders are up to 9 times more likely to be misdiagnosed with
schizophrenia than otherwise similar white individuals in clinical (as opposed
to research) settings. Similar differences are observed in Afro-Caribbeans in
the United Kingdom. Recent studies suggest that these diagnostic differences
result from clinicians overemphasizing psychotic symptoms while minimizing
affective symptoms in people of African descent, leading to misidentifica-
tion of mood disorders as schizophrenia. The use of structured interviews,
which forces a more systematic approach to diagnosis, seems to improve
this problem, although it does not eliminate it entirely. Clinicians of differ-
ent ethnic and racial backgrounds from their patients must also be aware of
differences in the way symptoms are described, that is, cultural differences
in “idioms of distress.” These studies remind clinicians to be sensitive to dif-
ferences in symptom expression among multicultural groups when assigning
a diagnosis.5–7

Key Point: Depression is similarly common among ethnic groups,

although African Americans with affective disorders are at high risk for
being misdiagnosed with schizophrenia.
Major Depressive Disorder 3.2.4. Socioeconomic Status
In general, depressive disorders are minimally associated with socioeconomic
status, occurring similarly across income and educational levels. One pos-
sible exception to this statement is that the poorest and least educated may
have a slight increased risk of depression.2 However, as discussed in Section
3.3., depression negatively impacts work and psychosocial function, so the
directionality of this relationship is unclear, that is, whether poverty “causes”
depression or depression “causes” poverty. Regardless, the additional risk is
modest.

Key Point: Depressive disorders are similarly common across socio-

economic strata.

3.3. Burden of Disease

3.3.. Morbidity and Disability
Although a depressive episode can be a singular event in a person’s life,
depressive disorders commonly progress into recurrent and even chronic
lifelong conditions. Moreover, as noted in Chapter 2, once a depressive
episode occurs, 50% of individuals develop subsequent episodes, and after
18

two episodes, the risk of yet another increases to 80%. Symptoms can per-
sist for many weeks, months, or even years in some individuals. Depressive
symptoms negatively impact psychosocial function, leading to impairments
across life domains including relationships, work, health, and even recreation.
Long-term follow-up studies suggest that depressive symptoms, even when
they no longer meet full syndrome criteria, are associated with impaired work
performance in more than 50% of affected individuals, including 20% who
are not able to work at all.8,9 Depression worsens the course of many major
medical conditions, including diabetes, heart disease, cancer, and stroke (see
Chapter 4). Consequently, major depression is recognized as one of the top
five leading causes of disability; specifically, a study from the Harvard School
of Public Health predicts that by the year 2020, depression will be the leading
cause of disability worldwide.0 Each year, more is spent on medical care for
depressive disorders than all cancers combined. Moreover, depression is
typically the leading cause of missed days at work. Consequently, the societal
costs of depressive disorders are staggering: between direct expenses for
medical care and indirect costs related to lost productivity, the United States
spends $00 billion annually on depression. These financial costs pale in com-
parison to the human toll in the lives of people affected by depression and
their friends and family.

Key Point: Depression is a leading medical cause of disability world-

wide, and is associated with lost productivity at work, impairments
in relationships, decline in general health, and loss of life enjoyment.
3.3.2. Mortality and Suicide

Epidemiology of Depressive Disorders

Depressive disorders are associated with premature death at virtually every
age. Suicide is a major component of this risk and is a common consequence
of depressive disorders. Up to 8% of individuals with depression commit sui-
cide; this percentage increases to 20% in the absence of treatment. Rates
of attempted suicide are approximately twice as high as completed suicides;
although women make more attempts, men are more likely to kill themselves,
primarily due to choosing more violent means of death. Finally, suicidal ide-
ation occurs in up to half of depressed individuals.
Several factors have been associated with an increased risk of suicide in
the course of depression. In particular, the presence of drug and alcohol
abuse, inadequate treatment, co-occurring anxiety disorders, and hopeless-
ness increase the risk of suicide. Chronic or recurrent depressive symptoms
increase the risk of suicide, as does the presence of other chronic medical or
psychiatric disorders. Suicide rates typically increase with age. The strongest
predictor of suicide is a history of previous suicide attempts. Nonetheless,

Chapter 3
preventing suicide remains difficult. Although risk factors may be useful to
predict the behavior of groups, they are often difficult to apply to a specific
individual at a specific time. The treatment of suicidal individuals with depres-
sion is discussed in more detail in Chapter 0.
In addition to its association with suicide, depression also appears to increase
the risk of all-cause mortality.2 Namely, depression is associated with higher

19
rates of many medical problems, including cardiovascular and cerebrovascular
disease and cancer. Moreover, depression is a common comorbidity across
many major medical illnesses, and it is typically associated with poorer general
outcomes and increased risk of premature death (see Chapter 4). Some of
these effects may be due to depressed individuals having higher rates than the
general population of cigarette use and drug and alcohol abuse, behaviors that
are known to increase the risk of cancer and cardio- and cerebrovascular dis-
eases. In fact, cigarette use may also independently increase the risk of suicide.
There is a complex relationship between heart disease and depression in
which the combination of conditions worsens the outcomes of both. For
example, in the Framingham heart study, although depression was not asso-
ciated with specific cardiac events per se, its presence increased the risk of
all-cause mortality in individuals with cardiovascular disease.3 Although the
specific mechanisms of these interactions between depression and heart dis-
ease are not known, several hypotheses have been proposed and are listed in
Box 3.. Similar findings have been observed following stroke.2
Through potentially a variety of associations and mechanisms, then,
depressive disorders increase morbidity and mortality. Because depression is
so common, it therefore is one of the world’s leading public health problems,
so effective treatment of depression becomes critical (see Chapter 9).

Key Point: Individuals with depressive disorders have higher mortal-

ity rates than their peers from the general population, and suicide is
a major contributor to this increased risk. Depression is one of the
world’s major public health problems.
Major Depressive Disorder
Box 3. Proposed Links Between Depression and
Cardiovascular Mortality
Stress-diathesis hypothesis
Increased activity of HPA axis in depression leads to
. chronic adrenaline release;
2. sustained blood pressure elevation;
3. damage to coronary arteries and heart disease.

Autonomic dysregulation
Sympathetic/parasympathetic imbalance of depression leads to
. reduced heart rate variability;
2. inability of heart to respond to demands;
3. increased rates of arrhythmias & sudden death.

Platelet aggregation
Depression is associated with serotonin abnormalities that
. alter platelet aggregation properties;
2. increase clot formation in coronary arteries;
3. increase risk of CAD and sudden death.
20

HPA = hypothalamic-pituitary-adrenal, CAD = coronary artery disease.

Adapted from Seymour & Benning2

References
. Weissman MM, Bruce ML, Leaf PJ, Florio LP, Holzer C. Affective disorders.
In: Robins LN, Regier DA, eds., Psychiatric Disorders in America: The Epidemiologic
Catchment Area Study, pp. 53–80. New York: Free Press, 99.
2. Kessler RC, McGonagle KA, Zhao S, Nelson CB, Hughes M, Eshleman S,
Wittchen HU, Kendler KS. Lifetime and 2-month prevalence of DSM-III-R psy-
chiatric disorders in the United States. Results from the National Comorbidity
Survey. Arch Gen Psychiatry 994; 5:8–9.
3. Merikangas KR, Akiskal HS, Angst J, Greenberg PE, Hirschfeld RM, Petukhova
M, Kessler RC. Lifetime and 2-month prevalence of bipolar spectrum disor-
der in the National Comorbidity Survey replication. Arch Gen Psychiatry 2007;
64(5):543–552.
4. Weissman MM, Bland RC, Canino GJ, Faravelli C, Greenwald S, Hwu H-G,
Joyce PR, Karam EG, Lee C-K, Lellouch J, Lepine J-P, Newman SC, Rubio-Stipec
M, Wells E, Wickramaratne PJ, Wittchen H-U, Yeh E-K. Cross-national epide-
miology of major depression and bipolar disorder. JAMA 996; 276:293–299.
5. Strakowski SM. Chapter 3: Epidemiology. In: Bipolar Disorder. Oxford American
Psychiatry Library. New York: Oxford University Press, 204. [Note: Segments
of section 3.2.2. are taken directly from this previous publication with permis-
sion of the author and the publisher.]
6. Strakowski SM, Keck PE Jr., Arnold LM, Collins J, Wilson R, Fleck DE, Corey
KB, Amicone J, Adebimpe VR. Ethnicity and diagnosis in patients with affective
psychoses. J Clin Psychiatry 2003; 64:747–754.
 7. Gara MA, Vega WA, Arndt S, Escamilla M, Fleck DE, Lawson WB, Lesser I,

Epidemiology of Depressive Disorders

Neighbors HW, Wilson DR, Arnold LM, Strakowski SM. Influence of patient
race and ethnicity on clinical assessment in patients with affective disorders.
Arch Gen Psychiatry 202; 69:593–600.
8. Judd LL, Schettler PJ, Solomon DA, Maser JD, Coryell W, Endicott J, Akiskal
HS. Psychosocial disability and work role function compared across the
long-term course of bipolar I, bipolar II and unipolar major depressive disor-
ders. J Affect Disord 2008; 08:49–58.
9. Judd LL, Akiskal HS, Zeller PJ, Paulus M, Leon AC, Maser JD, Endicott J, Coryell
W, Kunovac JL, Mueller TI, Rice JP, Keller MB. Psychosocial disability during the
long-term course of unipolar major depressive disorder. Arch Gen Psychiatry
2000; 57:375–380.
0. Murray CJ, Lopez AD. The Global Burden of Disease: A Comprehensive
Assessment of Mortality and Disability from Diseases, Injuries and Risk Factors
in 990 and Projected to 2020. Cambridge, MA: Harvard School of Public
Health, 996.
. National Network of Depression Centers. “The Facts.” http://www.nndc.
org/the-facts.

Chapter 3
2. Seymour J, Benning TB. Depression, cardiac mortality and all-cause mortality.
Adv Psychiatr Treatment 2009; 5:07–3.
3. Wulsin LR, Evans JC, Vasan RS, Murabito JM, Kelly-Hayes M, Benjamin EJ.
Depressive symptoms, coronary heart disease, and overall mortality in the
Framingham Heart Study. Psychosom Med 2005; 67:697–702.

21
Chapter 4

Illness Comorbidity and

Co-occurrence with
Depressive Disorders

4.. What Is Comorbidity?

In medical parlance, “comorbidity” refers to the concurrent presence of two
or more distinct medical conditions. For example, if someone with coronary
artery disease develops streptococcal pharyngitis, since these two illnesses
are etiologically unrelated, they are distinct and therefore are comorbid. It
is expected that people with any one illness will develop second unrelated
illnesses at essentially the base population rate. When this expectation is vio-

23
23
lated, it suggests that the conditions share risks. In contrast, if an individual
with diabetes experiences renal failure, since these conditions share an under-
lying vascular pathology, rates of each are expected to occur at higher than
population base rates. Although this latter situation is often called comorbid-
ity, technically that is a misuse of the term, with “co-occurrence” being more
accurate. Therefore, the term “co-occurrence” is often preferred.
Because the specific etiologies of depressive disorders are both variable
and largely unknown, defining comorbidity is relatively difficult, although sec-
ondary illnesses occurring at population base rates that are unrelated to the
central nervous system (e.g., again, streptococcal pharyngitis) likely meet the
strict definition. Individuals with depression are not protected from illnesses
that affect the general population. However, individuals with depression also
exhibit elevated rates of a number of conditions that suggest common eti-
ologies or risk factors. Alternatively, depression may be the most common
co-occurring “secondary” illness in medicine, with increased rates in a wide
variety of psychiatric, neurologic, and medical conditions.2 In this chapter we
will discuss some of these reciprocal relationships.

Key Point: Depressive disorders are commonly complicated by other

psychiatric and medical conditions and, conversely, frequently compli-
cate the courses of other illnesses.
Major Depressive Disorder 4.2. Co-occurrence of Depression and Other
Psychiatric Conditions
Major depression occurs commonly with other psychiatric disorders.
Whether depression is viewed as a consequence (secondary) or cause
(primary) of another illness depends on which condition is used to define a
particular case. In fact, determining whether depression is “primary” or “sec-
ondary” is often difficult, so this definition is typically based on which condi-
tion began first or which is more severe. In many instances, it is not possible
to retrospectively make this determination; moreover, this categorization is
based upon an assumption of causality, that is, that one condition produces
the other, when perhaps it is more likely that these syndromes share com-
mon risk factors leading to the expression of both. Indeed, the individual
symptoms of many psychiatric syndromes are nonspecific, almost guaran-
teeing overlap among the various disorders defined in DSM-5 or ICD-0.2
That said, when cases are specifically defined by a psychiatric disorder other
than depression, elevated rates of depression occur almost universally (see
Table 4.), supporting suggestions that the syndrome of depression is par-
ticularly nonspecific.2 Conversely, when depression is used to define cases
(i.e., depression is primary), elevated rates of other conditions are some-
what limited and include anxiety, substance use and impulse control disorders
24

(Table 4.2).
Table 4. lists rates of depression in several common psychiatric conditions
that were derived from best estimates of variable rates across publications
(see Strakowski et al.2 for details). A similar “best estimate” approach was used
to create Table 4.2. As illustrated in Table 4., co-occurring major depression
is common in virtually every major psychiatric illness with increased risks of

Table 4. Lifetime Prevalence of Co-occurring Major

Depression in Common Psychiatric Disorders
Condition Lifetime Prevalence of
Depression
Bipolar I disorder 90%
Schizophrenia 50%
Obsessive compulsive disorder 30%
Panic disorder 50%
Generalized anxiety disorder 67%
PTSD 37%
ADHD 25%
Alcohol use disorders 40%
Drug use disorders 40%
Personality disorders 23%
PTSD = post-traumatic stress disorder; ADHD = attention deficit hyperactivity disorder;
PD = personality disorder.
Adapted from: Strakowski SM, Adler CM, DelBello MP. Is depression simply a non-specific
response to brain injury? Curr Psychiatry Rep 203; 5:386–393.
 Illness Comorbidity and Co-occurrence
Table 4.2 Psychiatric Conditions Co-occurring with
Primary Depression
Condition Lifetime Prevalence in
Primary Depression
Any anxiety disorder 60%
GAD 50%
Social phobia 30%
PTSD 20%
Impulse control disorder 30%
Personality disorder 40%
Alcohol use disorder 7%
Drug use disorder 8%
GAD = generalized anxiety disorder; PTSD = post-traumatic stress disorder.
See references 3–7.

2 to 5 times (or greater) compared to the general population base rate of

Chapter 4
0–5% (Chapter 3). As noted by Strakowski et al.,2 it is actually rather dif-
ficult to identify a psychiatric disorder in which an increased risk of depres-
sion is absent. Consequently, it appears that any psychiatric illness increases
the risk for developing major depression. When depression develops dur-

25
ing the course of another psychiatric illness, this co-occurrence is associated
with earlier age at onset and poorer outcomes that include decreased rates
of recovery, increased rates of suicide, and worse psychosocial function.2
Moreover, multiple co-occurring illnesses (i.e., 2 or greater) are common.3
Conversely, the co-occurrence of anxiety, substance use, and impulse control
disorders in the course of depression similarly worsens outcomes. Several of
these common co-occurrences warrant additional comment.
4.2.. Bipolar Disorder
Bipolar I disorder is defined by the occurrence of mania. However, in up to
90% of individuals, major depressive episodes also occur; in fact, the depres-
sive symptoms dominate the long-term course of illness and morbidity asso-
ciated with bipolar disorder. Bipolar II disorder requires the occurrence of
depression by definition, so there is a 00% overlap.
4.2.2. Anxiety Disorders
Anxiety disorders are exceptionally common in people with “primary” depres-
sive disorders, occurring in up to 60% of individuals, and depression even
more commonly develops during the course of primary anxiety disorders. In
particular, there is a very strong relationship between major depression and
generalized anxiety disorder (GAD), specifically, such that co-occurrence is
the rule rather than exception. For example, in a New Zealand birth cohort
study,4 037 individuals were followed for up to 32 years; 2% developed
co-occurring GAD and major depression by adulthood. Among those who
developed depression, half also experienced GAD; in those with GAD, more
than 70% developed depression. Individuals who developed both conditions
were essentially equally as likely to have either one develop first. Similarly,
Major Depressive Disorder depression commonly co-occurs with social phobia, obsessive-compulsive
disorder (OCD), panic disorder, and post-traumatic stress disorder (PTSD),
suggesting shared mechanisms underlying anxiety and depressive disorders
(see Chapters 5 and 6).
4.2.3. Substance Use Disorders
Drug and alcohol abuse are elevated during the course of major depression,
occurring at perhaps twice the rates of the general population. Conversely,
rates of depression in primary drug- and alcohol-dependent individuals are
elevated up to 4 times the general population rates. Most individuals who
abuse alcohol will develop depressive symptoms, with many of those pro-
gressing to a major depressive episode or dysthymia. This co-occurrence can
be lethal, as the combination of depression and substance abuse significantly
increases the risk for suicide over either condition alone.
4.2.4. Personality Disorders
Up to 40% of individuals with personality disorders experience major depres-
sion. Although studies will report this co-occurrence with either condition
as the “primary” illness, since personality disorders are defined as lifelong,
in general they are probably the primary condition. However, some posit
that chronic affective symptoms may lead to the development of a personal-
ity disorder that was not present prior to the depressive illness. Regardless,
26

among the personality disorders, the Cluster C group, especially avoidant

personality disorder, appears to carry the highest risk, although depression
is also common in the course of borderline personality disorder and other
Cluster B conditions.5 The presence of a personality disorder is associated
with decreased treatment response of depression.
4.2.5. Dysthymia (Persistent Depressive Disorder)
Current diagnostic criteria sets permit the concurrent diagnosis of both
major depression and dysthymia, distinguished primarily by the relative chro-
nicity of the symptoms (i.e., dysthymia is more chronic; see Chapter 2). This
co-occurrence is common and has been referred to as “double depression.”
It is associated with poor treatment response.

Key Point: The course of depression is complicated by anxiety, sub-

stance use, and impulse control disorders. Conversely, co-occurring
depression is ubiquitous in other psychiatric conditions.

4.3. Co-occurrence of Depression and Other

Neurological and Medical Illnesses
In addition to co-occurring in most, if not all, psychiatric conditions, depres-
sive disorders are also commonly part of the course of neurological illnesses.
As illustrated in Table 4.3, rates of depression are elevated 2 to 5 times higher
in most common neurologic conditions, such as stroke, epilepsy, migraine,
and dementia, as up to half of individuals are affected.2 In fact, coupled with
 Illness Comorbidity and Co-occurrence
Table 4.3 Lifetime Prevalence of Co-occurring Major
Depression in Common Non-Psychiatric Neurologic Conditions
Condition Lifetime Prevalence of
Depression
Stroke 30%
Epilepsy 35%
Parkinson’s disease 40%
Alzheimer’s disease 50%
Multiple sclerosis 50%
Migraine 47%
Adapted from: Strakowski SM, Adler CM, DelBello MP. Is depression simply a non-specific
response to brain injury? Curr Psychiatry Rep 203; 5:386–393.

the findings in psychiatric disorders, this co-occurrence is so common as to

suggest that depression can be a consequence of any condition that impacts
brain function. As with psychiatric conditions, depression worsens the course

Chapter 4
of illness of neurological conditions and is associated with treatment failure
and poor functional recovery.
The risk for increased depression associated with medical illness is not lim-
ited to conditions that directly impact brain function. For example, as listed in
Table 4.4, rates of depression are elevated across a wide variety of medical

27
conditions including, for example, coronary artery disease, cancer, autoim-
mune disorders, metabolic disorders, and chronic pulmonary and renal dis-
ease.2 The specific mechanisms underlying these associations are not known;
although the occurrence of stress from chronic illness has been proposed
as one common link, the risk appears to be greater in illnesses that impact
brain function, as evidenced by comparing Table 4.4 with Tables 4. and 4.3.
Importantly, although rates of depression are elevated in these various medi-
cal, neurological, and psychiatric conditions, co-occurrence is not 00%, so
that it is likely there are additional underlying shared genetic or neurobio-
logical risks leading to depression. Conversely, causes of depression may also
increase the risk of other medical conditions. These possibilities are discussed

Table 4.4 Lifetime Prevalence of Co-occurring Major

Depression in Common Non-Psychiatric Medical Conditions
Condition Lifetime Prevalence of
Depression
Cardiovascular disease 35%
COPD 40%
Chronic renal disease 30%
Cancer 30%
Diabetes 33%
COPD = chronic obstructive pulmonary disease.
Adapted from: Strakowski SM, Adler CM, DelBello MP. Is depression simply a non-specific
response to brain injury? Curr Psychiatry Rep 203; 5:386–393.
Major Depressive Disorder in Chapters 5 and 6. Several of these medical conditions warrant additional
comment.
4.3.. Dementia
In older individuals, particularly in those with no prior history, the develop-
ment of a new depressive episode may be the first indication of an evolving
dementing illness (e.g., Alzheimer’s disease). In particular, the presence of
significant cognitive impairment during the depressive episode, or a strong
family history of dementia, should initiate a high index of suspicion for the
possibility of dementia. However, depression in old age is common, indepen-
dent of dementia, so it should not be assumed to be the latter. Moreover,
depression causes cognitive impairments, especially decrements in concen-
tration, that may be misinterpreted as dementia in older patients, sometimes
termed “pseudodementia.” Conversely, depression may also develop during
the course of dementia and may contribute to worsening cognitive symp-
toms; again, in this circumstance a high index of suspicion of the combina-
tion is warranted, and careful neuropsychological evaluation is necessary in
order to make maximally effective treatment decisions. Finally, there is some
evidence, albeit less strong, that recurrent major depression earlier in life
increases the risk of developing dementia in senescence.
4.3.2. Parkinson’s Disease
28

As with dementia, a new onset of a depressive episode in older age might

herald the onset of Parkinson’s disease, particularly in the presence of the
other neurological symptoms. Likewise, depression commonly occurs during
the course of Parkinson’s disease and can be easily missed as a contributor to
sudden failure to respond to treatment or make psychosocial progress. Again,
a high index of suspicion for this co-occurrence is warranted.
4.3.3. Cardiovascular Disease
There is now a vast medical literature bidirectionally linking depressive and
cardiovascular disorders. Heart disease is more common in people with
depression and is associated with developing depression. Outcomes in
people with both are typically worse than either condition alone. Several
hypothesized mechanisms underlying the associations between cardiac
mortality and depression have been proposed that include increased
hypothalamic-pituitary-adrenal (HPA) axis reactivity, autonomic dysregula-
tion, and platelet aggregation abnormalities due to serotonin dysregulation;
these are outlined in Chapter 3 (Box 3.) but none has been firmly estab-
lished or has produced novel treatment interventions as yet. As with the
other medical conditions in Table 4.4, failure of an individual with cardiovas-
cular illness to predictably progress with treatment warrants a careful review
for depression.

Key Point: Rates of depression are elevated in a wide variety of medical

illnesses, but particularly those that affect the brain. A high index of
suspicion for co-occurring depression should be maintained in these
illnesses, particularly when treatment is less effective than expected.
 4.4. Depression Is Nonspecific

Illness Comorbidity and Co-occurrence

As suggested throughout this chapter, depression occurs within the context
of a wide variety of medical, psychiatric, and neurological conditions. It is
a particularly common secondary illness in any condition that impacts brain
function. Together, these findings suggest that depression represents a non-
specific response to brain injury or insult, expressed through a shared neu-
robiological final pathway, but arising from a wide variety of causes.2 Possible
models for these neurobiological pathways and etiologies are discussed in
Chapters 5 and 6. Importantly, one implication of this possibility is that the
putative underlying cause may need to be first identified and managed in
order to maximize treatment outcomes for people suffering from depression.
This consideration is discussed additionally in Chapters 7–0.

Key Point: Depression occurs commonly in the context of any condi-

tion that impacts brain function, suggesting that, in many cases, it is a
nonspecific response to brain insult or injury.

Chapter 4
References

29
. Strakowski SM. Chapter 4: Illness comorbidity and co-occurrence in bipo-
lar disorder. In: Bipolar Disorder. Oxford American Psychiatry Library.
New York: Oxford University Press, 204.
2. Strakowski SM, Adler CM, DelBello MP. Is depression simply a non-specific
response to brain injury? Curr Psychiatry Rep 203; 5:386–393.
3. Rush AJ, Zimmerman M, Wisniewski SR, Fava M, Hollon SD, Warden D,
Biggs MM, Shores-Wilson K, Shelton RC, Luther JF, Thomas B, Trivedi MH.
Comorbid psychiatric disorders in depressed outpatients: demographic and
clinical features. J Aff Disord 2005; 87:43–55.
4. Moffit TE, Harrington H, Caspi A, Kim-Cohen J, Goldberg D, Gregory AM,
Poulton R. Depression and generalized anxiety disorder: cumulative and
sequential comorbidity in a birth cohort followed prospectively to age 32 years.
Arch Gen Psychiatry 2007; 64:65–660.
5. Mantere O, Melartin TK, Suominen K, Rytsala HJ, Valtonen HM, Arvilommi P,
Leppamaki S, Isometsa ET. Differences in Axis I and II comorbidity between
bipolar I and II disorders and major depressive disorder. J Clin Psychiatry 2006;
67:584–593.
6. Kessler RC, Berglund P, Demler O, Jin R, Koretz D, Merikangas KR, Rush AJ,
Walters EE, Wang PS. The epidemiology of major depressive disorder: Results
from the National Comorbidity Survey Replication (NCS-R). JAMA 2003;
289:3095–305.
7. Regier DA, Farmer ME, Rae DS, Locke BZ, Keith SJ, Judd LL, Goodwin
FK. Comorbidity of mental disorders with alcohol and other drug abuse.
Results from the Epidemiologic Catchment Area (ECA) Study. JAMA 990;
264:25–258.
Chapter 5

Neurophysiology of
Depressive Disorders

5.. Clinical Considerations for Models of the

Neurophysiology of Depression
As discussed in Chapters 2 and 4, depression is a heterogeneous condition
with a wide range of symptoms that commonly occur within the context of
other psychiatric and medical illnesses. Consequently, it appears that multiple
etiologies lead to the common “end-state” syndrome we call major depres-
sion. As we discuss the neurobiology of depression, then, we will primarily
focus on the features of this “end-state,” rather than the various co-occurring
syndromes that are beyond the scope of this handbook. With these thoughts

31
31
in mind, neurobiological models of depression must consider the following:
() a wide range of cognitive, affective, and neurovegetative symptoms and
signs; (2) a significant risk for recurrence after a first episode; (3) respon-
siveness to antidepressants; (4) a lifelong risk period; and (5) the assump-
tion of multiple and diverse precipitants. These clinical considerations suggest
that neurophysiological models of depression must describe a dysfunction
of mood and cognitive brain systems that are susceptible to interruption at
various points along pathways, and that have a genetic basis, at least in part
(reviewed clinically in Chapter 2).

5.2. Depression Arises from Abnormalities in

Emotional and Cognitive Brain Networks
5.2.. Emotional Brain Networks and Depression
Based upon this brief review, the expression of depression almost cer-
tainly includes abnormalities in mood regulation and associated cognitive
processes.,2 Like most complex human behaviors, emotional states are con-
trolled by networks originating in the prefrontal cortex (Figure 5.).,2 The
prefrontal cortex is heterogeneous, composed of multiple histologically dis-
tinct regions that share a common general functional architecture. Namely,
each prefrontal area maps to specific regions of striatum then pallidum then
thalamus before connecting back to the originating prefrontal area to form
iterative brain networks with both feedback and feed-forward properties.
The various structures that comprise these networks receive sensory and
other processed information from throughout the brain—information that
Major Depressive Disorder
Dorsolateral Striatum
prefrontal cortex Nucleus accumbens

Globus pallidus

Anterior cingulate
Thalamus

Orbitofrontal
(ventral) prefrontal
cortex

Amygdala

Figure 5. Schematic of key areas involved in the expression of depression

(adapted from Strakowski).

is integrated within prefrontal cortex. From a comparative evolutionary per-

32

spective, with increasing complexity of the prefrontal cortex, animal species

demonstrate increasingly nuanced variations of primitive “fight/flight” and
reward-seeking behaviors—behaviors driven by amygdala and ventral stria-
tum, respectively, which are perceived by humans as emotions.
Humans are distinguished from other animals by relatively excessive pre-
frontal development that supports the complex emotional-social behaviors
characterizing our species. Two prefrontal networks specifically modulate
human emotional function, and, like most prefrontal networks, follow the
previously reviewed pattern of organization. The ventrolateral prefrontal
network manages external emotional cues, such as correctly interpreting
facial expressions in others.,2 The ventromedial prefrontal network pro-
cesses internally referenced emotional states, that is, how we “feel.”,2 These
networks are illustrated in Figures 5.2 and 5.3.
Cognitive networks are similarly organized, but they originate in dorsal pre-
frontal areas (Figure 5.3). However, because they are reciprocally connected
to emotional (ventral) networks via the anterior cingulate, when emotional
prefrontal systems are activated, dorsal (cognitive) networks are deactivated.
It is this deactivation that may underlie the cognitive symptoms of depression.
Conversely, when cognitive networks are activated, they decrease emotional
network activity. This latter situation may be the neurobiological basis for suc-
cessful psychotherapy. Knowledge of these networks, then, forms a context
for functional neuroanatomic models of depression.

Key Point: Human emotional behavior is supported by ventral prefron-

tal cortical iterative networks that are reciprocally connected to dorsal
(cognitive) networks.
 of Depressive Disorders
External Emotional Control Internal Emotional Control

Thalamus Thalamus

G. pallidus G. pallidus
Amygdala

Ventromedial Nucleus
striatum accumbens

Chapter 5 Neurophysiology
Ventrolateral Ventromedial
PFC PFC/OFC
(BA 10, 47) (BA 11)
Anterior
temporal cortex Rostral
(BA 38, 20) insula

Anterior cingulate Subgenual cingulate

(BA 24, 32) (BA 25)

Cognition (Dorsal PFC)

33
Figure 5.2 Schematic of the proposed ventrolateral and ventromedial prefrontal
networks underlying human emotional brain networks (adapted from Strakowski,2).

5.2.2. Prefrontal Cortical Regions Are Dysfunctional

in Depression
Research consistently demonstrates that dysfunction of or disruption within
the prefrontal cortical networks contributes to the expression of depres-
sion. In particular, imaging studies find that the ventromedial prefrontal
cortex, which modulates internal mood states, as noted in Figure 5.2., is
over-activated in depression.3 Injuries localized to this brain region may actu-
ally eliminate depressive symptoms. The ventromedial prefrontal cortex is
heavily connected to the amygdala (see Section 5.2.3). It also heavily projects
to hypothalamic nuclei; these nuclei control the autonomic nervous system
and likely are the effector regions that create the physical sensations of emo-
tions (i.e., “feelings”).
Conversely, dorsolateral, and perhaps ventrolateral, prefrontal regions are
commonly under-activated in imaging studies of depression, and injuries to
these brain areas increase the risk of developing depression.3 The dorsolateral
prefrontal cortex is responsible for cognitive activities such as working mem-
ory, attention, and executive functions (e.g., planning and problem-solving).
This brain area is strongly connected to the hippocampus, which also sub-
serves memory and is abnormal in depression (see Section 5.2.5). As noted,
the dorsolateral prefrontal cortex is reciprocally connected to ventral (emo-
tional) prefrontal regions, so a decrease in dorsolateral prefrontal activation
may “release” excessive activation in the ventral prefrontal cortex. Indeed,
the opposite activation abnormalities noted between dorsolateral and
Major Depressive Disorder
Cognitive Control Emotional Control

Thalamus Thalamus

G. pallidus G. pallidus

Hippocampus Amygdala

Dorsal Ventral
striatum striatum/NA

Dorsolateral Ventrolateral/
PFC medial PFC
(BA 45) (BA10,11,47)

Anterior cingulate
(BA 24,32)
(Reciprocal connection)
34

Figure 5.3 Schematic of relationship between a cognitive (dorsal) and emotional

(ventral) brain networks. The latter are consolidated from Figure 5.2, simplified for this
diagram.

ventromedial prefrontal areas in depression suggest an imbalance between

cognitive and emotional brain networks such that extreme negative mood
states are associated with attentional and memory impairments (i.e., the
symptoms of depression). Of note, effective treatment corrects many of
these prefrontal abnormalities.
This reciprocal connection between prefrontal areas appears to occur within
the anterior cingulate. The cingulate is an integrative structure that manages
conflicting stimuli; its most anterior and ventral parts (i.e., subgenual cingulate)
are primarily responsive to emotional cues with increasing (non-emotional)
cognitive modulation as one moves dorsally and posteriorly (see Figure 5.).
The subgenual cingulate has been shown to be smaller and to have abnor-
mal metabolic activity in depressed subjects compared with healthy subjects.
Abnormalities in other areas of the anterior cingulate are also observed in imag-
ing studies of people with depression performing a variety of cognitive tasks.

5.2.3. In Depression, the Amygdala Is Overly Negative

As noted, the amygdala is responsible for “fight or flight” behavioral responses
to threats. It can be conceptualized as sending emotional signals (anger and
fear, respectively) as part of those responses. In humans, ventral prefrontal
networks nuance this response to contribute to the wide range of human
emotional states that characterize our species and that have gone awry in
depression (e.g., guilt, frustration, irritability, embarrassment). Imaging studies
suggest that during depression the amygdala is overly responsive to negative

of Depressive Disorders
emotional cues and, conversely, demonstrates blunted activation to positive
cues.4 Consequently, these findings suggest that, during depression, the amyg-
dala is sensitized toward negative emotional experiences. Successful antide-
pressant treatment appears to correct this amygdala bias.
5.2.4. Connections among Prefrontal Regions and
Amygdala Are Disrupted in Depression
As noted, in humans our excessively developed prefrontal cortex nuances
our emotional behaviors and experiences. In depression, this nuance is lost. In
part, this loss may reflect the specific regional abnormalities noted—that is, an

Chapter 5 Neurophysiology
overly activated emotional brain (i.e., ventral prefrontal cortex and amygdala)
with a hypo-responsive cognitive correction (i.e., dorsolateral prefrontal cor-
tex). However, depression does not simply localize to specific brain regions,
but instead appears to result from a more extensive network failure—a fail-
ure of the integrative processes of the prefrontal cortical circuits. Consistent
with this suggestion, a number of recent imaging studies report that during
depression, functional connections among the various brain regions of the
networks illustrated in Figures 5.2 and 5.3 appear to be lost, particularly those
between amygdala and prefrontal areas.4 Although the actual physical con-
nections among neurons are intact, the functionality of these connections fails.
Moreover, these studies suggest that disruptions anywhere in these networks

35
may increase the risk for depression. For example, in late-onset depression
in the elderly, abnormalities in white matter (i.e., the “connections”) occur
throughout these networks, consistent with this observation. With treat-
ment, as with the other abnormalities, functional connectivity improves.

5.2.5. The Hippocampus Is Smaller in Depression

A final common neuroimaging finding in depression is decreased hippocam-
pal volume. This finding appears to be associated primarily with recurrent or
chronic illness and may represent a consequence of a more severe course
of illness.4 The hippocampus is critical for memory functions, which are dis-
rupted in depression, as noted. The hippocampus is also closely integrated
into amygdala such that the two structures work together to consolidate
emotional memories and social behaviors. However, decreased hippocampal
volumes are also associated with chronic stress; stress is a common precipi-
tant for depression (Section 5.6), so that hippocampal volume findings may
simply reflect stress directly, rather than depression per se.

5.2.6. Functional Neuroanatomy of Depression: Summary

Taken together, neuroimaging research, coupled with studies of brain inju-
ries, suggests that the symptoms of depression arise from a loss of dorsal
and ventral prefrontal modulation of each other, the amygdala, and other
brain regions; that is, depression arises from a functional failure within these
prefrontal systems. Evidence that treatments modulate these abnormalities
provides validity of the model. Moreover, given the multiple components of
these networks, it is relatively straightforward to imagine disruptions from a
variety of causes impacting their function, consistent with a syndrome arising
Major Depressive Disorder from multiple etiologies. Some of these abnormalities may exist in individuals
at genetic risk for depression (see Chapter 6), consistent with an underlying
vulnerability in some families, but they also may occur de novo (e.g., with a
stroke). This model, then, provides a substrate to consider molecular and
other underlying causes of depression.

Key Point: The functional neuroanatomy of depression is characterized

by dysfunction of prefrontal cortical brain networks that modulate
human emotional and cognitive behaviors.

5.3. Neurotransmitter Hypotheses

of Depression
5.3.. Monoamines: Serotonin and Norepinephrine
For decades, investigators hypothesized that mood disorders result from
dysfunctional monoamine neurotransmission, namely abnormalities in sero-
tonin and norepinephrine function and metabolism. These hypotheses arose
primarily from the neurochemical effects of antidepressants that typically
increase the availability of synaptic serotonin and, in some instances, nor-
epinephrine. Although monoamines originate in a limited number of specific
36

brainstem nuclei, they are widely distributed throughout the prefrontal net-
works described previously (Figures 5., 5.2, and 5.3).
Serotonergic abnormalities have been observed in studies of depressive
disorders for decades, driven in large part, as noted, by the observation
that most antidepressants alter aspects of serotonergic neurotransmission
(see Chapter 7). Some of the more common findings supporting the role of
serotonergic neurotransmission abnormalities in depression include the fol-
lowing: reduced serotonin metabolites (namely 5-hydroxyindoleacetic acid;
5-HIAA) in the cerebrospinal fluid of depressed and especially suicidal indi-
viduals; precipitation of depression with tryptophan depletion in individuals
with histories of depression (tryptophan is a metabolic precursor of sero-
tonin); abnormalities in serotonin transporter (5-HTT) function; and reduced
concentration of 5-HTA serotonin receptors.,4,5 Of note, 5-HTA receptors
are widely distributed throughout the prefrontal cortex as well as the amyg-
dala, hippocampus, and hypothalamic nuclei.4 The concentrations of these
receptors are decreased in imaging and postmortem studies in depressed
persons compared with healthy individuals. Similarly, imaging studies report
regionally specific abnormalities in 5-HTT function in these prefrontal net-
works, although there are inconsistencies in these reports. Animal models
of depression also demonstrate down-regulation of 5-HTA receptors and
abnormalities in 5-HTT function in brain structures homologous to those of
the human prefrontal networks that underlie the expression of emotions.4
Moreover, metabolism of the 5-HTA receptor and 5-HTT is regulated by
genes that have been, albeit inconsistently, associated with familial depression
(Chapter 6); these genes likely confer a risk for developing depression that
does not occur until other processes further disrupt the relevant prefrontal
Other documents randomly have
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gelten statt Siegel, wanns ihm no mo net recht is, glei hinpappen —
alleweil glei hinpappen, da kann er fei nix machen.“
Er duckte hämisch gegen den Götzen. Der aber mußte den
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neugerüsteten Feind an sich herankommen, dann klappte das
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„Abrechnen tut er,“ raunte es ringsum, und klägliche Blicke hingen
sich an den Minutenzeiger, daß er nicht springe: vier Fünfersprünge
und das Postamt schloß. Der Zeiger schüttelte die Augentraube ab
und sprang zum ersten Mal. Das Milchglas rührte sich noch immer
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durch das Götzenloch und sah jenseits der niedren Zwischenwand
den mit dem rändigen Karneol am Mittelfinger sich noch immer die
schwarzen Nagelplatten ausstochern, während er einer
kanariengelben Mitbeamteten aus dem Abendblatt vorlas. Da riß ihm
die Geduld. Gut: diesem Lande Gast, hatte er sich seinen Bräuchen
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geballter Faust drang er gegen das Milchglasfenster vor, dem frechen
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einzig Gegebene. Welche Erlösung für die mißhandelte Herde, wenn
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bespiene Menschenwürde, nur einen, der ihnen allen zu Hilfe kam:
der gemeinsame Feind.
 Ach so: sie liebten das also offenbar, bezahlten es eigens. „Pardon,
ein Mißverständnis.“ Eben ganz wie in dem Masochistenbordell zu
Paris. Sir Osmond hatte ihn der Kuriosität halber einmal dort
eingeführt — Zuschauer beide — denn manche Kunden wünschten
ausdrücklich auch Publikum zu dem etwas gewaltsamen Empfang,
den sie sich bis auf jeden Handgriff genau, brieflich und um
schweres Geld vorausbestellt hatten.
An jenem Abend hatte sich nun, der Himmel mochte wissen wieso,
ein schlichter outsider hierher verirrt. Offenbar fehl am Ort und
durchaus nicht im Bilde, war der brave Mann in heller Empörung
einem Habitué zu Hilfe geeilt, als dieser, seiner innersten Neigung
nach, schon an der Türe, nachdem er lange vergeblich gewartet, mit
einer Flut von Injurien durch eine Beamtete des Unternehmens
empfangen worden war. Der in seinem Vergnügen Bedrohte, an
Ureigenstem verstört und gehemmt, zeterte nun seinerseits los:
„Wo die Ordnung bleibe — Wirtschaft —! Ob man meine, er zahle
sein Geld für nichts? Sacré nom d’un petit chien marron! — Wozu
unterhalte man denn sonst den ganzen Betrieb!“
Und nun begannen alle: Handelnde und Behandelte über den
schlichten outsider herzufallen und warfen ihn die Treppe hinab.
Sogar ein Ölreisender in Pyjamas war, wie aus der Kanone
geschossen, plötzlich dabei und beteiligte sich unter Beteuerungen,
daß er ganz normal sei, aber sicher noch seinen Nachtzug nach Lyon
versäumen werde, an dem Strafgericht. Stürzte dann wieder zurück
— — fait vite — fait vite — rief es aus dem Zimmer, machte bei
halboffener Türe ein paar Griffe an seiner Dame, fuhr herein, heraus
und in seine Kleider, fand zwischendurch noch Zeit, sich bei der
Direktion über „cette grue“ zu beschweren. Frechheit, während
seiner Liebe habe sie einen Apfel vom Nachtkästchen genommen,
hineingebissen und die Kerne zum Plafond gespuckt, wie um zu
zeigen, auch sie wolle eben ein Vergnügen dabei haben. Kränkend
sei das! „Freche Hure“. Er spuckte aus und sauste mit zwei
Musterkoffern die Treppe hinab. Vielleicht hatte er vor dem Tor gar
den Hinausgeworfenen noch überholt und im Vorüberstürzen Zeit
gefunden, diesen über den Grund des Treppenflugs sexuell
aufzuklären.
 Ein Mißverständnis eben. Nein, Horus würde in deutschen
Amtslokalen nicht mehr „schlichten outsider“ zu spielen versuchen.
Staunte auch nicht, als jetzt ein neues System teuflischer Netze den
schäumenden Haufen, knapp vor seinem Ziel: dem Bahnsteig,
abfing, daß er davor zu einem Block Unluststoffe gerann, dessen
Lodenhülse unter dem Druck sich durch die Gitterstäbe spannte als
platzende Ballonhaut. Drei Zentimeter jenseits, vor Himmel und
Schienen, gähnten ein paar Götzen mit Zwickzangen im Leeren, vor
der leeren, längst bereiten Zugsgarnitur.
Samossy, in die Ecke getrieben, bis an den Hals im Pöbel, starrte
dunkel und süchtig hinüber. Hatte die Ohren zurückgelegt, spannte
die Stirnhaut, röchelte dumpf und eingespeichelt glücklich. Dann wie
zu schlechtem Gewissen erwachend:
„So ein moderner Verkehr hat doch etwas Imponierendes, diese
musterhafte Ordnung, daß alles so klappt.“
Und sank wieder in träumende Starre.
Im Block unter der Lodenhülse aber brodelte Ärgernis: unerzogene
Mütter trieben mit Püffen Anstand in ihre falschgebornen Kinder
hinein, den diese wieder schreiend erbrachen. Männer rissen sich
immer wieder viehisch Wege zu Büfett und Zeitungsstand. Den
Raubmord von heute gierig schwingend, den Raubmord von gestern
achtlos um den Leberkäs gewickelt, ritten sie dann,
zurückgaloppierend, Schinkenstullen unter dem Rucksack mürbe.
Jeder Ankömmling aber stieß auf wutgerundete Rücken der
Abwehr. Wieviel so üble Zweibeiner gab es denn noch, wie man
selber einer war? Fassungslose Empörung! Man konnte das eigne
Zahlreichsein offenbar noch nicht meistern, hatte sich schneller
vermehrt als daß dem Einzelnen seine persönliche Gleichung
gestattet hätte, sich dieser Verdichtung anzupassen.
Pöbeldichte ist das Infernalische hier, fühlte der Fremde; dieses
geistig und leiblich einander auf die Hufe spucken. Pöbeldichte, nicht
Menschendichte, denn diese schafft ja positive Qualitäten: etwa
Chinas Rücksicht und Diskretion, kann doch bei Übervölkerung die
unersetzliche Einsamkeit dem Einzelnen nur durch zarte und
kultivierte Manieren der Vielen gewährleistet werden. Er träumte sich
zurück in das südliche Blütenland, das „Land der Lebendigen“.
Wieder stieg die Paganinipyramide auf, doch diesmal trug sie ihn
durch Stunden und über diese ganze Fahrt hinweg, wie zum Dank
für einst. Manchmal schrak er glücklich lächelnd auf, wog seinen
Reichtum: „Wieviel war meiner Jugend beschieden“. Auch „geflügelte
Perle“ kam.
„Ich will dich das Geheimnis des Fußes lehren und meiner älteren
Schwester das Geheimnis der Blume Lan.“
Seidnes Wesen!
Sie hatte ihr Versprechen gehalten.
Aus der Zahnradbahn keuchte es jetzt, sich überrennend, dem
Hotel unter dem Gipfelkopf zu, einer im Kielschweiß des Andern,
Kinder und Rucksäcke schleiften nach. Im Tor schäumten Wirt und
Pilgrime gegeneinander an.
„Zu fünft drei Betten — ausgeschlossen, da sorcht ja schon die
Behörde jejen!“
„Aber Ludwig, ich bitte dich, Trude und Hans in einem Zimmer!“
„Bleibste in der Depandanxe — nöch?“
„Na, denn nich.“ — Und auf einmal ließ man das ganze
Übernachten stehen, riß sich angstvoll um die Speisekarte — zu
reservieren, was zu reservieren war. Familienväter bestanden auf
fünf Kalbshaxen, Kinder grölten nach Apfeltorte; es ging um Tod und
Leben, als eine Person mit angekettetem Kropf zwei graue Beete aus
Krügen in den Männerarmen hereintrug.
Auf einmal waren alle Mehmkes da, samt Töchtern,
Schwiegersohn und Enkel Fritz, von Krause flankiert. Dallmeyer blies
schon Bierschaum in den Ausschnitt von Margrinchens rosa taffet
Bluse über dem Lodenrock.
Samossy, gänzlich verwildert, umwieherte indes die Kellnerin.
Doch ihre rotpunktierten Männerarme in den kalkharten
Puffärmelchen waren jetzt frei und schützten sie erfolgreich
ringsherum.
Langsam mit dem Speisendunst ging die Stimmung ins Breite,
Qualm nikotinisierte den Verdruß. Schon war die Luft fast so dick wie
zu Hause, und nahrhaft von vergastem Fett.
Jetzt hieben ein paar Tatzen voll Töne in den Brodem. Ein
Auswendighämmerer begann Kraut und Rüben durcheinander zu
hacken, riß dem Klavier die Stockzähne aus, schmiß sie der Dulliöh-
Stimmung in den Rachen: aus einer Art Beethoven cake walk
schmalzte er in ein Carmen-Meistersinger-Potpourri hinein, schlang
diesem den Liebestod als Boa um und markierte dem wiehernden
Saal die Glocken aus Parsifal, mit dem Gesäß auf der Klaviatur,
landete dann mit einem Flohsprung mitten im letzten Satz der
Neunten Symphonie, boxte sich durch bis an die Menschenstimme —
— —:

„Nee, so was Gemütliches, nee so was Gemütliches,

Mir wackelt vor Lachen der Bauch,
Na siehste, dir wackelt er auch.“

Und die Sonnenpilgrime fielen mit der zweiten Strophe des

Sensations-Schlagers der Saison ein:
„Vor Gericht zur Ehescheidung ist zur Sühne heut Termin.
Er in eleganter Kleidung, sie sehr schick, Hut voll Jasmin.
‚Wollen Sie sich nicht vertragen?‘ fragt der Richter ehrfurchtsvoll.
Als sie grade ja woll’n sagen, schreit ein Weib: ‚Paul, bist wohl toll!
Laß die alte Zicke türmen!‘ ‚Was, Sie Mensch!‘ schreit darauf die
Frau;
Nun geht’s los mit Regenschirmen, alles schlägt ein’n Mordsradau.
Zähne, Zöpfe umherliegen und der Richter bietet Ruh.
Süße Schmeichelworte fliegen. Ekel, Lulatsch, alte Kuh!
Selbst der Richter kriegt zum Schluß im Gewühl eins auf die Nuß.
Nee, so was Gemütliches etc.“
Draußen — draußen standen irgendwo Sterne — groß und weit
weg.
Um Morgengrauen barsten Wecker auf Tellern, kreischten spitze
Trichter hinein. Ein finstrer Knöchel kam von Tür zu Tür, zerklopfte
durch Holz hindurch Träume im Hirn. Das Hemmungslose der
Aufstehgeräusche stand plötzlich mitten in fremden Zimmern. Durch
Korridore schlurfte es ohne Kragen, in Hemd und Unterhosen. Wie
ertrugen sie nur eine Tracht, die tagtäglich durch dieses
entwürdigende Stadium hindurch mußte?
 „So mach doch vorwärts — noch nicht fertig?“ — Dann wieder in
seltsamem Hedonismus: „Na, freu’ Dich bis wir nach Haus kommen!“
Türen knallten; grün vom Fleisch und Bier der Nacht, stolperte es in
karierten Plaids durch die silberne Frühe. Ein Pfahl im
Schotterhaufen und eine Ansichtskartenbude markierten den Gipfel.
Jetzt war es so weit:
Ungezogenes Gebrüll verkündete das Herannahen der Sonne.
Männer riefen: „Na also!“ Frauen: „Ach wie süß.“ Jeder rief irgend
etwas.
„Ja, so ein Sonnenaufgang bleibt doch ein Sonnenaufgang,“
begann Fräulein Mehmke — dann ward es ihr bleich vor dem
anämischen Hirn, sie hätte gestern nicht so viel Schlagsahne zu den
Birnen essen sollen.
Dallmeyer stieß indes aus den Wolken seines Bartes die ersten
Töne von Brünhildens Erwachen: „Heil dir, Sonne!“
Krause war dagegen:
„Nee, nee, lassen Se se lieber in alter Weise tönen.“
Und Margrinchen, die wieder funktionierte, ratschte weiter:
„In Brudersphären Wettgesang, und ihre vorgeschriebne Reise —“
„Reise“ — erinnerte sich Frau Geheimrat, im Rucksack kramend —
„hast du am Ende das Reisebesteck vergessen? — Vater braucht den
Pfropfenzieher.“
„Nun, Fritz, wie geht es weiter,“ examinierte Mehmke, „in deinem
‚Goethe für Jungens‘ hast du’s ja beinahe unverkürzt.“
Aber Fritz maulte: „jetzt is Ferien.“ Und er intonierte das
Lieblingslied von jung und alt:

„Mariechen,
Du süßes Viechen,
Sie ist eine ne—te—te—te,
Diva von der Oper—e—te—te—te.“

Da es ihm seine Mutter oben verwies, quäkte er es um so lauter

etwas weiter unten bei den Kühen, kam aber bald zurück, denn man
leerte aus den Rucksäcken Konserven in die Natur, die Fransen von
Mehmkes Plaid schwammen schon im Sardinenöl. Man kaute und
schrieb zwischendurch Ansichtskarten. Männer entfalteten markig
das Abendblatt; weise diesem zeitungslosen Sonnenaufgang
entgegengespart. Es war voll der neuesten Pariser Sensation: dem
Hosenrock. Seit Wochen flossen die Gazetten aller Parteirichtungen
über von Bulletins. Würde er sich wirklich auch außerhalb
Frankreichs als Mode durchsetzen? Unmöglich ... bei keiner
anständigen Frau ... die Entrüstung war allgemein.
„Geiler, welscher Tand.“ Dallmeyer röhrte auf germanisch.
Margrinchen zeigte ihm, wie mühelos ihr eigner Rock
aufzuknöpfen sei: entarteter Abkömmling eines verjährten Pariser
Schlitzmodells, nur daß sein planlos Affenhaftes hier ins stockend
Barbarische geraten war.
„Echt weiblich und doch praktisch,“ lobte Dallmeyer, „echt
deutsch!“
„Auch malerisch,“ ergänzte ihre verheiratete Schwester, die den
gleichen trug, und drapierte einen Batikschal über den Wettermantel
und die auseinander geronnenen Hüften.
Wer ohne Zeitung, hatte anders vorgesorgt für die langen Stunden
hier draußen, wo nichts los war: „Wollen wir n’en Skat dreschen?“
Und aus Handflächen sprangen karierte Blätter per Kopf auf
gebreitete Lodenflecke ringsum. Manchmal zorniges Grunzen:
„Rindvieh dappigs, so paß schon auf.“ — „Halts Mäu!“
Akademisch Gebildete spielten hier nicht Karten. Wußten, daß man
in der Natur natürlich zu sein und sich in ihr zu lagern hatte. So
lagerten sie erst angezogen, als Fremdkörper umher, begannen dann
aber, als es wärmer wurde, auf grauenhafte Weise Bekleidung von
sich abzustoßen, unter andauernd witzigen Bemerkungen über
diesen Vorgang. Die Rhododendren hingen schon voll Hosenträger,
und das schlurfende Stadium von den Korridoren war wieder
erreicht; selbst halbe Akte tauchten vorübergehend auf,
verschwanden wieder: nein, es war allerdings kaum anzunehmen,
daß die Natur das zum sichtbarlich außen Tragen bestimmt haben
sollte.
„Mal bißchen Natur kneipen.“ Auf dem Rücken liegend, hob Krause
das Gesäß und klappte die Hufe in der Luft erlaubnisheischend
gegen die Damen zusammen. Oben die Sonne wiederkäuend, buk er
unten die gelbliche Riesensemmel seines Bauches gar, im eignen
säuerlichen Speck. Der Geheimrat kraute mit dem kleinen
Fingernagel seine grauen Achselhaare:
„Was Samossy, dieser Intrigant wieder ausgeheckt habe — ein
Narr — ein gemeingefährlicher Narr, ob Dallmeyer den Angriff ...“
Aber Dallmeyer hatte die Stiefel ausgezogen und war längst Jung-
Siegfried; dahin rollten die Stücke des morschen Speers, an Notung
zerschellt. Keine Abfindung für die Schwarzalbin, jüdische Mitläuferin
und was ihr entsprossen. Seine männische Kraft sollte eine reine
Jungfrau erwecken ... nur wer durch das Feuer bricht ... als
korrespondierendes Mitglied mußte er heuer noch in die Akademie
hinein.
Kein Gruß aus der Kreatur klang in diesem Äther. Kein
aufjubelndes Fluidum aus wilden, freien, vielgestaltigen Herzchen
entzündete sein zeugendes Netz. Leergescheucht auch er: ein übler
Doppelspat, auch er, durch den das Un-Sein hereingebrochen kam.
Kinder machten auf ein paar glücklose Kriechtiere Jagd, die nicht
Beine genug gehabt, sich rechtzeitig einzugraben. Fritz kroch umher,
kratzte aus dem Moos, was er an Fühlern und Flügeln erwischen
konnte, brachte es in seiner scheußlichen Gymnasiastenmütze
Margrinchen. Sie sonderte die männlichen Tiere aus, und er durfte
sie in eine Glasflasche füllen, während das Fräulein ihr biologisches
Besteck auspackte.
„Unten nicht so zerquetschen,“ mahnte sie, wenn seine
Fingerstummel mit den verkehrt eingesetzten Nägeln ihr eine
Kreatur nach der andern reichten. Dann sah er mit abstehenden
Ohren zu, wie sie hineinschnitt.
„Immer fleißig,“ schmeichelte Dallmeyer. Er war endgültig durch
das Feuer gebrochen und näherte sich bereits Margrinchen auf ihrem
Fels: „Immer eifrig bei unsrer Wissenschaft.“
Vom Hotel herauf schellte es jetzt Mittag. Sie warf das
angeschnittene Tier weg und begann ihre Frisur zu richten.
Dallmeyer stöhnte in Stiefel hinein, Krause suchte nach
Hosenträgern — Plaidfransen blieben an Uhrketten hängen, rissen
Geld und Karten ins Gras, alles knöpfte sich zu — stob abwärts zu
Hauf.
 In die lange, neue Stille hob sich aus Gebüsch mit eins ein
verschlafener Kopf, blinzelte ins Leere — begriff dann. Maßloser
Schreck ging in seinen Zügen auf, er blickte wirr um sich, dann
schreiend:
„Ist es schon losgegangen?“
„Wenn Sie die table d’hôte meinen, so glaube ich: ja.“
Der Europäer warf die Arme gen Himmel und wollte fortstürzen,
da vertrat ihm Horus den Weg, packte ihn vor der Brust:
„Was ist das jetzt eigentlich für ein Fest heute?“
„Na, Pfingsten doch.“
„Was ist das: Pfingsten?“
Dem Andern wurde ängstlich, er klammerte sich an seine
Brieftasche:
„Die Ausgießung des Geistes natürlich, oder so was Ähnliches.“ Riß
sich los und machte im Lauf kopfschüttelnd vage Gebärden vor dem
Hirn, wie er sie in irgendeinem verlogenen Theater gesehen.
Jetzt waren also endlich alle hinuntergeflossen, diese Ohne-
Hunger-Esser, zu ihren dicken Suppen, die ihnen wieder ausbrachen
als unmäßiger Schweiß, und der Gipfel tauchte frei empor; der
getötete Äther um ihn aber trug keine Seeligkeit mehr. — Vielleicht
das Moos? Er bückte sich: Enzian sah ihm in die Augen herauf, dann
ein kleines Gelbes, das sehr keck schien, rötliche Röllchen rochen
gut. Vielleicht enthielt die Erde für ihn die antäische Stärkung eines
Grußes.
Wie einst zwischen die aufrauschenden Ohren Rama-Krishnas,
warf er sich nach vorn, preßte das Gesicht ins Lebendige, fuhr auf
und mit der Hand an die Stirn: dort klebte quer eine Wursthaut.
Worin lag er da? Eine Bergwiese? — ein Kehrichthaufen? — ein
Magengeschwür? — ein ungemachtes Bett? Zerwälzt ohne Wonne, in
dem Frigidität, Geile und Feigheit aneinandergeklebt hatten! — War
das noch Enzian oder schon ein Tintenklex, roch die zerknüllte
Stanniolkugel da oder das Kohlröschen? Er suchte nach dem
angeschnittenen Versuchstier der jungen Dame. Tötete das sich
Windende rasch, fest, ehrfürchtig.
Samossy kam erst knapp vor der Rückfahrt aus einer Tür zum
Vorschein, an der geschrieben stand:
 „Nur für das Personal, Gästen ist der Eintritt nicht gestattet.“ Beim
Abstieg rieb er äußerst animiert die knorpeligen Enden seiner langen
Finger aneinander, als wollte er Feuer aus ihnen schlagen, wieherte
in der Fistel:
„Ja — ja, man muß vom Weibe loskommen.“
Die Kellnerin hatte ihm aus kalkharten Puffärmeln mit einer roten
Pranke nachgewunken, die kein goldnes Kettenarmband trug.
Zarathustra war ungelesen im Rucksack geblieben.
Abends entließ der Ostbahnhof die Ausflügler in fahle Vororte
hinein. Aus einem politischen Keller stank eben strukturloses Gewölle
breit in den Platz, jenem gleich, das im Hafen von Marseille, als
Ballen von Mißgunst, das rhythmische Arbeiten der asiatischen
Bemannung mit hämischer Überheblichkeit zu zergaffen versucht.
Hier schien es in Fluß geraten, in stumme, maßlose Geschwollenheit
hinein. Sah man näher zu, zerfiel es in einzelne, aus allen Angeln
gedrehte graue Brocken, die torkelnd neben ihren Stiefeln gingen.
Weiber hakten sich in Männer, reckten die abgebundenen
Spitzbäuche, stampften auf kolossalen Füßen eine namlos verlogene
Degagiertheit einher. Junge, mit wilden Papuafrisuren lachten wie
aus Grammophonen. Allen stand käsiger Schweiß aus Wurst und
dicken Phrasen um die eingetriebene Nase und den sackförmigen
Mund.
Es waren die abstoßendsten Geschöpfe, die er je erblickt. Nicht so
sehr durch das Übelgeratene selbst, nein, durch eine beispiellose
Überheblichkeit weltgültigen Rüpeltums, mit der jeder gerade dies
Übelgeratene, wie eine hohe Rechnung präsentierend, an sich zur
Schau trug; Gesitteteren damit schadenfroh unter der Nase
herumzufuchteln nicht müde ward, als wäre er das Unmaß aller
Dinge.
Auch hier wieder der typisch europäische Blick: er, der nicht sah,
als bliebe die ganze Umwelt dauernd in den gelben Fleck der
Netzhaut gerückt.
Auf dem andern Gehsteig kam jetzt eine einsame Frau dem
Haufen entgegen, strebte, dunkel gekleidet, unauffällig und still —
etwas eilig auch — ihres Wegs.
 Schon waren die Vorderbrocken blind über sie hinausgetappt: das
ausrangierte Schachrössel mit der roten Schleife an der Spitze, einer
der fanatischen Nasenbohrer aus der Russenecke im Café und ein
kleiner Herr mit Zwicker von außerordentlich semitischem Typus.
Da erspähten zwei Halbwüchsige die Einsame, vertraten ihr aus
der Flanke des Zugs heraus den Weg — noch probeweise — wie
suchend vorerst, tänzelten von Bein auf Bein — endlich glaubten sie
etwas gefunden zu haben:
„Mir scheint gar, dös is a Hosenrock.“
Und der eine blähte hämisch vorn seinen Latz, ganz wie die
Crapule in Marseille vor Gargi getan. Der Unflat, der auf seinem Hals
an Stelle des Gesichtes saß, stank ihm dabei aus den Augen.
Der andre, gebückt, Zigarettenstummel im eckigen Maul, tat, als
inspiziere er streng von unten.
Die unscheinbare Frau hob sanfte Hände der Abwehr:
„Lassen Sie mich vorbei, bitte, ich muß nach Hause.“
Aber schon kreischte es rundum:
„A Hosenrock, a Hosenrock.“
Spitzbäuche und Papuafrisuren rissen die Mannsleute heran:
„A soa Weibstuck, a soa ganz ausg’schaamts, a soa Großkopfate!“
„A soa Madame.“
„Oin iebermietiger Adel und ein verrottetes Bürgertum“ ... begann
das ausrangierte Schachrössel — —
„Eiterbeule am Pestleib des Kapitalismus“ ... fuchtelte der kleine
Leitjude. „Schamlose Provokation des klassenbewußten Proletariats
... Genossen, setzt euch zur Wehr ... der gesunde Sinn des
werktätigen Volkes darf nicht dulden ...“
„Geiler welscher Tand,“ röhrte es jetzt dazwischen aus dem
wallenden Dallmeyer-Schädel, den Häusern angeklemmt im Trupp
der Ausflügler.
Nur helleingesehene Unmöglichkeit, sich dorthin durchzuboxen,
hielt Horus ab, sich gerade auf diesen reißend Verpöbelnden zu
werfen, doch auch seine Glieder waren eingekeilt zwischen Mauer
und Mob.
Einen Moment duckte sich Stille im Raum. Bogenlampen flirrten
hoch darüber. Dann grellte ein Ton auf, dem sich in der ganzen Natur
an Gemeinheit nichts vergleicht. Der infernalische Ton eines
johlenden Europäerhaufens pfiff hinter dem hingespienen
Zigarettenstummel drein, zwischen Fingerstumpen hinausgegellt als
onanierende Niedertracht.
„Der Hosenrock muaß aver ... übern Hintern gspannt, ghörat er
ihr, der Hosenrock.“ Ein Stierkerl mit Wurstpratzen hatte es gebrüllt.
Temperamentlose Wut aus eiskaltem Schweinespeck gebar zuerst
Moralsadismus. Die Weiber heulten Triumph. Das wieherte, spie,
trampelte im Rudel heran um die weinende Frau. Unter gingen ihre
Hilferufe im Gegröle des Mob. Von der Welle aus Feigheit in
Frechheit hinübergespült, warfen sich die zwei Halbwüchsigen platt
auf den Bauch, krochen ihr unter den Rock, hoben ihn rechts und
links mit den Köpfen hoch, zerrten die Beine der Wimmernden
auseinander, daß sie mit dem Gesicht platt in den Kot fiel ... Mit
haßkrummen Pfoten stürzten sich die Weiber über die Liegende,
rissen ihr die Kleider in die Höhe, die Hose auseinander ... der
russische Nasenbohrer fanatisierte die Herde rechts und links, wie
ein anspringender Hetzhund.
Vorn der kleine Leitjude kniff sich eilig einen zweiten Zwicker auf,
reckte feixend den Hals, um besser sehen zu können.
Eine Megäre heulte wehleidig auf: „A soa Kanalli.“ Sie hatte sich
an der Hutnadel ihres Opfers geritzt.
„Volksgericht ... Volksgericht,“ das ausrangierte Schachrössel zerriß
sich fast in der Luft, doch keiner scherte sich drum. Eine Blase
grüner Gier, schwoll die Pöbelgeile über ihrem Opfer, immer höher
aufgetrieben von den fanatisierenden Sprüngen des slawischen
Nasenbohrers.
Auf einmal stach ein Polizeipfiff die Blase an, feig und flach fiel sie
zu einer Linse zusammen, gerann immer dünner, bis das
Straßenpflaster aus ihr aufstieg, in dem ganz allein, in Qual und
namenloser Scham, sich die gemobte Frau mit grellentblößtem
Unterkörper wand.
Außer ihr fand die Wache eigentlich niemanden mehr zum
Verhaften vor. Zwei Polizisten führten die Halbohnmächtige ab, ein
Dritter bückte sich nach dem Hosenrock. Mit strenger Hand hielt er
das „Ärgernis“ in sittlichem Ekel weithin von sich ab. Wies es
anklagend rundum, begann plötzlich zu gluren, zu grinsen, und alle
rings im Kreise grinsten mit. Man schlug sich auf die Schenkel vor
Vergnügen.
Das war ja gar kein Hosenrock.
Auf die entleerte Straße schlich es sich jetzt hinter einem
Häuserblock schlacksig heran, alle Körperknochen eckig unter die
engen Augen gehäuft: der Hetzhund des Haufens warf sich platt
nieder, windelweich auf einmal. Begann das glitschige Frauenblut
aus dem Straßenschmutz zu saugen, umarmte das Pflaster,
quetschte seine Seele wie einen verschnapsten Schwamm über den
Brei aus Blut und Kot, in greinendem Gefasel, menschheitsduselnd
aus.
Da stieß ihm Horus Elcho in sternblanker Wut den Fuß ins
Rückgrat:
„Auf — Schwein — aufhören mit dem sentimentalen Dreck.“
„Bruderherz,“ harnte es flennend naß von unten herauf — „laß
dich umarmen, Bruderherz, wir sind ja alle gleich, mein Seelchen, —
alle, alle gleiche Menschen.“
„Nein — Gott sei Dank — nein!“
Und der goldäugige Exote schritt auf den andern Gehsteig. Der
Erdradius war nicht so lang, als jetzt diese Vorstadtstraße breit war.
Viele Stunden lief er noch durch die milde Nacht, in den Anlagen
Fluß auf und ab, mit heißen Adern. Als schwefelige Blitze standen
ihm die Nervenfäden um das bewölkte Herz. Und dann trieb ihn
Trotz unwiderstehlich, ein Stück Maskerade seiner Zugehörigkeit zu
dieser weißen Köterrasse nach dem andern wegzuwerfen — einfach
weg ... Erst die Fußschachteln in eine Wiese, den Rock ins Wasser,
den albernen Stoffkopf hing er an einen Strauch, kam zurück, drehte
ihn um zu einem Nest zwischen drei Astgabeln; vielleicht diente er
so einem anständigen Vogel zur Brutstatt — tat es in vagem Trieb,
süßes Leben als Gegengewicht zu fördern.
Ins silberduffe Gras auf die Flanken gekauert, überdehnte er dann
die zehn Gliedspitzen wie ein gähnender Jaguar — wehende Halme
streichelten den Stromkreis zu, leiteten das ausgetriebene Übel
erdwärts, da löste es sich über die makellose Riesenkugel hin auf.
So mochte es zwei Uhr geworden sein.
 „Das gibts nicht da. Das ist Vagabundage, — im Freien darf nicht
übernachtet werden.“ Ein Ordnungsgötze voll Blech am Kopf türmte
schwarz und lotrecht in die Natur.
Langsam drehte er sich auf den Rücken, sah was zwischen ihm
und dem Polarstern stand, bekam einen gelachten Wutanfall.
„Also nur im Unfreien darf hier übernachtet werden? Jetzt sagen
Sie, was darf man in dieser europäischen Dreifalt von Schlachthaus,
Irrenhaus und Zuchthaus denn eigentlich? Leben verhunzen, was?
Natur verhunzen! süße Tiere zermartern! Pöbel züchten! Bosheit
mästen! Moralsadismus treiben? Kurz, auf jegliche Art ein
Schweinkerl sein: das darf man. Will aber einmal der Arme eine
Nacht lang Sterne statt Wanzen über seinem Kopf haben, so heißt
ihr das Vagabundage. Oh eure Lügenworte. Eure schiefgemaulten
Lügenworte! Da laufen Asphaltstraßen, rein wie Schnitte an einem
Tortenüberguß durch eure glatte Welt. Was hilft’s, sind sie allesamt
mit bürokretinistischem Sekret überzogen, nur im Härtegrad, nach
den Ländern wechselnd, von Eisenbeton zu fromage de Brie:
stinkender wenn weicher — drückender wenn härter;
lebensundurchlässig alle.“
„Habt ihr denn so ganz des göttlichen Kontinents, aus dem ihr
kamt, vergessen? Seine jahrelangen Straßen sind staubig und
trockenen Büffelmistes voll, der in die Augen brennt. Über diesen
Büffelmist aber schreiten mit Mantel und Schale Hunderttausende in
die Vergottung hinein — frei und unbefragt. Hier an dem weißen
Rand ins Nirvana tut jeder das herrlich züchtende Joch der Kaste von
sich ab, das ihn herangeleitet, steigt aus der tiefen Farbenmulde
seiner Art und verbrennt zu Gott, wandernd im Anhauch dieser
freien Straßen.“
„Sie gehen jetzt mit,“ sagte das Triefauge des Gesetzes, noch
uneins, ob das mit dem Büffelmist Amtsehrenbeleidigung oder nicht.
Im Polizeigebäude hingen an verwanzten Wänden schwachsinnige
Zettel in Rahmen herum: „wir wollen helfen, nicht strafen“ — „nach
eignem Sinne leben ist gemein“ und ähnlicher Fibelschund.
Daß er Seidenwäsche aber keine Stiefel trug, rettete die Situation.
Auch das Pfingstfest.
 „Nun ja, der Feiertag! total besoffen eben — aber sonst ein feiner
Herr.“ So ließ man den kuriosen Fang nach Abnahme seiner
Personalien gehen, machte ihn aber auf die Folgen eventueller
doloser Irreführung der Behörden aufmerksam.
Europa hatte nur eben probeweise ein paar Maschen ihres
Jusgarns ein bißchen um ihn zugezogen, so zum Spaß, nur um zu
zeigen, was sie alles konnte. Ließ ihn dann wieder laufen, — weiter
in gesenktem Netz, das über die klebriggespannte Ballonhaut dieser
ganzen aufgetriebenen Welt schleppte.
Seit der „Hosenrock“-Episode begriff er mit eins den Geldkrampf
aller. Ihre schlotternde Angst. Das an eignem oder andrer Geld
Kleben, hemmungslos, zum Gemeinsten bereit, aber nur
mitschwimmen dürfen im Oberflächenhäutchen, sich mit Dreck dort
anpappen — oh, alles — nur nicht heruntergestürzt werden zu
diesem aus seinem stinkenden Brodem aufschnappenden Mob.
Schicksal eines Beutetiers war Adel und Wohltat dagegen.
Hier hieß arm sein ja nicht in veredelnde Einsamkeit wandern, mit
vollkommenen Tieren frei durch Flur und Licht spielen, die
Diademgestirnte zur Genossin haben, bei Ganapati Sastriar hocken,
mit dem Schikari schweifen, im sanften Gewimmel blauer Kulis
unbelästigt leben oder sterben, unbeschnüffelt von der taktlosen
Tyrannei behördlichen Humanitätsschnauzentums.
Ging es einem Hindu schlecht, umgab ihn immer noch Distinktion
der Gebärde, Zartsinn, Niveau der Kaste, durch die das Individuum
mehr — schon dem Typus nach mehr ist — als es aus sich selbst zu
sein vermöchte. Arm sein hieß daher nur: Form der Gesittung
tauschen.
In Europa aber hieß es, dank diesem sadistischen Wohnzwang,
wirklich in der Hölle sein: bis zum Tod eingesperrt leben mit Roheit,
Bosheit, Intoleranz und Gekeif, umlauert von hämischer Neugier.
Hieß statt süßer Kinder falschgeworfene, verzogene, gröhlende
Mißgeburten haben, hingesudelt im Fuseldunst, denn nie könnten
klare Sinne den Ekel vor erotisch so ungepflegten Weibern, wie sie
dem Armen hier einzig zur Verfügung stehen, überwinden.
Hier ohne Geld sein, hieß also für einen Menschen von nur
durchschnittlichem Feingefühl: Selbstmord. Nicht Entbehrungen der
Armut, des Niveaus der Mitarmen wegen. Denn so etwas wie einen
entrassten europäischen Mob, das hat ja die Welt noch nicht
gesehen, hat es nie und nirgends noch gegeben! Lag es an Löhnen?
Lebenshaltung? Keine Spur. Gab doch das Volk hier nebenbei für
Alkohol und Tabak täglich mehr aus, als ein Chinese für den
Unterhalt einer ganzen Woche. Der kroch morgens aus seinem
Kanalloch, eine halbzerkaute Ratte zwischen den Zähnen und war
doch ein Wesen an Courtoisie und Herzenshaltung von den Höchsten
seiner Rasse, einem Li-Hung Tschang etwa, nicht gar zu sehr
verschieden, übte wie sie die Selbstzucht eines komplizierten
Zeremoniells, lebte wie sie das „Buch der Riten“ und die „Religion
des guten Bürgers“. Lag es an psychischer Qual? Beweis, daß diese
europäische Masse nicht wirklich litt, war ihre Taktlosigkeit: erste
Frucht des Leidens ist der Takt.
Eine unbegreifliche latente Bosheit bildete hier durch alle
Schichten hindurch Knoten, um gelegentlich an der Stelle geringsten
Widerstandes durchzubrechen: dem Sehen.
Aber warum sahen sie nicht? Warum waren alle am hellsten Sinn
verkümmert, aus dem die Liebe erfließt und die Vision? Konnten
Hose von Rock nicht unterscheiden, echt von unecht, Kunst von
Kitsch, fielen und legten einander rastlos wechselseitig optisch
herein.
Gargi, die nie Fragende, hatte einmal schüchtern gemutmaßt.
„Ist es ein Gelübde?“
Meinte den ersten Backenzahn, den die meisten golden trugen,
neben vorderen Porzellankronen.
Nein, sie glaubten eben, man sehe das nicht, weil der Zahnarzt,
der auch nicht sah, es beteuerte. Ein Blick hätte das Gegenteil
erwiesen, aber es war eben kein Blick da. Anfangs konnte er in Paris
immer wieder über die schleierlose Roheit erschrecken, mit der
Menschen in Sehweite übereinander medisierten, vermeinend, das
merke sich nicht, außer Hörweite zu sein genüge. Lang hatte er
gebraucht, um an solch optische Verstumpfung faktisch glauben zu
können. Alles was die Europäer in ihrer Biologie von den niedren
Tieren behaupteten, war wirklich ganz richtig — auf die Behaupter
selbst angewendet. Reagierten auch so automatisch mechanistisch,
wie sie es den Amöben zuschrieben; auch ihre Fundstelle (das Heim)
der einzig völlig reizlose Ort, wo sie ihr Futter fanden.
Hing mit dem flächlichen: oberflächlichen Sehen nicht auch die
Überschätzung des „Malerischen“ hier zusammen? Welt der niederen
Tiere, die sich in verschieden belichtete Flecke auflöst; noch nicht
aufgestiegen in die dritte Dimension. Daher vor allem der Hang ihrer
überkleideten konturscheuen Weibchen zur palettenumschweinzten
Aura. Dieser ewige Kunstschwatz und in Bilderausstellungen Rennen
der Europäerin, was sie gar nichts anging, statt was sie unmittelbar
angehen sollte zu beherrschen: die Raumschöpfung des Heims. —
Schaukraft fehlte eben: Durchschauung des dreifältig Gefügten:
Architektur.
Ja, die Überschätzung des „Malerischen“ lebte von zerronnenen
Weibern.
Nur konturreine Maschinen waren hier auch zu würdigen
Behausungen gelangt. Er hatte sich die modernsten
Architekturwerke kommen lassen, da herrliche Bahnhöfe, Silos,
Fabriken, Betriebsstätten gefunden, dabei gedacht:
„Wäre ich eine Turbine, ließe ich mir mein Heim von Behrens
einrichten.“ Auch Rösser und Exkremente hatten es gut. Ställe und
Kanäle gelangen manchmal wunderbar. Nur Menschenheime im Sinn
und Rang des Hauses Elcho fehlten, denn es fehlten die Menschen
dazu. Langsam begann er die Leistung seiner Mutter zu begreifen.
Diese jahrelange, zähe, unbeirrbare Treue zum Ideal. Das einzig im
höchsten Sinne europäische Heim war am Herzen des Dschungls
erschaffen worden.
Welche Selbstverlöschung, ihn in diesem Werk Europa anbeten zu
lassen, statt sie. Wie weise lang hatte sie ihm die sprühenden
Sporen dieser Illusion bewahrt, die ihn hinaufgebäumt aus goldner
Sinnenmulde in die herbe Kraft lotrechter Geistigkeit.
Langsam drehte sich die ganze Kuppel an seiner Jugend
Wunderbau in einen neuen Aspekt hinein. Manche Absicht klärte
sich, überraschend gelöst — mehr noch blieb vieldeutig, doch war er
ohne Ungeduld. Zog wie auf Wolken über diesen Kontinent dahin,
unangreifbar in seinem Kraftfeld: fern, stark und unberührt als ein
Schauender.
 Seit der Hosenrock-Episode schnitt er Dallmeyer. Schämte sich zu
sehr für ihn. Saß denn bei so einem kastenlosen, durch ewige
Bastardierung Entzüchteten keine einzige Hemmung, keine einzige
Qualität mehr generationenfest? Hatte man so einen Mischkerl allein,
war er meist ganz leicht besserem Niveau zugänglich, schon seiner
affenartigen Charakterlosigkeit wegen, mimte unter der Hypnose
eines Vornehmeren Verständnis ohne Heuchelei, um sich dann, bei
der ersten Probe, fiel Einzelverantwortung weg, der Masse: „dem
Vieh ohne Großhirn“ gleich zu benehmen. Das erklärte dieser
furchtbaren Vibrionen der Verpöbelung Virulenz und leichte
Übertragbarkeit auf scheinbar Immune. Immer waren eben hier die
wichtigsten Dinge einem schauerlichen Zufall, einem schamlosen
Ungefähr ausgeliefert. Heiratete man etwa eine Frau, die einem
gefiel, wünschte sich gleiche Kinder, krochen vielleicht Wechselbälge
aus ihr, nicht von Hexen in der Wiege, von üblen Tanten im
Mutterleib vertauscht, weil der Typus nicht feststand, die Frau selbst
nur ein freundlicher Zufall war, aus einem qui pro quo gemischter
Akzidenz zusammengewürfelt.
Natürlich hatten sie wieder aus ihrer torkelnden Planlosigkeit eine
wissenschaftliche Theorie gemacht. Samossy versuchte ihm einmal
so einen Humbug mit dem Ahnenverlust einzureden: da das
Individuum die Summe aller Eigenschaften und Erfahrungen seiner
sämtlichen Vorfahren sei, bedeute jede Inzucht: jeder Vater und
Mutter gemeinsame Ahne eine Verminderung des möglichen
Eigenschafts- und Erfahrungskomplexes: Mensch. Je heterogener
daher an Stamm, Rasse, Kaste, Blut, Heimat, die Vorfahren, desto
reicher die Nachkommen.
Da hatte er nicht mehr an sich zu halten vermocht:
„Mein Gott, was für ein Verköterungsschwindel! Auf Stoßkraft und
Richtkraft der Erbmassen kommt es doch an, auf Qualität und
Intensität, nicht auf einen möglichst hohen Kehrichthaufen von
Anlagen und Erfahrungen, die, wenn nicht gleichgerichtet wie
Eisenfeilspäne im magnetischen Feld, einander hemmen, schwächen,
aufheben, und das Endglied ist dann schließlich nichts als eine ganz
volle Null. Bei euren Pferden und Hunden wißt ihr doch recht gut,
worauf es ankommt, wollt ihr hohe Geldpreise gewinnen aus
gezüchteter Form und Leistung. Höchstens, daß fremdes Blut bei
gleicher Kaste möglicherweise vielseitige und doch gleichgerichtete
Erbmassen ergibt.“
Samossy hatte langsam das hilflos verschrobene Schülergesicht
bekommen, wieherte dann wie erwachend manisch in der Fistel:
„Vorfahren, was Vorfahren! Der einzig vernünftige Fundort der
Spezies Mensch ist doch die Drehlade. In einem Findelhaus
aufwachsen!“ Dann schadenfroh geduckt sein Unvermitteltes:
„Man muß vom Weibe loskommen.“
Horus gedachte Lizzi Beermanns, der Raeburn girls, Margots; ihrer
weihelos beschnupperten und doch versperrten Körper, jahrelang
saumseligen Reflektanten von trägen Müttern hingeködert:
„Eltern haben ist ja höchstwahrscheinlich ein Unglück,“ bemerkte
er, „keine haben aber ganz bestimmt eins. Auch soll ja das Heim eine
Art Placenta für das geborene Kind bedeuten.“
Sagte es eigentlich vorbei an dem hohen Vierziger da, dem
Kinderlosen; dieser Frage Brennen wohl zwiefach Fernen. Hatte er
überhaupt Anverwandte? Wer stand ihm nahe? Wer war ihm
Freund? Fachfeinde überall. Blieb das Weibstück mit dem
Kettenarmband sein einzig menschlicher Verkehr? Vor Gargis
Erscheinung wurde er linkisch, voll gereizten Unbehagens. Wußte
mit ihr so wenig anzufangen wie ein Mandrill mit einer Kamee. Da
frug Krause eines Tages aus kondolenzbeflissenen Mundwinkeln:
„Wie geht es Ihrem Vater?“
Samossy machte eine frivol hoffnungslose Geste:
„Von Tag zu Tag besser.“
Krause, mit verkniffenem Zwicker, bekundete Freude. Man habe
Fälle gesehen, wo Wassersucht jahrelang fast stationär geblieben ...
Das Geschäftsjubiläum würde also doch in der elterlichen Villa
gefeiert. Und Horus erfuhr, daß dieser Vater Gründer einer seit
fünfzig Jahren bestehenden Kattunfabrik und offenbar sehr
wohlhabend war. Er gedachte jenes Armschwunges zwischen Abort-
und Küchengeruch: „wohlbestallter Professor? Das ist der Stall, den
ich mir leisten kann.“
Nun kam polternd und verlegen auch an ihn die Einladung zu
dieser Feier im Vaterhaus.
 „Man hat dort schon so viel von Ihnen gehört“ — dann halb
entschuldigend: „nicht durch mich.“
Er lauerte, schülerhaft geniert, gelangweilt und wieder ängstlich
um ein Ja. Schlug, als er es hatte, sein zerfahrenes Gewieher an und
empfahl sich.
Der Mann war unberechenbar. Doch machte das den Verkehr nur
ermüdender, nicht reicher, ließ nie schöpferische Kontinuität der
Stimmung sich entwickeln, es sei denn in seinem engsten Fach.

Man stand leer herum in der großen Backsteinvilla. Wartete auf das
Jubiläumsessen.
Manchmal beklopfte ein zugereister Geschäftsfreund, geneigten
Ohres, mit dem Zeigefingerknöchel prüfend den bronzenen
„Lauscher“ in der Ecke auf Metallstärke hin, oder versuchte
Signaturen unter Ölbildern zu entziffern. Niemand saß.
Unverrückbare Fauteuilarrangements hinter Tischen waren von
vornherein dagegen, nur zwei Rollstühle an den Salonenden, um die
wechselnde Gruppen sich stauten, schienen besetzt.
In dem einen ragte ein riesiger Greis aus Stein und Wasser.
Die Beine zu Blöcken geschwollen, trugen flach auf den Knien
violette Hände, schwer wie Porphyr. Bis an die Hüften war er zu
einem mit Wasser gefüllten Sarkophag geschlossen. Darüber
kämpfte das harte alte Bauernherz zäh um jeden Zentimeter Leben,
gegen das innere Ertrinken an. Ganz oben, aus blutigem Blauauge
troff schon immer ein wenig Feuchtigkeit über, sickerte die fahlen
Wangenfalten herab. Er biß in seinen weißen Bart vor barbarischem
Starrsinn: da sein, nur da sein. Fuhr manchmal aus den
schauerlichen Vorgängen in sich auf, zu wahnwitziger Eitelkeit über
die eigne Zähe. Sah allen der Reihe nach in die Augen, trotzig,
lauernd, wie ein erliegender Gladiator, im Gefühl drohend gesenkter
Daumen ringsum.
War er vor Lebenswut hellhörig geworden an den schweren
Birnenohren?
 Seine blutigen Blauaugen drohten leuchtend hinüber zu dem
andern Rollstuhl am Ende des Saales.
„Oh, er ist schon kalt bis zu den Knien,“ schmunzelte die greise
Frau mit ruhiger Genugtuung Horus Elcho zu.
Ein goldnes Kettenarmband klirrte erledigend an der ganz
verkrümmten Hand. Der restliche Körper hing: ein gerunzelter Strick,
an den Enden mit Gicht verknotet, im Sessel. Hinter ihr stand ein
erloschener Mensch mit geduckten Augen: der zweite Sohn und
nunmehr Inhaber der Fabrik. Ihm schien auch die zerpatschte Frau
daneben mit den drei kleinen Kindern anzugehören. Das älteste,
einen schweren Bleichkopf im Phantasie-Matrosenkostüm aus Satin,
hielt sie zwischen den Schenkeln aufgepflanzt, memorierte angstvoll
etwas Gereimtes mit ihm und es zupfte an seinen Nagelwurzeln.
Jetzt hatte es zu tief geschält, heimlich wischte der blutende Finger
über den weißen Seidenslips.
Nun trollte sich Oskar Samossy, fast ebenso verdonnert wie das
satinene Kind, hinter den Greis aus Stein und Wasser. Und beide
Brüder schoben die elterlichen Rollstühle an die Têten der
Speisezimmertafel.
Drei Menus wurden gereicht — nacheinander. Das erste wie es der
Gründer der Fabrik anfangs gehabt: dicke Suppe, Erbswurst, Käse.
Dazu Bier. Beim zweiten, dem 25jährigen Bestand entsprechend,
erschien schon Fisch, Kalbsbraten mit Salat und eine süße Speise.
Dazu leichter Mosel. Das dritte endlich zeigte voll und ganz, was
man sich der heutigen Bilanz entsprechend leisten konnte, durfte
und sollte. Begann mit Austern und wollte schier kein Ende nehmen
an primeurs und durablen Weinen. Vom sechsten Gang mit
Champagner aufwärts, stand immer jemand auf, der nicht stehen
konnte, und sprach, ohne sprechen zu können: etwas, das man sich
wohl würdig, witzig oder feierlich zu denken hatte. Manchmal wurde
dazwischen „hoch“ geschrien, manchmal nur am Ende. Männer
erhoben sich dabei halb. Frauen saßen ganz da; schienen einzig und
ausschließlich zum Sitzvorgang geschaffen. Die Schwüle stieg. Eine
Dame lüftete ihr Kollier.
„Perlen machen so heiß, besonders echte.“
Eben schloß ein Stehender:
 „Nichts lobenswerter am Manne als recht reinliche Triebfedern.“
Über die Enden des Beifalls weg schnatterte es aus einer
arroganten kleinen Person laut in ihren Tischherrn hinein:
„Und denn is mal so’n schmieriger kleiner Jude gekommen und
hat gefragt, ob ich ihn heiraten will. Waschen Sie sich erst, hab’ ich
ihm gesagt. Na, sehen Sie, dort sitzt er — das ist mein Mann.“
Der riesige Greis aus Stein und Wasser war unterdessen wieder
ganz in die schauerlichen Vorgänge seines Inneren versunken, wies
mit Grauen alles Getränk weit ab, würgte nur ein wenig Kaviar auf
Zwieback hinunter, lauerte ihm schweigend nach. Langsam stieg
Triumph in den blutigen Blaublick. Dann aber trieb die aufdrängende
Flüssigkeitssäule das Kaviarbrötchen aus dem erstorbenen Magen in
den Schlund zurück. Triumph im Aug oben zerfiel. Der Hausarzt
näherte sich rasch — eben jener Mann, den die arrogante junge
Person zu ihrem Gatten reduziert — öffnete ihm rasch das
Frackhemd, bohrte eine Spritze mit irgend etwas: Kampfer oder
Theobromin dem Aufstöhnenden unter die lederzähe Haut. Dunst,
Schnaps und Schwatz hatten den Vorgang nahezu vernebelt.
Eben stand Dallmeyer da, spann aus seinem Bart heraus einen
Phrasenstrang über das dreifache Festessen hin: wie der verehrte
Gastgeber hier, erfolgreicher Mann der Arbeit, Leuchte modernen
Handelsgeistes, unentwegt die Fahne des Idealismus hochgehalten,
und wiewohl selbst geistig und körperlich noch ungebrochen — als
zärtlichster Vater dem einen Sohn den Fruchtgenuß seiner
Lebensarbeit überlassen: dem Nachfolger solcherart in selbstloser
Weise ein frei fröhliches Schaffen aus dem Vollen gönnend, seinen
Erstgeborenen hinwiederum auf das Großzügigste der hehren
Forschung geweiht habe, gleichsam mit dem Öl seiner Bilanzen das
reine Licht der Wissenschaft speisend. Und Dallmeyer schloß mit
einem „Hoch“ auf seinen genialen Kollegen und der Hoffnung, daß
dessen epochaler Bedeutung — in engstem Kreise längst neidlos
anerkannt — endlich auch offiziell die verdiente Sanktion durch ein
Ordinariat und Aufnahme in die geweihten Hallen der Akademie
zuteil werden möge.
Samossy sah ihn an und er verschluckte sich.
 Der greise Riese war unterdessen an der Injektion aufgelebt, stieg
aus seinen Gebresten wieder empor, diesmal in eine Art
erzieherischen Tropenkollers. Schüttelte herrisch das Haupt bei der
Wendung vom „Fruchtgenuß“ und „Gönnen aus dem Vollen“:
„Sind froh, wenn sie trocken Brot haben.“
Er sah gerührt über die eigne Härte auf die Familie seines
Nachfolgers, wie feindliche Erwachsene auf ein gedemütigtes Kind
blicken. Und dann hub dieser Memnonsblock auf einmal an in
greisenhafter Geschwätzigkeit zu tönen:
„Ja, der Idealismus“ — er konnte nur gradaus sprechen, doch galt
es wohl Horus Elcho, dem exotischen Ehrengast an seiner Seite —
„und dann immer möglichst billig kaufen und teuer verkaufen, das
habe er den Jungens von früh gepredigt. Aber der Idealismus, der
sei ihnen direkt eingebläut worden, fast von der Wiege an. Schon im
vierten Jahr habe der Oskar die längsten Schillerschen Gedichte
auswendig heruntersagen müssen, wo es besonders edel zuging: die
Bürgschaft, den Drachenkampf, den Taucher. Ein einziges
Steckenbleiben und er habe ihn jämmerlich durchgehauen.
„Das Lied an die Freude, das konnte er sich lang halt gar nicht
merken.“ Der Greis lebte in Erinnerungen auf.
„Da durfte er schon gar keine Hosen mehr dabei anhaben, drei
spanische Rohre sind für dieses einzige Gedicht draufgegangen. Mit
fünf Jahren konnte er dann auch schon die ganze Glocke. Eine
vorzügliche Schulung fürs Gedächtnis nebenbei, weil ja der Oskar ein
berühmter Gelehrter werden sollte, so habe er es schon bei der
Geburt bestimmt. Leider sei ja nur Mathematik draus geworden,
darauf gebe er nicht viel, das entziehe sich seiner Kontrolle. Chemie,
große Erfindungen wären besser gewesen. Philologie und so, das
habe er von vornherein verboten.“ Der Greis hielt nichts von
klassischer Bildung:
„Siebzig-Einundsiebzig war doch viel blutiger,“ sagte er mit Tränen
des Stolzes im Aug.
„Wozu Griechen und Römer, wozu immer noch diese Lappalien bei
Homer lesen, das kann man ja gar nicht vergleichen mit unsern
modernen Schlachten.“
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