Emotions - Robert Kohn and Martin B. Keller

Emotions
Robert Kohn and Martin B. Keller
Contents
Behavioral, Neurological, and Cognitive Components of Emotion ................. 2
Assessment of Mood and Affect in the Clinical Interview ........................... 10
Emotional Expression of Personality Disorders ...................................... 12
Emotional Expression of Anxiety ...................................................... 14
Spectrum of Anxiety ...................................................................... 14
Etiology of Anxiety ....................................................................... 14
Clinical Presentation of Anxiety .......................................................... 16
Emotional Expression of Depression .................................................. 20
Spectrum of Depression .................................................................. 20
Etiology of Depression ................................................................... 20
Clinical Presentation of Depression ...................................................... 23
Emotional Expression of Euphoria .................................................... 25
Emotional Expression of Fear .......................................................... 25
Emotional Expression of Apathy ....................................................... 26
Emotional Expression of Hostility, Anger, and Rage ................................. 28
This chapter is an update from the fourth edition. Previous
edition authors were Robert Kohn and Martin B. Keller
R. Kohn (*)
Department of Psychiatry and Human Behavior, The
Warren Alpert Medical School of Brown University,
Providence, RI, USA
Miriam Hospital, Brown University, Providence, RI, USA
e-mail: Robert_Kohn@brown.edu
M. B. Keller
Warren Alpert Medical School of Brown University,
Providence, RI, USA
e-mail: Martin_Keller@brown.edu
© Springer Nature Switzerland AG 2023
A. Tasman et al. (eds.), Tasman’s Psychiatry,
https://doi.org/10.1007/978-3-030-42825-9_111-1
1

Disturbances of Affect Incongruent with Mood ...................................... 28
The Emotional Experience of Empathy ............................................... 29
Conclusion ............................................................................... 29
References ................................................................................ 29
Abstract
Emotions are subjective feelings related to
mood and affect. Emotions are biologically
basic, present at birth, and universally experi-
enced, but can be shaped by culture and learn-
ing. A competing theory suggests that
emotions emerge when people make meaning
out of sensory input and from their environ-
ment using knowledge and prior experience.
Neuronal models have been implicated in the
automatic and voluntary components of emo-
tion regulation. Emotion regulation refers to
the strength of an emotion being amplified,
attenuated, or maintained. Affect is the observ-
able behavior seen in the expression of emo-
tion. Mood is frequently the reported
emotional state. Mood is evaluated through
the clinical interview though inquiry and
observation. Emotions are a defining charac-
teristic of most psychiatric disorders, in partic-
ular anxiety, depression, euphoria, fear, apathy,
and anger.
Keywords
Emotion · Affect · Mood · Anxiety ·
Depression · Fear · Euphoria · Emotion
regulation · Learning theory · Appraisal theory
Behavioral, Neurological,
and Cognitive Components of Emotion
Emotion is a subjectively experienced feeling that
is related to affect and mood. The experience of
emotion occurs through a set of expressive behav-
iors, the function of the nervous system, and cog-
nitive perception or appraisal. Appraisal is a
process that detects and assesses the significance
of the environment for well-being (Moors et al.,
2013). Emotion has behavioral, somatic, and psy-
chic components.
Emotions are not a single response but a col-
lection of responses and are always varied and
complex. Emotions are induced by objects or
situations that come from interactions with the
environment, or from within as representations
of internal milieu states. Both internal and exter-
nal perceptual recall can occur outside of con-
sciousness and induce an emotional response.
Emotions are linked to certain inducers and result
in consistent responses suggesting their early
specification in the nervous system (Damasio,
2000).
Charles Darwin’s (1872) work on facial
expression pioneered the role of expressive
behaviors in emotion. Darwin stated that the com-
plex behavioral actions associated with emotions
occur to relieve or gratify sensations or desires and
that the same movements are repeatedly
performed through force of habit. Furthermore,
when the opposite state of mind is induced, there
is an involuntary tendency to perform movements
of the opposite nature. He believed that the behav-
ioral expression of emotion is driven by the ner-
vous system independent of will and, to a large
part, independent of habit.
Basic emotions are critical in early develop-
ment and due to learning and cognition develop
into the more complex emotional states that are
experienced by adults. Basic emotions are consid-
ered primitive in that they originate in the subcor-
tical brain structures. Higher order structures are
involved in emotional processes processing.
The basic patterns of emotional expression are
present at birth and vary little with age and across
cultures. By 3 months of age, infant and adult
facial expressions of certain emotions are similar
(Emde, 1980; Emde et al., 1978). The facial
expressions and emotions of infants differ little
cross-culturally (Bowlby, 1973), although this has
2 R. Kohn and M. B. Keller

been brought into question (Camras et al., 2006;
Scherer et al., 2011). It is this nonverbal expres-
sion of emotion that the infant uses to communi-
cate with the parent and that the parent uses to
determine the needs of the infant. Although emo-
tional expression is considered innate, it can be
modified through learning and maturation (Bar-
low, 1988). Culture in adults may shape the adap-
tiveness of emotional regulation and result in
nonverbal and verbal expression (Ford and
Mauss, 2015; Kawahara et al., 2021).
Emotional regulation is the processes by which
any individual assesses, inhibits, maintains, or
modifies the intensity, frequency, or duration of
emotional reactions in order to have appropriate
social behavior or to achieve goals (Thompson,
1994). Emotional dysregulation is composed of
an inappropriate and excessive emotional reaction
compared to social norms, uncontrolled and rapid
shifts in emotions, and an abnormal allocation of
attention to emotional stimuli (Carmassi et al.,
2022).
Izard (1977) has proposed ten basic fundamen-
tally different expressions of emotion: anger, con-
tempt, disgust, fear, guilt, interest, joy, sadness or
distress, shame, and surprise (Fig. 1). Since, Izard
(2009) further divided emotions into two broad
categories basic emotion episodes and emotion-
cognition interactions or emotion schemas. Basic
emotions include positive (interest, joy) and neg-
ative emotions (sadness, anger, disgust, fear), as
well as shame, guilt, and contempt. These differ-
ent emotions can be combined with one another to
produce distinct behavioral reactions within and
between individuals (Barlow, 1988). The basic
emotions are differentiated not only by behavioral
expression but also at the psychophysiological
and neurobiological levels. The expressive behav-
ioral tradition for the study of emotion assumes
that it is the expressive behavior that results in the
experience of affect through autonomic or central
nervous system activation and that facial expres-
sion is the primary component of emotion (Bar-
low, 1988). This is referred to as a locationist
account of emotion. These emotions are biologi-
cally basic, and universally experienced, but can
be shaped by culture and learning.
Emotional schemas refer to emotions
interacting with the cognitive processes to influ-
ence mind and behavior. Emotional schemas are
elicited by appraisal, images, memories, and
thoughts and neurocognitive processes such as
changes in neurotransmitters and hormone levels
(Izard, 1993). Reoccurring emotional schemas
may stabilize as emotion traits or as components
of personality traits. Through learning basic emo-
tions can transition to emotion schemas. They
constitute the primary motivational system for
human behavior. Others have argued that emo-
tions do not necessarily lead to behavior directly,
and when it does it is often irrational and self-
defeating (Baumeister et al., 2007).
A related theory, known as the James–Lange
theory (James, 1890), proposes that body changes
that differ between the basic emotions are a
response to a predisposing event, but the sensa-
tions of these body changes, and not the event,
leads to the expression of the emotion. The view
that emotional expression is hardwired is incom-
plete because the behavioral, experiential, and
somatic or physiological components of emotion
are often not correlated (Barlow, 1988). This is a
constructionist model that emotions emerge when
people make meaning out of sensory input and
from their environment using knowledge and
prior experience (Lindquist et al., 2012) or the
conceptual act theory (Barrett, 2006). Unlike the
locationist approach, which would suggest that
emotions correspond to specific brain regions,
the constructionist approach argues for the exis-
tence of general brain networks that may result in
discrete emotions.
The role of the nervous system in the study of
emotion was initiated in experiments where Wal-
ter Cannon (1929) surgically removed areas of
animal brains. These studies of emotion as pri-
marily a function of the brain suggested that the
areas of the brain associated with emotion are
phylogenetically more ancient and primitive.
Pathological emotions involve the deep brain
structures more than the cerebral cortex. Emo-
tional activation may occur without the activation
of higher cognitive processes and perhaps through
connections with the retina (Moore, 1973; Zajonc,
1984). The deep brain structures that may mediate
Emotions 3

emotions include the limbic system (including the
hypothalamus, septum, hippocampus, amygdala,
and cingulum), as well as other bodies (such as the
thalamus, locus coeruleus, median raphe nuclei,
and dentate nuclei of the cerebellum) and the
connections between them. Papez (1937) origi-
nally posited this general neuroanatomical path-
way for emotion. MacLean (1949), who
introduced the concept of the limbic system, pro-
posed that there was an integration with bodily
sensations from the outside world. Research
attempting to locate brain structures associated
with specific emotions has been conducted in
humans through insertion of electrodes that stim-
ulated or coagulated different parts of the cortex
and the deep brain (Delgado, 1972; Smirnov,
1966). The subjective emotions elicited in these
studies were accompanied by motor and auto-
nomic changes only in the deep brain structures.
Site-specific emotional expression has not been
demonstrated; the emotion expressed varies
under somewhat different conditions, and differ-
ent structures may produce similar emotional
responses (Izard, 1977; Mukamel & Fried, 2012;
Panksepp, 1982; Plutchik, 1980).
The neocortex and the cortex also have a role in
emotion. Orbitomedial frontal leucotomy, for
example, reduces anxiety (Marks et al., 1966;
Tan et al., 1977). Some investigators have dem-
onstrated laterality of cortical involvement,
although the evidence is conflicting (Leventhal
& Tomarken, 1986). The right side of the cortex
is more involved in unpleasant emotions and the
left in pleasurable emotions (Fox & Davidson,
1986; Mayes, 1979). Perception and expression
of emotion may be a right hemisphere function.
Right hemisphere damage impairs the ability to
express emotions through inflection of the tone of
voice (Ross & Mesulam, 1979). The roles of right
and left hemispheres can be grouped into four
categories of theories (Kolb & Taylor, 2000).
The right hemisphere is dominant over the left
with respect to various aspects of emotions
(Gainotti, 1988; Ley & Bryden, 1982); the two
hemispheres have complementary specialization
for control of mood (Sackeim et al., 1982), such as
the left hemisphere being dominant for positive
emotions and the right for negative emotions;
right hemisphere is dominant for emotional
expression parallel to the left’s dominance for
language (Ross, 1984); and the right hemisphere
is dominant for the perception of emotion-related
cues including facial expression, body posture,
Fig. 1 Izard’s basic emotions. (Guilt not illustrated; with permission from Carroll E. Izard )

and prosody (Adolphs et al., 1996; Rapcsak et al.,
1989).
The frontal lobe is involved in the process of
interpreting the emotions of others, in particular
those from facial expressions. The temporal lobe,
in particular the amygdala, has a role in altering
the response to emotional stimuli, such as fear
(Feinstein et al., 2011). The amygdala is involved
in processing facial expression (Dalgleish et al.,
2009). The recall of past experiences requires an
intact temporal lobe memory system (Squire et al.,
1993). When the hippocampus and related corti-
cal areas are damaged, conscious memories can-
not be formed; however, learning not involving
conscious memories remains intact, such as
unconscious emotional memories formed in the
amygdala. Intense stress may alter the function of
the hippocampus even in adults with a normal
hippocampus (Diamond & Rose, 1994), resulting
in failure to form conscious memories of a trauma,
while at the same time forming unconscious emo-
tional memories (LeDoux & Muller, 1997). The
anterior cingulate cortex is associated with moni-
toring of errors and detecting completeness or
responses, as well as reappraisal of negative emo-
tional stimuli (Carter et al., 1998; Gerhring &
Knight, 2000). It is one of the points of integration
of visceral, attentional, and emotional informa-
tion. The anterior cingulate cortex is involved
with regulation of mood. The insula is involved
in a number of emotional experiences including
recognition and experience of disgust and empa-
thy (Papagno et al., 2016).
The prefrontal cortex is involved with regula-
tion of emotions, as demonstrated by the famous
case of Phineas Gage (Harlow, 1868), who
became impulsive, restless, and disrespectful
after damage to the anterior part of his frontal
lobe by a railroad iron bar exiting through his
forehead from an explosion. The prefrontal cortex
is divided into six regions: dorsal lateral, ventro-
lateral (inferior frontal cortex), anterior prefrontal
cortex (frontopolar), orbital frontal cortex, ventro-
medial, and dorsomedial. Activation in the
orbitofrontal and ventrolateral cortex is associated
with suppressing and reappraising negative emo-
tional stimuli. Increased prefrontal cortex activity
is believed to decrease amygdala activity, a key
brain region related to extinction – the weakening
of a response to a stimulus, during regulation of
emotions (Quirk & Beer, 2006). The ventromedial
prefrontal cortex integrates cognitive affective
information and regulates the hypothalamic pitu-
itary adrenal axis in response to emotional stress
(Radley et al., 2006). The regulation of fear after
extinction has been found to involve the
hippocampal–prefrontal cortex (Kalisch et al.,
2006). The role of the prefrontal cortex in extinc-
tion has broad clinical implication. Some emo-
tional disorders are characterized by a resistance
to extinction of learned emotional anxiogenic
stimuli and an avoidance of situations with the
potential to induce extinction (Sotres-Bayon
et al., 2006). Table 1 provides a summary of
damage to speciﬁc areas of the brain associated
with emotional regulatory deﬁcits (Beer, 2007).
Phillips et al. (2008) proposed a neuronal
model implicated in the automatic and voluntary
components of emotion regulation. Emotion reg-
ulation refers to the heterogeneous set of pro-
cesses by which emotions themselves are
regulated (Gross, 2014). Voluntary behavioral
control involves the inhibition of ongoing
emotive-expressive behavior. Automatic atten-
tional control involves the automatic ability to
overcome interference from emotional distracters
that may unconsciously divert attention from cog-
nitive task performance (Rive et al., 2013).
According to Phillips et al. (2008) there may be
two systems at work in the prefrontal cortex in
emotion regulation. One is a lateral prefrontal
cortical system (dorsolateral prefrontal cortex,
ventrolateral prefrontal cortex) that is neocortical
in origin involved in voluntary subprocess oper-
ating on a feedback mechanism. The second is a
medial prefrontal cortex system (orbitofrontal cor-
tex subgenual anterior cingulate gyrus, rostral
anterior cingulate gyrus, dorsomedial prefrontal
cortex) that is paleocortical in origin that sub-
verses automatic subprocess. This medial prefron-
tal cortex uses feed-forward inputs from
orbitalfrontal cortex to monitor internal states
and select appropriate behaviors during automatic
cognitive change paradigms. Both neural systems
involved in voluntary and automatic control of
emotions may operate simultaneously in emotion
Emotions 5

regulation and behavior that are initially generated
by the emotion perceptual process of the amyg-
dala, ventral striatum, and thalamus. Figure 2
illustrates a neuronal model of emotional pro-
cessing and regulation (Phan & Sripada, 2013;
Wessa & Linke, 2009) focused on successive
and recurrent mechanisms. A special class of
motor neurons, mirror neurons, found in the pos-
terior superior sulcus, inferior parietal lobule, pre-
motor cortex, and the inferior frontal gyrus are
believed to be involved with emotion recognition
(Lamm & Majdandzic, 2015).
Neurotransmitters and their presynaptic and
postsynaptic receptors seem to mediate emotion
within the central nervous system. The possible
role of norepinephrine in depression has been
suggested by the catecholamine deficiency
hypothesis. Many antidepressant drugs increase
synaptic concentrations of norepinephrine,
whereas reserpine, a catecholamine-depleting
drug, causes depressive symptoms (Bunney &
Davis, 1965; Schildkraut, 1965). The indolamine
hypothesis postulates that depression results from
deficits in serotonin. The gamma-aminobutyric
acid, noradrenergic, glumatergic, and serotoniner-
gic systems have all been shown to mediate forms
of anxiety. Monoamines have been hypothesized
to be associated with both basic emotions and
facial expression (Lövheim, 2012).
A third approach to the study of emotion has
been based on the cognitive characterization of
emotion. Two competing cognitive explanations
have been posited: the appraisal theory and Lang’s
bioinformational approach. The appraisal theory
(Schacter & Singer, 1962) suggests that emotion
is a result of the individual’s appraising the con-
text of a situation, attributing a causal relationship
after the perception of a generalized,
undifferentiated arousal state. There is little evi-
dence to support this theory in its entirety as
emotion can occur in the absence of arousal (Bar-
low, 1988). Emotion has also been viewed by
Table 1 Areas of anatomical damage associated with impairment in regulation of emotion
Impaired response to social rewards Temporal lobe, OFC, DIPFC
Inappropriate filtering of emotional stimuli OFC
Inability to appreciate positive emotion OFC
Poor reversal learning OFC
Inability to achieve goals DIPFC, OFC
Decreased response to anticipated startle OFC
Abnormal sexual behaviors Temporal lobe, amygdala, OFC
Poor control of age, violence, explosive temper, aggression, hostility,
anger, irritability, irreverence, lability
Temporal lobe, amygdala, caudate, ACC,
OFC
Increased anxiety OFC, PFC
Increased pride OFC
Increased impulsiveness VMPFC
Altered subjective emotional experience OFC, ACC
Increased placidity, passivity, apathy Temporal lobe, amygdala, caudate, ACC,
OFC, lateral PFC
Increased depression, less happy OFC and DIPFC
Blunted affect Temporal lobe, OFC, DIPFC
Reduced anger, fear Temporal lobe, amygdala, thalamus,
ACC, OFC
Inability to demonstrate embarrassment OFC
Impaired reflexive smiling Corticomotor strip, corticobulbar
connections
Exaggerated crying, laughing OFC, lateral PFC, caudate, temporal lobe
Impaired posed facial expressions Extrapyramidal system (basal ganglia)
ACC anterior cingulate cortex, DIPFC dorsolateral prefrontal cortex, OFC orbitofrontal cortex, PFC prefrontal cortex,
VMPFC ventromedial prefrontal cortex
Source: Based on data obtained from Beer (2007)

alternative appraisal theories as an adaptive
behavior, which follows changes in the environ-
ment that are evaluated in terms of their potential
impact on the individual (Lazarus et al., 1970;
Lazarus, 1968). The appraisal model suggests
that an evaluation or appraisal of the environment
is connected to the initial stimulus preceding and
modifying the emotion. For subsequent stimuli, a
reappraisal of the earlier situation may ensue. The
emotional response is case-based on associative
reasoning and provides a preparedness function
(Ortony et al., 1988). Appraisal theory has diffi-
culty explaining irrational emotions (Barlow,
1988) unless information is appraised and pro-
cessed by use of an unconscious process (Mac-
Leod et al., 1986). A modification of this theory is
the modal model of emotion that has three
elements: first, emotions arise when an individual
attends to a situation and sees it relevant to their
goals; second, emotions result in changes in sub-
jective experience, behavior, and central and
peripheral physiology; and third, a response that
may be modulated. Five families of processes
regulate emotions: situation selection, situation
modification, attentional deployment, cognitive
change, and response modification (Gross, 2014)
(see Fig. 3).
An alternative cognitive explanation of emo-
tion is the bioinformational approach (Lang,
1985). Emotion involves processing and
accessing information stored in memory. Informa-
tion on both the stimulus and the response is
stored in memory. This information is then
interpreted on the basis of the significance of the
Emotional
Stimulus
Amygdala
Ventral visual
corex
Pre-attentive
Parietal cortex
frontal eye
fields
Thalamus
Attention
Deployment
Visual
processing
areas
Amygdala
Situation
Perception
Amygdala
Insula
Ventral
striatum
OFC
vmPFC
Transient and
Automatic
emotional
response
Amygdala
Insula
OFC
vmPFC
Subgenual CC
Facial
expression
Experience and
expression of
emotion
Emotional
Response
Cognitive
Physiological
Motivational
responses
Broken arrows are enhancing or suppressive effects; Solid
arrows indicate different emotion regulation strategies at
different time points during emotional processing; OFC
orbitofrontal cortex; mPFC medial prefrontal cortex;
vmPFC ventromedial prefrontal cortex; vlPFC ventrolateral
prefrontal cortex; dIPFC dorsolateral prefrontal cortex;
dACC dorsal anterior cingulate cortex; CC cingulate cortex
High level
appraisal
Emotion
regulation
Behavior
Early Emotional Processing
ACC vlPFC OFC
Inhibition of irrelevant emotional
information
ACC dlPFC vlPFC mPFC OFC
Reappraisal of stimulus meaning
dACC DIPFC OFC
Suppression of
activated emotion
Fig. 2 Mechanisms in emotional processing and regulation
Emotions 7

event, allowing expression of the appropriate
emotion in intensity consistent with the stimulus.
Research into emotional states based on factor-
analytical approaches has resulted in various
models to characterize the range of emotional
expression. Factor analysis of dimensions of affect
and personality has given rise to dimensional
models, which are considered theoretical models
to describe not only emotion but also personality.
Dimensional models usually attempt to describe
emotions in only two or three bidirectional dimen-
sions, such as Eysenck (1967) two-factor model.
One axis is called introversion–extroversion, and
the other neuroticism–stability. In Eysenck’s bio-
logical theory, emotions are associated with an
individual’s level of arousal that is set either too
high or too low by the reticular-activating system.
Extroverts seek out greater stimulation because of
low levels of arousal, whereas introverts, who have
high levels of arousal, need less stimulation. Neu-
roticism is theorized to involve the autonomic ner-
vous system; neurotic individuals have increased
reactivity in the autonomic nervous system. Emo-
tion results from the interaction of these two axes
and the limbic system.
An alternative approach is the circumplex
model, in which emotions are placed in a circular
order reflecting their relationship to other emo-
tions. The opposite emotion is on the other side
of the circle. Tellegen (1985) created a circumplex
model that is divided into eight sections: strong
engagement, high negative affect, unpleasantness,
low positive affect, disengagement, low negative
affect, pleasantness, and high positive affect
(Fig. 4). This model can be used to capture the
distinction between an anxious, depressed, or
manic mood and affect, as well as to demonstrate
that these moods are a continuum. An anxious
mood is considered to be a high negative affect,
with descriptors such as distressed, fearful, hos-
tile, jittery, nervous, and scornful. A depressed
mood in the circumplex model would be a low
positive affect, including descriptors such as
being drowsy, dull, sleepy, and sluggish. A
manic affect would be captured by terms in the
high positive affect dimension: active, elated,
enthusiastic, excited, peppy, and strong. Revised
versions of the circumplex model have been con-
tinuously proposed (Yik et al., 2011).
The strength of an emotion may be amplified,
attenuated, or maintained, emotion regulation
(Thompson, 1994), or affective style (Davidson,
1998). Through this process the individual can be
distracted from aversive stimuli and generate
imagery to replace unwanted emotions
(Derryberry & Reed, 1996), making it difficult to
interpret where emotions end and regulation
begins. Emotion regulation has been character-
ized into five distinct processes (Table 2)
(DeStano et al., 2013). Emotional functioning or
Situation
Selection
Situation
Modification
SITUATION
Attentional
Deployment
ATTENTION
Cognitive
Change
APPRAISAL
Response
Modulation
RESPONSE
Fig. 3 Modal model using a feedback loop highlighting five families of emotion regulation strategies. (Reproduced from
Gross (2014, p. 7) with permission of Guilford Press)

emotional competence refers to a broad range of
processes related to inferring emotional states,
understanding causes and consequences of emo-
tions, modulating, appraising, and expressing
emotion. This allows the ability to guide decisions
amid behaviors. Five domains of emotional func-
tioning have been identified: (1) expression –
facial, bodily and vocal behaviors; (2) perception
– ability to infer emotional expression of others;
(3) knowledge – beliefs about how emotions
work; (4) reactivity – response to stimuli,
appraisal of emotional triggers, or emotional sen-
sitivity, emotion intensity, and emotional persis-
tence or the time to return to baseline; and
(5) regulation – internal and external processes
involved in initiating, maintaining, and modulat-
ing the occurrence emotional expression and
Fig. 4 The two-factor structure of self-rated mood. (Reproduced from Tellegen (1985) with permission from Taylor &
Francis)
Table 2 Categories of emotion regulation
Situation
selection
Taking actions that may lead to a
situation where emotions we would
like to have occur or emotions we
would like not to have
Situation
modification
Modifying the environment to alter
the emotional response to that
environment
Attentional
deployment
Influencing emotional response by
redirecting attention within a given
situation
Cognitive
change
Changing one or more of the
appraisals that give rise to different
emotions
Response
modulation
Influencing physiological,
experiential or behavioral responses
directly to a generated emotional
response
Emotions 9

regulation either consciously or automatic
(Milojevich et al., 2021) (Fig. 5).
Assessment of Mood and Affect
in the Clinical Interview
Two terms are often used to refer to an individ-
ual’s emotion: affect and mood (Table 3). In the
absence of a psychopathological process, affect
fluctuates with time and context and ranges from
sadness to anger to elation, depending on the
emotional state. Affect can be expressed through
autonomic responses, body movements, and alter-
ations in speech to concrete or abstract stimuli.
Observing a violent act exemplifies a concrete
stimulus that could lead to the expression of fear;
hearing the abstract term love could result in the
expression of an elated affect. Speech changes
that reflect affect include tone of voice, vocaliza-
tion, and word selection. Visible autonomic
changes that may reflect changes in affect include
sweating, trembling, blushing, and becoming
flush. Changes in posture, alterations in facial
expression, reactive responses, and grooming
movements are body changes seen in expression
of affect. Reactive movements include move-
ments of the body and face made in response to
a novel stimulus, such as in a startle response,
when an individual jumps or turns and looks at
the stimulus. Changes in facial movements of the
mouth, nose, and eyes are found with different
affective states. Manipulation of one’s appearance
is common in states of discomfort; individuals
may fix their hair, clean their nails, scratch, or
straighten their clothes.
Affect has three functions: self-perception,
communication, and motivation (Othmer &
Othmer, 1994). Self-perception is the emotional
value judgment, or the affective response associ-
ated with affect. This function of affect tells one
whether an experience is good or bad. A smile or
an accelerated heart rate is an example of self-
perception. The expression of affect communi-
cates to others our emotional response to events,
interactions, behavior, and situations. Affect pre-
cedes a behavioral response or motivates it. For
Fig. 5 Domains of emotional function (based in part on Milojevich et al., 2021)
Table 3 Affect and mood
Affect The observable behavior seen in the expression
of emotion resulting from sensorial experience
in response to internal or external stimuli
expressed with physiological and motor
responses. Affect responds to changes in
emotional states
Mood A sustained and pervasive emotion. Mood is
frequently the reported emotional state

example, anger is a precursor to aggression. The
valence of the affect or emotion, positivity versus
negativity, depends on whether the condition that
brought the emotion is pleasant or unpleasant;
whether the consequence of the emotion is adap-
tive or maladaptive; or the emotion feels subjec-
tively pleasant or unpleasant (Lazarus, 1991).
Social and cultural norms determine whether
an affect is appropriate or disturbed for a given
situation. Disturbances in affect (Table 4) may be
a pattern of observable behaviors that is the
expression of a subjectively experienced feeling
state or emotion and include blunted, flat, inap-
propriate, labile, and restricted or constricted
affect. An appropriate affect, the normal condi-
tion, is exemplified by people who are able to
express the full range of emotions in a manner
consistent with their thoughts and speech.
Evaluation of affect consists of monitoring
gestures, body movements, and facial expres-
sions. Because adults are frequently capable of
controlling facial expression in attempts to inten-
tionally or unintentionally suppress their affect,
other behavioral gestures may give clues to the
underlying affect. The quality, duration or mobil-
ity, appropriateness, intensity, range, and reactiv-
ity or control over the affect should be considered.
The range of the affect is characterized by the
variety of emotional expressions noted in a clini-
cal session. Normal individuals express different
feelings at different times. Patients who appropri-
ately express many different emotions have a full
or broad range of affect. A restricted range of
affect is seen in individuals who have a limited
emotional expression, whereas a fixed or immo-
bile affect is found in those who display only one
type of emotion. The intensity of affect (the
strength of the emotional expression) normally
varies according to the situation. Those with lim-
ited emotional expression may have a blunted or a
flattened affect. The mobility of affect is the ease
and speed with which one moves from one type of
emotion to another. Changes in the type and inten-
sity of emotional expression normally occur grad-
ually. Reduced mobility in affect is also referred to
as constricted affect. When the affect is extremely
constricted to one emotion, it is called a fixed or
immobile affect. When no affect is displayed, it is
reported to be flat. Pathologically increased
mobility of affect is referred to as labile. The
reactivity is the extent to which the affect changes
in response to an environmental stimulus. When
the patient does not respond to the examiner’s
provocation, such as joking, the affect is non-
reactive (Manschreck & Keller, 1989; Trzepacz
& Baker, 1993) (Table 5).
Mood and affect are related but differ in their
pattern of stability over time. Affect fluctuates,
whereas mood is a more pervasive and sustained
emotional state. Unlike affect, which is observed,
mood is not always readily discernible or
Table 4 Disturbances in affect
Blunted Marked reduction in the intensity of
emotional expression
Fixed Display of only one particular
emotion, and absence of range and
mobility of affect
Flat Absence or near absence of signs of
affective expression
Inappropriate Discordance between affective
expression and the content of speech
or thought content
Labile Abnormal variability in affect with
repeated, rapid, and abrupt shifts in
affective expression
Restricted or
constricted
Mild reduction in the range and
intensity of emotional expression
Table 5 Description of affect
Parameter of Affect Normal Abnormal
Appropriateness Appropriate Inappropriate
Congruent Incongruent
Intensity Normal Blunted
Exaggerated
Flat
Heightened
Overly dramatic
Mobility Mobile Constricted
Fixed
Immobile
Labile
Range Full range Restricted range
Reactivity Reactive Nonreactive
Responsive Nonresponsive
Source: Reproduced from Trzepacz and Baker (1993) with
permission of Oxford University Press
Emotions 11

observed but may need to be reported. An
alexithymic person is unable to verbalize or has
difficulty describing or being aware of emotions
or moods. Mood colors an individual’s perception
of the environment. Mood can be characterized as
dysphoric, elevated, expansive, irritable, or
euthymic (Table 6). Mood is described by its
quality, stability, reactivity, intensity, duration,
and congruence with thought content (Table 7).
A particular mood is not necessarily abnormal or
pathological but must be evaluated in the context
of the patient’s entire history and psychiatric men-
tal status examination.
Emotional Expression of Personality
Disorders
Emotions are not only defining characteristics of
anxiety and depression, but also of personality
disorders. Almost all personality disorders con-
tain at least one specific emotion that is affect
related. There are two primary competing views
on the role of personality and emotions. The pre-
dispositional approach suggests that personality
characteristics are antecedent to the affective
state, such as depression. The complication
approach theorizes that as a result of the affective
state changes in personality are noted. A long-
term longitudinal follow-up study of individuals
with affective disorders showed support for the
complication approach; pessimism and depen-
dency may become permanent features of person-
ality following multiple depressive episodes
(Hirschfeld, 2013).
The general criterion for personality disorder
in the Diagnostic and Statistical Manual of
Mental Disorders, Fifth Edition, Text Revision
(DSM-5-TR) includes affectivity, the range,
intensity, lability, and appropriateness of emo-
tional response (American Psychiatric Associa-
tion, 2022). Table 8 lists the specific criteria that
are affect related for each of the personality disor-
ders. In borderline personality disorder emotional
dysregulation, the inability to change or regulate
emotional cues, experiences, actions, verbal
responses, and nonverbal expression has been
proposed to explain their greater emotional sensi-
tivity, greater emotional reactivity, and slower
return to baseline arousal (Fig. 6) (Linehan, 1993).
The DSM-5-TR includes a proposed alterna-
tive model for personality disorders. In this model
disturbances of self (identity and self-direction)
and interpersonal functioning (empathy and inti-
macy) constitute the core symptoms. Distur-
bances in self-identity include the ability to
regulate a range of emotional experiences (Amer-
ican Psychiatric Association, 2022). Each of the
proposed personality disorders includes a descrip-
tion of the specific emotional characteristics asso-
ciated with identity and empathy.
Table 6 Mood states
Dysphoric Includes sustained emotional states such as
sadness, anxiety, or irritability
Elevated Exaggerated feeling of well-being,
euphoria, or elation
Expansive Lack of restraint in expressing feelings,
frequently with an over-valuation of one’s
significance or importance
Irritable Easily annoyed or angered
Euthymic Mood in the normal range
Table 7 Clinical assessment of mood
Evaluate its quality How do you feel? What is
your mood like?
Evaluate its stability Do you always feel like
this?
Evaluate its reactivity Does your mood ever
change? When does your
mood change?
Evaluate its intensity What is it like to feel this
way? On a scale of 1–10,
how would you rate your
mood?
Evaluate its duration How long have you felt
this way?
Evaluate whether the
mood is congruent with
the thought content

Table 8 Affect-related personality disorder criteria based on DSM-5-TR
Disorder Criteria
Anger/irritability
Paranoid Quick to react angrily to perceived character attacks
Antisocial Irritability and aggressiveness
Borderline Inappropriate, intense anger or difficulty controlling anger
Anxiety
Schizotypal Excessive social anxiety associated with paranoid fears
Paranoid Unwarranted fear
Avoidant Avoids interpersonal contact because of fears of criticism, disapproval, or rejection
Fears of being shamed or ridiculed
Dependent Fears of separation
Fears of being unable to take care for self
Restricted emotionality
Schizoid Restricted range of expression of emotions
Emotional coldness, detachment, or flattened reactivity
Schizotypal Inappropriate or constricted affect
Emotional deficits
Antisocial Lack of remorse
Narcissistic Lack of empathy
Emotion related
Borderline Affective instability due to marked reactivity of mood
Chronic feelings of emptiness
Dependent Uncomfortable and helpless when alone because of fears of being unable to care for self
Histrionic Rapidly shifting and shallow expressions of emotions
Obsessive-compulsive Shows rigidity and stubbornness
Emotion Vulnerability
Emotion Dysregulation
Intense Response
to Emotional
Stimuli
Inability to Regulate
Physiological
Arousal
Slow Return to
Emotional
Baseline
Inability to
Organize Non-
Affective Goals
High Sensitivity to
Emotional Stimuli
Inability to
Disengage
Attention from
Emotional Stimuli
Emotional
Response
Emotional
Stimuli
Distorted
Cognitions
Hypervigelence
Low Distress
Tolerance Suicidal Behavior
Emotionally Shuts
Down
Inability to Control
Impulsive Behaviors
Related to Affect
Fig. 6 Pervasive emotion dysregulation in borderline personality disorder (based in part on Linehan et al., 2007, p. 584)
Emotions 13

Emotional Expression of Anxiety
Spectrum of Anxiety
Anxiety is an emotion characterized by apprehen-
sive anticipation of future danger or misfortune
accompanied by a feeling of worry, distress, or
somatic symptoms of tension. The perceived dan-
ger may be either an internal or an external fear.
The physiological manifestations of anxiety
(Table 9) may present as symptoms of activation
of the autonomic nervous system. Anxiety is a
normal reaction to a situation where immediate
danger exists and may result in physical harm.
Anxiety is also a normal response to situations
that pose a threat to self-esteem or psychological
well-being. Pathological anxiety occurs in situa-
tions where there is no real physical or psycho-
logical danger or when the emotional reaction is
disproportionate in intensity to the actual danger
(Spielberger & Rickman, 1990).
Etiology of Anxiety
Traditionally, the emotion of anxiety has been
dichotomized into fear and neurotic anxiety.
Fear, or objective anxiety, as conceptualized by
Freud (1936, 1959), consisted of three compo-
nents: a real external danger, an accurate percep-
tion of the danger as potentially harmful, and an
emotional response of anxiety, which varied in
intensity proportional to the magnitude of the
objective danger. Neurotic anxiety, as Freud
described it, was also a psychobiological process;
however, the danger was from within, in the form
of forbidden instinctual drives that were punished
in childhood, repressed, and subsequently about
to escape from the individual’s control
(Spielberger, 1966). Fear and anxiety may be pre-
sent in varying proportions in a given situation.
Elucidating the cause of the affect is more impor-
tant clinically than determining whether the emo-
tion is fear or anxiety (Uhde & Nemiah, 1989).
More recent theories of the emotion of anxiety
can be divided into stimulus- and response-
oriented theories. The former construct suggests
that stimulus events serve to initiate the emotional
response. It is the nature of the event (the
thoughts, feelings, and situation associated with
the event) that precipitates the response. An exam-
ple of a stimulus-oriented theory is Goldstein
(1940) catastrophic reaction. A situation that rep-
resents a threat to the individual’s existence, phys-
ical or psychological, is necessary for impairment
of objective behavior resulting in the subjective
experience of anxiety.
Fear may result in anxiety disorder when it
becomes greater than warranted or occurs in inap-
propriate situations. LeDoux (2000) has proposed
that anxiety may develop as a conditioned
response to fear following exposure to the
unconditioned stimuli, not dissimilar to condi-
tioned response proposed by Pavlov (1927).
Subsequently, exposure to a conditioned stimulus
meditated by the amygdala leads to activation
of a defensive behavior, autonomic arousal,
hypoalgesia, somatic reﬂex potentiation, and
pituitary–adrenal axis activation.
The response-oriented approach focuses on the
resultant affect. The response-oriented theorists
hold that the anxiety response is the same regard-
less of the stimulus. Anxiety is an innate emotion
resulting from a neurophysiological response that
can be modiﬁed through learning. Pathological
anxiety differs from normal anxiety by the
increased intensity, frequency, and duration of
the neurophysiological response.
The trait–state dichotomy (Cattell & Scheier,
1961) of anxiety is an outgrowth of the response-
oriented theorists. Trait is viewed as a personality
Table 9 Physiological manifestations of anxiety
Elevated blood pressure
Cardiac discomfort
Palpitations
Tachycardia
Diaphoresis
Dizziness
Dry mouth
Irregularities in breathing
Hyperventilation
Musculoskeletal disturbances
Restlessness
Tremors
Weakness

feature, whereby the individual consistently
behaves anxiously despite the situation. State
refers to momentary feelings of anxiety. Despite
some detractors to this theoretical distinction
(Allen & Potkay, 1981), the validity of this dichot-
omy has been shown in research demonstrating
trait anxiety to remain stable over time and to be
impervious to stress, despite circumstances
(Spielberger & Rickman, 1990). The stimuli that
elicit anxiety, according to trait–state anxiety the-
ory (Fig. 7), may be either intrapsychic or from
environmental sources. Anxiety from situations
that threaten personal adequacy is found more
often in individuals with high trait anxiety.
Other cognitive theories of anxiety are out-
growths of the response-oriented view. Beck and
colleagues (1974) believed that anxiety results
from a misperception of danger or an unrealistic
heightened expectation of harm. The degree of the
anxiety is directly proportional to the anticipated
severity of the adversity and the degree to which
the individual cognitively distorts these fears
(Table 10). The phenomenology and maintenance
of anxiety has been proposed to be a result of
counterproductive efforts to regulate emotions.
That core features of anxiety, such as worry and
behavioral avoidance, are maladaptive attempts to
regulate uncomfortable or unwanted emotions
(Campbell-Sills & Barlow, 2007).
Kagan and colleagues (1984) have suggested
that behavioral inhibition in childhood, initial
negative emotional and motor reactivity to nov-
elty during infancy, may be an antecedent of anx-
iety disorders in adulthood. Children with an
inhibited temperament tend to be timid with peo-
ple, objects, and situations that are novel or unfa-
miliar. They have found that children of parents
with panic disorder with agoraphobia, including
those with comorbid major depressive disorder,
are at increased risk of behavioral inhibition. Chil-
dren identiﬁed as having behavioral inhibition
have high rates of childhood-onset anxiety disor-
ders; behavioral inhibition is associated with
familial risk for anxiety disorders; children with
behavioral inhibition and anxiety disorders have
greater familial anxiety disorders; and children
Sensory and cognitive feedback
Internal stimuli
Thoughts, feelings,
biological needs
Subjective feelings
of applehension,
anxious expectation
A-state
Activation (arousal)
of the autonomic
nervous system
A-trait
Individual differences
in anxiety proneness
Highly overleamed responses
to threat stimuli
Defense mechanism
Adjustive processes
for avoiding or
reducing A-states
Response to stimuli appraised as nonthreatening
Alteration of cognitive appraisal by defense mechanisms
B
e
h
a
v
i
o
r
Cognitive
appraisal
External
stimuli
(stressors)
Fig. 7 A trait–state conception of anxiety. (Reproduced from Spielberger (1966, p. 17) with permission from Elsevier)
Emotions 15

who remain inhibited over time are at highest risk
of anxiety disorders including panic disorder and
social phobia (Lehat et al., 2011; Rosenbaum
et al., 1993).
Attachment is a lasting psychological connec-
tion between human beings (Bowlby, 1969). Four
types of attachment styles have been described:
secure, ambivalent-secure, avoidant-insecure, and
disorganized-insecure (Ainsworth et al., 1978;
Main & Solomon, 1986). Insecure attachment
may have an impact on later adult relationships
and development of anxiety, as well as depression
(Lee & Hankin, 2009).
Clinical Presentation of Anxiety
Anxiety is an emotion that may be present in
many psychiatric disorders as well as other med-
ical conditions (Table 11). Anxiety may be a
prominent feature in numerous neurological dis-
orders, hypoxic states, and endocrine disorders.
Uremia, posthepatitis syndrome, infectious mono-
nucleosis, porphyria, febrile illnesses and chronic
infections, systemic malignancies, carcinoid syn-
drome, and hypoglycemia have been implicated
in producing states of anxiety. Inflammatory dis-
eases and some vitamin deficiencies have also
been implicated. A number of toxic agents have
been shown to result in anxiety (Cummings,
1985).
Anxiety is a common symptom in psychosis,
mood disorders, neurocognitive disorders, and
somatoform disorders. Anxiety is the prevailing
mood state in DSM-5-TR anxiety disorders
(Table 12).
The clinical presentation of anxiety symptoms
varies with the specific disorder. Panic attacks
may be present in nearly all the specific anxiety
disorders. A panic attack is described as a sudden,
Table 10 Theories of anxiety
Objective-neurotic
Stimulus oriented
Response oriented
Trait-state
Cognitive
Table 11 Anxiety presenting in medical conditions
Neurological
disorders
Cerebral malaria, cerebral
neoplasms, cerebral syphilis,
cerebrovascular disease,
encephalitis, epilepsy,
Huntington’s disease, migraine,
multiple sclerosis, Parkinson’s
disease, postconcussional
syndrome, posttraumatic
encephalopathy, stroke,
subarachnoid hemorrhage,
Wilson’s disease
Cardiopulmonary
disease
Anemia, acute asthma, angina,
cardiac arrhythmias,
cardiovascular disease, congestive
heart failure, mitral valve prolapse,
pneumothorax, pulmonary
embolisis
Endocrine
disorders
Adrenal dysfunction, disorders of
female virilization, carcinoid
syndrome, Cushing’s syndrome
with hyperadrenalism,
hyperthyroidism, hypoglycemia,
hypoparathyroidism, multiple
endocrine neoplasms, parathyroid
dysfunction, pheochromocytoma
Gastrointestinal
disease
Gastrointestinal reflux, peptic
ulcer, ulcerative colitis
Inflammatory
diseases
Polyarteritis nodosa, rheumatoid
arthritis, systemic lupus
erythematous, temporal arteritis
Vitamin
deficiencies
Folic acid, niacin, pellagra,
vitamin B1, vitamin B6, vitamin
B12
Other systemic
disorders
Brucellosis, chronic fatigue
syndrome, chronic infections,
febrile illnesses, hepatic failure,
hypocalcemia, hypercalcemia,
infectious mononucleosis,
nephritis, tuberculosis, porphyria,
posthepatitis syndrome, uremia,
systemic malignancies
Pharmocological
agentsa
Antiparkinson agents, caffeine,
corticosteroids, isoniazid,
interferon, digitalis, niacin,
penicillin, sulfonamides,
salicylates, sulfonamides,
sympathomimetic agents,
theophylline, thyroid hormones,
vasopressors, yohimbine
Toxic substances Carbon disulfide, heavy metals,
mercury, organophates, organic
solvents
Source: Cummings (1985, p. 214) and Cummings and
Mega (2003, pp. 246–247)
a
Psychopharmacological, anticonvulsants, and illicit sub-
stances are not listed

Table 12 DSM-5 diagnoses which have anxiety, depression, euphoria, anger, fear, or apathy as part of the diagnostic
criteria or diagnostic features
Diagnostic category Anxiety Depression Euphoria Anger Fear Apathy
Neurodevelopmental disorder
Childhood-onset fluency disorder Anxiety
Schizophrenia spectrum and other psychotic
disorders
Schizophrenia Anxietya
Depressiona
Angera
Schizoaffective disorder Depression Euphoria
Bipolar and related disorders
Bipolar I disorder Anxiety Depression Euphoria Angera
Cyclothymic disorder Anxiety Depression Euphoria
Bipolar and related disorder due to another
medical condition
Anxiety Depression Euphoria
Other specified bipolar and related disorder Anxiety Depression Euphoria
Unspecified bipolar and related disorder Anxiety Depression Euphoria
Depressive disorders
Disruptive mood dysregulation disorder Anxiety Depression Anger
Major depressive disorder Anxiety Depression
Premenstrual dysphoric disorder Anxiety Depression Anger
Depressive disorder due to another
medical condition
Anxiety Depression
Other-specified depressive disorder Anxiety Depression
Unspecified depressive disorder Anxiety Depression
Anxiety disorders
Separation anxiety disorder Anxiety Depressiona
Depressiona
Fear Apathya
Selective mutism Anxiety
Specific phobia Anxiety Fear
Social anxiety disorder Anxiety Fear
Panic disorder Anxiety Depression Fear
Agoraphobia Anxiety Depressiona
Fear
Generalized anxiety disorder Anxiety
Substance/medication-induced anxiety
disorder
Anxiety
Anxiety disorder due to another medical
condition
Anxiety
Other specified anxiety disorder Anxiety
Unspecified anxiety disorder Anxiety
Obsessive-compulsive and related disorders
Obsessive–compulsive disorder Anxiety
Body dysmorphic disorder Anxietya
Depressiona
Trichotillomania disorder Anxietya
Excoriation (skin-picking) disorder Anxietya
Trauma- and stressor-related disorders
Reactive attachment disorder Depression Fear
Posttraumatic stress disorder Anxiety Depression Anger Fear
Acute stress disorder Anxiety Depression Anger
Adjustment disorders Anxiety Depression
Somatic symptom and related disorders
Somatic symptom disorder Anxiety
(continued)
Emotions 17

Table 12 (continued)
Illness anxiety disorder Anxiety Fear
Other speciﬁed somatic symptom and
related disorder
Anxiety
Feeding and eating disorders
Anorexia nervosa Depressiona
Fear
Binge eating disorder Depression
Sleep-wake disorders
Nightmare disorder Anxiety
Substance/medication-induced sleep
disorder
Anxietya
Depressiona
Sexual dysfunctions
Genito-pelvic pain/penetration disorder Anxiety Fear
Disruptive, impulse-control, and conduct
disorders
Oppositional deﬁant disorder Anger
Intermittent explosive disorder Anger
Conduct disorder Anger
Substance-related and addictive disorders
Alcohol use disorder Anxietya
Depressiona
Alcohol intoxication Depressiona
Anger
Alcohol withdrawal Anxiety Anger
Caffeine intoxication Euphoria
Caffeine withdrawal Depressiona
Cannabis use disorder Euphoria
Cannabis intoxication Euphoria
Cannabis withdrawal Anxiety Depressiona
Anger
Inhalant intoxication Euphoria
Opioid intoxication Euphoria
Opioid withdrawal Depression
Sedative, hypnotic, or anxiolytic
withdrawal
Anxiety Anger
Stimulant use disorder Anxietya
Depressiona
Stimulant intoxication Anxiety Depression Euphoria Anger
Stimulant withdrawal Depressiona
Tobacco withdrawal Anxiety
Other (or unknown) substance intoxication Anxiety Euphoria
Gambling disorder Depression Euphoria
Neurocognitive disorders
Delirium Anxietya
Depressiona
Euphoriaa
Angera
Feara
Apathya
Major or mild neurocognitive disorder Anxiety Depression Euphoria Apathya
Personality disorders
Paranoid personality disorder Anger Fear
Schizotypal personality disorder Anxiety Depressiona
Fear
Borderline personality disorder Anxiety Depression
Histrionic personality disorder Depressiona
Narcissistic personality disorder Depressiona
Angera
Antisocial personality disorder Anger
Avoidant personality disorder Anxietya
Fear
(continued)

discrete period of intense apprehension, fearful-
ness, or terror associated with physical symptoms
including shortness of breath, palpitations, and
chest discomfort. During a panic attack, the indi-
vidual frequently has feelings of impending
doom, a fear of losing control, a sense of immi-
nent danger, and an urge to escape. Panic attacks
are divided into two characteristic types by the
onset of the attack in relation to the presence or
absence of a situational stimulus: expected and
unexpected (Table 13). Unexpected panic attacks
occur spontaneously, unassociated with a situa-
tional trigger. Expected panic attacks can be situ-
ationally bound or anticipated. Situationally
bound panic attacks occur immediately on expo-
sure to or in anticipation of a situational cue.
Situationally predisposed panic attacks are more
likely to occur on exposure to a specific stimulus
but do not necessarily occur immediately. Unex-
pected panic attacks are necessary for a diagnosis
of a panic disorder. Situationally bound panic
attacks are characteristic of social and specific
phobias. The situationally predisposed panic
attack occurs in panic disorder, specific phobias,
or social anxiety disorder. Panic attacks are not
limited to anxiety disorders but may also occur in
posttraumatic stress disorder, depressive
disorders, and substance use disorders, as well as
other mental disorders.
The characteristic presentation of anxiety in
phobic disorders is a persistent, irrational fear of
a specific object, activity, or situation that results
in a desire to avoid it. When exposed to the stim-
ulus, the phobic individual experiences intense,
autonomic symptoms associated with fear. The
response is frequently difficult to distinguish
from the anxiety of panic disorder, which is char-
acteristically spontaneous and not situationally
provoked. Anxiety symptoms associated with
increased arousal, reexperience of a traumatic
event, and avoidance of stimuli reminiscent of
the trauma are characteristic of both acute and
posttraumatic stress disorders.
Generalized anxiety disorder is characterized
by excessive worrying, often about routine life
circumstances. The object of worry may shift
from one concern to another. Associated with
generalized anxiety disorder are physiological
symptoms, including muscle tension presenting
as trembling, twitching, feeling shaky, or muscle
aches or soreness. Autonomic aspects to the anx-
iety may be present, including cold, clammy
hands, dry mouth, sweating, nausea or diarrhea,
urinary frequency, and trouble swallowing.
Table 12 (continued)
Dependent personality disorder Anxietya
Fear
Obsessive compulsive personality disorder Angera
Personality change due to another medical
condition
Anger Apathy
a
Not found in the diagnostic criteria or diagnostic features of DSM-5 but in associated features supporting diagnosis,
comorbidity excluded
Table 13 Types of panic attacks and DSM-5-TR anxiety disorder
Type Onset Situational trigger DSM-5-TR diagnoses
Unexpected Spontaneous Unassociated Panic disorder
Agoraphobia
Expected
Situationally bound Immediate On exposure Social anxiety disorder
Specific phobia
Situationally predisposed Not always
Immediate
On exposure Generalized anxiety disorder
Panic disorder
Social anxiety disorder
Emotions 19

Individuals with generalized anxiety disorder fre-
quently have an exaggerated startle response.
Although not classified under the anxiety dis-
orders, obsessive compulsive and related disor-
ders present with obsessions, persistent ideas,
thoughts, impulses, or images that are intrusive
and inappropriate that result in distress and anxi-
ety. The associated compulsion is a repetitive
behavior or mental act, the goal of which is to
prevent or reduce anxiety resulting from the
obsession.
Emotional Expression of Depression
Spectrum of Depression
Depression refers not only to an emotional state
that is characterized by brief or mild periods of
sadness or being “down” but also to a clinical
condition characterized by depressed mood. A
sense of helplessness or loss of self-esteem is
often present in a depressed mood. Sadness,
dejection, self-reproach, helplessness, despair,
feelings of rejection, pessimism, and boredom
may be terms used to describe the dysphoric,
painful, or unpleasant feelings associated with
depression (Hamilton, 1982). Depressed mood
states are present in simple unhappiness, grief or
bereavement, demoralization, and mood
disorders.
Demoralization is characterized by subjective
incompetence, helplessness, hopelessness, an
inability to cope, a sense of failure, and a loss of
meaning (Zhu et al., 2021). Demoralization is
experienced in a variety of situations including
severe physical illness, chronic illness, and con-
ditions of marginalization as well as psychiatric
disorders, and may be a risk factor for developing
psychiatric disorders such as post-traumatic stress
disorder (Kohn, 2013). The degree to which an
individual is demoralized can be considered her or
his psychological temperature and may provide a
conceptual continuity of depressive symptoms
from normalcy to clinical disorder.
Sadness appropriate to a real loss is part of
mourning or grief. The depressed affect accompa-
nying grief differs from other depressed states by a
sense of relief felt with the expression of grief
(Jacobson, 1974). A depressed mood accompa-
nied by poor appetite, weight loss, and insomnia
commonly occurs during bereavement. If
bereavement is also associated with morbid pre-
occupation with worthlessness, guilt about things
other than actions taken or not taken by the survi-
vor at the time of death, thoughts of death other
than the survivor feeling that he or she would be
better off dead or should have died with the
deceased person, prolonged and marked func-
tional impairment, marked psychomotor retarda-
tion, or hallucinatory experiences other than
thinking that he or she hears the voice of or tran-
siently sees the image of the deceased person, this
suggests that the bereavement is beyond the
expected norm and that a major depressive epi-
sode is present. The duration and expression of
normal bereavement vary considerably among
different cultural groups.
Etiology of Depression
Theories of the origins of pathological depressed
mood states can be found in the Hippocratic writ-
ings of the fourth and fifth centuries. These early
writings defined melancholia to be a prolonged
state of depression, with associated aversion to
food, despondency, sleeplessness, irritability, and
restlessness. Of the four humors, blood, yellow
bile, black bile, and phlegm, an excess of black
bile was thought by the ancient Greeks to play a
distinct role in the development of melancholia.
The introduction of the term depression as a sub-
stitute for melancholia in the mid-1800s began to
signify a psychological and not merely physiolog-
ical understanding of depressive mood states.
Modern conceptualizations of the etiological ori-
gins of the emotion of depression encompass a
broad theoretical spectrum, including early envi-
ronmental, personality, psychodynamic, cogni-
tive, life events and social stress, and
neurobiological theories.
Early environmental theories considered
parental loss, parental separation, and parental
style to be risk factors for depression. There is
little evidence in experimental controlled studies

to support a relationship between parental loss by
death in childhood and depression in adulthood
(Canetti et al., 2000; Crook & Eliot, 1980;
Tennant et al., 1980). The role of parental separa-
tion appears to be more complex; separations
involving family discord, such as divorce, may
have a long-term impact (Canetti et al., 2000);
and studies that have suggested a role for parental
death in major depression in adulthood have
found a more robust role for parental separation
(Agid et al., 1999). However, methodological
issues in this area of research continue to create
speculation as to the validity of such findings
(Tennant, 1988), in particular, the lack of adequate
accounting of the effects of genetic and environ-
mental factors preceding the loss. Parental styles
from rejecting and indifferent to overprotective
and controlling have been posited to predispose
to adult depression; however, evidence of a causal
relationship is yet to be demonstrated. Adult
attachment, insecure attachment, has been shown
to lead to depressive symptoms in adulthood
through its impact on self-worth contingencies
and self-esteem (Roberts et al., 1996).
There are four major models for the role of
personality in depression: vulnerability model,
complication model, spectrum model, and
pathoplasty model. The distinction between
these five models may not always be clear and
combinations may be seen (Kendler & Neale,
2010). The vulnerability or predispositional
model considers that certain antecedent personal-
ity characteristics render an individual vulnerable
to the development of depression. An example of
this model is Cloninger (1987) theory that neuro-
biological processes interact with heritable per-
sonality traits. He stated that there are three
underlying dimensions of personality defined by
their stimulus-response characteristics that are
genetically and neuroanatomically based: novelty
seeking, harm avoidance, and reward dependence
(Fig. 8). Susceptibility to reactive dysphoria is
primarily determined by high reward dependence
and reduced by high harm avoidance and high
novelty seeking (Cloninger, 1986).
The complication model is the reverse of the
predispositional model. According to this model,
clinical depression leads an individual to change
Fig. 8 Three-way interaction of personality and monoaminergic transmission. (Reproduced from Cloninger (1986) with
permission of Oxford University Press)
Emotions 21

the way she or he interacts with others or per-
ceives herself or himself. The spectrum model
proposes a continuum between temperament and
mood disorders. Pessimism, moodiness, passivity,
negativity, and low energy may be personality
characteristics that represent the same genetic
endowment in normal or milder depressive states
as in pathological syndromes. Akiskal and
Akiskal (1992) have suggested that cyclothymic,
depressive, and hyperthymic temperaments repre-
sent the subclinical foundations from which affec-
tive episodes arise (Table 14). The mechanism
postulated by the fourth model, the pathoplasty
model, that symptomatic expression and course of
depression are inﬂuenced by personality charac-
teristics has not been demonstrated in studies
measuring personality attributes before the devel-
opment of a depressive episode (Angst & Clayton,
1986; Hirschfeld et al., 1989; Lewinsohn et al.,
1988; Nystrom & Lindegard, 1975).
The psychodynamic understanding of depres-
sion has evolved with the development of psycho-
analytic theory. It holds that depression is the
result of disturbance of self-esteem in the context
of failed interpersonal relationships. These child-
hood relationships are internalized and reactivated
with the onset of depression. These object rela-
tionships are also externalized into current rela-
tionships. There is a close relationship between
the individual’s intimate interpersonal interactions
and the maintenance of self-esteem in depression
(Gabbard, 1994).
The best-known cognitive theory of depression
is put forward by Beck (1967). Beck claimed that
the principal etiological agent in the development
of depression is inaccurate cognitions. It is these
distorted thoughts that result in the self-defeating
and pathological emotional responses experi-
enced by individuals with depression. The study
of dogs exposed to inescapable shock has led to
the learned helplessness model of depression.
Seligman (1974) found that animals developed a
passive acceptance of the condition in subsequent
situations when escape was possible. In the
learned helplessness condition, the animal was
unable to initiate adaptive responses. This model
was thought to apply to depression, when
individuals perceive themselves as helpless and
behave passively.
Individuals with depression have been shown
to exhibit an attentional bias toward negative
emotional cues, an attentional bias away from
positive emotional cues, and an enhanced mem-
ory for negative emotional material (Altgassen
Table 14 Spectrum of temperament and mood
Temperament Clinical features
Cyclothymic
temperament
Hypersomnia vs. decreased
sleep
Introverted vs. uninhibited
Taciturn vs. talkative
Unexplained tearfulness
vs. jocularity
Psychomotor inertia
vs. restlessness
Lethargy vs. eutonia
Dulling of senses vs. keen
perceptions
Slow witted vs. sharp thinking
Shaky self-esteem
Pessimistic brooding
vs. optimism
Depressive
temperament
Gloomy, humorless, or
incapable of fun
Given to worry, brooding, or
pessimistic
Introverted, passive, or lethargic
Long sleeper or insomnia
Preoccupied with inadequacy
and failure
Skeptical, overcritical, or
complaining
Self-critical, self-reproachful,
and guilty
Reliable, dependable, and
devoted
Hyperthymic
temperament
Cheerful, overoptimistic, or
exuberant
Warm, people seeking, and
extroverted
Overtalkative and jocular
Overconﬁdent, self-assured, or
grandiose
Short sleeper
High energy level and full of
plans
Overinvolved and meddlesome
Uninhibited and stimulus
seeking

et al., 2011; Leppänen, 2006). Some of these
abnormalities in the processing of emotional
information have been noted in healthy controls
that are at risk of developing mood disorders.
Responsiveness to positive emotional cues is
blunted in depression, although this is not
supported by all studies and there is a question
as to whether this reflects comorbid anxiety.
Theories of social stress have examined stress-
ful life events (Brown & Harris, 1978) and social
support (Aneshensel & Stone, 1982; Williams
et al., 1981) as etiological factors in the develop-
ment of depression. The role of life events has
been confirmed using the stringent test of inde-
pendent and fateful events that cannot be linked to
the individual’s depression or personality other
characteristics (Shrout et al., 1989). In addition,
chronic stress has been associated with risk of
depression (Hammen, 2005). Social support is
defined as provision of psychological and material
resources by a social network intended to benefit
an individual’s ability to cope with stress (Cohen,
2004). There is stronger evidence to support the
role of perceived (subjective) rather than enacted
(objective) social support in the role of depression
(Marroquín, 2011). Such studies have demon-
strated a cause-and-effect role for these social
risk factors; however, these models can explain
only a small proportion of the variance for the
occurrence of depression.
Based on epidemiological studies of twin pairs,
men and women have been shown to have more
similarities than differences. Three pathways to
depression in men and women were suggested,
characterized by internalizing symptoms (genetic
risk factors, neuroticism, low self-esteem, early-
onset anxiety, and past history of major depres-
sion), externalizing symptoms (males: genetic
risk factors, conduct disorder, and substance mis-
use; females: conduct disorder, substance misuse,
and past history of major depression), and adver-
sity and interpersonal difficulty (low parental
warmth, childhood sexual abuse and parental
loss, low education, lifetime trauma, low social
support, history of divorce, past history of major
depression, marital problems, and stressful life
events) (Kendler et al., 2002, 2006). In both
sexes, genetic factors were important in the
pathways to neuroticism, substance misuse, life-
time traumas, past history of major depression,
and risk of major depression in the past year.
The genetic factors for both genders are mediated
partially by personality, increased exposure to
traumatic events, and substance misuse. Child-
hood parental loss and low self-esteem had a
more potent effect on men than on women.
Physiological explanatory models have
become the primary focus in understanding the
origins of depression. Subcortical and limbic
brain structures and their ascending projections
are believed to mediate depression. Biochemical
theories have implicated disturbances in norepi-
nephrine, serotonin, and dopamine in the patho-
genesis of depression. Dysfunction of the
hypothalamic–pituitary–adrenal (HPA) axis has
been consistently observed in patients with
major depression, presenting as elevation of
basal cortisol dexamethasone-mediated negative
feedback resistance, increased cerebrospinal fluid
levels of corticotrophin-releasing factor (CRF),
and a blunted adrenocorticotropic hormone
(ACTH) response to challenge with exogenous
CRF (Plotsky et al., 1998). None of these etiolog-
ical mechanisms, biological or psychological, is
sufficient to explain the development of the path-
ological expression of the emotion of depression.
Clinical Presentation of Depression
A dominating depressed mood state may be seen
in numerous general medical disorders (Table 15)
as well as in psychiatric disorders. A number of
neurological conditions may result in a depressed
mood including Parkinson’s disease. In cerebro-
vascular disease, depression is more common
with frontal lobe lesions than with posterior hemi-
sphere lesions, and it is more common with left-
rather than right-sided infarcts (Robinson et al.,
1984). Cardiopulmonary disease, renal disease
and uremia, systemic neoplasms, porphyria,
Klinefelter’s syndrome, postoperative states, and
acquired immunodeficiency syndrome may all
present with disorders of emotion, often depres-
sion. Less common but documented are deficien-
cies of vitamin B12, folate, and vitamin C resulting
Emotions 23

in depression. Endocrine disorders, inflammatory
diseases, bacterial and viral infections, and a
broad spectrum of pharmaceutical agents may
result in development of depressed mood states.
Of the hypertensive drugs, reserpine, methyldopa,
and propranolol have been the most widely
implicated in the literature, although the evidence
for the latter is weak (Kohn, 2001).
Depression is a mood state that is at some point
present in all of the DSM-5-TR depressive disor-
ders. In addition, depression may be a presenting
symptom in bipolar and related disorders. A
depressed mood is a specifier for adjustment dis-
orders and schizoaffective disorder. Depressed
mood may also color other psychiatric disorders
(Table 12).
The mood disturbance characterized by a
major depressive episode involves both cognitive
and vegetative symptoms. These vegetative
symptoms, referred to as such because they are
unconscious and involuntary, include changes in
appetite or weight, sleep, energy, and psychomo-
tor activity. The cognitive changes include feel-
ings of worthlessness or guilt; difficulty in
thinking, concentrating, or making decisions;
and recurrent thoughts of death or suicidal idea-
tion, plans, or attempts. Loss of interest or anhe-
donia, the inability to experience pleasure, is
another cardinal feature. Although not necessary
for a diagnosis of a major depressive episode, a
depressed mood is usually present. The mood in a
major depressive episode is often described as
depressed, sad, hopeless, empty, discouraged, or
down. The depressed mood is not always
acknowledged or recognized by the patient and
may need to be inferred from the patient’s
demeanor or facial expression. The affect is
revealed by the slowed and hypophonic speech
produced (Greden et al., 1981). “Facial masking”
with little or no facial muscle response to emo-
tional stimuli is often seen (Schwartz et al., 1976).
The posture is frequently bowed, steps are short-
ened, and there is a general lack of spontaneous
activity (Kupfer et al., 1974). In children and
adolescents, an irritable mood rather than a sad
mood may be present. Individuals with major
depressive episodes may also demonstrate other
emotional states including irritability, anxiety,
phobias, obsessive ruminations, and excessive
worry, in particular about physical complaints.
The depressed mood seen in individuals with
persistent depressive (dysthymia) disorder differs
little from that found in major depressive disorder,
except in the number and duration of the
Table 15 Depression presenting in medical conditions
Neurological
disorders
Atrovenous malformations,
cerebral neoplasms, cerebral
trauma, cerebrovascular disease,
corticobasal degeneration, epilepsy,
Fahr’s disease, Huntington’s
disease, hydrocephalus, multiple
sclerosis, narcolepsy, narcolepsy,
Parkinson’s disease, progressive
supranuclear palsy, stroke, white
matter ischemia, Wilson’s disease
Infections Creutzfeldt-Jakob disease, Lyme
encephalitis, systemic bacterial
infections, systemic viral
infections, viral encephalitis
Endocrine
disorders
Acromegaly, Addison’s disease,
Cushing’s syndrome, diabetes
mellitus, hyperaldosteronism,
hyperparathyroidism,
hyperthyroidism,
hypoparathyroidism,
hypopituitarism, hypothyroidism,
prolactinoma
Inflammatory
diseases
Polyarteritis nodosa, rheumatoid
arthritis, Sjögren’s syndrome,
systemic lupus erythematous,
temporal arteritis
Vitamin
deficiencies
Folate, niacin, vitamin B12, vitamin
C
Other systemic
disorders
Acquired immunodeficiency
syndrome, cardiopulmonary
disease, Klinefelter’s syndrome,
porphyria, postoperative states,
renal disease, uremia, systemic
neoplasms
Pharmacological
agents
Analgesics, antibacterial and
antifungal agents, anti-
inflammatory agents, antineoplastic
drugs, cardiac and hypertensive
drugs, interferon, neurological
agents, psychotropic drugs,
sedatives and hypnotics, steroids
and other hormonal agents,
stimulants and appetite
suppressants, varenicline
Mega (2003, p. 204)

associated cognitive and vegetative features. Cog-
nitive symptoms are more characteristic of persis-
tent depressive than vegetative symptoms (Keller
et al., 1995). The depressed mood found in per-
sistent depressive disorder is typically described
as sad or “down in the dumps” and is chronic
(at least 2 years in duration).
The depression specifier in adjustment disor-
ders is a response to an identifiable psychosocial
stressor but is not severe enough to meet criteria
for a depressive disorder. The dominant features
include a depressed mood, tearfulness, and feel-
ings of hopelessness.
Emotional Expression of Euphoria
Euphoria is defined as intense elation often asso-
ciated with feelings of grandeur. Euphoria, ela-
tion, exultation, and ecstasy are synonyms that
describe an exceedingly pleasurable mood.
These emotions can be a part of normal experi-
ence. Euphoric states are achieved during sexual
pleasure, when one is in love, after achieving a
long-sought goal, or just when life is going well.
Religious experiences can also result in feelings
of euphoria. When euphoria goes beyond the
range of normal experience and becomes a psy-
chiatric problem, mania or hypomania is present.
Euphoric mood states may be induced by
numerous drugs, neurological conditions, sys-
temic medical disorders (Table 16), and psychiat-
ric illnesses. The psychiatric conditions in which
euphoric mood predominates are among the
DSM-5-TR bipolar and related disorders
(Table 12). Euphoria is also characteristic of
schizoaffective disorder, bipolar type, and in
substance-related intoxication.
The elevated mood of a manic episode is
described as euphoric, unusually good, cheerful,
or high. It is viewed as excessive and may seem to
have an infectious quality. The quality of the
mood is expansive with indiscriminate enthusi-
asm for interpersonal, sexual, and occupational
interactions. Speech during a manic episode is
pressured, loud, rapid, and difficult to interrupt.
Lability and irritability of mood are often seen in
manic episodes. The expression of the euphoric
mood seen in a hypomanic episode is similar to
that of a manic episode; however, it is not as
severe and consequently does not result in psy-
chotic features, hospitalization, or marked impair-
ment in social or occupational functioning as seen
in manic episodes.
Emotional Expression of Fear
Fear is an emotion that is caused by threat-related
stimuli, and thereby causes particular patterns of
adaptive behaviors to avoid or cope with that threat.
The most common distinction is between fear and
anxiety. Fear is usually conceptualized as an adap-
tive, but transient state elicited through confronta-
tion with a threatening stimulus, while anxiety is a
more tonic state related to prediction and prepared-
ness for possible upcoming negative events, a dis-
tinction is similar to the one between emotions and
Table 16 Euphoria presenting in medical conditions
Neurological
disorders
Cerebral neoplasms, cerebral
trauma, cerebrovascular accidents,
Huntington’s disease, general
paresis of syphilis, idiopathic basal
ganglia calcification, idiopathic
dystonia, Kleine–Levin syndrome,
multiple sclerosis, Parkinson’s
disease, Pick’s disease,
postencephalitic Parkinson’s
disease, temporal lobe epilepsy,
thalamotomy, Wilson’s disease
Infections Cryptoccocosis, herpes simplex
virus, HIV encephalopathy,
influenza, mononucleosis,
neurosyphilis, Q-fever, viral
encephalitis
Systemic
disorders
Carcinoid syndrome, cerebral
anoxia, fragile X syndrome,
hemodialysis, hyperthyroidism,
Klinefelter’s syndrome, pellagra,
uremia, vitamin B12 deficiency
Pharmacological
agents
Antihypertensive and
cardiovascular compounds,
anticonvulsants, antidepressants,
atypical antipsychotics,
dopaminergic antiparkinsonian
agents, hallucinogens, some
antimicrobials, stimulants, steroids,
sympathomimetic amines
Mega (2003, pp. 214–217)
Emotions 25

moods. Exposing an anxious patient to situations
that elicit fear that results in reducing fear following
repeated exposures is a commonly used technique
in exposure-based psychotherapies.
Lang (1968) classified fear into three
responses: verbal subjective – thoughts of immi-
nent threat; overt motor acts – escape; and
somato-viceral activity – autonomic surge
resulting in physical symptoms such as sweating,
trembling, heart palpitations, and nausea
(Table 17). In the Pavlovian model or classical
associative learning theory conditioned fear is
acquired through associations with aversive
events, experienced directly, vicariously, or thor-
ough informational transmission. An innocuous
stimulus, the conditional stimulus, is followed
by an aversive stimulus, the unconditional stimu-
lus, resulting in a conditional fear reaction or
conditional response. If the conditional stimulus
is presented continuously without the uncondi-
tional stimulus a gradual decay, extinction, of the
conditional response may occur. Individuals who
develop anxiety disorders and trauma- and
stressor-related disorders may have impaired fear
extinction (Vervliet et al., 2013). The experience
of fear or a traumatic event do not necessarily
result in permanent memories of the trauma but
undergo a period of consolidation in which they
shift from a labile state to a more permanent state
(Ressler & Mayberg, 2007). After memories
become consolidate, they may become labile
again, a process called reconsolidation. The trau-
matic memories in fear-related disorders are
reduced through extinction with repeated expo-
sure to the fear related cues that reduce fear mem-
ories. However, avoidance of exposure with
intrusive and uncontrollable memories leads to
sensitization of the fear response as seen in
trauma- and stressor-related disorders (Fig. 9).
The amygdala has a central role in the condi-
tioning of fear reactions. Sensory information
from the conditional and unconditional response
is transmitted from the thalamus to the basolateral
nucleus us of the amygdala (Vervliet et al., 2013).
Transmitting signals to the central nucleus of the
amygdala leads to the expression of fear. Threat
anticipation involves the dorsal anterior cingulate
cortex, and the insular cortex is related to intro-
spection, awareness, and sensitivity to visceral
activity. Fear extinction involves the coordinated
activity of the amygdala, hippocampus, and ven-
tromedial prefrontal cortex.
Fear is present in the criteria description of
numerous DSM-5-TR mental disorders
(Table 12). Although the term fear is not specifi-
cally mentioned in the DSM-5-TR criteria due to
the avoidant behavior, researchers frequently use
obsessive compulsive disorder in models of fear.
In addition, acute stress disorder perhaps should
be considered among the disorders characterized
by fear.
Posttraumatic stress disorder is the principal
diagnosis used to illustrate a fear response. In
posttraumatic stress disorder the restraining influ-
ence of the medial prefrontal cortex, especially the
anterior cingulate gyrus and the orbitofrontal cor-
tex, is compromised. The consequent disinhibi-
tion of the amygdala increases the likelihood of
recurrent fear conditioning, as ambiguous stimuli
are possibly misinterpreted as threatening. The
counterbalance to inhibitory prefrontal cortex
restraint no longer functions and sensitization of
key limbic nuclei may occur, therefore lowering
the threshold for fearful emotions (Friedman &
Karam, 2009).
Emotional Expression of Apathy
Apathy is characterized by a dulled emotional
tone associated with detachment or indifference.
The apathetic individual has a qualitative
Table 17 Comparison of symptoms of fear, anxiety, and depression
Response system Fear Anxiety Depression
Verbal-subjective Thoughts of eminent danger Thoughts of future threat Thoughts of loss, failure
Somato-visceral Sympathetic arousal Muscle tension Energy loss
Overt motor Escape Avoidance Withdrawal
Source: Reproduced from Craske et al. (2009, p. 1068) with permission of Wiley-Liss

reduction in goal directed activity often described
as a “bump on a log” or seen as having loss of
motivation, interest or concern; there is reduced
emotional responsiveness to positive and negative
events. Abulia refers to conditions of severe apa-
thy, the loss of will-to-act, and inability to make
decisions or to set goals. It is characterized by
reduced spontaneous, verbal, motor, cognitive,
and emotional behaviors. This differs from
avolition, one of the negative symptoms of
schizophrenia, in that the wish to do something
is present, but the desire is without energy
(Edgerton & Campbell, 1994). The abulic patient
may be immobile, be virtually unresponsive, or
appear even comatose. Harry Stack Sullivan intro-
duced a psychodynamic explanation for the exis-
tence of apathy as an emotion expressed in
personality development (Mullahy, 1952). He
considered apathy an early security operation, a
means of reducing awareness and susceptibility to
interpersonal tension and of dealing with anxiety.
Bleuler (1924) pointed out that apathy to the
extent that there is no affect probably does not
even occur in psychoses or in the most severe
organic brain injury. However, lack of interest in
almost everything that occurs is seen among some
individuals with schizophrenia and neurocognitive
disorders as described by Bleuler (1911) and
Kraepelin (1919). Apathy is the strongest predictor
of poor functional outcome in schizophrenia
(Kiang et al., 2003) and identiﬁed as one of the
most bothersome symptoms (Selten et al., 2000).
DSM-5-TR includes negative symptoms as a char-
acteristic of schizophrenia, which has more clinical
complexity than apathy (Starkstein & Leetjens,
2008).
Affective ﬂattening, alogia, and avolition may
all characterize the emotional expression of
Fig. 9 Emotional learning
process related to fear.
(Reproduced from Ressler
and Mayberg (2007,
p. 1120) with permission of
Nature Publishing Group)
Emotions 27

apathy (Table 18). Individuals with severe major
depressive episode and in particular those with late-
life depression may also present as apathetic
(Alexopoulos et al., 2013), because they may not
be able to discern their own feelings. Several other
DSM-5-TR diagnosis present with apathy
(Table 12). Frontal lobe syndromes involving the
orbital regions typically result in unresponsiveness
to environmental stimuli. Individuals with frontal
lobe syndromes often lack initiative and are
unmotivated and disinterested in their daily activi-
ties. Apathy is also characteristically seen in major
and minor neurocognitive disorder, hypoactive
delirium, Huntington’s disease, Korsakoff’s syn-
drome, and Parkinson’s disease. Individuals with
right hemisphere strokes compared with left-sided
lesions have a greater risk of presenting with apathy
(Marin et al., 1995).
Emotional Expression of Hostility,
Anger, and Rage
Hostility, anger, and rage are aggressive emotions.
These emotions are characterized by heightened
vigilance in response to a sense of threat. Often
there is a tendency to act and engage the threaten-
ing stimulus. There is heightened physiological
tone in preparation for a behavioral response.
This behavioral response varies with societal and
cultural norms and ranges from the adaptive-
constructive response of assertiveness to the
destructive response of violence (Yager, 1989).
Anger may present as a symptom in a number of
DSM-5-TR disorders (Table 12).
Individual differences in expressing and
experiencing aggressive emotions may be cul-
tural, developmental, and temperamental. An
infant’s temperament at birth may predispose to
increased expression of aggressive emotions in
adulthood (Chess & Thomas, 1986). Organic
brain injuries may result in violent acts. Psycho-
logical and social contributions may increase the
likelihood that an individual will express anger,
hostility, or rage. For example, children from vio-
lent families or who are abused often become
violent and abusive themselves (Kempe & Helfer,
1980). Males with schizophrenia may misinter-
pret neutral faces as angry, whereas women with
schizophrenia misinterpreted them as sad (Weiss
et al., 2007). This ﬁnding suggests that gender
differences in aggressive behavior in schizophre-
nia may be related to cognitive styles. Stimulant
use, alcohol use, and other drugs of abuse can
increase the experience of aggressive emotions;
additionally, disinhibition increases the risk of
violent behavior.
Aggressive emotions are present in aspects of
everyday life and as part of the range of emotional
expression in many psychiatric disorders. There
are a number of psychiatric disorders in which the
behavioral outcome of aggressive emotions is
violence either directed toward others as in anti-
social personality disorder, intermittent explosive
disorder, and sexual sadism disorder or directed
toward oneself as in borderline personality disor-
der. In general, there is evidence that there is a
modest relationship between violence and severe
mental illness, and a stronger one with comorbid
substance-related and addictive disorders (van
Dorn et al., 2012).
Disturbances of Affect Incongruent
with Mood
In certain neuropsychiatric disorders, the emotion
expressed by the patient, the mood, is dissociated
from the affect, what is observed. There are pri-
marily three conditions in which this is seen:
Table 18 Characteristics of apathy
Affective
ﬂattening
The face appears immobile,
unresponsive with poor eye contact and
reduced body language
Range of emotional expression is
diminished most of the time
Alogia Poverty of speech is manifested by
brief, laconic, and empty replies
Fluency and productivity of speech are
decreased
Avolition There is inability to initiate and persist
in goal-directed activities
Cognition Lack of interest in learning new things
or having new experiences
Lack of concern for one’s personal
problems

pseudobulbar affect, ictal affective alterations,
and dysprosody.
Patients with pseudobulbar affect have exag-
gerated emotional expression with unintended
laughing or unmotivated crying, and sometimes
a mixture of both, that lacks an appropriate envi-
ronmental trigger. The emotion expressed may be
unrelated to the mood or in disproportionate inten-
sity to the emotion experienced. The emotions
expressed are difficult for the patient to discon-
tinue. Dysarthria and dysphagia are associated
features in many individuals with pseudobulbar
palsy. Although seen in a number of brain disor-
ders and brain injuries, it is commonly seen in
amyotrophic lateral sclerosis, cerebrovascular
accidents, multiple sclerosis, Parkinson’s disease,
Alzheimer’s disease, and traumatic brain injury
(Miller et al., 2011). Bilateral interruption of
descending cortical fibers disinhibits responses
integrated at the lower central nervous system.
Exaggerated emotional expression results from
release of intrinsic motor programs of the limbic
system and related subcortical structures. More
specifically, pseudobulbar affect is believed to be
a dysfunction in a cortico-pontine-cerebellar cir-
cuit (Parvizi et al., 2009).
Mood changes may be induced by focal seizure
activity. Laughter is more common than crying as
an ictal manifestation, but both may occur in the
same patient. The laughter is stereotyped, inap-
propriate, and not stimulus induced. The patient
views the expressed affect not as pleasurable, but
rather as disagreeable (Sethi & Rao, 1976).
Prosody is the affective and inflectional color-
ing of speech. Prosody involves speech melody,
pauses, intonation, stresses, and accents during
articulation. Neurological insults to the basal
ganglia, cerebellum, and brain stem may result
in dysprosody as well as dysarthria. Dysprosody
reduces the patient’s ability to communicate
emotion.
The Emotional Experience of Empathy
Empathy refers to the cognitive ability to experi-
ence and recognize the emotions and motivations
of others. In addition, empathy involves the
identification of one’s own feelings after identifi-
cation and awareness of the emotion of others.
Empathy involves affective arousal, the ability to
automatic discrimination of stimulus as hostile or
hospitable, unpleasant or pleasant, and threaten-
ing or nurturing; emotional awareness or under-
standing; and emotional regulation (Decety,
2011). Mirror neurons have a role in empathy.
Conclusion
Emotions are a feeling state that is described in the
psychiatric mental status examination by affect
and mood. Affect and mood are not separate enti-
ties, although they are often considered as such.
Any observable event or body feeling from which
the psychiatrist makes an inference about affect
could also be incorporated into determining the
mood (Owens & Maxmen, 1979). The important
point in the description of emotions in the mental
status examination is to obtain both a subjective
report and an objective evaluation. It is the
patient’s described and observed emotion that
allows the psychiatrist to properly distinguish
and subsequently make a diagnosis of disorders
that are related to anxiety, depression, euphoria,
fear, apathy, hostility, and anger. Emotional
dysregulation is seen in most psychiatric
disorders.
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