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Neurophysiology of Emotions

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Emotions are automatic and primary patterns of purposeful cognitive-behavioral organizations. They have three main functions: coordination, signaling, and information. First, emotions coordinate organs and tissues, thus predisposing the body to peculiar responses. Scholars have not reached a consensus on the plausibility of emotion-specific response patterns yet. Despite the limitations, data support the hypothesis of specific response patterns for distinct subtypes of emotions. Second, emotional episodes signal the current state of the individual. Humans display their state with verbal behaviors, nonverbal actions (e.g., facial movements), and neurovegetative signals. Third, emotions inform the brain for interpretative and evaluative purposes. Emotional experiences include mental representations of arousal, relations, and situations. Every emotional episode begins with exposure to stimuli with distinctive features (i.e., elicitor). These inputs can arise from learning, expressions, empathy, and be inherited, or rely on limited aspects of the environment (i.e., sign stimuli). The existence of the latter ones in humans is unclear; however, emotions influence several processes, such as perception, attention, learning, memory, decision-making, attitudes, and mental schemes. Overall, the literature suggests the nonlinearity of the emotional process. Each section outlines the neurophysiological basis of elements of emotion.
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Chapter
Neurophysiology of Emotions
Maurizio Oggiano
Abstract
Emotions are automatic and primary patterns of purposeful cognitive-behavioral
organizations. They have three main functions: coordination, signaling, and informa-
tion. First, emotions coordinate organs and tissues, thus predisposing the body to
peculiar responses. Scholars have not reached a consensus on the plausibility of
emotion-specific response patterns yet. Despite the limitations, data support the
hypothesis of specific response patterns for distinct subtypes of emotions. Second,
emotional episodes signal the current state of the individual. Humans display their
state with verbal behaviors, nonverbal actions (e.g., facial movements), and
neurovegetative signals. Third, emotions inform the brain for interpretative and eval-
uative purposes. Emotional experiences include mental representations of arousal,
relations, and situations. Every emotional episode begins with exposure to stimuli
with distinctive features (i.e., elicitor). These inputs can arise from learning, expres-
sions, empathy, and be inherited, or rely on limited aspects of the environment (i.e.,
sign stimuli). The existence of the latter ones in humans is unclear; however, emotions
influence several processes, such as perception, attention, learning, memory,
decision-making, attitudes, and mental schemes. Overall, the literature suggests the
nonlinearity of the emotional process. Each section outlines the neurophysiological
basis of elements of emotion.
Keywords: emotion, emotion definition, emotion faces, facial expressions, emotional
experience, elicitor, sign stimuli, reward system, James-Lange theory, Cannon-Bard
theory
1. Introduction
The study of emotions has fascinated scholars from all over the world for
millennia. Socrates and Plato dealt with it about two thousand five hundred years ago,
and they probably were not even the first [1]. Although there have been considerable
advances since then, our knowledge is far from complete.
In this chapter, the term emotion refers to automatic and primary patterns of
purposeful cognitive-behavioral organizations.[2] Although there is no consensus,
data suggest that emotions are automatic modelssince each subtype probably has
specific neurophysiological layouts [3]. Furthermore, every emotional process is pri-
marybecause, in certain situations, it coordinates the activity of the nervous system
(e.g., perception, attention, and memory) [4]. The expression cognitive-behavioral
organizationsdescribes the coordinating nature of emotion and its ability to facilitate
distinctive behavioral responses [5], while maintaining central control. In particular,
1
brain processing makes it possible to learn (see Section 5.1), inhibit, and regulate emo-
tional responses [6]. Emotions are then purposefulbecause they aim to prepare the
body to respond to situations that have occurred repeatedly throughout evolution [4].
On the whole, these features reveal the essential functions of emotions, namely [7]:
Coordination: Emotions coordinate organs and tissues, thus predisposing the
body to peculiar responses (see Section 2).
Signaling: Although the central nervous system (CNS) maintains the faculty of
control (e.g., inhibition), coordination activities facilitate the production of
distinctive behavioral responses and expressive signals of the individuals current
emotional state (see Section 3).
Information: The CNS interprets and evaluates emotional episodes. That allows
individuals to partly consciously perceive emotions, learn from them, and direct
behaviors (see Section 4).
2. Coordination
One of the first scientists to define the nature of emotions was probably William
James. Until then, the prevalent idea was that situations evoke emotions that, in turn,
trigger bodily changes. James instead claimed that bodily changes follow directly the
PERCEPTION of the exciting fact, and that our feeling of the same changes as they
occur IS the emotion(pp. 189190) [8]. The Danish psychologist Lange developed
similar concepts in the same period. Therefore, today, scholars refer to this idea as the
James-Lange theory. Sensory systems send data about the current situation to the
central nervous system. Subsequently, the CNS induces physiological changes (e.g.,
heartbeat and muscle tone). The following feeling of these changes is the emotion. In
other words, there is no emotion without physiological changes. It seemed a counter-
intuitive thesis even then. Nevertheless, several scholars accepted the James-Lange
theory [9].
Some years later, Walter Bradford Cannon falsified Jamess idea. He considered
that stopping sensory sensitivity would impair the central perception of physiological
changes, thereby eliminating emotions. Thus, Cannon resected the animalsspinal
cords. Results suggested that surgically operated individuals still felt emotions,
though. Furthermore, it seemed the same physiological changes accompanied various
emotions. Cannon concluded that emotions disturb the activity of the autonomic
nervous system (ANS) [10], and Philip Bard enriched this view. In brief, this hypoth-
esis (i.e., the Cannon-Bard theory) [9] is an all-or-noneapproach with only two
autonomic patterns: non-activated versus diffusely activated [5].
Neither theory has disappeared over the years. Indeed, they have led to two
contrasting approaches.
First, nonstate theories and general arousal models suggest the inexistence of
specific internal states of emotions [11]. The two-factor theory [12], the component
process model [13], and other hypotheses [14] reach the same conclusion. Empirical
evidence does not support the idea that emotions have specific ANS patterns. Part
of the data instead suggests that undifferentiated arousal accompanies emotional
experiences [3]. Something in the body happens, but are the people who label
it as an emotional experience (e.g., fear, joy, and sadness) [15]. Therefore,
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Neurophysiology
proponents of these theories (i.e., cognitive models) claim that emotions result from
brain activity [5].
The second approach supports the existence of discrete emotions, each one char-
acterized by specific neurophysiological and behavioral routines. In this case, scholars
usually view emotions as an adaptive mechanism, a product of evolution [4]. Charles
Darwin was probably the first to search for the cause of expressions [16]. Subse-
quently, several scientists focused on the link between emotions, autonomic activity,
and behavioral responses (e.g., facial expressions) [17]. Proponents of this functional-
evolutionary approach claim the existence of different emotions associated with bio-
behavioral layouts [5].
There is a lively debate still today. In particular, scholars did not reach a consensus
on the existence of emotion-specific response patterns. One explanation for this dia-
tribe lies in the methodological challenges the study of emotions entails. Individual
differences (e.g., emotion recognition skills), the choice of elicitor (e.g., there is no
certainty that a given stimulus elicits a given emotion in people), indicators (e.g., a
continuous recording of different physiological and behavioral measures) [5], and
statistical methods are among these [18].
Despite the issues, data support the hypothesis of specific response patterns for
distinct subtypes of emotions [3]. For example, in rodents, different types of fear
correspond to independent neural substrates [19]. Indeed, emotional families are sets
of states that share elicitors (see Section 5), autonomic patterns, expressions, and
behavioral reactions [17]. The neural substrates of emotional subtypes facilitate
different behavioral responses. As an illustration, consider the Fight Flight Freeze
System [20]:
The flight depends on norepinephrine activity from the locus coeruleus.
Moreover, the amygdaloid complex (Amg) activates periaqueductal gray and
brainstem autonomic nuclei.
The fight has its neurobiological basis in the hypothalamic-pituitary-adrenal axis
(HPA). In particular, the release of cortisol stimulates gluconeogenesis (i.e., the
conversion of substrates into glucose) and glycogenesis (i.e., glycogen synthesis).
That provides fuel for metabolism and activates the sympathetic division of the
autonomic nervous system [21].
Freezing also relies on a specific neural network. In brief, the central nucleus of
the amygdala has connections to the lateral hypothalamus (i.e., which mediates
autonomic sympathetic responses), medullar nuclei (i.e., that control
parasympathetic response), and the ventrolateral periaqueductal gray [22].
3. Signaling
The bodily activity that occurs with emotions has a high signaling value. For
example, organs and tissues, as well as the nervous system, can signal emotional
states [20].
Furthermore, emotions and motor activation often correlate. That can affect the
striated muscles of the neck, back, arms, or the smooth muscles of the blood vessels and
alimentary tract. Similarly, facial muscles can also be part of the emotion [23]. All these
activities can be expressions, namely, distinctive signals of emotional episodes [6].
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However, emotions are not the only determinants of bodily signals. In particular,
contextual and cognitive factors make it challenging to distinguish expressions from
cues attributable to other causes. Individual differences (e.g., age, gender and learn-
ing) are often decisive in expression regulation. Indeed, the nervous system (e.g.,
premotor cortex and primary motor cortex) has the flexibility to adjust actions already
planned to the current situation [9]. That means individuals can generally inhibit,
mask, or even simulate expressions [6].
In brief, emotional signals can belong to three macro categories. First, verbal
behavior refers to emotional expression through natural-historical languages. The
second category, nonverbal behavior (NVB), concerns any type of action except the
use of words. Gestures, gait, and posture are examples of NVB. Although facial
expressions also fall into this category, they will be examined separately, given their
significance to humans. Finally, autonomic activity can produce external manifesta-
tions (neurovegetative signals) interpretable as expressions (e.g., pupil diameter, heart
rate, and breathing).
3.1 Verbal behavior
Voice and speech are the two components of the act of speaking. The voice
features are pitch, volume, intensity, and rhythm. Instead, speech is the content of
discourses. It includes vocabulary, grammar style, and structure [24].
Humans can use verbal behavior to express emotions [25]. Speaking is a faculty
that recruits several anatomical structures: cerebral regions (e.g., the frontal lobe) [9]
and the digestive and respiratory systems (e.g., lungs, larynx, sinus cavities of the
vocal tract, palate, tongue, and teeth) [26]. Noteworthy, dysfunction of the frontal
lobe is one of the determinants of alexithymia, a condition that involves among other
things, difficulty or inability to verbalize emotions [27]. However, a vast cerebral
network underpins verbal expression of emotion. The right inferior frontal cortex, the
right posterior superior temporal cortex, the left mid-fusiform gyrus, the right inferior
prefrontal and bilateral fusiform cortices, and the amygdaloid complex are part of this
network [25].
3.2 Nonverbal behavior
Behavioral responses can be emotional clues. For example, gait (e.g., arm swing,
length, and speed of stride) can reveal whether an individual is happy, sad, or angry
[28]. Furthermore, the emotional state can influence posture (i.e., the position of the
body or its parts) [29], produce acoustic signals, such as laughter [30], and alter the
sound of voice (e.g., pitch, intensity, and tension) [31].
However, humans can voluntarily signal and fake emotional states through their
bodies (e.g., facial expressions, gestures, and posture) [30]. Birds also have this
ability. For example, the wild fork-tailed drongos (Dicrurus adsimilis) produce false
mimicked alarm calls that scare meerkats (Suricata suricatta). Thereby, these birds
steal meerkatsfood [32].
It is unclear whether emotional expression management relies on a single
neurocognitive system. The intentional inhibition of human motor responses depends,
at least in part, on the activation of the right inferior frontal cortex (rIFC). Indeed, the
activity of the rIFC is often associated with the deactivation of other brain regions
important for emotions, such as the amygdaloid complex [33].
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Neurophysiology
3.3 Facial expressions
The face is informative in several ways. For example, humans get clues about
peoples health through skin color [34]. Nonetheless, the main source of information is
the activity of the facial muscles. Their contraction, in specific combinations, pro-
duces skin movements, namely, facial expressions. Moreover, they assume complex
patterns according to the movement of the head and eyes.
The muscles of the face include two large groups. First, the mastication muscles (i.e.,
temporalis, masseter, and pterygoid muscles) have the primary task of moving the
jaws and chewing. However, they can even participate in emotional expression. It is
the trigeminal nerve that innervates these muscles (Figure 1).
The expressive or mimetic muscles are the second group. The facial nerve innervates
these muscles. Indeed, their function is to configure the expression of the face. The
temporofacial division of this nerve connects the muscles of the upper part of the face
to both cerebral hemispheres. Instead, the cervicofacial facial nerve links the lower
face only to the contralateral hemisphere (Figure 2).
The cerebral cortex controls voluntary movements through the corticospinal (or
pyramidal) tract [23]. Two-thirds of this tract receives input from the motor cortex
and the rest from the somatosensory areas, such as the parietal lobe [9]. For these
reasons, emotional facial expressions seem to depend on the other trait, the extrapy-
ramidal one.
The right side of the face could be dominant for emotional expressions. That is the
idea of some scholars, based on some clinical evidence. For example, several people
show a left bias during posed expressions [23]. Nevertheless, the empirical results are
ambiguous, and academic speculations are divergent [35]. For instance, the approach-
withdrawal model hypothesizes that emotions of approach(e.g., joy) coincide with
more activity of the left frontal brain, and the withdrawalones (e.g., fear) activate
the right frontal brain to a superior extent [36].
Moreover, humans can exhibit brief, local contractions (i.e., microexpressions).
Their duration varies from about 40 to 335 ms [37]. Microexpressions mainly involve
Figure 1.
Schematic representation of the motor pathways of mastication.
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the upper face muscles (e.g., the frontalis) and occur unconsciously, at least in part.
Indeed, it is the extrapyramidal tract that mediates their production [23]. However,
their alleged unintentional nature has stretched their informative potential. In partic-
ular, several scholars believe that microexpressions are reliable signals of spontaneous
emotions and lies. For example, law enforcement and airport security use
microexpressions as lie-detecting clues. All this despite the experimental data being
inconclusive and practical applications ineffective [38]. However, microexpressions
could be functional in other fields (e.g., to survey the quality of the patient-therapist
relationship) [39]. Noteworthy, only a few microexpressions seem unmanageable. For
example, the eyebrow flash and contempt expression are more controllable [38].
Although the prototypical patterns are well known, there is a low coherence
between facial displays and emotions. Specifically, the likelihood of a person showing
an expression (e.g., the Duchenne smile) when feeling the corresponding emotion
(e.g., joy) is often lower than chance, in the both laboratory [40] and naturalistic
settings [41]. One of the determinants of this low emotion-expression coherence lies
in display rules. In brief, they are laws of expression management based on various
factors (e.g., context, roles, gender, and age). Learning these rules usually takes place
in the first years of life. Thereby, humans learn to repeat, amplify, and inhibit the
expression of emotions [42]. It is the cerebral cortex that mediates the voluntary
inhibition of facial movements [23].
3.4 Neurovegetative signals
Despite limitations and still open questions, there are enough data to state that
physiological changes accompany emotions (see Section 2).
Activities of the autonomic nervous system can induce appearance variations. For
example, vasodilation can cause blood vessels to bulge and alter the color of the skin.
Blushing (i.e., in embarrassment) and reddering (e.g., in anger) are two typical
neurovegetative signals of an increase in the caliber of blood vessels. Conversely,
vasoconstriction (e.g., in fear) produces blanching.
The body can also secrete various substances. For example, tear glands provoke
crying [43] related to some types of sadness [44]. Similarly, the sweat glands produce
Figure 2.
Schematic representation of the pathways of human facial expressive muscles.
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Neurophysiology
sweat (e.g., in fear), and the salivary ones are responsible for the secretion of saliva,
which is typical of certain emotional states, such as disgust and anger.
Other neurovegetative signals are piloerection and the change in pupil diameter.
They can be cues to emotions (e.g., anger and fear) or other states (e.g., sexual
appetite) [43].
At the central level, these ANS activities are outcomes of a neural network that
involves the hypothalamus (Hy), which is essential for homeostasis. The Hy links with
periaqueductal gray, the reticular formation, parabrachial nucleus, ventral tegmental
area (VTA), and the raphe nuclei [45].
4. Information
Rather than describing the whole emotional process, the James-Lange theory
focuses on the emotional experience, namely, what the individual perceives of
emotion [11].
In particular, emotional experiences consist of mental representations that can relate
to different aspects of emotions. First, the individual can perceive, even if only
partially, arousal [46]. The central nervous system processes the information it
retrieves from the bodys activity. For example, reactions, such as wrinkles, blushing,
and tearing are all signals, that potentially influence the perception of emotions [47].
Indeed, autonomic feedback (e.g., from sweating and respiration) is another essential
feature of the emotional experience [48]. The second aspect is about the relational
content (e.g., mental representations of dominance and submission). Third, the situ-
ational content is an integral part of the emotional experience. For example, people
often link psychological situations to their emotions.
The elements of the emotional experience concern the appraisal, at least in part
[46]. In brief, it consists of the cognitive assessments (e.g., of valence) accompanying
emotions (e.g., positive or negative) [48]. According to the cognitive approach,
the appraisal is necessary to elicit emotions, and it can also occur quickly and
involuntarily [49].
The neurophysiological basis of emotional experience may rely on two distinct
networks. A first circuit seems to allow value-based representation. The essential
brain regions of this network are the basolateral amygdala (BLA), the anterior insula,
and the orbitofrontal cortex (OFC). In particular, the BLA provides an initial assess-
ment of a stimulus. The anterior insula instead allows the representation of intero-
ceptive inputs. Finally, the OFC makes processing more flexible by including
information regarding the context. BLA and OFC are interconnected with each other,
as well as have connections with the cortical regions responsible for sensory repre-
sentations. The second circuit of emotional experience seems to be a sort of affective
working memory that holds and processes emotive information for short periods. Its
neurophysiological basis lies in the amygdaloid complex and the reciprocal connec-
tions between the prefrontal cortex (PFC) and the anterior cingulate cortex [46].
5. Elicitors of emotions
An emotional episode begins through exposure to stimuli with specific features.
For example, loss causes sadness [50]. In this sense, emotion is a process, and these
stimuli (i.e., elicitors) are the inputs that initiate it.
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Animals learn to feel certain emotions in specific situations. However, it is not just
environmental cues that trigger an emotional episode. The state of the organism,
behavior, and other complex faculties (e.g., thoughts and empathy) can be elicitors too.
5.1 Learning
Stimuli internal and external to the body can become elicitors of emotion through
classical and operant conditioning. In particular, animals learn to associate a stimulus
(S) with a specific emotional response (R). With an S-R association established,
exposure to S may be sufficient to elicit the emotional response.
Yet, S-R associations can take complex forms. For instance, emotional reactions
can even be self-reinforcing. An individual may experience a pleasant state that elicits
behavior, which fuels repetition in a sort of loop [51]. However, the S-R associability is
not absolute. For example, it seems impossible to teach a hungry pigeon to fly away by
presenting it with food [52].
At the basis of emotional learning is a vast neural network that includes the reward
system. Its architecture is complex and involves circuits for the cost/benefit assess-
ment of specific reward values, reward expectations, and action selection (Figure 3).
The amygdaloid complex and ventral striatum (vStr) underpin the appetitive
Figure 3.
Schematic representation of reward system. One: cost/benefit assessment of specific reward value. Two: cortical
loop. Three: limbic loop. Four: reward expectation. Five: action selection. Six: go and stop processes. Abbreviations:
Amg, Amygdaloid complex; DA, dopamine; dlPFC, dorsolateral prefrontal cortex; dStr, dorsal striatum; GP,
globus pallidus; Hip, hippocampus; OFC, orbitofrontal cortex; SNc, substantia nigra pars compacta; SNr,
substantia nigra pars reticulata; STN, subthalamic nucleus; vStr, ventral striatum; VTA, ventral tegmental area.
This article was published in [53] Copyright Elsevier (2020).
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Neurophysiology
processing of reward expectations. Moreover, dopamine (DA) pathways modulate
motivation and behavior by connecting the ventral tegmental area, the substantia
nigra pars compacta (SNc), and the striatum. The reward system is also capable of
inhibiting the behavior. Specifically, five sub-circuits (or sub-loops) of the basal
ganglia (BG) are essential for various functions, including action cancelation [53].
5.2 Expressions
Even emotional signals (see Section 3) can be elicitors. For example, breathing
[54], vocalizations [55], and postures [56] may elicit emotions. Indeed, some experi-
ments suggest that an expansive pose lowers cortisol and increases testosterone levels.
That would be enough to produce feelings of power and increase risk tolerance [57].
However, attempts to replicate such data have failed [58].
In general, peripheral feedback theories propose the idea that emotional expressions
can become elicitors [56]. For example, facial expressions could trigger emotions.
According to this idea (i.e., the facial feedback hypothesis), movements of the face
influence the release of some neurotransmitters, thus acting as an elicitor [59]. There-
fore, feedback theories follow the path traced by the James-Lange theory (see Section 2).
Observing signals and behaviors in others can also initiate the emotional process.
In this sense, indirect experience (e.g., imitation and emotional contagion) is a poten-
tial elicitor of emotion. The anterior insula and the rostral cingulate cortex are part of
the neural network responsible for these mechanisms [60].
5.3 Empathy
Empathy consists of the emotional states produced by observation of individuals
and situations. Thus, it is an elicitor of emotion per se. Scholars usually distinguish
between cognitive empathy (CE) and emotional empathy (EE). The CE deals with
mental perspective-taking, mentalizing, and the theory of mind. Instead, EE consists
of the vicarious sharing of emotions [61].
The resulting emotion may be the same as that of the observed individual, but not
necessarily. Indeed, the emotional experience can be so intense as to produce an
empathic overarousal, which often induces disengagement [62]. That happens, for
example, to paramedics who, being exposed to traumatic events, adopt coping strate-
gies, such as emotional detachment [63]. In other cases, emotions felt may be diverse
from those observed. That is the case of Schadenfreude (i.e., the pleasure caused by the
misfortune of others) [64].
Given the complexity of empathy as a faculty, it seems clear that its neurobiolog-
ical basis is equally complex. For example, its neural substrate includes the insula,
cingulate cortex, and the interoceptive network [65]. Furthermore, empathic
responses probably depend on various processes (e.g., emotional contagion and affec-
tive mentalizing) that underpin distinct neural mechanisms. The temporoparietal
junction, medial temporal lobe, prefrontal cortex, and dopamine pathways are part of
the circuits of cognitive empathy. Instead, the neural substrates of emotional empathy
include the frontal gyrus, insula, anterior cingulated cortex, and oxytocin paths [66].
5.4 Sign stimuli
Animals can feel emotions even when exposed to stimuli they have never encoun-
tered. For instance, the smell of predators they have never seen before scares rats [67].
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Some scholars claim that humans also have innate fears (e.g., snakes) [68]. However,
experimental results are controversial [69].
Several animals can respond to limited aspects of the environment (i.e., sign stimuli),
ignoring the rest [70]. The common toad (Bufo bufo) produces defensive responses
(e.g., stiff-legged) when faced with relatively simple perceptual patterns (dummies)
with specific configurational features reminiscent of their predators (i.e., snakes) [71].
Moreover, newborn babies prefer and imitate human face schematizations (i.e., facelike
patterns)[72].
From a neurobiological point of view, it is unlikely that there are cells in the
nervous system specialized in innately identifying specific stimuli. The determinants
of any sign stimuli as elicitors could lie, then, in the biological predisposition [52].
6. Outcomes
Emotions influence several processes, including [4]:
Perception: Emotional states can magnify some perceptual aspects to the
detriment of others. For instance, afraid-of-falling people overestimate the
steepness of hills [73].
Attention: According to a theoretical approach, the central nervous system
allocates more cognitive resources to selective attention and vigilance under the
influence of negative emotions. Instead, positive ones spread these resources.
That hypothesis (i.e., broaden-and-build theory) [74] is subject to debate,
however [75]; in this sense, each emotion may have selective effects on
attentional performance [76].
Learning: Emotions heighten some mnemonic aspects at the expense of others.
In particular, several factors (e.g., personality and age) define the enhancement
and impairment of learning due to emotional influences [77].
Memory: Considering their relationship with attention and learning, it seems
logical that emotions influence memory. The flashbulb memory (i.e., the vivid
remembering of details of when a person learned about a specific dramatic event)
is an excellent example of this [78].
Decision making: Emotions impact the evaluation and interpretation processes.
For example, sadness may lead people to overestimate difficulties [2].
Attitudes and mental schemes: Some emotional episodes can shape attitudes,
mentalities, and values. For instance, awe produces overwhelming and elevating
experiences that strengthen the sense of unity. In particular, those who
experience emotional experiences of this type usually develop a new vision of life
and the universe [79].
The neurophysiological basis of the relationship between emotions and cognitive pro-
cesses is not yet fully understood. In brief, neurophysiological superimposition of emotions
and other mechanisms may underpin emotional outcomes. For example, amygdala, hip-
pocampus, and orbitofrontal cortex have a role in several neural functions [80].
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Neurophysiology
7. Emotional and mood disorders
Some emotion-based symptoms may appear in various conditions, such as schizo-
phrenia (e.g., anhedonia), borderline personality disorder (e.g., emotional instabil-
ity), addiction (e.g., euphoria and dysphoria), and so on. These conditions can be
related to several features of emotions, such as intensity, frequency, adaptivity, phys-
iology, expression, and experience [81]. However, some scholars disagree with placing
these disorders in the same category. Indeed there is the risk of generalizing qualita-
tively diverse states (e.g., emotions, moods, and affect) [7].
Several scholars use the term emotional disturbanceto refer to psychopathologies
that include emotion-related symptoms, such as regulation problems, phobias, spe-
cific deficits (e.g., lack of empathy), and so on [81]. It is challenging to briefly
delineate the etiology of these emotion-related psychopathologies. In brief, there are
hereditary, epigenetic, developmental, environmental, and behavioral determinants.
From a neurophysiological point of view, emotion disturbances usually result from
cerebral peculiar functioning. Indeed, the bases of such conditions often include
inefficient reuptake [82], irregularities in synaptic proteins, and neuronal density
[83]. Even social activities (e.g., play) can influence the development of these brain
mechanisms and shape cerebral maturation [84]. These factors can influence the
functioning of a vast neural network that includes the prefrontal cortex, limbic sys-
tem, striatum, thalamus, and brainstem [83].
8. Conclusions
Albeit limitations [5], the literature suggests that emotions predispose the body to
timely recognition and response to specific circumstances. Situations identify ancestral
problems, and the responses illustrate the solutions that have proved most profitable for
evolutionary success [4]. In this sense, the emotional process has as its central themes the
bodys coordination [5], the signaling of the individuals state [17], and the processing by
the central nervous system of both endogenous and exogenous information [46].
The literature does not allow a conclusive illustration of the neurophysiology of
emotions. Nevertheless, each emotional subtype likely has its patterns [3]. It seems
then better to speak of families rather than single emotions [17].
Due to several factors, the emotional process affects performance in different
domains (e.g., perception and attention). These factors include the partial overlap of
the neural basis of emotion and other faculties and the numerous brain interconnec-
tions. Furthermore, elicitors are heterogeneous and even include the essential ele-
ments of emotion (e.g., expressions). That suggests the nonlinearity of the emotional
process. In other words, emotions could have stochastic or aleatory progress: In
probabilistic terms, each element can initiate, be a part of, or be their outcome [7].
Conflict of interest
The authors declare no conflict of interest.
Thanks
Thanks to every enthusiast, scholar, and researcher who came before me. Thanks
to those who deal with emotions today, and to those who will do so in the future.
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Everyones contribution is a step forward in the path of knowledge. Thanks to every
reader, without whom the effort of writing this chapter would have been futile.
Ideologies separate us, and emotions bring us together.
Abbreviations
Amg amygdaloid complex
ANS autonomic nervous system
BG basal ganglia
BLA basolateral amygdala
CE cognitive empathy
CNS central nervous system
DA dopamine
dlPFC dorsolateral prefrontal cortex
dStr dorsal striatum
EE emotional empathy
GP globus pallidus
Hip hippocampus
Hy hypothalamus
HPA hypothalamic-pituitary-adrenal axis
NVB nonverbal behavior
OFC orbitofrontal cortex
PFC prefrontal cortex
rIFC right inferior frontal cortex
SNc substania nigra pars compacta
STN subthalamic nucleus
vStr ventral striatum
VTA ventral tegmental area
Author details
Maurizio Oggiano
European Mind and Metabolism Association, Via Valtellina, Rome, Italy
*Address all correspondence to: maurizio.oggiano.79@gmail.com
© 2022 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of
the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0),
which permits unrestricted use, distribution, and reproduction in any medium, provided
the original work is properly cited.
12
Neurophysiology
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We often assume that the autonomic nervous system (ANS) sends genuine signals of emotions. Nonetheless, people can misunderstand autonomic cues (e.g., blinking, pallor, blushing, salivation, sweating). These responses are usually the outcome of multiple factors. The ANS tasks go beyond homeostasis: other tasks are predisposition to specific actions, delivery of signals for social purposes, and monitoring digestive processes. These functions are not entirely independent of central control. Indeed, several brain regions (e.g., the hypothalamus, the amygdaloid complex, and the insular cortex) and neurotransmitters (e.g., dopamine) can exert some influence on autonomic activity.
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A considerable amount of research has investigated the effect of emotion on visual attention. One prominent model in the field is the broaden-and-build theory, which suggests positive emotions broaden the scope of attention. In addition, the theory proposes positive emotions increase the amount of resources available to a person, which can thus accumulate to enhance life skills and well being. However, while there is evidence to support this theory, other research has critiqued certain aspects of the model. Some studies propose that the methods used to investigate the broaden-and-build theory do not accurately measure the broadening of attention, while others highlight that a broadening of attentional resources is not always advantageous. Moreover, evidence has shown that different types of positive and negative emotions impact differently on the scope of attention. This paper will discuss the different aspects of research in the area, and explore the influence of emotion on the spread of visual attention.
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Sadness is characterized by raised inner eyebrows, lowered corners of the mouth, reduced walking speed and slumped posture. Ancient subcortical circuitry provides a neuroanatomical foundation, extending from dorsal periaqueductal grey to subgenual anterior cingulate, the latter of which is now a treatment target in disorders of sadness. Sadness is often context dependent, yet electrophysiological studies emphasise a role for reduced left relative to right frontal asymmetry in sadness, fueling interest in the transcranial stimulation of left dorsolateral prefrontal cortex as an antidepressant target. Neuroimaging studies – including meta-analyses – indicate that sadness is associated with reduced cortical activation, which may contribute to reduced inhibitory control over medullary cardioacceleratory circuits. Increased stress system activity including reduced parasympathetic cardiac control may – in part – contribute to epidemiological reports of reduced life expectancy in affective disorders, effects equivalent to heavy smoking. We suggest that the field may be moving toward a theoretical consensus, in which different models may be considered as complementary, working at different levels of phylogenetic hierarchy.
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Introduction: The significance of psychotherapeutic micro-processes, such as nonverbal facial expressions and relationship quality, is widely known, yet hitherto has not been investigated satisfactorily. In this exploratory study, we aim to examine the occurrence of micro-processes during psychotherapeutic treatment sessions, specifically facial micro-expressions, in order to shed light on their impact on psychotherapeutic interactions and patient-clinician relationships. Methods: In analyzing 22 video recordings of psychiatric interviews in a routine/acute psychiatric care unit of Vienna General Hospital, we were able to investigate clinicians' and patients' facial micro-expressions in conjunction with verbal interactions and types. To this end, we employed the Emotion Facial Action Coding System (EmFACS)-assessing the action units and microexpressions-and the Psychodynamic Intervention List (PIL). Also, the Working Alliance Inventory (WAI), assessed after each session by both patients and clinicians, provided information on the subjective quality of the clinician-patient relationship. Results: We found that interpretative/confrontative interventions are associated with displays of contempt from both therapists and patients. Interestingly, displays of contempt also correlated with higher WAI scores. We propose that these seemingly contradictory results may be a consequence of the complexity of affects and the interplay of primary and secondary emotions with intervention type. Conclusion: Interpretation, confrontation, and working through contemptuous microexpressions are major elements to the adequate control major pathoplastic elements. Affect-cognitive interplay is an important mediator in the working alliance.
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The p-value has long been the figurehead of statistical analysis in biology, but its position is under threat. p is now widely recognized as providing quite limited information about our data, and as being easily misinterpreted. Many biologists are aware of p's frailties, but less clear about how they might change the way they analyse their data in response. This article highlights and summarizes four broad statistical approaches that augment or replace the p-value, and that are relatively straightforward to apply. First, you can augment your p-value with information about how confident you are in it, how likely it is that you will get a similar p-value in a replicate study, or the probability that a statistically significant finding is in fact a false positive. Second, you can enhance the information provided by frequentist statistics with a focus on effect sizes and a quantified confidence that those effect sizes are accurate. Third, you can augment or substitute p-values with the Bayes factor to inform on the relative levels of evidence for the null and alternative hypotheses; this approach is particularly appropriate for studies where you wish to keep collecting data until clear evidence for or against your hypothesis has accrued. Finally, specifically where you are using multiple variables to predict an outcome through model building, Akaike information criteria can take the place of the p-value, providing quantified information on what model is best. Hopefully, this quick-and-easy guide to some simple yet powerful statistical options will support biologists in adopting new approaches where they feel that the p-value alone is not doing their data justice.
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Dopamine is essential to many functions like reward, motivation, and attention; when its neural pathways do not function properly, various disorders (e.g., anxiety, depression, hyperactivity, compulsions) can arise. Truncated-DAT rats display persistent stereotypies and aggressiveness; hence they are a new valuable animal model to study the pathogenesis of these disorders. The focus of research is often on the individual epigenetic determinants and much less on the impact of social experiences. Here, we investigate the developmental impact of the social environment on adolescent wild type (WT) rats. We divided subjects at weaning into three groups: living with another adolescent (WT Peer), with a WT adult, or with a truncated-DAT one, and we observed homecage social behavior of these pairs (play, jump, victory, and "bullying") during whole adolescence. When adult, we observed the same subjects in plus maze, forced swim, and social preference tests to measure levels of anxiety, depression, and quality of social interactions. Compared to the other groups, WT rats that had spent their adolescence with a truncated-DAT adult as companion show more anxious, depressive, hyperactive, impulsive, and compulsive behaviours. Results confirm that social interactions and healthy play (i.e., when play has behavioural, social, and psychomotor rewards that support the cognitive, emotional and physical development of the individual) are essential to neurobehavioral maturation. Conversely, anomalous interactions like poor play and "bullying" in developing rats may impact onto their dopaminergic system. Consequently, an impoverished social play could be one of the factors contributing to the appearance of putative indexes of attention deficit hyperactivity disorder (ADHD) and obsessive-compulsive disorder (OCD), such as depression, hyperactivity, impulsive behavior, compulsive behavior, and anxiety.
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The Naples High Excitability (NHE) is a validated rat strain to model for a mesocortical variant of Attention Deficit Hyperactivity Disorder (ADHD). NHE rats' brains have a tuned-down cortical and a potentiated limbic loop (Zoratto et al. 2017). ADHD and comorbid pathological gambling (PG) involve similar deficits of prefrontal-striatal dialogue. This work aimed to understand if NHE rats (compared to normal random-bred rats, NRB) can be a useful model for gambling vulnerability in ADHD. Experiment 1 evaluated gambling proneness in NHE rats, namely attraction/avoidance in nose-poking for a "Large & Luck-Linked" (LLL) reward (versus a "Small & Sure" one, SS), when the probability of LLL delivery was progressively reduced. Experiment 2 assessed (by phMRI) differential responsivity of ventral (vStr) versus dorsal (dStr) striatum following a methylphenidate (MPH, 4 mg/kg IV) challenge. In NHE rats, reduced attraction by secondary cues (associated with uncertain, intermittent, rarefying LLL delivery) comes along with little or no activation of dStr and enhanced activation of vStr by MPH. Together, such evidences from NHE rats indicate distinctive roles of ventral (enhanced value given to actual primary reward) and dorsal (lower encoding of repeated stimulus-reward associations into a habit) striatum. In conclusion, the dynamics of reward systems could link an attention deficit with a decreased vulnerability to pathological gambling.