9 Emotion 04/02/2014
S.M. was a young patient who lived a normal life but started having what appeared to be seizures;
however, brain scans revealed severe bilateral atrophy in her amygdala.
S.M. had an autosomal recessive genetic disorder, called UrbachWiethe disease.
This disease causes an accumulation of glycoprotein calcium in the medial temporal lobe, leading to the
degeneration of the amygdalae.
S.M. also had no other structural abnormalities, making this condition highly specific.
S.M. had normal intelligence, no perceptual or motor problems, but she only had the specific lack of
emotional knowledge in terms of fear.
In neurological assessment batteries, S.M. had to distinguish emotions in faces, however, she could
accurately describe every emotion except fear.
If shown a fearful face, she would report some other emotion.
Researchers though she was unable to process the concept of fear, but she was able to describe situations
that would elicit fear, and used words describing fear properly, and could label fearful prosody (fearful
S.M. was found to not be able to create a picture that depicted fear (she drew a baby crawling), but she
could depict every other emotion.
A Freudian might say this was a fearful experience from her childhood, but she could not say why she
Two lessons can be learned from a study of S.M.
The amygdala must play a critical role in the identification of facial expressions of fear.
This is not surprising since the amygdala was previously known to do other forms of emotional processing.
The fact that people could fail to comprehend one emotion with little impairment in their other emotions
helped inspire new views in thinking about the neural bases of emotion.
THE COGNITIVE NEUROSCIENCE OF EMOTION
The cognitive neuroscience of emotion has been slow to emerge because emotion is a behavior that is
difficult to study systematically. Issues in the Cognitive Neuroscience of Emotion
In an effort to apply some order and uniformity to the definition of emotion, researchers have focused on
two primary categories of emotion.
Basic emotions, as seen trough facial expression.
Dimensions of emotions, seen as reactions to events.
One of them ore recent attempts to characterize basic emotions examined the universality of facial
Paul Ekman of the University of California, San Francisco, studied cultures around the world, and found that
the means by which emotion is conveyed does not vary from culture to culture.
From his work, him and others suggested that anger, fear, disgust, happiness, sadness and surprise are the
six basic emotions.
Most people agree on the idea that there are basic, universal human emotions.
Basic emotions such as fear and rage have largely been confirmed in animals, which show dedicated
subcortical circuitry for these emotions.
Thus, scientists have adopted this notion of basic emotion in order to investigate emotional states, and
neural systems underlying it, as well as the developmental basis of facial expression and evaluation.
DIMENSIONS OF EMOTION
Another way to approach the categorization of emotion is to describe them as reactions to events in the
world that vary along a continuum, and not as discrete states.
For example, we could be happy finding a penny on the sidewalk, or winning 10 million dollars on the
lottery, even though the feeling is the same, the intensity is different.
One type of dimensional approach to categorization proposes that emotional reactions to stimuli and events
can be characterized by two factors: valence (pleasant—unpleasant or good—bad) and arousal (the
intensity of the internal emotional response, high—low.
A second dimensional approach is to characterize emotions by the actions and goals they motivate. Richard Davidson and colleagues (1990) at the University of Wisconsin—Madison suggested that different
emotional reactions or states can motivate us either to approach or withdraw from a situation.
Happiness may excite a tendency to approach, and disgust or anger may motivate us to withdraw.
No consensus has been reached on how to define emotion, so researchers must be clear in their results.
NEURAL SYSTEMS IN EMOTIONAL PROCESSING
Early Concepts: The Limbic System
One goal of cognitive neuroscience research is to identify and understand the neural systems underlying
different emotional states and processes.
The notion of a network of brain structures is not new.
In 1937, James Papez proposed a circuit theory of the brain and emotion, suggesting that emotional
responses involve a network of brain regions, including the hypothalamus, anterior thalamus, cingulate
gyrus, and hippocampus.
Paul MacLean (1949,1952) later described these structures as the Papez circuit, and included the
amygdala, orbitofrontal cortex, and portions of the basal ganglia (calling this inclusion the limbic system).
The structures of the limbic system roughly form a ring around the corpus callosum.
Although several of the limbic structures are known to play a role in emotion, it has been impossible to
determine criteria for defining which structures and pathways should be included in the limbic system.
Classic limbic areas such as the hippocampus, have also been shown to be more important for other, non
Thus, MacLean’s concept seems less functional in the current understanding of the neural basis of
Early attempts to identify neural circuits of emotion tended to view emotion as a unitary concept that could
be localized to one specific circuit, separating the emotional brain from the rest of the brain.
Research now focuses on specific types of emotional tasks and on identifying then neural systems
underlying specific emotional behaviors. Depending on the emotional task or situation, we can expect different neural systems to be involved.
The amygdala is a small, almondshaped structure in the medial temporal lobe adjacent to the anterior
portion of the hippocampus.
Structures in the medial temporal lobe were first proposed to be important for emotion in the early 20
century, when Heinrich Klüver and Paul Bucy at the University of Chicago (1939) documented unusual
emotional responses in monkeys following damage to this region.
The observed deficit was psychic blindness, with a prominent characteristic being a lack of fear,
characterized by a tendency to approach objects that would normally elicit a fear response.
In the 1950s, the amygdala was finally thought to be the primary structure in the monkey’s fear deficits, in
what is now called Klüver–Bucy syndrome.
The amygdala has now become a focus on research in emotional processing in the brain.
Humans with Klüver–Bucy syndrome, only show, as S.M. demonstrates, more subtle deficits in fear
IMPLICIT EMOTIONAL LEARNING
Recall the introductory story of the young man.
Although the young man in the story could first not be able to consciously identify the party guest as the
fellow commuter, when the party guest started talking to him, his emotional response indicated that he had
some memory of this person.
He showed signs of physiological arousal that left him feeling uneasy and nervous, indicating that the
image of his fellow commuter/party guest was linked to the train on that fateful day and the aversive
consequences of the accident.
This type of learning, in which a neutral; stimulus acquires aversive properties by virtue of being paired with
an aversive event is called fear conditioning, which is a form of classical conditioning in which the
unconditioned stimulus is aversive.
One advantage of the fearconditioning paradigm to investigate emotional learning is that it works
essentially the same across a wide range of species.
This paradigm applies to rats, in which a rat receives training to have a conditioned startle response to a
light, by pairing the flash of a light with a shock. Once the rat is conditioned to react to the light with a startle response, another natural stimulus occurs that
creates a startle response as well, like a loud sound, with the light, causing a potentiated startle (amplified
Damage to the amygdala impairs conditioned fear responses, but lesions to the amygdala do not usually
block the unconditioned response to an aversive event, showing that the amygdala is not needed to exhibit
a fear response.
Thus, damage to the amygdala blocks the ability to acquire and express a conditioned response to the
neutral conditioned stimulus that is paired with the aversive unconditioned stimulus.
Using the fear conditioning paradigm, researchers fond that the amygdala consists of several nuclei.
The lateral nucleus of the amygdala serves of a convergence area for information from multiple brain
regions, allowing for the formation of associations underlying fear conditioning.
The lateral nucleus then projects to the central nucleus of the amygdala.
Projections to the central nucleus initiate an emotional response if a stimulus, after being analyzed and
placed in the appropriate context is determined to represent something threatening or potentially
An important aspect of the circuitry of fear conditioning is that information about a unconditioned stimulus or
a conditioned stimulus can reach the amygdala through two separate and simultaneous pathways.
One is sometimes called he low road (quick but dirty).
This is a subcortical pathway in which sensory information about a stimulus projects to the thalamus, which
in turn sends a signal directly to the amygdala.
The thalamus does not produce a sophisticated analysis of sensory information, but it sends a crude signal
to the amygdala indicating whether this stimulus roughly resembles the conditioned stimulus.
The low road allows for the amygdala to receive information quickly in order to prime, or ready the
amygdala so it can respond right away, if the information from the high road confirms that the sensory
stimulus is the conditioned stimulus.
At the same time sensory information about the stimulus is being projected to the amygdala via another
cortical pathway, sometimes referred to the high road.
The sensory information analysis is more thorough and complete.
The sensory information projects to the thalamus, then it moves to the sensory cortex for a finer analysis.
The sensory cortex projects the results of this analysis to the amygdala.
The role of the amygdala in learning to respond to stimuli that have come to represent aversive events
through fear conditioning is said to be implicit. It is referred to as implicit because the learning is expressed indirectly through a behavioral or physiological
response, such as autonomic nervous system arousal or potentiated startle.
Although patients with amygdala damage fail to demonstrate an indirect conditioned response, when they
are asked to report the parameters of fear conditioning explicitly or consciously, they demonstrate no deficit
(intact latter ability).
This concept was shown in patient S.P., who has bilateral amygdalar damage.
Her right half was removed but her left half was already damaged, and she could not recognize fear in the
faces of others like S.M.
She probably had mesial temporal sclerosis, causing neuronal loss in the medial temporal regions of the
Much like the rats who were getting fear conditioned, S.M. was attempted to be fear conditioned to a blue
She showed a normal fear response to the shock, but not when the blue square was presented, meaning
she failed to acquire a conditioned response.