Congratulations. Now that you've reached Chapter 6, you may be happy to learn that it's mostly down hill from here. The previous chapter on mood represents the heaviest lifting in this book. This is because the human PFC, which processes mood, is the seat of almost everything that makes us animals uniquely human. As such, that region of the brain is the greatest contributor toward human personality — the subject of this book.
The present chapter deals with fear. When speaking of fear and the brain, the star of the show for all vertebrates is the amygdala. Moreover, processing fear seems to be by far the predominant role of this brain region. So whereas the previous chapter ranged well beyond mood, this chapter, more or less, huddles close to fear.
The other reason this chapter is lighter than the previous one is that the research on amygdala asymmetry is more straightforward. Recall that the previous chapter lacked even a single study directly finding optimism/pessimism to be the core model of PFC asymmetry in emotion. Due to this absence, the previous chapter painstakingly cobbled together this model from a range of authorities.
In this chapter, the central model holds that aware fear and unaware fear are mediated by left and right amygdala, respectively. In support of this model, this chapter presents a relatively compelling (and circa the present, un-contradicted) study directly on this point.
However, on the question of persistent individual differences regarding asymmetry, the research in this chapter is far less developed than it was in the previous chapter. The best the current amygdala research can do on this question is to suggest provocative clues.
So take heart. If the previous chapter bogged you down, the present one should roll along.
What Mr. Davidson is to the study of mood and the PFC, Mr. LeDoux seems to be to the study of fear and the amygdala. In addition to his myriad papers, Mr. LeDoux has published two recent, leading books in his field of specialty: The Emotional Brain and Synaptic Self. The first book confines its analysis pretty much to the amygdala and fear. The second book extends the work of the first book, addressing subjects beyond the amygdala and fear.
Although Mr. LeDoux has focused his research on rats, rather than humans, that research has served as the principal foundation for much of the human amygdala research. This reliance on the rat research appears valid because the newer brain technologies — PET and fMRI — have "been very successful in showing that many of the basic fear conditioning observations in animals apply equally to the human brain."[1] In fact, all vertebrates (reptiles, birds, and mammals) have an amygdala.[2]
The principle function of the amygdala is the mediation of fear. But as Mr. LeDoux makes clear, the amygdala plays the lead role in the unconscious processing of fear,[3] rather than in the conscious experience of fear:
[E]motion can be defined as the process by which the brain determines or computes the value of a stimulus. Other aspects of emotion then follow from this computation. First, emotional reactions occur. These overt bodily responses and associated changes in internal body physiology are the advance guard of emotional responsivity. Subsequently (at least in humans), a feeling emerges as we become aware that our brain has determined that something important is present and we are reacting to it.[4]
In the preceding paragraph, Mr. LeDoux defined "emotion" to concern the unconscious processing of fear — the domain of the amygdala. He used the term "feeling" to refer to the conscious experience of it — the domain of the PFC. Moreover, he makes clear that feeling follows emotion.
With Mr. LeDoux's seminal work serving as a touchstone, a mountain of research has grown in recent years concerning the human amygdala. Attempting to make some sense of this explosion in the volume of published papers, some researchers have recently published reviews of this emerging field. One such review is by M. Davis and P.J. Whalen[5], and another by David H. Zald[6]. These reviews serve as excellent starting points for diving into the field.
One point these reviews make clear is that the amygdala processes not only aversive, negative stimuli. While that seems to be its dominant function, the amygdala also seems to play some role in the processing of certain attractive, positive stimuli.[7] Evidence for this latter function is relatively scant, albeit persistent. It seems that experimentally inducing this positive effect is difficult to achieve consistently. Still, some patterns seem to be emerging here. Positive stimuli for which amygdala activation has been observed include:
viewing cocaine paraphernalia by a cocaine addict[8]
viewing pornography by males[9]
smelling food by hungry subjects[10]
Although this "positive valence" research is scant compared with the "negative valence" research, it does serve a crucial function. It serves to illuminate the amygdala as a fundamental tool of survival. It is a tool that scans the environment and identifies potential punishments and rewards. Apparently, the amygdala is the common seat of both fear and desire.
Notice, however, that the amygdala does not process the experience of reward/pleasure or of punishment/pain. That function is left to the pain/pleasure centers of our brain. Those centers register the actual "ouch!" or "aaah" sensations that we feel. The amygdala serves instead to recognize situations in which big "ouches" and certain "aaahs" are likely to arise.[11]
For the most part, this chapter confines its focus to the voluminous fear/punishment branch of amygdala research, and leaves aside the scant research on the amygdala's role with respect to desire/reward. However, in Part Three, this latter research will be re-introduced in a discussion on the interaction between the amygdala and PFC, and how that interaction may give rise to personality.
But for now, there is much to be discussed concerning the amygdala and fear. The discussion begins with the observation that the amygdala progresses through five principal stages in response to aversive stimuli. These stages are:
1. Implicit learning
2. Recognition
3. Expression
4. Termination
5. Habituation
The process begins with the experience of pain (or expected pain). Upon this experience, implicit learning is the process through which the amygdala associates surrounding stimuli with the pain. At a later time, when the same or sufficiently similar stimuli reappear, recognition occurs — i.e. the amygdala recognizes the stimuli as ones harkening pain. Once recognition has been made, the amygdala engages in expression by "sounding an alarm" within the body. With this alarm ringing, termination involves deactivating the amygdala in the case that the alarm proves false. Finally, after a number of such false alarms, habituation is the process through which the amygdala "unlearns" the association between the stimuli and pain. The following five sections walk through these five stages of amygdala processing in greater detail.
## Morris (2002) -- PAF
## Adolphs (2001)
## Buchanan/Adolphs (2001)
## Dolan (2002)
Implicit learning is the subconscious association of perceived stimuli with experienced pain. In this definition, there are three relevant concepts: subconscious, association, and perception.
On the issue of perception, Mr. LeDoux's research on the mammalian brain[12] reveals a "high road" and a "low road" of information traveling to the amygdala. The low road ferries stimuli registered by passive perception (see Chapter 5) directly to the amygdala. Specifically, the low road reaches the amygdala via the nearby thalamus. The thalamus serves as a sort of crossroads for sensory stimuli. That is, sensations of sight, sound, taste, touch, and smell all make their way from the sensory organs to the thalamus. From there, these sensations are relayed to different regions of the brain. One such region is the amygdala.
Mr. LeDoux discovered the low road through his research on rats. In 1999, other researchers discovered the same low road in humans.[13] Those researchers used "subliminal" stimuli of which the subjects were subconsciously aware, but not consciously aware. Mr. LeDoux explains:
[The researchers] asked which brain areas seemed changed in a way that would indicate connectivity with the amygdala. They found that across the whole brain amygdala activity during conditioning was most directly related to activity in subcortical visual processing areas, including an area of the visual thalamus. Particularly significant was the fact the amygdala activity was not at all related to activity in the area of the visual cortex. This finding thus indicates that unconscious emotional learning occurs through the path from visual sensory areas of the thalamus to the amygdala. The low road is indeed used in both the rat and human brain (emphasis added).[14]
Apparently, we all have more than a little bit of rat in us.
The high road is a path between the PFC and the amygdala. Via this path, the PFC sends processed stimuli to the amygdala.
So the amygdala perceives stimuli through at least two different sources: directly via the passive perception low road; and indirectly and in a pre-processed form via the PFC high road.[15] Mr. LeDoux says that the low road provides "quick and dirty" information to the amygdala. The high road, in contrast, provides "slower but accurate" information.
The second concept at issue here is association. With the stimuli perceived by the amygdala via the low road, the job of the amygdala is to associate that stimuli with the experienced pain, and facilitate the recording of that association in memory. But since the low road ferries "quick and dirty" information, the association is broad and crude.
Mr. LeDoux offers an example of a person walking down a
street.[16]
Suddenly, a dog races out from a side yard and bites the person. The bite is
painful. The person's amygdala will associate not only that particular dog with
pain, but it may also associate many other
circumstances surrounding the painful situation — including sights, smells,
sounds, tactile sensations, and emotional states, both directly concerning the
painful stimulus and generally concerning the environment. For example, the
next time the person turns the corner to walk down that same block, he may feel
his heart jump even if doesn't see the dog. Or the next time he sees any dog,
his heart may jump, even though that dog is different from the biting dog. The point here is that the amygdala
casts a wide net around the circumstances surrounding pain.
The third issue here is the subconscious nature of association.[17] This means that implicit learning
happens outside of our conscious awareness. Via the amygdala, we learn things
we don't even know we are learning.
This is the case even for the high
road from the PFC to the amygdala. Recall that the PFC consciously processes
stimuli. The high road ferries this consciously processed stimuli to the
amygdala. Although that aspect is conscious, the subconscious aspect comes in
when the amygdala implicitly learns that the stimuli harkens pain. Moreover, as
we'll see below, the initiation of amygdala expression is also a subconscious
dynamic.
This suggests that we humans are
about much more than simply what goes on inside our conscious minds.
With implicit learning having drawn an association between
pain and certain stimuli, the amygdala is now ready to recognize those stimuli
should they arise again in the future. With
recognition, the amygdala says: "Hey, isn't that stimulus the same one I
perceived earlier during that painful time?"
Interestingly, the amygdala is more prone to recognize ambiguous stimuli, than unambiguous stimuli.[18] The notion here is that while the amygdala is trying to recognize certain stimuli that it previously associated with pain, it is especially alert to ambiguous stimuli that only might turn out to be that certain stimuli. The amygdala says: "I'm treating that squiggly thing on the ground as a snake" (even though it might turn out to be only a curved stick). Notice that this heightened activation for ambiguous stimuli highlights our common experience with scary movies. The scariest movies are not the ones in which the frightening presence is displayed in detail. The scariest ones are those in which the door handle is turning but we don't know for sure whether that harkens the frightening presence.
Footnotes: [## AMG mediates
perception - tells us what to look at; Dolan (2002) at 1192; better memory goes
to survival, at 1192; AMG used for both learning and remembering fearful
events, at 1193]
Once the amygdala has recognized certain stimuli as ones associated with pain, the amygdala activates, sounding an alarm bell to which expression responds.[19] Mr. Davidson describes this "alarm bell" function as follows:
Extant evidence is consistent with the argument that the amygdala is critical for recruiting and coordinating cortical arousal and vigilant attention for optimizing sensory and perceptual processing of stimuli associated with undetermined contingencies, such as novel, "surprising" or "ambiguous" stimuli [citations omitted].[20]
Stated another way, amygdala
activation sounds an alarm, and sends that alarm upstream, toward the rest of
the brain, and downstream, toward the body. The purpose of the upstream signal
is to marshal the brain's attention on the ambiguous stimuli.[21]
The
purpose of the downstream signal is to mobilize the body for action —
specifically, for fight or flight. "Expression" refers to this heightened
response of mind and body.
Think of being jolted awake in the
middle of the night by a sound, our heart pounding. In that circumstance, we
are experiencing amygdala expression. Our hearing has become acute, registering
every squeak. Our attention has become rapt; our entire mind focused on the
disturbance.[22] Although we conclude there is no danger, we still have
difficulty getting back to sleep. In the coming days and even years later, we
may retain a vivid memory of that disturbance.[23]
But these are just the powerful effects on our mind. In our bodies, not only is
our heart thumping, our palms have become moist. And these are just the bodily
effects we notice. There are others that we don't even notice.
This process is automatic; its
initiation is subconscious. While implicit learning and recognition
involve learning, expression is simply part of the human condition. We don't learn amygdala expression.[24] As Mr. LeDoux explains:
We don't have to learn to freeze or raise blood pressure in the presence of dangerous stimuli, for the brain is programmed by evolution to do these things. We have to learn what to be afraid of, but not how to act afraid.[25]
The preceding discussion describes "loud" episodes of amygdala expression. But the amygdala is capable of initiating "quieter" expressions too. Like all brain regions, the amygdala depends for its activation on blood flow. Blood flow can vary in terms of both rate and duration. These variances modulate the degree and duration of amygdala activation, and thus expression.
With mind and body on high alert due to amygdala expression, a mechanism is needed for calming things down if the excitement turns out to be a false alarm (or, at least, if the ambiguities have been resolved). This mechanism is "termination". Termination involves deactivating the amygdala. Research suggests that the high road from the PFC is critical to termination. Mr. LeDoux explains:
[Research] suggests that the prefrontal cortex and amygdala are reciprocally related. That is, in order for the amygdala to respond to fear reactions, the prefrontal region has to be shut down. By the same logic, when the prefrontal region is active, the amygdala would be inhibited, making it harder to express fear.[26]
Consistent with this, recent studies with humans have shown that a conscious effort to reduce a negative mood dampens activity in the amygdala.[27] Recall that consciousness appears to do its work within working memory of the PFC. So during scary movies, telling us ourselves "it's only a movie, it's only a movie," actually does work.
Repeated "false alarms" tend to result in amygdala habituation. Habituation is the flip-side of the amygdala's propensity to react to novel or ambiguous stimuli. That is, after repeated exposure to the novel or ambiguous stimuli, the novelty has worn off, and the ambiguity has been resolved. Thus, the subject has become "habituated" to the stimulus, and the amygdala does not activate.
Habituation would tend to throw a wrench into amygdala studies. The point of any study is to demonstrate a phenomenon through repeatable experiment. But repetition is the trigger for habituation. Yet some degree of repetition is needed because the amygdala of some subjects activates in response to the experimental setup alone. That is, with amygdala experiments, subjects place their heads inside of large, imposing PET and/or fMRI machines. This makes some people nervous, which results from their amygdala activating.
So the subtle challenge for the researcher is to get the subject's amygdala to habituate to the experimental setup before recording the activation sought in the experiment. But that activation must be recorded before the amygdala habituates to the experimental stimulus. Add to this pressure the large expense of PET and fMRI testing environments, and as of this writing, amygdala research would seem to amount to the mythical challenge of sailing between Scylla and Charybdis.
The preceding five sections canvassed the five principal stages of amygdala activation: implicit learning, recognition, expression, termination, and habituation. Mr. Davidson has encouraged a rigorous, systematic approach to studying individual differences with respect to these stages. He has used different terms — "affective chronometry", "affective reactivity", and "affective style" — to refer to various aspects of this approach. Roughly speaking, this approach seeks to record attributes such as how "touchy" a subject is, how high his "stack blows", and how long it takes him to "get over it". These factors contribute plenty to our personalities. Common experience tells us that different people score differently on these measures. However, as of this writing, I am unaware of researchers following this promising suggestion of Mr. Davidson.
Up to this point in this chapter, the discussion has treated the amygdala as a single brain region. Actually, just as with the PFC, there are two sides to this region. For the next few sections, this chapter will focus on the differences between the left and right amygdala.
Concerning asymmetry, there are two key questions:
1. What is the functional difference between left and right?
2. Do individuals exhibit persistent patterns of asymmetric dominance?
In the previous chapter concerning the PFC, the answers to these questions were, respectively, optimism/pessimism, and "yes". On the second question, research revealed some subjects to be lefties, others righties, and still others as middies.
Concerning the amygdala, the second question is still unresolved. When it comes to amygdala activation, are some people lefties, others righties, and still others middies? As of this writing, the field of neuroscience offered no direct answer to this question. Still, as the following discussion indicates, the research seems to suggest that the answer is "probably".
But first, the next section addresses the first question. Presently, it appears there is a reasonably solid answer to the question of functional asymmetry in the amygdala. That answer is: aware fear versus unaware fear.
In 2003, researchers Jan Glaescher of Hamburg, Germany, and Ralph Adolphs of Iowa published a study entitled Processing of the Arousal of Subliminal and Supraliminal Emotional Stimuli by the Human Amygdala.[28] A primary conclusion arising from this study is that the left amygdala mediates aware fear, while the right mediates unaware fear. The authors themselves describe their conclusion as follows:
[This study] suggest[s] different and complementary roles for the left and right amygdala in the processing of emotional stimuli. Whereas the right amygdala seems to provide an overall level of physiological arousal in response to stimuli (Davidson et al., 1992), the left amygdala provides the better discrimination between different magnitudes of arousal. ... There might be an initial, perhaps automatic and relatively undifferentiated emotional, reaction that is mediated by the right amygdala, followed by a more differentiated emotional reaction that discriminates differences in arousal magnitude mediated by the left amygdala.[29]
Although this paragraph refers to a left/right dichotomy of "differentiated"/"undifferentiated", this section explains how that formulation gives rise to the aware/unaware dichotomy.
In their experiment, the researchers studied four types of subjects:
8 brain-damaged subjects with a left amygdala, but no right amygdala (the "Only Left" subjects);
12 brain-damaged subjects with a right amygdala, but no left amygdala (the "Only Right" subjects);
3 brain-damaged subjects lacking both amygdale (the "Neither" subjects); and
38 normal people with both amygdalae intact (the "Normal" subjects).
The study focused on the recognition and expression stages of amygdala processing. Specifically, the researchers presented certain stimuli to the subjects in order to trigger amygdala recognition. Then they recorded certain effects of the resulting amygdala expression. They did not employ an implicit learning phase, nor did they test for amygdala termination or habituation[30].
The stimuli used in the study comprised various pictures. [31] The pictures were selected to cover a wide range of arousal potential. They were classified into the following categories: nudes, threat, mutilation, household, sad scenes, sweet foods, neutral scenes, and babies/animals.
These stimuli were presented to the subjects in supraliminal mode, as well as subliminal mode. [32] The difference between the two modes depended upon how long the particular picture was presented to the subject. Subliminal mode was achieved by presenting the pictures for only 30 milliseconds, followed by a second picture presented for 2 seconds. Most subjects did not consciously perceive the subliminal pictures. But in the few cases that they did, the researchers threw out that data in order to keep their results clean.
In addition to this supraliminal/subliminal dichotomy, the researchers also varied the presentation of pictures along the lines of left versus right hemisphere.[33] Recall from Chapter 5 that our left eye feeds light to our right hemisphere, while our right eye serves the left hemisphere. So, by displaying a picture only to, say, the right eye, the researchers were able to discern what was happening in the left hemisphere.
As you can see, the study was highly complex. It involved different kinds of subjects, different kinds of pictures, supraliminal vs. subliminal presentation, and left versus right presentation. All of this complexity allowed the researchers to tease out just what the left amygdala was doing, and what the right was doing, during recognition and expression.
For assessing what the "amygdala was doing", the researchers recorded a certain form of amygdala expression known as skin conductance response (SCR).[34] SCR refers to the ability of the skin to transmit electricity. It is well known in the field that amygdala activation increases SCR level. In fact, the higher the activation, the higher the SCR level.
In addition to SCR, the researchers recorded self-report data.[35] Self-report involves a subject reporting what he or she believes to be going on in his or her own mind. This study polled different kinds of self-report. The kind that is of particular interest here is level of arousal. That is, subjects were asked to rate how arousing they found each picture to be.
SCR served to indicate how aroused each subject actually had become. Self-report, on the other hand, served to indicate how aroused each subject thought he or she had become. Comparing what had actually happened with what the subjects thought had happened was the particularly elegant maneuver of this study.[36] Had the researchers relied solely on self-report, they would have had no way of knowing whether the subjects were reporting accurately or not. Similarly, had the researchers relied on SCR alone, they would have had no way of knowing whether the subjects were aware of their own arousal. But by comparing these two sets of data — self report and SCR — the researchers revealed the level of awareness in the subjects.
In the study, the researchers found that the Normal subjects and the Only Right subjects showed the highest level of amygdala expression.[37] That is, they showed the highest SCR to the emotional stimuli (e.g. nudes, threat, mutilation). In comparison, the SCR of the Only Left subjects was significantly muted, and SCR for the Neither subjects was negligible. This meant that, among all subjects, the Normal and Only Right subjects were actually aroused the most. In fact, the researchers found that the mean arousal level of the Only Right subjects was slightly higher than even that of the Normal subjects.
But when the researchers obtained self-report data from the subjects, it turned out that the Only Right subjects rated their arousal level the lowest among all four types of subjects.[38] So the Only Right subjects were actually aroused the most, but they thought they were aroused the least. This powerfully and elegantly suggests that the right amygdala surpasses the left in generating amygdala expression, but is relatively lax in helping consciousness to become aware of that amygdala expression.
The researchers found the reverse pattern for the left amygdala. This finding relied on the left versus right presentation aspect of the study. The researchers found that the Normal subjects were able to accurately report their actual level of arousal only when the stimuli were presented to their left hemispheres.[39] This was true whether the stimuli were presented in supraliminal mode or subliminal mode. It didn't matter so long as the stimuli were available to the left side. But when the stimuli were presented to the right side, the Normal subjects joined the brain- damaged subjects in their inability to correctly report their arousal level. This, together with the SCR results, suggests that the left amygdala surpasses the right in helping consciousness to become aware of our amygdala expression, but trails the right in generating amygdala expression.
How the left amygdala helps consciousness is suggested by the performance of the Only Left subjects. Recall from above that the SCR response for these subjects was significantly muted compared to the response of Normal and Only Right subjects. Despite this muted somatic response, the Only Left subjects performed better than did the Only Right and Neither subjects in reporting their actual arousal level.[40] Still, the Only Left subjects were not quite as accurate in doing so as were the Normal subjects.
This suggests that, in reporting what they believed to be their arousal level, consciousness of the Only Left subjects had some information that was unavailable to the Only Right and Neither subjects, but it was missing some additional information that the Normal subjects had. It follows from the nature of this study that the available information was left amygdala recognition, and that the missing information was right amygdala expression. The following discussion explains this.
The left amygdalae of both Normal and Only Left subjects obtained visual information about the stimuli via both the high road (supraliminal presentation) and the low road (subliminal presentation). This enabled left amygdala recognition. Since both the Only Right and Neither subjects were missing left amygdalae, they were missing left amygdala recognition.
However, the left amygdalae of the Normal subjects also received additional information not available to the Only Left subjects. This additional information was the somatic response that resulted from expression of the right amygdala. Recall that amygdala expression involves effects such as increased heart rate, increased attention, and elevated SCR. These effects comprise additional information available to the left amygdalae of the Normal subjects. This information was not available to the Only Left subjects. This would explain why they didn't perform as well as the Normal subjects on self-report. And even though this somatic response information might have been available to the right amygdalae of Only Right subjects, it does not appear that the right amygdala uses this information to inform consciousness.
The final element of the story concerns the valence ratings by the subjects. In addition to self-report on arousal, subjects reported on how positive or negative they found the pictures to be. The study found that all four kinds of subjects performed similarly on the valence rating task. So it doesn't appear that either amygdala plays a role with respect to awareness of the positive or negative aspect of stimuli. It would seem that other parts of the brain perform this function.
Summing up, the Glascher/Adolphs study found that, in general:
the right amygdala surpasses the left amygdala in generating a subconscious fear response; but
the left surpasses the right in informing consciousness as to the existence and level of fear; and
neither amygdala is required for awareness of the valence of stimuli.
The first finding was not necessarily new. Other researchers had suggested the same thing. But the second finding — left versus right amygdala activation parallels aware versus unaware fear — was new. This new finding was made possible by the elegant comparison maneuver described above. This maneuver positioned the Glascher/Adolphs study in an emerging special class of neuroscience research.
The Glascher/Adolphs study lines up nicely against a persistent, emerging theme in neuroscience. This theme concerns the relative prominence of subjective processing, compared with objective processing. This theme has previously emerged in the fields of PFC asymmetry in cognition and PFC asymmetry in emotion.
Recall from Chapter 5 that the dominant model of left/right PFC asymmetry in cognition depends upon the conscious field of the subject. With this subjective field defined, meaning accrues to notions like global versus local, whole versus parts, analytical versus holistic. But shift the subjective conscious field, and the meanings of these dichotomies shift as well.
For example, consider the word "example" in this sentence. Is that word text or context? The answer depends on your conscious field. If you were looking at the word "example" in the context of the sentence or the paragraph, then it would be text. But if you were focusing solely on that word, it would be context and the letters of the word (i.e. e-x-a-m-p-l-e) would be text.
Now ask a second person to look at that same word. In the conscious field of that second person, "example" could be text, whereas in your conscious field it could be context. The point here is that is asymmetry in cognition does not depend upon objective stimuli. Rather, it depends entirely upon subjective processing of the objective stimuli.
A similar pattern was observed with respect to left/right PFC asymmetry in emotion. Chapter 5 concluded that the sensitivity model concerning optimism and pessimism was correct. This subjective theory was contrasted with the objective valence theory. The latter theory ascribed objective positive or negative attributes to stimuli and argued that left versus right PFC tracked these objective attributes. But recent research has rejected this objective notion in favor of a subjective notion. Neuroscience is now saying that one subject's reward can be another's punishment, and that the same stimuli presented to the same subject can be perceived as a reward one moment, and as a punishment the next.
This finding emerged through comparing the responses of subjects to two stimuli that differed with respect to their reward/punishment potential.[41] When the researchers studied responses to any single stimuli, the PFC asymmetry data remained silent. But when the researchers compared responses to one stimuli with responses to the preceding stimuli, that same data suddenly spoke up. It said: "optimism and pessimism distinguishes left from right PFC in emotion."
This same subjective dynamic exists here in Chapter 6 with the Glascher/Adolphs study. That study found awareness emerging from certain amygdala asymmetry data. That finding emerged from comparing two different data points: how the subjects actually responded, and how the subjects said they responded. The comparison of these two measures revealed subjective "awareness" as a core metric differentiating the function of the left amygdala from that of the right.
Note that it is entirely consistent with the Glascher/Adolphs model for some normal subjects to respond to stimuli with a relatively high level of amygdala activation (i.e. relatively jumpy people), while others respond with a relatively low level (i.e. relatively calm people). Despite these objective differences, the model says that the left amygdalae of all subjects will contribute more toward subjective awareness of that level, while the right amygdalae will contribute more toward generation of that subjective level.
Similarly, it is entirely possible under the Glascher/Adolphs model that given any stimuli, for some people, their left amygdala is more prone to respond, for others, it is their right amygdala, and for still others, it is both. But despite these objective differences, the model says that the left, if it does activate, will serve to assist subjective consciousness, while the right, if it does activate, will generate a subjective response without assisting consciousness.
Note further that these three subjective metrics defining asymmetry of cognition, asymmetry of mood, and asymmetry of fear, all place the "observer" in the paramount position. That is, in all three areas of research, the objective stimuli of the experiment is not nearly as important as the subjective perception of that stimuli by the subject (the "observer"). This subjective property seems to line up neuroscience rather nicely with the branch of physics known as "quantum mechanics".
Almost a century ago, led by the work of men like Albert Einstein, Werner Heisenberg, and Neils Bohr, physicists discovered that what we perceive as objective reality is actually a subjective illusion. That is, the common-sense notion that we are merely passive observers of the world around us was proven false decades ago. Still, until recently, statements like this made sense only in the domain of arcane mathematics applied to subatomic workings. But with the emergence of PET and fMRI, neuroscientists are now able to probe the depths of the human mind. And their findings are beginning to hint at these astonishing revelations of quantum mechanics. The skit from Monty Python and the Holy Grail could well have been the following:
Bridge Keeper: What
is the airspeed velocity of reality?
King Arthur: What
do you mean? Your reality or mine?
Bridge Keeper: I
don't know that.
(The Bridge Keeper is catapulted into the Gorge of Death)
The subjective nature of the Glascher/Adolphs model contrasts it with the vast bulk of recent research on amygdala asymmetry. A 2004 study[42] performed a comprehensive review of this research. Specifically, this study reviewed 54 papers that reported activation of left and right amygdale separately. Forty-six of these 54 papers were published since 2001. So this review provides a current understanding of this highly active field.
The authors of this review analyzed the 54 papers with respect to the models of amygdala asymmetry proposed by them. The authors identified four classes of models being pursued in these papers. In these classes, amygdala asymmetry depended upon:
1. stimulus type (pictorial versus verbal stimuli);
2. elaborate processing (plenty of thinking required versus little or no thinking);
3. task instructions (explicit versus implicit instructions); or
4. habituation as a function of stimulus nature (variety in stimuli versus same kind of stimuli)
Notice that all four of these classes describe objective models. That is, under each of the classes, asymmetric amygdala activation is presumed to be a function of objective factors residing outside of the subjective self-appraisal of the subjects.
The authors of this review found that the 54 papers supported none of these classes. Thus, as of this writing, there exists no generally accepted objective model of amygdala asymmetry. It would seem that, generally speaking, the field of amygdala asymmetry is presently barking up the wrong tree.
As for the subjective findings of the 2003 Glascher/Adolphs study, the 54 amygdala asymmetry papers neither support nor contradict them. This is because these papers looked for objective responses whereas Glascher/Adolphs found subjective perception. Toward the end of the 2004 review, the authors called for further study of the Glascher/Adolphs model. The authors stated that the collective findings of the 54 papers "remain[] inconclusive" concerning this model. Accordingly, it's too soon for the Glascher/Adolphs model to be considered "generally accepted."
To assess whether this model is valid, a study must, at a minimum, record and report amygdala activation data at an individual level. Second, for each individual, it must compare conscious self report against somatic response. Of the dozens of amygdala asymmetry papers I have found on the Internet, none, besides the Glascher/Adolphs paper, perform these two procedures.
I did, however, find two papers that satisfied only the first criterion. That is, they recorded and reported amygdala activation data at an individual level. The first study, conducted in 2001, reported that:
... 11 of 12 subjects showed significant activity in the left amygdala. ... Although the group composite revealed left amygdala activity, the pattern of amygdala response varied somewhat across individuals, and 7 of 12 individuals showed less extensive but significant right amygdala activation.[43]
Assuming that the one subject out of 12 who did not show significant activity in the left amygdala did show significant activity in the right, the above results can be equivalently described as: 1 out of 12 with right activation, 5 out of 12 with left activation, and 6 out of 12 with activation of both left and right.
The second study, conducted in 2002, looked for differences between men and women with respect to asymmetric amygdala activation. The study reported:
The reported left-lateralized amygdala memory correlations were seen in 72% of the [12] women and reported right-lateralized correlations in 50% of the [12] men, with the remaining subjects exhibiting very minor to modest lateralization in the opposite direction.[44]
Another way of saying this is the following: 9 women and 6 men showed relative left activation; 3 women and 6 men showed relative right activation.
Whatever the researchers in these two studies were trying to show, one thing they did show was that, presented the same stimuli and given the same instructions, individuals can demonstrate different patterns of asymmetric amygdala activation. This is certainly consistent with the Glascher/Adolphs model.
I anticipate that, in the future, more researchers will continue to report asymmetric amygdala activation at an individual level. Further, consistent with the Glascher/Adolphs model, these researchers will probe the righties for their conscious awareness of arousal, as compared with that of the lefties and middies.
The previous chapter explained that it is settled science that individuals differ according to persistent patterns of asymmetric PFC activation. When it comes to the PFC, some people are righties, others lefties, and still others middies.
But as of this writing, I am unaware of any analogous direct findings in the amygdala asymmetry research. To my knowledge, no one has yet set out to show that, when it comes to amygdala activation, some people are righties, others lefties, and still others "bothies."
Still, the research offers provocative suggestions that this is indeed the case. First, as the previous section showed, studies that report amygdala activation at an individual level have reported different patterns of amygdala activation (left, right, or both) among different individuals despite the identical stimuli and instructions.
Second, the 2004 review of the 54 amygdala asymmetry papers also supports this provocative suggestion. Recall that that review found that no proposed objective model of amygdala asymmetry was supported by the research as a whole.
Yet most of these studies did in fact report dominant patterns of activation — whether that pattern was left, right, or both. This means that different studies using the same kind of stimuli or same kind of experimental procedure each reported a pattern, but collectively, the patterns conflicted. This suggests that the subjects for different studies differed, in the aggregate, according to dominant patterns of amygdala asymmetry. That is, some studies seemed to have used subjects who, in the aggregate, tended to be lefties, while other studies used subjects tending to be righties or bothies.
But this is more speculation than firm conclusion. The most that can be said at present about trait amygdala asymmetry is: "probably".
Up until now, this chapter has discussed research that mostly concerns physical fear or desire. For example, as stimuli, some fear studies used angry faces; others used pictures of mutilations. Similarly, desire studies used pictures of nudes, the smell of food, and cocaine paraphernalia. All of these studies can be said to have mined the amygdala's role in mediating physical fear and desire. But the amygdala also responds to social stimuli.
For example, the stimuli in a 1999 study[45] consisted of displayed "neutral" and "threat" words. The study reported amygdala activation in response to the threat words. In addition to words with a physical aspect (e.g. "molest", "kill", "mutilate"), the threat words also included notions of a predominantly social nature. These social words included "blame", "distrust", "opposition", "disturb", "betrayal", "conspiracy", "deceive", "corruption", "suspicion", "follow", "intrude", "conspire", and "stare". In a repressive totalitarian regime, these words could well evoke physical fear. But in present-day America, these words would more likely evoke only social fear.
Similarly, Mr. Davidson mentioned[46] a 2000 amygdala study[47] that used money as the stimuli. The study reported amygdala activation upon the winning and losing of money. Except for the indigent, the prospect of winning and losing money is a matter of pure social desire and fear.
So the amygdala seems to mediate social fear as well as physical fear.
In the previous chapter, we saw that there was a difference between left and right PFC with respect to physical health. Specifically, right PFC dominance, in contrast with left PFC dominance, is associated with a dampened immune system.
As for the amygdala, there appears to be no significant distinction between left and right amygdala concerning physical health. Presently, it is believed that either or both amygdalae have roughly the same impact on physical health. That impact arises from the "fight or flight" state that amygdala expression induces.
Is this state positive or negative regarding our physical health? The answer is: It depends. It depends on whether that bump in the night is evidence of a violent home intruder, or just a creak in an old house. In the former case, the "fight or flight" responses initiated by amygdala expression just might save our lives. Certainly, the home intruder scenario seems to be among the favorite of the gun lobby in America. Whenever such a scenario does occur, rare though it is, we are sure to see it on the nightly news.
Of course, for every such home invasion scenario in the nation, there are probably at least millions of "false alarm" harmless creaks in the night. In those cases, our sleep is ruined. But this scenario describes just one sleepless night. If this "false alarm" persists every night, we can soon find ourselves quite ill.
This is because amygdala
expression is a relatively "expensive" operation within our bodies. It is expensive because it consumes
substantial resources and expends significant energy. Moreover, it shuts down
other systems critical to our long-term health, in particular, the immune
system.
Amygdala expression achieves these
effects through the release of hormones like adrenalin and cortisol. The
amygdala itself doesn't release these hormones. But it initiates a cascade of
signals that make their way to the organs that release these hormones.
Recall from the previous chapter that cortisol acts to shut down the immune system. [##SS at 223] Adrenaline serves to raise the heart rate and elevate blood pressure. Chronically weakened immune systems and chronically elevated blood pressure are believed by many to be key factors over the past century in the prevalence of degenerative disease (e.g. heart disease, cancer, stroke) in America.
In sum, activation of either or both left and right amygdala is detrimental to our long-term health. Of course, this long-term detriment is the price we pay for short-term survival. Yet in an age when, for most Americans, the risk of violent death is relatively remote, one may well ask whether this short-term benefit is worth the cost.
## Davis (2000): detail on AMG nuclei
Currently, there seems to be very little data on the role that genes play in amygdala activation. This includes questions of asymmetric dominance, as well as "affective chronometry". This is not surprising given that current evidence of trait amygdala asymmetry is scant. If trait asymmetry is still an open question, genetic bases for these unproven traits are naturally further off.
But when neuroscience does get around it, I predict that the field will find what it seems to be finding concerning the genetic basis of trait PFC asymmetry. Namely, I expect that these traits will be found to be established, at latest, in early childhood.
## gene for R AMG; Hariri (2002)
With the PFC, the issue of plasticity concerns whether patterns of asymmetric dominance can be changed. In other words, can the brains of lefties learn to use their right PFC more? Can the brains of righties change to increase left PFC activation?
Since both left and right PFC are intimately involved in consciousness, the thrust of the plasticity literature concerns activating both sides of the PFC, rather than in decreasing activity in one side or the other. The reverse pattern is the case for the amygdala.
The previous section discussed the negative physical health implications of amygdala over-activity. The next chapter discusses some negative mental health implications of this over-activity. These negative implications concern both left and right amygdala. So the plasticity question regarding the amygdala is: Can amygdala activation be decreased? The current answer is the literature is "yes, but ...".
Some of the "but" part arises from the finding that the experiences of early childhood seem to play a significant role concerning amygdala activation.
## mom rat licking & grooming, Francis & Meaney, 1999; see Davidson (2003) at 662
## Teicher (2002): effect of childhood abuse on AMG
These findings concerning early childhood have significant implications for all of us. This is because memories of our own experiences that occurred before the age of three our four are usually quite vague to us at best. So few if any of us possess direct knowledge whether, when we were toddlers, we were sufficiently "licked and groomed" by our own caregivers. If we hadn't been, and our amygdala is therefore frequently over-active, we might not be aware of that. This is because amygdala activation is an unconscious process, and if the experience of an over-active amygdala is all we've ever known since before memory, then that might serve as what we perceive as reality.
Being unaware that our own reality does not accord with the reality perceived by others, or with objective reality (if such a thing exists), we inevitably run into health problems — mental and/or physical. When those problems grow big enough, we visit doctors — mental and/or physical. And some us patients end up being subjects of the neuroscience studies cited by this book.
## overcoming our fears
## Field (1998)
## Davidson/Jackson (2000)
## neurogenesis in adult animal hippocampus, see Davidson (2003) at 662
## but can't just cut out the amygdala
One implication of the automatic nature of amygdala expression is the conclusion that (natural) therapies for settling down an over-active amygdala work upstream of the amygdala, not downstream. That is, such therapies seek to have the amygdala unlearn the overbroad pain associations, and relearn more narrow and accurate associations. The idea is to encourage the amygdala to forego firing when firing is unnecessary. But if the amygdala does fire, there is little that can be (naturally) done to stem the initial cascade of expressive effects.[48]
## acupuncture: Hui et al (1999)
## meditation: Lazar et al (2000)
This concludes the discussion of this chapter that was focused upon solely the amygdala. To this point, we have seen that:
the amygdala is a the seat of fear in the human brain;
aware versus unaware fear seems to be the most persuasive theory of left versus right amygdala asymmetry;
excessive amygdala activation is unhealthy; and
the amygdala is a relatively plastic region in the brain.
From here on, this chapter shifts its focus from solely the amygdala, to the interaction of the amygdala with the PFC. While the amygdala may be the seat of fear in the brain, it is the interaction between the PFC and amygdala that fills out the full story of fear. Moreover, this interaction also reveals how the "survival instinct" in us humans operates. Finally, this chapter concludes by looking at how this interaction may give rise to human personality. Accordingly, the next three sections address fear, survival, and personality.
When it comes to processing fear, the amygdala and PFC play roles that are independent but complementary. Roughly speaking, it appears that the amygdala serves as an early warning system — one that scans the environment looking out for significant rewards, but especially for significant punishments. It gets its information both in a form that is quick and dirty, and in a form that is slow but accurate. Either way, if the amygdala recognizes the information as sufficiently potentially dangerous or thrilling, it sounds an alarm waking up the body, including the PFC.
Meanwhile, in another corner of the brain, the PFC is also engaged in scanning the environment. The PFC sends what it finds to the amygdala so that the amygdala can have slow but accurate data. When the amygdala sounds the alarm, the PFC goes on heightened alert. During those times, the PFC scans the environment intently, assessing the rewarding and/or punishing aspects of the situation at hand. Once the PFC has resolved the ambiguity of the general alarm, the PFC switches off the amygdala, thus quieting the alarm.
So the amygdala and PFC serve different, although related, functions in the processing of fear. In addition, the processing of the amygdala is unconscious, while that of the PFC is typically quite conscious. Think again of being startled awake by a bump in the night. Our ears have pricked up, and we are consciously listening for any further sounds. This is the PFC on heightened alert. When we determine that the source of the bump is benign, we may begin to relax, although returning to sleep may take some time. This is the PFC switching off the amygdala.
This dynamic describes our common understanding of fear. This familiar response feels unitary when we are experiencing it. However, as we have seen, this response actually results from the seamless melding of two independent processes — amygdala processing and PFC processing.
This independence is reflected in the observation that each process can operate without the other. That is, we are able to experience conscious PFC-based fear without the amygdala firing and our body responding. Indeed, a 2002 study[49] showed that the amygdala is not necessary for the conscious experience of fear, whereas the PFC is necessary.[50]
Conversely, we are capable of experiencing bodily fear, mediated by the amygdala, but without the conscious feeling of fear. This second observation — amygdala independence — is critical to the hypothesis of this book. Thus it bears further explanation.
Recall from early in this chapter the study in which subjects were presented with frightening faces, but in a subliminal manner.[51] Although the subjects did not consciously perceive the subliminal faces (i.e. their PFC did not respond), their amygdala did respond. In other words, their amygdala seems to have issued an early warning, but their PFC seems to have missed the warning.
This dynamic is even clearer in the Glascher/Adolphs study that lies at the crux of this chapter. Recall that the Only Right subjects — brain damaged subjects with a functioning right amygdala but with damage to the left — exhibited the highest amygdala response among all subjects, yet they displayed the lowest level of conscious awareness of arousal.
This Glascher/Adolphs study suggests a refinement of amygdala-PFC independence. It suggests that where the amygdala generates a fear response of which the PFC is not conscious, it is specifically the right amygdala that is generating this response. In other words, this section began by describing a partnership between the amygdala and PFC in the mediation of fear. The Glascher/Adolphs study suggests that as between the left and the right amygdala, the left is a more forthcoming partner of the PFC than is the right. Apparently, the right tends to "go off and do it's own thing."
In the preceding discussion on fear, the PFC served to heighten attention and resolve ambiguity. But this discussion didn"t explore the nature of the resolution. Specifically, it wasn"t considered how and whether optimism and pessimism inform this process.
This section approaches this question by looking closer at the PFC"s mood processor. In Chapter 5, we saw that the PFC generates the mental states of optimism and pessimism. Optimism is sensitivity toward reward; pessimism, sensitivity toward punishment. Survival enters the picture due to the fact that insufficient rewards and excessive punishments both lead to death (i.e. non-survival). So optimism and pessimism are simply tools of survival.
In addition to the PFC"s mood processor, two other brain regions also play a central role with respect to survival. One is the amygdala. As seen in this chapter, the amygdala serves as an early warning system for potential punishments and rewards. The third brain region of interest here is the pain/pleasure centers. These centers in our brain mediate the experience of pleasure that arises from a reward received, and the experience of pain that arises from punishment received.
So we see three brain regions — the PFC's mood processor, the amygdala, and the pain/pleasure centers — all playing a central role with regard to reward and punishment. But the role of each is quite different. Further, this difference tracks along the dimension of time abstraction. The following table begins to explain this:
|
|
Role in Reward
& Punishment |
|
Pain/Pleasure
Centers |
experience |
|
Amygdala |
recognition |
|
PFC's Mood Processor |
attention bias |
Different Functions Concerning Reward and Punishment
The pain/pleasure centers are the least abstracted from reward/punishment. These centers register the actual sensations arising from rewards and punishments at the time they are being received.
The amygdala is more abstracted. Instead of registering the experience of reward and punishment, the amygdala serves only to recognize situations in which reward or punishment seems imminent. "Imminent" is the moment before "now". What may seem imminent may not in fact arise. But the job of the amygdala is not to wait to find out whether its hunches play out. Instead, its job is to "jump the gun" — to anticipate whether the current stimulus harkens impending reward or punishment.
The PFC's mood processor is the most abstracted from reward punishment. Its role is to bias attention toward prospective or historical rewards and punishments. In others words, there may be no reward or punishment present. There may not even exist the imminent potential for reward or punishment. Yet the PFC's mood processor is still active, looking out for reward and punishment.[52]
This difference between recognition (amygdala) and attention bias (PFC mood processor) bears further exploration. In addition to time abstraction, these processes differ in terms of granularity. Specifically, the processing of the amygdala is relatively crude, while that of the PFC's mood processor is relatively refined.
This crude/refined difference between recognition and attention bias was the subject of a 1999 study.[53] The study included brain-damaged subjects, as well as normal controls. There were two kinds of brain-damaged subjects: people with damage to their amygdala; and people with damage to the mood processor of their PFC. The subjects were instructed to play a gambling game with monetary rewards and punishments. This was the same game that was used in the 2001 O'Doherty optimism/pessimism study discussed in Chapter 5. As the researchers in the 1999 study explained, this gambling game is "a paradigm designed to simulate real-life decisions in terms of uncertainty, reward, and punishment."[54]
The researchers found that the amygdala patients (i.e. subjects lacking the amygdala) were impaired in generating bodily responses (i.e. no internal "alarm bell") to rewards and punishments in the game. The effect of this impairment was that the amygdala patients didn't feel much when they experienced losses in the game. This made them poor players. As the researchers explained:
The notion that bilateral damage to the amygdala is associated with decision-making impairments in the gambling task also is supported by the observation that amygdala patients demonstrate poor judgment and decision-making in their real-life social behavior.[55]
In contrast with the amygdala patients, the PFC patients (i.e. subjects lacking the PFC mood processor) did generate bodily responses upon winning or losing money. In other words, they did feel something. However, like the amygdala patients, they also played the game poorly. But their reason for doing so was different. As the researchers explained:
After the somatic states [bodily responses] of reward and punishment are evoked with individual card draws, each deck becomes associated with numerous and conflicting states of reward and punishment. The role of the [PFC] comes into play when subjects sort out this conflict and decide whether to seek or avoid the deck. The poor decision making associated with the [PFC] patients is related to an inability to integrate effectively all of the somatic state information triggered by the amygdala ... .[56]
This experiment elegantly showed that while the amygdala helps us recognize a situation as important (i.e. rewarding or punishing), the PFC helps us sort out the complex rewarding and punishing aspects of that situation.
This study showed that the amygdala and PFC collaborate on decision-making with respect to reward and punishment. Another way of getting to the same conclusion involves looking closer at the high road between the PFC and amygdala. One "lane" of this road travels between the OFC region of the PFC and the amygdala.[57] The OFC region is the same region that was issue in this 1999 decision-making study, as well as in the 2001 Wellcome Department optimism/pessimism study. So the OFC seems to be part of the PFC's mood processor. That the OFC and amygdala are directly connected corroborates the finding that the two regions collaborate with respect to reward/punishment decision-making.
Further, it is from this collaboration that personality begins to emerge. This is the subject of the next section.
Human personality begins to emerge from the interaction of PFC and amygdala asymmetry. Chapter 5 concluded that left and right PFC asymmetry seems to track along optimism versus pessimism. This chapter finds support for the theory that left and right amygdala asymmetry tracks along aware versus unaware fear. Personality pokes it head out of the mixing and matching of these four attributes.
One word of caution seems in order before we begin the analysis of this section. This section contains my own analysis of how the findings of the 2001 O'Doherty study on optimism/pessimism and the PFC might relate to the findings of the 2003 Glascher/Adolphs study on aware/aware fear and the amygdala. As of this writing, I am unaware of any researchers looking into possible relationships between these two studies. So for this section, we're in uncharted territory.
With this caveat, recall from Chapter 5 that people apparently differ with respect to trait PFC asymmetry. That is, some people are "lefties", others "righties", and still other "middies" of one degree or another.
For the analysis of this section, let's begin by considering a lefty. This is a person who tends to experience more activity in her left PFC than in her right PFC. According to the O'Doherty study and others, this person would tend more toward optimism than pessimism. We might even call this person an optimist. This means that her attention is biased more toward potential personal rewards than toward punishments.
Now consider what should happen when this person's left amygdala activates out of fear. According to the Glascher/Adolphs study, this would generate arousal in the person of which she is quite aware. Since she is an optimist, and she is aware of her feeling of discomfort, it seems reasonable to conclude that she would typically act to avoid the stimulus that is causing the discomfort. To be sure, sometimes she would challenge the stimulus; other times, attempt negotiation. But, being aware of her discomfort, the easiest thing to do most of the time will be to withdraw with optimism that the withdrawal will relieve the discomfort. Being an optimist, she wouldn't typically view her withdrawal as surrender. Instead, she would see it as wise self-preservation.
Now consider what should happen when this person's right amygdala activates out of fear. According to the Glascher/Adolphs study, this would generate arousal in the person of which she is not aware. Being aroused, this person would become more animated, with heightened attention — even though she doesn't know she is aroused. Being an optimist, being aroused, but being unaware of her own discomfort, she seems likely to approach proximate stimuli with optimism. In other words, she seems likely to approach with attention tuned toward potential rewards.
Thus, two different personalities seem to emerge from the intersection of these two studies. The left PFC/left amygdala personality would seem to be an optimist who tends to float smoothly away from and around trouble. In contrast, the left PFC/right amygdala personality would seem to be an optimist who wades headlong into trouble, crashing into it unawares. The first is the confident, elegant matador; the second, the confident, determined, albeit a bit thick headed, bull.
Now, if you've been reading this book closely, you might recognize these two personalities as the Enneagram Seven and Eight, respectively. Recall that the Seven is a smooth, confident, optimist, expert in deftly slipping past and around trouble. The Eight, meanwhile, is a blunt, confident, optimist, who, often unknowingly, barges headlong into trouble.
If these parallels seem apt, perhaps you may suspect that this book is preparing to wrap up. However, this is not the case. It is the job of Part Three to draw these connections between the findings of neuroscience and the Enneagram. An entire part is needed because these connections are still relatively loose as of this writing. So they require careful explanation.
For example, these personalities could exist only if the Glascher/Adolphs model (assuming it is correct) applies to trait amygdala asymmetry, not just state asymmetry. Presently, this is an open question. That study looked only at state asymmetry. No one, to my knowledge, has yet studied whether individuals exhibit persistent patterns of left versus right dominance in the amygdala.
This sort of trait asymmetry seems necessary for personalities to emerge. For example, for the confident, elegant matador to be described as just that, it would require persistent, consistent, relative dominance of her left PFC and left amygdala. Otherwise, this matador would, during other times, seem also to be a thick headed bull, a pessimistic self defeatist, a shy bookish introvert, and so on. But if she was all that, her personality would defy description. So trait asymmetry is required for personality.
Well, that's all this chapter will say on personality. The story of how personalities seem to emerge from the neuroscience findings will continue in Part Three. Still, this section should have given you a flavor of the Enneagram-brain analysis to come.
With reasonable confidence, this chapter concludes that the Glascher/Adolphs model of amygdala asymmetry is likely to be sound. Under this model, the left amygdala mediates aware fear; the right, unaware fear.
Still, an open question in the field is whether amygdala asymmetry is a trait-like feature, akin to PFC asymmetry. With respect to amygdala asymmetry, are some people lefties, other righties, and still others "bothies"? The most we can say at present is: "probably".
Beyond the Glascher/Adolphs model, this chapter explained that the normal amygdala exhibits an "on-off" pattern of activation. This is in contrast with the PFC which is an "always-on" brain region (at least during waking hours). This on-off nature of the amygdala impacts plasticity (can we train "off"?) and health (too much "on" spells trouble).
Finally, this chapter delved into the interaction between PFC and amygdala. It is within this rich interaction that fear, survival processes, and human personality emerge.
[1] SS at ##.
[3] SS at ##.
[4] SS at ##.
[5] ##
[6] ##
[7] Davis & Whalen (2001) at 13, 20.
[8] ##
[9] ##
[10] ##
[11] Davis & Whalen (2001) at 19 (amygdala involved in "process[ing] the social signals of fear") and 24 ("anticipation of shock often leads to more fear — compared to the actual receipt of shock").
[12] SS at 123: Figure 5.7; at 214
[13] Morris (1999).
[14] SS at 220.
[15] Actually there are three inputs to the amygdala — thalamus, hippocampus and cortex — corresponding, roughly, to perception, memory, and consciousness, respectively. Davis & Whalen (2001) at 13.
[16] ## cite LeDoux
[17] SS at 224 - no explicit memory, but strong implicit memory. Davis & Whalen (2001) at 14.
[18] Adams (2003); Adolphs (1998) (amygdala necessary for fear of novel threatening faces); Davis & Whalen (2001) at 24 ("amygdala is especially sensitive to the uncertainty of stimulus contingencies") and 26.
[19] Davis & Whalen (2001) at 14.
[20] Davidson (2003) at 657
[21] SS at 226-229
[22] "In fact, an attention or orienting reflex was the most common response elicited by electrical stimulation of the amygdala." Davis & Whalen (2001) at 17.
[23] ## amplification of memory; SS at 221-223; Davis & Whalen (2001) at 23.
[24] Davis & Whalen (2001) at 17.
[25] SS at 213.
[26] SS at 217
[27] Schaefer et al. 2002; see Davidson (2003) at 662; see also Beauregard (2001) (conscious effort to dampen arousal response from viewing pornography dampened amygdala).
[28] Glascher/Adolphs (2003).
[29] Glascher/Adolphs (2003) at 10281.
[30] In fact, the researchers recorded "large interindividual differences in the habituation rate". But they performed data massaging to "remove the effect of habituation". Glascher/Adolphs (2003) at 10277. This procedure allowed them to conduct "apples to apples" comparisons between the subjects.
[31] Glascher/Adolphs (2003) at 10275,77.
[32] Glascher/Adolphs (2003) at 10276.
[33] Glascher/Adolphs (2003) at 10276.
[34] Glascher/Adolphs (2003) at 10276-77.
[35] Glascher/Adolphs (2003) at 10276.
[36] Glascher/Adolphs (2003) at 10278-79.
[37] Glascher/Adolphs (2003) at 10277-78.
[38] Glascher/Adolphs (2003) at 10279-80.
[39] Glascher/Adolphs (2003) at 10278-79.
[40] Glascher/Adolphs (2003) at 10279.
[41] O'Doherty (2001) at ##.
[42] Baas/Aleman/Kahn (2004).
[43] Phelps et al. (2001) at 438.
[44] Canli et al. (2002).
[45] Isenberg at al (1999).
[46] Davidson (2004) at 1400.
[47] Zalla et al (2000).
[48] Davis & Whalen (2001) at 17 ("plasticity during fear conditioning probably results from a change in synaptic inputs prior to or in the basolateral amygdala, rather than from a change in its efferent target areas").
[49] Anderson (2002)
[50] Davis & Whalen (2001) at 26 ("reported emotion and amygdala activation should not be equated").
[51] Morris (1998).
[52] Davis & Whalen (2001) ("cells in the ... amygdala encode the associative significance of cues, whereas cells in the [PFC] are active when that information, relayed from the ... amygdala, is required to guide choice behavior") at 24.
[53] Bechara/Damasio (1999)
[54] Bechara/Damasio (1999) at 5473
[55] Bechara/Damasio (1999) at 5480
[56] Bechara/Damasio (1999) at 5480
[57] SS at 226-229