watching her body “acting out” the murder without personal involvement.)
The dissociative state involves the deployment of some of the same neural structures already discussed, but in addition two other structures: the hypothalamus and the anterior cingulate.11 Ordinarily, when confronted with a threat, two outputs flow out from the hypothalamus: a behavioral output, such as running away or fighting; and an emotional output, such as fear or aggression. (We already mentioned the third output: autonomic arousal leading to sweating GSR, blood pressure, and heart-rate elevation.) The anterior cingulate is simultaneously active; it allows you to remain aroused and ever vigilant for new threats and new opportunities for fleeing. But the degree of threat determines the degree to which each of these three subsystems is engaged. When one is confronted with an extreme threat, it is sometimes best to lie still and do nothing at all. This could be regarded as a form of “playing possum,” shutting down both the behavioral and emotional output. The possum becomes completely still when a predator is so close that escape is no longer an option, and in fact any attempt would only activate the carnivore’s instinct to chase down fleeing prey. Nonetheless, the anterior cingulate remains powerfully engaged the whole time to preserve vigilance, just in case the predator isn’t fooled or a quick escape route becomes available.
A vestige of this “possum reflex,” or an exaptation of it, may manifest itself as dissociative states in humans in extreme emergencies. You shut down overt behavior as well as emotions and view yourself with objective detachment from your own pain or panic. This sometimes happens in rape, for example, where the woman gets into a paradoxical state: “I was viewing myself being raped as a detached external observer might—feeling the pain but not the agony. And there was no panic.” The same thing must have occurred when the explorer David Livingstone was mauled by a lion chewing his arm off; he felt no pain or fear.
The ratio of activation among these circuits and interactions between them can also give rise to less extreme forms of dissociation in which action is not inhibited but emotions are. We have dubbed this the “James Bond reflex”: his nerves of steel allow him to remain unperturbed by distracting emotions as he pursues and tackles the villain (or has sex with a woman without paying the “penalty” of love).
Social Embedding
The self defines itself in relation to its social environment. When that environment becomes incomprehensible —for example, when familiar people suddenly seem unfamiliar or vice versa—the self can experience extreme distress or even feel that it is under threat.
THE MISIDENTIFICATION SYNDROMES:
DOCTOR, THAT’S NOT MY MOTHER
A person’s brain creates a unified, internally consistent picture of his social world—a stage occupied by different selves like you and me. Seems like a banal statement, but when the self is deranged you begin to realize there are specific brain mechanisms at work to clothe the self with a body and an identity.
In Chapter 2, I offered an explanation for the Capgras syndrome in terms of visual pathways 2 and 3 as they diverge from the fusiform gyrus (Figures 9.1 and 9.2). If pathway 3 (the “so what” stream, which evokes emotions) is compromised while pathway 2 (the “what” stream, which enables identification) remains intact, the patient can recall facts and memories about his nearest and dearest—in a word, he can recognize them—but, jarringly, distressingly, he does not get the warm fuzzy feelings that he “should.” The mismatch is either too painful or too bewildering to accept, so he embraces the delusion of an identical imposter. Going further down the path of delusion, he may say things like “my other mother,” or even assert that there are several mother-like beings. This is called duplication, or reduplication.
Now think about what happens when the Capgras scenario is reversed: intact pathway 3, compromised pathway 2. The patient loses her ability to recognize faces. She becomes face blind, a condition called prosopagnosia. And yet her pure unconscious discrimination of people’s faces continues to be carried out by her intact fusiform gyrus, which can still send signals down her intact “so what” stream (pathway 3) to her amygdala. As a result, she still responds emotionally to familiar faces—she gives a nice big GSR signal when seeing her mother, for example—even though she has no idea who she is looking at. Strangely, her brain—and skin—“knows” something that her mind is unaware of consciously. (This was shown in an elegant series of experiments by Antonio Damasio.) So you can think of the Capgras and prosopagnosia disorders as mirror images of each other, both structurally and in terms of clinical symptoms.12
To most of us with our undamaged brains, it seems counterintuitive that identity (facts known about a person) should be segregated from familiarity (emotional reactions to a person). How can you recognize someone yet not recognize her at the same time? You might get an inkling of what this is like if you think back to an occasion when you ran into an acquaintance somewhere completely out of context, such as an airport in a foreign country, and could not for the life of you remember who he was. You experienced familiarity with lack of identity. The fact that such dissociation can occur at all is proof that separate mechanisms are involved, and in such “airport” moments you experience a miniature, fleeting “syndrome” that is the converse of Capgras. The reason you don’t experience this cognitive discrepancy as unpleasant (except briefly as you buy time with small talk while racking your brain) is because such episodes do not last long. If this acquaintance continued to look strange all the time, irrespective of context and no matter how much or how often you spoke with him, he might start looking sinister and you might indeed develop a strong aversion or paranoia.
FIGURE 9.1 A highly schematic diagram of the visual pathways and other areas invoked to explain symptoms of mental illness: The superior temporal sulcus (STS) and supramarginal gyrus (SM) are probably rich in mirror neurons. Pathways 1 (“how”) and 2 (“what”) are identified anatomical pathways. The split of the “what” pathway into two streams—“what” (pathway 2) and “so what” (pathway 3)—is based mainly on functional considerations and neurology. The superior parietal lobule (SPL) is involved in the construction of body image and visual space. The inferior parietal lobule (IPL) is also concerned with body image, but also with prehension in monkeys and (probably) apes. The supramarginal gyrus (SM) is unique to humans. During hominin development, it split off from the IPL and became specialized for skilled and semiskilled movements such as tool use. Selection pressure for its split and specialization came from the need to use hands for making tools, wielding weapons, hurling missiles, as well as fine hand and finger manipulation. Another gyrus (AG) is probably unique to us. It split off from IPL and originally subserved cross-modal abstraction capacities, such as tree climbing, and matching visual size and orientation with muscle and joint feedback. The AG became exapted for more complex forms of abstraction in humans: reading, writing, lexicon, and arithmetic. Wernicke’s area (W) deals with language (semantics). The STS also has connections with the insula (not shown). The amygdaloid complex (A, including the amygdala) deals with emotions. The lateral geniculate nucleus (LGN) of the thalamus relays information from the retina to area 17 (also known as V1, the primary visual cortex). The superior colliculus (SC) receives and processes signals from the retina that are to be sent via the old pathway to the SPL (after a relay via the pulvinar, not shown). The fusiform gyrus (F) is involved in face and object recognition.
FIGURE 9.2 An abbreviated version of Figure 9.1, showing the distinction between emotions and semantics (meaning).
SELF DUPLICATION: DOCTOR, WHERE IS THE OTHER DAVID?
