and come and see us.”
Over the next few months Ali’s seizures disappeared, and as an added bonus his mood swings diminished and he became less depressed. Yet even three years later he continued to maintain that he was dead.14
What would be causing this Kafkaesque disorder? As I noted earlier, pathways 1 (including parts of the inferior parietal lobule) and 3 are both rich in mirror neurons. The former is involved in inferring intentions and the latter, in concert with the insula, is involved in emotional empathy. You have also seen how mirror neurons might not only be involved in modeling other people’s behavior—the conventional view—but may also turn “inward” to inspect your own mental states. This could enrich introspection and self-awareness.
The explanation I propose is to think of Cotard syndrome as an extreme and more general form of Capgras syndrome. People with Cotard syndrome often lose interest in viewing art and listening to music, presumably because such stimuli also fail to evoke emotions. This is what we might expect if all or most sensory pathways to the amygdala are totally severed (as opposed to Capgras syndrome, in which just the “face” area in the fusiform gyrus is disconnected from the amygdala). Thus for a Cotard patient, the entire sensory world, not just Mum and Dad, would seem derealized—unreal, as in a dream. If you added to this cocktail a derangement of reciprocal connections between the mirror neurons and the frontal lobe system, you would lose your sense of self as well. Lose yourself and lose the world—that’s as close to death in life as you can get. No wonder severe depression frequently, though not always, accompanies Cotard syndrome.
Note that in this framework it is easy to see how a less extreme form of Cotard syndrome could underlie the peculiar states of derealization (“The world looks unreal as in a dream”) and depersonalization (“I don’t feel real”) that are frequently seen in clinical depression. If depressed patients have selective damage to the circuits that mediate empathy and the salience of external objects, but intact circuitry for self-representation, the result could be derealization and a feeling of alienation from the world. Conversely, if self-representation is mainly affected, with normal reactions to the outside world and people, the sense of internal hollowness or emptiness that characterizes depersonalization would be the result. In short, the feeling of unreality is attributed to either oneself or the world depending on differential damage to these closely linked functions.
The extreme sensory-emotional disconnection and diminishment of self I am proposing as an explanation for Cotard syndrome would also explain such patients’ curious indifference to pain. They feel pain as a sensation but, like Mikhey (whom we met in Chapter 1), there is no agony. As a desperate attempt to restore the ability to feel something—anything!—such patients may try to inflict pain on themselves in order to feel more “anchored” in their bodies.
It would also explain the paradoxical finding (not proven, but suggestive) that some severely depressed patients commit suicide when first put on antidepressant drugs such as Prozac. It is arguable that in extreme Cotard cases suicide would be redundant, since the self is already “dead” there is no one there who can or should be put out of her suffering. On the other hand, an antidepressant drug may restore just enough self-awareness for the patient to recognize that her life and world are meaningless; now that it matters that the world is meaningless, suicide may seem the only escape. In this scheme, Cotard syndrome is apotemnophilia for one’s entire self, rather than just one arm or leg, and suicide is its successful amputation.15
DOCTOR, IAMONE WITH GOD
Now consider what would happen if the extreme opposite were to occur—if there were a tremendously overactivation of pathway 3 caused by the kind of kindling one sees in temporal lobe epilepsy (TLE). The result would be an extreme heightening of empathy for others, for the self, and even for the inanimate world. The universe and everything in it become deeply significant. It would feel like union with God. This, too, is frequently reported in TLE.
Now, as in Cotard syndrome, imagine adding into this cocktail some damage to the system in the frontal lobes that inhibits mirror-neuron activity. Ordinarily this system preserves empathy while preventing “overempathy,” thus preserving your sense of identity. The result of damaging this system would be a second, even deeper sense of merging with everything.
This sense of transcending your body and achieving union with some immortal, timeless essence is also unique to humans. To their credit, apes are not preoccupied with theology and religion.
DOCTOR, I’M ABOUT TO DIE
Incorrect “attribution” of our internal mental states to the wrong trigger in the external world is very much a part of the complex web of interactions that lead to mental illness in general. Cotard syndrome and “merging with God” are extreme forms of this.16 A far more common form is the syndrome of panic attacks.
A certain proportion of otherwise normal people are seized for forty to sixty seconds by a sudden feeling of impending doom—a sort of transient Cotard syndrome (combined with a strong emotional component). The heart starts beating faster (felt as palpitations, an intensification of heartbeats), palms sweat, and there is an extreme sense of helplessness. Such attacks can occur several times a week.
One possible source of panic attacks might be brief miniseizures affecting pathway 3, especially the amygdala and its emotional and autonomic arousal outflow through the hypothalamus. In such a case, a powerful fight-or- flight reaction would be triggered, but since there is nothing external you can ascribe the changes to, you internalize it and start to feel as if you’re dying. It’s the brain’s aversion to discrepancy again—this time between the neutral external input and the far-from-neutral internal physiological feelings. The only way your brain can account for this combination is to ascribe the changes to some indecipherable and terrifying internal source. The brain finds free- floating (inexplicable) anxiety less tolerable than anxiety which can be clearly attributed to a source.
If this is correct, one wonders if it might be possible to “cure” panic attacks by taking advantage of the fact that the patient often knows a few seconds ahead of time that an attack is about to occur. If you are the patient, then as soon as you sense the attack coming on, you could quickly start watching a horror movie on your iPhone, for example. This might abort the attack by allowing your brain to ascribe the physiological arousal to the external horror, rather than to some terrifying but intangible inner cause. The fact that you “know” that it’s only a movie at some higher intellectual level doesn’t necessarily rule out this treatment; after all, you do feel fear when watching a horror movie even while recognizing that it’s “only a movie.” Belief is not monolithic; it exists in many layers whose interactions one can manipulate clinically using the right trick.
Continuity
Implicit in the idea of the self is the notion of sequentially organized memories accumulated over a lifetime. There are syndromes that can profoundly affect different aspects of memory formation and retrieval. Psychologists classify memory (the word is used loosely synonymous with learning) into three distinct types that might have separate neural substrates. The first of these, called procedural memory, allows you to acquire new skills, such as riding a bicycle or brushing your teeth. Such memories are summoned up instantly when the occasion demands; no conscious recollection is involved. This type of memory is universal to all vertebrates and some invertebrates; it certainly isn’t unique to humans. Second, there are memories that comprise your semantic memory, your factual knowledge of objects and events in the world. For example, you know that winter is cold and bananas are yellow.
