Descartes’ Error1 can be read in 2 ways. To start, it works as an engagingly written, accurate piece of science journalism (which is something that we need more of; it’s hard to imagine running a democracy without it).
Even before Oliver Sacks reconstructed the genre as high literary art, pop neurology books—often just compendia of freakish cases and brilliant diagnoses—had great entertainment value. But these books make their subject matter sound more frivolous than it is. Before functional MRI and implantable brain stimulators, neurology was an essentially passive and observational science. It was built from observation and clinicopathological correlation of just those odd “experiments of nature,” with their uncanny dissociations and disconnections, that make for a ripping yarn.
Damasio parades some spectacularly freakish cases, but he doesn’t stop there. As a reflective practitioner, he uses those cases to argue a distinctive and original theory of mental functioning. Descartes’ Error should also be read as serious and original scientific research.
His first example is a classic. Phineas Gage was a bright, industrious 25-year-old in 1848, until an iron rod penetrated his frontal lobes in an industrial accident. Amazingly, he survived, with sensation, movement, speech, and reasoning apparently intact. But Gage’s personality changed. He became vulgar, emotionally shallow, shiftless, and unreliable. A completely different man.
Damasio’s second case, the index patient that launched his theorizing, is “Elliot,” formerly an intelligent, successful professional in his 30s, who lost parts of both frontal lobes to a meningioma. Elliot emerged from surgery as an impulsive, stimulus- bound, sleazy, unemployable jerk. Like Gage, he’d become cool and unemotive—transitory annoyance was his strongest remaining affect. And like Gage, his impairments were invisible to standard neuropsychological assessment: nothing worse than decreased autonomic response to fearful stimuli was detected.
From these 2, and a few other cases, Damasio and others extracted the key insight that acquired social incompetence and mood flattening were not dissociable; they always occurred together. They also localized a constellation of symptoms, “Gage syndrome,” to the ventromedian frontal lobes. Similar problems occur after bilateral amygdala damage and, in patients with anosognosia, after nondominant hemisphere strokes. In these cases, however, defective social reasoning is overshadowed by more gross neurological deficits.
In explaining Gage syndrome, Damasio distinguishes between primary and secondary emotions. The primary emotions, such as fear, elation, and disgust, seem to be hardwired and generated by phylogenetically old structures in the limbic system. What is more important, they evoke stereotypical, predictable body responses such as sweating and tachycardia. Secondary emotions by contrast are learned, variable, and nuanced. They originate in the frontal regions, but they work through the older primary circuitry rather than parallel to it.
The idea that the evolutionary process has built neocortical systems of regulation on top of older ones is crucial for Damasio. In this view, judging, reasoning, and subtle affective responses serve the same purposes—survival, homeostasis, reproduction—as the ancient limbic and endocrine systems. As we go about our lives, frontal mechanisms create associations between images in primary sensory cortices and physiological states of the body; images get somatically marked (the “somatic marker hypothesis”). Then, when we have to decide among competing courses of action, images of potential outcomes evoke the physiological states they’ve been marked with. In turn, these physiological states are themselves subliminally perceived, with the result that alternative actions with negative somatic markings are rapidly rejected and those with positive markings receive extra attention.