Descartes' Error: Emotion, Reason, and the Human Brain

Damasio elaborates on the scientific discoveries at the time of Gage’s accident. Doctors Paul Broca and Carl Wernicke individually proposed that lesions in the left frontal lobe at the third frontal gyrus caused aphasia, or language impairment. Although acceptance was not immediate, the scientific world endorsed this theory after some revision and clarification. Dr. Harlow’s hypothesis (that damage to certain areas of the brain affect social behavior), however, was not as easily accepted: No autopsy was performed after Gage’s death, and the precise location of the legion in his brain was uncertain. Five years after his death, Dr. Harlow convinced Gage’s family to retrieve his skull and the tampering iron from his grave, which are now under the safeguard of the Harvard Medical School.

More recently, neuroscientist Hanna Damasio attempted to reconstruct the path of the tampering iron. Using Brainvox, a technique she developed to depict images of the brain in three dimensions, she narrowed the possible paths that the tampering iron could have taken. She concluded that the regions of the brain dedicated to language and movement were intact, that the left hemisphere was affected more than the right, and that the ventromedial prefrontal region (which recent research has confirmed affects decision-making) was damaged. Thus, she confirmed that the accident affected select areas of Gage’s prefrontal cortices and that this rendered him incapable of adhering to social rules and making advantageous decisions for the future.

In a subsection of Chapter 2 called “An Aside on the Anatomy of Nervous Systems,” the author explains for the lay audience the basics of neuroanatomy. The human nervous system contains central and peripheral divisions. The central nervous system (CNS), which is mainly operated by the cerebrum (brain), also includes the diencephalon, midbrain, brain stem, and spinal cord. It connects to all parts of the body by nerves, which collectively form the peripheral nervous system (PNS). Substances that travel through the bloodstream, such as hormones and peptides, chemically connect the body and brain.

The brain itself contains gray and white matter. Gray matter can form a cortex or a nucleus depending on its organization. Gray matter below the cortex is subcortical; the most modern part of the cortex is the neocortex; and the oldest Part is the limbic cortex. When Damasio refers to the cerebral cortex, he means the neocortex. The limbic system has cortical and subcortical divisions, and its main components are the cingulate gyrus, amygdala, and basal forebrain.

Neurons are cells that regulate brain activity. Collectively, they can be arranged to form cortical regions or nuclei, which in turn form systems and systems of systems that are increasingly complex. Neurons have a cell body, dendrites, and an axon. When neurons are active, they fire electric currents from the cell body to the axon. Once this current reaches the synapse, if action potential exists, chemicals called neurotransmitters are released onto the receptors of the adjacent neuron, allowing the current to circulate to the target neuron.

Damasio sees the brain as a “supersystem of systems” (49). These macroscopic systems interconnect through cortical regions and subcortical nuclei, which in turn comprise local circuits composed of thousands of microscopic neurons. In later chapters, Damasio refers to systems as macroscopic and circuits as microscopic.

This chapter introduces Elliot, an anonymous patient whom Damasio evaluated when his personality changed dramatically after prefrontal cortex damage. Elliot’s case was “an especially pure version” of Phineas Gage’s condition: His intellect remained unchanged, but his decision-making skills took a turn for the worse. He could no longer retain his job, but because his condition was invisible, the government denied him disability benefits. Consequently, his physician wanted to confirm whether his change in behavior was a “real” disease (52).

Elliot was a smart person with good social status but had a tumor that damaged the frontal lobe tissue of his brain. After surgery, Elliot’s personality began to shift. Although he was just as intelligent and discerning as before, he could no longer reliably perform specific tasks within a set timeframe due to his inability to reach decisions. He began collecting junk. His first and second marriages failed. Elliot could no longer effectively plan his future, and this compromised his free will. After Damasio performed a computerized tomography and several magnetic resonance studies, he concluded that both the right and left frontal lobes had sustained damage, with an emphasis on the right side. No other areas were affected.

Elliot arrived at Damasio’s clinic after psychological evaluations proved unsuccessful in assessing his condition. He performed better than average in standard intelligence tests and did not have memory problems, so psychotherapy did not help. Damasio believes this demonstrates the inadequacy of psychological tests of the time, which failed to account for invisible disabilities (diseases of the mind) as opposed to physical ones (diseases of the brain). In the end, Elliot emerged as a perfectly sensible individual whose only “defect” was that he could not make appropriate decisions on social and intrapersonal matters.

Damasio eventually realized his mistake: He had focused all his efforts on understanding Elliot’s rationality and had overlooked his emotions. When recounting his lived tragedies, Elliot seemed distant, to the point that Damasio felt he experienced more pain than his patient just from listening to him. Elliot confirmed this change himself: He noticed that after his illness, he no longer reacted to situations that merited a strong emotional response even if he knew what a typical response would be.

At this stage, Damasio wished to confirm whether Elliot was still aware of what constituted appropriate social behaviors even if he no longer followed them. After tests in which Elliot offered responses to social situations, predicted their outcome, and performed value judgment, Damasio realized that his patient always did well in the laboratory but continued to make poor decisions in real life.

Damasio began trying to account for this discrepancy. He soon noticed that the laboratory tests only required reasoning through a problem; they did not force decision-making. Even if they had, those decisions would not have brought about a new scenario with a new set of constraints as in real life. Furthermore, the laboratory tests he had given Elliot had no time constraint, whereas in real life people often have choices and reach decisions quickly. By this stage, Damasio was certain that his patient knew the rules of social behavior but could not follow them. He began thinking that Elliot’s reduced emotional reactivity may be the key to understanding his condition.

Damasio prefaces this chapter by offering instances in which a strong emotional response may cloud judgment. For example, people—including the highly educated—are more likely to accept a surgery if doctors tell them that it has a 90% success rate rather than a 10% death rate, even though the statistical outcomes are identical. Damasio posits that a reduction in emotional feeling may similarly induce irrational behavior and uses experimental neuropsychology to prove this theory but cautions that his approach does not involve localizing specific conditions to specific areas of the brain. Rather, he attempts to explain how certain neural systems as a whole can correspond to specific cognitive operations. In Elliot’s condition, this occurred whenever something compromised the systems that process emotion, feeling, reason, and decision-making. Such compromise may result from prefrontal cortex damage or something else; therefore, it is not fully understandable through brain localization.

Damasio presents four cases of patients in whom prefrontal cortex damage markedly reduced decision-making skill and emotion-based feeling. He labels them as being in the “Phineas Gage matrix” (71).

Like Elliot, “Patient A,” whom Columbia University neurologist Dr. Brickner studied in 1932, developed a brain tumor that damaged his frontal lobe. After surgery, he was no longer a modest man and boasted about his musculature and virility even though he did not exercise and stopped having sex. He elaborately planned a professional comeback but never tried to return to work. Damasio summarizes his emotional range as “shallow” (71).

The second case, whom doctors Donald Hebb and Wilder Penfield of McGill University studied in 1940, was a patient who had prefrontal cortex damage at age 16. Unlike Elliot and Patient A, he was still in the process of physical and social development. After his injury, his interpersonal skills ceased to progress, and his social behavior worsened.

The third case, which doctors S. S. Ackerly and A. I. Benton recorded in 1948, was a patient who had frontal lobe damage after birth and always displayed abnormal behavior. He could not hold a steady job even though he was not stupid. He would sometimes steal or act disorderly. Reward or punishment could not influence his actions, and his feelings were shallow. He had many of the same symptoms as the Hebb-Penfield patient, including the inability to hold employment or organize future activity, a reduced sex drive, and a diminished emotional life.

The fourth example in Damasio’s Phineas Gage matrix comes from early records of prefrontal leucotomy. This surgical procedure, developed by Portuguese neurologist Egas Moniz, produced “small areas of damage in the deep white matter of both frontal lobes” (73). Leucotomy was meant to treat severe psychiatric conditions such as schizophrenia without compromising locomotion, language, perception, or memory. Patients who underwent the procedure lost their state of heightened anxiety but were abnormally quiet and became less creative and decisive. Damasio concludes that impairment of decision-making and emotion-based feelings is associated with prefrontal cortex damage, especially when it affects the ventromedial sector.

The discussion then turns to examining instances in which damage elsewhere than the prefrontal cortex brought about the same dual impairment of reasoning/decision-making and emotion/feeling. Damasio believes that two other sites in the brain fit this description: the area in the right cerebral hemisphere that processes signals from the body, and certain structures of the limbic system (including the amygdala).

First, Damasio presents anosognosia as a neurological condition that shares the Phineas Gage matrix. Anosognosia is an inability to gauge one’s own physical changes after neurological damage. For example, it can accompany left-side paralysis and manifests in patients’ inability to recognize their own paralysis even if someone points it out. This lack of self-awareness is not a result of psychological denial but the consequence of impaired cognitive functions. Like patients in the Phineas Gage matrix, people with anosognosia exhibit a lack of emotion over their own misfortunes and have difficulty arriving at decisions and planning a future.

The second type of damage that can result in conditions in the Phineas Gage matrix occur in the limbic system, particularly in the amygdala. However, patients who sustain this type of injury are incredibly rare, and Damasio has access to only one example from the records of his colleagues. The person in question is a woman who, like every other example in the Phineas Gage matrix, has an average IQ but displays abnormal social behavior and inappropriate emotional range. Research on monkeys and rats show without a doubt that the regulation of emotion involves the amygdala.

Damasio proposes the anterior cingulate cortex in the limbic system is a “fountain” region that links emotion/feeling, attention, and working memory. These forces interact so intimately that “they constitute the source for the energy of both external action (movement) and internal action (thought animation, reasoning” (84). For example, Mrs. T, a patient who had a stroke that damaged the dorsal and medial regions of her frontal lobe, became immobile, speechless, and displayed no emotion. Although she could move, such as to rearrange her bed covers, she did so infrequently and had a blank facial expression. As she gradually recovered, she expressed that her body had not trapped her mind but that she had little mental activity at all. Damasio concludes that these cases in this chapter sufficiently show the relation between these specific brain regions and reasoning/decision-making.