Psychopathology

According to Eysenck (1995), Aristotle claimed, "No great genius has ever been without some madness." According to Simonton (1999), Aristotle also wrote, "Those who have become eminent in philosophy, politics, poetry and the arts all had tendencies toward melancholia." John Adams said, "Genius is sorrow's child." In his book, Eysenck tried to make the argument that there is a strong relationship between creativity, psychosis, and schizophreniform thinking, but then quoted Eisenman's studies that demonstrate that schizophrenics are even less creative than normal hospital employees, who Eysenck noted are not "particularly creative." Kraepelin in 1921 noted that manic-depressive psychosis was often associated with enhanced creativity (Weisberg, 1994). Post (1996) studied the biographies of a large group of world-famous creative people, such as composers, scientists, artists, and writers. To classify these people, Post used the diagnostic criteria found in the Diagnostic and Statistical Manual of Mental Disorders (3rd ed.) (DSM-III) (American Psychiatric Association, 1980). He found that scientists had the lowest percentage of psychopathology and writers had the most, but in all these groups the percentage of people classified as having psychopathology was relatively high. For example, he found that 18% of the scientists, 38% of artists, and 46% of writers had severe psychopathology. He also found, however, that actual psychosis was very low in this group (1.7%), and there was an almost complete absence of schizophrenia. Andreasen (1987) studied a group of 30 creative writers and compared them with 30 matched controls who were not creative writers. She also examined their families. The writers had a very high rate of mental illness, especially affective disorders such as bipolar disease and depression. In addition, she found that there was a high rate of affective disorders in these people's relatives. Jamison (1989) studied British writers and found that 38% of his experimental participants had been treated for affective disorders and that about three quarters of these writers had received either antidepressants or lithium (used to treat bipolar or manic-depressive disorder). Other investigators have also reported that many of our most creative writers, composers, painters, and scientists have suffered with mood disorders, either bipolar or monopolar (Andreasen & Glick, 1988; Poldinger, 1986; Post, 1996; Richards, Kinney, Lunde, Benet, & Merzel, 1988; Slaby, 1992).

Scientists who perform research with human participants must have their research approved by an institutional review board (IRB). These boards are so concerned with government regulations and government threats that some board members do everything they can to prevent an investigator's research from being approved. For the most part, the research that we do in our laboratories is behavioral. For example, we test the ability of people who have suffered with a stroke to learn if they might have more trouble naming objects than actions (nouns versus verbs). There is not even a remote possibility that we could harm these people by this type of testing, but to get protocols for research such as this approved by the IRB might take months to a year, with requests for multiple revisions. Most of these requests for revisions are trivial. For example, the IRB has asked us, "What will you do if someone gets anxious because they cannot find the correct name of an object?" Anybody who has to deal with bureaucrats such as those found on the IRB or has to work with granting agencies such as the National Institutes of Health might argue that it is dealing with these organizations while attempting to be creative that induces psychopa-thology. Most scientists who work at universities at least get paid (but for many it is not much and when they do invent something that might bring them financial reward, this invention is usually the property of the government or the university). But although scientists usually get paid, the life for the artist or writer is usually much more difficult. After writing novels, biographies, and other types of books, many authors cannot find anyone who will publish their work. There are only a limited number of galleries and only a few people who buy nondecorative art. In addition, museums show the works of well-known artists only. Thus, artists have difficulty getting their works shown. When a small but fortunate few do get their works published or shown, they must then deal with harsh critics who seem only to know who became great after they died.

Newton's law of inertia (bodies at rest tend to remain at rest) appears to also be true for science and art. People and society are resistant to change, and because the creative person is attempting to implement change, he or she often comes up against resistance, and, usually, the greater the change the greater the resistance. In the 35 years that I have been performing research and publishing papers, I have found that there appears to be a negative correlation between the degree of creativity of a research project or report and the difficulty I have either receiving funding to support this research or getting this research published.

Disappointment and frustration can lead to mood changes, and it is possible that the attempt to implement and gain recognition of creative acts leads to the mood disorders observed in creative people. Many creative acts also require solitude and introspection, and these conditions can also lead to mood disorders. Thus, although there is little question that creative people subject themselves to conditions that might induce mood changes, most investigators and theorists believe that the mood disorders experienced by creative people are not reactive but are endogenous, and it is the psychopathology that leads to creativity.

Sigmund Freud (1908/1959) suggested one of the first theories that attempted to account for the relationship between psychopathology and creativity. Freud suggested that as adults we learn that libidinal energy must be expressed by socially acceptable means and that creative expression might be one means of sublimating this energy. Unfortunately, like many psychodynamic theories, these hypotheses are difficult to test and do not explain the brain mechanisms that account for creativity. In addition, as I wrote in the introduction, an explanation of the brain mechanisms underlying creativity should be ideally reductionistic such that one theory should account for a myriad observations that appear to be independent, but are not finding the thread that unites.

In contrast to the psychodynamic theories of Freud, one thread that might unite those states that lead to creativity—including resting, relaxing, dreaming, and depression—are alterations of the brain's neurotransmitter systems, primarily a reduction of catecholamines, including norepinephrine (McCarley, 1982). Brain levels of norepinephrine might influence creativity because they moderate the size of neuronal networks.

Behavioral support for the postulate that catecholamines modulate the size of neuronal networks comes from the priming studies of Kis-chka and coworkers (1996). These investigators used a lexical priming task in which either real words or pseudowords are flashed on a screen and the participants are asked to press a computer key, as rapidly as possible, when they determine that the word on the screen is a real word, but they are not to press a key if a pseudoword is seen. Sometimes these real words and pseudowords are preceded by another word that is called a prime. The preceding word is called a prime because if this preceding word is related to the real target word, the prime word will help the participant recognize the real target word and thus reduce the response time. The more highly associated the prime word is to the target word (e.g., doctor and nurse), the more efficient the word recognition and the more rapid the response time or key press. In contrast, the less the two real words are related, the less influence the prime word has on word recognition or response time. In our brains we have neuronal networks that store knowledge about words and their meaning (lexical-semantic representations). When these lexical-semantic networks are activated or excited by the prime, if the representation of the target word is also stored in this activated network, recognition will be more efficient than if the word is unrelated to the prime because with related words, the lexical-semantic networks that are needed for recognition are already activated. When a prime is unrelated to the target, however, the prime activates a network, but because the target word is not part of this activated network, recognition of the target word requires that a new network be activated before the person can recognize that the target word is a real word.

When Kischka et al. (1996) administered L-dopa to normal participants and tested priming, they found that direct semantic priming (e.g., winter-summer) was only marginally influenced by this medicine. The administration of L-dopa, however, significantly reduced the effects of indirect priming (summer-snow). On the basis of these results, Kischka et al. suggested that dopamine increases the signal-to-noise ratio in semantic networks by reducing the spread of semantic activation. Although Kischka et al. attributed this effect to the dopaminergic system, L-dopa is a precursor of both dopamine and norepinephrine, and the administration of L-dopa to these individuals may have also increased the level of norepinephrine.

In the Remote Associates Test, participants are presented with a series of word triads (e.g., blue, American, and goat) and are requested to find a word that is associated with all three words (e.g., cheese). Like the priming task, this test might assess the size or breadth of lexical-semantic networks. During stress, performance on this test deteriorates (Martindale & Greenough, 1973). One of the reasons why stress can reduce performance on this task is that stress is associated with increased activity of the noradrenergic system. Further support for this postulate comes from the results of a study in which students with test anxiety dramatically improved their scores on the Scholastic Aptitude Test when they took the beta-adrenergic blocker propranolol (Faigel, 1991). The Scholastic Aptitude Test tests crystallized intelligence (knowing facts, such as that Albany is the capital of New York State) and fluid intelligence (e.g., How are a zebra and a tree similar?). Perhaps the beta-blockade reduced the influence of norepinephrine on neuronal networks, allowing for activation of larger networks, and the activation of large networks enhances cognitive flexibility.

The basal forebrain (including the nucleus of Meynert, diagonal band of Broca, and the medial septum) sends neurons that contain the neurotransmitter acetylcholine to almost the entire cerebral cortex (see Figure 8.1). There are several lines of evidence that these cholin-ergic neurons in the basal forebrain modulate cortical activation or the degree of cortical arousal. Cape and Jones (1998) injected the neurotransmitter norepinephrine into the basal forebrain. When recording brain activity, by using an EEG, they found that these injections induced high-frequency EEG activity at between 30 and 60 Hz

Fornix

Basal Forebrain (Medial Septal Nucleus and Diagonal Band of Broca)

-Hippocampus

Basal Forebrain (Nucleus of Meynert)

Figure 8.1. Diagram of the basal forebrain, which contains cholinergic neurons that project to the cerebral cortex (from the nucleus of Meynert) and parts of the limbic system, such as the hippocampus (from the medial septum and the diagonal band of Broca).

Fornix

Basal Forebrain (Medial Septal Nucleus and Diagonal Band of Broca)

-Hippocampus

Basal Forebrain (Nucleus of Meynert)

Figure 8.1. Diagram of the basal forebrain, which contains cholinergic neurons that project to the cerebral cortex (from the nucleus of Meynert) and parts of the limbic system, such as the hippocampus (from the medial septum and the diagonal band of Broca).

(gamma activity) and reduced the amount of slower EEG activity. This gamma frequency is found during states of high vigilance or arousal (e.g., when an animal orients or alerts to a novel or highly significant stimulus). Thus, they concluded that norepinephrine regulates the activity of the basal forebrain, which in turn influences the activity or arousal of the cerebral cortex.

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