428 Vestiges of the Bicameral Mind in the Modern World nated voices of the bicameral mind were amalgams of stored admonitory experiences that were somehow organized in the right temporal lobe and conveyed to the left or dominant hemisphere over the anterior commissures and perhaps the corpus callosum.
Further, I have suggested that the advent of consciousness necessitated an inhibition of these auditory hallucinations originating in the right temporal cortex. But what precisely this means in a neuro-anatomical sense is far from clear. We definitely know that there are specific areas of the brain that are inhibitory to others, that the brain in a very general way is always in a kind of complicated tension (or balance) between excitation and inhibition, and also that inhibition can occur in a number of different ways. One way is an inhibition of an area in one hemisphere by excitation of an area in the other. The frontal eye fields, for example, are mutually inhibitory, such that stimulation of the frontal eye field on one hemisphere inhibits the other.37
And we may suppose that some proportion of the fibers of the corpus callosum which connects the frontal eye fields are inhibitory themselves, or else excite inhibitory centers on the opposite hemisphere. In behavior, this means that looking in any direction is programmed as the vector resultant of the opposing excitation of the two frontal eye fields.38 And this mutual inhibition of the hemispheres can be presumed to operate in various other bilateral functions.
But to generalize this reciprocal inhibition to asymmetrical unilateral functions is a more daring matter. Can we suppose, for example, that some mental process on the left hemisphere is paired in reciprocal inhibition with some different function on the 37 A. S. F. Layton and C. S. Sherrington, “Observation on the excitable cortex of chimpanzees, orangutan, and gorilla,” Quarterly Journal of Experimental Physiology, 1917, 11: 135.
38 The phrasing here is that of Marcel Kinsbourne in “The control of attention by interaction between the cerebral hemispheres,” Fourth International Symposium on Attention and Performance, Boulder, Colorado, August 1971.
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right, so that some of the so-called higher mental processes could be the resultants of the two opposing hemispheres?
At any rate, the first step in bringing some credence to these ideas about the relationship of schizophrenia to the bicameral mind and its neurological model is to look for some kind of laterality differences in schizophrenics. Do such patients have different right-hemispheric activity from the rest of us? Research on this hypothesis is only beginning, but the following very recent studies are at least suggestive:
• In most of us, the total E E G over a long time period shows slightly greater activity in the dominant left hemisphere than in the right hemisphere. But the reverse tends to occur in schizophrenia: slightly more activity in the right.39
• This increased right hemisphere activity in schizophrenia is much more pronounced after several minutes of sensory deprivation, the same condition that causes hallucinations in normal persons.
• If we arrange our E E G machine so that we can tell which hemisphere is more active every few seconds, we find that in most of us this measure switches back and forth between the hemispheres about once a minute. But in those schizophrenics so far tested, the switching occurs only about every four minutes, an astonishing lag.
This may be part of the explanation of the “segmental set” I have previously referred to, that schizophrenics tend to “get stuck” on one hemisphere or the other and so cannot shift from one mode of information processing to another as fast as the rest of us. Hence their confusion and often illogical speech and behavior in interaction with us, who switch back and forth at a faster rate.40
39 Arthur Sugarman, L. Goldstein, G. Marjerrison, and N. Stoltyfus, “Recent Research in EEG Amplitude Analysis,” Diseases of the Nervous System, 1973, 34: 162-181.
40 This is the preliminary work on a few subjects of Leonide E. Goldstein, “Time Domain Analysis of the EEG: the Integrated Method,” Rutgers Medical School preprint, 1975. I am grateful to him for discussing these suggestions with me.
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• It is possible that the explanation of this slower switching in schizophrenia is anatomical. A series of autopsies of long-term schizophrenics have, surprisingly, shown that the corpus callosum which connects the two hemispheres is i mm. thicker than in normal brains. This is a statistically reliable result. Such a difference may mean more mutual inhibition of the hemispheres in schizophrenics.41 The anterior commissures in this study were not measured.
• If our theory is true, any extensive dysfunction of the left temporal cortex due to disease, circulatory changes, or stress-induced alteration of its neurochemistry should release the right temporal cortex from its normal inhibitory control. When temporal lobe epilepsy is caused by a lesion on the left temporal lobe (or on both the left and right), thus (presumably) releasing the right from its normal inhibition, a full 90 percent of the patients develop paranoid schizophrenia with massive auditory hallucinations. When the lesion is on the right temporal lobe alone, fewer than 10 percent develop such symptoms. In fact this latter group tend to develop a manic-depressive psychosis.42
These findings need to be confirmed and explored further. But together they indicate without doubt and for the first time significant laterality effects in schizophrenia. And the direction of these effects can be interpreted as partial evidence that schizophrenia may be related to an earlier organization of the human brain which I have called the bicameral mind.
In Conclusion
Schizophrenia is one of our most morally prominent problems of research, such the agony of heart that it spreads both in those 41 Randall Rosenthal and L. B. Bigelow, “Quantitative Brain Measurements in Chronic Schizophrenia,” British Journal of Psychiatry, 1972, 121: 259-264.
42 P. Flor-Henry, “Schizophrenic-like Reactions and Affective Psychoses Associated with Temporal Lohe Epilepsy: Etiological Factors,” American Journal of Psychiatry, 1969, 126: 400—404.
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afflicted and in those who love them. Recent decades have watched with gratitude a strong and accelerating improvement in the way this illness is treated. But this has come about not under the banners of new and sometimes flamboyant theories such as mine, but rather in the down-to-earth practical aspects of day-today therapy.
Indeed, theories of schizophrenia — and they are legion — because they have too often been the hobbyhorses of competing perspectives, have largely defeated themselves. Each discipline construes the findings of others as secondary to the factors in its own area. The socio-environmental researcher sees the schizophrenic as the product of a stressful environment. The biochemist insists that the stressful environment has its effect only because of an abnormal biochemistry in the patient. Those who speak in terms of information processing say that a deficit in this area leads directly to stress and counterstress defenses. The defense-mechanism psychologist views the impaired information processing as a self-motivated withdrawal from contact with reality. The geneticist makes hereditary interpretations from family history data. While others might develop interpretations about the role of schizophrenogenic parental influence from the same data. And so on. As one critic has expressed it, “Like riding the merry-go-round, one chooses his horse. One can make believe his horse leads the rest. Then when a particular ride is finished, one must step off only to observe that the horse has really gone nowhere.43