Schizophrenia as a Brain Defect
“Know syphilis in all its manifestations and relations, and all things clinical will be added unto you.” These often quoted words of Sir William Osler (1849-1919) graphically and succinctly sum up the late-nineteenth and early-twentieth-century view concerning the nature and cause of schizophrenia and other forms of madness.
Since the early 1980s views similar to those of Osler’s have been becoming increasingly fashionable.
One of the most vociferous
proponents of this germ theory of schizophrenia is Dr. E. Fuller Torrey1 Another one of
his pet theories is his belief that you can catch the schizophrenia bug from
cats.2 In 1983, Dr. Torrey
appeared on the Phil Donahue Show where he gave a presentation of his views on
schizophrenia. When Donahue remarked that Torrey’s views would hardly earn
him a standing ovation in every quarter of the psychiatric community, Dr.
I think the
psychiatric community that are reading their medical journals are almost
unanimous now that schizophrenia is a brain disease. Unfortunately there is a
segment of the psychiatric community that reads only the National Geographic. They have not got the word yet.3
To lend substance to his
claim that schizophrenia is a brain disease, Dr. Torrey displayed and described pictures
taken by a computerized axial tomographic (CAT) scanner:
This is two pictures. The top row
are CAT scans from the brain of a normal person. This is taken as showing the
black is the fluid in the ventricles. That’s what a normal brain looks like.
The bottom row is the brain of a person with schizophrenia. You can see how
much larger the
ventricles are. That’s fluid you’re looking at. That means this loss of
brain tissue. That’s the brain disease you are looking at.4
To get some idea of the deceptiveness of Dr. Torrey’s presentation, let’s imagine the following: instead of Dr. Torrey, suppose that either Pat Robertson or Jerry Falwell appeared on the Phil Donahue Show. After lecturing the audience on the evils of secular humanism, Rev. Falwell shows two pictures. One of these pictures is a CAT scan taken of a brain of a born-again Christian. This picture reveals the utter flawlessness of that person’s brain. Then Falwell shows a CAT scan taken of the brain of a secular humanist. This picture reveals that the brain of that godless individual has grossly enlarged ventricles: a clear sign of brain atrophy . From this, Falwell comes to the thundering conclusion that secular humanism is a brain disease.
However, had either Robertson or Falwell presented the above argument as “proof” that secular humanism is a brain disease, his claim would have been met with almost total disbelief—and for three very good reasons. First, it would have been obvious to nearly everyone that the vast majority of secular humanists would have normal brains. Second, it would have been equally obvious that those suffering from brain atrophy would include a proportionate number of born-again Christians. Third, it would seem highly unlikely that any correlation would exist between secular humanism and brain atrophy .
But the same sorts of objections which can be brought against this purely hypothetical or imaginary claim that secular humanism is a brain disease can also be brought against a similar claim made by Torrey in regard to schizophrenia. First of all, in every computerized tomographic (or magnetic resonance imaging ) brain scan study which has been done using schizophrenic patients and normal controls, it has been found that a clear majority of the schizophrenics had normal-sized ventricles. For example, in a 1983 review of such studies, it was found that anywhere from 60 to 95 percent of the schizophrenics showed no sign of brain atrophy or enlarged ventricles.5 In fact, at least a dozen brain scan studies exist which reveal no differences at all between the ventricular size of schizophrenics and that of normal controls.6
Among the twelve brain scan studies mentioned above is one done by Terry L. Jernigan.; and her associates at the Stanford University School of Medicine.7 This study involved 30 schizophrenics and 33 normal volunteers. Jernigan’s study is particularly noteworthy in that the methods used in calculating the ventricular-brain ratio (VBR) are far more sophisticated than those of any previous study.8 Furthermore, Dr. Jernigan sent the brain scans from her study to two other research groups—groups led by Drs. Daniel R. Weinberger and Charles Golden. All three of these groups blindly measured the VBRs of the subjects’ brain scans and could find no difference between the VBRs of the schizophrenics and those of the controls.9
Significantly enough, while none of the three groups could find any relative difference between the VBRs of the schizophrenics and the controls, the absolute values of the VBRs measured by Dr. Golden were, on the average, almost twice those measured by Drs. Jernigan and Weinberger.10 Such discrepant results clearly indicate the inherent subjectivity involved in interpreting data derived from CAT scans.
Another brain scan study of special interest was done by William R. Yates and his coworkers at the University of Iowa College of Medicine. Yates’ study is the largest study of its kind to date. His study involves 108 schizophrenic patients, 50 patients with affective disorder, and 74 age- and sex-matched controls. Yates and his group found that neither the schizophrenic patients nor the patients with affective disorder had ventricles larger than those of the control subjects.11
The twelve brain scan studies that have found no differences between schizophrenic subjects and normal controls include four studies utilizing magnetic resonance imaging (MRI)—a technique capable of producing far clearer and more detailed pictures of the brain than is possible with computerized tomography. The four MRI studies include two studies done by Robert C. Smith and his associates at the Texas Research Institute of Mental Sciences in Houston;12 a study done by Roy C. Matthew and C. Leon Partain of the Vanderbilt University School of Medicine in Nashville, Tennessee;13 and a study done by Eve C. Johnstone and her colleagues at the Clinical Research Centre in Harrow, Middlesex, England.14
Although the twelve studies mentioned above are contradicted by other studies showing that some schizophrenics do have enlarged ventricles, the contradiction is more apparent than real since all the studies that have ever been done support the conclusion that the vast majority of schizophrenics have normal-sized ventricles and show no sign of brain atrophy whatsoever.
Moreover, it is equally important to bear in mind that there are groups of people who have enlarged ventricles but who still have no psychiatric problems. For example, it is known that ventricular enlargement is much more common in left-handed people than in right-handed people.15 This is due to the fact that left-handed people have a tendency to develop brain lesions as a result of their brains being organized differently from right-handed people.16 Yet no sensible person would claim that left-handedness is a brain disease. On the contrary, left-handed people tend to be gifted and contribute a disproportionate number of professional athletes, artists, architects, engineers, and mathematicians.17
Finally, various attempts have been made to establish meaningful correlations between ventricular enlargement (VE) and schizophrenic symptomatology. For example, VE is associated with the presence of negative symptoms (blunted affect , lack of motivation) and the absence of positive symptoms ( delusions, hallucinations ).18 Other authorities such as Farmer have found just the opposite: that VE is associated with the presence of positive symptoms and the absence of negative symptoms.19 Yet there are also other authorities such as Nasrallah,20 Pandurangi,21 Owens,22 Obiols,23 and Bankier,24 who have found no correlation at all between VE and the presence or absence of positive and negative symptoms, or between VE and the degree of cognitive impairment or mental disorder in their schizophrenic subjects. For instance, Owens has found that “Some of the most handicapped schizophrenic patients had ventricles in the smallest range of ventricle size,”25 while Obiols has found in some cases that the schizophrenic patients with the most VE have the least cognitive impairment.26 Moreover, while Pandurangi has found significant correlations between VE and impairment on several parameters traditionally associated with brain damage, he—like Nasrallah and Owens—is unable to find any correlation between VE and clinical variables indicative of schizophrenia.27 Finally, as a result of his own study which found a total lack of any significant differences between schizophrenics with and without VE, Bankier has come to the conclusion that VE must be totally unrelated to schizophrenia.28Andreasen and others have found that
Rather than being the
result of a brain disease, the VE seen in schizophrenic patients can readily
be accounted for by such factors as the effects of prolonged emotional stress,
the effects of institutionalization, an inadequate diet, repeated and
prolonged sleep deprivation
, and the effects of neuroleptic drugs. For example, it is known that
emotional stress can cause a hypersecretion of cortisol which decreases the
water content of the brain and causes the brain to shrink.29 Furthermore, two very
recent studies have presented hard evidence that neuroleptic drugs cause brain
atrophy. In one study, conducted by Madsen and associates in Denmark, 31
psychotic patients who had never taken neuroleptic drugs underwent
computerized tomographic scans upon being hospitalized, and then again after
five years of being on neuroleptic drugs. The authors of this study state,
“The estimated risk of atrophy increases by 4 to 6% for each additional 10 g
of neuroleptic drug.”30 The other study was conducted by Raquel E. Gur and her
colleagues at the University of Pennsylvania in Philadelphia. In using
magnetic resonance brain imaging to monitor 20 first-episode schizophrenic
patients over a 31-month period, these researchers found “higher medication
dose was associated with greater reduction in frontal and temporal volume (r =
-.075 and -0.66, respectively; P < .001).”31
Some psychiatrists are not content with merely claiming that schizophrenia is a brain disease, but have attempted to locate the exact spot in the brain where schizophrenia does its sinister work. Schizophrenia has been described by various authorities as a frontal-lobe disease32 as a temporolimbic disease,33 as a left-hemisphere disease,34 and as a right-hemisphere disease.35
One of the claims encountered most often in psychiatric journals these days is the notion that schizophrenia is a disease localized in the hippocampus .36 This theory stems from the work of Sarnoff A. Mednick, now at the University of California at Los Angeles, who has hypothesized that a lack of oxygen occurring prior to birth causes hippocampal damage—a condition that ultimately leads to schizophrenia.37 More recently, in 1987, Nestor A. Schmajuk of Boston University has suggested that the behavioral disorders of rats with hippocampal lesions are an adequate model for understanding humans suffering from schizophrenia.38 More to the point are the findings of two UCLA medical researchers, Arnold Scheibel and Joyce A. Kovelman. These investigators have found gross cellular disarray in the hippocampi of some schizophrenic patients.39
However, in a study similar to that of Scheibel and Kovelman’s, Daniel R. Weinberger of the National Institute of Mental Health found just as much cellular disarray in the hippocampi of normal controls as he did in the hippocampi of schizophrenics.40 Furthermore, in a more recent study, Scheibel and Kovelman have themselves been unable to find significant differences between the hippocampi of schizophrenics and nonpsychotic controls.41
It is, moreover, highly speculative at best to use the behavioral disorders of hippocampal-lesioned rats as a model for understanding schizophrenia. Certainly it would seem self-evident to anyone that the behavior of hippocampal-lesioned human beings would be of far more relevance in assessing the truth or falsity of the hippocampal theory of schizophrenia than the behavior of brain-damaged rats. An ideal test of this theory would be to surgically remove the hippocampus of a human being and observe the results. If that person becomes schizophrenic as a result of this operation, then the hippocampal theory of schizophrenia stands confirmed. If not, then the theory has been decisively refuted.
According to Jonathan
Winson, such an operation—resulting in the removal of nearly the entire
—was performed on a twenty-nine-year-old epileptic man by a psychosurgeon,
Dr. William Scoville, on September 1, 1953, at the Hartford Hospital in
Hartford, Connecticut. In referring to this patient, Winson writes:
preoperative personality was not affected by the operation, nor were his
capacity to understand and reason.42
In fact, that patient did not exhibit any psychotic or schizophrenic symptoms during the entire twenty-five year period following his operation in which he was under intense scientific scrutiny.43 But if schizophrenia is caused by damage to the hippocampus , then this man should have become a schizophrenic. That he didn’t is a clear refutation of the hippocampal theory of schizophrenia if ever there was one!
However, as a result of having his hippocampus removed, the above patient did have one prominent symptom: his memory was severely affected. Although this man’s old memories were completely intact, he suffered from a complete inability to learn new things or to remember events in his immediate past.
From cases such as the one mentioned above it has been learned that the hippocampus is that portion of the brain where new memories are stored.44
Therefore if (a) the ability to remember depends upon having an intact functioning hippocampus , and (b) schizophrenia is the result of a damaged hippocampus , then it follows logically that schizophrenics must suffer from severe memory impairment. Yet it has been known for a long time that schizophrenia leaves one’s ability to remember totally intact. (If this were not the case, it would have been impossible for me to have written this book.) The mere fact that schizophrenia does not affect the memory is another reason that the hippocampal theory of schizophrenia is totally without any scientific basis.
Finally, we are presented
with the pitiful spectacle of reputable medical researchers damaging the
brains of rats, and fantasizing about these animal’s “schizophrenic
symptoms,” when it has been known for decades (since 1953) that damage to
has no bearing upon whether or
not a person becomes schizophrenic!
By no means is psychiatry content with pointing to structural defects in the brains of schizophrenics. Recently, psychiatry has acquired a wonderful new tool—positron emission tomography (PET)—which allows it to point with pride to brain defects of a wholly functional nature.
Just as it has been claimed that CAT scans have revealed that schizophrenics have atrophied brains, it has likewise been claimed that PET scans have demonstrated that the brains of schizophrenics function in a grossly abnormal way. It has been claimed, for example, that while the brains of normal people burn relatively more energy in the frontal cortex and relatively less energy in the posterior areas of the brain, the brains of schizophrenics exhibit the exact opposite pattern—the so-called hypofrontal pattern —and burn relatively less energy in the frontal and relatively more energy in the posterior regions of the brain.45
This hypofrontal metabolic pattern is by far the best documented functional brain abnormality that psychiatric researchers have found in schizophrenics while using the PET scanning technique. Moreover, as with the CAT scan studies, the results in these PET scan studies have been very widely publicized, and claims have been made that such studies offer conclusive proof that schizophrenia is a bona fide brain disease.
Despite these claims, however, all the available evidence seems to indicate that the diminished metabolism encountered in the frontal lobes of schizophrenic patients is totally unrelated to their psychiatric disorders. Among the studies that support this conclusion is one done by Drs. DeLisi, Buchsbaum, and Holcomb and their associates at the National Institute of Mental Health.46 In this study involving 21 chronic schizophrenics and 21 age- and sex-matched controls, the investigators found that one of the controls and eight of the patients exhibited the hypofrontal pattern . These researchers were unable to find any correlation at all between schizophrenic symptoms and hypofrontality, or between the presence of the hypofrontal pattern and the severity of the so-called “illness.”47
The NIMH investigators found that hypofrontality was correlated with symptoms more characteristic of depression than schizophrenia: emotional withdrawal, disorientation, distractibility, and feelings of hopelessness and helplessness.48 This is consistent with the fact that the hypofrontal pattern is also found in cases of major depression.49
Furthermore, not only is hypofrontality nonspecific to schizophrenia, the hypofrontal pattern is totally absent in most cases of schizophrenia. In fact, many research teams utilizing PET scans have been unable to find hypofrontality in their schizophrenic subjects.50 For example, a research team headed by G. Sheppard at the Charing Cross Hospital in London, England, was unable to find any evidence of hypofrontality in twelve acute schizophrenic patients—most of whom had never been treated with neuroleptic drugs.51 Moreover, like Sheppard, Raquel E. Gur and her associates at the University of Pennsylvania in Philadelphia were also unable to detect hypofrontality in twelve schizophrenic subjects who were not under medication.52
Since the hypofrontal pattern has been found to be associated with depression, and since many of the drugs used in treating schizophrenia are depressants,53 it is only reasonable to suspect that these drugs might be a contributing factor to the hypofrontality encountered in schizophrenia. This suspicion is supported by two lines of evidence. First, three independent research teams led by Widen,54 Volkow,55 and Wolkin,56 have done PET scans on schizophrenics both before and after the administration of neuroleptic drugs and have found that these drugs contribute to the hypofrontal metabolic pattern . Second, G. Geraud and his coworkers at Chu Rangueil in Toulouse, France, found that they were able to reverse the hypofrontal pattern in their schizophrenic subjects by administering a weak dose of piribedil, a drug whose effects are the direct opposite of the drugs used in treating schizophrenia.57 Dr. Geraud and his associates also found that they were able to effect a similar change in some of their schizophrenic patients by merely taking them off neuroleptic drugs for a prolonged period of time.58
However, at this point it
must be stressed that no amount of evidence will ever convince the majority of
psychiatrists that schizophrenics have normally functioning brains. Whenever a
theory about the supposed defectiveness of schizophrenic brains is abandoned,
another similar theory always immediately takes its place. For instance,
recently Henry Szechtman and his colleagues at McMaster University at
Hamilton, Ontario in Canada, have proposed replacing the hypofrontal with hyperfrontal
theory of schizophrenia. According to these investigators, schizophrenia is a
pathological condition characterized by a hyperactive frontal cortex—a
condition which can be corrected by prolonged medication with
“It should be
remembered that, except for their brains, schizophrenics are basically like
other people.”60 This remarkable piece of doublethink is from a
prize-winning essay by John S. Allen, a postdoctoral fellow in the Department
of Psychiatry and Behavioral Sciences at Stanford University. The sole
evidence cited by Dr. Allen in support of his claim that schizophrenics have
brains basically different from those of normal people is the now widely
publicized observation that schizophrenics exhibit jerky
eye movements when tracking the movements of a swinging pendulum, instead of
the smooth-pursuit movements that are considered normal. However, these
eye-tracking movements are known to be controlled by the pontine reticular
formation which is part of the brain stem. Since no psychiatric researcher
seriously believes that schizophrenia is a disease localized in the brain
stem, it is therefore hard to imagine what possible relevance the poor
eye-tracking performance of schizophrenics could have in regard to their
mental problems—unless, of course, one regards the entire
brain of the schizophrenic as being defective. Furthermore, studies show that
anywhere from 14 to 48 percent of schizophrenics do not exhibit these aberrant
eye tracking movements,61 while as much as 8 or 9 percent of normal people
do.62 Moreover, in an
experimental study, Brezinova and Kendell have demonstrated that when normal
people are bored or distracted, their eye tracking performance is
indistinguishable from that of schizophrenics.63
Finally, we are confronted with the astonishing discovery that schizophrenics have smaller brains and smaller craniums than normal people—a finding which accounts for the feeble-mindedness of people such as myself. This earth-shaking discovery was made by 64Nancy Andreasen and her colleagues both at the University of Iowa College of Medicine and at Ohio State University, and was published in the February 1986 issue of the Archives of General Psychiatry.
Upon reading 65 Upon his death Morton was also eulogized in the pages of the Charleston Medical Journal: “We of the South should consider him as our benefactor, for aiding most materially in giving to the negro his true position as an inferior race.”66Dr. Andreasen’s report on how the cognitive impairment of her schizophrenic subjects is correlated with the smallness of their craniums, I am reminded of the work of Dr. Samuel George Morton. Dr. Morton was an eminent nineteenth-century Philadelphia scientist and physician who “proved” that black men have smaller brains and craniums than white men. From his anatomical and anthropological studies, Dr. Morton came to the conclusion that black men were inferior to white men—a conclusion which no one disputed. When Morton died in 1851 his obituary in the New York Tribune noted that “probably no scientific man in America enjoyed a higher reputation among scholars throughout the world, than Dr. Morton.”
Just as the work of Dr.
Morton was used as a scientific justification for slavery, the results of a
variety of psychiatric studies—including studies utilizing CAT and PET
scanners—have been used as
scientific justification for involuntary commitment
. Here, for example, are the words of E. Fuller Torrey
a disease of the brain, the body organ charged with the responsibility of
recognizing sickness and the need for treatment—the same organ which is
sick. Out of this unfortunate coincidence arises the frequent need for
schizophrenic persons to be committed to psychiatric treatment settings
against their will.67
From Dr. Torrey’s reference to “treatment settings” it is obvious that not only does he approve of involuntary commitment , he also believes in treating schizophrenic individuals against their will. (Indeed, more than any other person, Dr. Torrey has been the driving force behind the enactment of the involuntary outpatient commitment laws making it illegal for mental patients to stop taking psychiatric drugs.*68)
The therapy most commonly
used in treating schizophrenic persons is the administration of neuroleptic drugs—drugs which are known to cause severe and often
irreversible damage to the brain. The use of such drugs is in turn justified
by the notion that schizophrenics suffer from a biochemical imbalance.
the third edition of his Surviving Schizophrenia, Dr. Torrey places
©2003/2009 John Modrow