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Still Crazy After All These Years 1



Even more convincing, in Andreasen's eye, are the five or six MRI studies of newly diagnosed schizophrenics conducted at centers in Australia, Asia, Europe, and North America. These have shown "substantial structural brain abnormalities," including overall smaller brain size, enlarged ventricles, and other anomalies. 

She says one cannot conclude, based on these studies, that schizophrenia damages any specific brain cells or regions." A diligent search by many talented neuroscientists has not identified any such specific regional abnormalities or nerve cell lesions," she writes. Instead, she theorizes that schizophrenia is a "misconnection syndrome," meaning that it's a disorder that "damages the way regions are connected to one another, so that a breakdown in signal transfer occurs.… Like a malfunctioning computer, the various nodes in brain networks send information back and forth in a way that causes file corruption, garbled information, or crashes." 

Andreasen says PET scans (which measure changes in blood-flow associated with brain function) have shown people with schizophrenia to have abnormal blood-flow patterns while performing a variety of tasks. "We now suspect that the cerebellum may be malfunctioning as a 'metronome' or timekeeper, causing signaling to lose its synchrony and coordination," she writes. "The thalamus, which functions as a filter or gatekeeper that helps determine how much information should be let in or out of the brain, may be failing to screen information out, so that the system becomes overwhelmed with so much data that the person's thinking becomes confused or sluggish." 

Brain chemistry is yet one more area where Andreasen and other psychiatrists see evidence of an organic disorder in schizophrenics. Andreasen says researchers early on noted that stimulants such as amphetamines, which cause the brain to release lots of the neurotransmitter dopamine, can produce schizophrenia-type symptoms. Conversely, nearly all antipsychotic drugs prevent dopamine molecules from delivering chemical messages to the nerve cell membranes that normally receive them. "These observations led to the formulation of the 'dopamine hypothesis of schizophrenia' " in the 1960s, writes Andreasen. "Simply stated, it suggested that the symptoms of schizophrenia were due primarily to hyperactivity in the dopamine system." 

Although this hypothesis "was universally accepted…for nearly thirty years," Andreasen says that in the past decade, "the plot has thickened" as antischizophrenic drugs that block the function of two other neurotransmitters, serotonin and glutamate, have hit the market. The newer drugs, known as "atypical neuroleptics," are believed to work as well as and have fewer serious side effects than the older generation of antipsychotics. Andreasen writes, "Clinician scientists now think that schizophrenia occurs as a consequence of a much more complex chemical imbalance that includes multiple neurotransmitter systems that interact with and modulate one another." 

Mosher finds none of this convincing. "There are very good critiques of the adoption studies and the twin studies," he asserts. The problem with explaining the higher concordance of schizophrenia among identical twins by pointing to their shared genes is that identical twins also share the same environment to a greater extent than even nonidentical twins. Mosher says a number of studies have demonstrated that they're "clearly raised more similarly than nonidentical twins or siblings. People tend to dress [identical twins] more alike. They look the same. They generate a similar response. And they do have this sense of being one person." So that shared environment may explain why a higher percentage of both of them go crazy than do nonidentical siblings. 

One traditional way of subtracting environment from the picture in identical-twin studies has been to look at pairs who've been raised separately. But, Mosher says, so few identical twins are separated at birth and later diagnosed with schizophrenia that there aren't enough of them to be statistically significant. 

On the other hand, you can find plenty of schizophrenic parents whose offspring were raised by adoptive parents, and a number of researchers have examined what happens in such cases. Andreasen cites two studies of adopted children who grew up in families considered normal or healthy. Both studies showed that the rate of schizophrenia among children with a schizophrenic parent was the same (about 10 percent) regardless of whether the children were raised by the adoptive family or the schizophrenic mother. 

Mosher, however, says both of these studies had major methodological flaws. In contrast, he says a twin study begun about 20 years ago by a Finn named Tienari and an American named Wynne is "one of the best pieces of research done this century." It compared the outcome of children who had a schizophrenic parent with that of children of normal parents when both groups were placed in normal adoptive families, and it found that the children of schizophrenics developed schizophrenia only slightly more often than the control group. "So you can say, well, there's a little genetic bit there, but it takes the family to make that bit be expressed," Mosher says. One's genetic makeup "at most may be a sort of background variable. But it's so weak and so indefinable as to be useless in terms of defining the condition." 

As for the abnormalities that researchers have found with brain scans, Mosher thinks the antischizophrenic medication accounts for much of this. He says, "The Germans, who invented neuropathology, looked at the brains of thousands of schizophrenics before there were any neuroleptics. And they were never able to find anything. They never reported increased ventricular volume, which at postmortem you can measure quite easily. And they also never reported any specific cellular pathology, and they studied many, many, many brains." He adds that "there are a whole lot of people who don't have schizophrenia and also have enlarged ventricles. And there are people who have other psychiatric conditions who have enlarged ventricles, and there are a number of known causes of enlarged ventricles that are not schizophrenia. So, yes, there is a statistical difference, but it is not specific."   

"On the other hand," Mosher continues, "there are studies that have shown that people treated with neuroleptics have changes in brain structure that are at least associated with drug treatment, dosage, and duration -- and have been shown to increase over time as drugs are given." He cites one "horrific study" of children between the ages of 10 and 15 in which the researchers measured the volumes of the kids' cortexes. "The cortex is what you think with, the part on the outside," Mosher explains. Over time, "They watched the cortical volume of these young people decline, while the cortical volume of the nonschizophrenic controls was expanding because they were adolescents and still growing." The researcher concluded that their schizophrenia had caused the decrease in the subjects. "And yet every single one was taking neuroleptic drugs," Mosher says. 

He concedes that the German neuropathologists working earlier in the last century didn't have access to PET scans, a tool that Mosher categorizes as being a significant advance. "They show you activity, not just structure. They show which parts of the brain are working at a given task. And okay -- there they do find differences between people who've been labeled schizophrenic and normal people." But how, Mosher asks, can anyone tell if those differences cause the psychotic behavior or result from it? He says he's not at all surprised that the frontal lobe metabolism of drug-naïve schizophrenics looks different on PET scans than that of normal people. "Because if you meet such people, you know that they are in an unusual state of consciousness. They may be going 100 miles a minute. They may be totally distractible. You could measure a lot of other things, and they'd all be different at that point in time. But you don't know if that's a cause or an effect of the way they are." 

Mosher insists he could still be convinced that schizophrenia is a disease. "If you show me something -- either a lesion, meaning a structural abnormality, or a particular neurophysiologic process that is identifiable, can be replicated, and is found only in those people who've been labeled as having schizophrenia, and it's there before the onset of the disorder -- I would change my mind tomorrow. I've held that position for 30 years." But lacking that sort of evidence, he argues that to label anyone as being schizophrenic is to sentence them to a life of discrimination. "It is a sticky label which, once given, is extraordinarily difficult to get rid of," Mosher says. If you have pneumonia and you get over it, you're not forever more considered to be a person with pneumonia. "You're fixed," he says. "But if you are once labeled schizophrenic, the tendency is you are always a person who will be called schizophrenic. This is totally crazy. It violates all the rules of medicine."    

It also flies in the face of a number of studies that have looked at how people fare many years after being given a diagnosis of schizophrenia. Perhaps the best-known American example of this research was conducted by a psychologist named Courtenay Harding. She decided to focus on a group of men and women who had once inhabited the back wards of Vermont State Hospital. "Middle-aged, poorly educated, [and] lower-class," these people had been hospitalized for an average of six years and given long courses of phenothiazines when they were chosen to be discharged and placed in a community rehabilitation program in the mid- to late 1950s. In the early 1980s, Harding and her colleagues at Yale University managed to track down what had happened to 97 percent of the 269 original subjects. Using their medical records, the researchers had independent experts rediagnose the subjects according to updated criteria. In the light of the more stringent modern standards, 118 subjects received a schizophrenia diagnosis, and 82 of them were still alive and willing to be interviewed. 

Contrary to the researchers' expectations, the former mental patients for the most part had encouraging stories to tell. They had evolved "into various degrees of productivity, social involvement, wellness, and competent functioning," the resulting 1987 article in the American Journal of Psychiatry reported. Some 68 percent displayed no signs or symptoms of their previous crazy behavior. Furthermore, Harding's group wasn't the only one to study long-term outcomes; at least four similar efforts have been made. "Together these studies found that one-half to two-thirds of more than 1300 subjects studied for longer than 20 years achieved recovery or significant improvement," Harding noted in another publication. 

Nonetheless, many doctors continue to believe that schizophrenia "is a disease that's always there," Mosher complains. People like John Nash -- the Nobel Prize-winning mathematician whose recovery from schizophrenia was dramatized in A Beautiful Mind -- are "a thorn under [their] saddle," he says. Mosher was appalled by the way the movie seemed to credit the pharmacological industry for Nash's return to sanity. This occurs when a representative of the Nobel committee comes to visit actor Russell Crowe at Princeton in the early 1990s, and Crowe/Nash declares, "I take the newer medications." Mosher points out that in fact Nash has stated on numerous occasions that he has not taken any antischizophrenic medication since 1970.

Harding's study of the former mental patients in Vermont offers confirmation that a drug-free recovery like Nash's was no fluke. Half the subjects interviewed in the 1980s never took any psychotropic medication, and an additional 25 percent said they took it only sporadically. All of those who had fully recovered had long since stopped taking medication, the American Psychiatric Association's Monitor quoted Harding as stating in February 2000. 

There's some debate over whether a massive study of schizophrenic outcomes conducted by the World Health Organization (WHO) shows a similar correlation between lower reliance on neuroleptic medication and recovery. Begun in 1968, this research identified schizophrenics in nine countries (China, Colombia, Czechoslovakia, Denmark, India, Nigeria, USSR, United Kingdom, and the U.S.) and tracked what happened to them over the next five to ten years. The most striking -- some might say astounding -- finding was that the patients from the three poorest countries -- India, Nigeria, and Colombia -- fared far better than their cohorts in the developed countries. Whereas more than three-quarters of the Indians, Nigerians, and Colombians were either recovered or doing fairly well five years after their diagnosis, only 25 percent of the patients in the rich countries enjoyed a similar level of success.  

Critics of this study charged that it must have suffered from design flaws. The patients from the poor countries must not have been as sick. So the World Health Organization launched another investigation, making every effort to use the same criteria in every country. It didn't matter. The new study "replicated in a clear and, possibly, conclusive way…the existence of consistent and marked differences in the prognosis of schizophrenia between the centres in developed countries and the centres in developing countries," the authors wrote. "It can now be said with a fair amount of confidence that they are not the result of differing sample composition in the two groups of centres." 

Muñoz, the San Diego psychiatrist and former president of the American Psychiatric Association, says he's familiar with the study. He's a good friend of the principal researcher. And Muñoz complains, "No matter what the criteria were, you are not comparing apples to apples.… To say that American schizophrenics have a poorer prognosis is just reading into the study things that the study was not studying.… If we are going to try to examine which country gets the best outcome, first you have to know the country." Americans live with a higher level of stress and more barriers to success, Muñoz contends. "For example, if someone is an anthropologist in Colombia, he's probably employed and very successful. If he's an anthropologist here, he's either dusting windows at the museum or doing research that makes him famous. Once you have a degree in this country, either you belong to the minority that is very successful or you will be unhappy for the rest of your life." 

Whitaker, the Boston medical journalist who wrote Mad in America, sees "an obvious flaw"Robert Whitaker in the notion that cultural differences account for the difference in outcomes spotlighted by the World Health Organization study. "The poor countries in the WHO studies -- India, Nigeria, and Colombia -- are not at all culturally similar," Whitaker argues in his book. "They are countries with different religions, different folk beliefs, different ethnic groups, different customs, different family structures." The developed countries studied also share no common culture or ethnic makeup -- but they do provide similar medical care. While in the poor countries, "Only 16 percent of the patients were maintained on neuroleptics. In rich countries, 61 percent of the patients were kept on such drugs," Whitaker points out. "Certainly if the correlation had gone the other way, with routine drug use associated with much better outcomes, Western psychiatry would have taken a bow and given credit to its scientific potions.… Yet, in the WHO studies, that was the model of care that produced the worst outcomes."    

Today the percentage of American schizophrenics taking neuroleptic drugs is much higher. Mosher says, "The standard practice is to treat all such persons with one or another neuroleptic drug and to advise them that they will need to take this drug for the rest of their lives." Concurs Michael McDaniel, a San Diego doctor who has practiced psychiatry for almost 20 years, "You've got to be on the medication. It's a mainstay of treatment." McDaniel asserts that schizophrenics who go off their medication have a relapse rate of 10 percent per month. "So yeah, you've got to be on the medication." 

McDaniel says he thinks that in most cases, the medication alone is not sufficient. Most patients also need to participate in a rehabilitation program. "The studies all show that rehabilitation helps patients coordinate the details of life." The local psychiatrist adds that when the county surveyed schizophrenia patients a few years ago, "The number-one thing the patients wanted was individual psychotherapy." However, few patients receive this, according to McDaniel, who cites several reasons. "One is the nature of the illness. People tend to be erratic. They don't come to appointments regularly. It's also partly historical. Time was when schizophrenia was seen as a psychological condition, and medicines were thought to be bad.… You had people describing the medications as chemical restraints." Today the pendulum has swung too far in the other direction, McDaniel says. "Now nobody really wants to talk or listen to these folks." Economics adds one final complication. "There's not a lot of money for therapists.… It can easily cost $300 to $400 a month for a single antipsychotic medication. And people often take several. The fact is that MediCal pays for medicines. But it pays very poorly for psychotherapy. I don't know if there's a cause and effect there. Probably there is." 

McDaniel estimates that as many as 95 percent of all schizophrenic patients today are taking the newer atypical neuroleptics, instead of the old-fashioned varieties such as Thorazine. "The advances in the medications are huge," he enthuses. Patients still dislike taking them, and "They don't necessarily work that much better. But they are a lot safer," he asserts. "And one of them -- clozapine -- probably is the best antipsychotic ever. It's in a different category. It works in different parts of the brain. The brain is enormously complex! It's three pounds of electronic oatmeal." Every cell connects to every other cell by as many as three connectors. "So a certain amount of what goes on in the brain has to do with timing. And there are wave phenomena because the body releases different chemicals at different times of the day and night. Clozapine seems to work with the brain in that sort of timed fashion. I think that makes a difference." 

McDaniel acknowledges that even clozapine has some drawbacks. In rare cases, "It can destroy someone's bone marrow. So that means you have to check the patient's blood count every two weeks. A lot of people don't like that. Patients still get a lot of other side effects. You have to take it more than once a day. You feel sick. You drool all night. You get sleepy," McDaniel says. "But when it works, it works great! And for your really sick people with schizophrenia, it's great." 

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San Diego Weekly Reader, Vol. 32, No. 2, Jan. 9, 2003
Jeanette De Wyze

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