Baby’s Growth May Warn of Schizophrenia

A UCLA psychiatrist has identified what she calls a clear-cut pattern of warning signs of schizophrenia that show up as early as the first year of life, perhaps making it possible in some cases for early diagnosis and treatment of the emotionally debilitating condition.

Analyzing the results of her four-year study of children of schizophrenic adults, Barbara Fish and her colleagues report today in the Archives of General Psychiatry that those children who developed schizophrenia displayed a characteristic set of symptoms during infancy.

Those symptoms included a distinct pattern of spurts and lags in weight gain, bone growth and mental development. Not all children who displayed the symptoms developed schizophrenia, whose victims lose touch with reality. But children who did not display the symptoms did not develop the disorder.

The study provides the strongest evidence yet that the severe mental disorder, which affects one in 100 people, has a biological basis. Moreover, it opens the door to a program of childhood screening that could be used to treat the disorder early, Fish said.

“The tests themselves (for detecting susceptibility to the disorder) are simple ones that pediatricians already do a little bit of in watching infants develop,” Fish said. “They are very straightforward.”

UCLA psychiatrist Daniel X. Freedman, editor of the Archives of General Psychiatry, said Fish “is a very careful and keen observer . . . and this paper is enormously convincing. We’ve always wished we had predictors of who will get ill (from schizophrenia). This is not a handy clinical predictor for everybody, but in certain populations it will be very useful.”

“This is a very good study,” said psychiatrist Samuel Keith of the National Institute of Mental Health, editor of the Schizophrenia Bulletin and former head of schizophrenia research at the institute.

The symptoms of schizophrenia include hallucinations and delusions, severely inappropriate emotional responses, erratic behavior, and problems in thinking and concentrating. Three-quarters of schizophrenics develop the disorder between ages 16 and 25.

On any given day, 600,000 people in the United States are in treatment for the disorder. Such treatment typically involves hospitalization and the use of powerful medications. The disorder cannot be adequately treated through psychotherapy alone.

There has been growing recognition that vulnerability to schizophrenia has a strong genetic component. About 15% of children in families with one schizophrenic parent will develop the disorder and 40% to 50% of those in families with two schizophrenic parents will develop it. Three years ago, scientists believed that they had found the vulnerability gene, but that proved to be a case of mistaken identity.

In most cases, a genetic component alone is not sufficient to cause the development of schizophrenia. Typically, some other injury or damage to the brain is required. USC psychologist Sarnoff Mednick and others have found that the mother’s exposure to the influenza virus during the second trimester of pregnancy, when crucial brain circuitry is being formed, is one such injury. Complications of pregnancy are another.

Fish’s study has its origins 40 years ago, when University of Chicago psychiatrist Joseph Marcus--one of the authors of the new paper--began studying Israeli children with at least one schizophrenic parent. At that time, researchers mistakenly believed that interactions between parents and children were the cause of schizophrenia, and Marcus hoped to show that the incidence was lower among children raised in commune-like kibbutzim than in those raised in nuclear families in Jerusalem.

But he found no differences between the two groups. Instead, he discovered that about half the children of schizophrenics had subtle neurological signs when they were of school age. “We were dealing with something that had to do with brain dysfunction rather than environment,” Marcus said.

The affected children had below-normal muscle coordination and were not good at paying attention in class. Some were hyperactive.

“These were things that you saw in a very careful examination,” he said. “They were not things that really made these kids stand out as being behaviorally disturbed.” These children had what is now called a “schizotypal personality disorder.”

When Marcus followed the 100 children enrolled in the project to adulthood, nine of the schizotypal children developed schizophrenia. None of the children who were not schizotypal developed the disorder.

But because they had started following the children when they were already past infancy, “we didn’t know whether it was genetic, related to problems in pregnancy, or what,” he said. Thus, they began studying a new group at birth who are now passing through elementary school.

Meanwhile, in the 1950s, Fish began studying a similar group of 12 children of schizophrenics and 12 children of non-schizophrenic parents in New York City. By tracking those in that group who have gone on to become schizophrenic, Fish has concluded that there are definite warning signs of schizophrenia in infancy.

Vulnerability to schizophrenia is foreshadowed in infancy by a condition she calls “pandysmaturation,” which requires that three problems be present in the first year:

* Development of muscle or visual functions slows briefly and then speeds up to return to normal levels.

* An infant may not have attained certain muscle functions that it should have by its age but does possess more complex functions that normally would occur later in development. For example, an infant might be able to support weight with his legs but not be able to lift his head--the reverse of the normal pattern of development.

* The lags in development of muscle or visual functions are accompanied by similar, temporary lags in skeletal growth.

To test her findings, Fish used her criteria to study data about 58 infants in Marcus’ new Jerusalem group. Without knowing the identity or parenthood of the children, she reported in today’s paper that she successfully identified which children went on to become schizotypal and are most likely to develop adult schizophrenia.

Fish emphasized that all three traits must be present in the child for schizotypal to be diagnosed. A child who is only a little late to walk or talk or who just shows lags and spurts in development is at no more risk of developing schizophrenia than any other child, she said.

Fish predicted that her criteria could soon be used as a screening test to identify children with a high risk of schizophrenia in affected families. “We don’t want it to scare parents because we don’t want any self-fulfilling prophecies,” she said.

But if a child is found to be schizotypal, Fish said, the child can be watched more carefully and steps taken to promote development, much as they would be for a brain-damaged child. The stimulation of play and intellectual activity might ameliorate the effects of a schizotypal personality during childhood but would not prevent adult schizophrenia.

Though psychiatrists cannot prevent schizophrenia, she said, the ability to identify those at high risk should make it possible to monitor them at an early stage when treatment should be more effective.