Adolescent Schizophrenia Physically Degenerates the Brain
Abstract & Commentary
Source: Thompson PM, et al. Mapping adolescent brain change reveals dynamic wave of accelerated gray matter loss in very early-onset schizophrenia. Proc Natl Acad Sci U S A. 2001;98:11650-11655.
Children and adolescents rarely develop schizophrenia. When they do, however, major crippling neurological abnormalities often develop. These reflect the presence of widespread cerebral areas of functional brain damage. Sometimes termed "adolescent onset schizophrenia" (AOS), the disease often overlaps puberty and generates serious cerebral abnormalities. These include: 1) bizarre delusions; 2) hallucinations, especially if perceived by internally generated vocal comments or visual objects; 3) disorganized speech; 4) grossly disturbing or catatonic behavior; and 5) negative symptoms such as a flattened affect, little speech, and absence of either an internal thought or an imagined self. Additional symptoms include hand flapping, echolalia, lack of attention, and lost short- and long-term memory. Until recent years, however, neither quantitative functional brain maps nor the specific evolving patterns of behavior have been strongly investigated in pre- or post puberty schizophrenic children.
Thompson and colleagues used a single MRI instrument to assure technical consistency in order to study dynamically a single group of schizophrenic and normal children. Using a 3-part protocol lasting for a 5-year period, they studied 12 AOS children, 6 boys and 6 girls, aged 13.9 ± 0.8 years at the start. The same protocol and imaging machine was also used on 12 healthy adolescents (6 boys and 6 girls) all of whom had similar ages, and tests compared to the AOS patients. At the onset and advancing time, all of the schizophrenic children expressed progressively serious psychotic symptoms, whereas the healthy adolescents’ brains grew normally and intelligently. Three quantitative MRI functional evaluations were applied to each subject: 1) age at the start averaged 13.9 ± 0.8 years; 2) a middle evaluation occurred at 2.3 ± 1.4 years from the start; and 3) final changes of brain and behavior were concluded at 4.6 years.
Functional MRI in the AOS patients identified a severe, steadily progressive loss of functional cerebral gray matter in 5 years. At the first baseline MRI, affected peaks of AOS dysfunction appeared in parietal cerebral areas normally devoted to generating visual-spatial thinking. As time (4.6 yrs) passed, degeneration proceeded into the anterior temporal lobes, the sensory-motor cortex, and, finally, the frontal eye fields . Average total annual cerebral functional losses amounted to 2.9 ± 0.5% in the abnormal superior parietal lobules; the right hemisphere 2.9 ± 0.5%; both superior frontal cortices at 2.6-.7 ± 0.5; and the lateral temporal cortices 2.3-2.4 ± 0.9. These unfavorable functional losses compared significantly to normal physiological reductions of 0.7 ± 2% and 1.1 ± 0.3% in the healthy controls. Group functional declines between the schizophrenics and normal adolescents equaled P < 0.003 and < 0.005 in degree of severity. Subtle functional changes over 5 years in normal adolescents of < 0.9-1.4% appeared in all areas. Presumably, anatomic patterns change a little as normal adolescents mature, leaving the adult brain with minor readjustments of shape derived from the genesis and storage of new memories as well as the perfection of more coordinated athletic behavior.
Commentary
These clinical-functional studies place schizophrenia squarely in the category of inherited, degenerative, cerebral brain diseases. Since 1980, both scientific neurology and psychiatry have refocused some of their best minds on this principle. Unfortunately, however, most investigators have focused most of their clinical efforts into the different categories of neurology and psychiatry. Neurologists primarily care for patients with Huntington’s disease, dementia, Parkinson’s disease, epilepsy, strokes, and peripheral neuropathy. Psychiatrists mainly care for manic-depressive illness, schizophrenia, and a raft of patients with life-long functional disorders that severely resist medical and psychiatric support.
Schizophrenia statistically reflects genetic trait(s), but not apparently single ones, since the disease has been known to attack only one carrier of monozygotic twins. (One example of this occurred in the above group.) Nevertheless, its patterns of genetic unevenness reflect those of neurological diseases such as Parkinson’s, elderly dementia, multiple sclerosis, and others.
This current report demonstrates fully the earlier that schizophrenia attacks a brain, the worse will become the future of the beholder. Postadolescent sufferers often develop schizophrenia between 17-25 years old but, when treated, many oscillate thenceforth from sick to fairly well for several years. Thompson et al’s exceptionally important report opens the door to the quantitative damage that schizophrenia does to the early maturing brain. Pursuing what they have found here invites additional studies to affirm this first study and extend it into adolescent-to-early adult groups of schizophrenics. An excellent discussion of children and adolescents with schizophrenia appeared in: McClennan J, et al. Practice parameter for the assessment and treatment of children and adolescents with schizophrenia. Supplement of the J Am Acad Child Adolesc Psychiatry (JAACA), July 1999. —Fred Plum
Dr. Plum, University Professor, Weill Medical College, and Attending Neurologist, New York Presbyterian Hospital, is Editor of Neurology Alert.
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