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By studying patients who developed abnormal hoarding behavior following brain injury, neurology researchers in the University of Iowa Roy J. and Lucille A Carver College of Medicine have identified an area in the prefrontal cortex that appears to control collecting behavior. The findings suggest that damage to the right mesial prefrontal cortex causes abnormal hoarding behavior by releasing the primitive hoarding urge from its normal restraints. The study was published online in the Nov. 17 Advance Access issue of the journal Brain.
Hoarding behavior is common among animals; around 70 species hoard and mostly they hoard food, which makes sense from a survival standpoint. Studies of hoarding behavior in rodents have shown that collecting is driven by certain primitive structures deep in the brain and most mammals, including humans, share these subcortical regions.
"But human collecting goes beyond items that are solely useful for survival," said Steven Anderson, Ph.D., UI associate professor of neurology and lead author of the study. "People often collect art or stamps or pretty much anything. Clearly there is some higher structure in humans that modulates the collecting drive and that's what we think we have tapped into."
The UI team studied 86 people with focal brain lesions - very specific areas of brain damage – to see if damage to particular brain regions could account for abnormal collecting behavior. Other than the lesions, the patients' brains functioned normally and these patients performed normally on tests of intelligence, reasoning and memory.
A questionnaire completed by a close family member was used to identify problematic collecting and the behavior was classified as abnormal if the collection was extensive; the collected items were not "useful" or aesthetic; the collecting behavior began only after the brain injury occurred; and the patient was resistant to discarding the collected items.
The questionnaire very clearly split the patients into two groups – 13 patients who had abnormal collecting behavior and a majority (73 patients) who did not. Unlike normal collecting behavior such as stamp collecting, the abnormal collecting behavior of these patients significantly interfered with their normal daily life. Patients with abnormal collecting behavior filled their homes with vast quantities of useless items including junk mail and broken appliances. Despite showing no further interest in the collected items, patients resist attempts to discard the collection.
To determine if certain areas of damage were common to patients who had abnormal collecting behavior, the UI researchers used high-resolution, three-dimensional magnetic resonance imaging to map the lesions in each patient's brain and overlapped all the lesions onto a common reference brain.
"A pretty clear finding jumped out at us: damage to a part of the frontal lobes of the cortex, particularly on the right side, was shared by the individuals with abnormal behavior," Anderson said. "Our study shows that when this particular part of the prefrontal cortex is injured, the very primitive collecting urge loses its guidance.
"This finding sheds some light on a ubiquitous, nearly universal human behavior that we really don't know much about, and we can use this as springboard to think about normal collecting behavior."
Anderson added that the findings also may have implications for understanding certain neurological conditions such as obsessive-compulsive disorder (OCD) where abnormal collecting behavior occurs but the patient has no readily detectable brain defect.
"Patients with OCD and some other disorders such as schizophrenia, Tourette's syndrome and certain dementias, can have similar pathological collecting behavior but we don't have a pointer to locate where in the brain the problem is occurring," Anderson said. "Our hope is that our findings with these brain lesion studies will lead to insights in these conditions as well."
Anderson's co-authors on the study were Antonio Damasio, M.D., Ph.D., the Maurice Van Allen Professor of Neurology and head of the department, and Hanna Damasio, M.D., UI Foundation Distinguished Professor in the Department of Neurology. The study was funded in part by a grant from the National Institute of Neurological Disorders and Stroke.
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