Bruce D. Perry

Childhood trauma, the neurobiology of adaptation, and “use-dependent” development of the brain: How “states” become “traits”

Childhood trauma has profound impact on the emotional, behavioral, cognitive, social, and physical functioning of children. Developmental experiences determine the organizational and functional status of the mature brain. The impact of rruumufic experiences on the development and function of the brain are discussed in context of basic principles of neurodevelopment. There are various adaptive mental and physical responses to trauma, including physiological hyperarousal and dissociation. Because the developing brain organizes and internalizes new information in a use-dependent fashion, the more a child is in a state of hyperarousal or dissociation, the more likely they are to have neuropsychiatric symptoms following trauma. The acute adaptive states, when they persist, can become maladaptive traits. The clinical implications of this new neurodevelopmental conceptualization of childhood trauma are discussed.

Homeostasis, stress, trauma, and adaptation. A neurodevelopmental view of childhood trauma.

All experiences change the brain, but not all experiences affect the brain equally. Because the brain is developing and organizing at such an explosive rate in the first years of life, experiences during this period have more potential to influence the brain in positive and negative ways. Traumatic events disrupt homeostasis in multiple areas of the brain that are recruited to respond to the threat. Use-dependent internalization of elements of the traumatic experience can result in the persistence of fear-related neurophysiologic patterns affecting emotional, behavioral, cognitive, and social functioning. A neurodevelopmental view of childhood trauma can help future clinical and research efforts to define and use child-specific and developmentally informed models to guide assessment, intervention, education, therapeutics, and policy.

Platelet serotonin measures in adolescents with conduct disorder

Dysregulation of serotonergic function has been associated with aggression in several studies involving children, adolescents, and adults. This study investigated the relationship of platelet serotonergic measures to conduct disorder type, severity of aggression, and social skills impairment. Standardized assessments of diagnosis, aggression, impulsivity, and social skills were obtained from 43 male adolescents (ages 13-17) incarcerated at an involuntary residential treatment facility for juvenile offenders. Blood samples were collected and assayed for whole blood serotonin (5-HT) and platelet [3H]-paroxetine-labeled 5-HT-transporter binding. Whole blood 5-HT was higher in adolescents with conduct disorder, childhood type than in subjects with conduct disorder, adolescent type. Whole blood 5-HT was positively correlated with violence rating of the current offense and total offense points, and staff ratings of social skills impairment. Our findings are consistent with a relationship between 5-HT dysregulation and aggressive behavior in incarcerated adolescent boys with conduct disorder, particularly of childhood onset.

Effects of chronic sleep deprivation on central cholinergic receptors in rat brain

Rats subjected to chronic total sleep deprivation (TSD) by the disk-over-water method have shown very large, sustained rebounds in paradoxical sleep (PS) (also known as REM sleep). Other studies have indicated that cholinergic mechanisms are involved in the instigation and maintenance of PS. Hypothetically, the large PS rebounds could be mediated by an upregulation of cholinergic receptors during TSD. To evaluate this hypothesis, regional brain cholinergic receptors were compared in rats subjected to 10-day TSD by the disk-over-water method (TSD rats), yoked control (TSC) rats which received the same physical stimulation but with much smaller reductions in sleep, and home cage control (HCC) rats. L-[3H]nicotine and [3H]quinuclidinyl benzilate were used as specific cholinergic radioligands for nicotinic and muscarinic receptor binding assays, respectively. Nicotinic receptor binding was not significantly different among groups for any of the brain regions assayed, including frontal cortex, parietal cortex, thalamus, amygdala, hippocampus, anterior hypothalamus, posterior hypothalamus, caudate, limbic system (including septal area, olfactory tubercle, and nucleus accumbens), midbrain, pons, and medulla. Thus, there was no evidence that changes in nicotinic receptors mediate the PS rebounds. For muscarinic receptor binding, TSD rats differed significantly from control rats only in showing a higher binding affinity than TSC rats in the limbic system and a lower binding density than HCC rats in the hippocampus. On the other hand, significant differences in muscarinic receptor binding sites between rats selectively deprived of PS and their yoked controls were found only for the septal area.(ABSTRACT TRUNCATED AT 250 WORDS)