PubMed · 14841605
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A B M SISON. 1951. Stress.. https://pubmed.ncbi.nlm.nih.gov/14841605/
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Medical care of the newborn or infant discharged from the neonatal intensive care unit is difficult and requires close co-operation between the primary care pediatrician and the team of specialists. The authors are trying to collect the rules of pediatric guidance of the high-risk patients to help in practical approach to such children and highlight the issues requiring special attention. The newborn should be discharged with precisely described plan of following treatment and controls. Despite careful discussion with parents on child's clinical status, many questions and daubts appear as sooll as the infant arrives home. All these problems have to be explained by the primary care pediatrician. Defining the subgroup of special care patients on the basis of perinatal and adaptive period risk factors can protect them from being "overseen" (the steadily progressing deterioration or problems occurring in the course of development). On the other hand, some non-typical symptoms are normal for these special patients and should be taken into consideration in the following evaluation of the development and recognition of changes in clinical condition. The attention is drawn to the meaning of corrected age and its use in growth monitoring and psychomotor development, and also the carefulness in recognizing mental psychomotor disability. Other problems, like early neurodevelopmental stimulation program, feeding difficulties, immunization questions and the care of children with chronic diseases are also discussed.
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The molecular and biochemical bases for interactions between the immune and central nervous systems are described. Immune cytokines not only activate immune function but also recruit central stress-responsive neurotransmitter systems in the modulation of the immune response and in the activation of behaviors that may be adaptive during injury or inflammation. Peripherally generated cytokines, such as interleukin-1, signal hypothalamic corticotropin-releasing hormone (CRH) neurons to activate pituitary-adrenal counter-regulation of inflammation through the potent antiinflammatory effects of glucocorticoids. Corticotropin-releasing hormone not only activates the pituitary-adrenal axis but also sets in motion a coordinated series of behavioral and physiologic responses, suggesting that the central nervous system may coordinate both behavioral and immunologic adaptation during stressful situations. The pathophysiologic perturbation of this feedback loop, through various mechanisms, results in the development of inflammatory syndromes, such as rheumatoid arthritis, and behavioral syndromes, such as depression. Thus, diseases characterized by both inflammatory and emotional disturbances may derive from common alterations in specific central nervous system pathways (for example, the CRH system). In addition, disruptions of this communication by genetic, infectious, toxic, or pharmacologic means can influence the susceptibility to disorders associated with both behavioral and inflammatory components and potentially alter their natural history. These concepts suggest that neuropharmacologic agents that stimulate hypothalamic CRH might potentially be adjunctive therapy for illnesses traditionally viewed as inflammatory or autoimmune.