Serologic evidence of prenatal influenza in the etiology of schizophrenia

CONTEXT: Some, but not all, previous studies suggest that prenatal influenza exposure increases the risk of schizophrenia. These studies used dates of influenza epidemics and maternal recall of infection to define influenza exposure, suggesting that discrepant findings may have resulted from exposure misclassification. OBJECTIVE: To examine whether serologically documented prenatal exposure to influenza increases the risk of schizophrenia. DESIGN: Nested case-control study of a large birth cohort, born from 1959 through 1966, and followed up for psychiatric disorders 30 to 38 years later. SETTING: Population-based birth cohort. PARTICIPANTS: Cases were 64 birth cohort members diagnosed as having schizophrenia spectrum disorders (mostly schizophrenia and schizoaffective disorder). Controls were 125 members of the birth cohort, had not been diagnosed as having a schizophrenia spectrum or major affective disorder, and were matched to cases on date of birth, sex, length of time in the cohort, and availability of maternal serum. MAIN OUTCOME MEASURES: Archived maternal serum was assayed for influenza antibody in pregnancies giving rise to offspring with schizophrenia and matched control offspring. RESULTS: The risk of schizophrenia was increased 7-fold for influenza exposure during the first trimester. There was no increased risk of schizophrenia with influenza during the second or third trimester. With the use of a broader gestational period of influenza exposure-early to midpregnancy-the risk of schizophrenia was increased 3-fold. The findings persisted after adjustment for potential confounders. CONCLUSIONS: These findings represent the first serologic evidence that prenatal influenza plays a role in schizophrenia. If confirmed, the results may have implications for the prevention of schizophrenia and for unraveling pathogenic mechanisms of the disorder.     

Studies on thyroid-catecholamine interactions in the isolated rabbit heart

Isolated atria and strips of ventricles from hyperthyroid and euthyroid rabbits were subjected to a series of pharmacologic tests in an attempt to demonstrate an interaction between the thyroid and the catecholamines on cardiac chronotropism and inotropism. These tests included dose response curves to norepinephrine and epinephrine; the use of cocaine to see whether there was a greater potentiation to norepinephrine in hyperthyroidism; dose response curves to tyramine to determine whether hyperthyroidism altered the development of tachyphylaxis to this agent; dose response curves to epinephrine in the presence of theophylline since these agents act at different sites in the cyclic-AMP system; dose response curves to mecholyl in the absence and presence of atropine to detect any hyperthyroid-induced change in cholinergic receptor sites. Our results do not support the concept of a thyroid-catecholamine interaction on cardiac chronotropism and inotropism.     

Subdural air collection: a likely source of radicular pain after lumbar epidural

This case conference reports two cases of epidural anesthesia in which air was used to identify the epidural space during a loss-of-resistance placement technique. Both patients subsequently complained of severe pain and subdural air was demonstrated in case 1 by computed tomography and in case 2 by magnetic resonance imaging. The possible causes of the pain syndrome experienced by both patients are discussed.