Genetic influence on laterality in schizophrenia? A twin study of neurological soft signs.

OBJECTIVE: This study explored the genetic basis of neurological soft signs in schizophrenia and addressed disturbed hemispheric lateralization. METHOD: The authors investigated neurological soft signs in 30 monozygotic twin pairs, 13 pairs discordant for schizophrenia or schizoaffective disorder and 17 healthy comparison twin pairs. RESULTS: The twins with schizophrenia showed higher total scores for neurological soft signs than did the comparison subjects. The total scores for neurological soft signs of the nonaffected discordant twins were significantly higher than those of the comparison twins. There was a significant difference between the nonaffected and affected discordant twins in total scores for neurological soft signs. In contrast to the comparison subjects, the nonaffected and affected twins of the discordant pairs showed a trend toward higher scores for neurological soft signs on the left body half. CONCLUSIONS: These results suggest that the occurrence of neurological soft signs and, more specifically, their lateralization to the left body half are genetically transmitted.

[Effectiveness of preventing hypotension with H1/H2 antagonists before protamine administration]. / Wirksamkeit einer Hypotensionsprophylaxe mit H1/H2-Antagonisten vor Protamingabe.

BACKGROUND: This prospective randomized study was undertaken to evaluate the effects of prophylactic administration of H1/H2 receptor blockers on histamine release and hemodynamic changes after administration of protamine in two groups of patients (n = 20) undergoing elective coronary artery bypass graft surgery. PATIENTS AND METHODS: Group 1 (n = 10) patients were pretreated intravenously with 1 mg/kg ranitidine and 0.1 mg/kg dimetinden 15 min before termination of the extracorporeal circulation; group 2 patients (n = 10) received no medication. After termination of the extracorporeal circulation, heparin was neutralized by administration of 350 U/kg protamine, injected during 4 min via a peripheral vein. Hemodynamic measurements were carried out before the administration of protamine and at 1-min intervals up to 10 min after the injection. Before administration of protamine and 2, 4, 6, 8, and 10 min thereafter, plasma histamine levels were measured using central venous blood samples. RESULTS: In group 1 patients, who were treated prophylactically with H1/H2 receptor blockers, the plasma histamine concentration was 0.21 +/- 0.15 ng/ml (mean +/- SD) and reached a peak value of 0.30 +/- 0.17 ng/ml within 4 min. In group 2 patients, the plasma histamine concentration increased from 0.17 +/- 0.15 to 0.26 +/- 0.24 ng/ml after 10 min. The hemodynamic reactions were comparable in both groups (group 1: decrease in systolic arterial pressure from 118 +/- 16 to 104 +/- 15 mm Hg; group 2: from 111 +/- 19 to 108 +/- 21 mm Hg; differences statistically not significant). The Spearman rank correlation revealed no statistically significant relationship between the slight plasma histamine release and clinically severe decreases of blood pressure that were observed in single patients. CONCLUSION: Histamine release appears unlikely as the mechanism of protamine-induced hypotension. Therefore, general prophylaxis using H1/H2 receptor antagonists does not seem to be justified and cannot be recommended.