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Prasad S. S. V. Vannemreddy and James L. Stone

Fifty years before a report on the complete bitemporal lobectomy syndrome in primates, known as the Klüver-Bucy syndrome, was published, 2 talented investigators working at the University College in London, England—neurologist Sanger Brown and physiologist Edward Schäfer—also made this discovery. The title of their work was “An investigation into the functions of the occipital and temporal lobes of the monkey’s brain,” and it involved excisional brain surgery in 12 monkeys. They were particularly interested in the then-disputed primary cortical locations relating to vision and hearing. However, following extensive bilateral temporal lobe excisions in 2 monkeys, they noted peculiar behavior including apparent loss of memory and intelligence resembling “idiocy.” These investigators recognized most of the behavioral findings that later came to be known as the Klüver-Bucy syndrome. However, they were working within the late-19th-century framework of cerebral cortical localizations of basic motor and sensory functions.

Details of the Brown and Schäfer study and a glimpse of the neurological thinking of that period is presented. In the decades following the pivotal work of Klüver and Bucy in the late 1930s, in which they used a more advanced neurosurgical technique, tools of behavioral observations, and analysis of brain sections after euthanasia, investigators have elaborated the full components of the clinical syndrome and the extent of their resections.

Other neuroscientists sought to isolate and determine the specific temporal neocortical, medial temporal, and deep limbic structures responsible for various visual and complex behavioral deficits. No doubt, Klüver and Bucy’s contribution led to a great expansion in attention given to the limbic system’s role in action, perception, emotion, and affect—a tide that continues to the present time.

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Prasad Vannemreddy, Christina Notarianni, Krishna Yanamandra, Dawn Napper and Joseph Bocchini Jr


Studies have shown decreased levels of nitric oxide (NO), the product of endothelial NO synthase (eNOS) gene activity, in infants with respiratory conditions and intraventricular hemorrhage (IVH). The authors evaluated the association of the eNOS gene promoter polymorphism T-786C with the cause of these conditions (respiratory conditions and IVH) in premature infants.


Blood samples from 124 African American premature infants were studied. The DNA was isolated and microplate polymerase chain reaction–restriction fragment length polymorphism assay was performed. Genotypes were scored as: TT homozygotes with 140 bp and 40 bp; CC homozygotes with 90 bp, 50 bp, and 40 bp; and TC heterozygotes with 140 bp, 90 bp, 50 bp, and 40 bp. Genotypes were stratified according to ethnicity, preterm status, and prematurity conditions.


The mutant allele -786C was present in 15.3% of premature infants with respiratory distress syndrome, bronchopulmonary dysplasia, and IVH, compared with 7.25% in those premature infants without these conditions. A significant 2-fold increase of the mutant allele in patients compared with controls (p = 0.04, OR 2.3) reveals that the eNOS -786C allele could be a significant risk factor in the origin of respiratory conditions and IVH in premature infants.


These results suggest that the mutant eNOS -786C allele is a significant risk factor in the origin of respiratory and IVH diseases, probably mediating an insufficient supply of endogenous NO in premature infants.