Autonomic and somatomotor responses to electrical stimulation of the posterior hypothalamus are reported in 51 patients with pathologically aggressive behavior. The stimulated area causing rise in blood pressure, tachycardia, and maximal pupillary dilatation lies in the posteromedial hypothalamus, more than 1 mm and less than 5 mm lateral to the lateral wall of the third ventricle, occupying a triangle formed by the midpoint of the intercommissural line, the rostral end of the aqueduct, and the anterior border of the mammillary body. Electrical stimulation of this (ergotropic) triangle resulted in desyncbronization of the electroencephalogram (EEG) with hippocampal theta waves, or diffuse irregular delta waves of high voltage.Cases with violent behavior showed higher plasma levels of non-esterified fatty acids (NEFA) in the fasting stage; these were markedly elevated by electrical stimulation of the ergotropic triangle.Points in the ergotropic triangle where signs of sympathetic discharge were most marked were electrocauterized bilaterally. This procedure produced marked calming effects (95% of the cases) during the follow-up period of more than 2 years. Postoperatively there was a tendency to a decrease in sympathicotonia or an increase in parasympathicotonia. The follow-up plasma level of NEFA was found to have decreased to approximately the normal value.Y. Neurosurg. / Volume 33 / December, 1970 69]
Embryonic stem (ES) cells are expected to be a potential donor source for neural transplantation. We have obtained motoneuron-enriched neural progenitor cells by culturing mouse ES cells with retinoic acid (RA). The cells also expressed mRNA of a neurotrophic factor, neurotrophin-3 (NT-3). The left motor cortex area of mice was damaged by cryogenic brain injury, and the neural cells were transplanted underneath the injured motor cortex, neighboring to the paraventricular region. We found that the cells expressing neuronal phenotypes not only remained close to the implantation site, but also exhibited substantial migration penetrating into the damaged lesion, in a seemingly directed manner up to cortical region. We found that some of the neural cells differentiated into Islet1-positive motoneurons. It seems likely that the ability of the ES cellderived neural progenitor cells to respond in vivo to guidance cues and signals that can direct their migration and differentiation may contribute to functional recovery of the recipient mice. We found that an "island of the mature neuronal cells" of recipient origin emerged in the damaged motor cortex. This may be associated with the neuroprotective effects of the ES cell-derived neural cells. The ES cells differentiated into CD31+ vasculoendothelial cells with the RA treatment in vitro. Furthermore, the grafted cells may provide sufficient neurotrophic factors such as NT-3 for neuroprotection and regeneration. The grafted neural cells that migrated into residual cortex and differentiated into neurons had purposefully elongated axons that were stained with anti-neurofilament middle chain (NFM) antibody. Our study suggests that motoneurons can be induced from ES cells, and ES cells become virtually an unlimited source of cells for experimental and clinical neural cell transplantation.
A case is reported of a 59-year-old man with a spinal arachnoid cyst accompanied by spinal arachnoiditis. The patient developed symptoms after treatment for a ruptured vertebral artery aneurysm, in which fibrin glue was used for reconstruction of the suboccipital bone defect. It is believed that the fibrin glue may have played a role in forming the arachnoid cyst. The authors urge the readers to keep in mind the possibility of subclinical spinal arachnoiditis in the patients with aneurysmal subarachnoid hemorrhage and suggest that care should be taken to avoid any possible adverse effect of fibrin glue.
We developed neural tube-like structures accompanying neural crest-like cells by treating embryonic stem (ES) cells with retinoic acid. The structures contained pseudostratified Nestin+Vimentin+ neuroepithelial cells surrounded by Masson staining+ basement membrane. betaIIItubulin+Synaptophysin+ mature neurons and glial fibrillary acidic protein (GFAP)+ glial cells dispersed outside of the membrane. Addition of Noggin to the culture induced prominent proliferation of the neuroepithelial cells, leading to epithelial hyperstratification of the structures. mRNAs of transcription factors essential for forebrain development such as Emx1/2 and Pax6 were specifically expressed and Islet1+Lim1/2- motoneurons appeared by the addition of Noggin. In contrast, basic fibroblast growth factor (bFGF) promoted enlargement of central lumen and elongation of the structures. mRNAs of caudal markers, Gbx2, Cdx2 and Hoxb4/9 were expressed and Lim1/2+ spinal motoneurons appeared by the addition of bFGF. Addition of BMP-4 similarly brought about mild enlargement of central lumen of the structures. Interestingly, the addition of BMP-4 induced Slug+ neural crest-like cells surrounding the tube-like structures. mRNAs of Snail and dHand, other markers for neural crest cells, were also expressed by the addition of BMP-4. These results suggest that Noggin lead the neural-tube like structures to forebrain fate, whereas bFGF was involved in the caudalization. BMP-4 was implicated in emergence of the neural crest-like cells. Differentiation of ES cells by the present methods may mimic neurulation and subsequent neural development of early embryos, and elucidates the opposite effects of Noggin and bFGF for the neural tube development.
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