Generation of human B-cell hybridomas secreting monoclonal anti–myelin-associated glycoprotein antibodies from a patient with neuropathy
✍ Scribed by Dr. Linda Spatz; Becky Lieberson; Judith Abraham; Orlando J. Miller; Dorothy A. Miller; Norman Latov
- Publisher
- John Wiley and Sons
- Year
- 1987
- Tongue
- English
- Weight
- 797 KB
- Volume
- 21
- Category
- Article
- ISSN
- 0364-5134
No coin nor oath required. For personal study only.
✦ Synopsis
This heterogeneity showed that all components of the infarcted area were not equally damaged. These isointensity transverse bands were probably the spared nerve fiber bundles projecting into the cerebellar hemisphere from the contralateral pontine nuclei.
In the cerebral hemispheres, the region most affected by a moderate reduction in perfusion pressure is white matter instead of cortex [9], but this vulnerability is presumably explained by the fact that white matter is supplied in part by penetrating arteries that traverse the cortex, and they will preferentially perfuse the cortex when perfusion pressure drops moderately 181. In the basis pontis, the cell bodies of the pontine nuclei intermingle with the transverse pontocerebellar fiber bundles. Thus, the reduced perfusion pressure of the cell bodies may be identical with that of the fiber bundles, and the metabolic rate may be the main factor that determines the severity of the ischemic damage. Therefore, on the basis of our case studies, we speculate that the cell bodies and synaptic structures of the pontine nuclei with a higher metabolic rate are severely damaged when the paramedian branch of the basilar artery is occluded. Also, the projecting fibers running through the ischemic area originating from the contralateral pontine nuclei are relatively spared and the medial pontine infarct causes contralateral rather than bilateral ataxia.