PubMed · 4026624
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L R Caplan. 1985. Vertebrobasilar transient ischemic attacks.. https://doi.org/10.1001/archneur.1985.04060080017006
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Schimke immunoosseous dysplasia (SID) is an autosomal recessive spondyloepiphyseal dysplasia that was first described by Schimke et al. [1971: Lancet 2:1088-1089]. It is associated with premature arteriosclerosis and cerebral ischemia; however, the cerebral vascular abnormalities causing ischemia have not been described [Spranger et al., 1991: J Pediatr 119:64-72; Ehrich et al., 1995: Clin Nephrol 43:89-95]. Based on magnetic resonance angiography (MRA) and magnetic resonance venography (MRV), we now report on 2 girls with SID who have cerebral ischemia associated with moyamoya phenomenon. In addition, one patient also has an absent or occluded left transverse sinus and diffuse aortic narrowing. This is the first characterization of the cerebral vascular abnormality found in SID and raises the possibility that cerebral moyamoya may represent another major manifestation of the underlying genetic defect in SID.
The so-called terminal negativity (TN) of the DC-potential is a characteristic reaction of neuronal tissue to hypoxia or ischemia. In a previous study on human neocortical slices, two types of TN with flat and steep slopes of rise (< or >10 mV/min) were found with hypoxia. The aim of the present study was to further investigate causes underlying the occurrence of flat and steep TN. Experiments were performed on 23 human neocortical slices (500 micron) resected from 13 patients (epilepsy and tumour surgery). DC-potential and evoked potentials (white matter stimulation) were recorded in layer III. The extracellular potassium concentration ([K+]o) was measured by K+-sensitive microelectrodes. In an interface type chamber, ischemic episodes were induced by oxygen and glucose deprivation. They were terminated when TN had peaked. Both flat and steep TN also existed with ischemic conditions. There was a linear correlation between the slope of rise of TN and the associated slope of rise in [K+]o, respectively, but none regarding latencies of TN or recovery of evoked potentials. Peak levels in [K+]o were 13.9+/-0.9 mmol/l. Compared to control, the slope of rise and latency of TN were clearly increased by addition of dimethyl sulfoxide (DMSO, 0.4%) to the bath solution, whereas nimodipine (40 micromol/l) in 0.4% DMSO had neither an effect on slope of rise of TN nor on latency of TN. As a whole, our observations suggest, that the actual metabolic state determines the occurrence of flat or steep TN.