The posterior crico-arytenoid muscle in two cases of Shy-Drager syndrome with laryngeal stridor. Comparison of the histological, histochemical and biometric findings.

The histological, histochemical and biometric findings in the posterior crico-arytenoid muscle in two patients with Shy-Drager syndrome were compared with those found in cases of carcinoma of the larynx. In biopsy specimens from the patients with laryngeal carcinoma, neurogenic atrophy and various structural changes in the muscle fibres were the prominent features. In the two patients with Shy-Drager syndrome these changes were not present and the only significant finding was the more pronounced type I fibre atrophy, with type II fibre predominance in the more severely affected case. These findings do not permit the vocal cord paralysis seen in the Shy-Drager syndrome to be explained by motorneuron loss and denervation. It is postulated that a possible cause may be a biochemical defect in the brain.

Ischemic lesions of the hippocampus and their relation to Ammon's horn sclerosis. A neuropathological study of two cases and a comparison to the vascular anatomy.

Two adult brains with small ischemic lesions in the hippocampus, due to impairment of the supply from the posterior cerebral artery, are presented. The first case corresponds to what is described in the literature as "incisural sclerosis" and shows no difference in vulnerability between the Sommer and the Spielmeyer sector. In the second case the hippocampal lesion is due to an embolic occlusion of the posterior cerebral artery and consists of selective necrosis of the subiculum, the Sommer sector and part of the endfolium of the pyramidal layer, the Spielmeyer sector remaining noninfarcted. The postmortem angiograms of 12l hippocampi of adults, as well as full term born and premature infants, show that the h1 and h2 sectors and part of the h3 sector of the hippocampus are supplied by the same "sulcus" arteries. Although there is a selective vulnerability to ischemia in some sectors of the hippocampus, which is typical for Ammon's horn sclerosis, this cannot be explained by a difference of arterial supply or by compression of arteries during the process of birth.

In vitro TNF-alpha, IL-2 and IFN-gamma production as markers of relapses in multiple sclerosis.

In 22 patients with definite multiple sclerosis (MS) we determined with monthly intervals over a period of 24 months the in vitro tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), and interleukin-2 (IL-2) production and the serum neopterin levels. The results were compared with normative data collected from 14 healthy controls over the same period. Twenty-nine relapses in 13 patients were noticed. We found increased in vitro TNF-alpha production from 4 weeks on prior to the day of an exacerbation. There was a significant correlation with in vitro IFN-gamma release, the absolute blood monocyte count and the serum neopterin levels, suggesting that monocytes stimulated by IFN-gamma play an important role in the TNF-alpha production. Serial analysis of in vitro TNF-alpha production proved to be a helpful tool in predicting relapses in MS patients. Furthermore, elevated levels of IFN-gamma and IL-2 after stimulation with OKT3 during exacerbations were demonstrated. Serial analysis of these two biological markers revealed to be of no value in predicting relapses.

Relapse markers in multiple sclerosis: are in vitro cytokine production changes reflected by circulatory T-cell phenotype alterations?

In vitro tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma) and interleukin-2 (IL-2) production, serum neopterin levels, and T-lymphocyte subpopulations were determined on a monthly basis in 22 MS patients. We found increased in vitro TNF-alpha production from 4 weeks on prior to the day of an exacerbation. There was a significant correlation with in vitro IFN-gamma release, the absolute blood monocyte count and the serum neopterin levels, suggesting that monocytes stimulated by IFN-gamma play an important role in the TNF-alpha production. Serial analysis of in vitro TNF-alpha production proved to be a helpful tool in predicting relapses in MS patients. Furthermore, elevated levels of IFN-gamma and IL-2 after stimulation with OKT3 during exacerbations were demonstrated. These increases were not reflected by changes in T-lymphocyte subpopulations. However, significant differences in T-cell subsets were observed between controls and relapsing progressive patients.