Treatment of vestibular disorders with weak asymmetric base-in prisms: An hypothesis with a focus on Ménière's disease.

BACKGROUND: Regular treatments of Ménière's disease (MD) vary largely, and no single satisfactory treatment exists. A complementary treatment popular among Dutch and Belgian patients involves eyeglasses with weak asymmetric base-in prisms, with a perceived high success rate. An explanatory mechanism is, however, lacking. OBJECTIVE: To speculate on a working mechanism explaining an effectiveness of weak asymmetric base-in prims in MD, based on available knowledge. METHODS: After describing the way these prisms are prescribed using a walking test and its effect reported on, we give an explanation of its underlying mechanism, based on the literature. RESULTS: The presumed effect can be explained by considering the typical star-like walking pattern in MD, induced by a drifting after-image comparable to the oculogyral illusion. Weak asymmetric base-in prisms can furthermore eliminate the conflict between a net vestibular angular velocity bias in the efferent signal controlling the VOR, and a net re-afferent ocular signal. CONCLUSIONS: The positive findings with these glasses reported on, the fact that the treatment itself is simple, low-cost, and socially acceptable, and the fact that an explanation is at hand, speak in favour of elaborating further on this treatment.

Motion sickness amelioration induced by prism spectacles.

A side effect of the prescription of prism glasses according to the principle of Utermöhlen to improve mechanical reading skills of certain types of learning disabled children was the alleviation of car sickness. Besides a decrease in reported symptoms after prescription of these glasses, the effect is quantified by a decrease in estimated number of emeses per year per patient. A placebo effect is unlikely because alleviation of car sickness was not the original intention of the prescription, and the symptoms returned as soon as the spectacles were discontinued.

Quantitation of human tumor-reactive monoclonal antibody 16.88 in the circulation and localization of 16.88 in colorectal metastatic tumor tissue using murine antiidiotypic antibodies.

Detection of administered human monoclonal antibodies in the tissues and circulation of patients requires special reagents to overcome interference by normal endogenous immunoglobulin. A practical approach is the development of antiidiotypic antibodies to the human monoclonal antibody and their application in immunoassays specific for the human monoclonal antibody. Accordingly, antiidiotypic antibodies were made to the monoclonal antibody 16.88, a human IgM class anti-colon carcinoma antibody being developed for applications in antibody-targeted immunotherapy of cancer. Three stable clones were obtained that produced antiidiotypic antibodies reactive with 16.88 but nonreactive with human polyclonal IgM or 16.52, a patient-matched IgM monoclonal antibody with different specificity than 16.88. One antiidiotypic antibody, MID 65, was used in a capture format radioimmunoassay to detect 16.88 in the sera of patients who had received 108-mg doses of unlabeled 16.88 coadministered with trace doses of 131I-16.88. Using this assay it was demonstrated that unlabeled 16.88 antibody and 131I-labeled 16.88 antibody did not differ significantly in blood retention for up to 24 h after administration, the period during which the immunoreactivity of the administered antibody remained over 90%. Indirect microautoradiography using exogenously applied 125I-MID 65 to localize 16.88 in frozen metastatic tumor tissue from patients given 16.88 8 days prior to surgery demonstrated the accumulation of 16.88 in areas of apparently healthy tumor cells. Much less 16.88 was detected in stroma or areas of tumor cell necrosis. The accumulation of antibody in nonnecrotic tumor sites encourages the further development of 16.88 for radioimmunotherapy of colon cancer and provides support for further development of human anticytokeratin monoclonal antibodies for cancer therapy.

Influence of the qualitative caloric composition of enteral diets on liver protein synthesis in normal and operated rats.

Protein synthesis L-(l-14C) leucine in liver was studied. Normal (n = 40) and operated (n = 40) Sprague-Dawley rats with an initial body weight of 161.18 +/- 12 g were divided into four groups (n = 10), respectively. Each group, subjected to the same conditions of temperature, light, noise and movement received a different commercial formula for human enteral nutrition and water for 8 days (normal rats) and six days (operated rats). All rats received the same caloric and protein intake per ml (l kcal; 6-7.10(-3) g protein), with no statistically significant differences among groups. The differences in diets were merely qualitative. The tolerance to all diets was similar, with rats attaining the expected weight. Losses of protein, alpha aminic nitrogen, total fat and non sterified fatty acid in faeces were negligible. In normal rats, different results in liver protein synthesis were obtained. No mass/synthesis rate correlation was found. Under these conditions it would appear that these results are due to the different diets used. In operated rats, a significantly different liver protein synthesis per gram of body weight was obtained, but not per gram of organ weight. These results suggest that the influence of the qualitative caloric intake, in the stress phase, is less than in the normal state.