[Acute vestibular syndrome in emergency departments : Clinical differentiation of peripheral and central vestibulopathy]. / Akutes vestibuläres Syndrom in der Notaufnahme : Klinische Differenzierung von peripherer vs. zentraler Vestibulopathie.

INTRODUCTION: The differentiation between central and peripheral vestibular disorders is difficult in some cases, especially during the clinical routine of an emergency department (ED) without otoneurological diagnostic equipment. This study evaluated the frequency of vestibular pseudoneuritis as distinguished from acute peripheral vestibular disorders in patients who were admitted to hospital with the suspicion of vestibular neuropathy (VN). METHODS: This retrospective study analyzed the results of anamnestic and clinical examinations of 315 patients admitted to the emergency department and the inpatient otoneurological examination results as well as the imaging of morphological alterations. In the ED, the clinical examination by a neurologist and an otorhinolaryngologist resulted in the characteristic signs of peripheral VN but no further evidence of a neurological disorder. Patients without signs of a peripheral vestibular disorder in the otoneurological diagnostics subsequently underwent cerebral magnetic resonance imaging scans (cMRI). RESULTS: Suspected isolated VN could be confirmed in 69% of the patients; however, in a further 29% of the patients neither the suspected isolated VN nor an ischemic pathology of the central nervous system as a cause of the vertigo could be confirmed. Additional cMRI scans revealed that 2% of patients suffered from an infarction of the mesencephalon, the pons, the medulla oblongata and the cerebellum. CONCLUSION: In rare cases central cerebral disorders mimic the pattern of a peripheral vestibular disorder. Despite thorough history taking, neurological and otolaryngological clinical examinations, it is not always possible to distinguish central and peripheral vestibular disorders of patients in emergency care suffering from acute vertigo. Video oculography-assisted caloric testing and the video head impulse test are recommended to confirm a peripheral VN. In cases without confirmation of suspected NV in otoneurological diagnostics, infarction of the mesencephalon, brain stem and cerebellum should be excluded by diffusion-weighted cMRI.

Expression of an immunoglobulin heavy chain transgene in macrophage as well as lymphocyte lineages in vivo.

A rearranged immunoglobulin heavy chain (IgH) transgene-encoded protein is expressed in macrophage lineage cells, in addition to B and T lineages, in transgenic mouse bone marrow. Peripheral macrophages also express transgenic IgH protein. Mature T cells express lower levels than immature thymocytes. Almost all B220+ cells in the bone marrow express transgenic IgH protein, and this early expression in the B lineage is accompanied by a reduction of cell frequency even in the early B220+ CD43+ BP-1- stages, although it is more prominent in BP-1+ pre-B cells. Thus, an IgH transgene can be expressed not only in lymphoid but also in myeloid cells, although its developmental effects are restricted to the B cell lineage.

Deletion of a recombined Ig heavy chain transgene in B-lineage cells of transgenic mice.

Fully recombined transgenes are stable in their transmission in the germline of transgenic mice, in common with the endogenous genetic complement of most mammalian somatic tissues, including the genes for lymphoid Ag receptors somatically generated from germline minigenes. There have, however, been isolated reports of unusual low frequency transgene losses in various transgenic mice. Here we show, using Southern blots and PCR-based assays, that plasmablast hybridomas and B cells from three independently derived founder lines of transgenic mice bearing a recombined heavy chain Ig transgene we have been studying show a significant net loss of transgene copies. This loss is more marked in the B cells expressing endogenous heavy chains than in those expressing transgenic heavy chains. We have also examined cells of the B lineage in the bone marrow, and a small degree of deletion is also evident in CD19+ CD23- IgM- immature B-lineage cells. As greater deletion is observed in mature B cells, it is possible that the deletion process either continues into B cell maturity and/or provides a selective advantage. We have investigated the relationship between transgene expression and deletion, and we find that while thymocytes in these mice express the transgene well, T cell hybridomas derived from transgenic thymus do not show any loss of the transgene. Thus, a recombined Ig heavy chain transgene prominently undergoes somatic deletion in B-lineage cells independent of its insertion site or expression. This transgenic instability is significant to the analysis of genomic stability as well as to the design of gene therapy strategies.