PubMed · 16821058
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G Ludwig, H Porst, U Wetterauer, H Sperling, U Hartmann. 2006. [Erectile dysfunction].. https://doi.org/10.1007/s00120-006-1109-4
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The concept of autoimmune myelinopathy as the primary pathology in multiple sclerosis (MS) is problematic. Vasculitis is seen in the MS brain, both within lesions and in adjacent normal-appearing white matter. The first observation in acute relapse is the sudden, orderly death of oligodendrocytes; inflammatory removal of unsupported myelin seems to be a secondary process. An alternative explanation for these findings is that oligodendrocyte infection might trigger an inflammatory response. Many pathogens, including Chlamydophila (Chlamydia) pneumoniae, have been associated with MS. MS might be an infectious syndrome in which C. pneumoniae has a role in a subset of patients. Mechanisms by which such a cryptic infection could engender relapsing-remitting and, ultimately, progressive disease patterns are discussed.
Glutamate excitotoxicity has been suggested to play a role in amyotrophic lateral sclerosis, since overstimulation of post-synaptic glutamate receptors by accumulated extracellular glutamate leads to motoneuron cell death. It is however unclear as to why some groups of motoneurons degenerate in this disease while other groups remain relatively intact even during terminal stages of the disease. Our previous studies in the rat showed differential expression of group I metabotropic glutamate receptors in motoneurons at low and high risk of degeneration in amyotrophic lateral sclerosis. Here we have extended this study to normal human brains. In situ hybridization showed that transcripts of both metabotropic glutamate receptor (mGluR) 1 and mGluR5 were expressed in motoneurons in both the resistant motor nucleus III and the vulnerable motor nucleus XII. Immunolabeling of mGluR1alpha and mGluR5 was found in both motoneurons and glia-like cells in all the motor nuclei and the ventral horn of the cervical spinal cord studied. Quantitative analysis of optical density measurements showed higher levels of mGluR1alpha protein expression but lower levels of mGluR5 protein expression in the vulnerable motoneuron pool (VII, XII and spinal cord) than in the resistant motoneuron pool (III, IV and VI). This differential expression of group I metabotropic glutamate receptor proteins within vulnerable motoneuron pools may predispose these neurons to degeneration as seen in amyotrophic lateral sclerosis.
Despite the longstanding conclusion that behavior can reveal aspects of underlying anatomy and function, no generalized antenatal behavior screening has been developed to identify fetuses that may have central nervous system defects requiring further evaluation. We devised a brief ultrasound examination to distinguish fetuses with compromised central nervous system function from the general population and evaluated it with this study. The study design compared behavioral findings obtained by retrospectively reviewing the ultrasound examinations of 5 fetuses that had abnormal behavior with prospectively obtained findings of 29 normal fetuses. Median time for brief examination criteria was 50 min (range, 30-60 min). The only case undetectable by this brief ultrasound examination has an eye-movement period significantly longer than the normal upper limit. Using this method as a screening test may make it possible to include assessment of fetal brain function as part of routine antenatal care.