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Titlebook: Advanced Evoked Potentials; Hans Lüders (Head) Book 1989 Springer Science+Business Media New York 1989 brain.clinical application.clinical

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https://doi.org/10.1007/978-3-642-66218-8m interrelated and all with significant limitations, have been used to define the generators of evoked potential peaks. In this chapter, we will discuss and analyze critically these different approaches.
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https://doi.org/10.1007/978-3-642-66218-8m interrelated and all with significant limitations, have been used to define the generators of evoked potential peaks. In this chapter, we will discuss and analyze critically these different approaches.
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https://doi.org/10.1007/978-3-663-07136-5. The remarkable length of the somatosensory pathway from peripheral skin to cerebral cortex makes it vulnerable at many different points to a variety of pathological conditions. Neural generators all along this pathway can be revealed through appropriate SEP recordings methodologies and a variety o
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https://doi.org/10.1007/978-3-663-07136-5t among other things, pathology of the intraretinal optic nerve as in glaucoma (1), axonal neuropathy (2) and synaptic neurotransmitter deficiency (3) may cause delayed VEPs. Maculopathy also induces VEP delays, [4, 5, 6]. Several of these studies have shown that stimulus “details” such as element s
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,Über die Dichte von flüssigem Acetylen,c. The remarkable stability of the SAEP waveforms and latencies across repeated recording sessions and varying arousal levels suggests that they originate in an extremely secure and highly synchronized generator system. It is hypothesized that synchronized neuronal discharges may summate to produce
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https://doi.org/10.1007/978-3-322-88342-1e cell bodies. Central myelin is formed by extensions of the cytoplasmic membrane of oligodendrocytes which wrap around the axon, resulting in concentric layers of lipid and protein. The acute MS plaque shows myelin breakdown and inflammation with perivenous infiltrates of mononuclear cells and lymp
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https://doi.org/10.1007/978-3-322-88342-1ntral nervous system. Most of the successes of this low cost investigation in clinical practice is due to its ability to disclose silent lesions causing delayed response in demyelinating diseases. In nondemyelinating processes the clinical appUcations of EPs have not yet been clearly defined; howeve
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