Acute and chronic inflammatory neuropathies--diagnosis
Autor(es): Köller H,Kieseier B C,Jander S,Hartung H-P
Resumo: Guillain-Barré syndrome (GBS) is the most frequent acute polyneuropathy with an annual incidence of 1-2 / 100000 [ 6 ]. In Europe and North America, approximately 85-90% are attributable to classic, acute, predominantly motor polyradiculoneuropathy, whereas in other areas the other subforms are much more frequently present. Because of the initially unspecific symptoms with distal tingling paresthesia and sensory disturbances, the patients are frequently presented in the reception centers of the general hospitals in the first few days, whereas the typical distally stressed ascending paresis occur only after a few days and then lead to the specific diagnosis. The chronic inflammatory demyelinating polyneuropathy (CIDP) differs from the GBS in terms of the course dynamics and the specific formation of the clinical deficits. The prevalence of CIDP is 1-2 / 100 000 [ 20 ]. In the last few years, the knowledge of the underlying immunopathogenesis has expanded considerably, especially in the case of the GBS as well as the CIDP [ 14 ]. In addition, diagnostic criteria for related subforms have also been defined and results of various therapies have been published which are to be presented in this overview. In the last few years, the knowledge of the underlying immunopathogenesis has expanded considerably, especially in the case of the GBS as well as the CIDP [ 14 ]. In addition, diagnostic criteria for related subforms have also been defined and results of various therapies have been published which are to be presented in this overview. In the last few years, the knowledge of the underlying immunopathogenesis has expanded considerably, especially in the case of the GBS as well as the CIDP [ 14 ]. In addition, diagnostic criteria for related subforms have also been defined and results of various therapies have been published which are to be presented in this overview.
Imprenta: Deutsche Medizinische Wochenschrift (1946), v. 128, n. 24, p. 1357-1360, 2003
Identificador do objeto digital: 10.1055/s-2003-39969
Descritores: Guillain-Barre Syndrome - Pathogenesis ; Guillain-Barre Syndrome - Proteins ; Guillain-Barre Syndrome - Antibodies
Data de publicação: 2003
