title: [Critical polyneuropathy].
abstract: Contrary to earlier belief, muscle weakness and atrophy in critically ill patients is not due to inactivity or disuse but rather caused by neuromuscular disorders arising de novo during the stay in the ICU. Clinical manifestations include delayed weaning from the respirator and prolongation of the rehabilitation phase. The available data indicate that critical illness polyneuropathy is the most frequent cause of such secondary neuromuscular problems. For differential diagnosis prolonged neuromuscular blockade and several myopathies have to be taken into consideration. The pathogenesis of critical illness polyneuropathy is unknown. It has been suggested that the factors mediating the systemic inflammatory response are also responsible for axonal damage in critical illness polyneuropathy. We recently described a neurotoxic activity present in the sera of affected patients, which can be reversed completely by NMDA antagonists. The critical illness per se is unrelated to the development of neuropathy. By contrast, occurrence of myopathies may be triggered by exogenous factors such as high-dose glucosteroids and non-depolarizing muscle blocking agents. Detailed electrodiagnostic studies are desirable in patients with long-lasting ICU stays, whenever possible as weekly monitoring. In doubtful cases, muscle biopsy might be necessary for proper diagnosis and management.
authors.affiliation: Neurologische Universitätsklinik, Heidelberg. ernst_hund@ukl.uni-heidelberg.de
authors.forename: E
authors.initials: E
authors.lastname: Hund
mesh_terms: D003422:Critical Care; D016638:Critical Illness; D018691:Excitatory Amino Acid Antagonists / Q000627:therapeutic use; D006801:Humans; D009422:Nervous System Diseases / Q000188:drug therapy / Q000209:etiology* / Q000503:physiopathology*
chemical_list: D018691:Excitatory Amino Acid Antagonists
vernacular_title: Intensivpolyneuropathie.