Chapter 7 Acute polyneuropathies encountered in the intensive care unit

Abstract

The diagnostic criteria of acute polyneuropathy are based on clinical, laboratory, and electrodiagnostic criteria. The clinical spectrum of Guillain–Barre syndrome (GBS) consists of acute inflammatory demyelinating polyradiculoneuropathy (AIDP), acute motor axonal neuropathy (AMAN), acute motor sensory axonal neuropathy (AMSAN), and Miller–Fisher syndrome (MFS). These heterogeneous groups of pathological entities have their own pathogenesis. In about two-thirds of the patients, GBS is preceded by infections. Campylobacter jejuni has been postulated to induce both acute motor neuropathy (AMN) and acute motor sensory neuropathy (AMSN) but can give a Miller–Fisher syndrome. In GBS, there seems a predisposition toward the proximal or nerve root regions. Central conduction times are essentially normal. The most frequently encountered abnormality early in GBS is conduction block. Such a block is present if there is a reduction in the peak-to-peak compound muscle action potential (CMAP) amplitude of more than 20%—a drop in proximal compared with distal CMAP), in the median, ulnar, and peroneal nerves.