Expanding the concept of inflammatory neuropathies.

Role of the innate immune system in the pathogenesis of multiple sclerosis. et al. Rituximab in patients with primary progressive multiple sclerosis: results of a randomized double-blind placebo-controlled multicenter trial. Differentiation block of oligodendroglial progenitor cells as a cause for remyelination failure in chronic multiple sclerosis. Retland E, et al. Differential effects of Th1, monocyte/macrophage and Th2 cytokine mixtures on early gene expression for molecules associated with metabolism, signaling and regulation in central nervous system mixed glial cell cultures. Freedman MS, et al. Autologous haematopoietic stem cell transplantation fails to stop demyelination and neurodegeneration in multiple sclerosis. et al. Primary and transitional progressive MS-a clinical and MRI cross-sectional study. Cognitive forms of multiple sclerosis: report of a dementia case. et al. Greater loss of axons in primary progressive multiple sclerosis plaques compared to secondary progressive disease. et al. Diagnostic criteria for primary progressive multiple sclerosis: a position paper. The natural history of multiple sclerosis: a geographically based study. I. Clinical course and disability. Brain 1989; 112: 133–46. Weiner HL. The challenge of multiple sclerosis: how do we cure a chronic heterogeneous disease? et al. PROMiSe Trial Study Group. Glatiramer acetate in primary progressive multiple sclerosis: results of a multinational, multicenter, double-blind, placebo-controlled trial. Expanding the concept of inflammatory neuropathies Inflammatory neuropathies include several clinical entities and constitute a major portion of peripheral neuropathies. Inflammatory neuropathies may be caused by immune-mediated mechanisms initiated by constituents of the peripheral nervous system. Among these neuropathies, Guillain–Barré syndrome and chronic inflammatory demyelinating polyneuropathy are especially well known. Although Guillain–Barré syndrome had been considered to be identical to acute inflammatory demyelinating polyradiculo-neuropathy (Asbury, 1981), recent studies have added acute motor axonal neuropathy as a component of Guillain–Barré syn-Although chronic inflammatory demyelinating poly-neuropathy usually manifests as a motor sensory neuropathy, a pure motor form, designated as multifocal motor neuropathy, and a pure sensory form, which is termed chronic immune sensory polyradiculopathy, may occur (Pestronk et al., 1988; Sinnreich et al., 2004). In addition to these mainly somatic neuropathies, the discovery of anti-ganglionic acetylcholine receptor antibodies has shed light on autonomic neuropathies in the field of immune-mediated neuropathies (Vernino et al., 2000). These immune-mediated neuropathies are caused by an abnormal