Idiopathic chronic inflammatory polyradiculoneuropathies are probably due to dysimmune mechanisms. They form a distinct entity defined by clinical, electrophysiological, histopathological criteria and by their evolution and response to treatment. The homogeneity of that syndrome, the exact nature of the underlying pathological processus, the natural history and the responses to treatment are still debated. Need to more studies, especially of immunologic nature, to precise limits and criteria of such a syndrome. Chronic polyradiculoneuropathy is different from acute form mainly by evolution. Within the chronic form, the progressive and relapsing forms can be distinguished with different electrophysiologic characteristics. These 2 forms share the same electrophysiologic aspect of chronic demyelination which is characterized by slowing of nerve conduction, conduction block and temporal dispersion. They had some specific different features such as the heterogeneity of the conduction failure and the multifocal distribution of demyelinating lesions. The histopathologic lesions are those of demyelination-remyelination with some degree of axonal damage, although inflammatory infiltrates are not frequent. In the majority of cases, the motor deficit is dominant although pure sensory forms have been reported. In few cases, central nervous system involvement is described. Idiopathic polyradiculoneuropathies had different electrophysiologic features than polyneuropathies associated with IgM monoclonal gammopathy and anti-MAG activity, these later presenting more distal and homogeneous abnormalities.