[Polyneuritis, polyradiculoneuritis, polyneuropathies: development of a concept]

The concept of polyneuritis, polyradiculoneuritis and polyneuropathy has changed considerably since the last century. Charcot-Marie-Tooth disease has been dismembered into hypertrophic, neuronal and spinal forms. Within the group of hereditary sensory neuropathies, to Thévenard's ulcero-multilating acropathy have been added recessive forms of early onset and various types of congenital analgesia. Other hereditary polyneuropathies result from inborn errors of metabolism; in adults, these are chiefly Refsum disease, Fabry's disease, porphyria, amyloidosis and adrenoleucodystrophy. Guillain-Barré acute primary polyradiculoneuritis has come to be associated with chronic and recurrent forms and, more recently, with multifocal demyelinating neuropathy with persistent conduction blocks and antibodies to GM1. Young and Adams acute pandysautonomia is close to polyradiculoneuritis. Finally, many polyneuropathies, formerly labelled polyneuritis, are subsequent to an ever increasing number of known causes, notably infections (e.g. borreliosis or HTLV viruses) and drug-induced or industrial toxicity. Advances in explatory techniques have generated new concepts, including small and large fibre neuropathy, distal and central degenerations, myelin diseases and neuronal diseases.