[Eaton-Lambert syndrome].

In the myasthenic syndrome sometimes associated with bronchogenic carcinoma (Eaton-Lambert syndrome) muscular weakness is caused by reduced acetylcholine release from motor nerve terminals (Elmqvist and Lambert, 1968). Guanidine is a potent drug in this condition (Lambert, 1966) but serious adverse reactions have been reported (Lambert and Howard, 1972; Cherington, 1976; Henriksson et al., 1977). We have treated a patient suffering from this syndrome with a new drug, 4-aminopyridine (4-AP). This drug powerfully increases neurally evoked transmitter release from motor nerves (Molgo et al., 1975) possibly by acting directly on the calcium channels in the nerve terminal membrane, allowing the inward calcium current during depolarisation of the nerve terminal to become regenerative (Lundh and Thesleff, 1977). The drug has recently been shown to restore neuromuscular transmission in paralysis produced by botulinum toxin in the rat (Lundh et al., 1977).