Lambert-Eaton syndrome is a paraneoplastic syndrome characterized by proximal muscle weakness that typically begins in the lower extremities but may spread to involve upper limb, bulbar, and respiratory muscles. It is usually associated with small cell carcinoma of the lung but may also be seen with other occult malignancies or as an idiopathic autoimmune disease. In contrast to myasthenia gravis, muscle weakness improves with repeated effort and is improved less dramatically by anticholinesterase drugs.
It results from a presynaptic defect of neuromuscular transmission. Antibodies to voltage-gated calcium channels on the nerve terminal markedly reduce the amount of acetylcholine released at the motor end plate. Small cell carcinoma cells express identical calcium channels, serving as a trigger for the autoimmune response in patients with paraneoplastic Lambert-Eaton. ACh release from the motor nerve terminal is impaired but the effect of ACh on the postsynaptic muscle membrane is normal.
Patients with Lambert-Eaton are very sensitive to both depolarizing and nondepolarizing NMBA’s. Volatile agents alone are often sufficient to provide muscle relaxation for both intubation and most surgical procedures. NMBAs should be given only in small increments and with careful neuromuscular monitoring.