What is the mechanism of Eaton-Lambert Syndrome?

Eaton-Lambert Syndrome, also known as Lambert-Eaton myasthenic syndrome (LEMS), involves an autoimmune response that primarily affects the presynaptic terminals at the neuromuscular junction. The correct mechanism that describes this condition is the inadequate release of acetylcholine.

In Eaton-Lambert Syndrome, there is a deficiency in the release of acetylcholine due to the autoimmune attack on voltage-gated calcium channels located on the presynaptic membrane of the neuromuscular junction. Under normal physiological conditions, these calcium channels facilitate the influx of calcium ions when a nerve impulse arrives, triggering the release of acetylcholine into the synaptic cleft. In LEMS, the impaired calcium channel function results in reduced acetylcholine release, leading to muscle weakness.

This understanding is crucial because the neuromuscular junction’s ability to transmit nerve impulses effectively is dependent on adequate levels of acetylcholine. In contrast to other options, such as the increased release of dopamine or the overproduction of serotonin, these do not directly relate to the pathophysiology of Eaton-Lambert Syndrome. Similarly, diminished release of GABA pertains more to inhibitory neurotransmission rather than the dysfunction at the neuromuscular junction associated with