Review
Classic diseases revisited
Lambert-Eaton myasthenic syndrome
Udaya Seneviratnea, Rajith de Silvab
a Department of
Neurology, Institute of Neurological Sciences, Southern General
Hospital, Glasgow G51 4TF, UK, b Department of Neurology, Essex Centre for
Neurological Sciences, Oldchurch Hospital, Romford, Essex RM7 0BE, UK
Correspondence to: Udaya Seneviratne, Institute of Neurology, National Hospital of Sri Lanka, Colombo 10, Sri Lanka
Accepted 16
April 1999
The Lambert-Eaton myasthenic syndrome is a neuromuscular
disorder characterised by defective neurotransmitter release at
autonomic neurones and presynaptic terminals of the neuromuscular
junction. It is caused by an IgG autoantibody formed against especially the P/Q type of voltage-gated calcium channels (VGCC) which is an
essential component of the mechanism of neurotransmitter release. Many
patients have an associated small cell carcinoma of the lung which
appears to provide the antigenic stimulus for antibody production, although there is another group with no underlying malignancy. Both
groups show an association with immunological disorders. Assay of VGCC
antibody titres and electrophysiological tests help to
differentiate Lambert-Eaton myasthenic syndrome from other disorders of
the neuromuscular junction. Several drugs and therapeutic interventions
capable of producing significant clinical improvement are currently
available. Patients should also be investigated for underlying tumours,
the specific treatment of which can result in remission or amelioration
of symptoms.
Keywords: Lambert-Eaton myasthenic syndrome; voltage-gated calcium channels
© 1999 by The Fellowship of Postgraduate Medicine
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