patient reviewing information on screen with healthcare provider

Cancer-Associated LEMS with SCLC

Timely detection of LEMS plays a pivotal role in ensuring appropriate oncology care1,2

Healthcare provider holding up chest xray

The impact of a delayed Lambert-Eaton myasthenic syndrome (LEMS) diagnosis extends beyond neuromuscular symptoms. LEMS is a paraneoplastic neurologic syndrome (PNS), in which autoantibodies target components of the peripheral nervous system involved in neuromuscular transmission. It is frequently associated with an underlying malignancy, most often small cell lung cancer (SCLC).1-4

In LEMS, the tumor induces an autoimmune response in which antibodies target presynaptic voltage-gated calcium channels (VGCCs) at nerve terminals. This disrupts calcium-mediated acetylcholine (ACh) release, impairing neuromuscular transmission and leading to muscle weakness.5,6

Neuromuscular symptoms often precede the detection of the cancer, highlighting the urgency of early diagnosis for both symptom management and timely cancer detection.1,2

Delayed diagnosis of LEMS may:

  • Allow cancer to progress undetected1
  • Increase morbidity1
  • Fail to target the presynaptic 
sources of LEMS7

of LEMS CASES are also ASSOCIATED WITH AN UNDERLYING cancer6,8-10

Patients with LEMS should be screened immediately for cancer with a computerized axial tomography (CAT) or positron emission tomography (PET) scan. If no cancer is found, symptomatic treatment should be initiated and follow-up cancer screening should be performed every 6 months for 2 years.1

Updated NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines®) for Small Cell Lung Cancer recommend VGCC-Ab testing, preferably in consultation with neurology in SCLC and suspected paraneoplastic neurologic syndrome.8

References: 1. Titulaer MJ, Lang B, Verschuuren JJ. Lambert-Eaton myasthenic syndrome: from clinical characteristics to therapeutic strategies. Lancet Neurol. 2011;10(12):1098-1107. 2. Kesner VG, Oh SJ, Dimachkie MM, Barohn RJ. Lambert-Eaton myasthenic syndrome. Neurol Clin. 2018;36(2):379-394. 3. Wirtz PW, Smallegange TM, Wintzen AR, Verschuuren JJ. Differences in clinical features between the Lambert-Eaton myasthenic syndrome with and without cancer: an analysis of 227 published cases. Clin Neurol Neurosurg. 2002;104(4):359-363. 4. Titulaer MJ, Wirtz PW, Willems LNA, et al. Screening for small-cell lung cancer: a follow-up study of patients with Lambert-Eaton myasthenic syndrome. J Clin Oncol. 2008;26(26):4276-4281. 5. Quartel A, Turbeville S, Lounsbury D. Current therapy for Lambert–Eaton myasthenic syndrome: development of 3,4-diaminopyridine phosphate salt as first-line symptomatic treatment. Curr Med Res Opin. 2010;26(6):1363-1375. 6. Titulaer MJ, Maddison P, Sont JK, et al. Clinical Dutch-English Lambert-Eaton myasthenic syndrome (LEMS) tumor association prediction score accurately predicts small-cell lung cancer in the LEMS. J Clin Oncol. 2011;29:902-908. 7. Shieh P, Sharma K, Kohrman B, Oh SJ. Amifampridine phosphate (Firdapse) is effective in a confirmatory Phase 3 clinical trial in LEMS. J Clin Neuromuscul Dis. 2019;20(3):111-119. 8. Referenced with permission from the NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines®) for Small Cell Lung Cancer V.2.2026. © National Comprehensive Cancer Network, Inc. 2025. All rights reserved. Accessed March 30, 2026. To view the most recent and complete version of the guideline, go online to NCCN.org. NCCN makes no warranties of any kind whatsoever regarding their content, use or application and disclaims any responsibility for their application or use in any way.