Case Report Describes Patient with LEMS, Myasthenia Gravis, and Advanced Lung Cancer

A new case study describes a patient with Lambert-Eaton myasthenic syndrome (LEMS), myasthenia gravis (MG), and metastatic small cell lung cancer (SCLC).

The report from Shandong, China, is titled “Coexistence of myasthenia gravis and Lambert-Eaton myasthenic syndrome in a small cell lung cancer patient: A case report.” It was published in the journal Medicine.

LEMS and MG are both autoimmune disorders of the neuromuscular junction, the site where specialized nerve cells called motor neurons communicate with muscle fibers. There is some controversy about whether these two conditions can exist at the same time.

While LEMS causes malfunctions at the cell transmitting the information (presynapse), myasthenia gravis leads to deficits at the cell receiving it (postsynapse).

The disorders are also characterized by different autoantibodies — P/Q type of voltage-gated calcium channels (VGCC) in LEMS and acetylcholine receptors (AChRs) in myasthenia gravis.

The authors described the case of a 60-year-old man who was admitted to a hospital in China with slurred speech, ptosis — drooping eyelid, a common manifestation in MG — and weakness of limbs that impaired his walking and balance.

Symptoms were milder in the morning. The patient had a four-decade history of smoking 60 cigarettes a day. His mother died of breast cancer, and one of his sisters died of pancreatic cancer.

Neurological examinations revealed weakness of the soft palate with a speaking impairment. His tendon reflexes were absent in the lower extremities, but normal in the upper limbs.

The prostigmin test — a diagnostic test for MG — was positive, and the patient showed AChR antibody production. He also showed decreased muscle action potentials (MAPs), transmitted at the neuromuscular junction from the nerve cell to the muscle, in his arms, legs, and left hand.

A chest computed tomography (CT) and cerebrospinal fluid exam — which takes a sample of the fluid that cushions the brain and fills the spinal cord — did not reveal abnormalities. The patient’s routine blood and biochemical tests were also normal.

But magnetic resonance imaging (MRI) revealed a type of ischemic stroke at multiple sites in the central nervous system, which did not match the patient’s symptoms.

His status became aggravated after admission, and a diagnosis of MG was considered. The patient’s symptoms gradually improved after treatment with Mestinon (pyridostigmine bromide) at 180 mg per day and methylprednisolone at 40 mg a day. He was then discharged.

The patient stopped taking the medications eight months later, which led to another hospitalization. His limb weakness, slurred speech, and ptosis worsened, while he also showed an inability to cough and swallow. MAPs were again reduced.

He was treated with Prostigmin (neostigmine), which is used to improve muscle strength in MG patients, and the steroid methylprednisolone.

Subsequent tests revealed increased tumor markers, abnormal liver enlargement, which was considered metastasis, as well as several enlarged lymph nodes in the area outside or behind the peritoneum in the abdomen.

A liver biopsy indicated a small-cell cancer, and the patient underwent chemotherapy while taking Mestinon and prednisone. Three months later, a lung mass was found on a chest CT, which was diagnosed as small-cell lung cancer (SCLC). He was finally diagnosed with LEMS, MG, and multiple metastases of SCLC.

Researchers concluded the patient’s symptoms were in line with criteria for MG LEMS overlap syndrome (MLOS), which include oculobulbar weakness (involving the eyes and the muscles innervated by cranial nerves), “good response to anti-cholinesterase for MG and limb weakness and decreased or absent reflexes for LEMS.”

The researchers said that when a patient is diagnosed with MG, LEMS, or the two diseases coexisting, clinicians should also consider the possibility of a malignant tumor.