The first concern should be the appropriate treatment of that malignancy. Secondarily, treatment of Lambert-Eaton myasthenic syndrome may include medications
Treatment of Lambert-Eaton myasthenic syndrome may include medications to improve transmission of nerve impulses across the synaptic junction and immunosuppressant agents
Patients with Lambert-Eaton myasthenic syndrome should be examined and then treated by both a neurologist and an appropriate cancer specialist (oncologist).
Lambert-Eaton myasthenic syndrome is an autoimmune disease that causes muscle weakness and easy fatigability, particularly in the pelvic muscles and thighs.
Family history of Lambert-Eaton myasthenic syndrome is a known risk factor for development of the disease, as is a personal history of smoking
Patients who develop Lambert-Eaton myasthenic syndrome should be thoroughly screened for the presence of a previously undetected cancer
Lambert-Eaton myasthenic syndrome may be diagnosed by demonstrating the presence of specific antibodies in the blood that are directed against aspects of the presynaptic nerve, such as the calcium channels.
The prognosis of individuals with Lambert-Eaton myasthenic syndrome varies widely. In fact, the most important element of prognosis involves the prognosis associated with any existing cancer.
The prognosis of individuals with Lambert-Eaton myasthenic syndrome varies widely. In fact, the most important element of prognosis involves the prognosis associated with any existing cancer.
about two-thirds of all people with Lambert-Eaton myasthenic syndrome will be diagnosed with some type of cancer, usually small-cell lung cancer, within two to three years
the immune system produces immune cells in response to the presence of early cancer cells which cross-react with the calcium channels on nerve cells
No, there is no treatment for Treacher Collins Syndrome.
Congenital myasthenic syndromes are a group of related disorders caused by inherited defects in the acetylcholine receptor.
The immune system accidentally attacks the calcium channels of the presynaptic nerve cells, preventing normal release of the neurotransmitter acetylcholine into the synaptic junction.