Neuromyotonia is a vague and generally not well-understood condition that could be due to a number of factors, such as neurochemical exposure, chronic neuro infection, neurotoxins, etc. Patients with such problems often are often eventually diagnosed with atypical ALS and other neurological diagnoses. When neuromuscular problems are present with no known etiology or exposures, we generally look for neurotrophic infections, such as Lyme Borrelia, Mycoplasma, etc. Such infections can invade the peripheral (and central) nervous system and cause all sorts of problems in nerve transmission and excitability. Usually such patients have major relief of signs and symptoms if the infections are properly treated. Unfortunately, in the UK there is not much in the way of expertise on the type of infections that could be involved and their treatment.
Neuromyotonia affects the peripheral nervous system of the body causing muscle pain and weakness. This disorder is rare in occurrence and incurable also. Acquired and hereditary are the two forms of neuromyotonia. This condition is also known as by the name continuous muscle fiber activity syndrome, quantal squander syndrome, Isaac-Mertens syndrome, and Isaac’s syndrome. Why this disorder appears is unknown. Some scientists say that if a person is exposed to toxins and has a genetic mutation then there may development of neuromyotonia. However, there are numerous clinical trials and research is going on to discover the exact causes of the disorder so that, there may be some scope for treatment. The government is conducting several trials on scheduled basis where a person can have diagnosis and if possible treatment also.
There is no known cure for neuromyotonia, but the condition is treatable. Anticonvulsants, including phenytoin and carbamazepine, usually provide significant relief from the stiffness, muscle spasms, and pain associated with neuromyotonia. Plasma exchange and IVIg treatment may provide short-term relief for patients with some forms of the acquired disorder. It is speculated that the plasma exchange causes an interference with the function of the voltage-dependent potassium channels, one of the underlying issues of hyper-excitability in autoimmune neuromyotonia. Botox injections also provide short-term relief. Immunosuppressants, such as prednisone may provide long term relief for patients with some forms of the acquired disorder.