Neuromuelitis optica is also known as Devic’s disease and it is a condition with several different possible causes. However, what is the same is that almost all patients, regardless of the cause, suffer from excessive inflammation and, at the same time, damage of the myelin sheath of the optic nerve which leads to hampered conduction of signals.
These problems come from autoantibodies from the body’s immune system which react against the cells in the body – in this case, optic nerves and spinal cord. The condition is often misdiagnosed as multiple sclerosis due to the fact that inflammation can also affect the brain. However, the lesions are not the same. Moreover, the difference can be seen from the fact that multiple sclerosis and neuromuelitis optica require different treatments.
In the case of neuromuelitis optica, the issues with the spinal cord result in a weakness in the legs and arms, or even paralysis, as well as problems with bladder, bowels and eyes, including blindness.
Due to the fact that there are similar conditions the term “neuromyelitis optica spectrum diseases” is being used increasingly.
The most probable cause is the attack of the immune system on the AQP4 water channel. They are used to transfer water between cell membranes and they are located in both the optic nerve and spinal cord. It has been discovered that almost 70% of patients with neuromyelitis optica have had positive results in tests which look for AQP4 antibody called NMO-IgG.
Neuromyelitis optica is more common in women than men. It is most often found in people between the ages of 40 and 50 but it is not limited to any age. It is estimated that about 250,000 people suffer from neuromyelitis optica.
Neuromyelitis optica symptoms
The most common symptoms include impairments of the spinal cord function and eyesight problems. The latter may include a number of different symptoms such as decreased vision clarity, lots of colour vision, defects in the visual field and even blindness.
The symptoms relates to spinal cord problems include loss of control over bladder and bowels, reduced sensation and weakness in muscles of limbs. Spastic weakness (both paraplegia and quadriplegia – impairments in motor functions in the legs and both arms and legs, respectively) is also very common.
Even though the symptoms increase in time, neuromyelitis optica really progresses through different stages. The increase in disabilities actually comes from an increased number of attacks on the AQP4 water channel, rather than any kind of worsening of the initial cause.
Neuromyelitis optica treatment
Diagnosing neuromyelitis optica as early as possible is essential because, unlike multiple sclerosis, the attacks of neuromyelitis optica are far more severe and they can quickly cause irreversible damage.
As with many other autoimmune diseases, there is currently no cure for neuromyelitis optica. Treating symptoms, on the other hand, can produce different results. For some patients they give complete recovery through successful symptoms management while the others suffer from various degrees of impairment of the limbs and vision.
Attacks can be very severe and in those cases patients are given high dosages of intravenous corticosteroids. In very rare cases when the attacks do not respond to corticosteroids, patients can be treated by plasmapheresis. However, this course of response to acute attacks has not undergone sufficient testing.
Corticosteroids are effective in most cases, but they come with side effects.
Immunosuppression is also necessary, but it does come with its dangers. It helps reduce the number of attacks and it can serve as prevention and having in mind that more than 90% of patients experience recurring attacks. Another downside is that this treatment needs to be ongoing.
This is why it is important to provide the patients with treatment options which can be used long-term, especially having in mind that there is no cure. Palmitoylethanolamide (PEA) is a treatment option which has several benefits for the patients suffering from neuromyelitis optica.
PEA treats pain and inflammation. Pain is treated through inhibition of iNOS and COX-2, while reduction in inflammation comes from calming of the inflamed cells. All of these effects come through PEA’s effects on several different nuclear receptors.
Moreover, due to its mutually rewarding cooperation with endogenous anandamide, PEA affects CB2 receptor which is spread throughout the immune system. This way PEA affects hematopoietic cells which give rise to all other blood cells, B cells which play a huge role in the immune system and creation of antibodies and macrophages which get rid of cellular debris and microbes.
Several different studies have shown that PEA affects mast and glial cells. Mast cells deal with inflammation and allergies and this is why PEA can help reduce inflammation and greatly diminish the negative effects of neuromyelitis optica.
Glial cells form myelin and restore homeostasis. Demyelination is a major part of neuromyelitis optica and proper operation of glial cells is essential.
In this way, PEA addresses the two most important aspects of neuromyelitis optica – inflammation and demyelination.
It is important to note that PEA is completely safe for prolonged use. It is actually pharmaceutical grade palmitoylethanolamide, which is an endogenous fatty acid amide. This makes it completely safe in any amounts. Moreover, there is no way to build up tolerance to PEA, so long-term usage only makes it more effective as well as completely safe.