Multiple sclerosis (MS) is a disease that has attacks affecting different locations in the nervous system. In addition to the requirement for multiple locations, to make a diagnosis of MS there must be multiple attacks at different times. This presents a problem for how to classify people who have had only a single attack. These patients are at high risk of having MS, but technically cannot be diagnosed with the disease until they have a second attack. This situation is called CIS.
Clinical examinations and MRI are the most common methods of following people with CIS. If the initial MRI is normal, then long term treatment is not indicated. Treatments to help with remaining symptoms may be needed however.
If the initial MRI is abnormal, then long term treatment for MS is recommended. Studies have shown benefit for Avonex, Betaseron, Copaxone and Rebif in CIS. In general, these studies indicate that the medications are likely to be more effective the earlier they are started. Also, patients who were on the placebo arms of these studies developed more disability than those on treatment. After 2 years, all patients in these studies were offered treatment with the real medication. In those patients on the placebo arms of the studies for 2 years, their rate of disease progression slowed after starting the medication, but they never caught up with those who started treatment early even several years later.
Neuromyelitis Optica is also called NMO, Devic’s disease or Devic disease. NMO was first described by Eugene Devic, a French neurologist, in 1894. It is often mistaken for multiple sclerosis (MS). Though it resembles MS in some aspects, it differs in several important ways. The cause of the disease and pathology of the disease differ from that of MS. The treatment is also different.
Acute attacks of NMO are treated with corticosteroids. The most commonly used steroid is methylprednisolone. If this fails and the symptoms are severe enough to warrant it, then plasma exchange can be used to treat acute attacks.
Without treatment to prevent attacks, virtually all NMO patients will have future attacks. Medications are generally recommended for life to prevent these future attacks.
The medications used for MS do not work well for NMO. NMO responds best to immunosuppressants. The most common treatment used for first line treatment is azathioprine (Imuran). If this fails, a number of other immunosuppressants have been used including mycophenolate (CellCept), rituximab (Rituxan), mitoxantrone (Novantrone), cyclophosphamide (Cytoxan), intravenous immunoglobulin (IVIG) or bone marrow transplant (stem cell transplant).
Optic neuritis (ON) is an inflammation of the optic nerve. It is also known as retrobulbar neuritis. The retina, in the back of the eye, senses light and converts this into a nerve signal. The optic nerve carries the nerve signal from the retina to the brain where it is interpreted into a visual image. If inflammation affects the optic nerve the signal between the retina and the brain is affected.
Acute attacks of ON are treated like MS attacks. This generally involves corticosteroids if the symptoms are severe enough to warrant it. If symptoms are severe and if they fail to respond to corticosteroids, then plasma exchange may be used.
If patients have an abnormal MRI, and thus have a high risk of having MS, treatment with medications to decrease the frequency of MS attacks may be warranted.
Transverse myelitis (TM) is an inflammation of the spinal cord. TM is usually noticed over a few hours and reaches a maximum severity over a few hours or days. The symptoms depend on what parts of the spinal cord are affected.
The spinal cord carries signals from the brain down the back. A second nerve then takes these signals from the back out to the rest of the body. Sensory signals from the body are brought to the spinal cord by nerves, and then are taken up the spinal cord to the brain. The spinal cord is the main connection between the brain and the rest of the body.
Motor nerves carry signals to muscles. If these nerves are affected, the result is referred to as spasticity. Spasticity will affect the muscles from the level of injury to the spinal cord downwards. For example, if the spinal cord is injured at the waist, then weakness will occur from the waist down. Spasticity has several components. This includes weakness, tightness/stiffness of the muscles, spastic leg jumps and brisk reflexes.
Sensory nerves carry signal from the skin, bones, joints and muscles to the brain. If these nerves are damaged, sensory symptoms will occur below the level of injury. If the injury is severe enough that no signal gets to the brain, then numbness results. If the signal gets to the brain, but is jumbled, then a number of odd sensations can result. These include pins and needles, burning, pain, tingling or other odd sensations. A feeling of tightness or constriction at the level of the injury is so common that patients have named it the “MS Hug”.
Damage to the nerves serving the bowels leads to constipation. Damage to the nerves serving the bladder can lead to a number of bladder symptoms including urgency, retention and hesitancy.
Sexual dysfunction can also be seen.
Acute attacks of TM are treated like MS attacks. This generally involves corticosteroids if the symptoms are severe enough to warrant it. If symptoms are severe and if they fail to respond to corticosteroids, then plasma exchange may be used. These treatments are discussed further in the section on treating acute attacks of MS. If patients have an abnormal MRI, and thus have a high risk of having MS, treatment with medications to decrease the frequency of MS attacks may be warranted.