For cell damage and for pain.
It appears that there are no totally adequate treatments.Some may alleviate the symptoms and help the patient's quality of life. Decisions about treatment may depend on the patient's general condition, age, the severity and progression of the neuropathy, tolerance of any disability and the time delay between onset and diagnosis.
It has been reported that for patients who fulfil CIDP diagnostic criteria, usually IgG and IgA patients, that generally the treatments are similar to those used for CIDP. Some may be tried with IgM cases.
- Corticosteroids such as Prednisone - an immunosuppressant.
- Plasma exchange (plasmapheresis) which aims to wash out nearly all the antibodies –‘good’ and ‘bad’ - and then replace with good ones.
- High dose intravenous immunoglobulin (IVIG), which floods the system with ‘good’ antibodies.
- The cytotoxic (cell poisons) drugs could be tried. The latter include Azathioprine, Cyclosporin and others. These drugs suppress T killer lymphocytes, interfere with cell division, or suppress B lymphocytes. Thus they reduce or inhibit the damage being done to the myelin sheath and in turn allow the myelin sheath to regrow.
The drug Rituxan or Rituximab, directed to treat B cell lymphocytes, is being used on trial especially for anti-MAG IgM cases, to improve strength and function and to reduce titers of paraprotein in the serum. This and all other treatments will be conducted under carefully controlled conditions.
Some PDN patients may respond to treatments , depending on a variety of factors, such as whether the neuropathy has become well established and/or is aggressive. They may produce mild or short-term but transient improvements whilst the benefits may not be very significant. A neurologist may have to decide whether any such treatment may be beneficial, as all these treatments can give rise to troublesome side effects. Benefit has to be balanced against risk. Often patients with relatively mild symptoms are not treated in order not to be subjected to the morbidity of some treatment regimes. Thus many specialists reserve treatment for patients experiencing a more aggressive disorder. The experience of some neurologists is that PDN may be very resistant to treatment.
Neuropathic pain management
Some PDN/MGUS-associated neuropathy sufferers experience a testing problem of the big demands made by neuropathic pain. Resulting from the damage to the peripheral nerves this pain is very complex and the most difficult type of chronic pain to treat. Because the damaged and malfunctioning nerve cells either become over stimulated or misfire, it means that an over abundance of pain messages are sent to the brain causing severe and often long lasting agony.
. The aching or pain in toes and feet reflects damage to the longest axons. The group of symptoms is typically described by patients in words including:
Sometimes it may begin by the patient describing feet sensations as tingling, feeling numb or tight, wooden or dead.
Shooting pains (like electric shock sensations).
Burning (sensations that the feet are on fire).
Sharp, stabbing pains (described as knife like, or pins and needles).
Cutting pains (like the pain experience from being cut on a finger by the sharp edge of a piece of paper – but like cuts from hundreds of pieces!).
This type of pain is very different to nociceptive pain – from burns, bumps, bruises, infections etcetera. A former UK GP with 36 years experience until acquiring CIDP has stated that "many of my medical colleagues are unaware of the intensity of this neuropathic pain". He has told of his experience of it building up "to almost screaming point, often in the latter part of the day."
Treatment or management of neuropathic pain.
Ordinary non-narcotic painkillers (opioids) generally do not ‘touch’ the problem, although there may be some initial success. After that the dose has to be greatly increased with sedative and other side-effects and decreasing value.
Tricyclics or anti depressants,
such as Amitriptyline, may be used but some people can not tolerate these, as is the case with the anti-convulsants. They work on the nerves dealing with the pain. Amitriptyline has been a first-line drug in this group but it is an old one with side effects, mainly sedation, dry mouth, fast heart rate, weight gain.
These anti-depressants drugs increase the levels of neuro-transmitter by blocking their re-absorption. Depressed people have fewer neuro-transmitters than normal being released, thus leading to reduced stimulation. Other drugs such as imipramine, dothiepin, dofepramine may also be used.
These are useful drugs that were originally designed for the treatment of epilepsy. The older ones such as carbamazepine, phenytoin and sodium valproate all have had a role. They have an inhibitory effect, reducing abnormal and excessive "electrical" excitability in the nervous system. There may be problems. Due to their side effect profile, they are becoming less popular. Sedation is a major concern, along with problems with concentration and memory at the dose levels required for controlling pain. They can cause dizziness, blurred vision, allergies, skin rashes and so on.
a relatively new anti-epileptic drug, has become more popular among pain clinicians. Having fewer side effects than other anti-convulsants it is better tolerated by patients and does not interfere with other medication being taken. It is now the first choice drug for neuropathic pain.
Please note: These notes are based on my experience and my reading of published professional material. They should not be understood as coming from any personal medical expertise. Should anyone, especially a professional neurologist, notice any error please contact me.