Lyme and CIDP

I have been treating a 45 year old male for several months. He has been sick for a very long time. He is seropositive for Lyme disease and Babesia. He has complained of searing total body pain, joint pain and cognitive difficulties for several years. he had become disabled. I tried treating him with a variety of oral and IV medications, with poor results. It has been a frustrating case and I have tried many different strategies. Finally he called me telling me that he had sudden weakness affecting his lower limbs and he was unable to stand. He went to the Hospital and was diagnosed with Guillan Barre syndrome. He was treated with plasmamapharesis. He had a reasonably positive response. He was able to walk but he was still in severe pain and had total body weakness. He was discharged to a rehabilitation facility before returning to see me in the office. I took another look at him. The diffuse, searing neuropathic pain had been ongoing for years. He had weakness of his legs- but there was also weakness of his arms. He had a diffuse loss of sensation to sharp touch in a diffuse pattern. His pain was also very diffuse. His deep tendon reflexes were diminished. He had evidence of mild muscle atrophy diffusely. The neurologist at the hospital had been dismissive. It was Guillan Barre syndrome. Both his intense pain and Lyme disease were dismissed. Unfortunately, my patients frequently get substandard care when they are admitted to the hospital: " Oh no- not another one of so and so's patients."

Guillan Barre is an acute syndrome. It is associated with an ascending neuropathy. This patient had a chronic neuropathy with an acute exacerbation. The plasmapheresis had bought him a little relief, but not much. I am a family doctor- not a neurologist. But it became clear to me what was going on with this patient. He has CIDP- chronic inflammatory demyelinating poly-neuropathy. The disease is a cousin of Guillan Barre, but it is different. It is a chronic disease. It is an autoimmune disease of the peripheral nervous system. Auto-antibodies attack the lipoprotein coat of peripheral neurons, causing diffuse demyelination of the motor and sensory peripheral nerves. In this case, I believe it was Lyme mediated- at least in part. Every time I had prescribed antibiotics for Lyme I only made matters worse. killing Lyme led to increased antigen presentation- feeding a malfunctioning immune response- cranking out noxious auto-antibodies. This is consistent with my model of how Lyme and other germs provide fuel for an autoimmune process. While many believe that autoimmunity is self perpetuating once it begins; it has been my experience that a reduction in germ load can frequently help quiet down the process.

A diffuse loss of myelin of sensory nerves could easily explain his uncontrollable pain. Similarly, the loss of myelin of motor nerves could easily explain the diminished reflexes, weakness and atrophy.

I temporized his therapy with intramuscular injections of steroids while introducing heomeopathic doses of Minocycline. I referred him to a neurologist- whom I believe will do a more thorough evaluation. EMG and NCV studies should confirm the diagnosis.

I also referred him to a hematologist whom I believe will soon start IViG therapy.

Physicians who treat Lyme disease you must be well versed in all of the autoimmune syndromes of the nervous system; It is clear that Lyme can be associated with any one of them.

The widely held injunction prohibiting the use of steroids is not necessarily the case with severe autoimmune disease. Plasmapheresis and IViG are not always practical. The main problem in this patient is not Lyme infection- it is autoimmune disease. A focus only on Lyme wold be a disservice to my patient. I also believe that a focus which excludes Lyme disease would also be a disservice. In my mind, it makes sense to temper steroid therapy with low doses of antibiotics. But of course this is theoretical and speculative. At least I now think we are headed in the right direction.