Here I am tackling a huge controversy. First of all keep in mind that the CPN camp tends to believe that CPN is the cause of MS and that many in the Lyme camp think it is Borellia. Physicians have suspected for decades that the underlying casuse of MS is an infectious disease. It has been known that MS is prevalent in temperant climates and non existant in the tropics, between the Tropic of Cancer and the Tropic of Capricorn. Spirochetal diseases exist in the tropics, but not Borellia species. Could there be a correlation? Many physicians focus on the MRI changes of MS. There are white matter lesions in the brain and central nervous system which correlate with demylinization, the destruction of the protective coat of neurons, brain cells. Neuroborreliosis, Lyme disease involving the brain, can show the identical MRI lesions. The lesions themselves are not diagnostic of multiple sclerosis. Then how is MS diagnosed? It is clinical diagnosis. The diagnosis is made on the basis of history and physical. Patients classically present with discrete neurological events involving a specific region of the central nervous system. The symptoms and signs tend to clear. Over time, a second event occurs involving another region of the central nervous system. The various events are separated by time and location. The characteristic pattern of demylinization on the brain MRI helps to confirm the clinical impression. The cause is MS is considered to be autoimmune. This means that the body's immune system for some unknown reason, attacks otherwise healthy tissues, such as the myelin sheath whic protects neurons. According to standard paradigms, the actual cause of the autoimmune response is unknown. The treatment which has been developed involves the administration of immune modulating drugs, such as the cytokine interferon, which help reduce the autoimmune destruction and reduce inflammation. These therapies have been shown to stabilize lesions and help prevent progression of the disease.
A novel idea is that infections may be the trigger which initiates the autoimmune reaction. If this is true, then treating the underlying infection may help reduce or cure the disease. Dr. David Wheldon has listed an fascinating compilation of studies relating MS to CPN. These studies show the presence of CPN genes and antibodies in the spinal fluid of MS patients. They show a relapse of symptoms after respiratory infections with CPN. They show an increase in CPN antibody levels when the disease shifts to a more progressive form. They show MRI improvements in patients treated with antibiotics, including Minocin. He reports some success in treating MS patients with antbiotic protocols, however there are no randomized controlled studies to prove his thesis.
Lets get back to Lyme. The MS of my medical school days has morphed into a different disorder. When I survey my 30 year old medical texts I discover, as I recalled, that the symptoms of MS included focal sensory (a loss of sensation in a specific location) and localized weakness represented the most common presentations. Other common signs were optic neuritis, pain in the eye with a loss of vision and swelling of the optic nerve, a loss of balance, thick speech, specific eye syndromes including "internuclear opthalmoplegial", bladder dysfunction, one sided facial twitching and some mood and personality changes. Patients did not have pain. They did not have fibromyalgia. They did not have migratory joint pain and swelling and they did not have diffuse numbness and tingling in a pattern suggesting peripheral neuropathy. They did not have changes in sensation which followed a stocking and glove distribution. And severe fatigue was not listed as a primary symptom. I have found that few MS patients today have a rapidly progressive course, yet this was formerly seen in one third of the patients. And I have found that most patients have some combination of these chronic Lyme type symptoms, which do not fit in with the classic description of MS. Yet it seems newer literature has incorporated many of the Lyme symptoms into modern day descriptions of MS. Somehow the disease has changed into something which over time has come to resemble chronic Lyme disease. I think doctors rely too much on diagnostic tests such as MRI enhanced with gadollinium, and have forgotted the basics of history and physical. Remember, the MRI characteristics are generally non-specific, and can be seen in both disorders. My suggestion here is not that MS is really Lyme. It seem more likey that many MS cases are misdiagnosed and are in fact really Lyme in the first place. I am more impressed by data which suggests that CPN may be involved in the pathogenesis (process of disease develpment) than Lyme. Of course having both infections simultaneously may complicate the picture and create a hybrid Lyme/MS presentation. Bottom line. Doctors should be aware of all the diagnostic possibilites before slapping on a label. If you are a hammer; everything looks like a nail.