Many patients are diagnosed with multiple sclerosis because they present to a neurologist with a variety of neurological symptoms and an abnormal MRI of the brain showing white matter lesions. A diagnosis cannot be made on the basis of an abnormal MRI. The findings in Lyme disease and MS can be identical. Medical diagnoses, including MS must be based on a history and clinical examination of the patient.
Most of the "MS" patients I see have a collection of symptoms which are not typically associated with MS. For example, MS patients do not have generalized muscle and joint pains. The two groups of patients usually have different histories and different physical.
MS is a disease of the brain, central nervous system and optic nerve. Neurological disease found in other areas is not compatible with MS. Many of the symptoms of MS and Lyme are the same: Optic neuritis, motor and sensory loss, vertigo, weakness, cognitive changes and many others. The history tends to be different however. Classically, MS is associated with discrete neurological events which tend to improve over time which is/are followed by additional discrete events involving different aspects of the central nervous system. Traditionally, MS is considered a relapsing and remitting disorder. Lyme tends to be a progressive disorder associated with a bewildering array of symptoms which tend to evolve in a progressive manner over time, without the relapsing and remitting feature.
With MS the neurological abnormalities are specifically associated with disease of the central nervous system. Lyme disease, on the other hand, tends to attack a wide spectrum of the nervous system. These diffuse, seemingly unrelated lesions are bewildering to neurologists, but par for the course for physicians accustomed to treating Lyme disease.
Lyme patients frequently have cranial nerve abnormalities of the type not seen in MS.
Lyme patients have upper motor neuron disease- as seen in MS, but may also have lower motor neuron disease, as seen with nerve entrapment syndromes or less frequently ALS. Lyme patients almost invariably have findings of sensory peripheral neuropathy, as seen with diabetes, hypothyroidism, Lyme disease and others. Sometimes neurologists perform EMG/NCV electrical studies to exclude the presence of peripheral neuropathy. These tests are relatively insensitive and are only revealing when the neuropathy is profound.
Despite proclamations made on the TV show House, there is no definitive diagnostic test for MS. It is a clinical diagnosis.
MS is an autoimmune disease. The neurological manifestations of Lyme disease are also for the most part mediated by autoimmune effects. The cause of MS is felt to be unknown. There are clear geographical differences in its prevalence. Many have felt that infections may be the root cause of the autoimmune process causing MS.
Dr. David Weldon in England, building on the work of Dr. Charles Stratton at Vanderbilt, has promoted the hypothesis that MS is causally related to infection with Chlamydia pneumonia. He has reported that his experimental therapy with antimicrobial therapy has shown benefits to patients with early MS.
The patient I refer to has had a protracted disabling illness. She has suffered with a progressive illness. She has had optic neuritis, vertigo, numbness and tingling, weakness, speech difficulties and progressive cognitive effects. She also lives in a wooded, Lyme endemic area and has suffered with severe muscle and joint pain. Her pain has required the use of narcotic pain killers. She had been treated for MS for several years, without much benefit. Her physical exam was not characteristic of MS. She has multiple neurological abnormalities which do not occur in MS. Recently, lab tests for Lyme and Babesia were positive. After several months of intensive antibiotic therapy she is now showing a great deal of improvement.
When I saw her last she was quite confused: "What do I have- is it Lyme or MS- I don't know what to tell my family?"
I stammered- and gave her a convoluted answer. I was soon clear that the technical details were contributing nothing to her understanding. Finally I said: "Just tell them that you have both."
Both Lyme and MS are associated with autoreactive T cells and autoantibodies directed against the lipoprotein coat of neurons called myelin. Both are Th1 mediated processes. Both are exacerbated by inter-current infections. MS therapies, like beta interferons, have anti-viral effects. They also may down regulate MHC molecules on antigen presenting cells and inhibit pro-inflammatory cytokines and T cell proliferation. These effects should benefit neuroborrelios patients. If a neurologists prescribes such drugs for MS they should dovetail nicely with antibiotic therapy prescribed by LLMDS.
Of course, LLMDS are concerned about the routine use of high dose intravenous steroids prescribed by many neurologists for MS exacerbations when "MS" co-exists with Lyme and neuroborreliosis.