This 40 year old woman saw a neurologist only once. She did have tingling on the right side of her face. At that point the neurologist stopped asking questions. He ordered am MRI. But she also had headache, joint pains (multiple and diffuse), cognitive issues and floaters. She spent a lot of time outdoors. The neurologist had no interest in this litany. Her neurological exam showed a typical pattern of sensory peripheral neuropathy, not the central nervous system findings one would expect to see in MS. I do not know what he found when he examined the patient.
The neurologist diagnosed MS. A brain MRI showed periventricular and subcortical white mattter disease. The radiology reports reads "While these are nonspecific these lesions are suspicious for demylinating plaques. Clinical correlation is needed to exclude......Lyme disease......"
These findings MRI findings are fairly classic as seen with MS. The neurologist informed the patient that she had MS. Not quite convinced, the patient sought my attention, seeking another opinion.
Again- MS cannot be diagnosed by MRI findings. There are diagnostic criteria listed in many text books. Per Harrison's Textbook of Medicine, 16th edition, page 2464:
There are 5 specific criteria listed. MRI findings are not a prominent aspect of the criteria. The fifth criteria is clear: "The patient's neurological condition could not better be attributed to another disease."
My history and exam pointed to Lyme disease- not MS: See criteria #5.
During a 6 month process of treatment, other symptoms became manifest. The patient had soaking sweats. She had profound fatigue, which increased with antibiotic therapy- a Herx response. She had muscle pains, diffuse numbness and tingling of the extremities, muscle twitching, tinnitus, floaters and sleep difficulties.
The cognitive difficulties were typical of what I have seen in numerous chronic Lyme patients. The patient had "brain fog," word retrieval difficulties, short term memory loss, slow cognitive processing and new ADD like symptoms- difficulty concentrating.
After 5 months of treatment which has focused on Lyme and Babesia she is feeling 80% better.
She never agreed to have labs run through a specialty lab. A limited Lyme WB showed a 23 IgM band. She has had alterations in vitamin D and high complement levels. Her CRP has remained very elevated. Let me comment on the Western Blot. There is much literature demonstrating the existence of sero-negative Lyme disease. This is denied by the IDSA- even though many of their physicians have authored and published papers in the past refuting their current stance. The 23 band is specific for Osp C. This is a specific antigen, outer surface protein C, which many consider diagnostic Bb- the Lyme bacteria, even in the absence of other bands. In truth, there are no universally accepted Western Blot criteria for the diagnosis of Lyme exposure. What exists is an assortment of surveillance criteria and individual guidelines espoused by a variety of physicians and laboratories familiar with the disease. The diagnosis is not cut and dried or black and white; and the treatment is murkier yet by many orders of magnitude. Perhaps as someone said in reference to Lyme and its controversies: "It is an exercise of nailing jello to the wall." This is true, but we still have to deal with the jello!
I ask physicians to try to do a better job, to keep an open mind- and to consider the fact that those of us who see patients in the northeast US and mid-atlantic region are operating in a Lyme endemic region. I also ask physicians to keep in mind that Lyme has aptly earned the title: "The great imitator." Patients with complex, multi-system complaints cannot be diagnosed with a single imaging study. The basic tools of history and examination are as essential now as they were 100 years ago. Something was ingrained into my mind by one of my mentors early in my medical training, something which has held me in good stead for all these years: Rule one- treat the patient, not the lab.