Dr. Nelson Mane States Lyme Disease is a Rare and Relatively Unknown Cause of Peripheral Neuropathy

The most common cause of neuropathy in the United States is Diabetes.  However, approximately 30% of patients with neuropathy are diagnosed with the term idiopathic neuropathy.  Idiopathic neuropathy is another way of saying “I don’t know why you have neuropathy.  The cause of your neuropathy is unknown.” As a physician who treats many patients who have failed conventional treatments for neuropathy (Neurontin, Cymbalta, Lyrica, Anodyne).  I see many patients who’s blood work has not been thoroughly evaluated or many times have not had blood work done at all. It seems many times patients come in saying, “I don’t know why I have neuropathy, I’m not diabetic”.  As if that were the only cause of neuropathy.  There are, in fact, many reasons to have neuropathy some more common than others.  Below I’ve included several articles from the scientific literature relating to a rare but possible cause of neuropathy that should be considered in your blood work up at least historically before you are labeled idiopathic.

Chronic neurologic manifestations of Lyme disease.

BACKGROUND AND METHODS. Lyme disease, caused by the tick-borne spirochete Borrelia burgdorferi, is associated with a wide variety of neurologic manifestations. To define further the chronic neurologic abnormalities of Lyme disease, we studied 27 patients (age range, 25 to 72 years) with previous signs of Lyme disease, current evidence of immunity to B. burgdorferi, and chronic neurologic symptoms with no other identifiable cause. Eight of the patients had been followed prospectively for 8 to 12 years after the onset of infection. RESULTS. Of the 27 patients, 24 (89 percent) had a mild encephalopathy that began 1 month to 14 years after the onset of the disease and was characterized by memory loss, mood changes, or sleep disturbance. Of the 24 patients, 14 had memory impairment on neuropsychological tests, and 18 had increased cerebrospinal fluid protein levels, evidence of intrathecal production of antibody to B. burgdorferi, or both. Nineteen of the 27 patients (70 percent) had polyneuropathy with radicular pain or distal paresthesias; all but two of these patients also had encephalopathy. In 16 patients electrophysiologic testing showed an axonal polyneuropathy. One patient had leukoencephalitis with asymmetric spastic diplegia, periventricular white-matter lesions, and intrathecal production of antibody to B. burgdorferi. Among the 27 patients, associated symptoms included fatigue (74 percent), headache (48 percent), arthritis (37 percent), and hearing loss (15 percent). At the time of examination, chronic neurologic abnormalities had been present from 3 months to 14 years, usually with little progression. Six months after a two-week course of intravenous ceftriaxone (2 g daily), 17 patients (63 percent) had improvement, 6 (22 percent) had improvement but then relapsed, and 4 (15 percent) had no change in their condition. CONCLUSIONS. Months to years after the initial infection with B. burgdorferi, patients with Lyme disease may have chronic encephalopathy, polyneuropathy, or less commonly, leukoencephalitis. These chronic neurologic abnormalities usually improve with antibiotic therapy.