The most common cause of neuropathy in the United States have diabetes. However, approximately 30% of patients with neuropathy are diagnosed with idiopathic neuropathy term. Idiopathic neuropathy is another way of saying "I do not know why you have neuropathy. The cause of the neuropathy is not known. "As a physician who treats many patients who have failed conventional therapies for neuropathy (Neurontin, Cymbalta, Lyrica, bland). I see many patients that the blood work has not been carefully evaluated and often have not had blood tests done at all. It seems that many times patients are told: "I do not know why I have neuropathy, I am not diabetic." As if it were the sole cause of the neuropathy. There are indeed many reasons to have a more common neuropathy than others. Below I have included many articles in the scientific literature on a rare but possible cause of neuropathy should be considered as a blood test at least before that historically have been labeled as idiopathic.
Chronic neurologic manifestations of Lyme disease.
Background and methods. Lyme disease, caused by the tick spirochete Borrelia burgdorferi, is associated with a variety of neurological manifestations. To define the chronic neurologic abnormalities of Lyme disease, we studied 27 patients (age, 25 to 72 years) with previous signs of Lyme disease, current evidence of immunity to B. burgdorferi, and chronic neurological symptoms with no other identifiable cause. Eight patients were prospectively followed 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 is characterized by memory loss, mood swings or sleep disturbances. Of the 24 patients, 14 had memory impairment on neuropsychological tests and 18 had increased levels of protein in the cerebrospinal fluid, evidence of intrathecal antibody production against 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 had encephalopathy. In 16 patients electrophysiologic testing showed an axonal polyneuropathy. One patient had spastic diplegia leukoencephalitis with asymmetrical lesions of the periventricular white matter, and intrathecal antibody production against B. burgdorferi. Among the 27 patients, associated symptoms were fatigue (74 percent), headache (48 percent), arthritis (37 percent), and hearing loss (15 percent). On examination, chronic neurologic abnormalities had been present from 3 months to 14 years, usually with little progression. Six months after a two-week course intravenous ceftriaxone (2 g / day), 17 patients (63 percent) had an improvement, 6 (22 percent) had improvement but then relapsed, and 4 (15 per percent) had no change in her condition. CONCLUSIONS. Of months or years after initial infection with B. burgdorferi, the Lyme disease patients may have chronic encephalopathy, polyneuropathy, or less commonly, leukoencephalitis. These chronic neurologic abnormalities usually improve with antibiotic therapy.
The clinical and electrophysiological findings in chronic neuropathy of Lyme disease.
We studied 25 patients with chronic Lyme disease and peripheral neuropathy. All had immunologic evidence of exposure to Borrelia burgdorferi and the absence of other identifiable causes of neuropathy. Neuropathic symptoms began a median of 8 months (range 0 to 165) after erythema migrans and had been present for a median of 12 months (range, 2 to 168) before evaluation. Twelve patients (48%) were usually symmetrical distal painful paraesthesias not, and 12 (48%) were generally asymmetric radicular pain. One patient (4%) had asymptomatic neuropathy. The most common physical multimodal sensory loss, which was observed in 13 patients (52%), weakness and hyporeflexia were less frequent. A motor or sensory nerve conduction was a bit "slow in 16 patients (64%). Paresthesia group most frequently detected abnormalities on physical examination and nerve conduction tests in comparison with group root. In 75% to 80% of patients in both groups, however, the needle examination showed denervation in the paraspinal muscles and limbs. Among the 20 patients who underwent lumbar puncture, only one had a mild pleocytosis of cerebrospinal fluid. Six months after treatment with intravenous ceftriaxone, 19 patients (76%) were clinically improved. We conclude that Lyme disease may be associated with a reversible, mild chronic axonal sensorimotor polyradiculoneuropathy or polyradiculopathy.
Chronic neurologic manifestations of Lyme disease.
Background and methods. Lyme disease, caused by the tick spirochete Borrelia burgdorferi, is associated with a variety of neurological manifestations. To define the chronic neurologic abnormalities of Lyme disease, we studied 27 patients (age, 25 to 72 years) with previous signs of Lyme disease, current evidence of immunity to B. burgdorferi, and chronic neurological symptoms with no other identifiable cause. Eight patients were prospectively followed 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 is characterized by memory loss, mood swings or sleep disturbances. Of the 24 patients, 14 had memory impairment on neuropsychological tests and 18 had increased levels of protein in the cerebrospinal fluid, evidence of intrathecal antibody production against 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 had encephalopathy. In 16 patients electrophysiologic testing showed an axonal polyneuropathy. One patient had spastic diplegia leukoencephalitis with asymmetrical lesions of the periventricular white matter, and intrathecal antibody production against B. burgdorferi. Among the 27 patients, associated symptoms were fatigue (74 percent), headache (48 percent), arthritis (37 percent), and hearing loss (15 percent). On examination, chronic neurologic abnormalities had been present from 3 months to 14 years, usually with little progression. Six months after a two-week course intravenous ceftriaxone (2 g / day), 17 patients (63 percent) had an improvement, 6 (22 percent) had improvement but then relapsed, and 4 (15 per percent) had no change in her condition. CONCLUSIONS. Of months or years after initial infection with B. burgdorferi, the Lyme disease patients may have chronic encephalopathy, polyneuropathy, or less commonly, leukoencephalitis. These chronic neurologic abnormalities usually improve with antibiotic therapy.
Dr. Marx is a board certified chiropractic orthopedist and neurologist.
For more information on the treatment of peripheral neuropathy or Dr. Nelson Mane DC please visit our website at http://www. manecenter. com / neuropathy. htm.
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(out of 14 reviews)
I spend much time in the woods. Lyme disease can cause a problem with a person swallow?
My dog was diagnosed with lyme disease today and is receiving a month’s dose of doxycycline for treatment. My question is whether or not his joints/muscles will suffer permanent damage from contracting the disease at all even after treatment is complete. He is 3 years old, the symptoms started Sunday and treatment began today (Tuesday). . . not sure if the timing would make a difference in the permanence of damage. Does anybody have experience with long term results of lyme disease in their dogs? Please help me, I’m confused by this disease. Thanks