Lyme disease, which is caused by the spirochetal bacterium Borrelia burgdorferi and transmitted by Ixodes ticks, has been known to mimic neurodegenerative disorders such as multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS), and Parkinson’s disease (PD). As a result, it has become known as “the great imitator", but is it actually the cause of other conditions?
There are several documented cases of patients with confirmed borrelia infection who went on to develop Parkinson’s disease, as well as anecdotal reports of the same. However, a causal relationship has been harder to establish, in part because pre and post mortem testing for borrelia infection (particularly within the central nervous system) had not been conducted in these cases. But in 2003, the first known documented case of Lyme-associated parkinsonism followed by an autopsy was published in the journal Archives of Pathology & Laboratory Medicine.
In 1995, a 63-year-old man with no history of neurological dysfunction presented with the classic Lyme-associated “bulls-eye” (erythema migrans) rash, tremors, joint pain, and swelling. It wasn’t until 12 months later that he was finally diagnosed with Lyme disease based on a positive Western blot (serum) test. Another 2 months went by before he was treated with IV antibiotics for 3 weeks. There was no improvement.
After an MRI was conducted and deemed normal, further testing confirmed antibodies to borrelia in both the serum and the cerebral spinal fluid, as well as a positive PCR (polymerase chain reaction) test. Several neurologists gave the patient the diagnosis of parkinsonism, attributable to Lyme neuroborreliosis. Antibiotic treatment was continued with little success except for a slight improvement in the tremors temporarily.
Over the course of the next few years, the patient continued to decline. He experienced cognitive dysfunction, chronic fatigue, musculoskeletal pain, progressive disability, rigidity, and pulmonary failure. Throughout the progression of his disease, the patient was periodically re-tested for Borrelia infection and continued to test positive (for Babesia as well, on at least one occasion). The patient ultimately passed away from pneumonia and respiratory failure in 2001 – six years after initially contracting Lyme disease.
While the autopsy did not turn up typical markers of Lyme encephalitis or meningitis, a western blot and ELISA were once again conducted and were positive for borrelia-specific IgM and IgG antibodies in samples of both the serum and cerebral spinal fluid. The autopsy also revealed mild atrophy of the basal ganglia and cerebellum, possible myocarditis (which has also been associated with Lyme disease), extensive neuronal loss, and other markers specifically associated with striatonigral degeneration (SND). SND is a sub-type of multiple system atrophy (MSA) that leads to parkinsonism. This is the first documented case of SND being linked to Borrelia infection and confirmed by autopsy. The authors hypothesize that the SND and resulting parkinsonism were either directly caused by infection or indirectly due to an immune response (against the infection).
Although the SND could have occurred independently of the infection, the authors cite that it is unlikely due to the timing of the onset of the patient’s symptoms. They concluded that the infection was probably sufficient enough to cause ongoing neuronal loss and astrogliosis, possibly due to the delayed treatment leading to irreversible neurological damage.
According to Dr. Eric Gordon, a physician who treats complex diseases, Lyme disease can trigger Parkinson’s disease in someone who is genetically predisposed and has a history of certain environmental exposures. Heavy metal is a common additional factor, he says. These other factors may be one of the reasons that some individuals with both Lyme and Parkinson’s disease respond to Lyme treatment, while others do not.
Lyme disease is known to cause neurological complications in its later stages, including meningitis, encephalitis, cranial neuropathy, cognitive dysfunction, and more rarely – parkinsonism and basal ganglia dysfunction. A recent study found that PD patients have higher rates of infection (than controls) with not only borrelia, but also other pathogens such as Epstein-Barr, h. pylori, and herpes simplex virus-1. The patients with higher infection loads also had higher levels of inflammatory markers and other indicators specifically associated with SND and PD.
This case study adds more definitive evidence to what was previously available in the literature, in terms of a causal link between Lyme disease and Parkinson’s disease. The account of this patient’s disease progression is disheartening and one has to wonder if the outcome would have been different had he received diagnosis and treatment for Lyme disease in a timely manner.
Case studies give a unique perspective of weaving a personal story with scientific data and hopefully more like these will help unravel the mystery of how Lyme disease fits into the complex paradigm of neurological conditions such as Parkinson’s.
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