What Causes Lyme Brain?

Since we’ve wrapped up our 10-week series on barriers to recovery from Lyme disease, I thought that I would give you a sneak peek into some of the topics that I’ll be covering in my new book entitled “Lyme Brain“, which should be released by the end of the summer.  The following excerpt is on the topic of “What Causes Lyme Brain?”.

Lyme Brain—brain fog, short-term memory loss, difficulty with focus and concentration, anxiety, depression and the host of other aspects that make up the cognitive and neuropsychiatric aspects of Lyme.

The causes of Lyme Brain can be grouped into four broad areas –

1. Direct damage to nerve cells
2. The inflammatory response
3. Neurotoxins
4. Neurotransmitter imbalance

Over the next four Wednesdays I will share these excerpts from my book, starting today with number one – direct damage to nerve cells.

We know that in the body, spirochetes can exist outside of cells or inside of cells. The intracellular invasion allows them some protection from host defenses, primarily our immune response.

Bacteria in the brain are invasive, too, and can invade neurons (nerve cells that conduct electrical impulses) and glial cells (supporting cells of the nervous system that do not conduct impulses).[i],[ii] The invasion, and the following inflammatory cascade that results, can lead to death of the nerve cells.

Researchers back this up. “The presence of B. burgdorferi DNA in tissue sample from areas with inflammatory changes indicates that direct invasion of B. burgdorferi may be the pathogenetic mechanism for focal encephalitis in LNB (Lyme Neuro-Borreliosis).”[iii]

Although this sounds dire—and not to make light of it, it can be—the neuronal death appears to be secondary to an inflammatory cascade triggered by the bacterial invasion. In other words, it appears to be the secondary inflammation rather than the pathogen itself that causes cell apoptosis.[iv] There are ways to mediate such inflammation, which we’ll discuss later. If we can mediate the inflammatory response, then we can minimize cell damage and death.

Borrelia may also cause demyelination of the white matter in the brain. The myelin sheath is a protective sheath that surrounds the axon of the nerve cell (the branch that juts out from the nerve cell and transmits the impulse). Myelin serves primarily to increase the speed of nerve transmission, getting the message from one cell to the next in the quickest, most efficient manner. There are several neurological diseases that involve demyelination, but the best known, perhaps, is multiple sclerosis (MS). Given that a subset of Lyme patients have been diagnosed with MS, it does raise the question of whether their primary diagnosis is truly Lyme disease but the diagnosis of MS was made based on similar findings on MRI studies. Unfortunately, there are no curative treatments for MS, and while Lyme treatment may not be quick or straightforward, I have seen Lyme patients who have also been diagnosed with MS improve with antibiotic treatment. This is often also evidenced by a reduction in white lesions on their brain MRI. So, determining whether MS is underlying Lyme disease can make all the difference in the world in a patient’s prognosis.

There are several studies that demonstrate demyelination in Lyme patients. Many of the studies are case reports, so it unclear exactly how prevalent this is, but as with anything in Lyme disease, my suspicion is that it most likely occurs more frequently than the literature would imply.[v]

One researcher, Vesna Briner, did make this statement:

“The diagnosis of multiple sclerosis (MS), despite well-defined clinical criteria is not always simple. On many occasions it is difficult to differentiate MS from various non-MS idiopathic demyelinating disorders, specific and infectious inflammatory diseases or non-inflammatory demyelinating diseases. Clinicians should be aware of various clinical and MRI “red flags” that may point to the other diagnosis and demand further diagnostic evaluation. It is generally accepted that atypical clinical symptoms or atypical neuroimaging signs determine necessity for broad differential diagnostic work up. Of the infectious diseases that are most commonly mistaken for MS the clinician should take into account Whipple’s disease, Lyme disease, Syphilis, HIV/AIDS, Brucellosis, HHV-6 infection, Hepatitis C, Mycoplasma and Creutzfeld-Jacob disease, among others.”[vi]

Another quote from a study out of Croatia:

“Demyelinating diseases of the central nervous system include a wide spectrum of different disorders that may resemble multiple sclerosis (MS). The diagnosis of MS is based on typical clinical and paraclinical criteria … If some of these criteria are atypical, diagnostic algorithm should be extended to some other procedures to exclude other diseases that can mimic MS not only in symptoms, signs or course of the disease but also in laboratory findings. In such a case, an alternative, better explanation for the clinical manifestations should be considered and performing specific tests is helpful to exclude alternative diagnoses.”[vii]

Certainly there are enough references and articles stating that infectious processes can be a cause of demyelination and that differential diagnosis must include those things. I wonder, then, why some doctors are still so reluctant to consider chronic infections such as Borreliosis in a patient presenting with MS?

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References:

[i] Miklossy, J, S Kasas, A D Zurn, S McCall, S Yu, and P L McGeer. “Persisting atypical and cystic forms of Borrelia burgdorferi and local imflammation in Lyme neuroborreliosis.” J Neuroinflammation 5, no. 4 (2008).

[ii] Miklossy, J, et al. “Beta-amyloid deposition and Alzheimer’s type changes induced by Borrelia spirochetes.” Neurobiol Aging 27 (2006): 228-236.

[iii] Oksi, J, et al. “Inflammatory brain changes in Lyme borreliosis. A report on three patients and review of literature.” Brain 119 (Pt 6) (December 1996): 2143-54.

[iv] Ramesh, G, L Santana-Gould, F M Inglis, J D England, and M T Philipp. “The Lyme disease spirochete Borrelia burgdorferi induces inflammation and apoptosis in cells from dorsal root ganglia.” J Neuroinflammation 10 (July 2013): 88.

[v] Durovska, J, S Bazovska, J Pancak, M Zaborska, M Derdakova, and P Traubner. “Infection with B. burgdorferi s.l., and the CNS demyelinating disease. A case report.” Neuro Endocrinol Lett 32, no. 4 (2011): 411-4.

[vi] Brinar, V V, and M Habek. “Rare infections mimicking MS.” Clin Nuerol Neurosurg 112 (2010): 625-628.

[vii] Dezmalj-Grbelja, L, R Covic-Negovetic, and V Demarin. “Differential diagnosis and diagnostic algorithm of demyelinating diseases.” Acta Clin Croat 48, no. 3 (2009): 345-8.