Lyme Neuroborreliosis: Known Knowns, Known Unknowns

John J. Halperin; Randi Eikeland; John A. Branda; Rick Dersch

Disclosures

Brain. 2022;145(8):2635-2647. 

In This Article

Conclusions

The goal of this paper has been to facilitate a common foundational understanding of LNB. Key to this is appreciating what does, and does not, constitute nervous system disease. As should be clear, it is highly unlikely that Bbsl infection causes neurodegenerative disorders—particularly in the absence of any evidence of CNS inflammation. A causal relationship with MUS or psychiatric disorders[114,125,137,138] seems highly unlikely—although becoming ill with inflammatory or infectious disorders in general might precipitate or aggravate symptoms of such disorders in individuals otherwise predisposed to them—i.e. this might reflect a class effect, true of any infection. Many questions remain. By what mechanism do spirochetes reach the nervous system? If a very small bacterial load triggers LNB, by what amplifying mechanism does this occur? Does this suggest other, non-antimicrobial interventions? Might this inform treatment of other infections? And if post-infectious symptoms occur, what is the pathophysiological mechanism and might this explain other post-infectious states? Hopefully the framework provided here will allow more focus on these fundamental questions.

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