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Neuroborreliosis
Classification and external resources
MeSH D020852

Neuroborreliosis is a disorder of the central nervous system caused by infection with a spirochete of the genus Borrelia.[1] The microbiological progression of the disease is similar to that of Neurosyphilis, another spirochete infection.[2] Neuroborreliosis is most often the late stage of Lyme disease, however it can also occur early during initial infection. The disease is controversial in regards to treatment, and is considered incurable by some. There are no official stages or specific identifying symptoms, however it is a progressive neurodegenerative disease. There is also no specific established way to manage symptoms, which is typical of most CNS infections. Unlike the similar spirochete infection Neurosyphilis, Neuroborreliosis does not cause (established) brain damage without immunosuppression (such as that caused by taking steroids), but rather causes progressive brain dysfunction as the spirochete load increases. Neuroborreliosis has been declared by the CDC as rarely fatal, however eventually disabling.

In 2004 German physician Fritz Schardt, specialist in internal medicine in Germany, published "Clinical effects of fluconazole in patients with neuroborreliosis" (Eur J Med Res. 2004 Jul 30;9(7):334-6). The daily protocol of 200 mg of fluconazole was a result of his own experience with neuroborreliosis and long-term antibiotics. As common to patients with a sustained antibiotic regimen, Dr. Schardt treated his resulting yeast infections with fluconazole (interview Jan Neimark, copyright 2005). Fluconazole inhibits cytochrome p450, particularly CYP3A4 (European Journal of Clinical Pharmacology,Effect of route of administration of fluconazole on the interaction between fluconazole and midazolam, Volume 51, Number 5 / January, 1997). Borrelia species, like other bacteria, require CYP 450 for metabolic processes. After a regimen of 25-50 days of fluconazole at 200 mg /day, followed by narrow spectrum penicillins such as cephalosporin, roxithromycin, cotrimTMPO, and clarithromycin, Schardt speculates that fluconazole may weaken spirochetes and enable such penicillins to kill the species, including those infecting the brain and CSF. Critically valuable to patients with neuroborreliosis is penetration of the blood-brain barrier, which fluconazole easily accomplishes (Pharm Res. 1996 Oct;13(10):1570-5, Fluconazole distribution to the brain: a crossover study in freely-moving rats using in vivo microdialysis). While his 2004 study documented 8 of 11 patients having a full recovery from neuroborreliosis one year following treatment, and three patients with greatly improved symptoms, Dr. Schardt attributes this protocol to the recovery of more than 80 patients and indicates that further refinement of the protocol is in order (Jan Neimark, 2005).

References

  1. ^ Rupprecht TA, Koedel U, Fingerle V, Pfister HW (2008). "The pathogenesis of lyme neuroborreliosis: from infection to inflammation". Mol. Med. 14 (3-4): 205–12. doi:10.2119/2007-00091.Rupprecht. PMID 18097481. PMC 2148032. http://www.molmed.org/pdfstore/205_212.Rupprecht.00091.PDF.  
  2. ^ Judith Miklossy, Sandor Kasas, Anne D Zurn, Shermann McCall, Sheng Yu, and Patrick L McGeer (2008). "Persisting atypical and cystic forms of Borrelia burgdorferi and local inflammation in Lyme neuroborreliosis". Journal of Neuroinflammation 5 (1): 40. doi:10.1186/1742-2094-5-40. http://www.jneuroinflammation.com/content/5/1/40.  

Template:Infectious-disease

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