Neuroimmunomodulators in neuroborreliosis and Lyme encephalopathy
Lyme encephalopathy, characterized by non-specific neurobehavioral symptoms including mild cognitive difficulties, may occur in patients with systemic Lyme disease and is often mistakenly attributed to CNS infection. Identical symptoms occur in innumerable other inflammatory states and may reflect the effect of systemic immune mediators on the CNS.
Multiplex immunoassays were used to characterize the inflammatory profile in serum and CSF from Lyme and non-Lyme patients with a range of symptoms to determine if there are specific markers of active CNS infection (neuroborreliosis), or systemic inflammatory mediators associated with neurobehavioral syndromes.
CSF CXCL13 was elevated dramatically in confirmed neuroborreliosis (n=8) and to a lesser extent in possible neuroborreliosis (n=11) and other neuroinflammatory conditions (n=44). Patients with Lyme (n=63) or non-Lyme (n=8) encephalopathy had normal CSF findings, but had elevated serum levels of IL-7, TSLP, IL-17A, IL-17F, and MIP-1α/CCL3.
CSF CXCL13 is a sensitive and specific marker of neuroborreliosis in individuals with Borrelia-specific intrathecal antibody (ITAb) production. However, CXCL13 does not distinguish individuals strongly suspected of having neuroborreliosis, but lacking confirmatory ITAb, from those with other neuroinflammatory conditions. Patients with mild cognitive symptoms occurring during acute Lyme disease, and/or following appropriate treatment, have normal CSF but elevated serum levels of T-helper 17 markers and T-cell growth factors. These markers are also elevated in non-Lyme disease patients experiencing similar symptoms. Our results support that in the absence of CSF abnormalities, neurobehavioral symptoms are associated with systemic inflammation, not CNS infection or inflammation, and are not specific to Lyme disease.
There is no question that inflammation plays a large role in Lyme/MSIDS. What is important to point out; however, is that persistence of infection is the issue that needs to be tackled.
Here’s some articles pointing to persistent infection:
Here’s a lengthy article Article Kicking and LLMDs Personal View coauthored by Halperin which states,
“Advocacy for LD has become an increasingly important part of an anti science movement that denies both the viral cause of AIDS and the benefits of vaccines and that supports unproven (sometimes dangerous) alternative medical treatments.”
Oh, and somehow patients, advocates, and their doctors pose a threat to public health.
Here’s a few telling Halperin quotes:
QUOTE- “When physicians who diagnose chronic Lyme disease obtain laboratory tests to provide support for their diagnoses, they often rely heavily on “Lyme specialty laboratories.” Such laboratories may perform unvalidated in-house tests that are not regulated by the Food and Drug Administration, or they may perform standard serologic tests interpreted with the use of criteria that are not evidence-based.1” Source
QUOTE- “Antibiotic therapy can cause considerable harm to patients treated for chronic Lyme disease or post–Lyme disease symptoms.” Source
QUOTE- “Although anecdotal evidence and findings from uncontrolled studies have been used to provide support for long-term treatment of chronic Lyme disease,18-20 a response to treatment alone is neither a reliable indicator that the diagnosis is accurate nor proof of an antimicrobial effect of treatment.” Source
QUOTE- “It is highly unlikely that post–Lyme disease syndrome is a consequence of occult infection of the central nervous system.” Source