Neuroprotection: Let the doctor speak!

Last night I heard a doctor try to tell Diane Rehm about neuroprotection. She cut him off. I think we should have heard him out.

Again we hear that there is no "evidence" to support chronic Lyme. There is no evidence to support the use of prolonged antibiotic therapy in patients with persistent Lyme related symptoms. Such are the proclamations made by "experts" who have evaluated the results of 3 NIH sponsored studies. These clinical studies sponsored by the NIH have been woefully misinterpreted. At any rate, none of these studies claim that the Lyme organisms have been eradicated or provide any scientific evidence to support this contention.

Then, when naysayers admit that such therapies seem to help patients, they claim it is due to other, non-specific effects of antibiotics.(Let the doctor speak) After all there are no germs to be killed. Based on what science have such experts concluded that there are no germs to be killed? Sounds like a bait and switch tactic to me.

How can the deniers have it both ways? Do the drugs help or don't they?

Beta-Lactam antibiotics may indeed offer neuroprotection. Included here are drugs in the penicillin family and the cephalosporin family. Animal studies have shown that Rocephin has neuroprotective properties in animal models. These drugs upregulate a molecule called GLT1 which in turn inhibits gluatamate. Glutamate is the principal "excitatory" neurotransmitter in the nervous system. Inflammation of the nervous system, both acute and chronic is associated with "glutamine toxicity." It is thought that drugs such as Rocephin may provide clinical benefits for a wide array of neurological disorders. For example,Rocephin has been shown to improve the clinical course of ALS in the mouse model.

Minocyline is reported to have neuroprotective effects due to inhibition of 5-lipoxygenases, a pro-inflammatory enzyme associated with the aging brain.

Antibiotics are reported to have anti-inflammatory properties independent of their germ killing effects. Some medical literature suggests that tetracycalines are inti-inflammatory because they inhibit nitric oxide. Cipro decreases inflammatory cytokines including: TNF-alpha, IL-6 and others. Erythromycins are said to inhibit cytokine production. And so on.

Naysayers, who deny chronic Lyme say patients improve because of these non-specific effects. Does this argument hold any water? NO!

Let us consider the use of Rocephin in a "neuroborreliosis" patient. This individual has an encephalopathy characterized by significant mental status changes. The brain MRI may be normal or abnormal. The SPECT/PET scan may be normal or abnormal. Something has caused a severe acquired brain disorder. If it is not Lyme disease they what else is it pray tell? After treatment with Rocephin the patients improves, perhaps to the point of baseline health. Here is a fantastic medical success story. Why would any physician be unhappy with the result for this patient regardless of one's beliefs?

My suspicion is that the neuroprotective effects may be playing a significant role. The primary effect of the drug however is to combat spirochetes in the brain.

The same arguments can be made down the line. If antibiotics have additional effects which benefit our patients great, what a plus!

None of this information "proves" that chronic Lyme is not real. The points are interesting but are not scientific evidence that chronic Lyme is not real. In fact they are irrelevant distractions from the debate at hand.

We know that chronic, persistent Lyme disease is real. Lyme hides in niches which cannot be accessed by the immune system. Bb binds to proteins in the intracellular matrix such as decorin. Bb can acquire antigen markers from host endothelial cells to camouflage itself. Bb can enter fibroblasts, an intracellular protected niche. Bb can enter immune privileged areas such as the brain where the immune responses are limited. It can morph into intracellular forms which cannot be accessed by the acquired immune responses. In this arena only primitive, innate immune responses are active; it has been established that such responses are unable to sterilize the cells of such organisms. Lyme spirochetes can morph into a cystic form not destroyed by immune responses. Bb can rearrange the structure of surface antigens by recombination with plasmids. All of these assertions are very well documented in peer reviewed literature and texts.

Animal models and human models have both demonstrated the persistence of the organism after large courses of antibiotic therapy in various tissues. This too is well documented in peer reviewed literature.

Patients with chronic Lyme have been shown to have consistent, reproducible clinical syndromes associated with characteristic physical and laboratory findings.

I treat these patient in my office every day, and for the most part they all get better.

Some of sickest patients I have encountered in my now lengthy medical career seem to be caught between the cracks of a dysfunctional medical system, the byproduct of misguided politics, and a stubborn refusal to really consider all the evidence.

Please let the doctor speak.