This is Part 3 of the series, The Complexities of Lyme Disease by Thomas Grier, M.S. Click here to read Part 1 and here to read Part 2. Part 4 is soon to come. ~ Michelle
When Lyme Bacteria Infects The Brain:
As we have previously discussed, the pathogen that causes Lyme disease is a highly motile spirochete within the Borrelia family of bacteria. This is the same group of bacteria that cause Relapsing Fevers in Africa and around the world. Like other Relapsing Fever bacteria, Borrelia burgdorferi (Lyme bacteria) has both an affinity for the brain and a mechanism to penetrate into it.
While Lyme may be a bit more subtle upon penetrating the brain, its silent but insidious invasion may be the reason that brain involvement can and is often overlooked by physicians for months or even years in neurological Lyme patients.
In the case of Lyme disease, every animal model to date shows that the Lyme spirochete can go from the site of the bite of an infected tick to the brain in just a few days. While we know this bacteria can break down individual cell membranes and capillaries, its entrance into the brain is too pronounced for such a localized effect.
When the Lyme bacteria enters the human body, we react by producing several immune regulatory substances known as cytokines and lymphokines. Several of these act in concert to break down the blood-brain barrier (e.g., IL-6, Tumor Necrosis Factor-alpha, IL-1, Transforming Growth Factor-beta, etc.). In addition to affecting the blood-brain barrier, these cytokines can make us feel ill and give us fevers.
Since the brain has no immune system, it prevents infection by limiting what can enter the brain. The capillary bed that surrounds the brain is so tight that not even white blood cells are allowed to enter. Many drugs can’t enter either, making treatment of the brain especially hard.
For the first ten days of a Lyme infection, the blood-brain barrier (BBB) is virtually nonexistent. This not only allows the Lyme bacteria to get in but also immune cells that can cause inflammation of the brain.
* Note: The breakdown of BBB was shown to occur by tagging WBCs, albumin, and other substances known not to cross the BBB with radioactive iodine. The CSF (cerebrospinal fluid) of mice was tested, and then they were infected with Bb (Borrelia burgdorferi). The CSF was then retested every day after for several weeks. The result? No crossover of iodine was present in the control group, but 100% crossover was in the infected group for 10 days. The infection had the same result on the BBB as if you were injecting the radioactive iodine directly into the brain.
Once the Lyme bacteria enter the brain, they continue to divide and become entrenched within the brain's tissues and cells. Borrelia burgdorferi is directly neurotoxic upon contact with neurons and also has a negative effect on glial cells trying to repair brain injury. This, in turn, further increases the permeability of the blood-brain barrier, allowing, even more, blood-borne agents to enter the brain. The immune system responds to the new flood of internal bacterial antigens and produces more inflammatory cytokines. The result can cause brain edema or encephalitis, intracranial pressure, and focal areas of demyelination.
Also, when the human brain becomes inflamed due to infection with the Lyme bacteria, cells called macrophages respond by releasing a neuro-toxin called quinolinic acid. This toxin is also elevated in Parkinson’s Disease, MS, and ALS. What quinolinic acid does is to stimulate neurons to repeatedly depolarize. If this goes on unabated, it eventually causes the neurons to demyelinate and die. Basically, people with elevated quinolinic acid have short-term memory problems.
This means: If we think of our brain cells like telephone lines, we can visualize the problem. If all of the lines coming in are busy, we can’t learn anything. If all of the lines going out are busy, we can’t recall any memories. Our thinking process becomes impaired.
A second impairment to clear thinking that Lymies can experience is the restriction of proper circulation within the blood vessels inside the brain. Using an instrument called the Single Photon Emission Computerized Tomography scanner (SPECT scans), we are able to visualize the blood flow throughout the human brain in 3-D detail. What was seen in the brains of chronic neurological Lyme patients was an abnormal “Swiss-Cheese” pattern of blood flow. The cortical or thinking region of the brain was being deprived of good circulation, while the occipital (eyesight) regions had an increased flow. This could help explain why most Lyme patients complain of poor concentration and overly sensitive eyes.
The Complexities of Lyme Disease (A Microbiology Tutorial) by Thomas Grier, M.S.
Neurocascade Events and Lyme by Thomas Grier, M.S.
When Lyme Bacteria Infects The Brain:
As we have previously discussed, the pathogen that causes Lyme disease is a highly motile spirochete within the Borrelia family of bacteria. This is the same group of bacteria that cause Relapsing Fevers in Africa and around the world. Like other Relapsing Fever bacteria, Borrelia burgdorferi (Lyme bacteria) has both an affinity for the brain and a mechanism to penetrate into it.
While Lyme may be a bit more subtle upon penetrating the brain, its silent but insidious invasion may be the reason that brain involvement can and is often overlooked by physicians for months or even years in neurological Lyme patients.
In the case of Lyme disease, every animal model to date shows that the Lyme spirochete can go from the site of the bite of an infected tick to the brain in just a few days. While we know this bacteria can break down individual cell membranes and capillaries, its entrance into the brain is too pronounced for such a localized effect.
When the Lyme bacteria enters the human body, we react by producing several immune regulatory substances known as cytokines and lymphokines. Several of these act in concert to break down the blood-brain barrier (e.g., IL-6, Tumor Necrosis Factor-alpha, IL-1, Transforming Growth Factor-beta, etc.). In addition to affecting the blood-brain barrier, these cytokines can make us feel ill and give us fevers.
Since the brain has no immune system, it prevents infection by limiting what can enter the brain. The capillary bed that surrounds the brain is so tight that not even white blood cells are allowed to enter. Many drugs can’t enter either, making treatment of the brain especially hard.
For the first ten days of a Lyme infection, the blood-brain barrier (BBB) is virtually nonexistent. This not only allows the Lyme bacteria to get in but also immune cells that can cause inflammation of the brain.
* Note: The breakdown of BBB was shown to occur by tagging WBCs, albumin, and other substances known not to cross the BBB with radioactive iodine. The CSF (cerebrospinal fluid) of mice was tested, and then they were infected with Bb (Borrelia burgdorferi). The CSF was then retested every day after for several weeks. The result? No crossover of iodine was present in the control group, but 100% crossover was in the infected group for 10 days. The infection had the same result on the BBB as if you were injecting the radioactive iodine directly into the brain.
Once the Lyme bacteria enter the brain, they continue to divide and become entrenched within the brain's tissues and cells. Borrelia burgdorferi is directly neurotoxic upon contact with neurons and also has a negative effect on glial cells trying to repair brain injury. This, in turn, further increases the permeability of the blood-brain barrier, allowing, even more, blood-borne agents to enter the brain. The immune system responds to the new flood of internal bacterial antigens and produces more inflammatory cytokines. The result can cause brain edema or encephalitis, intracranial pressure, and focal areas of demyelination.
Also, when the human brain becomes inflamed due to infection with the Lyme bacteria, cells called macrophages respond by releasing a neuro-toxin called quinolinic acid. This toxin is also elevated in Parkinson’s Disease, MS, and ALS. What quinolinic acid does is to stimulate neurons to repeatedly depolarize. If this goes on unabated, it eventually causes the neurons to demyelinate and die. Basically, people with elevated quinolinic acid have short-term memory problems.
This means: If we think of our brain cells like telephone lines, we can visualize the problem. If all of the lines coming in are busy, we can’t learn anything. If all of the lines going out are busy, we can’t recall any memories. Our thinking process becomes impaired.
A second impairment to clear thinking that Lymies can experience is the restriction of proper circulation within the blood vessels inside the brain. Using an instrument called the Single Photon Emission Computerized Tomography scanner (SPECT scans), we are able to visualize the blood flow throughout the human brain in 3-D detail. What was seen in the brains of chronic neurological Lyme patients was an abnormal “Swiss-Cheese” pattern of blood flow. The cortical or thinking region of the brain was being deprived of good circulation, while the occipital (eyesight) regions had an increased flow. This could help explain why most Lyme patients complain of poor concentration and overly sensitive eyes.
The Complexities of Lyme Disease (A Microbiology Tutorial) by Thomas Grier, M.S.
Neurocascade Events and Lyme by Thomas Grier, M.S.
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