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Neurocascade
Events and Lyme
By,Tom Grier
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The
human brain is by far the most complex and least understood organ of the
body. The brain stores and organizes data far more efficiently than
any computer in the world; it isolates itself from the rest of the body
including the immune system, and acts as an endocrine organ sending hormones
and chemical messages into the far reaches of the body affecting every
cell in our body. When the brain is sick or injured our whole body is
affected.
Our brains allow us to use our muscles by shear will of thought. The electrical impulses we command are rushed through our spine and filter through our limbs to the exact set of muscles we need to control. Equally important the brain will take care of our basic bodily needs like breathing, and heart rate, when we are unconscious.
Our brain works when we sleep, but requires rest. We see images when we open our eyes and again when we dream, and each image that we see is a construct of the brain. Our thoughts, our dreams, our memories are all stored patterns within our brain. So what happens to the essence of us, when the brain is damaged?
More specifically what can we expect when our brain is traumatized by a bacterial infection of the brain as can happen in Lyme Encephalitis?
The bacterium 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 around the world. Like other Relapsing Fever bacteria, Borrelia burgdorferi the causative agent of Lyme disease has both an affinity for the brain and a mechanism to penetrate into the brain.
Other neurogenic strains of Borrelia that cause Relapsing Fevers in Africa can be deadly within mere weeks of entering the brain. While Lyme disease may be a bit more subtle upon penetrating the brain, its silent and insidious invasion may be the reason that brain involvement can and is often be overlooked by physicians for months or even years in neurological Lyme patients.
Just like the spirochete that causes syphilis can remain active within the brain for decades in tertiary Syphilis, there is equal cause for concern that the Lyme bacteria can also become a sequestered unwelcome interloper to the central nervous system.
How does the Lyme bacteria enter the brain when the blood brain barrier fights against foreign invasion?
(The blood brain barrier is simply a network of capillaries that selectively feeds nutrients to the brain. The walls of the capillaries in the blood brain barrier are so tight, that they do not allow most things from the blood to pass into the brain. Also the vessels respond differently from the peripheral vessels and selectively allow some things into the brain. Some things pass through freely but many things like vitamin-C requires the brain to expend energy to pump it across the cell membranes. This selective process probably prevents infections of the brain on a weekly basis.)
Once the Lyme spirochete enters the peripheral blood circulation through an infected tick bite, the bacteria fights to escape the confines of the blood vessel walls. The spirochete’s motility allows it to swim in the blood stream until it lodges a wiggling tip into a endothelial cell junction, where it bores between endothelial cells lining the capillaries and causes a specific inflammation and irritation that causes the endothelial cells to release digestive proteins that create holes within the capillary bed.
(Borrelia burgdorferi actives the tissue plasminogen activation pathway (PAS) and soon other enzymes are involved in degrading the integrity of the vessels walls. It has been observed the proteases such as basement laminase; urokinase, metallomatrix proteases, the fibrinolytic pathway, and lipases all play a role in degrading human brain micro-endothelial cell integrity. In mice and other animal models the PAS pathway in Lyme disease plays a critical role in developing carditis and other inflammatory states including arthritis.)
In 1989 experiments were done using umbilical cord vein to show that Borrelia burgdorferi attaches tip first to endothelial cells and microscopic examination found holes near the areas of attachment. If these vessels were within the heart or brain it would be clear that there is nothing to stop Borrelia and other blood stream components from entering those sites. In the case of the brain, allowing bacteria and white blood cells access to the brain is setting up the brain for a series of events to occur which we can call neurocascade events. This is where one event will trigger another, which in turn will trigger another and so on until a small nonsymptomatic event becomes noticeable.
To see if Borrelia burgdorferi truly breaks down the blood brain barrier, several animal experiments were done. Since blood albumin protein should not be in the cerebral spinal fluid (CSF) researchers tagged normal albumin with radioactive Iodine. In mice, hamsters, and dogs without infection the radioactive Iodine never penetrated into the CSF of the normal control animals. But when the animals were infected with Lyme disease, within mere hours the blood brain barrier became permeable and radioactive iodine was found within the CSF of infected animals usually for about two weeks following initial infection. This window of permeability certainly gives ample time for the Lyme bacteria to establish itself within the brain. Detailed collection of CSF from recently bitten Lyme patients reveals that sub clinical infections of the CNS occurs often before the infection in the body is even detected.
Before we talk about the neurotoxic effects of Borrelia burgdorferi within the brain, lets first look at some other neurocascade events that occur in acute brain trauma and repeated brain trauma such as in sports accidents like soccer, football and boxing.
Repeated concussions in football players and boxers can cause a slow onset of a syndrome sometimes called Pugilistic Dementia, or Sports Related Encephalopathy. Common symptoms begin months to years after injury occurs and usually includes: headaches, muscle twitches, tics, sensitivity to bright lights and loud noises, inability to retrieve words, loss of time, depression, suicidal thoughts. Later these symptoms can progress to fatigue, lethargy, loss of interest, severe depression, Parkinson-like tremors, loss of motor control, and overall slowness, and finally dementia.
An interesting comparison between Lyme encephalitis and Pugilistic dementia besides sharing similar symptoms is that both patients can have global-cerebral-atrophy years after their initial trauma. In other words the brain shrinks, and appears to have lost the ability to properly repair damage that accumulates over many years. These abnormal MRIs of the brains of boxers and Lyme patients may be caused by different mechanisms, but the end result can appear similar in both the symptoms and pathology of the two conditions.
Our brains allow us to use our muscles by shear will of thought. The electrical impulses we command are rushed through our spine and filter through our limbs to the exact set of muscles we need to control. Equally important the brain will take care of our basic bodily needs like breathing, and heart rate, when we are unconscious.
Our brain works when we sleep, but requires rest. We see images when we open our eyes and again when we dream, and each image that we see is a construct of the brain. Our thoughts, our dreams, our memories are all stored patterns within our brain. So what happens to the essence of us, when the brain is damaged?
More specifically what can we expect when our brain is traumatized by a bacterial infection of the brain as can happen in Lyme Encephalitis?
The bacterium 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 around the world. Like other Relapsing Fever bacteria, Borrelia burgdorferi the causative agent of Lyme disease has both an affinity for the brain and a mechanism to penetrate into the brain.
Other neurogenic strains of Borrelia that cause Relapsing Fevers in Africa can be deadly within mere weeks of entering the brain. While Lyme disease may be a bit more subtle upon penetrating the brain, its silent and insidious invasion may be the reason that brain involvement can and is often be overlooked by physicians for months or even years in neurological Lyme patients.
Just like the spirochete that causes syphilis can remain active within the brain for decades in tertiary Syphilis, there is equal cause for concern that the Lyme bacteria can also become a sequestered unwelcome interloper to the central nervous system.
How does the Lyme bacteria enter the brain when the blood brain barrier fights against foreign invasion?
(The blood brain barrier is simply a network of capillaries that selectively feeds nutrients to the brain. The walls of the capillaries in the blood brain barrier are so tight, that they do not allow most things from the blood to pass into the brain. Also the vessels respond differently from the peripheral vessels and selectively allow some things into the brain. Some things pass through freely but many things like vitamin-C requires the brain to expend energy to pump it across the cell membranes. This selective process probably prevents infections of the brain on a weekly basis.)
Once the Lyme spirochete enters the peripheral blood circulation through an infected tick bite, the bacteria fights to escape the confines of the blood vessel walls. The spirochete’s motility allows it to swim in the blood stream until it lodges a wiggling tip into a endothelial cell junction, where it bores between endothelial cells lining the capillaries and causes a specific inflammation and irritation that causes the endothelial cells to release digestive proteins that create holes within the capillary bed.
(Borrelia burgdorferi actives the tissue plasminogen activation pathway (PAS) and soon other enzymes are involved in degrading the integrity of the vessels walls. It has been observed the proteases such as basement laminase; urokinase, metallomatrix proteases, the fibrinolytic pathway, and lipases all play a role in degrading human brain micro-endothelial cell integrity. In mice and other animal models the PAS pathway in Lyme disease plays a critical role in developing carditis and other inflammatory states including arthritis.)
In 1989 experiments were done using umbilical cord vein to show that Borrelia burgdorferi attaches tip first to endothelial cells and microscopic examination found holes near the areas of attachment. If these vessels were within the heart or brain it would be clear that there is nothing to stop Borrelia and other blood stream components from entering those sites. In the case of the brain, allowing bacteria and white blood cells access to the brain is setting up the brain for a series of events to occur which we can call neurocascade events. This is where one event will trigger another, which in turn will trigger another and so on until a small nonsymptomatic event becomes noticeable.
To see if Borrelia burgdorferi truly breaks down the blood brain barrier, several animal experiments were done. Since blood albumin protein should not be in the cerebral spinal fluid (CSF) researchers tagged normal albumin with radioactive Iodine. In mice, hamsters, and dogs without infection the radioactive Iodine never penetrated into the CSF of the normal control animals. But when the animals were infected with Lyme disease, within mere hours the blood brain barrier became permeable and radioactive iodine was found within the CSF of infected animals usually for about two weeks following initial infection. This window of permeability certainly gives ample time for the Lyme bacteria to establish itself within the brain. Detailed collection of CSF from recently bitten Lyme patients reveals that sub clinical infections of the CNS occurs often before the infection in the body is even detected.
Before we talk about the neurotoxic effects of Borrelia burgdorferi within the brain, lets first look at some other neurocascade events that occur in acute brain trauma and repeated brain trauma such as in sports accidents like soccer, football and boxing.
Repeated concussions in football players and boxers can cause a slow onset of a syndrome sometimes called Pugilistic Dementia, or Sports Related Encephalopathy. Common symptoms begin months to years after injury occurs and usually includes: headaches, muscle twitches, tics, sensitivity to bright lights and loud noises, inability to retrieve words, loss of time, depression, suicidal thoughts. Later these symptoms can progress to fatigue, lethargy, loss of interest, severe depression, Parkinson-like tremors, loss of motor control, and overall slowness, and finally dementia.
An interesting comparison between Lyme encephalitis and Pugilistic dementia besides sharing similar symptoms is that both patients can have global-cerebral-atrophy years after their initial trauma. In other words the brain shrinks, and appears to have lost the ability to properly repair damage that accumulates over many years. These abnormal MRIs of the brains of boxers and Lyme patients may be caused by different mechanisms, but the end result can appear similar in both the symptoms and pathology of the two conditions.
Ticks carry more than just
Lyme disease! Including:
0 -Ehrlichia;
o -Bartonella;
0 -Babesia;
o -Q- Fever;
0 -Tularemia;
o -Tick-borne Encephalitis;
0 -Mycoplasma;
o -Relapsing Fever;
0 -Rocky Mountain Spotted Fever and others.
Never WAIT and SEE about a tick bite, please! Quickly and properly treated infections are less likely to progress to later stage or chronic disease.
Sometimes tick bites are
mistaken for spider bites!
Some diseases may be spread by animal bites or scratches and from mosquitoes, fleas or lice.
There is still so much to learn about Lyme disease and related infections.
Sometimes Lyme disease and related infectious diseases are undiagnosed for years, even decades!
Watch closely for symptoms after tick bites. Some never see a tick or a bulls-eye rash.
Don't ignore tick-borne disease symptoms!
If you feel sick, ask a doctor!
SYMPTOMS may include:
0 -Tick bites;
o -Fever; Flu symptoms;
0 -All kinds of Rashes;
o -Muscle; Joint; Neck Pain;
0 -Body Aches; Weakness
o -Light /Sound Sensitivity;
0 -Bells Palsy; Nerve pain;
o -Insomnia; Poor memory
0 -Headaches; Numbness;
o -Mood disorders; Confusion;
0 -Extreme Fatigue; Exhaustion
Never let tick-borne diseases progress!
Lyme and associated diseases are often MISTAKEN FOR OTHER ILLNESSES, Including:
0 -Chronic Fatigue;
o -Fibromyalgia;
0 -Hypochondria;
o -Multiple Sclerosis;
0 -Lupus;
o -Rheumatoid Arthritis;
0 -Lou Gehrig's disease (ALS);
o -Alzheimer's and
0 -Parkinson's disease
******************
Don't be fooled about ticks and their diseases.
******************
Directly affecting humankind, worldwide:
W H A T H A P P E N E D
when the U.S. Senate addressed the Centers for Disease Control regarding Lyme disease?
Consult a good doctor!
Visit ILADS, LDF, LymeNet or LDA to find a specialist in your location.
Protect your children and your family.
Learn about ticks and their many diseases.
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- TICKS KNOW NO BOUNDARIES -
Tick-borne diseases are spreading rapidly in many countries across the world -not only in Scandinavia, UK, Hungary, Scotland, USA, France, Germany, China, and Australia.
- ONE BIG PROBLEM WITH TESTS -
There is NO 100% accurate Lyme disease test currently available to detect infection or cure. more...
- WHERE TICKS LIVE -
Ticks can be found in and around leaf litter; grass; logs; animal fur; bird feeders; and deer, mice, squirrel, and other small animal habitats.
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Ticks travel on mice!
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Never let tick-borne
infections progress !
Tick-borne diseases can
affect any body part,
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of the body.
Lyme disease and Syphilis are both caused by a type of bacteria called a spirochete.
Tick-borne diseases can KILL!
Ticks travel on mice!
ALWAYS Get Ticks Tested!
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