How Lyme Kills 

The Dangers of Neurological Lyme and Lyme Carditis: The Two largest causes of death- suicide and heart attacks. 

What is the difference, you may ask, between Lyme disease and Neurological Lyme Disease? The answer is far more complex than it may first seem. 

From the earliest days of the discovery and spread of Lyme disease, it was very evident that swollen joints indicated a rheumatological illness. Further cementing this view of Lyme disease was the way in which Lyme disease was first discovered and diagnosed by the Yale researchers, in particular Rheumatologist Dr. Alan Steere. (See Definition/History) 

What was not understood by the Yale doctors at the time (although I would wager the parents were well aware of the neurological impact of the disease on their children), the neurological symptoms are not visible, they are felt.  And as with other neurological diseases, the function of the brain is impaired by the disease which hinders the patient from being able to clearly articulate what is wrong. 

So doctors – very busy, many times with more patients waiting to be seen than they have time in the day - look at what they can see. They also rely on a diagnostic protocol that the IDSA and insurance companies require, and have no current way to distinguish where the bacteria are amassing other than swelling, rashes, sores and those types of outward symptoms. 

A good example would be Lyme Carditis (Borrelia infection in the heart). Many doctors, including Dr. Forrester a spokesman from the CDC, consider Lyme carditis as extremely rare. Dr Forrester even claims that it occurs in less than 1% of patients. However, there are several causes for alarm in spite of this seemingly insignificant percentage.: 

·       the number of people with Lyme disease is unknown (and the CDC agrees with that statement) 

·       the antibody tests used to diagnose Lyme are unreliable (see Testing), 

·       there is really no way to measure who has Borrelia infecting their heart without a specific biopsy, or during an autopsy because heart problems are not associated with Lyme disease. 

This last point is especially frightening as three people between the ages of 26 and 38 died from Lyme induced heart attacks between November 2012 and July of 2013 in New England (NY, CT and MA) who didn’t even know they had Lyme disease. 

These fatalities caused by Lyme disease would never have been discovered whout the experienced New England pathologist  Dr. Thadeus Schulz who worked at Cryolife ( a medical device company in Georgia that processes tissue and provides heart valves and patches for cardiac surgery), and happened to notice that one of the hearts had an unusual pattern of inflammation around blood vessels in the heart that was similar to features he had seen in biopsies from people with Lyme disease in New York. He showed his boss, Dr. Gregory Ray, and together they soon found two other hearts with similar distinction. The three hearts were infected with Borrelia.  

How many heart attacks are being caused by Lyme disease and being attributed to something else? 

2,200 people die every day in the US from heart disease according to US Department of Health and Human Services. That is 800,000 people every year or 1 in 3 deaths (including accidents and war.) Certainly if this many people are dying from heart attacks, it should be a federal mandate to examine hearts for Lyme disease to be proactive with the most fatal aspect of Lyme disease (besides suicide). 

In fact, another heart fatality was avoided in a 17 year old boy who went to the ER after experiencing chest discomfort. It is to the young man’s credit (or his parents) that the matter was pursued and he was later diagnosed with complete atrioventricular block due to lyme carditis which required immediate surgery and the placement of a pacemaker. He was treated with IV Rocephin and appears to be recovered at this time. 

Also, with spirochetes infecting all bodily fluids, sexual transmission is adding to the "Tsunami" of chronic neurological disease that is spreading all over the world. 

NeuroLyme (Neuroborreliosis) 

Neuroborreliosis (the correct term for Neuro-Lyme), encompasses any type of Lyme disease that has invaded the central nervous system, and there are over 90 species of Borrelia with more being discovered with frightening regularity.  And yet the CDC only tests for one species, and they only look for 10 proteins out of a possible 25 in one strain. 

According to Dr. Luft at SUNY School of Medicine, to make the Western Blot accurate, every genome in every currently known species of Borrelia would have to be mapped - 1800 proteins in all - a far cry from the 10 we now test. 

More alarming, studies at the SUNY Medical Center have proven that Lyme spirochetes can infiltrate the central nervous system within 24 hours of infection, so even though neurological symptoms may take weeks or months to appear, the number of victims is certainly much higher than presently recognised. 

Given the fact that there are very few experienced and knowledgeable specialists treating Lyme disease, there are even fewer capable of understanding and treating neuroborreliosis. 

As with Lyme arthritis and other forms of chronic Lyme disease, the patients most often requires access to the most recent developments in science and medicine with respect to their unique presentation of the disease. 

This can be a lonely and frightening aspect of an already terrifying illness 

Diagnostic Biomarkers for Persisting Brain and Nervous System Symptoms in Lyme Disease This study is led by Steven Schutzer, MD, a physician-scientist and Professor of Medicine at the University of Medicine and Dentistry of New Jersey. The study utilizes the most advanced mass spectroscopy and protein separation techniques in the United States. He has established a comprehensive list of proteins in cerebrospinal fluid (CSF, the liquid window of the brain) of normal healthy people. He has done the same in people with persisting brain and nervous system symptoms in Lyme disease. Through advanced proteomics, Dr. Schutzer has found that post-treatment Lyme encephalopathy patients possess a unique subset of spinal fluid proteins. These proteins may one day serve as biomarkers. This number can be narrowed down to the top ones in a Verification Phase using samples from separate individual patients. That analysis is ongoing. 

 

"Brain on Fire" =autoimmune encephalitis or =stealth infection? 

They both have the same, unique, CSF marker, CXCL13. 

{IMHO...there are no auto-immune driven diseases...but there are lots of stealth(hard to detect) infections...medicine is slowly killing people with over use of immune suppressants} 

Aggression and Lyme Disease 

by Robert C. Bransfield, M.D. 

  

Several years ago, I admitted a patient with Lyme disease (LD) to a psychiatric unit. He was para­noid and assaulted five police officers in an episode of rage. During the hospital stay, the patient went to the river behind the hospital to watch the Fourth of July fireworks display. When the fireworks began, the patient jumped into the river. It appeared the loud noise was responsible for an acoustic startle reaction. 

At the same time, a female patient with LD was also on the unit. She described puzzling symp­toms that consisted of episodes of rage and intrusive, horrific homicidal images. In both cases, the aggres­sive tendencies improved with treatment. 

In reviewing cases involving LD patients, another patient described an incident where some­one else pulled into a parking space that he wanted. Jumping out of his car, he knocked the other driver unconscious. Still another patient stated he was driv­ing on the highway when a motorist beeped their horn. He lunged out of his car and began pounding on the windshield of the car, then suddenly stopped in bewilderment because he did not understand or recall why he was behaving in this manner. 

A female patient was arrested for shoplifting during a state of confusion. Another patient was accused of pedophilia. I can cite many more examples. When we look at cases of aggression associated with LD, were all of these cases merely a coincidence or a causal relationship between LD and some of this aggressive behavior? 

Adler methodically interviewing hundreds of patients over a period of years, it was clear that cer­tain patterns were emerging. The same problems were being seen in too many patients. A causal link was becoming increasing apparent. I would like to em­phasize that the vast majority of patients who know they have LD are not violent. It is not my intention to draw attention to an issue that further increases the stigma that LD patients already receive. However, it is my intention to methodically look at the association that does seem to exist between LD and aggressive behavior in a minority of chronic LD patients. 

Clearly violence is a very complex issue. Many different factors have contributory or deterrent effects. One study of death row inmates demonstrated that 100% were neurologically impaired. Many also had a history of abuse Sometimes the abuse precedes or causes the neurological impairment. Sometimes the neurological impairment precedes or causes the abuse. Neurological impairments and abuse either alone or in combination are significant risk factors that increase the potential for violence. Other risk factors are significant in some cases. 

A triggering event(s) may then occur which provokes violent behavior in a person who is at risk. A normal person given the same level of provocation does not act in a violent manner. In some cases, the trigger is an intrusive, violent image, an obsession or compulsion to do harm, or it may be a perception of threat. 

In addition to a provocative factor, there are many deterrents to violence, which include a neuro­logical capacity for restraint, social bonding, victim response, and social structures. When violence occurs, we need to consider some combination of increased risk factors, triggering events, or a failure of deterrents to violence. 

It is well recognized that LD causes dysfunc­tion of the central nervous system (CNS). Many other conditions which cause CNS dysfunction are some­times also associated with violent behavior, i.e.: strokes, brain tumors, lupus, MS. head injuries, developmen­tal disabilities, carbon monoxide poisoning, syphilis and other CNS infections. When reviewing the pathology associated with aggression, we can see dysfunction of a number of different brain areas. 

To briefly review the physiology, there is a hi­erarchy of functioning within the CNS, which has de­veloped through evolution. When we go from the most advanced to the most primitive areas of the brain, the hierarchy consists of the prefrontal cortex, other cor­tical regions, para limbic asso­ciative areas, the limbic system, and the brain stem and hypo­thalamus. These centers func­tion together with many feed forward and feed back path­ways that are both stimulatory and inhibitory. Injury to a higher center can result in a dysfunction or a loss of a function. Injury to an inhibit­ing pathway will cause a decline or an inability to in­hibit that function. As a result, brain injury leads to a decline in our ability to fine-tune our adaptive abilities in an effective manner. 

In the case of aggressive functioning, injury can lead to apathy (a failure of stimulation) and/or aggres­sion (a failure a inhibition, modulation, or association) Since circuits controlling aggression are often parallel with sex and feeding, we often see aggressive disor­ders in combination with sexual dysfunction and eat­ing disorders. Different patterns of brain injury result in different patterns of symptoms. 

Now let’s look at the association between Lyme and aggression. The first reference on this sub­ject in the medical literature I could find was made by Fallon, et al in 1992 in ‘The Neuropsychiatric Mani­festations ofLyme Borreliosis”, in which he described a man acutely sensitive to sound was so intensely both­ered by the noise his three-year-old son was making that he picked him up and shook him in a sudden and unprecedented fit of violence. Other cases can be found in medical literature cited at Lyme meetings and in newspaper reports. The phrase “Lyme rage” continues to appear on the Internet. There are discussions that some “road rage” is caused by “Lyme rage”. 

I would estimate aggressive behavior has been a significant issue for approximately fifty patients with LD that I have evaluated or treated, although many more have reported some symptoms associated with aggressive potential. When aggression does occur, it may only be present for an interval in the progression of the illness. 

Deficits caused by LD that are sometimes as­sociated with increased risk for aggressive behavior may include: 

  

1. Decreased frustration tolerance. (This is magnified by the increased frustration caused by a chronic illness). 

2. Decreased impulse control. 

3. When mild, the combination of decreased frustra­tion tolerance and decreased impulse control leads to irritability. When more extreme, this combination can result inexplosive anger. 

4. Hyposexuality and hypersexuality caused by LD, both of which cause increased interpersonal frus­tration. 

5. Dysfunction causing different forms of obsessive compulsive disorder, which results in intrusive thoughts, images, and compulsions that sometimes are of an aggressive nature. 

6. Some dysfunction results in a decreased bonding capacity. 

7. Increased startle reflex - particu­larly increased acoustic startle. 

8. Hypervigilance and paranoia 

9. Delusions and hallucinations. 

          10. Some patients acquire impairment in their ability to regulate the arousal level of an emotion. As a result, emotions such as anger may be all or none, excessively intense, and not proportionate to the current situa­tion. This also leads to a decline in the ability to integrate concurrent emotions that exist either within the patient or in a relationship with another person. This symptom may in turn intensify other psychiat­ric syndromes such as post-traumatic stress disor­der, dissociative disorders, borderline personality, and narcissistic personality disorders. 

 Any combination of the above impairments can result in aggressive behavior. When these changes occur in a mature adult, the patient is surprised by the symptoms - they recognize it is pathological and attempt to compensate for the deficits. However, children who never had the reference point of a mature level of functioning are at a greater risk. Some of the most threatening cases were patients who were infected at a young age. 

The following is a quote from a patient describing horrific intrusive images, which many patients withLyme have described to me: 

“Frightening, stabbing, horrific images -usually of death, dying or pain and suffering. Often gory and unreal as in a horror story. Faces mostly with blood or terror exaggerated awful expressions. Visions of stabbing or killing often of those close to you or familiar. These penetrating images add to the already anxious condition of a Lymey. Episodic, not continuous. Fleeting faces most usually of the worse possible situation Helpless stumped bodies perhaps close to death. These images don’t seem to neces­sarily be associated with a particular occasion, place or time, but come and invade the privacy of my mind. Control over physical well-being is lost with Lyme, but much more disturbing and debilitating is the lack of control or normalcy of the mind both emotionally and cognitive - perhaps worse during a flair when all symptoms often rear their ugly heads. It is a crushing experience to survive these images feeling possessed or evil. If they were to be continuous and not fleeting, no-one could or would survive. 

In another case, a patient had no prior history of mental illness suicidal or homicidal tendencies. -The patient went to their HMO --primary care physician complaining of an apparent tick bite. It is reported that the doctor neither sent the patient for testing nor initially offered antibiotic treatment. As symptoms progressed, the patient was diagnosed with fibromyalgia. Subsequent symptoms included word substitutions, getting lost, losing items, and an inability to find their car in a parking lot. Eventual tests confirming LD included a Western Blot, brain SPECT, and an ophthalmologic exam. 

The patient improved with treatment of several weeks on IV antibiotics and was stopped as per the managed care guidelines. The patient relapsed and further treatment was denied. Their mental state declined and subsequently there was a combined homicide-suicide. 

In conclusion, based on my observations and clinical judgment, chronic relapsing LD at times causes aggressive behavior, which can manifest in a number of different forms. Since this is aggression associated with a CNS infection, it can potentially be treated and prevented. If only a small percent of chronic LD patients are affected, the total number of cases is still quite significant. Since this is a late stage manifestation, the increasing number of individuals infected with Bb raises serious concern that violence associated with or caused by LD will increase in the future. 

What can we do now to prevent a possible future epidemic of violence? Suggestions include high index suspicion for Lyme disease in rageful people, adequate testing for Lyme disease in those who are enraged, adequate treatment of LD, contin­ued LD advocacy efforts, research into the link between aggression and LD, evaluation of violent offenders who demonstrate some of the aggressive patterns seen with LD prior to their release into the community, and vaccinations. When regional epidemics of violence occur, LD and other causes of encephalopathy should be considered. We should exercise every option to prevent crime with medical treatment. 

 

SOURCES: 

http://www.bostonglobe.com/lifestyle/health-wellness/2013/12/13/three-deaths-reported-from-heart-inflammation-caused-lyme-disease/tA55TpWGXEjFKqnev6bB8N/story.html  

Karmacharya P, Aryal MR. Heart stopping tick. World J Cardiol. 2013;5(5):148-50.  http://www.ncbi.nlm.nih.gov/pubmed/23710302
http://www.2minutemedicine.com/cxcl13-shows-potential-anti-nmda-receptor-encephalitis-biomarker/

https://www.yumpu.com/en/document/view/8164839/the-chemokine-cxcl13-in-acute-neuroborreliosis 

 

 

   

Jenna Seaver author of lyme disease resource

Jenna in Maui

 

        

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