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Lyme is able to enter the brain in ten days.

It has powerful effects on brain tissue. These are easily seen on a wide range of blood tests, neuropsychological tests and nuclear scans of the head that look at how the brain is functioning.

It is stunning to me how grossly ignorant defense attorneys are to this common vector illness and how often it is involved in causing explosive rage, impulsive behavior and addiction.

Patients with Lyme disease and the toxins that come from the Lyme report emotional extremes. People who never considered homicide, suicide, excess drinking, an affair, reckless driving, running away from home, fighting, smashing objects or doing drugs. Report that after their infection with Lyme they because "extreme and unstable." Some become afraid of themselves.

Here are some small tastes of further material. More is also on my web site.


The link between Lyme neuroborreliosis (LN) and aggression is reviewed from multiple perspectives. Cases are presented and discussed. It appears Lyme disease (LD) and other related tick-borne diseases contribute towards causing human aggression and violence. Greater attention to this area has the potential of reducing crime and saving lives. Narrow and restrictive opinions on the diagnosis and treatment of Lyme disease can contribute to the increased consequences of late stage disease, which includes aggression and violence associated with Lyme disease and other related tick-borne diseases.

[NEUROBORRELIOSIS is Lyme in the Brain]
By Robert C. Bransfield, MD

For the article go to:

An unusual defense: Lyme-caused crime?

In 1996, seventeen-year-old Michael Griffon knocked on the door of a stranger. When the man opened his door, Griffon attacked him with an ax. The victim drove his attacker off, and police later located Griffon hiding in the closet of his own house with a knife.

The crime was somewhat unusual, but Griffon's defense is far stranger: he claims that late-stage Lyme disease mentally impaired him.

Brian Fallon, a Lyme disease expert at the New York Psychiatric Institute, has confirmed Griffon's diagnosis, and says, "In certain circumstances, [Lyme] causes normal inhibitions to stop working and violent behavior to occur. It can cause someone to develop full-blown mania."

Griffon's acquaintances say that he was happy, athletic, and studious before contracting Lyme disease, but afterward developed problems including insomnia, weight gain, and an explosive temper. Since the crime he has been treated with antibiotics, and has s returned to school. His attorney says he now has no behavioral problems.

The medical literature includes reports of a number of cases in which patients with late-stage Lyme became dangerous to themselves or others. "Common psychiatric symptoms are irritability, panic attacks, depression, suicidal thoughts, fluctuating moods, and depersonalization," Fallon says. "Less common are mania, paranoia, obsessions, compulsions, and occasionally a disorder that resembles schizophrenia." Several of Fallon's Lyme patients have become violent, including a woman who stopped treatment due t to side effects and developed severe depression, hallucinations, manic episodes, and paranoid delusions. The woman became violent, Fallon reports, "slapping her son repeatedly and breaking furniture." Another of Fallon's patients exhibited mania, panic at attacks, paranoia, verbal aggression, violent impulses, irritability, and hallucinations.

For the full article go to:


Med Hypotheses. 2005 May 27; [Epub ahead of print]

Munchausen's syndrome by proxy and Lyme disease: Medical misogyny or diagnostic mystery?

Sherr VT.

47 Crescent Drive, Holland, PA 18966-2105, USA.

Chronic, tertiary Lyme disease, a vector-borne infection most accurately designated neuroborreliosis, is often misdiagnosed. Infectors of the human brain, Lyme borrelial spirochetes are neurotropic, similar to the spirochetes of syphilis. Symptoms of either disease may be stable and persistent, transient and inconsistent or severe yet fleeting. Characteristics may be incompatible with established knowledge of neurological dermatomes, appearing to conventional medical eyes as anatomically impossible, thus creating confusion for doctors, parents and child patients. Physicians unfamiliar with Lyme patients' shifting, seemingly vague, emotional, and/or bizarre-sounding complaints, frequently know little about late-stage spirochetal disease. Consequently, they may accuse mothers of fabricating their children's symptoms - the so-called Munchausen's by proxy (MBP) "diagnoses." Women, following ancient losses of feminine authority in provinces of religion, ethics, and healing - disciplines comprising known fields of early medicine, have been scapegoated throughout history. In the Middle Ages, women considered potentially weak-minded devil's apprentices became victims of witch-hunts throughout Europe and America. Millions of women were burned alive at the stake. Modern medicine's tendency to trivialize women's "offbeat" concerns and the fact that today's hurried physicians of both genders tend to seek easy panaceas, frequently result in the misogyny of mother-devaluation, especially by doctors who are spirochetally naive. These factors, when involving cases of cryptic neuroborreliosis, may lead to accusations of MBP. Thousands of children, sick from complex diseases, have been forcibly removed from mothers who insist, contrary to customary evaluations, that their children are ill. The charges against these mothers relate to the idea they believe their children sick to satisfy warped internal agendas of their own. "MBP mothers" are then vilified, frequently jailed and publicly shamed for the "sins" of advocating for their children. In actuality, many such cases involve an unrecognized Lyme borreliosis causation that mothers may insist is valid despite negative tests. Doctors who have utilized MBP tactics against mothers are likely to be unaware that in advanced borreliosis, seronegativity is often the rule, a principle disagreed upon by its two extant, published, peer-reviewed, Standards of Care. These are guidelines for Lyme disease management - the older system questioning the existence of persistent Lyme and the newer system relying on established clinical criteria. Mothers must be free to obtain the family's preferred medical care by choosing between physicians practicing within either system without fear of reprisal. Doctors and mothers together may then explore medical options with renewed mutual respect toward the best interest of children's health.

  1. Neuropediatrics. 2005 Apr;36(2):104-7.
    Neuroborreliosis causing focal cerebral arteriopathy in a child.

    Cox MG, Wolfs TF, Lo TH, Kappelle LJ, Braun KP.

    A 9-year-old girl presented with an acute right-sided hemiparesis [right side is paralyzed]. Initially, the clinical presentation and stable vasculopathic abnormalities on MR and conventional angiography were suspicious of a so-called "transient cerebral arteriopathy". Mild but persistent pleocytosis and an elevated CSF IgG index led to an extensive search for infectious and immunological causes of cerebral vasculitis, eventually revealing neuroborreliosis. Although rare, infectious and potentially treatable causes of arterial ischemic stroke should be considered in every child with a documented cerebral arteriopathy.
  2. Neurology. 2005 Feb 22;64(4):758-9.

    Delayed resolution of white matter changes following therapy of B burgdorferi encephalitis.

    Steinbach JP, Melms A, Skalej M, Dichgans J.
  3. Diagn Microbiol Infect Dis. 2005 Feb;51(2):127-30.

    Severe neuroborreliosis: The benefit of prolonged high-dose combination of antimicrobial agents with steroids--an illustrative case.

    Massengo SA, Bonnet F, Braun C, Vital A, Beylot J, Bastard J.

    Neuroborreliosis frequently occurs in endemic areas, whereas encephalomyelitis is uncommon. Treatment consists classically of 2 to 4 weeks of recommended antimicrobial agents with a generally good outcome. A severe case is reported combining an encephalomyelitis with an axonal polyneuropathy. Clinical improvement was observed only with the use of prolonged high dose of 2 antimicrobial agents combined with steroids.
  4. Curr Treat Options Neurol. 2005 Mar;7(2):167-170.

    The Therapy of Lyme Neuroborreliosis.

    Pachner AR.

    The challenge for the neurologist in the treatment of Lyme neuroborreliosis is not in the treatment per se, but in the diagnosis. Neurological manifestations of Lyme disease can present in many forms, and diagnostic techniques which detect the spirochete directly; the culture or polymerase chain reaction of the spirochete in cerebrospinal fluid, are of disappointingly low yield. Therefore, the diagnosis is frequently not easy. After the diagnosis is made, antibiotic therapy is straightforward; Lyme neuroborreliosis should be treated with at least 2 weeks of antibiotics. In the United States, intravenous therapy with ceftriaxone or penicillin for 2 weeks is the standard, whereas in Europe oral doxycycline therapy is commonly administered. Either is effective, and my choice of therapy generally depends on the patient. Many patients have symptoms which continue after antibiotic therapy referable to persistent inflammation, and, for those patients, I will commonly prescribe nonsteroidal anti-inflammatory medications.
  5. Infect Immun. 2005 Feb;73(2):1014-22.

    Borrelia burgdorferi, host-derived proteases, and the blood-brain barrier.

    Grab DJ, Perides G, Dumler JS, Kim KJ, Park J, Kim YV, Nikolskaia O, Choi KS, Stins MF, Kim KS.

    Neurological manifestations of Lyme disease in humans are attributed in part to penetration of the blood-brain barrier (BBB) and invasion of the central nervous system (CNS) by Borrelia burgdorferi. However, how the spirochetes cross the BBB remains an unresolved issue. We examined the traversal of B. burgdorferi across the human BBB and systemic endothelial cell barriers using in vitro model systems constructed of human brain microvascular endothelial cells (BMEC) and EA.hy 926, a human umbilical vein endothelial cell (HUVEC) line grown on Costar Transwell inserts. These studies showed that B. burgdorferi differentially crosses human BMEC and HUVEC and that the human BMEC form a barrier to traversal. During the transmigration by the spirochetes, it was found that the integrity of the endothelial cell monolayers was maintained, as assessed by transendothelial electrical resistance measurements at the end of the experimental period, and that B. burgdorferi appeared to bind human BMEC by their tips near or at cell borders, suggesting a paracellular route of transmigration. Importantly, traversal of B. burgdorferi across human BMEC induces the expression of plasminogen activators, plasminogen activator receptors, and matrix metalloproteinases. Thus, the fibrinolytic system linked by an activation cascade may lead to focal and transient degradation of tight junction proteins that allows B. burgdorferi to invade the CNS.
  6. MMW Fortschr Med. 2004 Jul 22;146(29-30):38-41.

    [Pain and neuroborreliosis]

    [Article in German]

    Berthele A, Tolle TR.

    Pain is one of the presenting symptoms in acute neuroborreliosis. Classically, acute neuroborreliosis--also known in Europe as Bannwarth's syndrome--is a combination of radicular pain, cranial neuritis and peripheral radiculitis and inflammatory changes of the CSF. The prognosis following antibiotic therapy is favorable. At least in its early stages, however, the diagnosis neuroborreliosis might be missed or mistaken. Thus, targeted assessment of typical signs is needed to expedite examination of the CSF which then permits definitive diagnosis.

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